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data/en.wikipedia.org/wiki/Abrasion_collar-0.md
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title: "Abrasion collar"
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source: "https://en.wikipedia.org/wiki/Abrasion_collar"
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category: "reference"
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tags: "science, encyclopedia"
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date_saved: "2026-05-05T07:25:38.336536+00:00"
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An abrasion collar, also known as an abrasion ring or abrasion rim, is a narrow ring of stretched, abraded skin immediately surrounding projectile wounds, such as gunshot wounds. It is most commonly associated with entrance wounds and is a mechanical defect due to a projectile's penetration through the skin. It is caused by a temporary over-stretching of the skin surrounding the projectile's point of penetration. Like all skin abrasions, the abrasion collar tends to dry out due to scraping away of the skin's outer layers and the collapse and dehydration of the underlying cells; it therefore becomes easier to discern with time. This defect is most often seen around rifled firearm entrance wounds due to the striations or grooves in the bullet's surface caused by the rifling on the inside of the weapon's barrel; however, certain other high-velocity projectile wounds can also have the same effect.
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An abrasion collar is usually found in association with a contusion collar of bruising caused by damaged blood vessels in the skin by hydrostatic forces from the bullet's entry. An abrasion rim defect is also possible in firearm exit wounds under certain circumstances, such as if the skin at the exit was crushed between the outgoing bullet and an unyielding object pressed against the skin over the exit site, or if the projectile exits at an extreme angle. Careful examination of the wound under magnification may show signs of everted (outward-turned) edges characteristic of an exit wound. Multiple projectiles impacting in close proximity together, such as in a close-range shotgun blast, will usually still produce an abrasion rim or artefact, though the wound will likely be irregular in shape.
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== Factors and characteristics ==
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=== Bullet wipe ===
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In the case of gunshot wounds from unjacketed lead alloy bullets or dirty bullets, a phenomenon known as bullet wipe may be observed, which forms a ring of greasy residue known as a grease or dirt collar that overlays the abrasion collar and is caused by deposits on the skin's surface. Generally, these deposits contain lead from the unjacketed projectile or oil from inside the weapon's barrel, but they may simply be dirty. Studies using high-speed photography have shown that bullet wipe is caused only by the head of the bullet—instead of the body—because the skin recoils away from the bullet as it penetrates due to the force of entry.
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=== Angle of trajectory ===
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The bullet's angle of trajectory at the point where it penetrates the skin can influence the shape of the abrasion collar. This can be used by forensic pathologists in discerning an approximate angle of entry and is important in investigations of gunshot wound victims, where evidence of the gunshot's origin is necessary to determine whether the death was homicidal, suicidal, or accidental. Generally, if the bullet impacts at an angle perpendicular to the skin surface, the abrasion collar will be symmetrical, concentric, round, and evenly-shaped. As the angle between the trajectory and the skin surface decreases, the abrasion collar becomes more distorted and often more distinct at the point of entry, having a semi-lunar or "half-moon" shape with the broadest width pointing in the direction of the gunshot's origin. This is caused by the exterior of the bullet contacting and scraping over the skin's surface for a certain distance before penetrating the skin.
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=== Bullet shape and velocity ===
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The bullet shape influences the size of the abrasion collar. High velocity bullets with pointed, narrow, or spitzer tips, such as rifle rounds, and full metal jacket bullets are less likely to produce abrasion collars compared to lower-velocity, semi-jacketed civilian bullets, such as bullets fired from handguns, which have rounded noses.
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If the wound is caused by a high-velocity rifle bullet, the abrasion collar may be smaller, but it may have minute tears in the surface of the skin surrounding the wound entrance. This is because the skin is not capable of stretching quickly enough if the bullet's velocity is too high. If the wound is made over bone, such as a head wound in the scalp, the abrasion collar may not be round at all; it instead becomes stellate or "star-shaped" with ragged and torn edges caused by the skin over-stretching and tearing. In the case of skull entrance wounds, the skin that includes the abrasion collar may be torn away because the underlying tissue is unable to flex away from the force of the bullet's entry.
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=== Wound distortions ===
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Towards the end of a bullet's effective range, it tends to lose axial stability and will begin to yaw or even tumble end-over-end. This means it may impact the skin while travelling sideways, and the resulting wound may be distorted, irregular in shape, or even slit-like, such that it does not resemble a conventional entrance wound. In this case, an abrasion artefact may be absent. Similarly misshapen wounds can be caused by the distortion of the bullet if it hits an intermediate object (including another part of the victim's own body, in what is known as a re-entrant wound) before penetrating the skin surface. However, careful examination of the wound under magnification may show the inverted wound edges and signs of an irregularly-shaped abrasion rim characteristic of entry wounds.
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== References ==
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data/en.wikipedia.org/wiki/Absolute_risk-0.md
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title: "Absolute risk"
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source: "https://en.wikipedia.org/wiki/Absolute_risk"
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category: "reference"
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tags: "science, encyclopedia"
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date_saved: "2026-05-05T07:25:39.613272+00:00"
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instance: "kb-cron"
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Absolute risk (or AR) is the probability or chance of an event. It is usually used for the number of events (such as a disease) that occurred in a group, divided by the number of people in that group.
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Absolute risk is one of the most understandable ways of communicating health risks to the general public.
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In difference to absolute risk, the relative risk (RR) is the ratio of the probability of an outcome in an exposed group to the probability of the outcome in an unexposed group.
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== See also ==
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Absolute risk reduction
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Relative risk reduction
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== References ==
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== Further reading ==
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Woloshin, Steven; Schwartz, Lisa M.; Welch, H. Gilbert (2008). Know Your Chances: Understanding Health Statistics. Berkeley (CA): University of California Press. PMID 23469386.
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data/en.wikipedia.org/wiki/Acholia-0.md
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title: "Acholia"
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source: "https://en.wikipedia.org/wiki/Acholia"
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category: "reference"
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tags: "science, encyclopedia"
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date_saved: "2026-05-05T07:25:40.769428+00:00"
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Acholia is pale feces, due to lack of bile which results in the normal brown colour. It is a sign of reduced conjugated bilirubin into the bowel, as a result of a problem in the liver itself or in the biliary tree.
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== Signs and symptoms ==
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Acholia results in pale feces.
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== Cause ==
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A condition in which little or no bile is secreted or the flow of bile into the digestive tract is obstructed. The acholia is a sign of many diseases, such as hepatitis.
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== Etymology ==
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Ancient Greek: a + chole (without bile).
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== See also ==
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Choluria
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== References ==
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== External links ==
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data/en.wikipedia.org/wiki/Active_placebo-0.md
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title: "Active placebo"
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source: "https://en.wikipedia.org/wiki/Active_placebo"
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category: "reference"
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tags: "science, encyclopedia"
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date_saved: "2026-05-05T07:25:41.989643+00:00"
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An active placebo is a placebo that produces noticeable side effects that may convince the person being treated that they are receiving a legitimate treatment, rather than an inert placebo.
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== Nomenclature ==
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According to a 1965 paper, the term "concealed placebo" (German: Kaschiertes Placebo) was suggested in a 1959 paper published in German.
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== Example ==
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An example of an active placebo is the 1964 work of Shader and colleagues who used a combination of low-dose phenobarbital plus atropine to mimic the sedation and dry mouth produced by phenothiazines.
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Morphine and gabapentin are painkillers with the common side effects of sleepiness and dizziness. In a 2005 study assessing the effects of these painkillers on neuropathic pain, lorazepam was chosen as an active placebo because it is not a painkiller but it does cause sleepiness and can cause dizziness.
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Testing from the late 1950s onwards on narcotic analgesics like morphine also has used dicyclomine as an active placebo, and on some occasions it was reported to cause the Straub mouse tail reaction, as do most narcotics. Clonidine is now finding more use as an active placebo for narcotics.
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== References ==
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Shader, R. I.; Cohler, J.; Elashoff, R.; Grinspoon, L. (October 1964). "Phenobarbital and atropine in combination, an active control substance for phenothiazine research". Journal of Psychiatric Research. 2 (3): 169–183. doi:10.1016/0022-3956(64)90018-4. PMID 14242375. Retrieved 7 September 2020.
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data/en.wikipedia.org/wiki/Acute_(medicine)-0.md
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data/en.wikipedia.org/wiki/Acute_(medicine)-0.md
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title: "Acute (medicine)"
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source: "https://en.wikipedia.org/wiki/Acute_(medicine)"
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category: "reference"
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tags: "science, encyclopedia"
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date_saved: "2026-05-05T07:25:43.224820+00:00"
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In medicine, describing a disease as acute denotes that it is of recent onset; it occasionally denotes a short duration. The quantification of how much time constitutes "short" and "recent" varies by disease and by context, but the core denotation of "acute" is always qualitatively in contrast with "chronic", which denotes long-lasting disease (for example, in acute leukaemia and chronic leukaemia).
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In the context of the mass noun "acute disease", it refers to the acute phase (that is, a short course) of any disease entity. For example, in an article on ulcerative enteritis in poultry, the author says, "in acute disease there may be increased mortality without any obvious signs", referring to the acute form or phase of ulcerative enteritis.
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== Meaning variations ==
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A mild stubbed toe is an acute injury. Similarly, many acute upper respiratory infections and acute gastroenteritis cases in adults are mild and usually resolve within a few days or weeks.
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The term "acute" is also included in the definition of several diseases, such as severe acute respiratory syndrome, acute leukaemia, acute myocardial infarction, and acute hepatitis. This is often to distinguish diseases from their chronic forms, such as chronic leukaemia, or to highlight the sudden onset of the disease, such as acute myocardial infarct.
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=== Related terminology ===
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Related terms include:
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== Acute care ==
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Acute care is the early and specialist management of adult patients who have a wide range of medical conditions requiring urgent or emergency care usually within 48 hours of admission or referral from other specialties.
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Acute hospitals are those intended for short-term medical and/or surgical treatment and care which is a medical speciality of acute medicine, as often primary care is not positioned to assume this role.
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== References ==
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data/en.wikipedia.org/wiki/Acute_abdomen-0.md
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title: "Acute abdomen"
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source: "https://en.wikipedia.org/wiki/Acute_abdomen"
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category: "reference"
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tags: "science, encyclopedia"
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date_saved: "2026-05-05T07:25:44.430078+00:00"
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instance: "kb-cron"
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An acute abdomen refers to a sudden, severe abdominal pain. It is in many cases a medical emergency, requiring urgent and specific diagnosis. Several causes need immediate surgical treatment.
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== Differential diagnosis ==
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Common causes of an acute abdomen include a gastrointestinal perforation, peptic ulcer disease, mesenteric ischemia, acute cholecystitis, appendicitis, diverticulitis, pancreatitis, and an abdominal hemorrhage. However, this is a non-exhaustive list and other less common causes may also lead to an acute abdomen. In pregnant patient, a tubo-ovarian abscess, ruptured ovarian cyst or a ruptured ectopic pregnancy are common causes of an acute abdomen.
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=== Ischemic acute abdomen ===
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Vascular disorders are more likely to affect the small bowel than the large bowel. Arterial supply to the intestines is provided by the superior and inferior mesenteric arteries (SMA and IMA respectively), both of which are direct branches of the aorta.
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Clinically, patients present with diffuse abdominal pain, bowel distention, and bloody diarrhea. On physical exam, bowel sounds will be absent. Laboratory tests reveal a neutrophilic leukocytosis, sometimes with a left shift, and increased serum amylase. Abdominal radiography will show many air-fluid levels, as well as widespread edema. Acute ischemic abdomen is a surgical emergency. Typically, treatment involves removal of the region of the bowel that has undergone infarction, and subsequent anastomosis of the remaining healthy tissue.
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== Diagnosis ==
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Traditionally, the use of opiates or other pain medications in patients with an acute abdomen has been discouraged before the clinical examination because of the concern that pain medications may mask the signs and symptoms of the condition and therefore may lead to a delay in diagnosis. However, the scientific literature has shown that early administration of pain medications, including opiates, in those with acute abdomen does not lead to delayed diagnosis, delayed treatment or errors in management (the incorrect surgical treatment administered or performing un-necessary surgery). In a meta-analysis of those with acute appendicitis, early administration of opiates was found to alter treatment approach (with a slightly higher rate of appendectomy in those who received opiates) but diagnostic accuracy and surgical outcomes were unaffected by pain medication use. Clinical guidelines also recommend early analgesic use before a cause is established.
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Medical imaging aids in the diagnosis of potential causes of an acute abdomen. A CT scan or ultrasound of the abdomen and pelvis are the preferred imaging modalities in the evaluate of an acute abdomen. The use of radiocontrast agents with CT scans improve diagnostic accuracy. Some authors advocate for the use of CT angiography with contrast of the abdomen and pelvis as the preferred imaging modality. An ultrasound is the preferred imaging modality in pregnant patients as CT scans expose the fetus to ionizing radiation which may lead to adverse pregnancy outcomes. An abdominal x-ray may show free air in the abdominal cavity due to a perforation in the gastrointestinal tract. However, abdominal x-ray is not recommended as part of the diagnostic evaluation in acute abdomen due to its low sensitivity and specificity. Delays in medical imaging acquisition and interpretation greater than 2 hours are associated with an increased risk of complications and death.
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== Society and culture ==
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In a population based study of Medicare patients in the United States, Black patients who were admitted to the hospital for an acute abdomen requiring general surgery consultation were 14% less likely to receive surgical consultation as compared to White patients. These racial disparities in care persisted (with an 11% difference) when socioeconomic factors were standardized. In another population based study in the United States, Black patients and patients from other racial minority groups were 22-30% less likely to receive pain medication for an acute abdomen as compared to White patients.
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== References ==
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== External links ==
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data/en.wikipedia.org/wiki/Acute_pericarditis-0.md
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title: "Acute pericarditis"
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source: "https://en.wikipedia.org/wiki/Acute_pericarditis"
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category: "reference"
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tags: "science, encyclopedia"
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date_saved: "2026-05-05T07:25:45.765948+00:00"
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instance: "kb-cron"
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---
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Acute pericarditis is a type of pericarditis (inflammation of the sac surrounding the heart, the pericardium) usually lasting less than 4 to 6 weeks. It is the most common condition affecting the pericardium.
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== Signs and symptoms ==
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Chest pain is one of the common symptoms of acute pericarditis. It is usually of sudden onset, occurring in the anterior chest and often has a sharp quality that worsens with breathing in or coughing, due to inflammation of the pleural surface at the same time. The pain may be reduced with sitting up and leaning forward while worsened with lying down, and also may radiate to the back, to one or both trapezius ridges. However, the pain can also be dull and steady, resembling the chest pain in an acute myocardial infarction. As with any chest pain, other causes must also be ruled out, such as GERD, pulmonary embolism, muscular pain, etc.
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A pericardial friction rub is a very specific sign of acute pericarditis, meaning the presence of this sign invariably indicates presence of disease. However, absence of this sign does not rule out disease. This rub can be best heard by the diaphragm of the stethoscope at the left sternal border arising as a squeaky or scratching sound, resembling the sound of leather rubbing against each other. This sound should be distinguished from the sound of a murmur, which is similar but sounds more like a "swish" sound than a scratching sound. The pericardial rub is said to be generated from the friction generated by the two inflamed layers of the pericardium; however, even a large pericardial effusion does not necessarily present a rub. The rub is best heard during the maximal movement of the heart within the pericardial sac, namely, during atrial systole, ventricular systole, and the filling phase of early ventricular diastole.
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Fever may be present since this is an inflammatory process.
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== Causes ==
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There are several causes of acute pericarditis. In developed nations, the cause of most (80–90%) cases of acute pericarditis is unknown but a viral cause is suspected in the majority of such cases. The other 10–20% of acute pericarditis cases have various causes including connective tissue diseases (e.g., systemic lupus erythematosus), cancer, or involve an inflammatory reaction of the pericardium following trauma to the heart such as after a heart attack such as Dressler's syndrome. Familial Mediterranean fever and TNF receptor associated periodic syndrome are rare inherited autoimmune diseases capable of causing recurring episodes of acute pericarditis.
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== Pathophysiology ==
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Acute pericarditis is an over-arching term to describe a set of clinical symptoms and findings associated with inflammation of the pericardium. The initial triggering event is variable and depends on the underlying etiology. In general, an inflammatory stimulus (virus, idiopathic, radiation, surgery) results in an injury that activates the immune system of the body. A structure known as the inflammasome (a large molecule cellular structure) begins to activate other smaller inflammatory molecules known as cytokines that eventually attack and damage the mesothelial cells of the pericardium. The differentiation in symptoms and presentation may depend on the patient-level variation of the adaptive and innate immune system. If a patient has adequate mechanisms to turn off pro-inflammatory processes, the acute pericarditis may not progress. If immune system is not regulated as well and is allowed to continue activating the inflammasome to damage the mesothelial cells, this may lead to the inflammation of the pericardium. The goal of medical treatment for this condition is to turn off or regulate the patients inflammatory system.
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== Diagnosis ==
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For acute pericarditis to formally be diagnosed, two or more of the following criteria must be present: chest pain consistent with a diagnosis of acute pericarditis (sharp chest pain worsened by breathing in or a cough), a pericardial friction rub, a pericardial effusion, and changes on electrocardiogram (ECG) consistent with acute pericarditis.
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A complete blood count may show an elevated white count and a serum C-reactive protein may be elevated. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB). and cardiac troponin I (cTnI), both of which are also markers for injury to the muscular layer of the heart. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances may occur when inflammation of the heart's muscular layer in addition to acute pericarditis. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 μg/L. Coronary angiography in those patients should indicate normal vascular perfusion. Troponin levels increase in 35-50% of people with pericarditis.
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Electrocardiogram (ECG) changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes
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title: "Acute pericarditis"
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chunk: 2/3
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source: "https://en.wikipedia.org/wiki/Acute_pericarditis"
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category: "reference"
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tags: "science, encyclopedia"
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date_saved: "2026-05-05T07:25:45.765948+00:00"
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instance: "kb-cron"
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---
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stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.
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stage 2 -- normalization of ST and PR deviations
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stage 3 -- diffuse T wave inversions (may not be present in all patients)
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stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted
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The two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization. As opposed to pericarditis, AMI usually causes localized convex ST-elevation usually associated with reciprocal ST-depression which may also be frequently accompanied by Q-waves, T-wave inversions (while ST is still elevated unlike pericarditis), arrhythmias and conduction abnormalities. In AMI, PR-depressions are rarely present. Early repolarization usually occurs in young males (age <40 years) and ECG changes are characterized by terminal R-S slurring, temporal stability of ST-deviations and J-height/ T-amplitude ratio in V5 and V6 of <25% as opposed to pericarditis where terminal R-S slurring is very uncommon and J-height/ T-amplitude ratio is ≥ 25%. Very rarely, ECG changes in hypothermia may mimic pericarditis, however differentiation can be helpful by a detailed history and presence of an Osborne wave in hypothermia.
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Another important diagnostic electrocardiographic sign in acute pericarditis is the Spodick sign. It signifies to the PR-depressions in a usual (but not always) association with downsloping TP segment in patients with acute pericarditis and is present in up to 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodick's sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome. The presence of a classical Spodick's sign is often a giveaway to the diagnosis.
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Rarely, electrical alternans may be seen, depending on the size of the effusion.
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A chest x-ray is usually normal in acute pericarditis but can reveal the presence of an enlarged heart if a pericardial effusion is present and is greater than 200 mL in volume. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.
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An echocardiogram is typically normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.
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== Differential Diagnoses ==
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There are many causes of acute pericarditis, so the first step in differentiating is taking a good patient history to determine likely and unlikely causes of acute pericarditis. To diagnose acute idiopathic pericarditis, one must rule out all other causes of acute pericarditis (diagnosis of exclusion).
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Common diagnoses to rule out when considering acute idiopathic pericarditis include the following:
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Pericarditis secondary to post-cardiac injury: Differentiate this from acute idiopathic pericarditis by timing. If the pericarditis results a few days or weeks post acute myocardial infarction, trauma to the chest wall, cardiac surgery or other cardiac perforation causes pericarditis secondary to post-cardiac injury is most likely the diagnosis.
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Pericarditis secondary autoimmune disease: Differentiate idiopathic pericarditis from common autoimmune diseases that present with pericarditis as just one of many complications. This list includes, systemic lupus erythematosus, rheumatoid arthritis, scleroderma, dermatomyositis, polymyositis, mixed connective tissue disease, vasculitis, Inflammatory bowel disease, sarcoidosis, Behçet's disease, Still disease, Immunoglobulin G4-related diseases, Erheim-Chester disease, polyarteritis nodosa, etc. Can be done by evaluating labs such as ANA, ESR, anti-rheumatoid factor, Anti-SSA/Ro, Anti-SSB/La, and p-ANCA/c-ANCA and so on
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Pericarditis secondary to drug toxicity: Pericarditis can result from the following medications: Procainamide, isoniazid, hydralazine, and cyclosporine.
|
||||
Pericarditis secondary to metabolic derangements: Differentiate pericarditis from causes resulting from both excretion of waste, such as uremia (dialysis associated) as well as from endocrine function including hyperthyroidism, hypothyroidism, cholesterol and anorexia. This can be obtained from a basic CMP, TSH and T4 levels.
|
||||
Pericarditis secondary to infection: Differentiate between viral, bacterial, fungal, and/or protozoal. Evaluate if the patient has a fever, chills, septicemia or any other evidence of infection.
|
||||
Pericarditis secondary to malignancy: Differentiate the result of acute pericarditis arising from invasion/activation of the immune system from a tumor such as malignant melanoma, lymphoma, leukemia, or solid tumors. If a pericardial effusion is present, malignant cells are often found in the pericardial fluid.
|
||||
|
||||
== Treatment ==
|
||||
Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include the following:
|
||||
|
||||
subacute onset
|
||||
high fever (> 100.4 F/38 C) and leukocytosis
|
||||
development of cardiac tamponade
|
||||
large pericardial effusion (echo-free space > 20 mm) resistant to NSAID treatment
|
||||
immunocompromised
|
||||
history of oral anticoagulation therapy
|
||||
acute trauma
|
||||
failure to respond to seven days of NSAID treatment
|
||||
Pericardiocentesis is a procedure whereby the fluid in a pericardial effusion is removed through a needle. It is performed under the following conditions:
|
||||
36
data/en.wikipedia.org/wiki/Acute_pericarditis-2.md
Normal file
36
data/en.wikipedia.org/wiki/Acute_pericarditis-2.md
Normal file
@ -0,0 +1,36 @@
|
||||
---
|
||||
title: "Acute pericarditis"
|
||||
chunk: 3/3
|
||||
source: "https://en.wikipedia.org/wiki/Acute_pericarditis"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:45.765948+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
presence of moderate or severe cardiac tamponade
|
||||
diagnostic purpose for suspected purulent, tuberculosis, or neoplastic pericarditis
|
||||
persistent symptomatic pericardial effusion
|
||||
NSAIDs in viral or idiopathic pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range. Depending on severity, dosing is between 300 and 800 mg every 6–8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6–8 hours. Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.
|
||||
Colchicine, which has been essential to treat recurrent pericarditis, has been supported for routine use in acute pericarditis by recent prospective studies. Colchicine can be given 0.6 mg twice a day (0.6 mg daily for patients <70 kg) for 3 months following an acute attack. It should be considered in all patients with acute pericarditis, preferably in combination with a short-course of NSAIDs. For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1–2 mg on first day followed by 0.5 daily or twice daily for three months. It should be avoided or used with caution in patients with severe chronic kidney disease, hepatobiliary dysfunction, blood dyscrasias, and gastrointestinal motility disorders.
|
||||
Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease.
|
||||
|
||||
== Clinical Complications ==
|
||||
Clinical complications of acute pericarditis may vary between:
|
||||
|
||||
Acute and recurrent pericarditis
|
||||
Pericardial effusion without major hemodynamic compromise
|
||||
Cardiac tamponade
|
||||
Constrictive pericarditis
|
||||
Effusive-constrictive pericarditis
|
||||
|
||||
== Prognosis ==
|
||||
One of the most feared complications of acute pericarditis is cardiac tamponade. Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. Signs of cardiac tamponade include distended neck veins, muffled heart sounds when listening with a stethoscope, and low blood pressure (together known as Beck's triad). This condition can be fatal if not immediately treated.
|
||||
Another longer term complication of pericarditis, if it recurs over a longer period of time (normally more than 3 months), is progression to constrictive pericarditis. Recent studies have shown this to be an uncommon complication. The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart.
|
||||
|
||||
== References ==
|
||||
|
||||
== Further reading ==
|
||||
Chugh, S. N. (2014-05-14). Textbook of Clinical Electrocardiography. Jaypee Brothers Publishers. ISBN 9789350906088.
|
||||
|
||||
== External links ==
|
||||
34
data/en.wikipedia.org/wiki/Adherence_(medicine)-0.md
Normal file
34
data/en.wikipedia.org/wiki/Adherence_(medicine)-0.md
Normal file
@ -0,0 +1,34 @@
|
||||
---
|
||||
title: "Adherence (medicine)"
|
||||
chunk: 1/5
|
||||
source: "https://en.wikipedia.org/wiki/Adherence_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:48.247796+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
In medicine, patient adherence describes the degree to which a person correctly follows medical advice. Most commonly, it refers to medication or drug compliance, but it can also apply to other situations such as medical device use, self care, self-directed exercises, therapy sessions, or medical follow-up visits. Patient compliance and patient adherence may be used interchangeably but adherence emphasizes the role of the patient in decision-making and factors that influence the ability to follow instructions. Concordance is the process by which a patient and clinician make decisions together about treatment. Differences in terminology reflect regional variation, deliberate distinctions, and the preferences of various groups and organizations.
|
||||
Both patient and health-care provider affect adherence, and a positive physician-patient relationship is the most important factor in improving compliance. Access to care plays a role in patient adherence, whereby greater wait times to access care contributing to greater absenteeism. The cost of prescription medication and potential side effects also play a role.
|
||||
Worldwide, non-compliance is a major obstacle to the effective delivery of health care. 2003 estimates from the World Health Organization indicated that only about 50% of patients with chronic diseases living in developed countries follow treatment recommendations with particularly low rates of adherence to therapies for asthma, diabetes, and hypertension. Major barriers to compliance are thought to include the complexity of modern medication regimens, poor health literacy and not understanding treatment benefits, the occurrence of undiscussed side effects, poor treatment satisfaction, cost of prescription medicine, and poor communication or lack of trust between a patient and his or her health-care provider. Efforts to improve compliance have been aimed at simplifying medication packaging, providing effective medication reminders, improving patient education, and limiting the number of medications prescribed simultaneously. Studies show a great variation in terms of characteristics and effects of interventions to improve medicine adherence. It is still unclear how adherence can consistently be improved in order to promote clinically important effects.
|
||||
|
||||
== Terminology ==
|
||||
In medicine, compliance describes the degree to which a patient correctly follows medical advice. Most commonly, it refers to medication or drug compliance, but it can also apply to medical device use, self care, self-directed exercises, or therapy sessions. Both patient and health-care provider affect compliance, and a positive physician-patient relationship is the most important factor in improving compliance.
|
||||
As of 2003, US health care professionals more commonly used the term "adherence" to a regimen rather than "compliance", because it has been thought to reflect better the diverse reasons for patients not following treatment directions in part or in full. Additionally, the term adherence includes the ability of the patient to take medications as prescribed by their physician with regards to the correct drug, dose, route, timing, and frequency. It has been noted that compliance may only refer to passively following orders. The term adherence is often used to imply a collaborative approach to decision-making and treatment between a patient and clinician.
|
||||
The term concordance has been used in the United Kingdom to involve a patient in the treatment process to improve compliance, and refers to a 2003 NHS initiative. In this context, the patient is informed about their condition and treatment options, involved in the decision as to which course of action to take, and partially responsible for monitoring and reporting back to the team. Informed intentional non-adherence is when the patient, after understanding the risks and benefits, chooses not to take the treatment.
|
||||
As of 2005, the preferred terminology remained a matter of debate. As of 2007, concordance has been used to refer specifically to patient adherence to a treatment regimen which the physician sets up collaboratively with the patient, to differentiate it from adherence to a physician-only prescribed treatment regimen. Despite the ongoing debate, adherence has been the preferred term for the World Health Organization, The American Pharmacists Association, and the U.S. National Institutes of Health Adherence Research Network. The Medical Subject Headings of the United States National Library of Medicine defines various terms with the words adherence and compliance. Patient Compliance and Medication Adherence are distinguished under the MeSH tree of Treatment Adherence and Compliance.
|
||||
|
||||
== Adherence factors ==
|
||||
In 2003 WHO estimated that half of those for whom long term treatment regimens are prescribed do not follow them as directed.
|
||||
In general, adherence is higher in diseases where people see a greater health threat, such as HIV/AIDS and cancer, and it is lower for chronic conditions such as hypertension, asthma or diabetes.
|
||||
Factors can be categorized on 3 levels: individual, cultural and healthcare system level.
|
||||
|
||||
=== Individual factors ===
|
||||
Depressive symptoms and perceived discrimination have been correlated with poor adherence.
|
||||
|
||||
=== Side effects ===
|
||||
Negative side effects of a medicine can influence adherence.
|
||||
|
||||
=== Socioeconomic status ===
|
||||
Medication adherence rates are typically lower with lower socioeconomic status, increased stress related to difficult life circumstances.
|
||||
Poverty is associated with Low levels of literacy and numeracy. Adults in more deprived areas, such as the North East of England, performed at a lower level than those in less deprived areas such as the South East. Local authority tenants and those in poor health were particularly likely to lack basic skills.
|
||||
34
data/en.wikipedia.org/wiki/Adherence_(medicine)-1.md
Normal file
34
data/en.wikipedia.org/wiki/Adherence_(medicine)-1.md
Normal file
@ -0,0 +1,34 @@
|
||||
---
|
||||
title: "Adherence (medicine)"
|
||||
chunk: 2/5
|
||||
source: "https://en.wikipedia.org/wiki/Adherence_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:48.247796+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Literacy ===
|
||||
In 1999 one fifth of UK adults, nearly seven million people, had problems with basic skills, especially functional literacy and functional numeracy, described as: "The ability to read, write and speak in English, and to use mathematics at a level necessary to function at work and in society in general." This made it impossible for them to effectively take medication, read labels, follow drug regimes, and find out more.
|
||||
In 2003, 20% of adults in the UK had a long-standing illness or disability and a national study for the UK Department of Health, found more than one-third of people with poor or very poor health had literary skills of Entry Level 3 or below.
|
||||
A study of the relationship of literacy to asthma knowledge revealed that only 31% of asthma patients with a reading level of a ten-year-old knew they needed to see the doctors, even when they were not having an asthma attack, compared to 90% with a high school graduate reading level.
|
||||
|
||||
=== Treatment cost ===
|
||||
In 2013 the US National Community Pharmacists Association sampled for one month 1,020 Americans above age 40 for with an ongoing prescription to take medication for a chronic condition and gave a grade C+ on adherence. In 2009, this contributed to an estimated cost of $290 billion annually. In 2012, increase in patient medication cost share was found to be associated with low adherence to medication.
|
||||
The United States is among the countries with the highest prices of prescription drugs mainly attributed to the government's lack of negotiating lower prices with monopolies in the pharmaceutical industry especially with brand name drugs. In order to manage medication costs, many US patients on long term therapies fail to fill their prescription, skip or reduce doses. According to a Kaiser Family Foundation survey in 2015, about three quarters (73%) of the public think drug prices are unreasonable and blame pharmaceutical companies for setting prices so high. In the same report, half of the public reported that they are taking prescription drugs and a "quarter (25%) of those currently taking prescription medicine report they or a family member have not filled a prescription in the past 12 months due to cost, and 18 percent report cutting pills in half or skipping doses". In a 2009 comparison to Canada, only 8% of adults reported to have skipped their doses or not filling their prescriptions due to the cost of their prescribed medications.
|
||||
|
||||
=== Health literacy ===
|
||||
Cost and poor understanding of the directions for the treatment, referred to as 'health literacy' have been known to be major barriers to treatment adherence. Misinformation from the internet and social media can also lead to a delay or lack of compliance in following medical advice.
|
||||
|
||||
=== Age ===
|
||||
The recent National Service Framework on the care of older people highlighted the importance of taking and effectively managing medicines in the elderly. Elderly individuals may face challenges, including multiple medications with frequent dosing, and potentially decreased dexterity or cognitive functioning. Patient knowledge is also a factor.
|
||||
In 1999 Cline et al. identified several gaps in knowledge about medication in elderly patients discharged from hospital. Despite receiving written and verbal information, 27% of older people discharged after heart failure were classed as non-adherent within 30 days. Half the patients surveyed could not recall the dose of the medication that they were prescribed and nearly two-thirds did not know what time of day to take them. A 2001 study by Barat et al. evaluated the medical knowledge and factors of adherence in a population of 75-year-olds living at home. They found that 40% of elderly patients do not know the purpose of their regimen and only 20% knew the consequences of non-adherence. Comprehension, polypharmacy, living arrangement, multiple doctors, and use of compliance aids was correlated with adherence.
|
||||
In children with asthma, self-management compliance is critical and co-morbidities have been noted to affect outcomes; in 2013 it has been suggested that electronic monitoring may help adherence.
|
||||
|
||||
=== Ethnicity ===
|
||||
People of different ethnic backgrounds have unique adherence issues through, for example, limited English language proficiency, their cultural belief system rooted in historical experience (Tuskegee experiment), resulting in medical mistrust. There are few published studies on adherence in medicine taking in ethnic minority communities. Ethnicity and culture influence some health-determining behaviour, such as participation in health screening programmes and attendance at follow-up appointments.
|
||||
Ethnic groups differ in their attitudes, values, culture and beliefs about health and illness, particularly with preventive treatments and medication for asymptomatic conditions. Additionally, some cultures fatalistically attribute their good or poor health to their god(s), and attach less importance to self-care than others. Complementary and alternative medicine may be taken with or instead of the prescribed medications especially in Mexican American and Vietnamese people.
|
||||
Studies have shown that black patients and those with non-private insurance are more likely to be labeled as non-adherent. An increased risk for non adherence was observed even after controlling for A1c, and socioeconomic factors.
|
||||
|
||||
=== Prescription fill rates ===
|
||||
Not all patients will fill the prescription at a pharmacy. In a 2010 U.S. study, 20–30% of prescriptions were never filled at the pharmacy. Reasons people do not fill prescriptions include the cost of the medication, A US nationwide survey of 1,010 adults in 2001 found that 22% chose not to fill prescriptions because of the price, which is similar to the 20–30% overall rate of unfilled prescriptions. Other factors are doubting the need for medication, or preference for self-care measures other than medication. Convenience, side effects and lack of demonstrated benefit are also factors.
|
||||
82
data/en.wikipedia.org/wiki/Adherence_(medicine)-2.md
Normal file
82
data/en.wikipedia.org/wiki/Adherence_(medicine)-2.md
Normal file
@ -0,0 +1,82 @@
|
||||
---
|
||||
title: "Adherence (medicine)"
|
||||
chunk: 3/5
|
||||
source: "https://en.wikipedia.org/wiki/Adherence_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:48.247796+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
==== Medication Possession Ratio ====
|
||||
Prescription medical claims records can be used to estimate medication adherence based on fill rate. Patients can be routinely defined as being 'Adherent Patients' if the amount of medication furnished is at least 80% based on days' supply of medication divided by the number of days patient should be consuming the medication. This percentage is called the medication possession ratio (MPR). 2013 work has suggested that a medication possession ratio of 90% or above may be a better threshold for deeming consumption as 'Adherent'.
|
||||
Two forms of MPR can be calculated, fixed and variable. Calculating either is relatively straightforward, for Variable MPR (VMPR) it is calculated as the number of days' supply divided by the number of elapsed days including the last prescription.
|
||||
|
||||
|
||||
|
||||
|
||||
V
|
||||
M
|
||||
P
|
||||
R
|
||||
=
|
||||
|
||||
|
||||
|
||||
All days' supply
|
||||
Elapsed days (inclusive of last prescription)
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle VMPR={\dfrac {\text{All days' supply}}{\text{Elapsed days (inclusive of last prescription)}}}}
|
||||
|
||||
|
||||
For the Fixed MPR (FMPR) the calculation is similar but the denominator is the number of days in a year whilst the numerator is constrained to be the number of days' supply within the year that the patient has been prescribed.
|
||||
|
||||
|
||||
|
||||
|
||||
F
|
||||
M
|
||||
P
|
||||
R
|
||||
=
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
All days' supply
|
||||
|
||||
≤
|
||||
365
|
||||
|
||||
365
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle FMPR={\dfrac {{\text{All days' supply}}\leq 365}{365}}}
|
||||
|
||||
|
||||
For medication in tablet form it is relatively straightforward to calculate the number of days' supply based on a prescription. Some medications are less straightforward though because a prescription of a given number of doses may have a variable number of days' supply because the number of doses to be taken per day varies, for example with preventative corticosteroid inhalers prescribed for asthma where the number of inhalations to be taken daily may vary between individuals based on the severity of the disease.
|
||||
|
||||
=== Contextual factors ===
|
||||
Contextual factors along with intrapersonal circumstances such as mental states affect decisions. They can accurately predict decisions where most contextual information is identified. General compliance with recommendations to follow isolation is influenced beliefs such as taking health precaution to be protected against infection, perceived vulnerability, getting COVID-19 and trust in the government. Mobility reduction, compliance with quarantine regulations in European regions where level of trust in policymakers is high can influence whether one complies with isolation rules. In addition, perceived infectiousness of COVID-19 is a strong predictor of rule compliance such that the more contagious people think COVID-19 is, the less willing social distancing measures are taken, while the sense of duty and fear of the virus contribute to staying at home. People might not leave their homes due to trusting regulations to be effective or placing it in a higher power such that individuals who trust others demonstrate more compliance than those who do not. Compliant individuals see protective measures as effective, while non-compliant people see them as problematic.
|
||||
|
||||
=== Course completion ===
|
||||
Once started, patients seldom follow treatment regimens as directed, and seldom complete the course of treatment. In respect of hypertension, 50% of patients completely drop out of care within a year of diagnosis. Persistence with first-line single antihypertensive drugs is extremely low during the first year of treatment. As far as lipid-lowering treatment is concerned, only one third of patients are compliant with at least 90% of their treatment. Intensification of patient care interventions (e.g. electronic reminders, pharmacist-led interventions, healthcare professional education of patients) improves patient adherence rates to lipid-lowering medicines, as well as total cholesterol and LDL-cholesterol levels.
|
||||
The World Health Organization (WHO) estimated in 2003 that only 50% of people complete long-term therapy for chronic illnesses as they were prescribed, which puts patient health at risk. For example, in 2002 statin compliance dropped to between 25 and 40% after two years of treatment, with patients taking statins for what they perceive to be preventative reasons being unusually poor compliers.
|
||||
A wide variety of packaging approaches have been proposed to help patients complete prescribed treatments. These approaches include formats that increase the ease of remembering the dosage regimen as well as different labels for increasing patient understanding of directions. For example, medications are sometimes packed with reminder systems for the day and/or time of the week to take the medicine. Some evidence shows that reminder packaging may improve clinical outcomes such as blood pressure.
|
||||
A not-for-profit organisation called the Healthcare Compliance Packaging Council of Europe] (HCPC-Europe) was set up between the pharmaceutical industry, the packaging industry with representatives of European patients organisations. The mission of HCPC-Europe is to assist and to educate the healthcare sector in the improvement of patient compliance through the use of packaging solutions. A variety of packaging solutions have been developed by this collaboration.
|
||||
|
||||
== World Health Organization Barriers to Adherence ==
|
||||
The World Health Organization (WHO) groups barriers to medication adherence into five categories; health care team and system-related factors, social and economic factors, condition-related factors, therapy-related factors, and patient-related factors. Common barriers include:
|
||||
|
||||
== Improving adherence rates ==
|
||||
|
||||
=== Role of health care providers ===
|
||||
Health care providers play a great role in improving adherence issues. Providers can improve patient interactions through motivational interviewing and active listening. Health care providers should work with patients to devise a plan that is meaningful for the patient's needs. A relationship that offers trust, cooperation, and mutual responsibility can greatly improve the connection between provider and patient for a positive impact. The wording that health care professionals take when sharing health advice may have an impact on adherence and health behaviours, however, further research is needed to understand if positive framing (e.g., the chance of surviving is improved if you go for screening) versus negative framing (e.g., the chance of dying is higher if you do not go for screening) is more effective for specific conditions.
|
||||
52
data/en.wikipedia.org/wiki/Adherence_(medicine)-3.md
Normal file
52
data/en.wikipedia.org/wiki/Adherence_(medicine)-3.md
Normal file
@ -0,0 +1,52 @@
|
||||
---
|
||||
title: "Adherence (medicine)"
|
||||
chunk: 4/5
|
||||
source: "https://en.wikipedia.org/wiki/Adherence_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:48.247796+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Technology ===
|
||||
In 2012 it was predicted that as telemedicine technology improves, physicians will have better capabilities to remotely monitor patients in real-time and to communicate recommendations and medication adjustments using personal mobile devices, such as smartphones, rather than waiting until the next office visit.
|
||||
Medication Event Monitoring Systems (MEMS), as in the form of smart medicine bottle tops, smart pharmacy vials or smart blister packages as used in clinical trials and other applications where exact compliance data are required, work without any patient input, and record the time and date the bottle or vial was accessed, or the medication removed from a blister package. The data can be read via proprietary readers, or NFC enabled devices, such as smartphones or tablets. A 2009 study stated that such devices can help improve adherence. More recently a 2016 scoping review suggested that in comparison to MEMS, median mediction adherence was grossly overestimated by 17% using self-report, by 8% using pill count and by 6% using rating as alternative methods for measuring medication adherence.
|
||||
The effectiveness of two-way email communication between health care professionals and their patients has not been adequately assessed.
|
||||
|
||||
==== Mobile phones ====
|
||||
As of 2019, 5.15 billion people, which equates to 67% of the global population, have a mobile device and this number is growing. Mobile phones have been used in healthcare and has fostered its own term, mHealth. They have also played a role in improving adherence to medication. For example, text messaging has been used to remind patients to take medication in patients with chronic conditions such as asthma and hypertension. Other examples include the use of smartphones for synchronous and asynchronous Video Observed Therapy (VOT) as a replacement for the currently resource intensive standard of Directly Observed Therapy (DOT) (recommended by the WHO) for Tuberculosis management. Other mHealth interventions for improving adherence to medication include smartphone applications, voice recognition in interactive phone calls and Telepharmacy. Some results show that the use of mHealth improves adherence to medication and is cost-effective, though some reviews report mixed results. Studies show that using mHealth to improve adherence to medication is feasible and accepted by patients. Specific mobile applications might also support adherence. mHealth interventions have also been used alongside other telehealth interventions such as wearable wireless pill sensors, smart pillboxes and smart inhalers
|
||||
|
||||
=== Forms of medication ===
|
||||
Depot injections need to be taken less regularly than other forms of medication and a medical professional is involved in the administration of drugs so can increase compliance. Depot's are used for oral contraceptive pill and antipsychotic medication used to treat schizophrenia and bipolar disorder.
|
||||
|
||||
=== Coercion ===
|
||||
Sometimes drugs are given involuntarily to ensure compliance. This can occur if an individual has been involuntarily committed or are subjected to an outpatient commitment order, where failure to take medication will result in detention and involuntary administration of treatment. This can also occur if a patient is not deemed to have mental capacity to consent to treatment in an informed way.
|
||||
|
||||
== Health and disease management ==
|
||||
A WHO study estimates that only 50% of patients with chronic diseases in developed countries follow treatment recommendations.
|
||||
Asthma non-compliance (28–70% worldwide) increases the risk of severe asthma attacks requiring preventable ER visits and hospitalisations; compliance issues with asthma can be caused by a variety of reasons including: difficult inhaler use, side effects of medications, and cost of the treatment.
|
||||
|
||||
=== Cancer ===
|
||||
200,000 new cases of cancer are diagnosed each year in the UK. One in three adults in the UK will develop cancer that can be life-threatening, and 120,000 people will be killed by their cancer each year. This accounts for 25% of all deaths in the UK. However while 90% of cancer pain can be effectively treated, only 40% of patients adhere to their medicines due to poor understanding.
|
||||
Results of a recent (2016) systematic review found a large proportion of patients struggle to take their oral antineoplastic medications as prescribed. This presents opportunities and challenges for patient education, reviewing and documenting treatment plans, and patient monitoring, especially with the increase in patient cancer treatments at home.
|
||||
The reasons for non-adherence have been given by patients as follows:
|
||||
|
||||
The poor quality of information available to them about their treatment
|
||||
A lack of knowledge as to how to raise concerns whilst on medication
|
||||
Concerns about unwanted effects
|
||||
Issues about remembering to take medication
|
||||
Partridge et al (2002) identified evidence to show that adherence rates in cancer treatment are variable, and sometimes surprisingly poor. The following table is a summary of their findings:
|
||||
|
||||
Medication event monitoring system - a medication dispenser containing a microchip that records when the container is opened and from Partridge et al (2002)
|
||||
In 1998, trials evaluating Tamoxifen as a preventative agent have shown dropout rates of around one-third:
|
||||
|
||||
36% in the Royal Marsden Tamoxifen Chemoprevention Study of 1998
|
||||
29% in the National Surgical Adjuvant Breast and Bowel Project of 1998
|
||||
In March 1999, the "Adherence in the International Breast Cancer Intervention Study" evaluating the effect of a daily dose of Tamoxifen for five years in at-risk women aged 35–70 years was
|
||||
|
||||
90% after one year
|
||||
83% after two years
|
||||
74% after four years
|
||||
|
||||
=== Diabetes ===
|
||||
Patients with diabetes are at high risk of developing coronary heart disease and usually have related conditions that make their treatment regimens even more complex, such as hypertension, obesity and depression which are also characterised by poor rates of adherence.
|
||||
40
data/en.wikipedia.org/wiki/Adherence_(medicine)-4.md
Normal file
40
data/en.wikipedia.org/wiki/Adherence_(medicine)-4.md
Normal file
@ -0,0 +1,40 @@
|
||||
---
|
||||
title: "Adherence (medicine)"
|
||||
chunk: 5/5
|
||||
source: "https://en.wikipedia.org/wiki/Adherence_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:48.247796+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Diabetes non-compliance is 98% in US and the principal cause of complications related to diabetes including nerve damage and kidney failure.
|
||||
Among patients with Type 2 Diabetes, adherence was found in less than one third of those prescribed sulphonylureas and/or metformin. Patients taking both drugs achieve only 13% adherence.
|
||||
Other aspects that drive medicine adherence rates is the idea of perceived self-efficacy and risk assessment in managing diabetes symptoms and decision making surrounding rigorous medication regiments. Perceived control and self-efficacy not only significantly correlate with each other, but also with diabetes distress psychological symptoms and have been directly related to better medication adherence outcomes. Various external factors also impact diabetic patients' self-management behaviors including health-related knowledge/beliefs, problem-solving skills, and self-regulatory skills, which all impact perceived control over diabetic symptoms.
|
||||
Additionally, it is crucial to understand the decision-making processes that drive diabetics in their choices surrounding risks of not adhering to their medication. While patient decision aids (PtDAs), sets of tools used to help individuals engage with their clinicians in making decisions about their healthcare options, have been useful in decreasing decisional conflict, improving transfer of diabetes treatment knowledge, and achieving greater risk perception for disease complications, their efficacy in medication adherence has been less substantial. Therefore, the risk perception and decision-making processes surrounding diabetes medication adherence are multi-faceted and complex with socioeconomic implications as well. For example, immigrant health disparities in diabetic outcomes have been associated with a lower risk perception amongst foreign-born adults in the United States compared to their native-born counterparts, which leads to fewer protective lifestyle and treatment changes crucial for combatting diabetes. Additionally, variations in patients' perceptions of time (i.e. taking rigorous, costly medication in the present for abstract beneficial future outcomes can conflict with patients' preferences for immediate versus delayed gratification) may also present severe consequences for adherence as diabetes medication often requires systematic, routine administration.
|
||||
|
||||
=== Hypertension ===
|
||||
Hypertension non-compliance (93% in US, 70% in UK) is the main cause of uncontrolled hypertension-associated heart attack and stroke.
|
||||
In 1975, only about 50% took at least 80% of their prescribed anti-hypertensive medications.
|
||||
As a result of poor compliance, 75% of patients with a diagnosis of hypertension do not achieve optimum blood-pressure control.
|
||||
|
||||
=== Mental illness ===
|
||||
A 2003 review found that 41–59% of patients prescribed antipsychotics took the medication prescribed to them infrequently or not at all. Sometimes non-adherence is due to lack of insight, but psychotic disorders can be episodic and antipsychotics are then use prophylactically to reduce the likelihood of relapse rather than treat symptoms and in some cases individuals will have no further episodes despite not using antipsychotics. A 2006 review investigated the effects of compliance therapy for schizophrenia: and found no clear evidence to suggest that compliance therapy was beneficial for people with schizophrenia and related syndromes.
|
||||
|
||||
=== Rheumatoid arthritis ===
|
||||
A longitudinal study has shown that adherence with treatment about 60%. The predictors of adherence were found to be more of psychological, communication and logistic nature rather than sociodemographic or clinical factors. The following factors were identified as independent predictors of adherence:
|
||||
|
||||
the type of treatment prescribed
|
||||
agreement on treatment
|
||||
having received information on treatment adaptation
|
||||
clinician perception of patient trust
|
||||
|
||||
== See also ==
|
||||
Drug withdrawal
|
||||
Patient participation
|
||||
|
||||
== References ==
|
||||
|
||||
== External links ==
|
||||
Adherence to long-term therapies, a report from the World Health Organization
|
||||
Technology report on NFC enabled smart medication packages
|
||||
46
data/en.wikipedia.org/wiki/Adhesion_(medicine)-0.md
Normal file
46
data/en.wikipedia.org/wiki/Adhesion_(medicine)-0.md
Normal file
@ -0,0 +1,46 @@
|
||||
---
|
||||
title: "Adhesion (medicine)"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Adhesion_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:49.521012+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Adhesions are fibrous bands that form between tissues and organs, often as a result of irritation of internal surfaces during surgery, infections or trauma. They may be thought of as internal scar tissue that connects tissues not normally connected.
|
||||
|
||||
== Pathophysiology ==
|
||||
Adhesions form as a natural part of the body's healing process after surgery in a similar way that a scar forms. The term "adhesion" is applied when the scar extends from within one tissue across to another, usually across a virtual space such as the peritoneal cavity. Adhesion formation post-surgery typically occurs when two injured surfaces are close to one another. According to the "classical paradigm" of adhesion formation, the pathogenesis starts with inflammation and activation of the coagulation system which causes fibrin deposits onto the damaged tissues.
|
||||
The fibrin then connects the two adjacent structures where damage of the tissues occurred. The fibrin acts like a glue to seal the injury and builds the fledgling adhesion, said at this point to be "fibrinous." In body cavities such as the peritoneal, pericardial, and synovial cavities, a family of fibrinolytic enzymes may act to limit the extent of the initial fibrinous adhesion, and may even dissolve it. In many cases, the production or activity of these enzymes are compromised because of inflammation following injury or infection, however, and the fibrinous adhesion persists. A more recent study suggested that the formation of "fibrinous" adhesions is preceded by the aggregation of cavity macrophages that may act like extravascular platelets in the abdominal cavity.
|
||||
If this is allowed to happen, tissue repair cells such as macrophages, fibroblasts, and blood vessel cells penetrate into the fibrinous adhesion and lay down collagen and other matrix substances to form a permanent fibrous adhesion. In 2002, Giuseppe Martucciello's research group showed a possible role could be played by microscopic foreign bodies (FB) inadvertently contaminating the operative field during surgery. These data suggested that two different stimuli are necessary for adhesion formation: a direct lesion of the mesothelial layers and a solid substrate foreign body (FB).
|
||||
While some adhesions do not cause problems, others may prevent muscle, nerve and other tissues and organs from moving freely, sometimes causing organs to become twisted or pulled from their normal positions.
|
||||
|
||||
== Regions affected ==
|
||||
|
||||
=== Adhesive capsulitis ===
|
||||
In the case of adhesive capsulitis of the shoulder (also known as frozen shoulder), adhesions grow between the shoulder joint surfaces, restricting motion.
|
||||
|
||||
=== Abdominal adhesions ===
|
||||
Abdominal adhesions (or intra-abdominal adhesions) are most commonly caused by abdominal surgical procedures. The adhesions start to form within hours of surgery and may cause internal organs to attach to the surgical site or to other organs in the abdominal cavity. Adhesion-related twisting and pulling of internal organs may result in complications such as abdominal pain or intestinal obstruction.
|
||||
Small bowel obstruction (SBO) is a significant consequence of post-surgical adhesions. A SBO may be caused when an adhesion pulls or kinks the small intestine and prevents the flow of content through the digestive tract. Obstruction may occur 20 years or more after the initial surgical procedure, if a previously benign adhesion allows the small bowel to twist spontaneously around itself and obstruct. Without immediate medical attention, SBO is an emergent, possibly fatal, condition.
|
||||
According to statistics provided by the National Hospital Discharge Survey, approximately 2,000 people die every year in the US from obstruction due to adhesions. Depending on the severity of the obstruction, a partial obstruction may relieve itself with conservative medical intervention. Many obstructive events require surgery, however, to loosen or dissolve the offending adhesion(s) or to resect the affected small intestine.
|
||||
|
||||
=== Pelvic adhesions ===
|
||||
Pelvic adhesions are a form of abdominal adhesions in the pelvis. In women they typically affect reproductive organs and thus are of concern in reproduction or as a cause of chronic pelvic pain. Other than surgery, endometriosis and pelvic inflammatory disease are typical causes.
|
||||
Surgery inside the uterine cavity (e.g., suction dilation and curettage, myomectomy, endometrial ablation) may result in Asherman's syndrome (also known as intrauterine adhesions, intra uterine synechiae), a cause of infertility.
|
||||
The impairment of reproductive performance from adhesions may happen through many mechanisms, all of which usually stem from the distortion of the normal tubo-ovarian relationship. This distortion may prevent an ovum from traveling to the fimbriated end of the fallopian tube.
|
||||
A meta-analysis in 2012 came to the conclusion that there is only little evidence for the surgical principle that using less invasive techniques, introducing fewer foreign bodies, or causing less ischemia reduces the extent and severity of adhesions in pelvic surgery.
|
||||
|
||||
=== Pericardial adhesions ===
|
||||
Adhesions forming between the heart and the sternum after cardiac surgery place the heart at risk of catastrophic injury during re-entry for a subsequent procedure.
|
||||
|
||||
=== Peridural adhesions ===
|
||||
Adhesions and scarring as epidural fibrosis may occur after spinal surgery that restricts the free movement of nerve roots, causing tethering and leading to pain.
|
||||
|
||||
=== Peritendinous adhesions ===
|
||||
Adhesions and scarring occurring around tendons after hand surgery restrict the gliding of tendons in their sheaths and compromise digital mobility.
|
||||
|
||||
== Association with surgical procedures ==
|
||||
Applying adhesion barriers during surgery may help to prevent the formation of adhesions. There are two methods that are approved by the U.S. Food and Drug Administration (FDA) for adhesion prevention: Intercede and Seprafilm. One study found that Seprafilm is twice as effective at preventing adhesion formation when compared to just surgical technique alone. Surgical humidification therapy may also minimise the incidence of adhesion formation. Laparoscopic surgery has a reduced risk for creating adhesions. Steps may be taken during surgery to help prevent adhesions such as handling tissues and organs gently, using starch-free and latex-free gloves, not allowing tissues to dry out, and shortening surgery time.
|
||||
An unfortunate fact is, that adhesions are unavoidable in surgery and a treatment for adhesions is more surgery. Besides intestinal obstructions caused by adhesions that may be seen in an X-ray, there are no diagnostic tests available to accurately diagnose an adhesion.
|
||||
27
data/en.wikipedia.org/wiki/Adhesion_(medicine)-1.md
Normal file
27
data/en.wikipedia.org/wiki/Adhesion_(medicine)-1.md
Normal file
@ -0,0 +1,27 @@
|
||||
---
|
||||
title: "Adhesion (medicine)"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Adhesion_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:49.521012+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Abdominal surgery ===
|
||||
A study showed that more than 90% of people develop adhesions following open abdominal surgery and that 55–100% of women develop adhesions following pelvic surgery. Adhesions from prior abdominal or pelvic surgery may obscure visibility and access at subsequent abdominal or pelvic surgery. In a very large study (29,790 participants) published in British medical journal The Lancet, 35% of patients who underwent open abdominal or pelvic surgery were readmitted to the hospital an average of two times after their surgery, due to adhesion-related or adhesion-suspected complications. Over 22% of all readmissions occurred in the first year after the initial surgery. Adhesion-related complexity at reoperation adds significant risk to subsequent surgical procedures.
|
||||
Certain organs and structures in the body are more prone to adhesion formation than others. The omentum is particularly susceptible to adhesion formation; one study found that 92% of post-operative adhesions were found in the omentum. It appears that the omentum is the chief organ responsible for "spontaneous" adhesion formation (i.e. no prior history of surgery). In another study, 100% of spontaneous adhesion formations were associated with the omentum.
|
||||
One method to reduce the formation of adhesions following abdominal surgery is hydroflotation, in which the organs are separated from one another by being floated in a solution.
|
||||
|
||||
=== Carpal tunnel surgery ===
|
||||
The long-term use of a wrist splint during recovery from carpal tunnel surgery may cause adhesion formation. For that reason, it is advised that wrist splints be used only for short-term protection in work environments, but otherwise, splints do not improve grip strength, lateral pinch strength, or bowstringing. Beyond adhesion they also may cause stiffness or flexibility problems.
|
||||
|
||||
== Types ==
|
||||
There are three general types of adhesions: filmy, vascular, and cohesive, however, their pathophysiology is similar. Filmy adhesions usually do not pose problems. Vascular adhesions are problematic.
|
||||
|
||||
== References ==
|
||||
|
||||
== External links ==
|
||||
|
||||
eMedicineHealth: Adhesions, General and After Surgery
|
||||
Smith, Orla M., Getting adhesions unstuck, Science, November 30, 2018, volume 362, issue 6418, pp. 1014-1016
|
||||
142
data/en.wikipedia.org/wiki/Admission_note-0.md
Normal file
142
data/en.wikipedia.org/wiki/Admission_note-0.md
Normal file
@ -0,0 +1,142 @@
|
||||
---
|
||||
title: "Admission note"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Admission_note"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:50.831652+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
An admission note is part of a medical record that documents the patient's status (including history and physical examination findings), reasons why the patient is being admitted for inpatient care to a hospital or other facility, and the initial instructions for that patient's care.
|
||||
|
||||
|
||||
== Purpose ==
|
||||
Admission notes document the reasons why a patient is being admitted for inpatient care to a hospital or other facility, the patient's baseline status, and the initial instructions for that patient's care. Health care professionals use them to record a patient's baseline status and may write additional on-service notes, progress notes (SOAP notes), preoperative notes, operative notes, postoperative notes, procedure notes, delivery notes, postpartum notes, and discharge notes. These notes constitute a large part of the medical record. Medical students often develop their clinical reasoning skills by writing admission notes. The traditional, rational definition of being admitted usually involves spending an overnight in the hospital. This definition is sometimes stretched in the U.S. medical billing industry, where hospital corporations may blur the definitions of "admission" and "observation" because of reimbursement rules under which healthcare payors pay less for the care if an "admission" was involved.
|
||||
|
||||
|
||||
== Components ==
|
||||
An admission note may sometimes be incorrectly referred to as an HPI (history of present illness) or H and P (history and physical), which include only portions of an admission note.
|
||||
An admission note can include the following sections:
|
||||
|
||||
|
||||
== Outline ==
|
||||
Not every admission note explicitly discusses every item listed below, however, the ideal admission note would include:
|
||||
|
||||
|
||||
=== Header ===
|
||||
Patient identifying information (maybe located separately)
|
||||
name
|
||||
ID number
|
||||
chart number
|
||||
room number
|
||||
date of birth
|
||||
attending physician
|
||||
sex
|
||||
admission date
|
||||
Date
|
||||
Time
|
||||
Service
|
||||
|
||||
|
||||
=== Chief complaint (CC) ===
|
||||
|
||||
Typically one sentence including
|
||||
|
||||
age
|
||||
race
|
||||
sex
|
||||
presenting complaint
|
||||
example: "34 yo white male with right-sided weakness and slurred speech."
|
||||
|
||||
|
||||
=== History of present illness (HPI) ===
|
||||
|
||||
statement of health status
|
||||
detailed description of chief complaint
|
||||
positive and negative symptoms related to the chief complaint based on the differential diagnosis the health care provider has developed.
|
||||
emergency actions taken and patient responses if relevant
|
||||
|
||||
|
||||
=== Allergies ===
|
||||
|
||||
first antigen and response
|
||||
second antigen and response
|
||||
etc.
|
||||
|
||||
|
||||
=== Past medical history (PMHx) ===
|
||||
List of the patient's on-going medical problems. Chronic problems should be addressed as to whether or not they are well controlled or uncontrolled. Include dates of pertinent items.
|
||||
|
||||
|
||||
=== Past surgical history (PSurgHx, PSxHx) ===
|
||||
List of surgeries in the past with dates of pertinent items.
|
||||
|
||||
|
||||
=== Family history (FmHx) ===
|
||||
|
||||
Health or cause of death for:
|
||||
|
||||
Parents
|
||||
Siblings
|
||||
Children
|
||||
Spouse
|
||||
|
||||
|
||||
=== Social history (SocHx) ===
|
||||
|
||||
In medicine, a social history is a portion of the admission note addressing familial, occupational, and recreational aspects of the patient's personal life that have the potential to be clinically significant.
|
||||
|
||||
|
||||
=== Medications ===
|
||||
|
||||
for each: generic name - amount - rate
|
||||
medications on arrival (aspirin, Goody's medicated powder, herbal remedies, prescriptions, etc.)
|
||||
medications on transfer
|
||||
|
||||
|
||||
=== Review of systems (ROS) ===
|
||||
|
||||
General
|
||||
Head
|
||||
Eyes
|
||||
Ears
|
||||
Nose and sinuses
|
||||
Throat, mouth, and neck
|
||||
Breasts
|
||||
Cardiovascular system
|
||||
Respiratory system
|
||||
Gastrointestinal system
|
||||
Urinary system
|
||||
Genital system
|
||||
Vascular system
|
||||
Musculoskeletal system
|
||||
Nervous system
|
||||
Psychiatric
|
||||
Hematologic system
|
||||
Endocrine system
|
||||
|
||||
|
||||
=== Physical exam ===
|
||||
|
||||
Physical examination or clinical examination is the process by which a health care provider investigates the body of a patient for signs of disease.
|
||||
|
||||
|
||||
=== Labs ===
|
||||
e.g.: electrolytes, arterial blood gases, liver function tests, etc.
|
||||
|
||||
|
||||
=== Diagnostics ===
|
||||
e.g.: EKG, CXR, CT, MRI
|
||||
|
||||
|
||||
=== Assessment and plan ===
|
||||
|
||||
Assessment includes a discussion of the differential diagnosis and supporting history and exam findings.
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== See also ==
|
||||
Admitting privileges
|
||||
28
data/en.wikipedia.org/wiki/Adrenergic_storm-0.md
Normal file
28
data/en.wikipedia.org/wiki/Adrenergic_storm-0.md
Normal file
@ -0,0 +1,28 @@
|
||||
---
|
||||
title: "Adrenergic storm"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Adrenergic_storm"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:52.151132+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
An adrenergic storm is a sudden and dramatic increase in serum levels of the catecholamines adrenaline and noradrenaline (also known as epinephrine and norepinephrine respectively), with a less significant increase in dopamine transmission. It is a life-threatening condition because of extreme tachycardia and hypertension, and is especially dire for those with prior heart problems. If treatment is prompt, prognosis is good; typically large amounts of diazepam or other benzodiazepines are administered alongside beta blockers. Beta blockers are contraindicated in some patients, so other antihypertensive medication such as clonidine may be used.
|
||||
Antipsychotics are also used to treat the most severe psychiatric reactions such as psychosis, paranoia or terror, after their use was formerly discouraged because of their potential to prolong the QT interval; however, more recent research performed since 2019 has revealed that this and other severe side effects are rare and their occurrence does not warrant banning antipsychotics from the treatment of adrenergic crises for which they can be extremely useful.
|
||||
Adrenergic storms are usually caused by overdoses of stimulants, especially cocaine or methamphetamine, or eating foods high in tyramine while taking monoamine oxidase inhibitors. A subarachnoid hemorrhage can also cause an adrenergic storm. A catecholamine storm is part of the normal course of rabies infection, and is responsible for the severe feelings of agitation, terror, and dysautonomia present in the pre-coma stage of the disease.
|
||||
|
||||
== Signs and symptoms ==
|
||||
The behavioral symptoms are similar to those of an amphetamine, cocaine, or caffeine overdose. Overstimulation of the central nervous system results in a state of hyperkinetic movement and unpredictable mental status including mania, rage and suicidal behavior; hyperthermia is also prominently present. Delirium can also be present but rarely.
|
||||
Physical symptoms are more serious and include heart arrhythmias as well as outright heart attack or stroke in people who are at risk of coronary disease. Breathing is rapid and shallow while both pulse and blood pressure are dangerously elevated.
|
||||
Other complications would include rhabdomyolysis, a breakdown of the voluntary muscles because of the excessive physical movement, causing the components of the muscle, most notably myoglobin, to be released into the bloodstream and then clog the kidneys, causing renal failure. In all, rhabdomyolysis is especially common in adrenergic storms caused by the use of stimulant drugs, most notably those of the phenethylamines such as cathinones or amphetamines.
|
||||
|
||||
== Causes ==
|
||||
There are several known causes of adrenergic storms; in the United States, cocaine overdose is the leading cause. Any stimulant drug has the capacity to cause this syndrome if taken in sufficient doses, but even non-psychotropic drugs can very rarely provoke a reaction.
|
||||
Monoamine oxidase inhibitors (MAOIs) are a class of drugs that inhibit the enzyme monoamine oxidase. This enzyme is responsible for breaking down many compounds; basically, anything with a primary amine moiety is likely to be oxidized by monoamine oxidase. An important substrate of the enzyme MAO is tyramine. MAOIs inhibit the enzyme either reversibly, in which MAO is inhibited only until the drug is cleared from the system, or irreversibly, in which the substrate binds permanently to the enzyme, rendering it inactive and effectively destroying it. Irreversible MAOIs are potentially more dangerous, because the body takes about two weeks to regenerate MAO enzymes to functional levels. Two subtypes of MAO exist: MAO-A and MAO-B; this is relevant to adrenergic storms, as there are significant differences between the two types, such as their differential expression throughout the body, and range of substrates. While both MAO-A and MAO-B metabolize tyramine, only MAO-A is present in the gastrointestinal tract and singularly metabolizes the majority of consumed tyramine. (The small portion normally passing into circulation is mostly degraded in the liver where both MAO types act.)
|
||||
Subarachnoid hemorrhage is an extremely serious condition in which a neural membrane is breached and the brain itself is compromised. The onset is sudden, described as "the worst headache of one's life," and many grave symptoms follow. Adrenergic storm is often present among these symptoms, and is responsible for some of the dangers, both long-term and short, of subarachnoid hemorrhage adrenergic storm, through a complex cascade of processes starting with the movement of subarachnoid blood into the brain. Apparently, as the intracranial pressure increases, the brain is squeezed and catecholamines are forced out of their vesicles into the synapses and extracellular space.
|
||||
|
||||
=== Rare causes ===
|
||||
Rarely, a pheochromocytoma (tumor of the medullar tissue of the adrenal glands, which are located anterior to the kidney), may result in an adrenergic storm. This type of tumor is not common to begin with, and furthermore, the subtype that can cause massive adrenaline release is rarer still. Patients with pheochromocytoma can unexpectedly fly into a rage or sink into trembling fear, possibly dangerous to themselves and others as their judgment is impaired, their senses and pain threshold are heightened, and the level of the adrenaline in their bloodstream is more than most people ever experience; pheochromocytoma can, very rarely, kill by internal adrenaline overdose. But overall, adrenergic storm is an uncommon but certainly not rare phenomenon associated with the also uncommon condition of pheochromocytoma.
|
||||
|
||||
== Diagnosis ==
|
||||
27
data/en.wikipedia.org/wiki/Adrenergic_storm-1.md
Normal file
27
data/en.wikipedia.org/wiki/Adrenergic_storm-1.md
Normal file
@ -0,0 +1,27 @@
|
||||
---
|
||||
title: "Adrenergic storm"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Adrenergic_storm"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:52.151132+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Differential diagnosis ===
|
||||
Because the adrenergic storm overlaps with so many other similar conditions, such as hypertensive crises, stimulant intoxication or overdose, or even panic attack, and because the treatments for these overlapping conditions are largely alike, it is not necessary to obtain a differential and definitive diagnosis before initiating treatment. However, analysis of the patient's medical history, checked against the possible causes of the adrenergic storm such as those above, should be done, because some adrenergic storms can be caused by serious underlying conditions. If a patient has an adrenergic storm and all or most of the other factors are ruled out, the adrenergic storm could lead to the discovery of a pheochromocytoma, which can become malignant. However, not all cases of adrenergic storm have an identifiable cause.
|
||||
Serotonin syndrome, in which an excess of serotonin in the synapses causes a similar crisis of hypertension and mental confusion, could be confused with an adrenergic storm. Serotonin, being a tryptamine (non-catecholamine) involved in higher brain functions, can cause dangerous hypertension and tachycardia from its effects on the sympathetic nervous system. Symptoms caused by excessive adrenergic signalling can occur alongside those of serotonergic signalling. Abnormal echocardiograms or chest pain are indicative of adrenergic storm. On the other hand, uncontrollable slow, rhythmic, or jerky movements, contractions and tension—often in every part of the body, dangerously high fever, eye rolling, and bruxism are more indicative of serotonin syndrome.
|
||||
|
||||
== Treatment ==
|
||||
If there is evidence of overdose or it is suspected, the patient should be given gastric lavage, activated charcoal, or both; this could make the difference between life and death in a close situation. It can however aggravate the patient which should be taken into account.
|
||||
The first-line treatments are diazepam and a non-selective beta blocker; other antihypertensive drugs may also be used. It is important to note that not all benzodiazepines and beta blockers are safe to use in an adrenergic storm; for instance, alprazolam and propranolol; alprazolam weakly agonizes dopamine receptors and causes catecholamine release while propranolol mildly promotes some catecholamine release – each worsening the condition.
|
||||
Antipsychotics are also used to treat the psychiatric symptoms such as aggression, agitation, psychosis, paranoia, or anxiety. Originally, the use of antipsychotics was discouraged because of their potential to prolong the QT interval; however, newer research has revealed that their careful use does not carry the potential for any significant side effects and today their judicious use is encouraged.
|
||||
Adrenergic storms are often idiopathic in nature; however if there is an underlying condition, then that must be addressed after bringing the heart rate and blood pressure down.
|
||||
|
||||
== See also ==
|
||||
Adrenal crisis
|
||||
Paroxysmal sympathetic hyperactivity
|
||||
Sympathomimetic drug
|
||||
Takotsubo cardiomyopathy
|
||||
|
||||
== References ==
|
||||
38
data/en.wikipedia.org/wiki/Adverse_effect-0.md
Normal file
38
data/en.wikipedia.org/wiki/Adverse_effect-0.md
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@ -0,0 +1,38 @@
|
||||
---
|
||||
title: "Adverse effect"
|
||||
chunk: 1/3
|
||||
source: "https://en.wikipedia.org/wiki/Adverse_effect"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:53.424672+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
An adverse effect is an undesired harmful effect resulting from a medication or other intervention, such as surgery. An adverse effect may be termed a "side effect", when judged to be secondary to a main or therapeutic effect. The term complication is similar to adverse effect, but the latter is typically used in pharmacological contexts, or when the negative effect is expected or common. If the negative effect results from an unsuitable or incorrect dosage or procedure, this is called a medical error and not an adverse effect. Adverse effects are sometimes referred to as "iatrogenic" because they are generated by a physician/treatment. Some adverse effects occur only when starting, increasing or discontinuing a treatment.
|
||||
Using a drug or other medical intervention which is contraindicated may increase the risk of adverse effects. Adverse effects may cause complications of a disease or procedure and negatively affect its prognosis. They may also lead to non-compliance with a treatment regimen. Adverse effects of medical treatment resulted in 142,000 deaths in 2013 up from 94,000 deaths in 1990 globally.
|
||||
The harmful outcome is usually indicated by some result such as morbidity, mortality, alteration in body weight, levels of enzymes, loss of function, or as a pathological change detected at the microscopic, macroscopic or physiological level. It may also be indicated by symptoms reported by a patient. Adverse effects may cause a reversible or irreversible change, including an increase or decrease in the susceptibility of the individual to other chemicals, foods, or procedures, such as drug interactions.
|
||||
|
||||
== Classification ==
|
||||
In terms of drugs, adverse events may be defined as: "Any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment."
|
||||
In clinical trials, a distinction
|
||||
is made between an adverse event and a serious adverse event. Generally, any event which causes death, permanent damage, birth defects, or requires hospitalization is considered a serious adverse event. The results of trials are often included in the labelling of the medication to provide information both for patients and the prescribing physicians.
|
||||
The term "life-threatening" in the context of a serious adverse event refers to an event in which the patient was at risk of death at the time of the event; it does not refer to an event which hypothetically might have caused death if it were more severe.
|
||||
|
||||
== Reporting systems ==
|
||||
In many countries, adverse effects are required by law to be reported, researched in clinical trials and included into the patient information accompanying medical devices and drugs for sale to the public. Investigators in human clinical trials are obligated to report these events in clinical study reports. Research suggests that these events are often inadequately reported in publicly available reports. Because of the lack of these data and uncertainty about methods for synthesising them, individuals conducting systematic reviews and meta-analyses of therapeutic interventions often unknowingly overemphasise health benefit. To balance the overemphasis on benefit, scholars have called for more complete reporting of harm from clinical trials.
|
||||
|
||||
=== United Kingdom ===
|
||||
The Yellow Card Scheme is a United Kingdom initiative run by the Medicines and Healthcare products Regulatory Agency (MHRA) and the Commission on Human Medicines (CHM) to gather information on adverse effects to medicines. This includes all licensed medicines, from medicines issued on prescription to medicines bought over the counter from a supermarket. The scheme also includes all herbal supplements and unlicensed medicines found in cosmetic treatments. Adverse drug reactions (ADRs) can be reported by a number of health care professionals including physicians, pharmacists and nurses, as well as patients.
|
||||
|
||||
=== United States ===
|
||||
In the United States several reporting systems have been built, such as the Vaccine Adverse Event Reporting System (VAERS), the Manufacturer and User Facility Device Experience Database (MAUDE) and the Special Nutritionals Adverse Event Monitoring System. MedWatch is the main reporting center, operated by the Food and Drug Administration.
|
||||
|
||||
=== Australia ===
|
||||
In Australia, adverse effect reporting is administered by the Adverse Drug Reactions Advisory Committee (ADRAC), a subcommittee of the Australian Drug Evaluation Committee (ADEC). Reporting is voluntary, and ADRAC requests healthcare professionals to report all adverse reactions to its current drugs of interest, and serious adverse reactions to any drug. ADRAC publishes the Australian Adverse Drug Reactions Bulletin every two months. The Government's Quality Use of Medicines program is tasked with acting on this reporting to reduce and minimize the number of preventable adverse effects each year.
|
||||
|
||||
=== New Zealand ===
|
||||
Adverse reaction reporting is an important component of New Zealand's pharmacovigilance activities. The Centre for Adverse Reactions Monitoring (CARM) in Dunedin is New Zealand's national monitoring centre for adverse reactions. It collects and evaluates spontaneous reports of adverse reactions to medicines, vaccines, herbal products and dietary supplements from health professionals in New Zealand. Currently the CARM database holds over 80,000 reports and provides New Zealand-specific information on adverse reactions to these products, and serves to support clinical decision making when unusual symptoms are thought to be therapy related
|
||||
|
||||
=== Canada ===
|
||||
In Canada, adverse reaction reporting is an important component of the surveillance of marketed health products conducted by the Health Products and Food Branch (HPFB) of Health Canada. Within HPFB, the Marketed Health Products Directorate leads the coordination and implementation of consistent monitoring practices with regards to assessment of signals and safety trends, and risk communications concerning regulated marketed health products.
|
||||
MHPD also works closely with international organizations to facilitate the sharing of information. Adverse reaction reporting is mandatory for the industry and voluntary for consumers and health professionals.
|
||||
29
data/en.wikipedia.org/wiki/Adverse_effect-1.md
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29
data/en.wikipedia.org/wiki/Adverse_effect-1.md
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@ -0,0 +1,29 @@
|
||||
---
|
||||
title: "Adverse effect"
|
||||
chunk: 2/3
|
||||
source: "https://en.wikipedia.org/wiki/Adverse_effect"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:53.424672+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Limitations ===
|
||||
In principle, medical professionals are required to report all adverse effects related to a specific form of therapy. In practice, it is at the discretion of the professional to determine whether a medical event is at all related to the therapy. As a result, routine adverse effects reporting often may not include long-term and subtle effects that may ultimately be attributed to a therapy.
|
||||
Part of the difficulty is identifying the source of a complaint. A headache in a patient taking medication for influenza may be caused by the underlying disease or may be an adverse effect of the treatment. In patients with end-stage cancer, death is a very likely outcome and whether the drug is the cause or a bystander is often difficult to discern.
|
||||
|
||||
== By situation ==
|
||||
|
||||
=== Medical procedures ===
|
||||
Surgery may have a number of undesirable or harmful effects, such as infection, hemorrhage, inflammation, scarring, loss of function, or changes in local blood flow. They can be reversible or irreversible, and a compromise must be found by the physician and the patient between the beneficial or life-saving consequences of surgery versus its adverse effects. For example, a limb may be lost to amputation in case of untreatable gangrene, but the patient's life is saved. Presently, one of the greatest advantages of minimally invasive surgery, such as laparoscopic surgery, is the reduction of adverse effects.
|
||||
Other nonsurgical physical procedures, such as high-intensity radiation therapy, may cause burns and alterations in the skin. In general, these therapies try to avoid damage to healthy tissues while maximizing the therapeutic effect.
|
||||
Vaccination may have adverse effects due to the nature of its biological preparation, sometimes using attenuated pathogens and toxins. Common adverse effects may be fever, malaise and local reactions in the vaccination site. Very rarely, there is a serious adverse effect, such as eczema vaccinatum, a severe, sometimes fatal complication which may result in persons who have eczema or atopic dermatitis.
|
||||
Diagnostic procedures may also have adverse effects, depending much on whether they are invasive, minimally invasive or noninvasive. For example, allergic reactions to radiocontrast materials often occur, and a colonoscopy may cause the perforation of the intestinal wall.
|
||||
|
||||
=== Medications ===
|
||||
|
||||
Adverse effects can occur as a collateral or side effect of many interventions, but they are particularly important in pharmacology, due to its wider, and sometimes uncontrollable, use by way of self-medication. Thus, responsible drug use becomes an important issue here. Adverse effects, like therapeutic effects of drugs, are a function of dosage or drug levels at the target organs, so they may be avoided or decreased by means of careful and precise pharmacokinetics, the change of drug levels in the organism in function of time after administration.
|
||||
Adverse effects may also be caused by drug interaction. This often occurs when patients fail to inform their physician and pharmacist of all the medications they are taking, including herbal and dietary supplements. The new medication may interact agonistically or antagonistically (potentiate or decrease the intended therapeutic effect), causing significant morbidity and mortality around the world. Drug-drug and food-drug interactions may occur, and so-called "natural drugs" used in alternative medicine can have dangerous adverse effects. For example, extracts of St John's wort (Hypericum perforatum), a phytotherapic used for treating mild depression are known to cause an increase in the cytochrome P450 enzymes responsible for the metabolism and elimination of many drugs, so patients taking it are likely to experience a reduction in blood levels of drugs they are taking for other purposes, such as cancer chemotherapeutic drugs, protease inhibitors for HIV and hormonal contraceptives.
|
||||
The scientific field of activity associated with drug safety is increasingly government-regulated, and is of major concern for the public, as well as to drug manufacturers. The distinction between adverse and nonadverse effects is a major undertaking when a new drug is developed and tested before marketing it. This is done in toxicity studies to determine the nonadverse effect level (NOAEL). These studies are used to define the dosage to be used in human testing (phase I), as well as to calculate the maximum admissible daily intake. Imperfections in clinical trials, such as insufficient number of patients or short duration, sometimes lead to public health disasters, such as those of fenfluramine (the so-called fen-phen episode), thalidomide and, more recently, of cerivastatin (Baycol, Lipobay) and rofecoxib (Vioxx), where drastic adverse effects were observed, such as teratogenesis, pulmonary hypertension, stroke, heart disease, neuropathy, and a significant number of deaths, causing the forced or voluntary withdrawal of the drug from the market.
|
||||
Most drugs have a large list of nonsevere or mild adverse effects which do not rule out continued usage. These effects, which have a widely variable incidence according to individual sensitivity, include nausea, dizziness, diarrhea, malaise, vomiting, headache, dermatitis, dry mouth, etc. These can be considered a form of pseudo-allergic reaction, as not all users experience these effects; many users experience none at all.
|
||||
The Medication Appropriateness Tool for Comorbid Health Conditions in Dementia (MATCH-D) warns that people with dementia are more likely to experience adverse effects, and that they are less likely to be able to reliably report symptoms.
|
||||
58
data/en.wikipedia.org/wiki/Adverse_effect-2.md
Normal file
58
data/en.wikipedia.org/wiki/Adverse_effect-2.md
Normal file
@ -0,0 +1,58 @@
|
||||
---
|
||||
title: "Adverse effect"
|
||||
chunk: 3/3
|
||||
source: "https://en.wikipedia.org/wiki/Adverse_effect"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:53.424672+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
==== Examples with specific medications ====
|
||||
Abortion, miscarriage or uterine hemorrhage associated with misoprostol (Cytotec), a labor-inducing drug (this is a case where the adverse effect has been used legally and illegally for performing abortions)
|
||||
Addiction to many sedatives and analgesics, such as diazepam, morphine, etc.
|
||||
Birth defects associated with thalidomide
|
||||
Bleeding of the intestine associated with aspirin therapy
|
||||
Cardiovascular disease associated with COX-2 inhibitors (i.e. Vioxx)
|
||||
Deafness and kidney failure associated with gentamicin (an antibiotic)
|
||||
Death, following sedation, in children using propofol (Diprivan)
|
||||
Depression or hepatic injury caused by interferon
|
||||
Diabetes caused by atypical antipsychotic medications (neuroleptic psychiatric drugs)
|
||||
Diarrhea caused by the use of orlistat (Xenical)
|
||||
Erectile dysfunction associated with many drugs, such as antidepressants
|
||||
Fever associated with vaccination
|
||||
Glaucoma associated with corticosteroid-based eye drops
|
||||
Hair loss and anemia may be caused by chemotherapy against cancer, leukemia, etc.
|
||||
Headache following spinal anaesthesia
|
||||
Hypertension in ephedrine users, which prompted FDA to remove the dietary supplement status of ephedra extracts
|
||||
Insomnia caused by stimulants, methylphenidate (Ritalin), Adderall, etc.
|
||||
Lactic acidosis associated with the use of stavudine (Zerit, for HIV therapy) or metformin (for diabetes)
|
||||
Mania caused by corticosteroids
|
||||
Liver damage from paracetamol
|
||||
Melasma and thrombosis associated with use of estrogen-containing hormonal contraception, such as the combined oral contraceptive pill
|
||||
Priapism associated with the use of sildenafil
|
||||
Rhabdomyolysis associated with statins (anticholesterol drugs)
|
||||
Seizures caused by withdrawal from benzodiazepines
|
||||
Drowsiness or increase in appetite due to antihistamine use. Some antihistamines are used in sleep aids explicitly because they cause drowsiness.
|
||||
Stroke or heart attack associated with sildenafil (Viagra), when used with nitroglycerin
|
||||
Suicide, increased tendency associated to the use of fluoxetine and other selective serotonin reuptake inhibitor (SSRI) antidepressants
|
||||
Tardive dyskinesia associated with use of metoclopramide and many antipsychotic medications
|
||||
|
||||
== Controversies ==
|
||||
Sometimes, putative medical adverse effects are regarded as controversial and generate heated discussions in society and lawsuits against drug manufacturers. One example is the recent controversy as to whether autism was linked to the MMR vaccine (or to thiomersal, a mercury-based preservative used in some vaccines). No link has been found in several large studies, and despite removal of thimerosal from most early childhood vaccines beginning with those manufactured in 2003, the rate of autism has not decreased as would be expected if it had been the causative agent.
|
||||
Another instance is the potential adverse effects of silicone breast implants, which led to class actions brought by tens of thousands of plaintiffs against manufacturers of gel-based implants, due to allegations of damage to the immune system which have not yet been conclusively proven. In 1998, Dow Corning settled its remaining suits for $3.2 Billion and went into bankruptcy.
|
||||
Due to the exceedingly high impact on public health of widely used medications, such as hormonal contraception and hormone replacement therapy, which may affect millions of users, even marginal probabilities of adverse effects of a severe nature, such as breast cancer, have led to public outcry and changes in medical therapy, although its benefits largely surpassed the statistical risks.
|
||||
|
||||
== See also ==
|
||||
|
||||
== References ==
|
||||
|
||||
== External links ==
|
||||
|
||||
Patient Safety Network – includes a glossary and articles on adverse effects, drug reactions, medical error, iatrogenesis, among others.
|
||||
Australian Adverse Drug Reactions Bulletin – published bimonthly
|
||||
MedEffect Canada (Health Canada)
|
||||
Medication Errors—from the U.S. Food and Drug Administration.
|
||||
Medical Product Safety Information – MedWatch lists safety alerts for drugs, biologics, devices and dietary supplements, recalls, market withdrawals, public health advisories and links
|
||||
Medical Devices Safety National Library of Medicine (Medline Plus, useful lists of conventional drug and medical device articles and websites)
|
||||
When Medicine Hurts Instead of Helps – June 1998 report by the Alliance for Aging Research.
|
||||
42
data/en.wikipedia.org/wiki/Adverse_outcome_pathway-0.md
Normal file
42
data/en.wikipedia.org/wiki/Adverse_outcome_pathway-0.md
Normal file
@ -0,0 +1,42 @@
|
||||
---
|
||||
title: "Adverse outcome pathway"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Adverse_outcome_pathway"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:55.006766+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
An adverse outcome pathway (AOP) is structured representation of biological events leading to adverse effects and is considered relevant to risk assessment. The AOP links in a linear way existing knowledge along one or more series of causally connected key events (KE) between two points — a molecular initiating event (MIE) and an adverse outcome (AO) that occur at a level of biological organization relevant to risk assessment. The linkage between the events is described by key event relationships (KER) that describe the causal relationships between the key events.
|
||||
AOPs are important for expanding the use of mechanistic toxicological data for risk assessment and regulatory applications with recent applications in further disciplines such as climate science.
|
||||
|
||||
|
||||
== Background ==
|
||||
In 2012, the Organisation for Economic Co-operation and Development (OECD) launched a new programme on the development of adverse outcome pathways. A guidance document describes in detail how AOPs are to be developed, reviewed, agreed and published at the OECD level. The AOP development and reviewing workflow is intended to take place via a web-based IT management tool: the Adverse Outcome Pathway Knowledge Base (AOP-KB) which is currently still under development. It is the wiki-based, user-friendly tool providing open-source interface for collaborative sharing of established AOPs and building new AOPs.
|
||||
The AOP-KB gives the scientific community the possibility to enter, share and discuss their AOP-related knowledge at one central point of information.
|
||||
The AOP-KB allows for building AOPs by entering and then linking information about MIEs, KEs, AOs and Chemical Initiators.
|
||||
Knowing that pathway elements are not necessarily unique to a single AOP, value is added to existing knowledge by facilitating the re-use of MIE, KE and AO information in multiple AOPs, which prevents redundancy and make the collective knowledge about those entities available in all AOPs in which they appear.
|
||||
The AOP-KB is a combination of individually developed applications, synchronised and orchestrated in a way that gives users the possibility to capture, review, browse and comment on AOPs shared by the AOP stakeholder community.
|
||||
The AOP-KB project is an Organisation for Economic Co-operation and Development initiative, which is executed as close collaboration between the Joint Research Centre of European Commission, the United States Environmental Protection Agency and the Engineer Research and Development Center of United States Army Corps of Engineers for the purpose of the Organisation for Economic Co-operation and Development's programme on the development of AOPs
|
||||
The AOP has also been recently applied to better understand the effects of climate related stressors, further expanding the potential of AOPs to other scientific disciplines
|
||||
More recent developments have focused on the analysis of AOP networks and the quantification of KERs with a view to developing mathematical models of AOPs, sometimes referred to as quantitative AOPs.
|
||||
Scientific workshops held for advancing the concept of AOP:
|
||||
|
||||
2013
|
||||
January 23–25, Baltimore, USA Building Shared Experience to Advance Practical Application of Pathway-Based Toxicology:Liver Toxicity Mode-of-Action
|
||||
2014
|
||||
March 2–7, Somma Lombardo, Italy Advancing Adverse Outcome Pathways (AOP) for Integrated Toxicology and Regulatory Applications
|
||||
August 24, Prague, Czech Republic AOPs 101: The How and Why of Development and Use
|
||||
September 3–5, Bethesda, USA Adverse Outcome Pathways: From Research to Regulation workshop held by NTP Interagency Center for the Evaluation of Alternative Toxicological Methods (NICEATM) and the Physicians Committee for Responsible Medicine. Materials from the workshop, including links to the plenary session videocasts and summaries of the breakout group discussions, are available on the NTP website
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
AOP KB Homepage
|
||||
OECD Adverse Outcome Pathways, Molecular Screening and Toxicogenomics Programme on the development of AOPs
|
||||
European Commission's Joint Research Centre
|
||||
Adverse Outcome Pathways: From Research to Regulation
|
||||
NTP Interagency Center for the Evaluation of Alternative Toxicological Methods
|
||||
27
data/en.wikipedia.org/wiki/Age_of_onset-0.md
Normal file
27
data/en.wikipedia.org/wiki/Age_of_onset-0.md
Normal file
@ -0,0 +1,27 @@
|
||||
---
|
||||
title: "Age of onset"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Age_of_onset"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:56.198547+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
The age of onset is the age at which an individual acquires, develops, or first experiences a condition or symptoms of a disease or disorder. For instance, the general age of onset for the spinal disease scoliosis is "10-15 years old," meaning that most people develop scoliosis when they are of age between ten and fifteen years.
|
||||
Diseases are often categorized by their age of onset as congenital, infantile, juvenile, or adult. Missed or delayed diagnosis often occurs if a disease that is typically diagnosed in juveniles (such as asthma) is present in adults, and vice versa (such as arthritis). Depending on the disease, ages of onset may impact features such as phenotype, as is the case in Parkinson's and Huntington's diseases. For example, the phenotype for juvenile Huntington's disease clearly differs from adult-onset Huntington's disease and late-onset Parkinson's exhibits more severe motor and non-motor phenotypes.
|
||||
|
||||
|
||||
== Causes ==
|
||||
Germ-line mutations are often at least in part the cause of disease onset at an earlier age. Though many germ-line mutations are deleterious, the genetic lens through which they may be viewed may provide insights to treatment, possibly through genetic counseling.
|
||||
In some cases, the age of onset may be the result of mutation accumulation. If this is the case, it could be helpful to consider ages of onset as a product of the hypotheses depicted in theories of aging. Even some mental health disorders, whose ages of onset have been found to be harder to define than physical illnesses may have a mutated component. The symptoms of standard mental disorders often start off non-specific. Pathological changes pertaining to disorders often become more detailed and less fickle before they can be defined in the American Psychiatric Association's DSM. The brain is a dynamic and complex system, it is constantly re-wiring itself and a major concern is what happens to the brain in earlier life that mirrors what occurs later in its psycho-pathological state. The typical onset of many mental disorders in late adolescence may reflect the critical development that happens at this time.
|
||||
|
||||
|
||||
== Theories of Aging ==
|
||||
The rate-of-living theory of aging states that senescence occurs because individuals accumulate damage to cells and tissues during cell division. This theory is not supported because its postulates that aging rate should be correlated with metabolic rate and organisms cannot evolve longer lifespans were not supported in trials. The rate-of-living theory may not be used to draw conclusions about age of onset based on this.
|
||||
There are two subsets to the evolutionary theory of aging: antagonistic pleiotropy hypothesis and the mutation accumulation hypothesis.
|
||||
The antagonistic pleiotropy hypothesis was tested by monitoring the age-1 gene in C. elegans. The age-1 gene plays a role in senescence; nematodes with mutations in this gene live up to 80% longer. Mutants in the age-1 gene for allele hx546 seem to be otherwise normal until placed under stressful conditions. Then, the carriers of the mutant gene appear to be at disadvantage—they do not lay eggs while being starved. This evidence supports antagonistic pleiotropy as a theory of aging, and therefore as an onset cause in some cases.
|
||||
The mutation accumulation hypothesis was tested by demonstrating how quickly deleterious mutations can accumulate in Musca domestica. Reed and Bryant demonstrated this by limiting the lifespan of the flies to a few days, which made late-life mutations invisible to selection since they occurred after reproduction. The lifespan of the flies was monitored by allowing them to carry out their complete lifespan every few generations, which was reported to decline substantially. Mutation accumulation is supported as a theory of aging, and therefore an onset cause in cases of diseases resulting from mutation accumulation.
|
||||
|
||||
|
||||
== References ==
|
||||
37
data/en.wikipedia.org/wiki/Agenesis-0.md
Normal file
37
data/en.wikipedia.org/wiki/Agenesis-0.md
Normal file
@ -0,0 +1,37 @@
|
||||
---
|
||||
title: "Agenesis"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Agenesis"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:57.418271+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
In medicine, agenesis () refers to the failure of an organ to develop during embryonic growth and development due to the absence of primordial tissue. Many forms of agenesis are referred to by individual names, depending on the organ affected:
|
||||
|
||||
Agenesis of the corpus callosum - failure in the development of the band of fibers connecting the cerebral hemispheres
|
||||
Renal agenesis - failure of one or both of the kidneys to develop
|
||||
Amelia - failure of the arms or legs to develop
|
||||
Penile agenesis - failure of penis to develop
|
||||
Müllerian agenesis - failure of the uterus and part of the vagina to develop
|
||||
Agenesis of the gallbladder - failure of the Gallbladder to develop. A person may not realize they have this condition unless they undergo surgery or medical imaging, since the gallbladder is neither externally visible nor essential.
|
||||
|
||||
|
||||
== Eye agenesis ==
|
||||
Eye agenesis is a medical condition in which people are born with no eyes.
|
||||
|
||||
|
||||
== Dental & oral agenesis ==
|
||||
Anodontia, absence of all primary or permanent teeth.
|
||||
Aglossia, absence of the tongue.
|
||||
Agnathia, absence of the jaw.
|
||||
Wisdom tooth agenesis - most adult humans have three molars (on each upper/lower left/right side), with the third being referred to as the wisdom tooth. But many people have less than the four total. Agenesis of wisdom teeth is a normal condition that can differ widely by population, ranging from practically zero in Tasmanian Aborigines to nearly 100% in indigenous Mexicans. (See research paper with world map showing prevalence.)
|
||||
|
||||
|
||||
== Ear agenesis ==
|
||||
Ear agenesis is a medical condition in which people are born without ears.
|
||||
Because the middle and inner ears are necessary for hearing, people with complete agenesis of the ears are totally deaf. Minor agenesis that affects only the visible parts of the outer ear, which may be called microtia, typically produces cosmetic concerns and perhaps hearing impairment if the opening to the ear canal is blocked, but not deafness.
|
||||
|
||||
|
||||
== References ==
|
||||
46
data/en.wikipedia.org/wiki/Agnosia-0.md
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||||
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||||
title: "Agnosia"
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||||
chunk: 1/2
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source: "https://en.wikipedia.org/wiki/Agnosia"
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||||
category: "reference"
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tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:58.633985+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Agnosia is a neurological disorder characterized by an inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is neither defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia affects only a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information.
|
||||
|
||||
== Types ==
|
||||
|
||||
=== Visual agnosia ===
|
||||
Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia.
|
||||
Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere.
|
||||
In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. However, individuals with prosopagnosia can recognize all other types of visual stimuli.
|
||||
|
||||
=== Speech agnosia ===
|
||||
Speech agnosia, or auditory verbal agnosia, refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they hear sounds being produced, but that the sounds are fundamentally unrecognizable or untranslatable.
|
||||
|
||||
EXAMINER: What did you eat for breakfast?
|
||||
PATIENT: Breakfast, breakfast, it sounds familiar but it doesn't speak to me. (Obler & Gjerlow 1999:45)
|
||||
Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speaker's voice (such as being a man or woman).
|
||||
|
||||
== Causes ==
|
||||
Agnosia can result from strokes, dementia, or other neurological disorders. It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders. Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved.
|
||||
Patients who experience dramatic recovery from blindness experience significant to total agnosia.
|
||||
The effect of damage to the superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individual's lexicon (vocabulary). For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface:
|
||||
|
||||
DOG activates 3, and inhibits 0 letters in DOG. – +3
|
||||
DOG activates 2, and inhibits 1 letters in FOG. – +2
|
||||
DOG activates 1, and inhibits 2 letters in DAN. – +1
|
||||
The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces 'pure word deafness' (Kussmaul, 1877), or as it is understood today, speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex.
|
||||
|
||||
== Diagnosis ==
|
||||
In order to assess an individual for agnosia, it must be verified that the individual does not have a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual has a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual has a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed.
|
||||
|
||||
=== Pure alexia ===
|
||||
|
||||
Individuals with pure alexia usually have difficulty reading words as well as difficulty with identifying letters. In order to assess whether an individual has pure alexia, tests of copying and recognition must be performed. An individual with pure alexia should be able to copy a set of words, and should be able to recognize letters.
|
||||
|
||||
=== Prosopagnosia ===
|
||||
|
||||
Individuals are usually shown pictures of human faces that may be familiar to them such as famous actors, singers, politicians or family members. The pictures shown to the patient are selected to be age- and culture-appropriate. The task involves the examiner asking the individual to name each face. If the individual cannot name whose face appears in the picture, the examiner may ask a question that would help to recognize the face in the picture.
|
||||
41
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||||
---
|
||||
title: "Agnosia"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Agnosia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:58.633985+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
== Treatment ==
|
||||
For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.
|
||||
Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia, which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment, such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies.
|
||||
|
||||
=== Verbal strategies ===
|
||||
Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues.
|
||||
|
||||
=== Alternate cues ===
|
||||
Alternate cues may be particularly useful to an individual with environmental agnosia or prosopagnosia. Alternate cues for an individual with environmental agnosia may include color cues or tactile markers to symbolize a new room or to remember an area by. Prosopagnosics may use alternate visual cues such as a scar on an individual's face or crooked teeth, or cues from other senses, like the sound of an individual's voice, in order to recognize the individual. Hair color and length can be helpful cues as well.
|
||||
|
||||
=== Organizational strategies ===
|
||||
Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues.
|
||||
|
||||
=== Current research ===
|
||||
There are clinical trials being done to further research for treatments. The National Institute of Neurological Disorders and Stroke (NINDS) supports research for rare diseases like agnosia. Some organizations recruit for trials via ClincalTrials.gov and provide status updates on the trials.
|
||||
|
||||
== History ==
|
||||
The term agnosia comes from the Ancient Greek ἀγνωσία (agnosia), 'ignorance, absence of knowledge'. It was introduced by Sigmund Freud in 1891: "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term 'agnosia'." Prior to Freud's introduction of the term, some of the first ideas about agnosia came from Carl Wernicke, who created theories about receptive aphasia in 1874. He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words. He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus. Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech.
|
||||
After Wernicke, came Kussmaul in 1877 who attempted to explain why auditory verbal agnosia, also known as word deafness, occurs. Contrary to Wernicke's explanations, Kussmaul believed auditory verbal agnosia was the result of major destruction to the first left temporal gyrus. Kussmaul also posited about the origins of alexia (acquired dyslexia) also known as word blindness. He believed that word blindness was the result of lesions to the left angular and supramarginal gyri.
|
||||
Heinrich Lissauer shared his ideas about agnosia after Wernicke and Kussmaul. In 1890, he theorized that there were two ways in which object recognition impairment could occur. One way in which impairment could occur was if there was damage to early perceptual processing or if there was damage to the actual object representation. If the actual object representation was damaged, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object. During the time of Wernicke, Kussmaul and Lissauer there was little known about the cerebral cortex. Today, new neuroimaging techniques have made it possible to expand our knowledge of agnosia greatly.
|
||||
|
||||
== See also ==
|
||||
Agnoiology – Study of ignorance
|
||||
Pyrrho – Greek philosopher and founder of Pyrrhonism (c.360-c.270 BC) who suspended judgement of the senses to attain freedom from disturbance
|
||||
|
||||
== References ==
|
||||
|
||||
== External links ==
|
||||
|
||||
Types and brain areas
|
||||
Total Recall: Memory Requires More than the Sum of Its Parts Scientific American (accessdate 2007-06-05)
|
||||
65
data/en.wikipedia.org/wiki/Agonist-0.md
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||||
---
|
||||
title: "Agonist"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Agonist"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:25:59.888594+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
An agonist is a chemical that activates a receptor to produce a biological response. Receptors are cellular proteins whose activation causes the cell to modify what it is currently doing. In contrast, an antagonist blocks the action of the agonist, while an inverse agonist causes an action opposite to that of the agonist.
|
||||
|
||||
|
||||
== Etymology ==
|
||||
The word originates from the Greek word ἀγωνιστής (agōnistēs), "contestant; champion; rival" < ἀγών (agōn), "contest, combat; exertion, struggle" < ἄγω (agō), "I lead, lead towards, conduct; drive."
|
||||
|
||||
|
||||
== Types of agonists ==
|
||||
Receptors can be activated by either endogenous agonists (such as hormones and neurotransmitters) or exogenous agonists (such as drugs), resulting in a biological response. A physiological agonist is a substance that creates the same bodily responses but does not bind to the same receptor.
|
||||
|
||||
An endogenous agonist for a particular receptor is a compound naturally produced by the body that binds to and activates that receptor. For example, the endogenous agonist for serotonin receptors is serotonin, and the endogenous agonist for dopamine receptors is dopamine.
|
||||
Full agonists bind to and activate a receptor with the maximum response that an agonist can elicit at the receptor. One example of a drug that can act as a full agonist is isoproterenol, which mimics the action of adrenaline at β adrenoreceptors. Another example is morphine, which mimics the actions of endorphins at μ-opioid receptors throughout the central nervous system. However, a drug can act as a full agonist in some tissues and as a partial agonist in other tissues, depending upon the relative numbers of receptors and differences in receptor coupling.
|
||||
A co-agonist works with other co-agonists to produce the desired effect together. NMDA receptor activation requires the binding of both glutamate, glycine and D-serine co-agonists. Calcium can also act as a co-agonist at the IP3 receptor.
|
||||
A selective agonist is selective for a specific type of receptor. E.g. buspirone is a selective agonist for serotonin 5-HT1A.
|
||||
Partial agonists (such as buspirone, aripiprazole, buprenorphine, or norclozapine) also bind and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist, even at maximal receptor occupancy. Agents like buprenorphine are used to treat opiate dependence for this reason, as they produce milder effects on the opioid receptor with lower dependence and abuse potential.
|
||||
An inverse agonist is an agent that binds to the same receptor binding-site as an agonist for that receptor and inhibits the constitutive activity of the receptor. Inverse agonists exert the opposite pharmacological effect of a receptor agonist, not merely an absence of the agonist effect as seen with an antagonist. An example is the cannabinoid inverse agonist rimonabant.
|
||||
A superagonist is a term used by some to identify a compound that is capable of producing a greater response than the endogenous agonist for the target receptor. It might be argued that the endogenous agonist is simply a partial agonist in that tissue.
|
||||
An irreversible agonist is a type of agonist that binds permanently to a receptor through the formation of covalent bonds.
|
||||
A biased agonist is an agent that binds to a receptor without affecting the same signal transduction pathway. Oliceridine is a μ-opioid receptor agonist that has been described to be functionally selective towards G protein and away from β-arrestin2 pathways.
|
||||
New findings that broaden the conventional definition of pharmacology demonstrate that ligands can concurrently behave as agonist and antagonists at the same receptor, depending on effector pathways or tissue type. Terms that describe this phenomenon are "functional selectivity", "protean agonism", or selective receptor modulators.
|
||||
|
||||
|
||||
== Mechanism of action ==
|
||||
As mentioned above, agonists have the potential to bind in different locations and in different ways depending on the type of agonist and the type of receptor. The process of binding is unique to the receptor-agonist relationship, but binding induces a conformational change and activates the receptor. This conformational change is often the result of small changes in charge or changes in protein folding when the agonist is bound. Two examples that demonstrate this process are the muscarinic acetylcholine receptor and NMDA receptor and their respective agonists.
|
||||
|
||||
For the muscarinic acetylcholine receptor, which is a G protein-coupled receptor (GPCR), the endogenous agonist is acetylcholine. The binding of this neurotransmitter causes the conformational changes that propagate a signal into the cell. The conformational changes are the primary effect of the agonist, and are related to the agonist's binding affinity and agonist efficacy. Other agonists that bind to this receptor will fall under one of the different categories of agonist mentioned above based on their specific binding affinity and efficacy.
|
||||
|
||||
The NMDA receptor is an example of an alternate mechanism of action, as the NMDA receptor requires co-agonists for activation. Rather than simply requiring a single specific agonist, the NMDA receptor requires both the endogenous agonists, N-methyl-D-aspartate (NMDA) and glycine. These co-agonists are both required to induce the conformational change needed for the NMDA receptor to allow flow through the ion channel, in this case calcium. An aspect demonstrated by the NMDA receptor is that the mechanism or response of agonists can be blocked by a variety of chemical and biological factors. NMDA receptors specifically are blocked by a magnesium ion unless the cell is also experiencing depolarization.
|
||||
These differences show that agonists have unique mechanisms of action depending on the receptor activated and the response needed. The goal and process remains generally consistent however, with the primary mechanism of action requiring the binding of the agonist and the subsequent changes in conformation to cause the desired response at the receptor. This response as discussed above can vary from allowing flow of ions to activating a GPCR and transmitting a signal into the cell.
|
||||
|
||||
|
||||
== Activity ==
|
||||
|
||||
|
||||
=== Potency ===
|
||||
Potency is the amount of agonist needed to elicit a desired response. The potency of an agonist is inversely related to its half maximal effective concentration (EC50) value. The EC50 can be measured for a given agonist by determining the concentration of agonist needed to elicit half of the maximum biological response of the agonist. The EC50 value is useful for comparing the potency of drugs with similar efficacies producing physiologically similar effects. The smaller the EC50 value, the greater the potency of the agonist, the lower the concentration of drug that is required to elicit the maximum biological response.
|
||||
|
||||
|
||||
=== Therapeutic index ===
|
||||
Therapeutic index is a measure of a drug's safety margin. When a drug is used therapeutically, it is important to understand the margin of safety that exists between the dose needed for the desired effect and the dose that produces unwanted and possibly dangerous side-effects (measured by the TD50, the dose that produces toxicity in 50% of individuals). This relationship, termed the therapeutic index, is defined as the ratio TD50:ED50. In general, the narrower this margin, the more likely it is that the drug will produce unwanted effects. The therapeutic index emphasizes the importance of the margin of safety, as distinct from the potency, in determining the usefulness of a drug.
|
||||
|
||||
|
||||
== See also ==
|
||||
Allosteric modulator
|
||||
Dose response curve
|
||||
Excitatory postsynaptic potential
|
||||
Functional selectivity
|
||||
Intrinsic activity
|
||||
Inverse agonist
|
||||
Mixed agonist/antagonist
|
||||
Receptor antagonist
|
||||
Receptor theory
|
||||
|
||||
|
||||
== References ==
|
||||
18
data/en.wikipedia.org/wiki/Allopathic_medicine-0.md
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|
||||
---
|
||||
title: "Allopathic medicine"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Allopathic_medicine"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:01.122654+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Allopathic medicine, or allopathy, from Ancient Greek ἄλλος (állos), meaning "other", and πάθος (páthos), meaning "pain", is a label originally used derogatorily by 19th-century homeopaths to describe heroic medicine. In its current usage, the term generally refers to contemporary conventional medicine. However, there are regional variations in usage of the term. For example, in the United States the term is primarily used in contrast with osteopathic medicine, especially in the field of medical education; whereas in India the term is used to distinguish modern medicine from Siddha medicine, Ayurveda, homeopathy, Unani and other alternative and traditional medicine traditions, especially when comparing treatments and drugs.
|
||||
The terms were coined in 1810 by the creator of homeopathy, Samuel Hahnemann. Heroic medicine was the conventional European medicine of the time and did not rely on evidence of effectiveness. It was based on the belief that disease is caused by an imbalance of the four "humours" (blood, phlegm, yellow bile, and black bile) and sought to treat disease symptoms by correcting that imbalance, using "harsh and abusive" methods to induce symptoms seen as opposite to those of diseases rather than treating their underlying causes: disease was caused by an excess of one humour and thus would be treated with its "opposite".
|
||||
A study released by the World Health Organization (WHO) in 2001 defined allopathic medicine as "the broad category of medical practice that is sometimes called Western medicine, biomedicine, evidence-based medicine, or modern medicine." The WHO used the term in a global study in order to differentiate Western medicine from traditional and alternative medicine, noting that in certain areas of the world "the legal standing of practitioners is equivalent to that of allopathic medicine" where practitioners can be separately certified in complementary/alternative medicine and Western medicine.
|
||||
The term allopathy was also used to describe anything that was not homeopathy. Kimball Atwood, an American medical researcher and alternative medicine critic, said the meaning implied by the label of allopathy has never been accepted by conventional medicine and is still considered pejorative. American health advocate and sceptic William T. Jarvis, stated that "although many modern therapies can be construed to conform to an allopathic rationale (e.g., using a laxative to relieve constipation), standard medicine has never paid allegiance to an allopathic principle" and that the label "allopath" was "considered highly derisive by regular medicine." Most modern science-based medical treatments (antibiotics, vaccines, and chemotherapeutics, for example) do not fit Hahnemann's definition of allopathy, as they seek to prevent illness or to alleviate an illness by eliminating its cause.
|
||||
|
||||
== History ==
|
||||
The practice of medicine in both Europe and North America during the early 19th century is sometimes referred to as heroic medicine because of the extreme measures (such as bloodletting) sometimes employed in an effort to treat diseases. The term allopath was used by Hahnemann and other early homeopaths to highlight the difference they perceived between homeopathy and the "conventional" heroic medicine of their time. With the term allopathy (meaning "other than the disease"), Hahnemann intended to point out how physicians with conventional training employed therapeutic approaches that, in his view, merely treated symptoms and failed to address the disharmony produced by underlying disease. Homeopaths saw such symptomatic treatments as "opposites treating opposites" and believed these methods were harmful to patients.
|
||||
Practitioners of alternative medicine have used the term "allopathic medicine" to refer to the practice of conventional medicine in both Europe and the United States since the 19th century. In that century, the term allopath was used most often as a derogatory name for the practitioners of heroic medicine, a precursor to modern medicine that itself did not rely on evidence of effectiveness.
|
||||
33
data/en.wikipedia.org/wiki/Allopathic_medicine-1.md
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|
||||
---
|
||||
title: "Allopathic medicine"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Allopathic_medicine"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:01.122654+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
James Whorton discusses this historical pejorative usage: One form of verbal warfare used in retaliation by irregulars was the word "allopathy". ..."Allopathy" and "allopathic" were liberally employed as pejoratives by all irregular physicians of the nineteenth century, and the terms were considered highly offensive by those at whom they were directed. The generally uncomplaining acceptance of [the term] "allopathic medicine" by today's physicians is an indication of both a lack of awareness of the term's historical use and the recent thawing of relations between irregulars and allopaths.
|
||||
The controversy surrounding the term can be traced to its original usage during a heated 19th-century debate between practitioners of homeopathy and those they derisively referred to as "allopaths."
|
||||
Hahnemann used "allopathy" to refer to what he saw as a system of medicine that combats disease by using remedies that produce effects in a healthy subject that are different (hence the Greek root allo- "different") from the effects produced by the disease to be treated. The distinction comes from the use in homeopathy of substances that are meant to cause similar effects as the symptoms of a disease to treat patients (homeo - meaning "similar").
|
||||
As used by homeopaths, the term allopathy has always referred to the principle of treating disease by administering substances that produce other symptoms (when given to a healthy human) than the symptoms produced by a disease. For example, part of an allopathic treatment for fever may include the use of a drug which reduces the fever, while also including a drug (such as an antibiotic) that attacks the cause of the fever (such as a bacterial infection). A homeopathic treatment for fever, by contrast, is one that uses a diluted dosage of a substance that in an undiluted form would induce fever in a healthy person. These preparations are typically diluted so heavily that they no longer contain any actual molecules of the original substance. Hahnemann used this term to distinguish medicine as practiced in his time from his use of infinitesimally small (or nonexistent) doses of substances to treat the spiritual causes of illness.
|
||||
The Companion Encyclopedia of the History of Medicine states that "[Hahnemann] gave an all-embracing name to regular practice, calling it 'allopathy'. This term, however imprecise, was employed by his followers and other unorthodox movements to identify the prevailing methods as constituting nothing more than a competing 'school' of medicine, however dominant in terms of number of practitioner proponents and patients".
|
||||
Contrary to the present usage, Hahnemann reserved the term "allopathic medicine" to the practice of treating diseases by means of drugs inducing symptoms unrelated (i.e., neither similar nor opposite) to those of the disease. He called the practice of treating diseases by means of drugs producing symptoms opposite to those of the patient "enantiopathic" (from the Greek ἐνάντιος (enántios), meaning "opposite") or "antipathic medicine".
|
||||
|
||||
== Current usage ==
|
||||
In the United States, the term is used in the modern era to differentiate between two types of US medical schools (both of which teach aspects of science-based medicine and neither of which teach homeopathy): Allopathic (granting the MD degree) and Osteopathic (granting the DO degree).
|
||||
In India the term is used principally to distinguish "Western medicine" from Ayurveda, especially when comparing treatments and drugs.
|
||||
A study released by the World Health Organization (WHO) in 2001 defined "allopathic medicine" as "the broad category of medical practice that is sometimes called Western medicine, biomedicine, evidence-based medicine, or modern medicine." The WHO used the term in a global study in order to differentiate Western medicine from traditional medicine, and from complementary/alternative medicine, noting that in certain areas of the world “the legal standing of practitioners is equivalent to that of allopathic medicine” where practitioners are certified in both complementary/alternative medicine and Western medicine.
|
||||
As of 2004, use of the term remained common among homeopaths and had spread to other alternative medicine practices. Kimball Atwood, an American medical researcher and alternative medicine critic, said the meaning implied by the label of allopathy has never been accepted by conventional medicine and is still considered pejorative by some. American health educator and skeptic William T. Jarvis, stated in 2008 that "although many modern therapies can be construed to conform to an allopathic rationale (e.g., using a laxative to relieve constipation), standard medicine has never paid allegiance to an allopathic principle" and that the label "allopath" was "considered highly derisive by regular medicine".
|
||||
Most modern science-based medical treatments (antibiotics, vaccines, and chemotherapeutics, for example) do not fit Samuel Hahnemann's definition of allopathy, as they seek to prevent illness, or remove the cause of an illness by acting on the cause of disease.
|
||||
|
||||
== See also ==
|
||||
Conservation medicine
|
||||
Ethnomedicine
|
||||
Evidence-based medicine
|
||||
|
||||
== References ==
|
||||
|
||||
== External links ==
|
||||
The dictionary definition of allopathy at Wiktionary
|
||||
33
data/en.wikipedia.org/wiki/Allow_natural_death-0.md
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33
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|
||||
---
|
||||
title: "Allow natural death"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Allow_natural_death"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:02.316918+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Allow Natural Death (AND) is a medical term defining the use of life-extending measures such as cardiopulmonary resuscitation (CPR). These orders emphasize patient comfort and pain management instead of life extension. Currently, American medical communities utilize "do not resuscitate," (DNR) orders to define patients' medical wishes. Those who propose to replace DNR with AND posit that DNR orders are ambiguous and require complex understanding between several parties, while AND orders are clearer. Proponents of replacing DNR with AND believe that AND terminology is more ethically conscientious DNR terminology. Research has been conducted regarding participant preference for AND vs. DNR terminology. The ease with which the terminology change can be practically incorporated depends on many factors such as costs and staff reeducation.
|
||||
|
||||
== DNR vs. AND ==
|
||||
DNR orders range in the extent of life-saving measures to be avoided, from solely prohibiting the use of resuscitation to prohibiting any action seen as life extending. Because there are many parties involved in a patient's end of life care - significant others, family, personal doctors, specialists and nurses - DNR orders are not always completely clear, leaving open possible violation of the patient's wishes. DNR terminology was replaced in 2005 by the American Heart Association with Do Not Attempt Resuscitation (DNAR) in an effort to make clearer the meaning of the order. However, DNR remains the popularly understood and used term in the medical and layperson settings. AND is yet another phrase for similar orders, and implementing it involves a term change.
|
||||
Those who propose to replace DNR orders with AND orders posit that AND is less ambiguous, clearly instructing medical personnel to not use any artificial, life extending measures. This would be especially helpful in regards to emergency care, when medical personnel who are unfamiliar with the patient must decide what medical practices should be used. Pros are that AND increases clarity on meaning and the choice of life or death. AND orders also don't use negative wording that could be confusing to interpret. Furthermore, proponents of AND claim that because it contains "death" in the title it is more clear to the patient and family exactly what the patient is agreeing to. Critics of AND claim it is simply the replacement of one ambiguous term with another. Cons include that death can be vague and CPR isn't mentioned in the phrase. Just as DNR particulars vary, so too would AND particulars vary. Thus, they argue that change would be ineffective.
|
||||
|
||||
== Ethics ==
|
||||
AND terminology represents an ideology of patient care that emphasizes bodily autonomy and respect of the individual. This is in contrast to the terminology associated with DNR, or "do not resuscitate," which has been criticized for placing emphasis on potential negative outcomes associated with hospitalization, i.e. the act of "not" resuscitating is a conscious decision to "not" engage in life-extending care. Proponents of AND argue that, by "allowing" natural death, the provider is, instead, consciously deciding to engage in care; although such care is not life-extending, this form of care respects the wishes of patients to die peacefully and without suffering.
|
||||
AND and DNR share similar ethical considerations with regards to end-of-life care. These considerations can involve the four main principles of biomedical ethics, including autonomy, beneficence, nonmaleficence, and justice. Autonomy can be thought of as a patient's right to self-determination and the right to decide what kind of care they should receive, which can be achieved through ANDs or DNRs. The principles of beneficence and nonmaleficence require that the healthcare providers are aware of their patient's AND and DNR statuses, and of their roles in that patient's end-of-life care. Lastly, the principle of justice refers to the obligation for healthcare providers to advocate for fair and appropriate treatment of their patients at the end of their lives, which requires abiding by the conditions expressed through AND and DNR.
|
||||
In the cases of attempted suicide or medical mismanagement, there are questions around the meaning of what a "natural" death is. It is argued that in these cases, physicians should have the capability to revoke a patient's DNR or AND, though a wide consensus has yet to be reached.
|
||||
|
||||
== Studies and Outcomes ==
|
||||
Most studies regarding AND are surveys based on hypothetical situations and are given to specific groups. One study gave a scenario regarding loved ones to nurses, nursing students, and people with no nursing background. Each group rated how likely they were to agree to end of life care when DNR or AND was used. Participants were significantly more likely to agree to end of life care when AND was used.
|
||||
Another study found similar results when giving a scenario to 524 adults- end of life care was more accepted when AND was used.
|
||||
However, when patients with cancer were given a scenario about how much time they had left to live (1 year, 6 months, or 1 month), the results were different. In two studies conducted by the same authors, there was no significant difference in choosing end of life care when AND or DNR was used.
|
||||
Finally, an anonymous survey asked residents and doctors about their experience with end of life care after their hospital switched to using AND over DNR. A majority agreed that using AND improved discussions about end of life care and decreased the burden of decision making.
|
||||
|
||||
== Future Directions ==
|
||||
There are barriers that exist in implementing "allow natural death". Some argue that costs will occur with the need to reeducate clinical staff and replace forms and edit electronic medical databases. People are looking into high-end care for when it comes to end of life decisions and AND can help provide more autonomy for patients.
|
||||
|
||||
== See also ==
|
||||
Letting die
|
||||
Coup de grace
|
||||
27
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27
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|
||||
---
|
||||
title: "Allow natural death"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Allow_natural_death"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:02.316918+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
== Bibliography ==
|
||||
Fan, S.-Y., Wang, Y.-W., & Lin, I.-M. (2018). Allow natural death versus do-not-resuscitate: Titles, information contents, outcomes, and the considerations related to do-not-resuscitate decision. BMC Palliative Care, 17(1). https://doi.org/10.1186/s12904-018-0367-4.
|
||||
This is a peer-reviewed scientific journal, so it should be a reliable source. It covers the topic in some depth, so it's helpful in establishing notability.
|
||||
Miljković, M. D., Emuron, D., Rhodes, L., Abraham, J., & Miller, K. (2015). "allow natural death" versus "do not resuscitate": What do patients with advanced cancer choose? Journal of Palliative Medicine, 18(5), 457–460. https://doi.org/10.1089/jpm.2014.0369.
|
||||
This is a peer-reviewed scientific journal, so it should be a reliable source. It covers the topic in some depth, so it's helpful in establishing notability.
|
||||
Wittmann-Price, Ruth; Celia, Linda M. (Nov–Dec 2010). "Exploring perceptions of "do not resuscitate" and "allowing natural death" among physicians and nurses". Holistic Nursing Practice. 24 (6): 333–337.
|
||||
This is a peer-reviewed scientific journal, so it should be a reliable source. It is an observational study that was used to understand the differences in perception of the terms "allow natural death" and "do not resuscitate."
|
||||
Akdeniz, Melahat; Yardımcı, Bülent; Kavukcu, Ethem (2021). "Ethical considerations at the end-of-life care". SAGE open medicine. 9: 20503121211000918.
|
||||
This is a peer-reviewed review article, so it should be a reliable source. It covers ethical considerations of end-of-life care, so it's helpful in providing context to the discussion of "allowing natural death."
|
||||
Knox, C., Vereb, J.A. (2005). "Allow Natural Death: A More Humane Approach to Discussing End-of-Life Directives". Journal of Emergency Nursing. 31 (6): 560-561. PMID 16308044
|
||||
This is an history of AND vs. DNR and argues for use of AND in a reputable journal.
|
||||
Venneman, S. S., Narnor-Harris, P., Perish, M., Hamilton, M. (2007). ""Allow natural death" versus "do not resuscitate": three words that can change a life". Journal of Medical Ethics. 34 (1): 2-6.
|
||||
This is a quantitative survey study in the Journal of Medical Ethics, which is a reputable and relevant source.
|
||||
Robinson, C., Kolesar, S., Boyko, M., Berkowitz, J., Calam, B., Collins, M. (2012). "Awareness of do-not-resuscitate orders". Canadian Family Physician. 58 (4): 229-233. PMID 22611610
|
||||
This is a primary cross-sectional study in a peer-reviewed journal on patient awareness of DNR and how and when they would like to decide on how or whether to use one.
|
||||
|
||||
== References ==
|
||||
35
data/en.wikipedia.org/wiki/Ambulatory-0.md
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|
||||
---
|
||||
title: "Ambulatory"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Ambulatory"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:03.561509+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
The ambulatory (Latin: ambulatorium 'walking place') is the covered passage around a cloister or the processional way around the east end of a cathedral or large church and behind the high altar. The first ambulatory was in France in the 11th century but by the 13th century ambulatories had been introduced in England and many English cathedrals were extended to provide an ambulatory.
|
||||
The same feature is often found in Indian architecture and Buddhist architecture generally, especially in older periods. Ritual circumambulation or parikrama around a stupa or cult image is important in Buddhism and Hinduism. Often the whole building was circumambulated, often many times. The Buddhist chaitya hall always allowed a path for this, and the Durga temple, Aihole (7th or 8th century) is a famous Hindu example.
|
||||
|
||||
The term is also used to describe a garden feature in the grounds of a country house. A typical example is the one shown, which stands in the grounds of Horton Court in Gloucestershire, England.
|
||||
|
||||
|
||||
== Medical term ==
|
||||
Ambulatory is also an adjective used to describe
|
||||
|
||||
patients who can walk despite their illness or injury.
|
||||
outpatients generally including those needing a wheelchair.
|
||||
medical staff providing outpatient care (see Ambulatory care nursing, Ambulatist).
|
||||
medical procedures that do not ordinarily require an overnight stay in hospital (see Ambulatory care).
|
||||
Canes or other walking aids can be called ambulatory assistive devices.
|
||||
|
||||
|
||||
== See also ==
|
||||
List of architectural vaults
|
||||
Scarcella
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
@ -4,7 +4,7 @@ chunk: 1/4
|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terminology"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:13:31.649291+00:00"
|
||||
date_saved: "2026-05-05T07:26:04.798609+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
|
||||
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|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terminology"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:13:31.649291+00:00"
|
||||
date_saved: "2026-05-05T07:26:04.798609+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
|
||||
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|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terminology"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:13:31.649291+00:00"
|
||||
date_saved: "2026-05-05T07:26:04.798609+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
|
||||
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|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terminology"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:13:31.649291+00:00"
|
||||
date_saved: "2026-05-05T07:26:04.798609+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
|
||||
50
data/en.wikipedia.org/wiki/Anatomical_terms_of_location-0.md
Normal file
50
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|
||||
---
|
||||
title: "Anatomical terms of location"
|
||||
chunk: 1/5
|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terms_of_location"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:06.044970+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Standard anatomical terms of location are used to describe unambiguously the anatomy of humans and other animals. The terms, typically derived from Latin or Greek roots, describe something in its standard anatomical position. This position provides a definition of what is at the front ("anterior"), behind ("posterior") and so on. As part of defining and describing terms, the body is described through the use of anatomical planes and axes.
|
||||
The meaning of terms that are used can change depending on whether a vertebrate is a biped or a quadruped, due to the difference in the neuraxis, or if an invertebrate is a non-bilaterian. A non-bilaterian has no anterior or posterior surface for example but can still have a descriptor used such as proximal or distal in relation to a body part that is nearest to, or furthest from its middle.
|
||||
International organisations have determined vocabularies that are often used as standards for subdisciplines of anatomy. For example, Terminologia Anatomica, Terminologia Neuroanatomica, and Terminologia Embryologica for humans and Nomina Anatomica Veterinaria for animals. These allow parties that use anatomical terms, such as anatomists, veterinarians, and medical doctors, to have a standard set of terms to communicate clearly the position of a structure.
|
||||
|
||||
== Introduction ==
|
||||
|
||||
Standard anatomical terms of location have been developed, usually based on Latin and Greek words, to enable all biological and medical scientists, veterinarians, medical doctors and anatomists to precisely delineate and communicate information about animal bodies and their organs, even though the meaning of some of the terms often is context-sensitive. Much of this information has been standardised in internationally agreed vocabularies for humans (Terminologia Anatomica, Terminologia Neuroanatomica, and Terminologia Embryologica), with Nomina Anatomica Veterinaria and Nomina Embryologica Veterinaria used for animal anatomy.
|
||||
Different terms are used for those vertebrates that are bipedal and those that are quadrupedal. The reasoning is that the neuraxis, and therefore the standard anatomical position is different between the two groups. Unique terms are also used to describe invertebrates, because of their wider variety of shapes and symmetries.
|
||||
|
||||
=== Standard anatomical position ===
|
||||
|
||||
Because animals can change orientation with respect to their environment, and because appendages like limbs and tentacles can change position with respect to the main body, terms to describe position need to refer to an animal when it is in its standard anatomical position, even when its appendages are in another position. This helps to avoid confusion in terminology when referring to the same animal in different postures. In humans, this refers to the body in a standing position with arms at the side and palms facing forward. In quadrupeds this is an animal standing upright with all four feet on the ground and the head facing forward. For a fish this is belly down with neutral appendages.
|
||||
|
||||
=== Planes ===
|
||||
|
||||
Anatomical terms describe structures with relation to three main anatomical planes. Anatomical planes are useful in a number of fields including medical imaging, embryology, and the study of movement.
|
||||
The three main plane orientations are:
|
||||
|
||||
The sagittal planes, also called the parasagittal planes or paramedian planes, are planes that divide the body into left and right. The central one of these is the median plane, also called the midsagittal plane, which passes through the head, spinal cord, navel and, in many animals, the tail.
|
||||
The coronal plane or frontal plane divides the body into front and back parts. In quadrupeds this plane is termed the dorsal plane and divides the body into dorsal (towards the backbone) and ventral (towards the belly) parts.
|
||||
The transverse plane, also called the axial plane or horizontal plane, is perpendicular to the other two planes.
|
||||
Sagittal planes and transverse planes are used as anatomical lines to delineate bodily regions. There are several transverse planes with clinical relevance in the division of the torso into sections. They include the transpyloric plane, the subcostal plane, and the transumbilical plane.
|
||||
|
||||
=== Axes ===
|
||||
|
||||
The three axes of a vertebrate, are formed in embryonic development before and during the gastrulation stage. Distinct ends of the embryo are chosen, and the axis is named according to those directions. The three main axes of a bilaterally symmetrical animal that intersect at right angles, are the left-right, the craniocaudal, and the anteroposterior axes.
|
||||
|
||||
The left-right axis, also known as the horizontal or frontal axis
|
||||
The craniocaudal axis, also known as the rostrocaudal, longitudinal or cephalocaudal
|
||||
The anteroposterior axis, also known as the dorsoventral, or sagittal axis
|
||||
An organism that is round, or asymmetrical may have different axes.
|
||||
|
||||
== Main terms ==
|
||||
|
||||
=== Superior and inferior ===
|
||||
In the standard human anatomical position, superior (from Latin super 'above') or cranial, describes something that is nearer to the head, and inferior (from Latin inferus 'below') or caudal describes what is below, and nearer to the feet. Examples are the superior mediastinum, and inferior mediastinum. Neuroanatomy examples are the superior colliculus, and the inferior colliculus. In veterinary anatomy, the terms superior and inferior are not used except to describe the eye, eyelids, lips and inner ear, using instead dorsal and ventral.
|
||||
|
||||
=== Anterior and posterior ===
|
||||
|
||||
Anterior (from Latin ante 'before') describes what is in front, and posterior (from Latin post 'after') describes what is to the back of something. For example, for many fish the gill openings are posterior to the eyes and anterior to the tail. In veterinary anatomy, these terms are reserved for some structures of the head, instead using cranial and caudal throughout the rest of the body.
|
||||
49
data/en.wikipedia.org/wiki/Anatomical_terms_of_location-1.md
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|
||||
---
|
||||
title: "Anatomical terms of location"
|
||||
chunk: 2/5
|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terms_of_location"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:06.044970+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Dorsal and ventral ===
|
||||
These two terms, used in veterinary anatomy, are also used in human anatomy mostly in neuroanatomy, and embryology, to describe something at the back (dorsal, posterior) or front (ventral, anterior) of an organ, or organism.
|
||||
The dorsal (from Latin dorsum 'back') surface, (also dorsum) of an organism or organ, refers to the back, or upper side, such as in the human, the dorsum of the tongue, the dorsum of the hand, and the dorsum of the foot. If talking about the skull, the dorsal side is the top.
|
||||
|
||||
The ventral (from Latin venter 'belly') surface refers to the front, or lower side, of an organism, or organ such as the undersurface of the tongue.
|
||||
In a fish, the dorsal fin is on the upper surface and its ventral fins (pelvic fins) are on the belly or undersurface.
|
||||
The terms are used in other contexts, for example in dorsal and ventral gun turrets on a bomber aircraft.
|
||||
|
||||
=== Medial and lateral ===
|
||||
These terms describe how close something is to the median plane. Lateral (from Latin lateralis 'to the side') describes something to the sides of an animal, as in "left lateral" and "right lateral". Medial (from Latin medius 'middle') describes structures close to the median plane, or closer to the median plane than another structure. For example, in a human, the arms are lateral to the torso. The genitals are medial to the legs. Temporal has a similar meaning to lateral but is restricted to the head.
|
||||
The terms "left" and "right", or sinistral and dextral, refer to the halves of a bilaterally symmetrical body divided by the median plane.
|
||||
Terms derived from lateral include:
|
||||
|
||||
Contralateral (from Latin contra 'against'): on the side opposite to another structure. For example, the right arm and leg are controlled by the left, contralateral, side of the brain.
|
||||
Ipsilateral (from Latin ipse 'same'): on the same side as another structure. For example, the left arm is ipsilateral to the left leg.
|
||||
Bilateral (from Latin bis 'twice'): on both sides of the body. For example, bilateral orchiectomy means removal of testes on both sides of the body.
|
||||
Unilateral (from Latin unus 'one') one-sided or single-sided: on one side of the body. For example, unilateral deafness is hearing impairment in one ear.
|
||||
Varus (from Latin 'bow-legged') and valgus (from Latin 'knock-kneed' ) are terms used to describe angulation or bowing of a bone or joint within the coronal plane, where the distal portion deviates towards (varus) or away from (valgus) the midline.
|
||||
|
||||
=== Proximal and distal ===
|
||||
|
||||
The terms proximal (from Latin proximus 'nearest') and distal (from Latin distare 'to stand away from') are used to describe parts of a feature that are close to or distant from the main mass of the body, respectively. Thus the upper arm in humans is proximal and the hand is distal. The main mass is taken as the center, the chest, or the heart.
|
||||
"Proximal and distal" are frequently used when describing appendages, such as fins, tentacles, and limbs. Although the direction indicated by "proximal" and "distal" is always respectively towards or away from the point of attachment, a given structure can be either proximal or distal in relation to another point of reference. Thus the elbow is distal to a wound on the upper arm, but proximal to a wound on the lower arm.
|
||||
This terminology is also employed in molecular biology and therefore by extension is also used in chemistry, specifically referring to the atomic loci of molecules from the overall moiety of a given compound.
|
||||
|
||||
=== Rostral, cranial, and caudal ===
|
||||
|
||||
Specific terms exist to describe how close or far something is to the head or tail of an animal. To describe how close to the head of an animal something is, three distinct terms are used:
|
||||
|
||||
Rostral (from Latin rostrum 'beak, nose') describes something situated toward the oral or nasal region, or in the case of the brain, toward the tip of the frontal lobe.
|
||||
Cranial (from Greek κρανίον 'skull') or cephalic (from Greek κεφαλή 'head') describes how close something is to the head of an organism.
|
||||
Caudal (from Latin cauda 'tail') describes how close something is to the trailing end of an organism.
|
||||
These terms are generally preferred in veterinary medicine and not used as often in human medicine. For example, in horses, the eyes are caudal to the nose and rostral to the back of the head.
|
||||
In humans, "cranial" and "cephalic" are used to refer to the skull, with "cranial" being used more commonly. The term "rostral" is rarely used in human gross anatomy and refers more to the front of the face than the superior aspect of the organism. But it is used in embryology, and neuroanatomy. Similarly, the term "caudal" is used more in embryology and neuroanatomy, and only occasionally in human gross anatomy. The "rostrocaudal axis" refers to the curved line of the neuraxis from the forehead (rostral) towards the tail end (caudal).
|
||||
|
||||
=== Central and peripheral ===
|
||||
Central and peripheral refer to the distance towards and away from the centre of something. That might be an organ, a region in the body, or an anatomical structure. For example, the central nervous system and the peripheral nervous systems.
|
||||
Central (from Latin centralis) describes something at, or close to the centre. For example, the great vessels run centrally through the body; many smaller vessels branch from these.
|
||||
Peripheral (from Latin peripheria, originally from Ancient Greek) describes something that is situated nearer to the body's surface, such as a peripheral nerve.
|
||||
47
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|
||||
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|
||||
title: "Anatomical terms of location"
|
||||
chunk: 3/5
|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terms_of_location"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:06.044970+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Superficial and deep ===
|
||||
These terms refer to the distance of a structure from the surface.
|
||||
Deep (from Old English) describes something further away from the surface of the organism. For example, the external oblique muscle of the abdomen is deep to the skin. "Deep" is one of the few anatomical terms of location derived from Old English rather than Latin – the anglicised Latin term would have been "profound" (from Latin profundus 'due to depth').
|
||||
Superficial (from Latin superficies 'surface') describes something near the outer surface of the organism. For example, in skin, the epidermis is superficial to the subcutis.
|
||||
|
||||
=== Combined terms ===
|
||||
|
||||
Many anatomical terms can be combined, either to indicate a position in two axes simultaneously or to indicate the direction of a movement relative to the body. For example, anterolateral indicates a position that is both anterior and lateral to the body axis (such as the bulk of the pectoralis major muscle), or to a named organ such as the anterolateral tibial tubercle. The term can also describe the direction and location of something that enters or courses through the body such as the anterolateral system in the spinal cord, and the anterolateral central arteries. Another term anteromedial is used for example in the anteromedial central arteries.
|
||||
In the more internal brain and spinal cord of the central nervous system the terms dorsal and ventral and their combinations are often used in place of anterior and posterior. In these organs numerous references need to be used, and in the brain for example the prefrontal cortex has the divisions of the dorsomedial prefrontal cortex, and the dorsolateral prefrontal cortex. And the dorsomedial region has subcompartments that make use of other terms such as the anterior cingulate cortex, and infralimbic cortex. Structures such as the anterior cingulate cortex may be divided anatomically based on cognitive (dorsal), and emotional (ventral) components.
|
||||
Proximodistal is the axis of an appendage such as an arm or a leg, taken from its tip at the distal part to where it joins the body at the proximal part.
|
||||
In radiology, various X-ray views uses terminology based on where the X-ray beam enters and leaves the body, including the front to back view (anteroposterior), the back to front view (posteroanterior), and the side view (lateral). Combined terms were once generally hyphenated, but typically the hyphen is omitted.
|
||||
|
||||
=== Modifiers ===
|
||||
|
||||
Several terms are commonly seen and used as prefixes:
|
||||
|
||||
Sub- (from Latin sub 'preposition beneath, close to, nearly etc') is used to indicate something that is beneath, or something that is subordinate to or lesser than. For example, subcutaneous means beneath the skin.
|
||||
Hypo- (from Ancient Greek ὑπό 'under') is used to indicate something that is beneath. For example, the hypoglossal nerve supplies the muscles beneath the tongue.
|
||||
Infra- (from Latin infra 'under') is used to indicate something that is within or below. For example, the infraorbital nerve runs within the orbit.
|
||||
Inter- (from Latin inter 'between') is used to indicate something that is between. For example, the intercostal muscles run between the ribs.
|
||||
Super- or Supra- (from Latin super, supra 'above, on top of') is used to indicate something that is above something else. For example, the supraorbital ridges are above the eyes.
|
||||
Ab- (from Latin ab 'away'), and ad- (from Latin ad 'towards') are used to indicate that something is towards (ad-) or away from (ab-) something else. For example abduction and adduction refer to muscular movement away from, and towards the midline of the body, respectively.
|
||||
Other terms are used as suffixes, added to the end of words:
|
||||
|
||||
-al (from Latin al 'pertaining to, of the') For example femoral neck.
|
||||
-ad (from Latin ad 'towards'), equivalent to '-ally', is a suffix creating the adverb form to indicate that something moves towards (-ad) something else. For example, "distad" means "in the distal direction," as in "arterial blood flows distad/distally." Further examples may include cephalad (towards the cephalic end), orad, craniad, and proximad. The terms "proximally" and "distally" are in more common use in human and veterinary anatomic textbooks, while "proximad" and "distad," are used commonly in insect anatomy.
|
||||
|
||||
== Other terms and special cases ==
|
||||
|
||||
=== Anatomical landmarks ===
|
||||
|
||||
The location of anatomical structures can also be described in relation to different anatomical landmarks used in anatomy, surface anatomy, surgery, and radiology.
|
||||
Structures may be described as being at the level of a specific vertebra, depending on the section of the vertebral column the structure is at. The position is often abbreviated. For example, structures at the level of the fourth cervical vertebra may be abbreviated as "C4", at the level of the fourth thoracic vertebra "T4", and at the level of the third lumbar vertebra "L3". Because the sacrum and coccyx are fused, they are not often used to provide the location.
|
||||
References may also take origin from surface anatomy, made to landmarks that are on the skin or visible underneath. For example, structures may be described relative to the anterior superior iliac spine, the medial malleolus or the medial epicondyle.
|
||||
Anatomical lines are theoretical lines, using either horizontal transverse planes, or vertical sagittal planes, used to describe anatomical location. For examples, the mid-clavicular line is used as part of the cardiac examination to feel the apex beat of the heart, and the axillary lines are reference lines for the underarm region. Other types of lines in anatomy include the curved nuchal lines on the occipital bone, and the gluteal lines on the ilium.
|
||||
|
||||
=== Mouth and teeth ===
|
||||
34
data/en.wikipedia.org/wiki/Anatomical_terms_of_location-3.md
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|
||||
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|
||||
title: "Anatomical terms of location"
|
||||
chunk: 4/5
|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terms_of_location"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:06.044970+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Special terms are used to describe the mouth and teeth. Fields such as osteology, paleontology and dentistry apply special terms of location to describe the mouth and teeth. This is because although teeth may be aligned with their main axes within the jaw, some different relationships require special terminology as well; for example, teeth also can be rotated, and in such contexts terms like "anterior" or "lateral" become ambiguous. For example, the terms "distal" and "proximal" (or "mesial") are used for surfaces of individual teeth relative to the midpoint of the dental arch, and "medial" and "lateral" are used in the standard sense relative to the median plane. Terms used to describe structures include "buccal" (from Latin bucca 'cheek') and "palatal" (from Latin palatum 'palate') referring to structures close to the cheek and hard palate respectively.
|
||||
|
||||
=== Hands and feet ===
|
||||
|
||||
Several anatomical terms are particular to the hands and feet. Additional terms may be used to avoid confusion when describing the surfaces of the hand and what is the "anterior" or "posterior" surface. The term "anterior", while anatomically correct, can be confusing when describing the palm of the hand; Similarly is "posterior", used to describe the back of the hand and arm. This confusion can arise because the forearm can pronate and supinate and flip the location of the hand. For improved clarity, the directional term palmar (from Latin palma 'palm of the hand') is commonly used to describe the front of the hand, and dorsal is the back of the hand. The palmar fascia is palmar to the tendons of muscles which flex the fingers, and the dorsal venous arch is so named because it is on the dorsal side of the foot.
|
||||
In humans, volar can also be used synonymously with palmar to refer to the palm of the hand, and can also be used to refer to the sole of the foot. But palmar is used exclusively for the palm of the hand, and plantar is used exclusively for the sole of the foot.
|
||||
Similarly, in the limbs for clarity, the sides are named after the bones. In the forearm, structures closer to the radius are radial, structures closer to the ulna are ulnar, and structures relating to both bones are referred to as radioulnar, such as the distal radioulnar joint. Similarly, in the lower leg, structures near the tibia (shinbone) are tibial and structures near the fibula are fibular (or peroneal).
|
||||
|
||||
=== Rotational direction ===
|
||||
|
||||
Anteversion and retroversion are complementary terms describing an anatomical structure that is rotated forwards (towards the front of the body) or backwards (towards the back of the body), relative to some other position. They are particularly used to describe the curvature of the uterus.
|
||||
|
||||
Anteversion (from Latin anteversus) describes an anatomical structure being tilted further forward than normal, whether pathologically or incidentally. For example, a person's uterus typically is anteverted, tilted slightly forward. A misaligned pelvis may be anteverted, that is to say tilted forward to some relevant degree.
|
||||
Retroversion (from Latin retroversus) describes an anatomical structure tilted back away from something. An example is a retroverted uterus.
|
||||
|
||||
=== Other directional terms ===
|
||||
Several other terms are also used to describe location. These terms are not used to form the fixed axes. Terms include:
|
||||
|
||||
Axial (from Latin axis 'axle'): around the central axis of the organism or the extremity. Two related terms, "abaxial" and "adaxial", refer to locations away from and toward the central axis of an organism, respectively
|
||||
Luminal (from Latin lumen 'light, opening'): on the—hollow—inside of an organ's lumen (body cavity or tubular structure); adluminal is towards, abluminal is away from the lumen. Opposite to outermost (the adventitia, serosa, or the cavity's wall).
|
||||
Terminal (from Latin terminus 'boundary or end') at the extremity of a usually projecting structure; forming the end of a structure such as an axon terminal.
|
||||
Visceral (from Latin viscera 'internal organs'): associated with the innermost layer of an organ within the body. For example, the visceral pleura covering the lungs, contrasted with the parietal pleura lining the thoracic cavity.
|
||||
Parietal (from Latin paries 'wall'): pertaining to the wall of a body cavity as the parietal pleura lining the thoracic cavity, contrasted with visceral pleura.
|
||||
Aboral (away from oral) is used to denote a location in an organism that is further from the mouth.
|
||||
42
data/en.wikipedia.org/wiki/Anatomical_terms_of_location-4.md
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|
||||
---
|
||||
title: "Anatomical terms of location"
|
||||
chunk: 5/5
|
||||
source: "https://en.wikipedia.org/wiki/Anatomical_terms_of_location"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:06.044970+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
== Other animals ==
|
||||
Different terms are used because of different body plans in animals, whether animals stand on two or four legs, and whether an animal is symmetrical or asymmetrical. For example, as humans are bilaterally symmetrical, anatomical descriptions usually use the same terms as those for other vertebrates. However, the standard human anatomical position means that their anterior/posterior and ventral/dorsal directions are the same, so the inferior/superior directions are used due to longstanding tradition instead of cranial/caudal, which apply regardless of position, as in other species. The term "rostral" used to refer to the beak or nose in some animals is used less frequently in humans, with the exception of parts of the brain; while humans do not have a visible tail (the coccygeal vertebrae are present and commonly called the "tailbone") the term "caudal" that refers to the tail-end is also sometimes used in humans and animals without tails to refer to the hind part of the body. Flounder and other flatfish which lie on the seabed on their left or right side are asymmetric, with both eyes on the 'up' side, making anatomical nomenclature a challenge.
|
||||
Invertebrates have a large variety of body shapes that can present a problem when trying to apply standard directional terms. Depending on the organism, some terms are taken by analogy from vertebrate anatomy, and appropriate novel terms are applied as needed. Some such borrowed terms are widely applicable in most invertebrates; for example proximal, meaning "near" refers to the part of an appendage nearest to where it joins the body, and distal, meaning "standing away from" is used for the part furthest from the point of attachment. In all cases, the usage of terms is dependent on the body plan of the organism.
|
||||
|
||||
=== Non-bilaterian organisms ===
|
||||
|
||||
In non-bilaterian organisms with a changeable shape, such as amoeboid organisms, most directional terms are meaningless, since the shape of the organism is not constant and no distinct axes are fixed. Similarly, in radially symmetrical organisms, there is nothing to distinguish one line through the centre of the organism from any other. An indefinite number of triads of mutually perpendicular axes could be defined, but any such choice of axes would be useless, as nothing would distinguish a chosen triad from any others. In such organisms, only terms such as superficial and deep, or sometimes proximal and distal, are usefully descriptive.
|
||||
|
||||
=== Elongated organisms ===
|
||||
|
||||
In organisms that maintain a constant shape and have one dimension longer than the other, at least two directional terms can be used. The long or longitudinal axis is defined by points at the opposite ends of the organism. Similarly, a perpendicular transverse axis can be defined by points on opposite sides of the organism. There is typically no basis for the definition of a third axis. Usually such organisms are planktonic (free-swimming) protists, and are nearly always viewed on microscope slides, where they appear essentially two-dimensional. In some cases a third axis can be defined, particularly where a non-terminal cytostome or other unique structure is present.
|
||||
|
||||
Some elongated protists have distinctive ends of the body. In such organisms, the end with a mouth (or equivalent structure, such as the cytostome in Paramecium or Stentor), or the end that usually points in the direction of the organism's locomotion (such as the end with the flagellum in Euglena), is normally designated as the anterior end. The opposite end then becomes the posterior end. Properly, this terminology would apply only to an organism that is always planktonic (not normally attached to a surface), although the term can also be applied to one that is sessile (normally attached to a surface).
|
||||
|
||||
Organisms that are attached to a substrate, such as sponges and animal-like protists also have distinctive ends. The part of the organism attached to the substrate is usually referred to as the basal end (from Latin basis 'support/foundation'), whereas the end furthest from the attachment is referred to as the apical end (from Latin apex 'peak/tip').
|
||||
|
||||
=== Radially symmetrical organisms ===
|
||||
Radially symmetrical organisms include those in the group Radiata – primarily Cnidarians (jellyfish, sea anemones and corals, and the comb jellies). Adult echinoderms, such as starfish, sea urchins, sea cucumbers and others are also included, since they have a pentamerous symmetry having five discrete symmetric parts arranged around a central axis. Echinoderm larvae are not included, since they are bilaterally symmetrical.
|
||||
Cnidarians have an incomplete digestive system, meaning that one end of the organism has a mouth, the oral end (from Latin ōrālis 'of the mouth'), and the opposite aboral end (from Latin ab- 'away from') has no opening from the gut (coelenteron). They are radially symmetric around the oral-aboral axis. Having only the single distinctive axis, "lateral", "dorsal", and "ventral" have no meaning, and all can be replaced by the generic term peripheral (from Ancient Greek περιφέρεια 'circumference'). Medial can be used, but in the case of radiates indicates the central point, rather than a central axis as in vertebrates. Thus, there are multiple possible radial axes and medio-peripheral (half-) axes.
|
||||
Comb jellies have a biradial symmetry about only two planes, a tentacular plane, and a pharyngeal plane.
|
||||
|
||||
=== Spiders ===
|
||||
|
||||
Special terms are used for spiders. Two such terms are useful in describing views of the legs and pedipalps of spiders, and other arachnids. Prolateral refers to the surface of a leg that is closest to the anterior end of an arachnid's body. Retrolateral refers to the surface of a leg that is closest to the posterior end of an arachnid's body. Most spiders have eight eyes in four pairs. All the eyes are on the carapace of the prosoma, and their sizes, shapes and locations are characteristic of various spider families and other taxa. Usually, the eyes are arranged in two roughly parallel, horizontal and symmetrical rows of eyes. Eyes are labelled according to their position as anterior and posterior lateral eyes (ALE) and (PLE); and anterior and posterior median eyes (AME) and (PME).
|
||||
|
||||
== See also ==
|
||||
Body relative direction
|
||||
Chirality
|
||||
Geometric terms of location
|
||||
Reflection symmetry
|
||||
|
||||
== References ==
|
||||
14
data/en.wikipedia.org/wiki/Anginal_equivalent-0.md
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14
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|
||||
---
|
||||
title: "Anginal equivalent"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Anginal_equivalent"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:07.251155+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
An anginal equivalent is a symptom such as shortness of breath (dyspnea), diaphoresis (sweating), extreme fatigue, or pain at a site other than the chest, occurring in a patient at high cardiac risk. Anginal equivalents are considered to be symptoms of myocardial ischemia. Anginal equivalents are considered to have the same importance as angina pectoris in patients presenting with elevation of cardiac enzymes or certain EKG changes which are diagnostic of myocardial ischemia.
|
||||
|
||||
|
||||
== References ==
|
||||
22
data/en.wikipedia.org/wiki/Anisomastia-0.md
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22
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|
||||
---
|
||||
title: "Anisomastia"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Anisomastia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:08.506878+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Anisomastia is a medical condition in which there is a severe asymmetry or unequalness in the size of the breasts, generally related to a difference in volume. In other words, when one of the breasts is much larger than the other. In contrast to anisomastia, a slight asymmetry of the breasts is common. Anisomastia may be corrected by surgical breast augmentation or reduction.
|
||||
|
||||
|
||||
== See also ==
|
||||
Micromastia
|
||||
Breast hypertrophy
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
64
data/en.wikipedia.org/wiki/Anophthalmia-0.md
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64
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|
||||
---
|
||||
title: "Anophthalmia"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Anophthalmia"
|
||||
category: "reference"
|
||||
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|
||||
date_saved: "2026-05-05T07:26:09.740164+00:00"
|
||||
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|
||||
---
|
||||
|
||||
Anophthalmia (Greek: ἀνόφθαλμος, "without eye") is the medical term for the absence of one or both eyes. Both the globe and the ocular tissue are missing from the orbit. The absence of the eye will cause a small bony orbit, a constricted mucosal socket, short eyelids, reduced palpebral fissure and malar prominence. Genetic mutations, chromosomal abnormalities, and prenatal environment can all cause anophthalmia. Anophthalmia is an extremely rare disease and is mostly rooted in genetic abnormalities. It can also be associated with other syndromes.
|
||||
|
||||
== Classifications ==
|
||||
There are three classifications for this condition:
|
||||
|
||||
Primary anophthalmia is a complete absence of eye tissue due to a failure of the part of the brain that forms the eye.
|
||||
Secondary anophthalmia the eye starts to develop and for some reason stops, leaving the infant with only residual eye tissue or extremely small eyes which can only be seen under close examination.
|
||||
Degenerative anophthalmia the eye started to form and, for some reason, degenerated. One reason for this occurring could be a lack of blood supply to the eye.
|
||||
|
||||
== Associations ==
|
||||
|
||||
There are a few conditions that are associated with anophthalmia. These include:
|
||||
|
||||
Trisomy 13
|
||||
Lenz syndrome
|
||||
Goldenhar-Gorlin syndrome
|
||||
Waardenburg syndrome
|
||||
Aside from these associative conditions, anophthalmia in only one eye tends to be associated with complications in the other eye. These risks include a higher chance of having glaucoma or a detached retina.
|
||||
|
||||
== Causes ==
|
||||
|
||||
=== SOX2 ===
|
||||
The most common genetic cause for anophthalmia is mutated SOX2 gene. Sox2 anophthalmia syndrome is caused by a mutation in the Sox2 gene that does not allow it to produce the Sox2 protein that regulates the activity of other genes by binding to certain regions of DNA. Without this Sox2 protein, the activity of genes that is important for the development of the eye is disrupted. Sox2 anophthalmia syndrome is an autosomal dominant inheritance, but the majority of patients who have Sox2 anophthalmia are the first in their family history to have this mutation. In certain cases, one parent will possess the mutated gene only in their egg or sperm cell and the offspring will inherit it through that. This is called germline mosaicism. There are at least 33 mutations in the Sox2 gene that have been known to cause anophthalmia. Some of these gene mutations will cause the Sox2 protein not to be formed, while other mutations will yield a non-functional version of this protein.
|
||||
|
||||
=== RBP4 ===
|
||||
RBP4 has recently been linked to autosomal dominant form of anophthalmia. This form of anophthalmia has variable penetrance and a unique maternal inheritance effect that is rooted in pregnancy. Specifically, the disease only occurs when a mother and fetus both carry a RBP4 mutation which predisposes the fetus to vitamin A deficiency (a known environmental risk factor for anophthalmia) during pregnancy. If Vitamin A deficiency occurs during the first several months when the eye is developing, it may lead to anophthalmia. This form of anophthalmia is the first that may be intervened upon with vitamin A supplementation of retinyl esters during the first several months of pregnancy. This strategy exploits an RBP-independent pathway. Clinical research is underway.
|
||||
|
||||
=== Other influential genes ===
|
||||
SOX2 and RBP4 are not the only genes that can cause anophthalmia. Other important genes include OTX2, CHX10 and RAX. Each of these genes are an important in retinal expression. Mutations in these genes can cause a failure of retinal differentiation. OTX2 is dominantly inherited. Mutation effects vary in severity, and can include microphthalmia. BMP4 is also linked to anophthalmia, as well as causing myopia and microphthalmia. It is dominantly inherited. BMP4 interacts with the Sonic hedgehog (SHH) pathway and can cause anophthalmia. Haploinsufficiency of PRR12 is also known to result in anophthalmia among other abnormalities.
|
||||
|
||||
=== Environmental influence ===
|
||||
Many environmental conditions have also been known to cause anophthalmia. The strongest support for environmental causes has been studies where children have had gestational-acquired infections. These infections are typically viral. A few known pathogens that can cause anophthalmia are Toxoplasma, rubella, and certain strains of the influenza virus. Other known environmental conditions that have led to anophthalmia are maternal vitamin A deficiency, exposure to X-rays during gestation, solvent abuse, and exposure to thalidomide.
|
||||
|
||||
=== Chromosome 14 ===
|
||||
An interstitial deletion of chromosome 14 has been known to occasionally be the source of anophthalmia. The deletion of this region of chromosome has also been associated with patients having a small tongue, and high arched palate, developmental and growth retardation, undescended testes with a micropenis, and hypothyroidism. The region that has been deleted is region q22.1-q22.3. This confirms that region 22 on chromosome 14 influences the development of the eye.
|
||||
|
||||
== Prenatal diagnosis ==
|
||||
|
||||
=== Ultrasounds ===
|
||||
Ultrasounds can be used to diagnose anophthalmia during gestation. Due to the resolution of the ultrasound, it is difficult to diagnose it until the second trimester. The earliest time to detect anophthalmia this way is approximately 20 weeks.
|
||||
|
||||
=== Amniocentesis ===
|
||||
It is possible to diagnose prenatally with amniocentesis, but it may not show a correct negative result. Amniocentesis can only diagnose anophthalmia when there is a chromosomal abnormality. Chromosomal abnormalities are only a minority of cases of anophthalmia.
|
||||
|
||||
== Postnatal diagnosis ==
|
||||
|
||||
=== MRI/CT ===
|
||||
MRIs and CTs can be used to scan the brain and orbits. Radiologists use this to assess the internal structures of the globe, the optic nerve and extraocular muscles, and brain anatomy.
|
||||
|
||||
=== Examination ===
|
||||
Physicians, specifically ophthalmologists, can examine the child and give a correct diagnosis. Some will do molecular genetics tests to see if the cause is linked with gene mutations.
|
||||
Genetic testing can include chromosomal microarray analysis, single-gene testing, or multigene-panel testing. Genomic testing including exome sequencing, genome sequencing, and mitochondrial sequencing may be considered if single-gene testing or use of a multigene panel fails to confirm a molecular diagnosis.
|
||||
|
||||
== Treatments ==
|
||||
30
data/en.wikipedia.org/wiki/Anophthalmia-1.md
Normal file
30
data/en.wikipedia.org/wiki/Anophthalmia-1.md
Normal file
@ -0,0 +1,30 @@
|
||||
---
|
||||
title: "Anophthalmia"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Anophthalmia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:09.740164+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Prosthetic eye ===
|
||||
Currently, there is not a treatment option for regaining vision by developing a new eye. There are, however, cosmetic options so the absence of the eye is not as noticeable. Typically, the child will need to go to an ocularist to have conformers fitted into the eye. Conformers are made of clear plastic and are fitted into the socket to promote socket growth and expansion. As the child's face grows and develops, the conformer will need to be changed. An expander may also be needed in anophthalmia to expand the socket that is present. The conformer is changed every few weeks the first two years of life. After that, a painted prosthetic eye can be fitted for the child's socket. The prosthetic eye can be cleaned with mild baby soap and water. Rubbing alcohol should be avoided because it may damage the prosthetic eye. Children need to be checked regularly to ensure the fit and size is appropriate.
|
||||
A Cochrane Review published in 2016 asked whether the type of material used to make the prosthetic eye affects the success of the operation. Prosthetic eyes can be made from two types of material; porous or non-porous material. "If the material is porous then the artificial eye can become integrated into the body because new blood vessels can grow into the material. If the material is non-porous, then the artificial eye remains separate from the rest of the body's tissue." After assessing three studies, the review concluded that there wasn't enough evidence to conclude which material was better.
|
||||
|
||||
=== Cosmetic surgery ===
|
||||
If the proper actions are not taken to expand the orbit, many physical deformities can appear. It is important that if these deformities do appear, that surgery is not done until at least the first two years of life. Many people get eye surgery, such as upper eyelid ptosis surgery and lower eyelid tightening. These surgeries can restore the function of the surrounding structures like the eyelid in order to create the best appearance possible. This is more common with people who have degenerative anophthalmia.
|
||||
|
||||
== Epidemiology ==
|
||||
Anophthalmia has been reported to be present in 3 out of every 100,000 births. Many instances of anophthalmia also occur with microphthalmia. A recent study in the UK indicated that anophthalmia and microphthalmia had a combined average of 1 in every 10,000 births. The annual rate of occurrence of anophthalmia/microphthalmia in the United States is about 780 children born/year. The most extensive epidemiological survey on this congenital malformation has been carried out by Dharmasena et al. and using English National Hospital Episode Statistics, they calculated the annual incidence of anophthalmia, microphthalmia and congenital malformations of orbit/lacrimal apparatus from 1999 to 2011. According to this study the incidence of congenital anophthalmia ranged from 2.4 (95% CI 1.3 to 4.0) per 100 000 infants in 1999 to 0.4 (0 to 1.3) in 2011. Parents that already have a child who has anophthalmia have a 1 in 8 chance of having another child with anophthalmia. Approximately two-thirds of all cases of anophthalmia are determined to be of genetic basis. Anophthalmia is one of the leading causes of congenital blindness and accounts for 3–11% of blindness in children. Anophthalmia and microphthalmia together make up 1.7–1.8% of reconstructive surgical cases in laboratory of plastic surgery and ocular prostheses.
|
||||
|
||||
== References ==
|
||||
|
||||
== External links ==
|
||||
|
||||
MAPS – Support group for parents with anophthalmic and microphthalmic children
|
||||
International Children's Anophthalmia and Microphthalmia Network (ICAN)
|
||||
Microphthalmia Anophthalmia & Coloboma Support (MACS) – Charity offering support and information for people affected by microphthalmia, anophthalmia, and coloboma
|
||||
National Eye Institute (NEI) – Resources
|
||||
GeneReviews/NCBI/NIH/UW entry on anophthalmia / microphthalmia
|
||||
NCBI/Molecular diagnosis of anophthalmia / microphthalmia
|
||||
76
data/en.wikipedia.org/wiki/Aplasia-0.md
Normal file
76
data/en.wikipedia.org/wiki/Aplasia-0.md
Normal file
@ -0,0 +1,76 @@
|
||||
---
|
||||
title: "Aplasia"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Aplasia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:11.073294+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Aplasia ( ; from Greek a, "not", "no" + plasis, "formation") is a birth defect where an organ or tissue is wholly or largely absent. It is caused by a defect in a developmental process.
|
||||
Aplastic anemia is the failure of the body to produce blood cells. It may occur at any time, and has multiple causes.
|
||||
|
||||
|
||||
== Types ==
|
||||
|
||||
|
||||
=== Pure red cell aplasia ===
|
||||
|
||||
Pure red cell aplasia (PRCA) is caused by the selective destruction or inhibition of erythroid progenitor or precursor cells. It is characterized by anemia and reticulocytopenia and can be chronic or acute. Diamond–Blackfan anemia is a type of PRCA that occurs at birth. PRCA can be acquired as a primary disorder or as a result of another disorder. Immunosuppressive drugs, particularly corticosteroids, will usually result in a temporary or permanent remission. The final outcome is primarily determined by the underlying disorder.
|
||||
|
||||
|
||||
=== Aplasia cutis congenita ===
|
||||
|
||||
Aplasia cutis congenita is a condition in which some or large portions of the skin is missing at birth. The disorder is most commonly seen on the scalp, often as a solitary lesion without other abnormalities. The condition may be caused by epidermolysis bullosa, specific teratogens, or intrauterine infections, or it may be caused by chromosomal abnormalities, ectodermal dysplasias, or other malformation syndromes.
|
||||
|
||||
|
||||
=== Radial aplasia ===
|
||||
|
||||
Radial aplasia is a condition in which the radius does not form. The radius runs from the elbow to the wrist, where the thumb is located. With radial aplasia, the arm can look misshapen and bent. The thumb could also be absent or shorter than usual.
|
||||
|
||||
|
||||
=== Sertoli cell-only syndrome ===
|
||||
|
||||
Sertoli cell-only syndrome (SCOS), also known as germ cell aplasia, is defined by azoospermia where the testicular seminiferous tubules are lined solely with sertoli cells. Sertoli cells contribute to the formation of the blood-testis barrier and aid in sperm generation. These cells respond to follicle-stimulating hormone, which is secreted by the hypothalamus and aids in spermatogenesis.
|
||||
Men often learn they have Sertoli cell-only syndrome between the ages of 20 and 40 when they are checked for infertility and found to produce no sperm. Other signs and symptoms are uncommon, yet in some cases, an underlying cause of SCO syndrome, such as Klinefelter syndrome, may produce other symptoms.
|
||||
Most cases of SCO syndrome are idiopathic, however, causes may include deletions of genetic material on Y-chromosome regions, particularly the azoospermia factor area. Other factors include chemical or toxin exposure, previous exposure to radiation therapy, and a history of severe trauma. A testicular biopsy confirms the diagnosis of SCO syndrome. Although there is no effective treatment at the moment, assisted reproductive technology may help some men with SCO syndrome reproduce.
|
||||
|
||||
|
||||
=== Pulmonary aplasia ===
|
||||
|
||||
Pulmonary aplasia is a rare congenital pathology characterized by the unilateral or bilateral absence of lung tissue. It is distinct from pulmonary agenesis, which, while similar, has a short-blind ending bronchus in aplasia. Because bilateral pulmonary aplasia is not feasible, it is usually unilateral. It is frequently associated with other congenital abnormalities, primarily cardiovascular, and has been shown to occur with the VACTERL syndrome.
|
||||
|
||||
|
||||
=== Thymic aplasia ===
|
||||
Thymic aplasia is a rare primary immunodeficiency with autosomal or X-linked recessive inheritance, characterized by thymus atrophy in the absence of other congenital abnormalities, profound T-cell deficiency, and normal or increased serum immunoglobulin levels. Patients present with chronic or recurring infections in infancy, such as candidiasis, skin, pulmonary, and urinary tract infections, chronic diarrhea, and failure to thrive.
|
||||
|
||||
|
||||
=== Optic nerve aplasia ===
|
||||
|
||||
Optic nerve aplasia (ONA) is a congenital optic nerve anomaly defined as the absence of the optic nerve head, the retinal blood vessels, ganglion cells of the retina, and optic nerve fibers in an otherwise normal eye. Clinically, the condition is characterized by a lack of light perception, an afferent pupillary defect, and a fundus appearance of an absent optic nerve head and retinal vessels, as well as other ocular and nonocular abnormalities. Bilateral ONA has been linked to systemic anomalies, whereas unilateral ONA is seen in otherwise healthy people.
|
||||
|
||||
|
||||
=== Aplastic anemia ===
|
||||
|
||||
Aplastic anemia is a bone marrow failure syndrome characterized by peripheral pancytopenia and bone marrow hypoplasia. Although the anemia is usually normocytic, mild macrocytosis can be seen in conjunction with stress erythropoiesis and raised fetal hemoglobin levels. Aplastic anemia patients present with symptoms related to a decrease in hematopoietic cell production in the bone marrow. The onset is gradual, and the first symptom is frequently anemia or bleeding, though a high temperature or infections may be present at the onset. The following are examples of specific manifestations:
|
||||
|
||||
Anemia: Pallor, headache, palpitations, dyspnea, fatigue, or foot swelling
|
||||
Thrombocytopenia: Mucosal and gingival bleeding, as well as petechial rashes, may occur.
|
||||
Neutropenia: Can cause overt infections, recurring infections, or mouth and pharyngeal ulcers.
|
||||
The majority of cases of aplastic anemia are idiopathic, and seeking a possible cause is frequently unproductive.
|
||||
|
||||
|
||||
== Epidemiology ==
|
||||
Aplasia is a rare condition. Radial aplasia and pure red cell aplasia, particularly the acquired form of pure red cell aplasia, are the most common types. Radial aplasia affects about one in every 30,000 newborns. Radial ray deficiencies, such as radial aplasia, are one of the most common congenital arm disabilities. Congenital pure red cell aplasia is uncommon, with an estimated 5 to 7 cases per million births. The acquired form is more prevalent.
|
||||
|
||||
|
||||
== See also ==
|
||||
Atrophy
|
||||
Hyperplasia
|
||||
Hypoplasia
|
||||
Neoplasia
|
||||
List of biological development disorders
|
||||
|
||||
|
||||
== References ==
|
||||
16
data/en.wikipedia.org/wiki/Arrested_development-0.md
Normal file
16
data/en.wikipedia.org/wiki/Arrested_development-0.md
Normal file
@ -0,0 +1,16 @@
|
||||
---
|
||||
title: "Arrested development"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Arrested_development"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:12.406155+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
The term "arrested development" has had multiple meanings for over 200 years. In the field of medicine, the term "arrested development" was first used, circa 1835–1836, to mean a stoppage of physical development; the term continues to be used in the same way.
|
||||
In contrast, the UK's Mental Health Act 1983 used the term "arrested development" to characterize a form of mental disorder comprising severe mental impairment, resulting in a lack of intelligence. However, some researchers have objected to the notion that mental development can be "arrested" or stopped, preferring to consider mental status as continuing to develop in other ways. Consequently, the term "arrested development" is no longer used when referring to a developmental disorder in mental health.
|
||||
In anthropology and archaeology, the term "arrested development" means that a plateau of development in some sphere has been reached. Often it is a technological plateau such as the development of high temperature ceramics without glaze because of a lack of materials, or copper smelting without the development of bronze, because of a lack of tin. Arrested development is key in the insight of self-domestication in the evolution of hominidae where it involves being in an environment that favors reduction in aggression, including interspecific and intraspecific antagonism, for survival, in favor of attitudes that favor living together in a group, social behavior, traits that favor the group as a whole to come to the front stage, elimination of bullies - individuals with an antisocial personality disorder.
|
||||
|
||||
|
||||
== References ==
|
||||
27
data/en.wikipedia.org/wiki/Assessment_and_plan-0.md
Normal file
27
data/en.wikipedia.org/wiki/Assessment_and_plan-0.md
Normal file
@ -0,0 +1,27 @@
|
||||
---
|
||||
title: "Assessment and plan"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Assessment_and_plan"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:13.697908+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
The assessment and plan (abbreviated A/P" or A&P) is a component of an admission note.
|
||||
|
||||
Assessment includes a discussion of the differential diagnosis and supporting history and exam findings.
|
||||
The plan is typically broken out by problem or system. Each problem should include:
|
||||
brief summary of the problem, perhaps including what has been done thus far
|
||||
orders for medications, labs, studies, procedures and surgeries to address the problem.
|
||||
problems are commonly derived from
|
||||
chief complaint
|
||||
history of present illness
|
||||
review of systems (rarely; these should have been picked up and incorporated as new chief complaints during the interview)
|
||||
physical exam (rarely; these should have been picked up and incorporated as new chief complaints during the exam)
|
||||
social history, including counseling for smoking, alcohol, and illicit drug use
|
||||
family history
|
||||
medications may indicate problems that need to be addressed in the treatment of the other problems, such as dyslipidemia controlled with a statin.
|
||||
|
||||
|
||||
== References ==
|
||||
44
data/en.wikipedia.org/wiki/Asymptomatic-0.md
Normal file
44
data/en.wikipedia.org/wiki/Asymptomatic-0.md
Normal file
@ -0,0 +1,44 @@
|
||||
---
|
||||
title: "Asymptomatic"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Asymptomatic"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:14.855425+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Asymptomatic (or clinically silent) is an adjective categorising the medical conditions (i.e., injuries or diseases) that patients carry but without experiencing their symptoms, despite an explicit diagnosis (e.g., a positive medical test).
|
||||
Pre-symptomatic is the adjective categorising the time periods during which the medical conditions are asymptomatic.
|
||||
Subclinical and paucisymptomatic are other adjectives categorising either the asymptomatic infections (i.e., subclinical infections), or the psychosomatic illnesses and mental disorders expressing a subset of symptoms but not the entire set an explicit medical diagnosis requires.
|
||||
|
||||
|
||||
== Examples ==
|
||||
An example of an asymptomatic disease is cytomegalovirus (CMV) which is a member of the herpes virus family. "It is estimated that 1% of all newborns are infected with CMV, but the majority of infections are asymptomatic." (Knox, 1983; Kumar et al. 1984) In some diseases, the proportion of asymptomatic cases can be important. For example, in multiple sclerosis it is estimated that around 25% of the cases are asymptomatic, with these cases detected postmortem or just by coincidence (as incidental findings) while treating other diseases.
|
||||
|
||||
|
||||
== Importance ==
|
||||
Knowing that a condition is asymptomatic is important because:
|
||||
|
||||
It may be contagious, and the contribution of asymptomatic and pre-symptomatic infections to the transmission level of a disease helps set the required control measures to keep it from spreading.
|
||||
It is not required that a person undergo treatment. It does not cause later medical problems such as high blood pressure and hyperlipidaemia.
|
||||
Be alert to possible problems: asymptomatic hypothyroidism makes a person vulnerable to Wernicke–Korsakoff syndrome or beri-beri following intravenous glucose.
|
||||
For some conditions, treatment during the asymptomatic phase is vital. If one waits until symptoms develop, it is too late for survival or to prevent damage.
|
||||
|
||||
|
||||
== Mental health ==
|
||||
Subclinical or subthreshold conditions are those for which the full diagnostic criteria are not met and have not been met in the past, although symptoms are present. This can mean that symptoms are not severe enough to merit a diagnosis, or that symptoms are severe but do not meet the criteria of a condition.
|
||||
|
||||
|
||||
== List ==
|
||||
These are conditions for which there is a sufficient number of documented individuals that are asymptomatic that it is clinically noted. For a complete list of asymptomatic infections see subclinical infection.
|
||||
|
||||
Millions of women reported lack of symptoms during pregnancy until the point of childbirth or the beginning of labor and did not know they were pregnant. This phenomenon is known as cryptic pregnancies.
|
||||
|
||||
|
||||
== See also ==
|
||||
Symptomatic
|
||||
Subclinical infection
|
||||
|
||||
|
||||
== References ==
|
||||
38
data/en.wikipedia.org/wiki/Asymptomatic_carrier-0.md
Normal file
38
data/en.wikipedia.org/wiki/Asymptomatic_carrier-0.md
Normal file
@ -0,0 +1,38 @@
|
||||
---
|
||||
title: "Asymptomatic carrier"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Asymptomatic_carrier"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:16.115969+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
An asymptomatic carrier is a person or other organism that has become infected with a pathogen, but shows no signs or symptoms.
|
||||
Although unaffected by the pathogen, carriers can transmit it to others or develop symptoms in later stages of the disease. Asymptomatic carriers play a critical role in the transmission of common infectious diseases such as typhoid, HIV, C. difficile, influenzas, cholera, tuberculosis, and COVID-19, although the latter is often associated with "robust T-cell immunity" in more than a quarter of patients studied. While the mechanism of disease-carrying is still unknown, researchers have made progress towards understanding how certain pathogens can remain dormant in a human for a period of time. A better understanding of asymptomatic disease carriers is crucial to the fields of medicine and public health as they work towards mitigating the spread of common infectious diseases.
|
||||
|
||||
== Types of asymptomatic carriers ==
|
||||
Asymptomatic carriers can be categorized by their current disease state. When an individual transmits pathogens immediately following infection but prior to developing symptoms, they are known as an incubatory carrier. Humans are also capable of spreading disease following a period of illness. Typically thinking themselves cured of the disease, these individuals are known as convalescent carriers. Viral diseases such as hepatitis and poliomyelitis are frequently transmitted in this manner. "Healthy carriers" never exhibit signs or symptoms of the disease, yet are capable of infecting others, and are often considered to be the "classic" asymptomatic carriers.
|
||||
While the mechanism of disease carrying is still unknown, researchers have made progress towards understanding how certain pathogens can remain dormant in a human for a period of time.
|
||||
|
||||
== Significance in disease transmission ==
|
||||
The limited information on the prevalence of asymptomatic carriers creates a considerable difficulty when planning public health initiatives. Given that disease surveillance is dependent on estimates for both the asymptomatic rates and symptomatic rates of disease, the lack of information on the prevalence of carriers can lead to insufficient initiatives for the mitigation of common public health concerns such as C. difficile or influenza.
|
||||
Researchers have expressed the desire to better predict transmission methods in order to determine the appropriate public health response. For example, a disease with a known low asymptomatic rate may lead to increased surveillance of symptomatic cases, whereas a higher asymptomatic rate could lead to more aggressive methods such as travel bans and compulsory quarantines, since the number of infectious, asymptomatic cases would be unknown.
|
||||
|
||||
== Possible explanations ==
|
||||
While an exact explanation for asymptomatic carriage is unknown, researchers have been dedicating their efforts towards understanding how specific bacteria thrive in human hosts in the hopes of determining a universal understanding of asymptomatic transmission.
|
||||
|
||||
=== A biological mechanism utilizing Salmonella ===
|
||||
Numerous research publications have demonstrated how salmonella is able to remain in immune cells and alter their metabolic systems in order to further transmit the disease. Utilizing a closely related strand of bacterium (S. typhimurium), scientists have been able to create a mouse model that mimics the persistent salmonella cases seen in carriers of typhoid. Knowing that the bacterium can reside in mice for their entire lives, researchers have been able to determine that the bacterium tends to reside in macrophages. Further examination of the gut lymph nodes of the mice reveals that S. typhimurium changes the inflammatory response of the macrophages. Instead of eliciting an inflammatory response from the attack cells, the bacterium is able to convert them into an anti-inflammatory macrophage, allowing for optimal survival conditions. In the words of lead scientist Denise Monack, "It wasn't that inflammatory macrophages were invulnerable to infection, but rather that, having infected a macrophage, S. typhimurium was much more able to replicate in the anti-inflammatory type".
|
||||
Investigators have also found that the presence of peroxisome proliferator-activated receptors (PPARs) correlated to the presence of salmonella bacterium. PPARs, thought of as roaming genetic switches, are responsible for the fat metabolism needed to sustain anti-inflammatory macrophages in which S. typhimurium hides.
|
||||
|
||||
== Asymptomatic bacteriuria ==
|
||||
Asymptomatic bacteriuria is a condition that typically impacts 3–5% of women, with the most vulnerable populations being the elderly and those diagnosed with diabetes. Within the female population, the risk of bacteriuria increases with age. Escherichia coli is the most common organism found during urine analysis, though the variety of potentially infectious organisms is diverse and can include Enterobacteriaceae, Pseudomonas aeruginosa, Enterococcus species, and group B streptococcus. The Agency for Healthcare Research and Quality has issued a set of screening recommendations as well as offered some insight into the mechanism of bacteriuria. Results of the meta-analysis produced no clear explanation for asymptomatic carriage, but did yield new evidence that strengthened the support for screening for asymptomatic bacteriuria in pregnant women only.
|
||||
|
||||
== Infectious diseases ==
|
||||
Asymptomatic carriers have furthered the spread of many infectious diseases. A common principle in epidemiology, the 80–20 rule, speculates that 80% of the disease transmission is conducted by only 20% of people in a population.
|
||||
|
||||
=== Typhoid fever ===
|
||||
Typhoid fever is an ailment caused by the bacterium Salmonella enterica ser. Typhi. An individual can acquire this infection from consuming risky foods or drinks, or by consuming foods or drinks prepared by an infected individual. Those who recover from this infection can still carry the bacteria in their cells, and therefore be asymptomatic.
|
||||
|
||||
==== Typhoid Mary ====
|
||||
45
data/en.wikipedia.org/wiki/Asymptomatic_carrier-1.md
Normal file
45
data/en.wikipedia.org/wiki/Asymptomatic_carrier-1.md
Normal file
@ -0,0 +1,45 @@
|
||||
---
|
||||
title: "Asymptomatic carrier"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Asymptomatic_carrier"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:16.115969+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Mary Mallon, known as "Typhoid Mary", was an asymptomatic carrier of Salmonella enterica serovar typhi, the causative agent of typhoid fever. She was a cook for several families and soldiers in New York City during the late 1800s, and several cases of typhoid fever were traced to her by the Health Department. At the time, there was no way of eradicating the disease, and it was spread primarily through fecal-oral transmission. Most of Mary Mallon's transmission risk was thought to arise from her continued involvement in occupations involving food preparation and handling. New York City's public health officials initially sought to merely restrict her from such employment rather than permanently quarantining her. When she continued to be non-compliant, the Health Commission ordered that she be quarantined on one of the islands surrounding Manhattan. She remained there until her death.
|
||||
Despite appearing perfectly healthy, it is estimated that Mallon infected about 50 people before she was quarantined on North Brother Island. Scientists calculate that between 1% and 6% of individuals infected with Salmonella typhi become chronic, asymptomatic carriers like Mary.
|
||||
|
||||
=== HIV ===
|
||||
|
||||
HIV infection has a long period during which the person is asymptomatic. Although the host may not be experiencing symptoms, the virus can still be passed on to others. It is also possible for the infection to become symptomatic after this incubation period. Whether the host is showing symptoms or not, opportunistic infections can take advantage of the weakened immune system and cause further complications.
|
||||
|
||||
=== Epstein–Barr virus ===
|
||||
Many carriers are infected with persistent viruses such as Epstein–Barr virus (EBV), a member of the herpes virus family. Studies show that about 95% of adults have antibodies against EBV, which means they were infected with the virus at some point in their life.
|
||||
|
||||
=== Clostridioides difficile ===
|
||||
Clostridioides difficile has also been shown to be spread by asymptomatic carriers, and poses significant problems in home-care settings. Reports indicating that over 50% of long-term patients present with fecal contamination despite a lack of symptoms have led many hospitals to extend the period of contact precautions until discharge.
|
||||
|
||||
=== Cholera ===
|
||||
For cholera the estimates of the ratio of asymptomatic to symptomatic infections have ranged from 3 to 100.
|
||||
|
||||
=== Chlamydia ===
|
||||
Chlamydia, an STI that affects both men and women, can also be asymptomatic in most individuals. Although the infection may not yield any obvious symptoms, it can still damage the reproductive system. If the infection goes unnoticed for a long time, infected individuals are at risk of developing pelvic inflammatory disease (PID). Like chlamydia, PID can also be asymptomatic.
|
||||
|
||||
=== Poliomyelitis ===
|
||||
A small number of asymptomatic carriers of polio (referred to as chronic excretors) continue to produce active virus for years (or even decades) after their initial exposure to the oral Sabin vaccine. Carriers of the attenuated virus unintentionally spread the attenuated virus, inoculating others, giving them contact immunity; however some adults with weak immune systems have contracted paralytic polio from contact with recently immunized children. Carriers of virulent strains spread polio, increasing the difficulty of poliomyelitis eradication.
|
||||
|
||||
=== Tuberculosis ===
|
||||
Tuberculosis (TB) is an infectious disease usually caused by the bacterium Mycobacterium tuberculosis (MTB). Tuberculosis generally affects the lungs, but can also affect other parts of the body. Active or symptomatic tuberculosis is spread from person to person through the air through bacterium spores that are released into the air following a cough or sneeze. Some individuals may be infected with the tuberculosis mycobacterium but never display symptoms. Called latent tuberculosis, these cases, while uncontagious, are particularly problematic from a public health perspective, since approximately 10% of those diagnosed with latent TB will go on to develop an active (and contagious) case.
|
||||
|
||||
=== COVID-19 ===
|
||||
A 2021 paper estimated that at least 50% of SARS-CoV-2 infections were a result of exposure to asymptomatic carriers.
|
||||
|
||||
== See also ==
|
||||
Vector (epidemiology)
|
||||
Viral load
|
||||
Virulence
|
||||
Jennie Barmore, "Typhoid Jennie"
|
||||
|
||||
== References ==
|
||||
55
data/en.wikipedia.org/wiki/Atresia-0.md
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|
||||
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|
||||
title: "Atresia"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Atresia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:18.542702+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Atresia is a condition in which an orifice or passage in the body is (usually abnormally) closed or absent.
|
||||
|
||||
== Types ==
|
||||
|
||||
=== Anotia ===
|
||||
|
||||
Anotia is characterized by the complete absence of the ear and is extremely rare. This condition may affect one or both ears, though one missing ear is more common. Anotia is also linked to conductive hearing loss, a condition in which sound waves do not travel well through the ear and sound is not efficiently conducted from the outer ear canal to the eardrum. Anotia has no known cause. An associated syndrome, such as Treacher Collins or Goldenhar syndrome, may affect up to 40% of patients. Anotia is typically diagnosed through a physical examination at birth. Prenatal ultrasounds may help with early detection. Total ear reconstruction is the standard treatment for Anotia.
|
||||
|
||||
=== Biliary atresia ===
|
||||
|
||||
Biliary atresia (BA) is a rare disease marked by an unknown-origin biliary obstruction that manifests in the neonatal period. The classic clinical triad of Biliary atresia is acholic stools, and dark urine, jaundice, and hepatomegaly. The clinical manifestations are used to make the diagnosis, which is supported by liver ultrasonography, cholangiography, and a liver biopsy. The initial treatment is surgical, with the obliterated extrahepatic bile duct resected and a hepatoportoenterostomy created.
|
||||
|
||||
=== Bronchial atresia ===
|
||||
|
||||
Bronchial atresia is a rare congenital disease characterized by segmental or lobar emphysema and, in some cases, mucoid impaction. The exact cause of bronchial atresia is unknown; the lobar bronchi, subsegmental bronchi, and distal bronchioles develop in the fifth, sixth, and sixteenth weeks of fetal development, respectively. Bronchial atresia is frequently discovered incidentally because it is asymptomatic. Recurrent pulmonary infections are among the most frequent clinical manifestations in symptomatic patients. Because such benign disease frequently affects young patients, minimally invasive surgery, such as thoracoscopic surgery, is advised.
|
||||
|
||||
=== Choanal atresia ===
|
||||
|
||||
Choanal atresia (CA) is a rare but well-known condition marked by the anatomical closure of the posterior choanae in the nasal cavity. CA presents clinically in a variety of ways, ranging from acute airway obstruction to chronic recurrent sinusitis, depending on whether it is unilateral, bilateral, or paired with other coexisting airway abnormalities, as is common in individuals who have CHARGE syndrome and craniofacial anomalies. The initial clinical evaluation consists of inserting a six or eight Fr suction catheter through the nostrils, performing a methylene blue dye test, a cotton wisp test, and a laryngeal mirror test. In patients with proper nasal preparation, a CT of the sinuses with 2-5 mm cuts provides a definitive evaluation.
|
||||
|
||||
=== Esophageal atresia ===
|
||||
|
||||
Esophageal atresia (EA) is a rare congenital malformation characterized by a lack of continuity between the lower and upper esophageal pouches, often associated with tracheoesophageal fistula. Esophageal atresia with or without tracheoesophageal fistula (TEF) is the most common birth defect of the esophagus. The diagnosis of EA usually occurs within the first 24 hours of life, but it can be made antenatally or later. Although environmental effects and genetic factors have been documented, the causes of EA remain largely unknown. Treatment is surgical and includes reconstruction of the continuity of the esophagus or replacement by other organs.
|
||||
|
||||
=== Follicular atresia ===
|
||||
|
||||
Follicular atresia refers to the process in which a follicle fails to develop, thus preventing it from ovulating and releasing an egg. It is a normal, naturally occurring progression that occurs as mammalian ovaries age. Approximately 1% of mammalian follicles in ovaries undergo ovulation and the remaining 99% of follicles go through follicular atresia as they cycle through the growth phases. In summary, follicular atresia is a process that leads to the follicular loss and loss of oocytes, and any disturbance or loss of functionality of this process can lead to many other conditions.
|
||||
|
||||
=== Imperforate anus ===
|
||||
|
||||
Imperforate anus is a somewhat common anomaly, with a newborn incidence ranging from 1: 1500 to 1:5000. There have been isolated cases of imperforate anus, but this condition is more commonly found as one among numerous anomalies. Imperforate anus is usually not diagnosed until after birth. There is no need for immediate reconstructive anorectal surgery. However, prompt evaluation is critical, and urgent decompressive surgery may be required.
|
||||
|
||||
=== Intestinal atresia ===
|
||||
|
||||
With an incidence of 1 in 5,000 newborns, intestinal atresias are one of the most common causes of neonatal intestinal obstruction. The majority of cases are small intestinal atresia, while colonic atresias are uncommon. There have been two main etiologies proposed for intestinal atresia: the first is a lack of re-vacuolization of the solid cord stage of intestinal development, and the second is a late intrauterine mesenteric vascular accident. Prenatal ultrasonography is the most reliable way to diagnose intestinal artesia. Pre-operative management includes primary resuscitation, correction of dehydration, and correction of electrolyte abnormalities. Kimura's diamond-shaped duodeno-duodenostomy is the most common surgical treatment.
|
||||
|
||||
=== Microtia ===
|
||||
|
||||
Microtia is a congenital deformity where the auricle (external ear) is underdeveloped. A completely undeveloped pinna is referred to as anotia. Because microtia and anotia have the same origin, it can be referred to as microtia-anotia. Microtia can be unilateral (one side only) or bilateral (affecting both sides). Microtia occurs in 1 out of about 8,000–10,000 births. In unilateral microtia, the right ear is most commonly affected. It may occur as a complication of taking Accutane (isotretinoin) during pregnancy.
|
||||
|
||||
=== Potter sequence ===
|
||||
|
||||
Potter's sequence is a fatal sporadic and autosomal recessive disorder with an incidence of 1 in 4000 births. Babies born with this defect are either stillborn or die very soon after birth. It primarily affects male babies and is associated with severe oligohydramnios, polycystic kidney, bilateral renal agenesis, and obstructive uropathy during the middle gestational weeks. The main defect in Potter's sequence is renal failure. Premature birth, breech presentation, atypical facial appearance, and limb malformations are other distinguishing characteristics. In most infants, severe respiratory insufficiency results in death.
|
||||
|
||||
=== Renal agenesis ===
|
||||
21
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|
||||
---
|
||||
title: "Atresia"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Atresia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:18.542702+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Renal agenesis occurs when the ureteric bud doesn't fuse with the metanephric blastema during embryogenesis, leading to the nephron and, in some cases, the ureter being absent. Unilateral renal agenesis occurs in 1 in 1000 live births, in contrast bilateral renal agenesis occurs in 1 in 3000 to 4000 pregnancies. Unilateral renal agenesis has a very good prognosis, whereas bilateral renal agenesis has a high rate of perinatal mortality and morbidity due to the lack of amniotic fluid, resulting in lethal pulmonary hypoplasia. The diagnosis of renal agenesis is usually made during a midgestation anatomy ultrasound examination. A genetic syndrome or other anomalies are linked to approximately 30% of cases of renal agenesis.
|
||||
|
||||
=== Tricuspid atresia ===
|
||||
|
||||
Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle. This defect is contracted during prenatal development, when the heart does not finish developing. It causes the systemic circulation to be filled with relatively deoxygenated blood. The causes of tricuspid atresia are unknown.
|
||||
|
||||
=== Vaginal atresia ===
|
||||
|
||||
Vaginal atresia is a birth defect that causes uterovaginal outflow tract obstruction. It happens when the urogenital sinus fails to form the caudal portion of the vagina. Fibrous tissue replaces the caudal portion of the vagina. Vaginal atresia is thought to affect one in every 5000-10,000 live female births. The anomaly is frequently undetected until adolescence, when primary amenorrhea or abdominal pain caused by an obstructed uterovaginal tract leads to a diagnostic evaluation.
|
||||
|
||||
== References ==
|
||||
45
data/en.wikipedia.org/wiki/Atypia-0.md
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|
||||
---
|
||||
title: "Atypia"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Atypia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:19.731619+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Atypia (from Greek, a + typos, without type; a condition of being irregular or nonstandard) is a histopathologic term for a structural abnormality in a cell, i.e. it is used to describe atypical cells.
|
||||
Atypia can be caused by infection or irritation. If, for example it were diagnosed in a Pap smear in the uterus it is more likely to be precancerous.
|
||||
The related concept of dysplasia refers to an abnormality of development, and includes abnormalities on larger, histopathologic scales.
|
||||
|
||||
|
||||
== Example features ==
|
||||
Features that constitute atypia have different definitions for different diseases, but often include the following nucleus abnormalities:
|
||||
|
||||
Enlargement
|
||||
Pleomorphism
|
||||
Nuclear polychromasia, which means variability in nuclear chromatin content. Polychromasia otherwise refers to a disease of immature red blood cells.
|
||||
Numerous mitotic figures
|
||||
|
||||
|
||||
=== Examples for Barrett's esophagus ===
|
||||
In Barrett's esophagus, features that are classified as atypia but not as dysplasia are mainly:
|
||||
|
||||
Nuclear stratification, wherein cell nuclei, which are normally located nearly at the same level between adjacent cells, are instead located at different levels.
|
||||
Crowding
|
||||
Hyperchromatism
|
||||
Prominent nucleoli
|
||||
|
||||
|
||||
== Prognosis ==
|
||||
It may or may not be a precancerous indication associated with later malignancy, but the level of appropriate concern is highly dependent on the context with which it is diagnosed.
|
||||
For example, already differentiated, specialised cells such as epithelia displaying "cellular atypia" are far less likely to become problematic (cancerous/malignant) than are myeloid progenitor cells of the immune system. The 'further back' in an already specialised, differentiated cell's lineage, the more problematic cellular atypia is likely to be. This is due to the conferring of such atypia to progeny-cells further down the lineage of that cell type.
|
||||
|
||||
|
||||
== See also ==
|
||||
|
||||
Irregularity
|
||||
List of biological development disorders
|
||||
|
||||
|
||||
== References ==
|
||||
13
data/en.wikipedia.org/wiki/Auditory_agnosia-0.md
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|
||||
---
|
||||
title: "Auditory agnosia"
|
||||
chunk: 1/5
|
||||
source: "https://en.wikipedia.org/wiki/Auditory_agnosia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:21.081452+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but rather a neurological inability of the brain to process sound meaning. While auditory agnosia impairs the understanding of sounds, other abilities such as reading, writing, and speaking are not hindered. It is caused by bilateral damage to the anterior superior temporal gyrus, which is part of the auditory pathway responsible for sound recognition, the auditory "what" pathway.
|
||||
Persons with auditory agnosia can physically hear the sounds and describe them using unrelated terms, but are unable to recognize them. They might describe the sound of some environmental sounds, such as a motor starting, as resembling a lion roaring, but would not be able to associate the sound with "car" or "engine", nor would they say that it was a lion creating the noise. All auditory agnosia patients read lips in order to enhance the speech comprehension.
|
||||
It is yet unclear whether auditory agnosia (also called general auditory agnosia) is a combination of milder disorders, such auditory verbal agnosia (pure word deafness), non-verbal auditory agnosia, amusia and word-meaning deafness, or a mild case of the more severe disorder, cerebral deafness. Typically, a person with auditory agnosia would be incapable of comprehending spoken language as well as environmental sounds. Some may say that the milder disorders are how auditory agnosia occurs. There are few cases where a person may not be able to understand spoken language. This is called verbal auditory agnosia or pure word deafness. Nonverbal auditory agnosia is diagnosed when a person's understanding of environmental sounds is inhibited. Combined, these two disorders portray auditory agnosia. The blurriness between the combination of these disorders may lead to discrepancies in reporting. As of 2014, 203 patients with auditory perceptual deficits due to CNS damage were reported in the medical literature, of which 183 diagnosed with general auditory agnosia or word deafness, 34 with cerebral deafness, 51 with non-verbal auditory agnosia-amusia and 8 word meaning deafness (for a list of patients see).
|
||||
21
data/en.wikipedia.org/wiki/Auditory_agnosia-1.md
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|
||||
---
|
||||
title: "Auditory agnosia"
|
||||
chunk: 2/5
|
||||
source: "https://en.wikipedia.org/wiki/Auditory_agnosia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:21.081452+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
== History ==
|
||||
A relationship between hearing and the brain was first documented by Ambroise Paré, a 16th century battlefield doctor, who associated parietal lobe damage with acquired deafness (reported in Henschen, 1918). Systematic research into the manner in which the brain processes sounds, however, only began toward the end of the 19th century. In 1874, Wernicke was the first to ascribe to a brain region a role in auditory perception. Wernicke proposed that the impaired perception of language in his patients was due to losing the ability to register sound frequencies that are specific to spoken words (he also suggested that other aphasic symptoms, such as speaking, reading and writing errors occur because these speech specific frequencies are required for feedback). Wernicke localized the perception of spoken words to the posterior half of the left STG (superior temporal gyrus). Wernicke also distinguished between patients with auditory agnosia (which he labels as receptive aphasia) with patients who cannot detect sound at any frequency (which he labels as cortical deafness).
|
||||
In 1877, Kussmaul was the first to report auditory agnosia in a patient with intact hearing, speaking, and reading-writing abilities. This case-study led Kussmaul to propose of distinction between the word perception deficit and Wernicke's sensory aphasia. He coined the former disorder as "word deafness". Kussmaul also localized this disorder to the left STG. Wernicke interpreted Kussmaul's case as an incomplete variant of his sensory aphasia.
|
||||
In 1885, Lichtheim also reported of an auditory agnosia patient. This patient, in addition to word deafness, was impaired at recognizing environmental sounds and melodies. Based on this case study, as well as other aphasic patients, Lichtheim proposed that the language reception center receives afferents from upstream auditory and visual word recognition centers, and that damage to these regions results in word deafness or word blindness (i.e., alexia), respectively. Because the lesion of Lichtheim's auditory agnosia patient was sub-cortical deep to the posterior STG (superior temporal gyrus), Lichtheim renamed auditory agnosia as "sub-cortical speech deafness".
|
||||
The language model proposed by Wernicke and Lichtheim wasn't accepted at first. For example, in 1897 Bastian argued that, because aphasic patients can repeat single words, their deficit is in the extraction of meaning from words. He attributed both aphasia and auditory agnosia to damage in Lichtheim's auditory word center. He hypothesized that aphasia is the outcome of partial damage to the left auditory word center, whereas auditory agnosia is the result of complete damage to the same area. Bastian localized the auditory word center to the posterior MTG (middle temporal gyrus).
|
||||
Other opponents to the Wernicke-Lichtheim model were Sigmund Freud and Carl Freund. Freud (1891) suspected that the auditory deficits in aphasic patients was due to a secondary lesion to cochlea. This assertion was confirmed by Freund (1895), who reported two auditory agnosia patients with cochlear damage (although in a later autopsy, Freund reported also the presence of a tumor in the left STG in one of these patients). This argument, however, was refuted by Bonvicini (1905), who measured the hearing of an auditory agnosia patient with tuning forks, and confirmed intact pure tone perception. Similarly, Barrett's aphasic patient, who was incapable of comprehending speech, had intact hearing thresholds when examined with tuning forks and with a Galton whistle. The most adverse opponent to the model of Wernicke and Lichtheim was Marie (1906), who argued that all aphasic symptoms manifest because of a single lesion to the language reception center, and that other symptoms such as auditory disturbances or paraphasia are expressed because the lesion encompasses also sub-cortical motor or sensory regions.
|
||||
In the following years, increasing number of clinical reports validated the view that the right and left auditory cortices project to a language reception center located in the posterior half of the left STG, and thus established the Wernicke-Lichtheim model. This view was also consolidated by Geschwind (1965) who reported that, in humans, the left planum temporale is larger in the left hemisphere than on the right. Geschwind interpreted this asymmetry as anatomical verification for the role of left posterior STG in the perception of language.
|
||||
The Wernicke-Lichtheim-Geschwind model persisted throughout the 20th century. However, with the advent of MRI and its usage for lesion mapping, it was shown that this model is based on incorrect correlation between symptoms and lesions. Although this model is considered outdated, it is still widely mentioned in Psychology and medical textbooks, and consequently in medical reports of auditory agnosia patients. As will be mentioned below, based on cumulative evidence the process of sound recognition was recently shifted to the left and right anterior auditory cortices, instead of the left posterior auditory cortex.
|
||||
|
||||
== Related disorders ==
|
||||
After auditory agnosia was first discovered, subsequent patients were diagnosed with different types of hearing impairments. In some reports, the deficit was restricted to spoken words, environmental sounds or music. In one case study, each of the three sound types (music, environmental sounds, speech) was also shown to recover independently (Mendez and Geehan, 1988-case 2). It is yet unclear whether general auditory agnosia is a combination of milder auditory disorders, or whether the source of this disorder is at an earlier auditory processing stage.
|
||||
18
data/en.wikipedia.org/wiki/Auditory_agnosia-2.md
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|
||||
---
|
||||
title: "Auditory agnosia"
|
||||
chunk: 3/5
|
||||
source: "https://en.wikipedia.org/wiki/Auditory_agnosia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:21.081452+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Cerebral deafness ===
|
||||
Cerebral deafness (also known as cortical deafness or central deafness) is a disorder characterized by complete deafness that is the result of damage to the central nervous system. The primary distinction between auditory agnosia and cerebral deafness is the ability to detect pure tones, as measured with pure tone audiometry. Using this test, auditory agnosia patients were often reported capable of detecting pure tones almost as good as healthy individuals, whereas cerebral deafness patients found this task almost impossible or they required very loud presentations of sounds (above 100 dB). In all reported cases, cerebral deafness was associated with bilateral temporal lobe lesions. A study that compared the lesions of two cerebral deafness patients to an auditory agnosia patient concluded that cerebral deafness is the result of complete de-afferentation of the auditory cortices, whereas in auditory agnosia some thalamo-cortical fibers are spared. In most cases the disorder is transient and the symptoms mitigate into auditory agnosia (although chronic cases were reported). Similarly, a monkey study that ablated both auditory cortices of monkeys reported of deafness that lasted 1 week in all cases, and that was gradually mitigated into auditory agnosia in a period of 3–7 weeks.
|
||||
|
||||
=== Pure word deafness ===
|
||||
Since the early days of aphasia research, the relationship between auditory agnosia and speech perception has been debated. Lichtheim (1885) proposed that auditory agnosia is the result of damage to a brain area dedicated to the perception of spoken words, and consequently renamed this disorder from 'word deafness' to 'pure word deafness'. The description of word deafness as being exclusively for words was adopted by the scientific community despite the patient reported by Lichtheim's who also had more general auditory deficits. Some researchers who surveyed the literature, however, argued against labeling this disorder as pure word deafness on the account that all patients reported impaired at perceiving spoken words were also noted with other auditory deficits or aphasic symptoms. In one review of the literature, Ulrich (1978) presented evidence for separation of word deafness from more general auditory agnosia, and suggested naming this disorder "linguistic auditory agnosia" (this name was later rephrased into "verbal auditory agnosia"). To contrast this disorder with auditory agnosia in which speech repetition is intact (word meaning deafness), the name "word sound deafness" and "phonemic deafness" (Kleist, 1962) were also proposed. Although some researchers argued against the purity of word deafness, some anecdotal cases with exclusive impaired perception of speech were documented. On several occasions, patients were reported to gradually transition from pure word deafness to general auditory agnosia/cerebral deafness or recovery from general auditory agnosia/cerebral deafness to pure word deafness.
|
||||
In a review of the auditory agnosia literature, Phillips and Farmer showed that patients with word deafness are impaired in their ability to discriminate gaps between click sounds as long as 15-50 milliseconds, which is consistent with the duration of phonemes. They also showed that patients with general auditory agnosia are impaired in their ability to discriminate gaps between click sounds as long as 100–300 milliseconds. The authors further showed that word deafness patients liken their auditory experience to hearing foreign language, whereas general auditory agnosia described speech as incomprehensible noise. Based on these findings, and because both word deafness and general auditory agnosia patients were reported to have very similar neuroanatomical damage (bilateral damage to the auditory cortices), the authors concluded that word deafness and general auditory agnosia is the same disorder, but with a different degree of severity.
|
||||
Pinard et al also suggested that pure word deafness and general auditory agnosia represent different degrees of the same disorder. They suggested that environmental sounds are spared in the mild cases because they are easier to perceive than speech parts. They argued that environmental sounds are more distinct than speech sounds because they are more varied in their duration and loudness. They also proposed that environmental sounds are easier to perceive because they are composed of a repetitive pattern (e.g., the bark of a dog or the siren of the ambulance).
|
||||
Auerbach et al considered word deafness and general auditory agnosia as two separate disorders, and labelled general auditory agnosia as pre-phonemic auditory agnosia and word deafness as post-phonemic auditory agnosia. They suggested that pre-phonemic auditory agnosia manifests because of general damage to the auditory cortex of both hemispheres, and that post-phonemic auditory agnosia manifests because of damage to a spoken word recognition center in the left hemisphere. A recent research on an epileptic patient supported this hypothesis. The patient undergone electro-stimulation to the anterior superior temporal gyrus, and demonstrated a transient loss of speech comprehension, while preserving intact perception of environmental sounds and music.
|
||||
21
data/en.wikipedia.org/wiki/Auditory_agnosia-3.md
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|
||||
---
|
||||
title: "Auditory agnosia"
|
||||
chunk: 4/5
|
||||
source: "https://en.wikipedia.org/wiki/Auditory_agnosia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:21.081452+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Non-verbal auditory agnosia ===
|
||||
The term auditory agnosia was originally coined by Sigmund Freud in 1891, to describe patients with selective impairment of environmental sounds. In a review of the auditory agnosia literature, Ulrich re-named this disorder as non-verbal auditory agnosia (although sound auditory agnosia and environmental sound auditory agnosia are also commonly used). This disorder is very rare and only 18 cases have been documented. In contradiction to pure word deafness and general auditory agnosia, this disorder is likely under-diagnosed because patients are often not aware of their disorder, and thus don't seek medical intervention.
|
||||
Throughout the 20th century, all reported non-verbal auditory agnosia patients had bilateral or right temporal lobe damage. For this reason, the right hemisphere was traditionally attributed with the perception of environmental sounds. However, Tanaka et al reported 8 patients with non-verbal auditory agnosia, 4 with right hemisphere lesions and 4 with left hemisphere lesions. Saygin et al also reported a patient with damage to the left auditory cortex.
|
||||
The underlying deficit in non-verbal auditory agnosia appears to be varied. Several patients were characterized by impaired discrimination of pitch whereas others reported with impaired discrimination of timbre and rhythm (discrimination of pitch was relatively preserved in one of these cases). In contrast, to patients with pure word deafness and general auditory agnosia, patients with non-verbal auditory agnosia were reported impaired at discriminating long gaps between click sounds, but impaired at short gaps. A possible neuroanatomical structure that relays longer sound duration was suggested by Tanaka et al. By comparing the lesions of two cortically deaf patients with the lesion of a word deafness patient, they proposed the existence of two thalamocortical pathways that inter-connect the MGN with the auditory cortex. They suggested that spoken words are relayed via a direct thalamocortical pathway that passes underneath the putamen, and that environmental sounds are relayed via a separate thalamocortical pathway that passes above the putamen near the parietal white matter.
|
||||
|
||||
=== Amusia ===
|
||||
Auditory agnosia patients are often impaired in the discrimination of all sounds, including music. However, in two such patients music perception was spared and in one patient music perception was enhanced. The medical literature reports of 33 patients diagnosed with an exclusive deficit for the discrimination and recognition of musical segments (i.e., amusia). The damage in all these cases was localized to the right hemisphere or was bilateral. (with the exception of one case.) The damage in these cases tended to focus around the temporal pole. Consistently, removal of the anterior temporal lobe was also associated with loss of music perception, and recordings directly from the anterior auditory cortex revealed that in both hemispheres, music is perceived medially to speech. These findings therefore imply that the loss of music perception in auditory agnosia is because of damage to the medial anterior STG. In contrast to the association of amusia specific to recognition of melodies (amelodia) with the temporal pole, posterior STG damage was associated with loss of rhythm perception (arryhthmia). Conversely, in two patients rhythm perception was intact, while recognition/discrimination of musical segments was impaired. Amusia also dissociates in regard to enjoyment from music. In two reports, amusic patients, who weren't able to distinguish musical instruments, reported that they still enjoy listening to music. On the other hand, a patient with left hemispheric damage in the amygdala was reported to perceive, but not enjoy, music.
|
||||
|
||||
=== Word meaning deafness / associative auditory agnosia ===
|
||||
In 1928, Kleist suggested that the etiology of word deafness could be due either to impaired perception of the sound (apperceptive auditory agnosia), or to impaired extraction of meaning from a sound (associative auditory agnosia). This hypothesis was first tested by Vignolo et al (1969), who examined unilateral stroke patients. They reported that patients with left hemisphere damage were impaired in matching environmental sounds with their corresponding pictures, whereas patients with right hemisphere damage were impaired in the discrimination of meaningless noise segments. The researchers then concluded that left hemispheric damage results in associative auditory agnosia, and right hemisphere damage results in apperceptive auditory agnosia. Although the conclusion reached by this study could be considered over-reaching, associative auditory agnosia could correspond with the disorder word meaning deafness.
|
||||
Patients with word meaning deafness are characterized by impaired speech recognition but intact repetition of speech and left hemisphere damage. These patients often repeat words in an attempt to extract its meaning (e.g., "Jar....Jar....what is a jar?"). In the first documented case, Bramwell (1897 - translated by Ellis, 1984) reported a patient, who in order to comprehend speech wrote what she heard and then read her own handwriting. Kohn and Friedman, and Symonds also reported word meaning deafness patients who are able to write to dictation. In at least 12 cases, patients with symptoms that correspond with word meaning deafness were diagnosed as auditory agnosia. Unlike most auditory agnosia patients, word meaning deafness patients are not impaired at discriminating gaps of click sounds. It is yet unclear whether word meaning deafness is also synonymous with the disorder deep dysphasia, in which patients cannot repeat nonsense words and produce semantic paraphasia during repetition of real words. Word meaning deafness is also often confused with transcortical sensory aphasia, but such patients differ from the latter by their ability to express themselves appropriately orally or in writing.
|
||||
26
data/en.wikipedia.org/wiki/Auditory_agnosia-4.md
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26
data/en.wikipedia.org/wiki/Auditory_agnosia-4.md
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@ -0,0 +1,26 @@
|
||||
---
|
||||
title: "Auditory agnosia"
|
||||
chunk: 5/5
|
||||
source: "https://en.wikipedia.org/wiki/Auditory_agnosia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:21.081452+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
== Neurological mechanism ==
|
||||
Auditory agnosia (with the exception of non-verbal auditory agnosia and amusia) is strongly dependent on damage to both hemispheres. The order of hemispheric damage is irrelevant to manifestation of symptoms, and years could take between the damage of the first hemisphere and the second hemisphere (after which the symptoms suddenly emerge). A study that compared lesion locations, reported that in all cases with bilateral hemispheric damage, at least in one side the lesion included Heschl's gyrus or its underlying white matter. A rare insight into the etiology of this disorder was reported in a study of an auditory agnosia patient with damage to the brainstem, instead of cortex. fMRI scanning of the patient revealed weak activation of the anterior Heschl's gyrus (area R) and anterior superior temporal gyrus. These brain areas are part of the auditory 'what' pathway, and are known from both human and monkey research to participate in the recognition of sounds.
|
||||
|
||||
== See also ==
|
||||
Amusia
|
||||
Aphasia
|
||||
Apraxia
|
||||
Auditory verbal agnosia
|
||||
|
||||
== References ==
|
||||
|
||||
== Further reading ==
|
||||
Polster MR, Rose SB (February 1998). "Disorders of auditory processing: evidence for modularity in audition" (PDF). Cortex; A Journal Devoted to the Study of the Nervous System and Behavior. 34 (1): 47–65. doi:10.1016/S0010-9452(08)70736-6. PMID 9533993. S2CID 2717085.
|
||||
|
||||
== External links ==
|
||||
Psychnet Definition
|
||||
85
data/en.wikipedia.org/wiki/Aura_(symptom)-0.md
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85
data/en.wikipedia.org/wiki/Aura_(symptom)-0.md
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@ -0,0 +1,85 @@
|
||||
---
|
||||
title: "Aura (symptom)"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Aura_(symptom)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:22.252744+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
An aura is a perceptual disturbance experienced by some with epilepsy or migraine. An epileptic aura is a form of minor seizure.
|
||||
Epileptic and migraine auras are due to the involvement of specific areas of the brain, which are those that determine the symptoms of the aura. Therefore, if the visual area is affected, the aura will consist of visual symptoms, while if a tactile sensory one, then tactile sensory symptoms will occur.
|
||||
Epileptic auras are subjective sensory or psychic phenomena due to a focal seizure, i.e. a seizure that originates from that area of the brain responsible for the function which then expresses itself with the symptoms of the aura. It is important because it makes it clear where the alteration causing the seizure is located. An epileptic aura is in most cases followed by other manifestations of a seizure, for example a convulsion, since the epileptic discharge spreads to other parts of the brain. Rarely it remains isolated. Auras, when they occur, allow some people who have epilepsy time to prevent injury to themselves and/or others when they lose consciousness.
|
||||
|
||||
|
||||
== Migraine ==
|
||||
The aura of migraine is visual in the vast majority of cases, because dysfunction starts from the visual cortex. The aura is usually followed, after a time varying from minutes to an hour, by the migraine headache. However, the migraine aura can manifest itself in without being followed by headache. The aura can stay for the duration of the migraine; depending on the type of aura, it can leave the person disoriented and confused. It is common for people with migraines to experience more than one type of aura during the migraine. Some people have the same type of aura every time.
|
||||
Auras can also be confused with sudden onset of panic, panic attacks or anxiety attacks, which creates difficulties in diagnosis. The differential diagnosis of patients who experience symptoms of paresthesias, derealization, dizziness, chest pain, tremors, and palpitations can be challenging.
|
||||
|
||||
|
||||
== Seizures ==
|
||||
An epileptic aura is the consequence of the activation of functional cortex by abnormal neuronal discharge. In addition to being a warning sign for an impending seizure, the nature of an aura can give insight into the localization and lateralization of the seizure or migraine.
|
||||
The most common auras include motor, somatosensory, visual, and auditory symptoms. The activation in the brain during an aura can spread through multiple regions continuously or discontinuously, on the same side or to both sides.
|
||||
Auras are particularly common in focal seizures. If the motor cortex is involved in the overstimulation of neurons, motor auras can result. Likewise, somatosensory auras (such as tingling, numbness, and pain) can result if the somatosensory cortex is involved. When the primary somatosensory cortex is activated, more discrete parts on the opposite side of the body and the secondary somatosensory areas result in symptoms ipsilateral to the seizure focus.
|
||||
Visual auras can be simple or complex. Simple visual symptoms can include static, flashing, or moving lights/shapes/colors caused mostly by abnormal activity in the primary visual cortex. Complex visual auras can include people, scenes, and objects which results from stimulation of the temporo-occipital junction and is lateralized to one hemifield. Auditory auras can also be simple (ringing, buzzing) or complex (voices, music). Simple symptoms can occur from activation in the primary auditory cortex and complex symptoms from the temporo-occipital cortex at the location of the auditory association areas.
|
||||
|
||||
|
||||
== Examples ==
|
||||
|
||||
An aura sensation can include one or a combination of the following:
|
||||
|
||||
|
||||
=== Visual changes ===
|
||||
Bright lights and blobs
|
||||
Zigzag lines
|
||||
Distortions in the size or shape of objects
|
||||
Vibrating visual field
|
||||
Scintillating scotoma
|
||||
Shimmering, pulsating patches, often curved
|
||||
Tunnel vision
|
||||
Scotoma
|
||||
Blind or dark spots
|
||||
Curtain like effect over one eye
|
||||
Slowly spreading spots
|
||||
Kaleidoscope effects
|
||||
Temporary blindness in one or both eyes
|
||||
Heightened sensitivity to light
|
||||
|
||||
|
||||
=== Auditory changes ===
|
||||
Hearing voices or sounds that do not exist: auditory hallucinations
|
||||
Modification of voices or sounds in the environment: buzzing, tremolo, amplitude modulation or other modulations
|
||||
Heightened sensitivity to hearing
|
||||
Vestibular dysfunction causing vertigo
|
||||
|
||||
|
||||
=== Other sensations ===
|
||||
Strange smells (phantosmia) or tastes (gustatory hallucinations)
|
||||
Heightened sensitivity to smell
|
||||
Synesthesia
|
||||
Déjà vu or jamais vu
|
||||
Cephalic aura, a perception of movement of the head or inside the head
|
||||
Abdominal aura, such as an epigastric rising sensation
|
||||
Nausea
|
||||
Numbness or tingling (paresthesia)
|
||||
Weakness on one side of the body (hemiparesis)
|
||||
Feelings of being separated from or floating above one's body (dissociation)
|
||||
Feeling of overheating and sudden perspiration
|
||||
Inability to speak (aphasia) or slurred speech
|
||||
|
||||
|
||||
== See also ==
|
||||
Focal seizure – Seizures which affect only one brain hemisphere
|
||||
Hallucination – Perception that only seems real
|
||||
Persistent aura without infarction
|
||||
Synesthesia – Neurological condition involving the crossing of senses
|
||||
CADASIL
|
||||
Retinal migraine – Medical condition of the eye
|
||||
Photopsia – Presence of perceived flashes of light in one's field of vision
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
27
data/en.wikipedia.org/wiki/Autoamputation-0.md
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27
data/en.wikipedia.org/wiki/Autoamputation-0.md
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@ -0,0 +1,27 @@
|
||||
---
|
||||
title: "Autoamputation"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Autoamputation"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:23.447574+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Autoamputation is the spontaneous detachment (amputation) of an appendage or organ from the body. This is not to be confused with self-amputation, which is performed at will. It is usually due to destruction of the blood vessels feeding an extremity such as the finger tips. Once the vessels are destroyed, the tissue is starved of oxygen and dies, which is often followed by gangrene.
|
||||
Autoamputation is a feature of ainhum, cryoglobulinemia and thromboangiitis obliterans. In 1881, Thornton made the case of autoamputation. Autoamputation could be the result of severe cases of certain chronic wounds, such as frostbite. These chronic wounds might be due to some vascular and pathogenic conditions like Buerger disease or Raynaud's phenomenon. Also, uncontrolled diabetes can predispose one to autoamputation. However, autoamputation has been described as spontaneous. Autoamputation has often been associated with fingers and toes but other parts of the body can suffer this condition as well. There have been reported cases of ovarian autoamputation in a newborn and also in a mature ovary of adults. Autoamputation has been reported to affect an infant of closely consanguineous parentage. Though autoamputation is often regarded as an acquired ailment, it could also be congenital. Chronic torsion or a delay in the diagnosis of acute adnexal torsion has been attributed as causes of acquired autoamputation.
|
||||
|
||||
|
||||
== Types of autoamputation ==
|
||||
Though its facts are being unraveled and analyzed, autoamputation can be categorized as acute, subacute or chronic. Acute autoamputation is characterized by tumor necrosis. This is accompanied by inadequate supply of blood to the heart and other body parts (ischemia) leading to the degeneration of the cells, a condition known as atrophy. Chronic or subacute autoamputation is evident in the attachment of the tumor to other cells surrounding it. There is a rare possibility of the tumor detaching itself from the pedicle. When this happens, it could be parasitic.
|
||||
|
||||
|
||||
== See also ==
|
||||
Autotomy
|
||||
|
||||
|
||||
== Notes ==
|
||||
|
||||
|
||||
== External links ==
|
||||
Media related to Autoamputation at Wikimedia Commons
|
||||
40
data/en.wikipedia.org/wiki/Autonomic_dysreflexia-0.md
Normal file
40
data/en.wikipedia.org/wiki/Autonomic_dysreflexia-0.md
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@ -0,0 +1,40 @@
|
||||
---
|
||||
title: "Autonomic dysreflexia"
|
||||
chunk: 1/3
|
||||
source: "https://en.wikipedia.org/wiki/Autonomic_dysreflexia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:24.727358+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Autonomic dysreflexia (AD) is a life-threatening medical emergency characterized by hypertension and cardiac arrhythmias. This condition is sometimes referred to as autonomic hyperreflexia. Most cases of AD occur in individuals with spinal cord injuries. Lesions at or above the T6 spinal cord level are more frequently reported, although there are reports of AD in patients with lesions as low as T10. Guillain–Barré syndrome may also cause autonomic dysreflexia.
|
||||
Hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache. Severe symptoms may result in life-threatening complications including seizure, intracranial bleeds (stroke), myocardial infarction, and retinal detachment.
|
||||
Both noxious and non-noxious stimuli can trigger AD. The result is stimulation and hyperactivity of the sympathetic nervous system. The noxious stimuli activate a sympathetic surge that travels through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion. The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge. This surge originates in the central nervous system to inhibit the sympathetic outflow. However, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion to reduce elevated blood pressure. This can result in bradycardia, tachycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion. Piloerection and pale, cool skin occur below the lesion due to the prevailing sympathetic outflow.
|
||||
The most common causes include bladder or bowel over-distension from urinary retention and fecal compaction. Other causes include pressure sores, extreme temperatures, fractures, undetected painful stimuli (such as a pebble in a shoe), sexual activity, and extreme spinal cord pain.
|
||||
Treating AD immediately involves removing or correcting the noxious stimuli. This entails sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), and rechecking blood pressure often. The inciting issue may require urinary catheterization or bowel disimpaction. If systolic blood pressure remains elevated (over 150 mm Hg) after these steps, fast-acting short-duration antihypertensives are considered, while other inciting causes must be investigated for the symptoms to resolve.
|
||||
Educating the patient, family, and caregivers about the avoidance of triggers and the cause, if known, is important in the prevention of AD. Since bladder and bowel are common causes, routine bladder and bowel programs and urological follow-up may help reduce the frequency and severity of attacks. These follow-ups may include cystoscopy/urodynamic studies.
|
||||
Prognosis of AD is generally good and mortality is rare, given that the trigger is identified and managed.
|
||||
|
||||
== Signs and symptoms ==
|
||||
This condition is distinct and usually episodic. An elevation of 20 mm Hg over baseline systolic blood pressure, with a potential source below the neurological level of injury, meets the current definition of dysreflexia.
|
||||
Common presenting symptoms include:
|
||||
|
||||
headache
|
||||
diaphoresis
|
||||
increased blood pressure
|
||||
facial erythema
|
||||
goosebumps
|
||||
nasal stuffiness
|
||||
a "feeling of doom" or apprehension
|
||||
blurred vision.
|
||||
|
||||
=== Complications ===
|
||||
Autonomic dysreflexia can become chronic and recurrent. This often occurs in response to longstanding medical problems like soft tissue pressure injuries or hemorrhoids.
|
||||
Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction, or cerebral hemorrhage. Other organs that may be affected include the kidneys and retinas of the eyes. Long-term therapy to decrease blood pressure may include alpha blockers or calcium channel blockers.
|
||||
|
||||
== Causes ==
|
||||
The first episode of autonomic dysreflexia may occur weeks to years after the spinal cord injury takes place. It may take place anytime after reflexes have returned following spinal shock. Most people at risk develop their first episode within the first year after the injury.
|
||||
There are many possible triggers of AD in patients who have had spinal cord injuries. The most common causative factor is bladder distention. Other causes include urinary tract infections, urinary retention, blocked catheters, constipation, hemorrhoids or fissures, skin damage, fractures, and sexual intercourse. It is important to note that not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli, e.g. broken bones, may not result in AD, and may in fact even go unnoticed. In the absence of clear triggering factors, recurrent episodes of AD can be important signs that there is an underlying pathology in a patient that has not yet been discovered.
|
||||
|
||||
== Mechanism ==
|
||||
40
data/en.wikipedia.org/wiki/Autonomic_dysreflexia-1.md
Normal file
40
data/en.wikipedia.org/wiki/Autonomic_dysreflexia-1.md
Normal file
@ -0,0 +1,40 @@
|
||||
---
|
||||
title: "Autonomic dysreflexia"
|
||||
chunk: 2/3
|
||||
source: "https://en.wikipedia.org/wiki/Autonomic_dysreflexia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:24.727358+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
The autonomic nervous system comprises the sympathetic, parasympathetic, and enteric nervous systems. The mechanism of autonomic dysreflexia has to do with the relationship of the sympathetic and parasympathetic systems.
|
||||
Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1-L2 segments of the spinal cord. The supraspinal neurons act on the SPN and its tonic firing by modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla. The sympathetic ganglia act directly on the blood vessels they innervate throughout the body. This controls vessel diameter and resistance. The adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine.
|
||||
In a patient with a spinal cord lesion, the descending autonomic pathways that are responsible for the supraspinal communication with the SPN are interrupted. This results in decreased sympathetic outflow below the level of the injury. In this circumstance, the SPN is controlled only by spinal influences.
|
||||
After a spinal injury, the decreased sympathetic outflow causes reduced blood pressure and sympathetic reflex. Eventually, synaptic reorganization and plasticity of the SPN develops into an overly sensitive state. Because of this, there is abnormal reflex activation of SPN due to afferent stimuli. Most commonly, bowel or bladder distension.
|
||||
Reflex activation then results in systemic vasoconstriction below the spinal cord disruption. This peripheral arterial vasoconstriction and hypertension activates the baroreceptors. There is a resultant parasympathetic surge originating in the central nervous system which inhibits the sympathetic outflow. This parasympathetic signal is unable to transmit below the level of the spinal cord lesion and there is a heightened sympathetic response. This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion. Below the lesion, piloerection, paleness, and cool skin occur due to the prevailing sympathetic outflow. This issue is much more prominent for lesions at or above the T6 level. This is because the splanchnic nerves emerge from the T5 level and below.
|
||||
|
||||
== Diagnosis ==
|
||||
Autonomic dysreflexia is diagnosed by documenting an increase in systolic blood pressure greater than 20 to 30 mmHg. The associated symptoms vary from life-threatening to asymptomatic.
|
||||
An essential step to diagnosing AD is careful monitoring of blood pressure and other vital sign changes. Having knowledge of the patient's baseline blood pressure can be helpful in diagnosing AD. Especially in cases of patients with baseline hypotension since the condition may not be recognized unless compared with their baseline levels.
|
||||
Apart from the increased blood pressure, additional symptoms help differentiate AD from other conditions. These include sweating, spasms, erythema (more likely in upper extremities), headaches, and blurred vision. Older patients with very incomplete spinal cord injuries and systolic hypertension may be experiencing essential hypertension, not autonomic dysreflexia, if they lack additional symptoms.
|
||||
|
||||
=== Differential Diagnoses ===
|
||||
Other diagnoses that should be considered due to similar presentation include:
|
||||
|
||||
Intracranial hemorrhage
|
||||
Ischemic stroke
|
||||
Hyperthyroidism
|
||||
Anxiety
|
||||
Essential hypertension
|
||||
Drug overdose
|
||||
|
||||
== Treatment ==
|
||||
Initial management of autonomic dysreflexia includes measuring and monitoring blood pressure and sitting the patient upright to attempt to lower their blood pressure. It is also important to search for and correct the triggering stimuli. Tight clothing and pressure stockings should be removed. Catheterization of the bladder should be performed as well as evaluation for possible urinary tract infection (UTI). Indwelling catheters should be checked for obstruction. Relief of a blocked urinary catheter tube may resolve the problem. A rectal examination can be performed to clear the rectum of any possible stool impaction. If the noxious stimuli cannot be identified or the systolic blood pressure remains above 150 mmHg, then pharmacologic treatment may be needed. In this situation, the aim is to decrease the elevated intracranial pressure until further studies can identify the cause.
|
||||
Pharmacologic treatment will include antihypertensive medications. Options include sublingual or topical nitrates as well as oral hydralazine or clonidine. Ganglionic blockers can also be used to control sympathetic nervous system outflow. Epidural anesthesia has been demonstrated to be effective in reducing AD in women in labor. However, there is less evidence for its use in reducing AD during general surgical procedures.
|
||||
If the episode of AD is triggered by bowel or bladder irritants, topical analgesics such as lidocaine and bupivacaine are commonly used. Yet, their effectiveness in reducing AD remains inconclusive. Because bladder distension is a common trigger of AD, botulinum toxin used to treat bladder dysfunction in SCI patients may be effective in reducing attacks. Prophylactic use of medications has also been reported to prevent attacks. Some examples include nifedipine, prazosin, and terazosin.
|
||||
Patients with AD should have a card or file about their medical history in case they have an episode in public. This will help the individuals responding to the episode manage the situation by looking for common triggers. Patients with history of AD should also carry their medications for easy access in emergency scenarios.
|
||||
|
||||
== Prognosis ==
|
||||
The prognosis of autonomic dysreflexia is generally good, given that the trigger is identified and managed. Attacks can be prevented by recognizing and avoiding triggering stimuli.
|
||||
Mortality is rare with AD, but morbidities such as stroke, retinal hemorrhage, and pulmonary edema if left untreated can be quite severe. The cause of autonomic dysreflexia itself can be life-threatening. There must be proper investigation and appropriate treatment of the inciting cause to prevent unnecessary morbidity and mortality.
|
||||
19
data/en.wikipedia.org/wiki/Autonomic_dysreflexia-2.md
Normal file
19
data/en.wikipedia.org/wiki/Autonomic_dysreflexia-2.md
Normal file
@ -0,0 +1,19 @@
|
||||
---
|
||||
title: "Autonomic dysreflexia"
|
||||
chunk: 3/3
|
||||
source: "https://en.wikipedia.org/wiki/Autonomic_dysreflexia"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:24.727358+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
== Research directions ==
|
||||
Most future work on the topic of autonomic dysreflexia is directed at earlier detection and intervention. Overall, the goal of these research projects involves minimizing complications that result from late detection of autonomic dysreflexia. Some research is aimed at investigating the use of non-invasive sensors to track nerve activity to detect signs of AD. Other work has begun to look at the use of AI for this role, although it has been limited to rat models. Results from a study showed that AI can serve as another non-invasive tool in combination with sensors that track nerve activity. Future work of studies such as these includes using more sensors to track other variables for increasingly accurate results.
|
||||
Other work revolves around increasing the understanding of the mechanism behind AD. While it is understood that spinal cord injury results in inhibited parasympathetic surges and a heightened sympathetic response that can lead to AD, other details are yet to be defined. It is also understood that the renin-angiotensin system (RAS) plays a significant role in cardiovascular function in addition to the autonomic nervous system (ANS), which includes the sympathetic and parasympathetic systems. What remains to be studied is the degree to which a spinal cord injury affects the relationship between RAS and ANS. It also remains to be determined whether targeting the RAS system can help manage symptoms of AD.
|
||||
|
||||
== References ==
|
||||
|
||||
== Further reading ==
|
||||
|
||||
== External links ==
|
||||
17
data/en.wikipedia.org/wiki/Azygos-0.md
Normal file
17
data/en.wikipedia.org/wiki/Azygos-0.md
Normal file
@ -0,0 +1,17 @@
|
||||
---
|
||||
title: "Azygos"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Azygos"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:25.966903+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Azygos (impar), from the Greek άζυξ, refers to an anatomical structure that is unpaired. This is relatively unusual, as most elements of anatomy reflect bilateral symmetry. Azygos may refer to:
|
||||
|
||||
Azygos anterior cerebral artery
|
||||
Azygos artery of vagina
|
||||
Azygos lobe
|
||||
Azygos vein
|
||||
Ganglion impar
|
||||
20
data/en.wikipedia.org/wiki/B_type_inclusion-0.md
Normal file
20
data/en.wikipedia.org/wiki/B_type_inclusion-0.md
Normal file
@ -0,0 +1,20 @@
|
||||
---
|
||||
title: "B type inclusion"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/B_type_inclusion"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:27.133905+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
B-type inclusions, formerly known as Guarnieri bodies are cellular features found upon microscopic inspection of epithelial cells of individuals suspected of having poxvirus (e.g. smallpox or vaccinia). In cells stained with eosin, they appear as pink blobs in the cytoplasm of affected epithelial cells. The absence of Guarnieri bodies cannot be used as to rule out smallpox, however, as more sensitive test need to be performed.
|
||||
B-type inclusions are the sites of viral replication and are found in all poxvirus-infected cells, unlike A-type inclusions which are more strongly eosinophilic and only found in infections with certain poxviruses.
|
||||
They are named after the Italian physician Giuseppe Guarnieri.
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== Further reading ==
|
||||
GOODPASTURE EW (1959). "Cytoplasmic inclusions resembling Guarnieri bodies, and other phenomena induced by mutants of the virus of fowlpox". Am. J. Pathol. 35 (2): 213–31. PMC 1934859. PMID 13627123.
|
||||
@ -0,0 +1,42 @@
|
||||
---
|
||||
title: "Ballard Maturational Assessment"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Ballard_Maturational_Assessment"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:28.282771+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
The Ballard maturational assessment, Ballard score, or Ballard scale, is a gestational age assessment technique. It was devised by Dr. Jeanne L. Ballard, professor emeritus of the Department of Pediatrics, Obstetrics, and Gynecology at the University of Cincinnati College of Medicine. It was developed in 1979.
|
||||
The assessment scores various criteria, the sum of which is then extrapolated to the gestational age of the fetus. These criteria are divided into physical and neuromuscular criteria, which allows for the estimation of age in the range of 26 weeks to 44 weeks. The new Ballard score is an extension of the above to include extremely preterm babies, i.e., up to 20 weeks.
|
||||
The scoring relies on the intrauterine changes the fetus undergoes during maturation. Whereas the neuromuscular criteria depend mainly upon muscle tone, the physical scale relies on anatomical changes. Neonate fetuses (less than 37 weeks of age) are in a state of physiological hypotonia, and since muscle tone increases throughout the fetal growth period, it can be used to identify fetal maturation.
|
||||
|
||||
|
||||
== Neuromuscular criteria ==
|
||||
Posture – score the infant's posture from flexed to extended
|
||||
Square window – assess the flexibility of the wrist
|
||||
Arm recoil – measure the angle of recoil after extending arm
|
||||
Popliteal angle – measure the angle formed between knees during flexed extension
|
||||
Scarf sign – record the resistance while stretching the infant's arm across the chest
|
||||
Heel to ear – note the location of the heel when stretching the infant's leg toward the ear
|
||||
|
||||
|
||||
== Physical criteria ==
|
||||
|
||||
|
||||
== Scoring system ==
|
||||
In the original Ballard score, each of the criteria is scored from 0 to 5. The scores were then ranged 5 to 50, with the corresponding gestational ages being 26 weeks and 44 weeks. A score increase of 5 advances the estimated age by 2 weeks. The new Ballard score allows scores of −1 for the criteria. The possible scores then range from −10 to 50, with the gestational range extending earlier to 20 weeks.
|
||||
|
||||
A simple formula to estimate age from the Ballard score is age = (2 * score + 120) / 5
|
||||
|
||||
|
||||
== See also ==
|
||||
Apgar score
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
BallardScore.com
|
||||
33
data/en.wikipedia.org/wiki/Benign_tumor-0.md
Normal file
33
data/en.wikipedia.org/wiki/Benign_tumor-0.md
Normal file
@ -0,0 +1,33 @@
|
||||
---
|
||||
title: "Benign tumor"
|
||||
chunk: 1/3
|
||||
source: "https://en.wikipedia.org/wiki/Benign_tumor"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:29.480012+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
A benign tumor is a mass of cells (tumor) that does not invade neighboring tissue or metastasize (spread throughout the body). Compared to malignant (cancerous) tumors, benign tumors generally have a slower growth rate. Benign tumors have relatively well differentiated cells. They are often surrounded by an outer surface (fibrous sheath of connective tissue) or stay contained within the epithelium. Common examples of benign tumors include moles and uterine fibroids.
|
||||
Some forms of benign tumors may be harmful to health. Benign tumor growth causes a mass effect that can compress neighboring tissues. This can lead to nerve damage, blood flow reduction (ischemia), tissue death (necrosis), or organ damage. The health effects of benign tumor growth may be more prominent if the tumor is contained within an enclosed space such as the cranium, respiratory tract, sinus, or bones. For example, unlike most benign tumors elsewhere in the body, benign brain tumors can be life-threatening. Tumors may exhibit behaviors characteristic of their cell type of origin; as an example, endocrine tumors such as thyroid adenomas and adrenocortical adenomas may overproduce certain hormones.
|
||||
The word benign means 'favourable, kind, fortunate, salutary, propitious'. However, a benign tumor is not benign in the usual sense; the name merely specifies that it is not "malignant", i.e. cancerous. While benign tumors usually do not pose a serious health risk, they can be harmful or fatal. Many types of benign tumors have the potential to become cancerous (malignant) through a process known as tumor progression. For this reason and other possible harms, some benign tumors are removed by surgery. When removed, benign tumors usually do not return. Exceptions to this rule may indicate malignant transformation.
|
||||
|
||||
== Signs and symptoms ==
|
||||
Benign tumors are very diverse; they may be asymptomatic or may cause specific symptoms, depending on their anatomic location and tissue type. They grow outward, producing large, rounded masses which can cause what is known as a "mass effect". This growth can cause compression of local tissues or organs, leading to many effects, such as blockage of ducts, reduced blood flow (ischaemia), tissue death (necrosis) and nerve pain or damage. Some tumors also produce hormones that can lead to life-threatening situations. Insulinomas can produce large amounts of insulin, causing hypoglycemia. Pituitary adenomas can cause elevated levels of hormones such as growth hormone and insulin-like growth factor-1, which cause acromegaly; prolactin; ACTH and cortisol, which cause Cushing's disease; TSH, which causes hyperthyroidism; and FSH and LH. Bowel intussusception can occur with various benign colonic tumors. Cosmetic effects can be caused by tumors, especially those of the skin, possibly causing psychological or social discomfort for the person with the tumor. Vascular tissue tumors can bleed, in some cases leading to anemia.
|
||||
|
||||
== Causes ==
|
||||
|
||||
=== PTEN hamartoma syndrome ===
|
||||
PTEN hamartoma syndrome encompasses hamartomatous disorders characterized by genetic mutations in the PTEN tumor suppressor gene, including Cowden syndrome, Bannayan–Riley–Ruvalcaba syndrome, Proteus syndrome and Proteus-like syndrome. Absent or dysfunctional PTEN protein allows cells to over-proliferate, causing hamartomas. Cowden syndrome is an autosomal dominant genetic disorder characterized by multiple benign hamartomas (trichilemmomas and mucocutaneous papillomatous papules) as well as a predisposition for cancers of multiple organs including the breast and thyroid. Bannayan–Riley–Ruvalcaba syndrome is a congenital disorder characterized by hamartomatous intestinal polyposis, macrocephaly, lipomatosis, hemangiomatosis and glans penis macules. Proteus syndrome is characterized by nevi, asymmetric overgrowth of various body parts, adipose tissue dysregulation, cystadenomas, adenomas, vascular malformation.
|
||||
|
||||
=== Familial adenomatous polyposis ===
|
||||
Familial adenomatous polyposis (FAP) is a familial cancer syndrome caused by mutations in the APC gene. In FAP, adenomatous polyps are present in the colon. The polyps progress into colon cancer unless removed. The APC gene is a tumor suppressor. Its protein product is involved in many cellular processes. Inactivation of the APC gene leads to the buildup of a protein called β-catenin. This protein activates two transcription factors: T-cell factor (TCF) and lymphoid enhancer factor (LEF). These factors cause the upregulation of many genes involved in cell proliferation, differentiation, migration and apoptosis (programmed cell death), causing the growth of benign tumors.
|
||||
|
||||
=== Tuberous sclerosis complex ===
|
||||
Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder caused by mutations in the genes TSC1 and TSC2. TSC1 produces the protein hamartin. TSC2 produces the protein tuberin. This disorder presents with many benign hamartomatous tumors including angiofibromas, renal angiomyolipomas, and pulmonary lymphangiomyomatosis. Tuberin and hamartin inhibit the mTOR protein in normal cellular physiology. Inactivation of the TSC tumor suppressors causes an increase in mTOR activity. This leads to the activation of genes and the production of proteins that increase cell growth.
|
||||
|
||||
=== Von Hippel–Lindau disease ===
|
||||
Von Hippel–Lindau disease is a dominantly inherited cancer syndrome that significantly increases the risk of various tumors. This includes benign hemangioblastomas and malignant pheochromocytomas, renal cell carcinomas, pancreatic endocrine tumors, and endolymphatic sac tumors. It is caused by genetic mutations in the Von Hippel–Lindau tumor suppressor gene. The VHL protein (pVHL) is involved in cellular signaling in oxygen starved (hypoxic) cells. One role of pVHL is to cause the cellular degradation of another protein, HIF1α. Dysfunctional pVHL leads to accumulation of HIF1α. This activates several genes responsible for the production of substances involved in cell growth and blood vessel production: VEGF, PDGFβ, TGFα and erythropoietin.
|
||||
|
||||
=== Bone tumors ===
|
||||
Benign tumors of bone can be similar macroscopically and require a combination of a clinical history with cytogenetic, molecular, and radiologic tests for diagnosis. Three common forms of benign bone tumors with are giant cell tumor of bone, osteochondroma, and enchondroma; other forms of benign bone tumors exist but may be less prevalent.
|
||||
42
data/en.wikipedia.org/wiki/Benign_tumor-1.md
Normal file
42
data/en.wikipedia.org/wiki/Benign_tumor-1.md
Normal file
@ -0,0 +1,42 @@
|
||||
---
|
||||
title: "Benign tumor"
|
||||
chunk: 2/3
|
||||
source: "https://en.wikipedia.org/wiki/Benign_tumor"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:29.480012+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
==== Giant cell tumors ====
|
||||
Giant cell tumors of bone frequently occur in long bone epiphyses of the appendicular skeleton or the sacrum of the axial skeleton. Local growth can cause destruction of neighboring cortical bone and soft tissue, leading to pain and limiting range of motion. The characteristic radiologic finding of giant cell tumors of bone is a lytic lesion that does not have marginal sclerosis of bone. On histology, giant cells of fused osteoclasts are seen as a response to neoplastic mononucleated cells. Notably, giant cells are not unique among benign bone tumors to giant cell tumors of bone. Molecular characteristics of the neoplastic cells causing giant cell tumors of bone indicate an origin of pluripotent mesenchymal stem cells that adopt preosteoblastic markers. Cytogenetic causes of giant cell tumors of bone involve telomeres. Treatment involves surgical curettage with adjuvant bisphosphonates.
|
||||
|
||||
==== Osteochondroma ====
|
||||
Osteochondromas form cartilage-capped projections of bone. Structures such as the marrow cavity and cortical bone of the osteochondroma are contiguous to those of the originating bone. Sites of origin often involve metaphyses of long bones. While many osteochondromas occur spontaneously, there are cases in which several osteochondromas can occur in the same individual; these may be linked to a genetic condition known as hereditary multiple osteochondromas. Osteochondroma appears on X-ray as a projecting mass that often points away from joints. These tumors stop growing with the closure of the parental bone's growth plates. Failure to stop growth can be indicative of transformation to malignant chondrosarcoma. Treatment is not indicated unless symptomatic. In that case, surgical excision is often curative.
|
||||
|
||||
==== Enchondroma ====
|
||||
Enchondromas are benign tumors of hyaline cartilage. Within a bone, enchondromas are often found in metaphyses. They can be found in many types of bone, including small bones, long bones, and the axial skeleton. X-ray of enchondromas shows well-defined borders and a stippled appearance. Presentation of multiple enchondromas is consistent with multiple enchondromatosis (Ollier Disease). Treatment of enchondromas involves surgical curettage and grafting.
|
||||
|
||||
=== Benign soft tissue tumors ===
|
||||
|
||||
==== Lipomas ====
|
||||
Lipomas are benign, subcutaneous tumors of fat cells (adipocytes). They are usually painless, slow-growing, and mobile masses that can occur anywhere in the body where there are fat cells, but are typically found on the trunk and upper extremities. Although lipomas can develop at any age, they more commonly appear between the ages of 40 and 60. Lipomas affect about 1% of the population, with no documented sex bias, and about 1 in every 1000 people will have a lipoma within their lifetime. The cause of lipomas is not well defined. Genetic or inherited causes of lipomas play a role in around 2-3% of patients. In individuals with inherited familial syndromes such as Proteus syndrome or Familial multiple lipomatosis, it is common to see multiple lipomas across the body. These syndromes are also associated with specific symptoms and sub-populations. Mutations in chromosome 12 have been identified in around 65% of lipoma cases. Lipomas have also been shown to be increased in those with obesity, hyperlipidemia, and diabetes mellitus.
|
||||
Lipomas are usually diagnosed clinically, although imaging (ultrasound, computed tomography, or magnetic resonance imaging) may be utilized to assist with the diagnosis of lipomas in atypical locations. The main treatment for lipomas is surgical excision, after which the tumor is examined with histopathology to confirm the diagnosis. The prognosis for benign lipomas is excellent and recurrence after excision is rare, but may occur if the removal was incomplete.
|
||||
|
||||
== Mechanism ==
|
||||
|
||||
=== Benign vs malignant ===
|
||||
|
||||
A tumor is classified as either benign or malignant based on its invasive potential. Benign tumors are non-invasive: They cannot invade adjacent tissues or metastasize (spread via metastasis). In contrast, malignant tumors are invasive or metastatic. For this reason, benign tumors are not classed as cancer. A benign tumor will grow in a contained area, usually a fibrous connective tissue capsule.
|
||||
The growth rates of benign and malignant tumors usually differ, with benign tumors growing more slowly than malignant tumors. However, cases of fast-growing benign tumors have been documented. Although benign tumors generally pose a lower health risk than malignant tumors, both can be life-threatening.
|
||||
Benign and malignant tumors differ in some general characteristics, but sometimes a benign tumor will exhibit some characteristics of a malignant tumor, or vice versa. For example, benign tumors are mostly well-differentiated, and malignant tumors are often undifferentiated. However, undifferentiated benign tumors can occur, as can differentiated malignant tumors. Certain malignant tumors, such as basal-cell carcinomas, are mostly non-metastatic.
|
||||
|
||||
=== Multistage carcinogenesis ===
|
||||
|
||||
Tumors are formed by carcinogenesis, a process in which cellular alterations lead to the formation of cancer. Multistage carcinogenesis involves the sequential genetic or epigenetic changes to a cell's DNA, where each step produces a more advanced tumor. It consists of three stages: initiation, promotion and progression. Multiple mutations may occur per stage.
|
||||
Initiation is where the first genetic mutation occurs in a cell. Promotion is the clonal expansion (repeated division) of this transformed cell into a visible tumor that is usually benign. Following promotion, progression may take place where more genetic mutations are acquired in a sub-population of tumor cells. Progression changes the benign tumor into a malignant tumor.
|
||||
A prominent and well studied example of this phenomenon is the tubular adenoma, a common type of colon polyp which is an important precursor to colon cancer. The cells in tubular adenomas, like most tumors that frequently progress to cancer, show certain abnormalities of cell maturation and appearance collectively known as dysplasia. These cellular abnormalities are not seen in benign tumors that rarely or never turn cancerous, but are seen in other pre-cancerous tissue abnormalities which do not form discrete masses, such as pre-cancerous lesions of the uterine cervix.
|
||||
|
||||
== Diagnosis ==
|
||||
|
||||
=== Classification ===
|
||||
21
data/en.wikipedia.org/wiki/Benign_tumor-2.md
Normal file
21
data/en.wikipedia.org/wiki/Benign_tumor-2.md
Normal file
@ -0,0 +1,21 @@
|
||||
---
|
||||
title: "Benign tumor"
|
||||
chunk: 3/3
|
||||
source: "https://en.wikipedia.org/wiki/Benign_tumor"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:29.480012+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Benign neoplasms are typically, but not always, composed of cells which bear a strong resemblance to a normal cell type in their organ of origin. These tumors are named for the cell or tissue type from which they originate. The suffix "-oma" (but not -carcinoma, -sarcoma, or -blastoma, which are generally cancers) is applied to indicate a benign tumor. For example, a lipoma is a common benign tumor of fat cells (lipocytes), and a chondroma is a benign tumor of cartilage-forming cells (chondrocytes). Adenomas are benign tumors of gland-forming cells, and are usually specified further by their cell or organ of origin, as in hepatic adenoma (a benign tumor of hepatocytes, or liver cells). Teratomas contain many cell types such as skin, nerve, brain and thyroid, among others, because they are derived from germ cells. Hamartomas are a group of benign tumors that have relatively normal cellular differentiation but exhibit disorganized tissue organization.
|
||||
Exceptions to the nomenclature rules exist for historical reasons. Malignant examples include melanoma (a skin cancer of pigmented melanocytes) and seminoma (a cancer of male reproductive cells).
|
||||
Not all benign growths are tumors. Skin tags, vocal chord polyps, and hyperplastic polyps of the colon are often called benign, but they are overgrowths of normal tissue rather than neoplasms.
|
||||
|
||||
=== Imaging ===
|
||||
Radiography can be used to image a tumor and determine whether it is malignant. Smaller tumors are more likely benign. For example, regarding lung cancer, 80% of lung nodules less than 2 cm in diameter are benign. Most benign nodules are smoothed radiopaque densities with clear margins, but these are not exclusive signs of benign tumors.
|
||||
|
||||
== Treatment ==
|
||||
Benign tumors typically need no treatment unless they cause problems such as seizures, discomfort or cosmetic concerns. Surgery is usually the most effective approach and is used to treat most benign tumors. In some cases, other treatments may be used. Adenomas of the rectum may be treated with sclerotherapy, in which chemicals are used to shrink blood vessels in order to cut off the blood supply. Most benign tumors do not respond to chemotherapy or radiation therapy, although there are exceptions; benign intercranial tumors are sometimes treated with radiation therapy and chemotherapy under certain circumstances. Radiation can also be used to treat hemangiomas in the rectum. Benign skin tumors are usually surgically resected but other treatments such as cryotherapy, curettage, electrodesiccation, laser therapy, dermabrasion, chemical peels and topical medication are used.
|
||||
|
||||
== References ==
|
||||
75
data/en.wikipedia.org/wiki/Bethesda_system-0.md
Normal file
75
data/en.wikipedia.org/wiki/Bethesda_system-0.md
Normal file
@ -0,0 +1,75 @@
|
||||
---
|
||||
title: "Bethesda system"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Bethesda_system"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:30.688221+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
The Bethesda system (TBS), officially called The Bethesda System for Reporting Cervical Cytology, is a system for reporting cervical or vaginal cytologic diagnoses, used for reporting Pap smear results. It was introduced in 1988 and revised in 1991, 2001, and 2014. The name comes from the location (Bethesda, Maryland) of the conference, sponsored by the National Institutes of Health, that established the system.
|
||||
Since 2010, the Bethesda system has been used for cytopathology of thyroid nodules, which is called The Bethesda System for Reporting Thyroid Cytopathology (TBSRTC or BSRTC). Like TBS, it was the result of a conference sponsored by the NIH and is published in book editions (currently by Springer). Mentions of "the Bethesda system" without further specification usually refer to the cervical system, unless the thyroid context of a discussion is implicit.
|
||||
|
||||
|
||||
== Cervix ==
|
||||
Abnormal results include:
|
||||
|
||||
Atypical squamous cells
|
||||
Atypical squamous cells of undetermined significance (ASC-US)
|
||||
Atypical squamous cells – cannot exclude HSIL (ASC-H)
|
||||
Low-grade squamous intraepithelial lesion (LGSIL or LSIL)
|
||||
High-grade squamous intraepithelial lesion (HGSIL or HSIL)
|
||||
Squamous cell carcinoma
|
||||
Atypical Glandular Cells not otherwise specified (AGC-NOS)
|
||||
Atypical Glandular Cells, suspicious for AIS or cancer (AGC-neoplastic)
|
||||
Adenocarcinoma in situ (AIS)
|
||||
The results are calculated differently following a Pap smear of the cervix.
|
||||
|
||||
|
||||
=== Squamous cell abnormalities ===
|
||||
|
||||
|
||||
==== LSIL: low-grade squamous intraepithelial lesion ====
|
||||
|
||||
A low-grade squamous intraepithelial lesion (LSIL or LGSIL) indicates possible cervical dysplasia. LSIL usually indicates mild dysplasia (CIN 1), more than likely caused by a human papillomavirus infection. It is usually diagnosed following a Pap smear.
|
||||
CIN 1 is the most common and most benign form of cervical intraepithelial neoplasia and usually resolves spontaneously within two years. Because of this, LSIL results can be managed with a simple "watch and wait" philosophy. However, because there is a 12–16% chance of progression to more severe dysplasia, the physician may want to follow the results more aggressively by performing a colposcopy with biopsy. If the dysplasia progresses, treatment may be necessary. Treatment involves removal of the affected tissue, which can be accomplished by LEEP, cryosurgery, cone biopsy, or laser ablation.
|
||||
|
||||
|
||||
==== HSIL: high-grade squamous intraepithelial lesion ====
|
||||
|
||||
High-grade squamous intraepithelial lesion (HSIL or HGSIL) indicates moderate or severe cervical intraepithelial neoplasia or carcinoma in situ. It is usually diagnosed following a Pap test. In some cases, these lesions can lead to invasive cervical cancer, if not followed appropriately.
|
||||
HSIL does not mean that cancer is present. Of all women with HSIL results, 2% or less have invasive cervical cancer at that time; however, about 20% would progress to having invasive cervical cancer without treatment. To combat this progression, HSIL is usually followed by an immediate colposcopy with biopsy to sample or remove the dysplastic tissue. This tissue is sent for pathology testing to assign a histologic classification that is more definitive than a Pap smear result (which is a cytologic finding). HSIL generally corresponds to the histological classification of CIN 2 or 3.
|
||||
HSIL treatment involves the removal or destruction of the affected cells, usually by LEEP. Other methods include cryotherapy, cautery, or laser ablation, but none are performed on pregnant women for fear of disrupting the pregnancy—the indication per 2006 American Society for Colposcopy and Cervical Pathology consensus guidelines being only invasive cancer. Any of these procedures is 85% likely to cure the problem.
|
||||
|
||||
|
||||
=== Glandular cell abnormalities ===
|
||||
|
||||
|
||||
==== Adenocarcinoma ====
|
||||
|
||||
Adenocarcinoma can arise from the endocervix, endometrium, and extrauterine sites.
|
||||
|
||||
|
||||
==== AGC ====
|
||||
AGC, formerly AGUS, is a term for atypical glandular cells of undetermined significance. Renamed AGC to avoid confusion with ASCUS.
|
||||
The management of AGC is colposcopy with or without an endometrial biopsy.
|
||||
|
||||
|
||||
== Thyroid nodules ==
|
||||
The Bethesda System for Reporting Thyroid Cytopathology is the system used to report whether the thyroid cytological specimen is benign or malignant on fine-needle aspiration cytology (FNAC). It can be divided into six categories:
|
||||
|
||||
Repeated FNAC is recommended for Category I, followed by clinical follow-up in Category II, repeat FNAC for Category III, and lobectomy for Category IV, near total-thyroidectomy/lobectomy for Category V, and near total thyroidectomy for Category VI. The risk of malignancy in a malignant FNAC report is 93.7% while for a suspicious FNAC report, it is 18.9%.
|
||||
|
||||
|
||||
== See also ==
|
||||
American Society for Clinical Pathology
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
ASCP: The Bethesda System Website Atlas
|
||||
Bethesda 2001 Workshop
|
||||
Bongiovanni, Massimo; Spitale, Alessandra; Faquin, William C.; Mazzucchelli, Luca; Baloch, Zubair W. (2012). "The Bethesda System for Reporting Thyroid Cytopathology: A Meta-Analysis". Acta Cytologica. 56 (4): 333–339. doi:10.1159/000339959. PMID 22846422. S2CID 14143335. Retrieved 24 November 2022.
|
||||
32
data/en.wikipedia.org/wiki/Biliary_microlithiasis-0.md
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32
data/en.wikipedia.org/wiki/Biliary_microlithiasis-0.md
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@ -0,0 +1,32 @@
|
||||
---
|
||||
title: "Biliary microlithiasis"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Biliary_microlithiasis"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:31.871930+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Biliary microlithiasis refers to the creation of small gallstones less than 3 mm in diameter in the biliary duct or gallbladder.
|
||||
It has been suggested as a cause of postcholecystectomy syndrome, or PCS, the symptoms of which include:
|
||||
|
||||
Upset stomach, nausea, and vomiting.
|
||||
Gas, bloating, and diarrhea.
|
||||
Persistent pain in the upper right abdomen.
|
||||
|
||||
|
||||
== Diagnostics ==
|
||||
Biliary Microlithiasis may be detectable by ultrasound using a Rapid Patient Rotation Ultrasound Protocol
|
||||
Analysis of biliary sludge obtained through endoscopic retrograde cholangiopancreatography (ERCP)
|
||||
|
||||
|
||||
== Treatment ==
|
||||
Oral ursodeoxycholic acid can be used to dissolve these crystals.
|
||||
|
||||
|
||||
== See also ==
|
||||
Biliary sludge
|
||||
|
||||
|
||||
== References ==
|
||||
23
data/en.wikipedia.org/wiki/Biliary_pseudolithiasis-0.md
Normal file
23
data/en.wikipedia.org/wiki/Biliary_pseudolithiasis-0.md
Normal file
@ -0,0 +1,23 @@
|
||||
---
|
||||
title: "Biliary pseudolithiasis"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Biliary_pseudolithiasis"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:33.115723+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Biliary pseudolithiasis is an unusual complication of ceftriaxone where the drug complexes with calcium and mimics gallstones. It is reversed when ceftriaxone administration is stopped. It was first described in 1988 by Schaad et al. as "reversible ceftriaxone-associated biliary pseudolithiasis". Ceftriaxone has been frequently associated with biliary sludge or biliary pseudolithiasis in subsequent reports. Ceftriaxone is excreted primarily through the urine, but also through the bile, up to 40% of its excretion, with concentrations in the bile 20-150 times higher than in the serum. It forms a calcium salt in the gallbladder, which can exceed its solubility and create precipitates that resemble gallstones on ultrasonography. The incidence of pseudolithiasis in children treated with ceftriaxone is up to 25%, but most patients are asymptomatic. Risk factors for biliary pseudolithiasis include age greater than 24 months, gram-negative sepsis, high doses of ceftriaxone, hypercalcemia, surgery, and decreased bile flow/increased ceftriaxone excretion in bile. Conservative management with serial ultrasounds is recommended until the "stones" completely resolve. If associated with ceftriaxone, it resolves on average about 2 weeks after the ceftriaxone is stopped.
|
||||
|
||||
|
||||
== Ceftriaxone ==
|
||||
|
||||
Ceftriaxone sold under the brand name Rocephin, is a third-generation cephalosporin antibiotic used for the treatment of a number of bacterial infections. These include middle ear infections, endocarditis, meningitis, pneumonia, bone and joint infections, intra-abdominal infections, skin infections, urinary tract infections, gonorrhea, and pelvic inflammatory disease. It is also sometimes used before surgery and following a bite wound to try to prevent infection. Ceftriaxone can be given by injection into a vein or into a muscle.
|
||||
|
||||
|
||||
== See also ==
|
||||
Biliary sludge
|
||||
|
||||
|
||||
== References ==
|
||||
53
data/en.wikipedia.org/wiki/Biliary_sludge-0.md
Normal file
53
data/en.wikipedia.org/wiki/Biliary_sludge-0.md
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@ -0,0 +1,53 @@
|
||||
---
|
||||
title: "Biliary sludge"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Biliary_sludge"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:34.361744+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Biliary sludge refers to a viscous mixture of small particles derived from bile. These sediments consist of cholesterol crystals, calcium salts, calcium bilirubinate, mucin, and other materials.
|
||||
|
||||
|
||||
== Signs and symptoms ==
|
||||
|
||||
|
||||
=== Complications ===
|
||||
Biliary sludge may cause complications such as biliary colic, acute cholecystitis, acute cholangitis, and acute pancreatitis.
|
||||
|
||||
|
||||
== Cause ==
|
||||
Biliary sludge has been associated with pregnancy, rapid weight loss, total parenteral nutrition, drugs such as ceftriaxone and octreotide, solid organ transplantation, and gastric surgery. In many of these conditions, it is thought that the impairment in the contractility of the gallbladder leads to the formation of the sludge.
|
||||
|
||||
|
||||
== Pathophysiology ==
|
||||
The pathophysiology of biliary sludge formation is likely related to gallbladder dysmotility. It is presumed that because the gallbladder is unable to effectively empty, the biliary sludge can start to accumulate.
|
||||
|
||||
|
||||
== Diagnosis ==
|
||||
|
||||
Biliary sludge is typically diagnosed by CT scan or transabdominal ultrasonography. Endoscopic ultrasonography is another more sensitive option. However, the gold standard is considered to be direct microscopy of aspirated gallbladder bile. This method is much more sensitive, although it is less practical.
|
||||
|
||||
|
||||
== Treatment ==
|
||||
For patients without symptoms, no treatment is recommended. If patients become symptomatic and/or develop complications, cholecystectomy is indicated. For those who are poor surgical candidates, endoscopic sphincterotomy may be performed to reduce the risk of developing pancreatitis.
|
||||
|
||||
|
||||
== Prognosis ==
|
||||
The clinical course of biliary sludge can do one of three things: (1) it can resolve completely, (2) wax and wane, or (3) progress to gallstones. If the biliary sludge has a cause (e.g. pregnancy), it oftentimes is resolved when the underlying cause is removed.
|
||||
|
||||
|
||||
== Epidemiology ==
|
||||
The prevalence of biliary sludge is low in the general population. It has been reported that the prevalence ranges from 0-0.20% in men and 0.18-0.27% in women. However, in patients with certain conditions, the prevalence may be higher.
|
||||
|
||||
|
||||
== See also ==
|
||||
Biliary microlithiasis
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
14
data/en.wikipedia.org/wiki/Biotrauma-0.md
Normal file
14
data/en.wikipedia.org/wiki/Biotrauma-0.md
Normal file
@ -0,0 +1,14 @@
|
||||
---
|
||||
title: "Biotrauma"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Biotrauma"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:36.815898+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Although the term has occasionally been used in other ways, in medical literature biotrauma is usually defined as a severe inflammatory response produced in the lungs of patients who breathe by means of a mechanical ventilator for a long period of time. The term was coined in a 1998 paper by L. N. Tremblay and A. S. Slutsky, titled Ventilator-induced injury: from barotrauma to biotrauma. The message of that paper was that barotrauma caused by pressure differentials is only one of several types of lung damage that a ventilator can produce.
|
||||
|
||||
|
||||
== References ==
|
||||
23
data/en.wikipedia.org/wiki/Bleb_(medicine)-0.md
Normal file
23
data/en.wikipedia.org/wiki/Bleb_(medicine)-0.md
Normal file
@ -0,0 +1,23 @@
|
||||
---
|
||||
title: "Bleb (medicine)"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Bleb_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:38.141600+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
In medicine, a bleb is a blister-like protrusion (often hemispherical) or vesicle filled with serous fluid. Blebs can form in a number of tissues by different pathologies, including frostbite and can "appear and disappear within a short time interval".
|
||||
In pathology, pulmonary blebs are small subpleural thin-walled air-containing spaces, not larger than 1-2 cm in diameter, found by the upper lobe of the lung, between the lung and the visceral pleura. Their walls are thin, being less than 1 mm thick. If they rupture, they allow air to escape into pleural space, resulting in a spontaneous pneumothorax and possibly a collapsed lung. Blebs can grow larger or join together to create a larger cyst, or bulla. There are usually no symptoms unless a pneumothorax occurs or the bulla grows very large. Blebs are usually associated with emphysema.
|
||||
In ophthalmology, blebs may be formed intentionally in the treatment of glaucoma. In such treatments, functional blebs facilitate the circulation of aqueous humor, the blockage of which will lead to increase in eye pressure. Use of collagen matrix wound modulation device such as ologen during glaucoma surgery is known to produce vascular and functional blebs, which are positively correlated with treatment success rate.
|
||||
In the lungs, a bleb is a collection of air within the layers of the visceral pleura.
|
||||
In breasts, a bleb is a milk blister (also known as blocked nipple pore, nipple blister, or "milk under the skin").
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
Medical definition
|
||||
Moorfields Bleb Grading System
|
||||
52
data/en.wikipedia.org/wiki/Body_fluid-0.md
Normal file
52
data/en.wikipedia.org/wiki/Body_fluid-0.md
Normal file
@ -0,0 +1,52 @@
|
||||
---
|
||||
title: "Body fluid"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Body_fluid"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:39.339802+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Body fluids, bodily fluids, or biofluids, sometimes body liquids, are liquids within the body of an organism. In lean healthy adult men, the total body water is about 60% (60–67%) of the total body weight; it is usually slightly lower in women (52–55%). The exact percentage of fluid relative to body weight is inversely proportional to the percentage of body fat. A lean 70 kg (150 lb) man, for example, has about 42 (42–47) liters of water in his body.
|
||||
The total body of water is divided into fluid compartments, between the intracellular fluid compartment (also called space, or volume) and the extracellular fluid (ECF) compartment (space, volume) in a two-to-one ratio: 28 (28–32) liters are inside cells and 14 (14–15) liters are outside cells.
|
||||
The ECF compartment is divided into the interstitial fluid volume – the fluid outside both the cells and the blood vessels – and the intravascular volume (also called the vascular volume and blood plasma volume) – the fluid inside the blood vessels – in a three-to-one ratio: the interstitial fluid volume is about 12 liters; the vascular volume is about 4 liters.
|
||||
The interstitial fluid compartment is divided into the lymphatic fluid compartment – about 2/3, or 8 (6–10) liters, and the transcellular fluid compartment (the remaining 1/3, or about 4 liters).
|
||||
The vascular volume is divided into the venous volume and the arterial volume; and the arterial volume has a conceptually useful but unmeasurable subcompartment called the effective arterial blood volume.
|
||||
|
||||
|
||||
== Compartments by location ==
|
||||
intracellular fluid (ICF), which consist of cytosol and fluids in the cell nucleus
|
||||
Extracellular fluid
|
||||
Intravascular fluid (blood plasma)
|
||||
Interstitial fluid
|
||||
Lymphatic fluid (sometimes included in interstitial fluid)
|
||||
Transcellular fluid
|
||||
|
||||
|
||||
== Health ==
|
||||
|
||||
|
||||
=== Clinical samples ===
|
||||
Clinical samples are generally defined as non-infectious human or animal materials including blood, saliva, excreta, body tissue and tissue fluids, and also FDA-approved pharmaceuticals that are blood products. In medical contexts, it is a specimen taken for diagnostic examination or evaluation, and for identification of disease or condition.
|
||||
|
||||
|
||||
== See also ==
|
||||
Basic reproduction number
|
||||
Blood-borne diseases
|
||||
Clinical pathology
|
||||
Humorism
|
||||
Hygiene
|
||||
Ritual cleanliness
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== Further reading ==
|
||||
Paul Spinrad. (1999) The RE/Search Guide to Bodily Fluids. Juno Books. ISBN 1-890451-04-5
|
||||
John Bourke. (1891) Scatalogic Rites of All Nations. Washington, D.C.: W.H. Lowdermilk.
|
||||
|
||||
|
||||
== External links ==
|
||||
De Luca LA, Menani JV, Johnson AK (2014). Neurobiology of Body Fluid Homeostasis: Transduction and Integration. Frontiers in Neuroscience. Boca Raton: CRC Press/Taylor & Francis. ISBN 9781466506930. PMID 24829987.
|
||||
41
data/en.wikipedia.org/wiki/Body_image_(neuroscience)-0.md
Normal file
41
data/en.wikipedia.org/wiki/Body_image_(neuroscience)-0.md
Normal file
@ -0,0 +1,41 @@
|
||||
---
|
||||
title: "Body image (neuroscience)"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Body_image_(neuroscience)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:40.513246+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Body image is a complex construct, often used in the clinical context of describing a patient's cognitive perception of their own body. The medical concept began with the work of the Austrian neuropsychiatrist and psychoanalyst Paul Schilder, described in his book The Image and Appearance of the Human Body first published in 1935. The term "body image" was officially introduced by Schilder himself and his widely used definition is: "body image is the picture of our own body we form in our mind, that is to say the way in which the body appears to ourselves". In research with the term "body image" we currently refer to a conscious mental representation of one's own body, which involves affects, attitudes, perceptual components and cognition. On the contrary, the term "body schema" was initially used to describe an unconscious body mental representation fundamental for action. Keizer and colleagues (2013) suggest the following definition: "[body schema is] an unconscious, sensorimotor, representation of the body that is invoked in action". In light of recent scientific developments regarding the multisensory integration of body sensations, the distinction between body image and body schema appears simplistic and probably no longer useful for scientific research and clinical purposes.
|
||||
|
||||
== Harms ==
|
||||
Engaging in social comparisons, particularly upward comparisons to individuals perceived as superior, can negatively affect self-evaluations and body image. Research indicates that exposure to idealized media images, such as models embodying cultural beauty standards, often leads to unfavorable body-image outcomes. Specifically for women, who are more likely to engage in upward appearance comparisons. Individual differences play a crucial role in which appearance comparison tendencies occur. Identifying modifiable risk factors linked to appearance comparisons is crucial for reducing their frequency and preventing body dissatisfaction. The Identity Disruption Model suggests that early adverse experiences, such as abuse or neglect, can disrupt identity development, leading to low self-concept clarity and an increased tendency to compare oneself to others.
|
||||
|
||||
== Clinical significance ==
|
||||
In the clinical setting, body image disturbances are relatively frequent and involve both psychiatric and neurological disorders. Disturbances in the perception of one's body are present in psychiatric disorders such as:
|
||||
|
||||
anorexia nervosa
|
||||
bulimia nervosa
|
||||
binge eating disorder
|
||||
psychotic spectrum disorders
|
||||
body dysmorphic disorder
|
||||
body integrity dysphoria (not included in DSM-5).
|
||||
Body image disorders are common in eating disorders and are referred to as "body image disturbance".
|
||||
|
||||
=== Anorexia nervosa ===
|
||||
There are three aspects pertaining to body image distortion in those with Anorexia nervosa. The first is Perception; this refers to the way in which someone views their own body. This is where the EBA and FBA come into play. Both the Extrastriate Body Area (EBA) and the Fusiform Body Area (FBA) in the brain are involved in how we perceive our own bodies. Those with Anorexia nervosa present an impaired functioning in these two brain regions which accounts for their inability to correctly describe their body. The second aspect is Affect; how satisfied or dissatisfied one is with their body. The third and final component is Cognition which alludes to what someone thinks about their own body and how they mentally picture themselves. Both the Affect and Cognition components use the insula in the brain; it creates our sense of "self" and self-awareness. This means that the insula plays a role in how we feel (Affect) and think (Cognition) about ourselves.
|
||||
Furthermore, The Allocentric Lock Theory states that those with eating disorders, such as Anorexia nervosa, are incapable of retaining new and updated views on their own bodies, therefore are unable to precisely report on their current body.
|
||||
|
||||
=== Bulimia nervosa ===
|
||||
Bulimia nervosa is a form of an eating disorder where one binge eats, and then forces themself to throw up in order to not gain weight. It can be caused by many things, such as stress, pressure, genetics, low self-esteem, obesity, and more. It is difficult to get diagnosed with as people tend to keep it to themselves, additionally, it is more common to get diagnosed with anorexia nervosa, so bulimia nervosa is often overlooked.
|
||||
|
||||
=== Binge eating disorder ===
|
||||
Binge eating disorder is a very serious form of eating disorder. Individuals with binge eating disorder often get the feeling of not being able to stop eating and eating much larger portions of food. Often after these binges, people with BED feel the need to cut back on their eating, but often this just results in more of the feeling to need to binge in the future. It can be caused by a number of things and is a lot of the time caused by a mix of things such as psychological things, environmental things, or biological things.
|
||||
|
||||
=== Psychotic spectrum disorders ===
|
||||
Psychotic spectrum disorder is a group of disorders that all have to do with psychosis. People with psychotic spectrum disorders often have trouble deciphering their thought which can lead to them being unable to tell what is real and what is fake. It is hard to define because each person who experiences it experiences it differently. There are many different types such as schizophrenia, schizophreniform disorder, delusional disorder, and many more. It is unknown for sure what causes psychotic spectrum disorders, but it is thought to be most likely a combination of genetics, brain development, traumas, and/or illnesses.
|
||||
|
||||
=== Body dysmorphia disorder ===
|
||||
Body dysmorphic disorder is a mental disorder in which a person hyper focuses on any possible flaws or defects that they see in themselves that in most cases aren't seen by others. It causes people that have it to care more and focus on body image and appearance. There's no known for sure cause of body dysmorphia, but like many other illnesses, it is most likely caused by a combination of things such as family history, negative experiences, and abnormal brain functions.
|
||||
26
data/en.wikipedia.org/wiki/Body_image_(neuroscience)-1.md
Normal file
26
data/en.wikipedia.org/wiki/Body_image_(neuroscience)-1.md
Normal file
@ -0,0 +1,26 @@
|
||||
---
|
||||
title: "Body image (neuroscience)"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Body_image_(neuroscience)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:40.513246+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
=== Body integrity disorder ===
|
||||
Body integrity dysphoria is a mental disorder in which a person gets the feeling that a certain part of their body no longer belongs on their body. People with this disorder know that the part is useful and healthy, but don't believe that they should be able to use it. It often causes people to try and get amputations or attempt to amputate themselves. There's no known cause of body integrity disorder, but it is thought to have to do with issues regarding the structure of the brain because multiple parts of the brain are involved in body perception.
|
||||
|
||||
=== Measurements ===
|
||||
Attempts by researchers to measure variances in body image include the FAI index, developed in a 2014 study (Zaccagni 2014). The FAI (feel-status minus actual-status inconsistency) index is used to assess someone's weight perception. FAI scores range from -3 to +3: Negative FAI values mean weight status underestimation, positive FAI values mean weight status overestimation and a FAI score of 0 means a realistic perception of one's weight status. The study found that women tend to have positive FAI values (overestimating their weight) while men had negative FAI values (underestimating their weight). Further studies have used the FAI index to study body image among natives and immigrants in Italy and North Africa.
|
||||
Another study (Zaccagni 2020) developed a refined version of the FAI index, called the FAIFAT index. This index (feel-fat-status minus actual-fat-status inconsistency) was meant to address possible fat status perception inconsistencies by bioelectrical impedance analysis (BIA).
|
||||
|
||||
== See also ==
|
||||
Body schema
|
||||
Gender dysphoria
|
||||
Mirror box
|
||||
Rubber hand illusion
|
||||
Body image—social concept
|
||||
|
||||
== References ==
|
||||
13. Vartanian, L. R., Pinkus, R. T., & Fardouly, J. (2025). Self-concept clarity and appearance comparisons in everyday life. Body Image An International Journal of Research, 52
|
||||
51
data/en.wikipedia.org/wiki/Bogart–Bacall_syndrome-0.md
Normal file
51
data/en.wikipedia.org/wiki/Bogart–Bacall_syndrome-0.md
Normal file
@ -0,0 +1,51 @@
|
||||
---
|
||||
title: "Bogart–Bacall syndrome"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Bogart–Bacall_syndrome"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:41.835054+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Bogart–Bacall syndrome (BBS) is a voice disorder that is caused by abuse or overuse of the vocal cords.
|
||||
|
||||
People who speak or sing outside their normal vocal range can develop BBS; symptoms are chiefly an unusually deep or rough voice, or dysphonia, and vocal fatigue. The people most commonly affected are those who speak in a low-pitched voice, particularly if they have poor breath and vocal control. The syndrome can affect both men and women.
|
||||
In 1988, an article was published describing a discrete type of vocal dysfunction which results in men sounding like actor Humphrey Bogart and women sounding like actress Lauren Bacall; Bogart and Bacall were married to each other and made several films together. BBS is now the medical term for an ongoing hoarseness that often affects actors, singers or TV/radio voice workers who routinely speak in a very low pitch.
|
||||
Treatment usually involves voice therapy by a speech language pathologist.
|
||||
|
||||
== Signs and symptoms ==
|
||||
Signs and symptoms of Bogart–Bacall Syndrome can appear differently depending on the vocal use of the individual. In singers, symptoms may appear more subtly due to their extreme sensitivity to small changes in the laryngeal mechanism and being able to control their laryngeal muscles more than the average person. This vocal control can compensate for irritation, weakness, or change in vibration patterns for the vocal folds. Signs and symptoms will vary on a case-by-case basis and will depend on vocal strain and the degree of daily use. Women are also more susceptible than men to experience heightened symptoms due to their increased likelihood of speaking at a lower pitch in professional settings.
|
||||
Signs and symptoms of Bogart–Bacall include the following:
|
||||
|
||||
Vocal fatigue
|
||||
Unnaturally deep or rough voice
|
||||
Hoarseness
|
||||
Sore larynx (tightness or muscle aches in the throat)
|
||||
Sudden breaks or fading of the voice
|
||||
Loss of vocal range when singing
|
||||
Feeling the need to clear the throat often
|
||||
Experiencing loss of speech
|
||||
|
||||
== Cause ==
|
||||
The cause of Bogart–Bacall syndrome is most commonly identified as abuse or overuse of the vocal cords. Individuals who speak or sing outside of their normal range can develop BBS over a long period of misuse. Individuals who develop this syndrome tend to speak or perform with poor breath support and laryngeal muscle tension. Causes include speech and communication disorders, throat conditions, and work-related conditions.
|
||||
Speech and communication disorders refers to issues involving language and related areas such as oral motor function. Some examples include expressive language disorder, receptive-expressive language disorder, phonologic disorder, and stuttering.
|
||||
Throat conditions can be any one of the following:
|
||||
|
||||
Vocal cord paralysis
|
||||
Vocal cord polyps
|
||||
Laryngitis
|
||||
Achalasia
|
||||
Throat cancer
|
||||
Hypopharyngeal cancer
|
||||
Larynx cancer.
|
||||
Work-related conditions typically affect individuals whose professions require extensive use or overuse of their vocal cords. Some examples include news and television broadcasters, radio hosts, as well as singers or actors. Teachers may also be susceptible to BBS depending on their volume and how much they talk on a regular basis.
|
||||
|
||||
== Mechanism ==
|
||||
There are many plausible reasons for how Bogart–Bacall and other vocal disorders occur, but it can not be determined for certain due to the many factors that play a role in speech production. Voice production requires the coordination of many muscles and other structures in the larynx. Many factors can cause the larynx to become tensed which changes the position of larynx. This affects the cartilaginous structures within the larynx leading to abnormal phonation. Bogart–Bacall refers to an unnaturally deep voice, so when lowering their voice, individuals may continue to speak even when the air in their lungs has been almost entirely expelled. Due to the effort exerted in lowering the pitch range, the muscles involved in respiration become tensed and strained along with speech.
|
||||
Bogart–Bacall syndrome is considered a secondary muscle tension dysphonia disorder, meaning that there is an abnormality in the voice box that causes the overuse of muscles to help produce your voice. This abnormality can be caused by an underlying medical reason or a physical exertion. By lowering vocal pitch, the larynx compresses the vocal folds which regulate air flow and production of the sounds used in speech which can cause damage to these muscles over time. Vocal fold lesions or nodules can cause changes in the vocal fold mucosa which leads to increased tension in the larynx, ultimately causing dysphonia.
|
||||
|
||||
== Diagnosis ==
|
||||
A speech-language pathology evaluation with a focus on understanding the patient's vocal use history, as well as an examination of the throat and larynx should be conducted. This evaluation potentially involves imaging to visualize the vocal cords in order to identify areas that have been heavily stressed. Imaging options can include a laryngoscope, videostroboscopy, or laryngeal electromyography. Diagnosis of Bogart–Bacall can be difficult due to the variance in symptom presentation and vocal use.
|
||||
Videostroboscopy provides a magnified, slow-motion view of the vocal cords and larynx in action which allows professionals to see any abnormal movement. Videostroboscopy can be used to visualize any swelling of the vocal folds, irritation, or polyps and growth. Occasionally, redness or bumps can be seen on vocal cords which is useful in making a correct diagnosis.
|
||||
Laryngeal electromyography is a test that measures the electrical signals from the voice box muscles (laryngeal muscles) during speaking, breathing, and swallowing. This evaluation is to check if vocal issues are related to any one of the following: partial paralysis resulting in muscle weakness, paralysis resulting in loss of muscle function, and the functionality of the motor unit of the laryngeal muscles. Laryngeal electromyography plays an important role in determining whether or not a nerve problem is the cause of a vocal disorder.
|
||||
27
data/en.wikipedia.org/wiki/Bogart–Bacall_syndrome-1.md
Normal file
27
data/en.wikipedia.org/wiki/Bogart–Bacall_syndrome-1.md
Normal file
@ -0,0 +1,27 @@
|
||||
---
|
||||
title: "Bogart–Bacall syndrome"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Bogart–Bacall_syndrome"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:41.835054+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
== Prevention and treatment ==
|
||||
Prevention of Bogart–Bacall syndrome aims to target the two main symptoms of this disorder, dysphonia and vocal fatigue. Having effective posture allows a person to shift the tension between the muscles allowing free movement of the larynx without blockage leading to effective voice production. Improvement of breath control with a professional vocal coach is also important for individuals who may have work-related conditions that require continuous strain on the vocal cords and larynx.
|
||||
Speech therapy with a speech-language pathologist is a very common method of treatment to return speaking level to its normal pitch range. Consultation with a speech-language pathologist will determine what levels of rest, fluid, and performance corrections are needed for the vocal cords and larynx to sustain a healthy voice. If there is a particular underlying cause of the condition that can be treated with medication, this can be coupled with speech therapy as a form of treatment.
|
||||
Individuals with persistent symptoms after speech therapy may require more invasive treatment. Invasive treatment may require the removal of lesions, nodules, or masses on the vocal cords if visualized during diagnostic imaging. If the disorder is found to be nerve related through electromyography the nerve in question may need to be replaced or the vocal cords can be pushed together with a bulk injection or thyroplasty. A bulk injection involves adding a filler substance to the paralyzed vocal cord to have it vibrate closer to the functioning vocal cord. Thyroplasty involves the insertion of an implant against the paralyzed vocal cord moving it closer to the other vocal cord.
|
||||
|
||||
== Prognosis ==
|
||||
Individuals with Bogart–Bacall syndrome that do not have an underlying condition are typically expected to make a vocal recovery through voice therapy. Having a form of muscle tension dysphonia go untreated, can cause further long-term disorders that require additional forms of treatment.
|
||||
|
||||
== Epidemiology ==
|
||||
Bogart–Bacall syndrome can develop in individuals at any age. It is more likely to develop in individuals who work in voice performance which can range from singers, actors, teachers or radio and television broadcasters. Women are more likely than men to develop BBS due to the tendency of lowering their voices in a professional environment. This syndrome is also more prevalent in the 40–50-year-old-age group as their vocal cords thin. Vocal disorders are prevalent in roughly 10% of the population and can range from muscle tension dysphonia to speech and language disorders.
|
||||
|
||||
== Research directions ==
|
||||
Further studies need to be conducted to further examine the long-term effects of Bogart–Bacall syndrome if left untreated. Studies that are currently ongoing aim to understand what the best course of treatment may be for individuals with muscle tension dysphonia, which includes individuals with Bogart–Bacall. It is currently understood that an interdisciplinary approach to target the causes such as poor breath support, overuse, and inappropriate intensity is most effective.
|
||||
Vocal disorders and misuse are currently being researched depending on work conditions and professions. A study based on over 1,200 teachers has indicated that voice disorders play a significant role in their profession. The study found that a substantial number of teachers have needed to take time off work or seek medical attention due to voice issues or to seek treatment. The study also found that women are more likely to develop these disorders over their male counterparts.
|
||||
There is more research available on vocal disorders and how they may be affected by additional lifestyle factors. A study was conducted to understand how reflux affected vocal disorders such as dysphonia in singers with bulimia. Singers tend to overuse their vocal cords which makes them very susceptible to a variety of vocal disorders. Dysphonia associated with bulimia has been linked to vocal fold edema and polypoid changes. The aim was to understand if bulimia was linked to laryngopharyngeal reflux as a plausible cause of dysphonia. In preliminary results, it was understood that reflux was the case in every singer with bulimia and dysphonia, indicating it may be a contributing factor to their vocal disorder.
|
||||
|
||||
== References ==
|
||||
24
data/en.wikipedia.org/wiki/Breast_atrophy-0.md
Normal file
24
data/en.wikipedia.org/wiki/Breast_atrophy-0.md
Normal file
@ -0,0 +1,24 @@
|
||||
---
|
||||
title: "Breast atrophy"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Breast_atrophy"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:43.043100+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Breast atrophy is the normal or spontaneous atrophy or shrinkage of the breasts.
|
||||
Breast atrophy commonly occurs in women during menopause when estrogen levels decrease. It can also be caused by hypoestrogenism and/or hyperandrogenism in women in general, such as in antiestrogen treatment for breast cancer, in polycystic ovary syndrome (PCOS), and in malnutrition such as that associated with eating disorders like anorexia nervosa or with chronic disease. It can also be an effect of weight loss.
|
||||
In the treatment of gynecomastia in males and macromastia in women, and in hormone replacement therapy (HRT) for trans men, breast atrophy may be a desired effect.
|
||||
|
||||
|
||||
== See also ==
|
||||
Mammoplasia
|
||||
Micromastia
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
@ -0,0 +1,52 @@
|
||||
---
|
||||
title: "Brief resolved unexplained event"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Brief_resolved_unexplained_event"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:44.192552+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Brief resolved unexplained event (BRUE), previously apparent life-threatening event (ALTE), is a medical term in pediatrics that describes an event that occurs during infancy. The event is noted by an observer, typically the infant's caregiver. It is characterized by one or more concerning symptoms such as change in skin color, lack of breathing, weakness, or poor responsiveness. By definition, by the time they are assessed in a healthcare environment they must be back to normal without obvious explanation after the clinician takes the appropriate clinical history and physical examination.
|
||||
The American Academy of Pediatrics (AAP) clarified the use of both terms in a 2016 consensus statement that recommended the term BRUE be used whenever possible as it is more specifically defined. Thus, it is more useful for assessing risk of further events. The cause for BRUEs is often unknown, although some of the more common causes include gastroesophageal reflux, seizure, and child maltreatment. Evaluation after an ALTE or BRUE is diagnostically important, as some events represent the first sign or symptom of an underlying medical condition. In most cases, assuming the infants are otherwise healthy and no underlying medical issue is found, the infants who have a BRUE are unlikely to have a second event and have an even smaller risk of death.
|
||||
|
||||
== Presentation ==
|
||||
A BRUE is a description of a self-limited episode. Usually a BRUE lasts for less than 1 minute. By definition, the episode must have resolved by the time the infant is evaluated by a medical professional. The caregiver may report observation of bluish skin discoloration, called cyanosis. Breathing abnormalities, such as lack of breathing, slow breathing, or irregular breathing may be noted. Differences in muscle tone, such as transient floppiness or rigidity can also be characterized as a BRUE. Changes in level of responsiveness such as abnormal eye contact or inability to interact can also fulfill the classification.
|
||||
A BRUE is a term used by a clinician to characterize an infant's self-limited episode witnessed by someone else. The AAP defines a BRUE as a sudden, brief episode that occurs to infants less than 1 year of age, lasts less than one minute, and resolves completely on its own prior to being evaluated by a health professional. The event must include at least one of the following:
|
||||
|
||||
skin color change to blue (cyanosis) or pale (pallor)
|
||||
abnormal breathing
|
||||
muscle weakness
|
||||
decreased responsiveness
|
||||
|
||||
== Causes ==
|
||||
Most infants who have a BRUE are never diagnosed with a definitive cause for the event. However, we use the literature on ALTEs, which is more extensive, to help explain the cause of a BRUE. These causes may also be considered conditions that can be confused with a BRUE.
|
||||
|
||||
=== Gastroesophageal reflux ===
|
||||
Vomiting or choking during feeding can trigger laryngospasm that leads to a BRUE or ALTE. This is a likely cause if the infant had vomiting or regurgitation just prior to the event, or if the event occurred while the infant was awake and lying down. In healthy infants with a suggestive GER event, no additional testing is typically done. In infants with repeated episodes of choking or repeated acute events, evaluation with a swallowing study can be helpful.
|
||||
|
||||
=== Other causes ===
|
||||
Other causes that are less common include meningitis, urinary tract infection, breath-holding spells, congenital central hypoventilation syndrome, cancer, intracranial bleed, apnea of infancy, periodic breathing of infancy, choking, obstructive sleep apnea, factitious disorder imposed on another (formerly Munchausen syndrome).
|
||||
|
||||
== Diagnosis ==
|
||||
Taking the history of the event is vital in the evaluation of a BRUE. The first step is determining whether this is truly a BRUE by looking for presence of abnormal symptoms or vital signs. If this is the case, then it cannot be labelled as a BRUE and the healthcare professional should treat accordingly.
|
||||
|
||||
=== Low-risk infants ===
|
||||
The next step in evaluation is distinguishing whether this BRUE is low- or high-risk. The American Academy of Pediatrics classifies an infant as low risk if they have a BRUE and meet the following characteristics:
|
||||
|
||||
infant is of age greater than 60 days
|
||||
gestational age greater than or equal to 32 weeks
|
||||
infant has had no prior BRUEs
|
||||
this BRUE did not occur in a cluster
|
||||
cardiopulmonary resuscitation (CPR) by a medical provider was not required
|
||||
no concerning features on history
|
||||
no concerning physical examination findings
|
||||
duration less than 20 seconds
|
||||
|
||||
=== High-risk infants ===
|
||||
If the infant does not meet all of these criteria, the BRUE is considered high-risk, and more likely represents an underlying medical condition. Characteristics of the infant that make this more likely include history of similar events or clustering, history of unexpected death in a sibling, need for CPR by a trained medical professional, ongoing lethargy, suspicion for child abuse or maltreatment, or existence of genetic syndrome or congenital anomalies.
|
||||
|
||||
== Management ==
|
||||
If the infant meets criteria for a low-risk BRUE and the clinician feels there are no concerning findings otherwise, treatment often involves simple short observation in the emergency department with pulse oximetry. For the cases where parents complain of specific symptoms at the time of the event, then follow-up testing may be done for the related conditions or diseases. Other tests are not typically recommended for low-risk infants.
|
||||
For infants that have concerning features on history or physical, and are thus categorized as high-risk, further evaluation is warranted. This will vary greatly depending on the infants symptoms, but may include, urinalysis, complete blood count, imaging with chest x-ray, and laboratory screening for ingestion of medications or poisons. Also, for infants in the high-risk category, clinicians should consider admission to the hospital for extended observation, depending on the benefits and risk of the case. The course of the admission provides an opportunity to witness a second event to better characterize it and narrow the list of possible diagnoses. The observation of infants at home with the help of medical devices after discharge is not recommended.
|
||||
@ -0,0 +1,20 @@
|
||||
---
|
||||
title: "Brief resolved unexplained event"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Brief_resolved_unexplained_event"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:44.192552+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
== Prognosis ==
|
||||
The risk of death of patients who have a BRUE has been studied by using the literature about ALTEs, since this data is more abundant. The studies concluded that there is no increased risk of death for these patients compared to the rest of the infant population. As for the prognosis of these infants into adulthood, research still needs to be conducted to assess for any long-term health effects.
|
||||
|
||||
== History ==
|
||||
In 1986, the National Institute of Health defined an apparent life-threatening event (ALTE) as an observed frightening event of an infant that includes at least one component of lack of breathing (apnea), skin color change (such as cyanosis), weakness, choking, or gagging. The term was invented to avoid previously used terms such as "near-miss SIDS" to dissociate the event from SIDS, a separate condition in infancy. There had been literature discussion in the past about the increased risk of SIDS in these infants, but more recently the research has concluded that there is no direct relationship between an ALTE and SIDS. It also was defined as part of an attempt to characterize the different forms of apnea, or sudden lack of breathing, in infants.
|
||||
In 2016, the American Academy of Pediatrics (AAP) published a clinical practice guideling recommending the replacement of ALTE with a new term, brief resolved unexplained event (BRUE). The guidelines state that the term ALTE is still applicable with key differences between ALTE and BRUE. The biggest difference is whether the infant is symptomatic at time of presentation to a health professional. If the infant is still showing symptoms, then the condition is termed an ALTE. In order to be considered a BRUE, the infant should be completely asymptomatic at time of presentation, which is more common. Because of this, a BRUE can also be considered as a subset of ALTE. The term change was also recommended in large part due to the "life-threatening" suggestion from the older term. The rate of death in infants following a BRUE has been studied and is relatively rare, about 1 in 800.
|
||||
|
||||
== References ==
|
||||
|
||||
== External links ==
|
||||
43
data/en.wikipedia.org/wiki/Calcinosis-0.md
Normal file
43
data/en.wikipedia.org/wiki/Calcinosis-0.md
Normal file
@ -0,0 +1,43 @@
|
||||
---
|
||||
title: "Calcinosis"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Calcinosis"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:45.452780+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Calcinosis is the formation of calcium deposits in any soft tissue. It is a rare condition that has many different causes. These range from infection and injury to systemic diseases like kidney failure.
|
||||
|
||||
|
||||
== Types ==
|
||||
|
||||
|
||||
=== Dystrophic calcification ===
|
||||
The most common type of calcinosis is dystrophic calcification. This type of calcification can occur as a response to any soft tissue damage, including that involved in implantation of medical devices.
|
||||
|
||||
|
||||
=== Metastatic calcification ===
|
||||
Metastatic calcification involves a systemic calcium excess imbalance, which can be caused by hypercalcemia, kidney failure, milk-alkali syndrome, lack or excess of other minerals, or other causes.
|
||||
|
||||
|
||||
=== Tumoral calcinosis ===
|
||||
The cause of the rare condition of tumoral calcinosis is not entirely understood. It is generally characterized by large, globular calcifications near joints.
|
||||
|
||||
|
||||
== See also ==
|
||||
Calcification
|
||||
Calcinosis cutis
|
||||
Dermatomyositis
|
||||
Fahr's syndrome
|
||||
Hyperphosphatemia
|
||||
Primrose syndrome
|
||||
Scleroderma
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
Media related to Calcinosis at Wikimedia Commons
|
||||
108
data/en.wikipedia.org/wiki/Calculus_(medicine)-0.md
Normal file
108
data/en.wikipedia.org/wiki/Calculus_(medicine)-0.md
Normal file
@ -0,0 +1,108 @@
|
||||
---
|
||||
title: "Calculus (medicine)"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Calculus_(medicine)"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:46.702674+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
A calculus (pl.: calculi), often called a stone, is a concretion of material, usually mineral salts, that forms in an organ or duct of the body. Formation of calculi is known as lithiasis (). Stones can cause a number of medical conditions.
|
||||
Some common principles (below) apply to stones at any location, but for specifics see the particular stone type in question.
|
||||
Calculi are not to be confused with gastroliths, which are ingested rather than grown endogenously.
|
||||
|
||||
|
||||
== Types ==
|
||||
|
||||
Calculi in the inner ear are called otoliths. Unlike other entries in this list, otoliths are not pathological but are a normal feature of the inner ear.
|
||||
Calculi in the urinary system are called urinary calculi and include kidney stones (also called renal calculi or nephroliths) and bladder stones (also called vesical calculi or cystoliths). They can have any of several compositions, including mixed. Principal compositions include oxalate and urate.
|
||||
Calculi in the prostate are called prostatic calculi.
|
||||
Calculi in the mammary gland are called breast microcalcifications or mammary microcalcifications.
|
||||
Calculi of the gallbladder and bile ducts are called gallstones and are primarily developed from bile salts and cholesterol derivatives.
|
||||
Calculi in the nasal passages (rhinoliths) are rare.
|
||||
Calculi in the gastrointestinal tract (enteroliths) can be enormous. Individual enteroliths weighing many pounds have been reported in horses.
|
||||
Calculi in the stomach are called gastric calculi (not to be confused with gastroliths which are exogenous in nature).
|
||||
Calculi in the salivary glands are called salivary calculi (sialoliths).
|
||||
Calculi in the tonsils are called tonsillar calculi (tonsilloliths).
|
||||
Calculi in the veins are called venous calculi (phleboliths).
|
||||
Calculi in the skin, such as in sweat glands, are not common but occasionally occur.
|
||||
Calculi in the navel are called omphaloliths.
|
||||
Calculi are usually asymptomatic, and large calculi may have required many years to grow to their large size.
|
||||
|
||||
|
||||
== Cause ==
|
||||
|
||||
From an underlying abnormal excess of the mineral, e.g., with elevated levels of calcium (hypercalcaemia) that may cause kidney stones, dietary factors for gallstones.
|
||||
Local conditions at the site in question that promote their formation, e.g., local bacteria action (in kidney stones) or slower fluid flow rates, a possible explanation of the majority of salivary duct calculus occurring in the submandibular salivary gland.
|
||||
Enteroliths are a type of calculus found in the intestines of animals (mostly ruminants) and humans, and may be composed of inorganic or organic constituents.
|
||||
Bezoars are lumps of indigestible material in the stomach and/or intestines; most commonly, they consist of hair (in which case they are also known as hairballs). A bezoar may form the nidus of an enterolith.
|
||||
In kidney stones, calcium oxalate is the most common mineral type (see nephrolithiasis). Uric acid is the second most common mineral type, but an in vitro study showed uric acid stones and crystals can promote the formation of calcium oxalate stones.
|
||||
|
||||
|
||||
== Pathophysiology ==
|
||||
Stones can cause disease by several mechanisms:
|
||||
|
||||
Irritation of nearby tissues, causing pain, swelling, and inflammation
|
||||
Obstruction of an opening or duct, interfering with normal flow and disrupting the function of the organ in question
|
||||
Predisposition to infection (often due to disruption of normal flow)
|
||||
A number of important medical conditions are caused by stones:
|
||||
|
||||
Nephrolithiasis (kidney stones)
|
||||
Can cause hydronephrosis (swollen kidneys) and kidney failure
|
||||
Can predispose to pyelonephritis (kidney infections)
|
||||
Can progress to urolithiasis
|
||||
Urolithiasis (urinary bladder stones)
|
||||
Can progress to bladder outlet obstruction
|
||||
Cholelithiasis (gallstones)
|
||||
Can predispose to cholecystitis (gall bladder infections) and ascending cholangitis (biliary tree infection)
|
||||
Can progress to choledocholithiasis (gallstones in the bile duct) and gallstone pancreatitis (inflammation of the pancreas)
|
||||
Gastric calculi can cause colic, obstruction, torsion, and necrosis.
|
||||
|
||||
|
||||
== Diagnosis ==
|
||||
Diagnostic workup varies by the stone type, but in general:
|
||||
|
||||
Clinical history and physical examination
|
||||
Imaging studies:
|
||||
Some stone types (mainly those with substantial calcium content) can be detected on X-ray and CT scan
|
||||
Many stone types can be detected by ultrasound
|
||||
Factors contributing to stone formation (as in #Etiology) are often tested:
|
||||
Laboratory testing can give levels of relevant substances in blood or urine
|
||||
Some stones can be directly recovered (at surgery, or when they leave the body spontaneously) and sent to a laboratory for analysis of content
|
||||
|
||||
|
||||
== Treatment ==
|
||||
Modification of predisposing factors can sometimes slow or reverse stone formation. Treatment varies by stone type, but, in general:
|
||||
|
||||
Healthy diet and exercise (promotes flow of energy and nutrition)
|
||||
Drinking fluids (water and electrolytes like lemon juice, diluted vinegar e.g. in pickles, salad dressings, sauces, soups, shrubs cocktail)
|
||||
Surgery (lithotomy)
|
||||
Medication / antibiotics
|
||||
Extracorporeal shock wave lithotripsy (ESWL) for removal of calculi
|
||||
|
||||
|
||||
== History ==
|
||||
The earliest operation for curing stones is given in the Sushruta Samhita (6th century BCE). The operation involved exposure and going up through the floor of the bladder.
|
||||
The care of this disease was forbidden to the physicians that had taken the Hippocratic Oath because:
|
||||
|
||||
There was a high probability of intraoperative and postoperative surgical complications like infection or bleeding
|
||||
The physicians would not perform surgery as in ancient cultures they were two different professions
|
||||
|
||||
|
||||
== Etymology ==
|
||||
The word comes from Latin calculus "small stone", from calx "limestone, lime", probably related to Greek χάλιξ chalix "small stone, pebble, rubble", which many trace to a Proto-Indo-European language root for "split, break up". Calculus was a term used for various kinds of stones. In the 18th century it came to be used for accidental or incidental mineral buildups in human and animal bodies, like kidney stones and minerals on teeth.
|
||||
|
||||
|
||||
== See also ==
|
||||
Bezoar
|
||||
Calculus (dental)
|
||||
Lithotomy
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
|
||||
"The Little Treatise on the Medical Treatment of the Back and of Hemorrhoids" is a manuscript, from the 18th-century, in Arabic, which discusses the treatment of calculi
|
||||
199
data/en.wikipedia.org/wiki/Cardiac_shunt-0.md
Normal file
199
data/en.wikipedia.org/wiki/Cardiac_shunt-0.md
Normal file
@ -0,0 +1,199 @@
|
||||
---
|
||||
title: "Cardiac shunt"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Cardiac_shunt"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:47.861966+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
In cardiology, a cardiac shunt is a pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system. It may be described as right-left, left-right or bidirectional, or as systemic-to-pulmonary or pulmonary-to-systemic. The direction may be controlled by left and/or right heart pressure, a biological or artificial heart valve or both. The presence of a shunt may also affect left and/or right heart pressure either beneficially or detrimentally.
|
||||
|
||||
|
||||
== Terminology ==
|
||||
|
||||
The left and right sides of the heart are named from a dorsal view, i.e., looking at the heart from the back or from the perspective of the person whose heart it is. There are four chambers in a heart: an atrium (upper) and a ventricle (lower) on both the left and right sides. In mammals and birds, blood from the body goes to the right side of the heart first. Blood enters the upper right atrium, is pumped down to the right ventricle and from there to the lungs via the pulmonary artery. Blood going to the lungs is called the pulmonary circulation. When the blood returns to the heart from the lungs via the pulmonary vein, it goes to the left side of the heart, entering the upper left atrium. Blood is then pumped to the lower left ventricle and from there out of the heart to the body via the aorta. This is called the systemic circulation. A cardiac shunt is when blood follows a pattern that deviates from the systemic circulation, i.e., from the body to the right atrium, down to the right ventricle, to the lungs, from the lungs to the left atrium, down to the left ventricle and then out of the heart back to the systemic circulation.
|
||||
A left-to-right shunt is when blood from the left side of the heart goes to the right side of the heart. This can occur either through a hole in the ventricular or atrial septum that divides the left and the right heart or through a hole in the walls of the arteries leaving the heart, called great vessels. Left-to-right shunts occur when the systolic blood pressure in the left heart is higher than the right heart, which is the normal condition in birds and mammals.
|
||||
|
||||
|
||||
== Congenital shunts in humans ==
|
||||
The most common congenital heart defects (CHDs) which cause shunting are atrial septal defects (ASD), patent foramen ovale (PFO), ventricular septal defects (VSD), and patent ductus arteriosi (PDA). In isolation, these defects may be asymptomatic, or they may produce symptoms which can range from mild to severe, and which can either have an acute or a delayed onset. However, these shunts are often present in combination with other defects; in these cases, they may still be asymptomatic, mild or severe, acute or delayed, but they may also work to counteract the negative symptoms caused by another defect (as with d-Transposition of the great arteries).
|
||||
|
||||
|
||||
== Acquired shunts in human ==
|
||||
|
||||
|
||||
=== Biological ===
|
||||
Some acquired shunts are modifications of congenital ones: a balloon septostomy can enlarge a foramen ovale (if performed on a newborn), PFO or ASD; or prostaglandin can be administered to a newborn to prevent the ductus arteriosus from closing. Biological tissues may also be used to construct artificial passages.
|
||||
Evaluation can be done during a cardiac catheterization with a "shunt run" by taking blood samples from superior vena cava (SVC), inferior vena cava (IVC), right atrium, right ventricle, pulmonary artery, and system arterial. Abrupt increases in oxygen saturation support a left-to-right shunt and lower than normal systemic arterial oxygen saturation supports a right-to-left shunt.
|
||||
Samples from the SVC & IVC are used to calculate mixed venous oxygen saturation using the Flamm formula
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
S
|
||||
|
||||
v
|
||||
|
||||
|
||||
|
||||
O
|
||||
|
||||
2
|
||||
|
||||
|
||||
=
|
||||
|
||||
|
||||
3
|
||||
4
|
||||
|
||||
|
||||
×
|
||||
S
|
||||
V
|
||||
C
|
||||
+
|
||||
|
||||
|
||||
1
|
||||
4
|
||||
|
||||
|
||||
×
|
||||
I
|
||||
V
|
||||
C
|
||||
|
||||
|
||||
{\displaystyle S_{v}O_{2}={\frac {3}{4}}\times SVC+{\frac {1}{4}}\times IVC}
|
||||
|
||||
|
||||
and Qp:Qs ratio
|
||||
|
||||
|
||||
|
||||
|
||||
Q
|
||||
p
|
||||
:
|
||||
Q
|
||||
s
|
||||
=
|
||||
|
||||
|
||||
change in oxygen concentration across the pulmonary circulation
|
||||
change in oxygen concentration across the systemic circulation
|
||||
|
||||
|
||||
=
|
||||
|
||||
|
||||
|
||||
|
||||
P
|
||||
|
||||
V
|
||||
|
||||
|
||||
−
|
||||
|
||||
P
|
||||
|
||||
A
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
S
|
||||
|
||||
A
|
||||
|
||||
|
||||
−
|
||||
|
||||
S
|
||||
|
||||
V
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle Qp:Qs={\frac {\text{change in oxygen concentration across the pulmonary circulation}}{\text{change in oxygen concentration across the systemic circulation}}}={\frac {P_{V}-P_{A}}{S_{A}-S_{V}}}}
|
||||
|
||||
|
||||
where
|
||||
|
||||
|
||||
|
||||
|
||||
P
|
||||
|
||||
V
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle P_{V}}
|
||||
|
||||
is the pulmonary vein,
|
||||
|
||||
|
||||
|
||||
|
||||
P
|
||||
|
||||
A
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle P_{A}}
|
||||
|
||||
is the pulmonary artery,
|
||||
|
||||
|
||||
|
||||
|
||||
S
|
||||
|
||||
A
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle S_{A}}
|
||||
|
||||
is the systemic arterial, and
|
||||
|
||||
|
||||
|
||||
|
||||
S
|
||||
|
||||
V
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle S_{V}}
|
||||
|
||||
is the mixed-venous The Qp:Qs ratio is based upon the Fick principle and it is reduced to the above equation and eliminates the need to know cardiac output and hemoglobin concentration.
|
||||
|
||||
|
||||
=== Mechanical ===
|
||||
Mechanical shunts such as the Blalock-Taussig shunt are used in some cases of CHD to control blood flow or blood pressure.
|
||||
|
||||
|
||||
== Reptile ==
|
||||
|
||||
All reptiles have the capacity for cardiac shunts.
|
||||
|
||||
|
||||
== References ==
|
||||
28
data/en.wikipedia.org/wiki/Carnoy's_solution-0.md
Normal file
28
data/en.wikipedia.org/wiki/Carnoy's_solution-0.md
Normal file
@ -0,0 +1,28 @@
|
||||
---
|
||||
title: "Carnoy's solution"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Carnoy's_solution"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:50.446534+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Carnoy's solution is a fixative composed of 60% ethanol, 30% chloroform and 10% glacial acetic acid, 1 gram of ferric chloride.
|
||||
Carnoy's solution is also the name of a different fixation composed of ethanol and glacial acetic acid (3:1).
|
||||
The invention of Carnoy's solution is attributed to Jean-Baptiste Carnoy, a pioneering 19th century cytologist.
|
||||
|
||||
|
||||
== Uses ==
|
||||
Some of the uses of Carnoy's solution are:
|
||||
|
||||
Enhancing lymph node detection during dissection of cadavers.
|
||||
Immunohistochemical fixation and detection of NMDA receptors within the murine hippocampus.
|
||||
Applied directly following enucleation for the treatment of odontogenic keratocysts.
|
||||
Direct application following enucleation (Cuba) for certain kinds of unicystic ameloblastomas. This appears to decrease the likelihood of recurrence over enucleation alone. Protein coagulation is thought to limit uptake of these toxic materials by surrounding tissues, however it is this fact that limits its usefulness as a treatment agent in general.
|
||||
As a fixative for pap smear samples.
|
||||
As a fixative agent for both nuclear and mitochondrial DNA in various tissues.
|
||||
As a fixative agent to preserve mucus, useful for tissue preparation before staining with periodic acid-Schiff base.
|
||||
|
||||
|
||||
== References ==
|
||||
40
data/en.wikipedia.org/wiki/Case_presentation-0.md
Normal file
40
data/en.wikipedia.org/wiki/Case_presentation-0.md
Normal file
@ -0,0 +1,40 @@
|
||||
---
|
||||
title: "Case presentation"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Case_presentation"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:51.626584+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
A case presentation is a formal communication between health care professionals such as doctors and nurses regarding a patient's clinical information.
|
||||
Essential parts of a case presentation include:
|
||||
|
||||
Identification
|
||||
Reason for consultation/admission
|
||||
Chief complaints (CC) - what made patients seek medical attention.
|
||||
History of present illness (HPI) - circumstances relating to chief complaints.
|
||||
Past medical history (PMHx)
|
||||
Past surgical history
|
||||
Current medications
|
||||
Allergies
|
||||
Family history (FHx)
|
||||
Social history (SocHx)
|
||||
Physical examination (PE)
|
||||
Laboratory results (Lab)
|
||||
Other investigations (imaging, biopsy etc.)
|
||||
Case summary and impression
|
||||
Management plans
|
||||
follow up in clinic or hospital
|
||||
Adherence of the patient to treatment
|
||||
success of the treatment or failure.
|
||||
causes of success or failure.
|
||||
|
||||
|
||||
== See also ==
|
||||
Case report
|
||||
Case series
|
||||
|
||||
|
||||
== References ==
|
||||
75
data/en.wikipedia.org/wiki/Case_report-0.md
Normal file
75
data/en.wikipedia.org/wiki/Case_report-0.md
Normal file
@ -0,0 +1,75 @@
|
||||
---
|
||||
title: "Case report"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Case_report"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:52.887502+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
In medicine, a case report is a detailed report of the symptoms, signs, diagnosis, treatment, and follow-up of an individual patient. Case reports may contain a demographic profile of the patient, but usually describe an unusual or novel occurrence. Some case reports also contain a literature review of other reported cases. Case reports are professional narratives that provide feedback on clinical practice guidelines and offer a framework for early signals of effectiveness, adverse events, and cost. They can be shared for medical, scientific, or educational purposes.
|
||||
|
||||
|
||||
== Types ==
|
||||
Most case reports are on one of six topics:
|
||||
|
||||
An unexpected association between diseases or symptoms.
|
||||
An unexpected event in the course of observing or treating a patient.
|
||||
Findings that shed new light on the possible pathogenesis of a disease or an adverse effect.
|
||||
Unique or rare features of a disease.
|
||||
Unique therapeutic approaches.
|
||||
A positional or quantitative variation of the anatomical structures.
|
||||
|
||||
|
||||
== Roles in research and education ==
|
||||
A case report is generally considered a type of anecdotal evidence. Given their intrinsic methodological limitations, including lack of statistical sampling, case reports are placed at the bottom of the hierarchy of clinical evidence, together with case series. Nevertheless, case reports do have genuinely useful roles in medical research and evidence-based medicine. In particular, they have facilitated recognition of new diseases and adverse effects of treatments. For example, the recognition of the link between administration of thalidomide to mothers and malformations in their babies was triggered by a case report. Case reports have a role in pharmacovigilance. They can also help understand the clinical spectrum of rare diseases as well as unusual presentations of common diseases. They can help generate study hypotheses, including plausible mechanisms of disease. Case reports may also have a role to play in guiding the personalization of treatments in clinical practice.
|
||||
Proponents of case reports have outlined some particular advantages of the format. Case reports and series have a high sensitivity for detecting novelty and therefore remain one of the cornerstones of medical progress; they provide many new ideas in medicine. Whereas randomized clinical trials usually only inspect one variable or very few variables, rarely reflecting the full picture of a complicated medical situation, the case report can detail many different aspects of the patient's medical situation (e.g. patient history, physical examination, diagnosis, psychosocial aspects, follow up).
|
||||
Because typical, unremarkable cases are less likely to be published, use of case reports as scientific evidence must take into account publication bias. Some case reports also contain an extensive review of the relevant literature on the topic at-hand (and sometimes a systematic review of available evidence). Reports adopting this sort of approach can be identified by terms such as a "case report and review of the literature". Reports containing broader active research such as this might be considered case studies in the true definition of the term.
|
||||
Case reports can also play a relevant role in medical education by providing a structure for case-based learning.
|
||||
A particular attraction of case reports is the possibility of quick publication (with respect to more extensive studies such as randomized control trials), allowing them to act as a kind of rapid short communication between busy clinicians who may not have the time or resources to conduct large scale research.
|
||||
|
||||
|
||||
== Reporting guidelines ==
|
||||
The quality of the scientific reporting of case reports is variable, and sub-optimal reporting hinders the use of case reports to inform research design or help guide clinical practice. In response to these issues, reporting guidelines are under development to facilitate greater transparency and completeness in the provision of relevant information for individual cases. The CARE (i.e. CAse REport) guidelines include a reporting checklist that is listed on the EQUATOR Network, an international initiative aimed at promoting transparent and accurate reporting of health research studies to enhance the value and reliability of medical research literature. This 13-item checklist includes indications regarding the title, key words, abstract, introduction, patient information, clinical findings, timeline, diagnostic assessment, therapeutic interventions, follow-up and outcomes, discussion, patient perspective, and informed consent. An explanation and elaboration article (a manual for writing case reports following the CARE guidelines) was published in the Journal of Clinical Epidemiology in 2017.
|
||||
|
||||
|
||||
== Publishing ==
|
||||
|
||||
Many international journals publish case reports, but they restrict the number that appear in the print run because this has an adverse effect on the journal's impact factor. Case reports are often published online, and there is often still a requirement for a subscription to access them. However, an increasing number of journals are devoted to publishing case reports alone, most of which are open access. The first of these to start publishing, in 2001, was Grand Rounds.
|
||||
There are a number of websites that allow patients to submit and share their own patient case reports with other people. PatientsLikeMe and Treatment Report are two such sites.
|
||||
|
||||
|
||||
== Use of terminology outside science ==
|
||||
The term is also used to describe non-scientific reports usually prepared for educational reasons.
|
||||
|
||||
|
||||
== Famous scientific case reports ==
|
||||
Sigmund Freud reported on numerous cases, including Anna O., Dora, Little Hans, Rat Man, and Wolf Man
|
||||
Frederick Treves reported on "The Elephant Man"
|
||||
Paul Broca reported on language impairment following left hemisphere lesions in the 1860s.
|
||||
Joseph Jules Dejerine reported on a case of pure alexia.
|
||||
William MacIntyre reported on a case of multiple myeloma (described in the 1840s).
|
||||
Christiaan Barnard described the world's first heart transplant as a case report
|
||||
W. G. McBride, Thalidomide Case Report (1961). The Lancet 2:1358.
|
||||
|
||||
|
||||
== See also ==
|
||||
Case series
|
||||
Case presentation
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
Riley DS, Barber MS, Kienle GS, Aronson JK, von Schoen-Angerer T; et al. (2017). "CARE 2013 Explanation and Elaborations: Reporting Guidelines for Case Reports". Journal of Clinical Epidemiology. 89: 218–235. doi:10.1016/j.jclinepi.2017.04.026. PMID 28529185. S2CID 205846029.{{cite journal}}: CS1 maint: multiple names: authors list (link)
|
||||
|
||||
|
||||
== Further reading ==
|
||||
Jamjoom, Aimun; Nikkar-Esfahani, Ali; Fitzgerald, J Edward (2010). "Writing a medical case report". BMJ. 340 b5274. doi:10.1136/sbmj.b5274. S2CID 164945175.
|
||||
Kidd, Michael; Hubbard, Charlotte (2007). "Introducing Journal of Medical Case Reports". Journal of Medical Case Reports. 1 (1): 1. doi:10.1186/1752-1947-1-1. ISSN 1752-1947. PMC 1839763. PMID 17411446.
|
||||
Richardson, Michael L.; Chew, Felix S. (2006). "Radiology Case Reports: a new peer-reviewed, open-access journal specializing in case reports". Radiology Case Reports. 1 (1): 1–3. doi:10.2484/rcr.v1i1.7. ISSN 1930-0433. PMC 4891400. PMID 27298670.
|
||||
"Talanow: A new interactive Radiology journal". Archived from the original on 2008-09-27.
|
||||
|
||||
|
||||
== External links ==
|
||||
Case reports – The CARE guidelines
|
||||
42
data/en.wikipedia.org/wiki/Cause_of_death-0.md
Normal file
42
data/en.wikipedia.org/wiki/Cause_of_death-0.md
Normal file
@ -0,0 +1,42 @@
|
||||
---
|
||||
title: "Cause of death"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Cause_of_death"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:54.150733+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
In law, medicine, and statistics, cause of death is an official determination of the conditions resulting in a human's death, which may be recorded on a death certificate. A cause of death is determined by a medical examiner. In rare cases, an autopsy needs to be performed by a pathologist. The cause of death is a specific disease or injury, in contrast to the manner of death, which is a small number of categories like "natural", "accident", "suicide", and "homicide", each with different legal implications.
|
||||
The standards for cause of death recording and reporting are set by WHO. All death certificates typically include a medical certificate of cause of death collecting information for disease prevention and health policy. The recommended international format for this certificate is established by the World Health Organization (WHO) and applies uniformly across member states. The World Health Organization's ICD-11 Reference Guide provides the authoritative specification for its design and completion. Extensive detail is also available in the format of a manual for medical certification.
|
||||
International Classification of Disease (ICD) codes are used to record manner and cause of death in a systematic way that makes it easy to compile statistics and more feasible to compare events across jurisdictions globally.
|
||||
|
||||
|
||||
== Accuracy concerns ==
|
||||
A study published in Preventing Chronic Disease found that only one-third of New York City resident physicians reported believing that the present system of documentation was accurate. Half reported the inability to record "what they felt to be the correct cause of death", citing reasons such as technical limitation and instruction to "put something else". Nearly four-fifths reported being unaware that determinations of "probable", "presumed", or "undetermined" could be made, and fewer than three percent reported ever updating a death certificate when conflicting lab results or other new information became available, and cardiovascular disease was indicated as "the most frequent diagnosis inaccurately reported".
|
||||
Causes of death are sometimes disputed by relatives or members of the public, particularly when some degree of uncertainty or ambiguity exists in relation to the cause of death. On occasion, such disputes may result from, or sometimes instigate, a conspiracy theory.
|
||||
Public perception of the relative risk of death by various causes is biased by personal experience and by media coverage. The phrase "hierarchy of death" is sometimes used to describe the factors that cause some deaths to get more attention than others.
|
||||
Though some opponents of abortion consider it a cause of death, conventionally medical authorities do not confer personhood on fetuses that are not viable outside the womb, and thus abortions are not reported as deaths in these statistics.
|
||||
|
||||
|
||||
== Aging ==
|
||||
|
||||
Health departments discourage listing "old age" as the cause of death because doing so does not benefit public health or medical research. Aging is not a scientifically recognized cause of death; it is currently considered that there is always a more direct cause (although it may be unknown in certain cases and could be one of a number of aging-associated diseases). As an indirect or non-determinative factor, biological aging is the biggest contributor to deaths worldwide. It is estimated that of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes. In industrialized nations the proportion is much higher, reaching 90%. In recent years, there have been official claims about a possibility of recognizing aging itself as a disease. If this would be so, the situation would change.
|
||||
|
||||
|
||||
== Emotional death ==
|
||||
There are also popular notions that someone can be "scared to death" or die of loneliness or heartbreak. Experiencing fear, extreme stress, or both can cause changes in the body that can, in turn, lead to death. For example, it is possible that overstimulation of the vagus nerve—which decreases heart rate in a mechanism related to the behavior of apparent death (also known as "playing dead" and "playing possum")—is the cause of documented cases of psychogenic death. The flight or fight response to fear or stress has the opposite effect, increasing heart rate through stress hormones, and can cause cardiovascular problems (especially in those with pre-existing conditions). This is the proposed mechanism for the observed increase in the death rate due to cardiac arrest after widely experienced acutely stressful events such as terrorism, military attacks, and natural disasters (even among those who are not in the affected area) and for documented deaths in muggings and other frightening events which caused no traumatic physical harm. The proximal medical cause of death in these cases is likely to be recorded as cardiac failure or vagal inhibition (which also has other potential causes such as blows to certain parts of the body and nerve injuries).
|
||||
One specific condition observed to result from acute stress, takotsubo cardiomyopathy, is nicknamed "broken heart syndrome", but the stress need not be relationship-related and need not be negative.
|
||||
These syndrome couldn't easily be diagnosed because it has less phisical evidence, when there are several volatile organic compounds developed. that can easily cause air polllution or poisenous gas.
|
||||
|
||||
|
||||
== See also ==
|
||||
Death by misadventure
|
||||
List of causes of death by rate
|
||||
List of preventable causes of death
|
||||
Manner of death
|
||||
Proximate and ultimate causation
|
||||
|
||||
|
||||
== References ==
|
||||
59
data/en.wikipedia.org/wiki/Central_venous_pressure-0.md
Normal file
59
data/en.wikipedia.org/wiki/Central_venous_pressure-0.md
Normal file
@ -0,0 +1,59 @@
|
||||
---
|
||||
title: "Central venous pressure"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Central_venous_pressure"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:55.347879+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Central venous pressure (CVP) is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. CVP is often a good approximation of right atrial pressure (RAP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope of the venous return (VR) plotted against right atrial pressure (where central venous pressure (CVP) increases, but right atrial pressure (RAP) stays the same; VR = CVP − RAP).
|
||||
CVP has been, and often still is, used as a surrogate for preload, and changes in CVP in response to infusions of intravenous fluid have been used to predict volume-responsiveness (i.e. whether more fluid will improve cardiac output). However, there is increasing evidence that CVP, whether as an absolute value or in terms of changes in response to fluid, does not correlate with ventricular volume (i.e. preload) or volume-responsiveness, and so should not be used to guide intravenous fluid therapy. Nevertheless, CVP monitoring is a useful tool to guide hemodynamic therapy.
|
||||
The cardiopulmonary baroreflex responds to an increase in CVP by decreasing systemic vascular resistance while increasing heart rate and ventricular contractility in dogs.
|
||||
|
||||
|
||||
== Measurement ==
|
||||
|
||||
Normal CVP in patients can be measured from two points of reference:
|
||||
|
||||
Sternum: 0–14 cm H2O
|
||||
Midaxillary line: 8–15 cm H2O
|
||||
CVP can be measured by connecting the patient's central venous catheter to a special infusion set which is connected to a small diameter water column. If the water column is calibrated properly the height of the column indicates the CVP.
|
||||
In most intensive care units, facilities are available to measure CVP continuously.
|
||||
Normal values vary between 4 and 12 cm H2O.
|
||||
|
||||
|
||||
== Factors affecting CVP ==
|
||||
Factors that increase CVP include:
|
||||
|
||||
Cardiac tamponade
|
||||
Decreased cardiac output
|
||||
Forced exhalation
|
||||
Heart failure
|
||||
Hypervolemia
|
||||
Mechanical ventilation and the application of positive end-expiratory pressure (PEEP)
|
||||
Pleural effusion
|
||||
Pulmonary embolism
|
||||
Pulmonary hypertension
|
||||
Tension pneumothorax
|
||||
Factors that decrease CVP include:
|
||||
|
||||
Deep inhalation
|
||||
Distributive shock
|
||||
Hypovolemia
|
||||
|
||||
|
||||
== See also ==
|
||||
Jugular venous pressure
|
||||
Pulmonary capillary wedge pressure
|
||||
|
||||
|
||||
== References ==
|
||||
|
||||
|
||||
== External links ==
|
||||
Venous function and central venous pressure: a physiologic story - a technical discussion of the more modern understanding of central venous pressure; this may well conflict with the sources below.
|
||||
Central Venous Pressure and Pulmonary Capillary Wedge Monitoring
|
||||
Cardiovascular Physiology
|
||||
Central+Venous+Pressure at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
|
||||
51
data/en.wikipedia.org/wiki/Cerebellar_degeneration-0.md
Normal file
51
data/en.wikipedia.org/wiki/Cerebellar_degeneration-0.md
Normal file
@ -0,0 +1,51 @@
|
||||
---
|
||||
title: "Cerebellar degeneration"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Cerebellar_degeneration"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:56.519839+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Cerebellar degeneration is a condition in which cerebellar cells, otherwise known as neurons, become damaged and progressively weaken in the cerebellum. There are two types of cerebellar degeneration; paraneoplastic cerebellar degeneration, and alcoholic or nutritional cerebellar degeneration. As the cerebellum contributes to the coordination and regulation of motor activities, as well as controlling equilibrium of the human body, any degeneration to this part of the organ can be life-threatening. Cerebellar degeneration can result in disorders in fine movement, posture, and motor learning in humans, due to a disturbance of the vestibular system. This condition may not only cause cerebellar damage on a temporary or permanent basis, but can also affect other tissues of the central nervous system, those including the cerebral cortex, spinal cord and the brainstem (made up of the medulla oblongata, midbrain, and pons).
|
||||
Cerebellar degeneration can be attributed to a plethora of hereditary and non-hereditary conditions. More commonly, cerebellar degeneration can also be classified according to conditions that an individual may acquire during their lifetime, including infectious, metabolic, autoimmune, paraneoplastic, nutritional or toxic triggers.
|
||||
|
||||
== Signs and symptoms ==
|
||||
|
||||
Patients with cerebellar degeneration experience a progressive loss of nerve cells (Purkinje cells) throughout the cerebellum. As well as this, it is common to incur an elevated blood protein level and a high volume of lymph cells within the cerebrospinal fluid, resulting in swelling and enlargement of the brain. The most characteristic signs and symptoms experienced by patients with cerebellar degeneration include:
|
||||
|
||||
muscle weakness
|
||||
an uncoordinated, staggering walk
|
||||
quivering of the torso
|
||||
jerky arm and leg movements
|
||||
tendency to fall over
|
||||
dysarthria (difficulty in articulating speech)
|
||||
dysphagia (difficulty in deglutition/swallowing of solids and liquids)
|
||||
vertigo (dizziness)
|
||||
nystagmus (rapid, involuntary eye movements), causing sleep disturbances
|
||||
ophthalmoplegia (paralysis of extraocular muscles)
|
||||
diplopia (double vision)
|
||||
Scientific studies have revealed that psychiatric symptoms are also common in patients with cerebellar degeneration, where dementia is a typical psychiatric disorder resulting from cerebellar damage. Approximately 50% of all patients experience dementia as a result of paraneoplastic cerebellar degeneration.
|
||||
|
||||
== Causes ==
|
||||
The root cause of incurring a cerebellar degenerative condition can be due to a range of different inherited or acquired (non-genetic and non-inherited) conditions, including neurological diseases, paraneoplastic disorders, nutritional deficiency, and chronic heavy alcohol use.
|
||||
|
||||
=== Neurological diseases ===
|
||||
A neurological disease refers to any ailment of the central nervous system, including abnormalities of the brain, spinal cord and other connecting nerve fibres. Where millions of people are affected by neurological diseases on a worldwide scale, it has been identified that the number of different types of neurological diseases exceeds six hundred, any of which an individual can incur. Some of the most prevalent types include Alzheimer's disease, cerebral palsy, epilepsy, Parkinson's disease and stroke. More specifically, the neurological diseases that can cause cerebellar degeneration include:
|
||||
|
||||
==== Inherited ====
|
||||
Spinocerebellar ataxia (SCA), which refers to a group of conditions caused by mutations in the genes of a human, and are characterised by degenerative changes to many parts of the central nervous system, inclusive of the cerebellum, brain stem, and spinal cord. If a parent is affected by SCA, each of their children will have a 50% risk of inheriting the mutated gene.
|
||||
|
||||
==== Non-inherited ====
|
||||
Multiple sclerosis (MS), a progressive and incurable condition caused by the combination of an individual's genetic influences and environmental circumstances. It occurs when the myelin sheath of the nerve cells becomes damaged. As the myelin sheath is responsible for protecting the nerves and conducting rapid impulses between them, any damage to this lipid-rich layer will result in delayed and interrupted nerve impulses to and from the brain.
|
||||
Transmissible spongiform encephalopathies (TSEs), which refers to a combination of diseases caused by the subsistence of foreign proteins in the blood, called prions. Prions originate in the bloodstream via ingestion of contaminated foods or through contact with contaminated medical instruments, body fluids, or infected tissue. This causes severe inflammation of the brain, impairing one's memory, personality and muscular coordination.
|
||||
Acute & haemorrhagic stroke, resulting in the death of neurons in the cerebellum due to a disrupted flow of oxygen to the brain. This disrupted flow may be due to one of two causes; either a narrowing or blocked artery which derives from a build-up of plaque in the inner walls of the coronary arteries, or a ruptured blood vessel, commonly deriving from high blood pressure or head trauma.
|
||||
|
||||
=== Paraneoplastic disorders ===
|
||||
Paraneoplastic disorders are a combination of non-inherited conditions that are activated by an individual's autoimmune response to a malignant tumour. These disorders prevail when T-cells (also known as white blood cells) begin to harm familiar cells in the central nervous system rather than the cancerous cells, resulting in degeneration of neurons in the cerebellum. Other signs and symptoms that commonly result from the incursion of a paraneoplastic disorder include an impaired ability to talk, walk, sleep, maintain balance and coordinate muscle activity, as well as experiencing seizures and hallucinations. Paraneoplastic disorders are prevalent among middle-aged individuals, typically those with lung, lymphatic, ovarian or breast cancer.
|
||||
|
||||
=== Nutritional deficiency ===
|
||||
Nutritional deficiency relates to an insufficient amount of macronutrients and micronutrients being provided to the body. Nutrient deficiencies are most prevalent among infants, the elderly, the poverty-stricken, and individuals with eating disorders. Alcohol use disorder is the diagnosis of which an individual frequently consumes excessive amounts of alcohol, and thus becomes dependent on the intoxicating substance. Studies show that men of every age group consume more alcohol than women, where the prevalence is higher in some regions of the world than others, such as across Western Europe and Australia. Nutritional deficiency is a non-inherited condition that lead to impaired absorption or utilisation of the vitamin thiamine (B-1) by the body, thus causing temporary or permanent damage to cerebellar cells. Alcoholic degeneration of cerebellar cells is one of the most common triggers of acquired cerebellar ataxia.
|
||||
|
||||
== Diagnosis ==
|
||||
25
data/en.wikipedia.org/wiki/Cerebellar_degeneration-1.md
Normal file
25
data/en.wikipedia.org/wiki/Cerebellar_degeneration-1.md
Normal file
@ -0,0 +1,25 @@
|
||||
---
|
||||
title: "Cerebellar degeneration"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Cerebellar_degeneration"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:56.519839+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
To select an appropriate and accurate diagnostic test for cerebellar degeneration, it is crucial that a range of factors specific to each patient are taken into consideration. These include; the patient's age, acuity of their signs and symptoms, associated neurological conditions, and family history of hereditary forms of cerebellar degeneration. A diagnosis for cerebellar degeneration is regarded after any of the aforementioned signs and symptoms surface. For genetically classified forms of cerebellar degeneration, genetic testing can be carried out in order to confirm or deny the diagnosis, where this form of testing is only possible if the gene responsible for the cause of the condition is recognised. In saying this, for most conditions the genetic cause of cerebellar degeneration is unidentified, hence these patients cannot proceed with genetic testing. In cases where cerebellar degeneration is acquired, a diagnosis can be established using imaging methods such as computerised tomography (CT scans) and magnetic resonance imaging (MRI), necessary to detect brain abnormalities in patients with cerebellar degeneration.
|
||||
|
||||
== Treatment ==
|
||||
Like any other disease, treatment for cerebellar degeneration is contingent on the underlying cause, unique to each patient. As of present time, hereditary forms of cerebellar degeneration are incurable, though they can be managed. Management is centred around coping with symptoms and improving a patient's quality of life. In these cases, immediate management of inherited cerebellum damage should involve consultation with a neurologist, followed by specific management approaches based on the signs and symptoms experienced by each unique patient. These management approaches aim to provide supportive care to the patient, consisting of physical therapy to strengthen muscles, occupational therapy, and speech pathology. Long-term management of inherited cerebellar degeneration involves an ongoing commitment to supportive care therapies, as well as a longitudinal relationship with a neurologist. In some instances adjustments need to be made in the patients home, to improve accessibility and mobility in and around their living environment, to optimise safety. The cerebellum is highly reactive to transcranial direct current stimulation, a technique which may improve ataxia.
|
||||
For non-hereditary types of cerebellar degeneration, some physical and mental indicators can be reversed by treating the fundamental cause. For instance, the signs and symptoms of paraneoplastic cerebellar degeneration can be managed by initially terminating the underlying cancer with treatments such as surgery, radiation therapy and chemotherapy. In cases of nutritional or alcoholic cerebellar degeneration, symptoms of these conditions can be relieved by initially consuming a balanced diet and discontinuing the consumption of alcohol respectively, followed by dietary supplementation with thiamine.
|
||||
|
||||
== Prognosis ==
|
||||
The long-term prospect for patients with cerebellar degeneration differs according to the underlying cause of the disease. Each inherited or acquired disease that results in cerebellar degeneration has its own specific prognosis; however, most are generally poor, progressive and often fatal.
|
||||
|
||||
== Epidemiology ==
|
||||
Cerebellar degeneration continues to carry a considerable burden on the health of the world population, as well as on health agencies and governing bodies across the globe. Cerebellum-related disorders generally transpire in individuals between the ages of 45 and 65 years; however, the age of symptomatic onset differs in accordance with the underlying cause of the degenerative disorder. For paraneoplastic cerebellar degeneration, the average age of onset is 50 years, generally affecting a greater population of males than females. Nutritional and alcoholic cerebellar degeneration, being more prevalent than paraneoplastic cerebellar degeneration, affects individuals with a thiamine deficiency and dipsomaniacs, respectively. Recent epidemiological studies on cerebellar degeneration estimated a global prevalence rate of 26 per 100,000 cases of cerebellar degeneration in children.
|
||||
|
||||
== References ==
|
||||
|
||||
== External links ==
|
||||
220
data/en.wikipedia.org/wiki/Cerebral_perfusion_pressure-0.md
Normal file
220
data/en.wikipedia.org/wiki/Cerebral_perfusion_pressure-0.md
Normal file
@ -0,0 +1,220 @@
|
||||
---
|
||||
title: "Cerebral perfusion pressure"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Cerebral_perfusion_pressure"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:57.755648+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Cerebral perfusion pressure (CPP) is the net pressure gradient causing cerebral blood flow to the brain (brain perfusion). It must be maintained within narrow limits because too little pressure could cause brain tissue to become ischemic (having inadequate blood flow), and too much could raise intracranial pressure (ICP).
|
||||
|
||||
|
||||
== Definitions ==
|
||||
The cranium encloses a fixed-volume space that holds three components: blood, cerebrospinal fluid (CSF), and very soft tissue (the brain). While both the blood and CSF have poor compression capacity, the brain is easily compressible.
|
||||
Every increase of ICP can cause a change in tissue perfusion and an increase in stroke events.
|
||||
|
||||
|
||||
=== From resistance ===
|
||||
CPP can be defined as the pressure gradient causing cerebral blood flow (CBF) such that
|
||||
|
||||
|
||||
|
||||
|
||||
C
|
||||
B
|
||||
F
|
||||
=
|
||||
C
|
||||
P
|
||||
P
|
||||
|
||||
/
|
||||
|
||||
C
|
||||
V
|
||||
R
|
||||
|
||||
|
||||
{\displaystyle CBF=CPP/CVR}
|
||||
|
||||
|
||||
where:
|
||||
|
||||
CVR is cerebrovascular resistance
|
||||
|
||||
|
||||
=== By intracranial pressure ===
|
||||
An alternative definition of CPP is:
|
||||
|
||||
|
||||
|
||||
|
||||
C
|
||||
P
|
||||
P
|
||||
=
|
||||
M
|
||||
A
|
||||
P
|
||||
−
|
||||
I
|
||||
C
|
||||
P
|
||||
|
||||
|
||||
{\displaystyle CPP=MAP-ICP}
|
||||
|
||||
|
||||
where:
|
||||
|
||||
MAP is mean arterial pressure
|
||||
ICP is intracranial pressure
|
||||
JVP is jugular venous pressure
|
||||
This definition may be more appropriate if considering the circulatory system in the brain as a Starling resistor, where an external pressure (in this case, the intracranial pressure) causes decreased blood flow through the vessels. In this sense, more specifically, the cerebral perfusion pressure can be defined as either:
|
||||
|
||||
|
||||
|
||||
|
||||
C
|
||||
P
|
||||
P
|
||||
=
|
||||
M
|
||||
A
|
||||
P
|
||||
−
|
||||
I
|
||||
C
|
||||
P
|
||||
|
||||
|
||||
{\displaystyle CPP=MAP-ICP}
|
||||
|
||||
(if ICP is higher than JVP)
|
||||
or
|
||||
|
||||
|
||||
|
||||
|
||||
C
|
||||
P
|
||||
P
|
||||
=
|
||||
M
|
||||
A
|
||||
P
|
||||
−
|
||||
J
|
||||
V
|
||||
P
|
||||
|
||||
|
||||
{\displaystyle CPP=MAP-JVP}
|
||||
|
||||
(if JVP is higher than ICP).
|
||||
Physiologically, increased intracranial pressure (ICP) causes decreased blood perfusion of brain cells by mainly two mechanisms:
|
||||
|
||||
Increased ICP constitutes an increased interstitial hydrostatic pressure that, in turn, causes a decreased driving force for capillary filtration from intracerebral blood vessels.
|
||||
Increased ICP compresses cerebral arteries, causing increased cerebrovascular resistance (CVR).
|
||||
FLOW
|
||||
Ranging from
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
20
|
||||
|
||||
|
||||
|
||||
mL
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
/
|
||||
|
||||
|
||||
100
|
||||
|
||||
|
||||
|
||||
g
|
||||
|
||||
|
||||
|
||||
⋅
|
||||
|
||||
|
||||
|
||||
min
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle ^{20\,{\textrm {mL}}}/_{100\,{\textrm {g}}{\cdot }{\textrm {min}}}}
|
||||
|
||||
in white matter to
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
70
|
||||
|
||||
|
||||
|
||||
mL
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
/
|
||||
|
||||
|
||||
100
|
||||
|
||||
|
||||
|
||||
g
|
||||
|
||||
|
||||
|
||||
⋅
|
||||
|
||||
|
||||
|
||||
min
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
|
||||
{\displaystyle ^{70\,{\textrm {mL}}}/_{100\,{\textrm {g}}{\cdot }{\textrm {min}}}}
|
||||
|
||||
in grey matter.
|
||||
|
||||
|
||||
== Autoregulation ==
|
||||
Under normal circumstances a MAP between 60 and 160 mmHg and ICP about 10 mmHg (CPP of 50-150 mmHg) sufficient blood flow can be maintained with autoregulation. Although the classic 'autoregulation curve' suggests that CBF is fully stable between these blood pressure values (known also as the limits of autoregulation), in practice spontaneous fluctuations can occur.
|
||||
Outside of the limits of autoregulation, raising MAP raises CBF and raising ICP lowers it (this is one reason that increasing ICP in traumatic brain injury is potentially deadly). In trauma some recommend CPP not go below 70 mmHg. Recommendations in children is at least 60 mmHg.
|
||||
Within the autoregulatory range, as CPP falls there is, within seconds, vasodilation of the cerebral resistance vessels, a fall in cerebrovascular resistance and a rise in cerebral-blood volume (CBV), and therefore CBF will return to baseline value within seconds (see as ref. Aaslid, Lindegaard, Sorteberg, and Nornes 1989: http://stroke.ahajournals.org/cgi/reprint/20/1/45.pdf). These adaptations to rapid changes in blood pressure (in contrast with changes that occur over periods of hours or days) are known as dynamic cerebral autoregulation.
|
||||
|
||||
|
||||
== Footnotes ==
|
||||
|
||||
|
||||
== References ==
|
||||
Sanders, MJ; McKenna, K (2001). "Ch. 22: Head and Facial Trauma". Mosby's Paramedic Textbook (2nd revised ed.). Mosby.
|
||||
Walters, FJM (1998). "Intracranial Pressure and Cerebral Blood Flow". Physiology (8, Article 4). Archived from the original on 2011-05-14. Retrieved 2011-02-10.
|
||||
30
data/en.wikipedia.org/wiki/Cervical_conization-0.md
Normal file
30
data/en.wikipedia.org/wiki/Cervical_conization-0.md
Normal file
@ -0,0 +1,30 @@
|
||||
---
|
||||
title: "Cervical conization"
|
||||
chunk: 1/2
|
||||
source: "https://en.wikipedia.org/wiki/Cervical_conization"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:59.084677+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Cervical conization refers to an excision of a cone-shaped portion of tissue from the mucous membrane of the cervix. Conization is used for diagnostic purposes as part of a biopsy and for therapeutic purposes to remove pre-cancerous cells (cervical intraepithelial neoplasia) or early stage cervical cancer. Ablative treatments are also available to treat abnormal cervical cells. The decision to perform a cervical conization procedure is made with consideration of a patient's pap smear, colposcopy, and HPV test results. The American College of Obstetricians and Gynecologists (ACOG) recommends that decisions regarding excision should be based on the risk of CIN3+. A conization can be performed in the office or the operating room, depending on the type of conization performed. This procedure carries few risks, with the most common one being bleeding after the procedure.
|
||||
|
||||
== History ==
|
||||
Before the introduction of the speculum, cervical cancer was only found once it was advanced. With the invention and use of a speculum, changes in the cervix could be appreciated. First, they were evaluated macroscopically and eventually were also assessed using a microscope. In 1927, H. Hinselmann discovered the transformation zone, where metaplastic squamous epithelium is found between the columnar epithelium of the endocervix and the squamous epithelium of the ectocervix. The transformation zone is clinically significant, as it is where almost all cervical cancers and precancerous lesions arise.
|
||||
All current cervical conization methods can be traced back to amputation of the ectocervix, which was developed by Marion Sims in 1861. Before this, any excisions of cervical carcinomas were mainly a palliative care treatment option. A. Sturmdorf was the first to describe an excision of a cone shape from the ectocervix; however, he utilized this as a treatment for cervicitis. J. E. Ayre was the first to introduce cold knife conization in 1948 and stressed the importance of evaluating the excised tissue in serial sections to assess the extent of invasion. This method of cold knife conization has been utilized, and eventually, options for excisions using electrocautery were developed as well. Initially, excised tissue utilizing electrocautery was not satisfactory for evaluation, but as the loops used have become finer, the quality of the surgical specimens has improved to rival those of cold knife conization. Presently, electrocautery methods are often preferred to cold knife conization due to the greater ease of procedure.
|
||||
|
||||
== Anatomy ==
|
||||
|
||||
The cervix connects the uterine cavity to the vagina. The cervix can be viewed by placing a speculum in the vagina. The part of the cervix that can be directly viewed upon placing a speculum in the vagina is the ectocervix. The beginning of the endocervix is called the cervical os. The endocervix leads from the vagina into the uterine cavity. The area where the columnar epithelium of the endocervix and the squamous epithelium of the ectocervix meet is called the transformation zone or the squamocolumnar junction (SCJ). This is the area of the cervix that is most susceptible to human papillomavirus (HPV) infection and is where the vast majority of cervical precancers and cancers arise. This is the tissue that is sampled during a pap smear as a screening test to find abnormal cells or the presence of an HPV infection.
|
||||
|
||||
== Types ==
|
||||
Types of conization include:
|
||||
|
||||
Cold knife conization (CKC)
|
||||
Loop electrical excision procedure (LEEP)
|
||||
|
||||
== Indications ==
|
||||
Abnormal cervical cells found on pap smear and colposcopy are the basis for the recommendation of a conization procedure. The amount of irregularity will be graded by the pathologist after the colposcopy as CIN1, CIN2, or CIN3. CIN3 represents the most irregularly appearing cells of the possible grading options. Conization may be recommended once the risk of CIN3 is greater than 25%. Conization before a radical hysterectomy is associated with better outcomes for early -stage cervical cancers as well, so it may be recommended even when hysterectomy will be the definitive surgical option. The American Society for Colposcopy and Cervical Pathology has developed a tool to aid in decision -making with abnormal cervical cancer screening and abnormal colposcopy results.
|
||||
|
||||
== Procedure ==
|
||||
23
data/en.wikipedia.org/wiki/Cervical_conization-1.md
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23
data/en.wikipedia.org/wiki/Cervical_conization-1.md
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@ -0,0 +1,23 @@
|
||||
---
|
||||
title: "Cervical conization"
|
||||
chunk: 2/2
|
||||
source: "https://en.wikipedia.org/wiki/Cervical_conization"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:26:59.084677+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
The vagina is prepped using antimicrobial scrub or iodine. Draping is placed to maintain a sterile surgical field. Some physicians may choose to drain the bladder using a catheter. The speculum will be placed, and the cervix visualized. The tissue is then excised from the cervix. The tissue will include the transformation zone and will be shaped like a cone, as the procedure name suggests. The physician will ensure hemostasis has been achieved before removing the speculum and ending the procedure. Typically, the physician will place a suture at the 12 o'clock position of the excised tissue to serve as a reference point during histological examination.
|
||||
The main difference between cold knife conization and LEEP is the instrument used to excise the tissue. In a LEEP, a thin wire loop electrode is used to remove the cone-shaped surgical specimen. During a cold knife cone, a scalpel is used to excise the tissue. Both LEEP and cold knife cone have shown equal effectiveness, so the decision for which procedure is often based on the physician's comfort with each procedure or other clinical considerations. Cold knife cone is performed with a scalpel, and one advantage of this procedure is that the margins of the excised tissue will be free from thermal damage that would be present in the excised tissue from a LEEP. This can allow for more accurate analysis of the margin of the specimen.
|
||||
Contraindications to completing the procedure are cervicitis, pelvic inflammatory disease, or anticoagulation. Pregnancy is a relative contraindication, meaning that decisions of whether to perform the procedure in pregnant patients would be made on an individual basis.
|
||||
After treatment, screenings will continue. HPV screening is recommended 6 months after conization. Regular cervical cancer screening will resume as well, with the schedule of screening being determined by the type of abnormal cells that were present in the cervix. HPV vaccination may also be recommended as a part of the treatment plan to reduce the chances of abnormal cervical cells developing again.
|
||||
|
||||
== Complications ==
|
||||
The most common complication of cervical conization is bleeding during the procedure or within a few weeks after the procedure. Infection after the procedure is possible but very rare. There is the possibility of cervical stenosis or cervical insufficiency. The data regarding the risk of preterm birth and low birth weight in future pregnancies is mixed; however, it is generally accepted that for patients desiring to carry future pregnancies, limiting the amount of cervical tissue that is excised is the best option to limit this risk. However, taking less tissue does produce an increased risk that the margins of the excised specimen will be positive, so the decision on how aggressively the excision is performed must be discussed between the patient and physician.
|
||||
Cervical conization effectively reduces the risk of cancer developing or spreading. The chances of cancer recurrence and premature birth depend on the type of conization. Cold knife conization is associated with 7% chance of the cancer recurring and a 16% chance of premature birth, laser conization comes with 6% cancer recurrence and 13% premature birth, and loop excision comes with a 10% recurrence and 11% premature birth.
|
||||
|
||||
== See also ==
|
||||
Cervicectomy
|
||||
|
||||
== References ==
|
||||
28
data/en.wikipedia.org/wiki/Cervical_dislocation-0.md
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28
data/en.wikipedia.org/wiki/Cervical_dislocation-0.md
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@ -0,0 +1,28 @@
|
||||
---
|
||||
title: "Cervical dislocation"
|
||||
chunk: 1/1
|
||||
source: "https://en.wikipedia.org/wiki/Cervical_dislocation"
|
||||
category: "reference"
|
||||
tags: "science, encyclopedia"
|
||||
date_saved: "2026-05-05T07:27:00.313128+00:00"
|
||||
instance: "kb-cron"
|
||||
---
|
||||
|
||||
Cervical dislocation is a common method of animal euthanasia. It refers to a technique used in physical euthanasia of small animals by applying pressure to the neck and dislocating the spinal column from the skull or brain. The aim is to quickly separate the spinal cord from the brain so as to provide the animal with a fast, painless, and easy death.
|
||||
|
||||
|
||||
== Technique ==
|
||||
Firm pressure is applied at the base of the skull, along with a sharp pinching and twisting of the thumb and forefinger. At the same time, the tail is pulled backward. This severs the spinal cord at the base of the brain or within the cervical spine area (the upper third of the neck). According to the Canadian Council on Animal Care (CCAC), cervical dislocation is normally only conducted on small animals.
|
||||
|
||||
|
||||
== Ethics ==
|
||||
The University of Iowa and some veterinary associations consider the technique to be an ethically acceptable method for killing small rodents such as rats, mice, squirrels, etc.
|
||||
|
||||
|
||||
== See also ==
|
||||
Cervical fracture
|
||||
Blunt trauma
|
||||
Slaughter (livestock)
|
||||
|
||||
|
||||
== References ==
|
||||
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