<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Myoclonus and explain in detail? [/INST] Myoclonus is a brief, involuntary, irregular (lacking rhythm) twitching  of a muscle or a group of muscles, different from clonus, which is rhythmic or regular. Myoclonus describes a medical sign and, generally, is not a diagnosis of a disease. These myoclonic twitches, jerks, or seizures are usually caused by sudden muscle contractions (positive myoclonus) or brief lapses of contraction (negative myoclonus).  The most common circumstance under which they occur is while falling asleep (hypnic jerk).  Myoclonic jerks occur in healthy people and are experienced occasionally by everyone.  However, when they appear with more persistence and become more widespread they can be a sign of various neurological disorders.  Hiccups are a kind of myoclonic jerk specifically affecting the diaphragm.  When a spasm is caused by another person it is known as a provoked spasm.  Shuddering attacks in babies fall in this category.
Myoclonic jerks may occur alone or in sequence, in a pattern or without pattern. They may occur infrequently or many times each minute.  Most often, myoclonus is one of several signs in a wide variety of nervous system disorders such as multiple sclerosis, Parkinsons disease, dystonia, cerebral palsy, Alzheimers disease, Gauchers disease, subacute sclerosing panencephalitis, Creutzfeldt–Jakob disease (CJD), serotonin toxicity, some cases of Huntingtons disease, some forms of epilepsy, and occasionally in intracranial hypotension.
In almost all instances in which myoclonus is caused by central nervous system disease it is preceded by other symptoms; for instance, in CJD it is generally a late-stage clinical feature that appears after the patient has already started to exhibit gross neurological deficits.
Anatomically, myoclonus may originate from lesions of the cortex, subcortex or spinal cord.  The presence of myoclonus above the foramen magnum effectively excludes spinal myoclonus; further localisation relies on further investigation with electromyography (EMG) and electroencephalography (EEG).

Types
The most common types of myoclonus include action, cortical reflex, essential, palatal, those seen in the progressive myoclonus epilepsies, reticular reflex, sleep and stimulus-sensitive.

Epilepsy forms
Cortical reflex myoclonus is thought to be a type of epilepsy that originates in the cerebral cortex – the outer layer, or "gray matter", of the brain, responsible for much of the information processing that takes place in the brain. In this type of myoclonus, jerks usually involve only a few muscles in one part of the body, but jerks involving many muscles may occur. Cortical reflex myoclonus can be intensified when patients attempt to move in a certain way or perceive a particular sensation.
Essential myoclonus occurs in the absence of epilepsy or other apparent abnormalities in the brain or nerves. It can occur randomly in people with no family history, or among members of the same family, indicating that it sometimes may be an inherited disorder. Essential myoclonus tends to be stable without increasing in severity over time. Some scientists speculate that some forms of essential myoclonus may be a type of epilepsy with no known cause.
Juvenile myoclonic epilepsy (JME) usually consists of jerking and muscle twitches of the upper extremities. This may include the arms, shoulders, elbows, and very rarely, the legs. JME is among the most common types of epilepsy and can affect one of every 14 people with the disease. These seizures typically occur shortly after waking up. Onset for JME can be seen around puberty for most patients. Administration of medications that also treat multiple seizure types is usually the most effective form of treatment.
Lennox-Gastaut syndrome  (LGS), or childhood epileptic encephalopathy, is a rare epileptic disorder accounting for 1–4% of childhood epilepsies. The syndrome has much more severe symptoms ranging from multiple seizures daily, learning disabilities, abnormal findings in electroencephalogram (EEG). Earlier age of seizure onset is correlated with higher risk of cognitive impairment.
Progressive myoclonus epilepsy (PME) is a group of diseases characterized by myoclonus, epileptic seizures, tonic-clonic seizures, and other serious symptoms such as trouble walking or speaking. These rare disorders often get worse over time and can be fatal. Studies have identified at least three forms of PME. Lafora disease is inherited as an autosomal recessive disorder, meaning that the disease occurs only when a child inherits two copies of a defective gene, one from each parent. Lafora disease is characterized by myoclonus, epileptic seizures, and dementia (progressive loss of memory and other intellectual functions). A second group of PME diseases belonging to the class of cerebral storage diseases usually involves myoclonus, visual problems, dementia, and dystonia (sustained muscle contractions that cause twisting movements or abnormal postures). Another group of PME disorders in the class of system degenerations often is accompanied by action myoclonus, seizures, and problems with balance and walking. Many of these PME diseases begin in childhood or adolescence. Treatment is not normally successful for any extended period of time.
Reticular reflex myoclonus is thought to be a type of generalized epilepsy that originates in the brainstem, the part of the brain that connects to the spinal cord and controls vital functions such as breathing and heartbeat. Myoclonic jerks usually affect the whole body, with muscles on both sides of the body affected simultaneously. In some people, myoclonic jerks occur in only a part of the body, such as the legs, with all the muscles in that part being involved in each jerk. Reticular reflex myoclonus can be triggered by either a voluntary movement or an external stimulus.

Diaphragmatic flutter
A very rare form includes the diaphragmatic flutter, the Belly Dancers Syndrome,: 2  or Van Leeuwenhoeks disease. It was first described by Antonie van Leeuwenhoek in 1723, who had it.: 2  The condition characterizes spoken communication that sounds like a short-breathed hiccup. These muscle spasms can recur dozens of times per day. Rate of diaphragmatic contraction ranges between 35 and 480 contractions per minute, with the average rate found to be 150.: 3  Studies show that possible causes include disruptions within the central or peripheral nervous systems, anxiety, nutritional disorder, and certain pharmaceuticals. No single treatment has proven effective, though blocking or crushing of the phrenic nerve can provide instantaneous relief when pharmacologic treatment has proven ineffective.: 11 Only about 50 people in the world have been diagnosed with diaphragmatic flutter.

Other forms
Action myoclonus is characterized by muscular jerking triggered or intensified by voluntary movement or even the intention to move. It may be made worse by attempts at precise, coordinated movements. Action myoclonus is the most disabling form of myoclonus and can affect the arms, legs, face, and even the voice. It is often associated with tonic-clonic seizures and diffuse neuronal disease such as post-hypoxic encephalopathy, uremia, and the various forms of PME, although, in the case of focal cerebral damage, the disease may be restricted to one limb. This type of myoclonus often is caused by brain damage that results from a lack of oxygen and blood flow to the brain when breathing or heartbeat is temporarily stopped. Over-excitement of the sensorimotor cortex (cortical reflex myoclonus) or reticular formation (reticular reflex myoclonus) is also a cause of action myoclonus. Serotonin and GABA neurotransmitters are thought to cause this lack of inhibition, which is a possible explanation as to why improvements are made with the administration of serotonin precursors. Systems involved include the cerebellodentatorubral, pyramidal, extrapyramidal, optic, auditory, posterior columns and gracile and cuneate nuclei, spinocerebellar tracts, motor neurons of cranial nerves and anterior horns, and muscle fibers.
Palatal myoclonus is a regular, rhythmic contraction of one or both sides of the rear of the roof of the mouth, called the soft palate. These contractions may be accompanied by myoclonus in other muscles, including those in the face, tongue, throat, and diaphragm. The contractions are very rapid, occurring as often as 150 times a minute, and may persist during sleep. The condition usually appears in adults and can last indefinitely. People with palatal myoclonus usually regard it as a minor problem; some complain of an occasional "clicking" sound, a noise made as the soft palate muscles contract.
Middle ear myoclonus occurs in the muscles of the middle ear. These muscles may include the tensor tympani and stapedius muscles. It can involve the muscles surrounding the Eustachian tube, which include the tensor veli palatini, levator veli palatini, and salpingopharyngeus. Those affected describe it as a thumping sound or sensation in the ear.
Spinal myoclonus is myoclonus originating in the spinal cord, including segmental and propriospinal myoclonus. The latter is usually due to a thoracic generator producing truncal flexion jerk. It is often stimulus-induced with a delay due to the slow conducting propriospinal nerve fibers.
Stimulus-sensitive myoclonus is triggered by a variety of external events, including noise, movement, and light. Surprise may increase the sensitivity of the patient.
Sleep myoclonus occurs during the initial phases of sleep, especially at the moment of dropping off to sleep, and include familiar examples of myoclonus such as the hypnic jerk. Some forms appear to be stimulus-sensitive. Some people with sleep myoclonus are rarely troubled by it, or need treatment. If it is a symptom of more complex and disturbing sleep disorders, such as restless legs syndrome, it may require medical treatment. Myoclonus can be associated with patients with Tourette syndrome.

Signs and symptoms
Myoclonic seizure can be described as "jumps" or "jolts" experienced in a single extremity or even the entire body.  The feeling experienced by the individual is described as uncontrollable jolts common to receiving a mild electric shock. The sudden jerks and twitching of the body can often be so severe that it can cause a small child to fall.
A myoclonic seizure (myo "muscle", clonic "jerk") is a sudden involuntary contraction of muscle groups.  The muscle jerks consist of symmetric, mostly generalized jerks, localized in the arms and in the shoulders and also simultaneously with a head nod; both the arms may fling out together and simultaneously a head nod may occur.  Symptoms have some variability amongst subjects.  Sometimes the entire body may jerk, just like a startle response.  As is the case with all generalised seizures, the patient is not conscious during the event but the seizure is so brief that the person appears to remain fully conscious.
In reflex epilepsies, myoclonic seizures can be brought on by flashing lights or other environmental triggers (see photosensitive epilepsy).
Familiar examples of normal myoclonus include hiccups and hypnic jerks that some people experience while drifting off to sleep.  Severe cases of pathologic myoclonus can distort movement and severely limit a persons ability to sleep, eat, talk, and walk.  Myoclonic jerks commonly occur in individuals with epilepsy.

Cause
Myoclonus in healthy individuals may indicate nothing other than arbitrary muscle contraction. Myoclonus may also develop in response to infection, hyperosmolar hyperglycemic state, head or spinal cord injury, stroke, stress, brain tumors, kidney or liver failure, lipid storage disease, chemical or drug poisoning, as a side effect of certain drugs (such as tramadol, quinolones, benzodiazepine, gabapentin, sertraline, lamotrigine, opioids), or other disorders.
Benign myoclonic movements are commonly seen during the induction of general anesthesia with intravenous medications such as etomidate and propofol. These are postulated to result from decreased inhibitory signaling from cranial neurons.  Prolonged oxygen deprivation to the brain, hypoxia, may result in posthypoxic myoclonus. People with benign fasciculation syndrome can often experience myoclonic jerking of limbs, fingers and thumbs.
Myoclonus can occur by itself, but most often as one of several symptoms associated with a variety of nervous system disorders, including multiple sclerosis, Parkinsons disease, Alzheimers disease, opsoclonus myoclonus, Creutzfeldt–Jakob disease, Lyme disease and lupus. Myoclonic jerks commonly occur in persons with epilepsy, a disorder in which the electrical activity in the brain becomes disordered leading to seizures. It is also found in MERRF (Myoclonic Epilepsy with Ragged Red Fibers), a rare mitochondrial encephalomyopathy.
Jerks of muscle groups, much of the body, or a series in rapid succession, which results in the person jerking bolt upright from a more relaxed sitting position is sometimes seen in ambulatory patients being treated with high doses of morphine, hydromorphone, and similar drugs, and is possibly a sign of high and/or rapidly increasing serum levels of these drugs. Myoclonic jerks caused by other opioids, such as tramadol and pethidine, may be less benign. Medications unrelated to opioids, such as anticholinergics, are known to cause myoclonic jerks.

Pathophysiology
Most myoclonus is caused by a disturbance of the central nervous system. Some are from peripheral nervous system injury. Studies suggest several locations in the brain are involved in myoclonus. One is in the brainstem, close to structures that are responsible for the startle response, an automatic reaction to an unexpected stimulus involving rapid muscle contraction.
The specific mechanisms underlying myoclonus are not yet fully understood. Scientists believe that some types of stimulus-sensitive myoclonus may involve overexcitability of the parts of the brain that control movement. These parts are interconnected in a series of feedback loops called motor pathways. These pathways facilitate and modulate communication between the brain and muscles. Key elements of this communication are chemicals known as neurotransmitters, which carry messages from one nerve cell, or neuron, to another. Neurotransmitters are released by neurons and attach themselves to receptors on parts of neighboring cells. Some neurotransmitters may make the receiving cell more sensitive, while others tend to make the receiving cell less sensitive. Laboratory studies suggest that an imbalance between these chemicals may underlie myoclonus.
Some researchers speculate that abnormalities or deficiencies in the receptors for certain neurotransmitters may contribute to some forms of myoclonus. Receptors that appear to be related to myoclonus include those for two important inhibitory neurotransmitters: serotonin, which constricts blood vessels and brings on sleep, and gamma-aminobutyric acid (GABA), which helps the brain maintain muscle control. Other receptors with links to myoclonus include those for benzodiazepines, drugs that induce sleep, and for glycine, an inhibitory neurotransmitter that is important for the control of motor and sensory functions in the spinal cord. More research is needed to determine how these receptor abnormalities cause or contribute to myoclonus.

Treatment
Concerning more serious conditions, the complex origins of myoclonus may be treated with multiple drugs, which have a limited effect individually, but greater when combined with others that act on different brain pathways or mechanisms. Treatment is most effective when the underlying cause is known, and can be treated as such. Some drugs being studied in different combinations include clonazepam, sodium valproate, piracetam, and primidone. Hormonal therapy may improve responses to antimyoclonic drugs in some people.
Some studies have shown that doses of 5-hydroxytryptophan (5-HTP) leads to improvement in patients with some types of action myoclonus and PME. These differences in the effect of 5-HTP on patients with myoclonus have not yet been explained.
Many of the drugs used for myoclonus, such as barbiturates, phenytoin and primidone, are also used to treat epilepsy. Barbiturates slow down the central nervous system and cause tranquilizing or antiseizure effects. Phenytoin and primidone are effective antiepileptics drugs, although phenytoin can cause liver failure or have other harmful long-term effects in patients with PME. Sodium valproate is an alternative therapy for myoclonus and can be used either alone or in combination with clonazepam. Some people have adverse reactions to clonazepam and/or sodium valproate.
When patients are taking multiple medications, the discontinuation of drugs suspected of causing myoclonus and treatment of metabolic derangements may resolve some cases of myoclonus. When pharmacological treatment is indicated anticonvulsants are the main line of treatment. Paradoxical reactions to treatment are notable. Drugs which most people respond to may in other individuals worsen their symptoms. Sometimes this leads to the mistake of increasing the dose, rather than decreasing or stopping the drug. Treatment of myoclonus focuses on medications that may help reduce symptoms. Drugs used include sodium valproate, clonazepam, the anticonvulsant levetiracetam, and piracetam. Dosages of clonazepam usually are increased gradually until the patient improves or side effects become harmful. Drowsiness and loss of coordination are common side effects. The beneficial effects of clonazepam may diminish over time if the patient develops a tolerance to the drug.
In forms of myoclonus where only a single area is affected, and even in a few other various forms, Botox injections (OnabotulinumtoxinA) may be helpful. The chemical messenger responsible for triggering the involuntary muscle contractions is blocked by the Botulinum toxins of the Botox.Surgery is also a viable option for treatment if the symptoms are caused by a tumor or lesion in the brain or spinal cord. Surgery may also correct symptoms in those where myoclonus affects parts of the face or ear. While DBS is still being studied for use with myoclonus, Deep Brain Stimulation has also been tried in those with this and other movement disorders.

Prognosis
The effects of myoclonus in an individual can vary depending on the form and the overall health of the individual. In severe cases, particularly those indicating an underlying disorder in the brain or nerves, movement can be extremely distorted and limit ability to normally function, such as in eating, talking, and walking </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Warfarin resistance and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pulmonary edema and explain in detail? [/INST] Pulmonary edema, also known as pulmonary congestion, is excessive liquid accumulation in the tissue and air spaces (usually alveoli) of the lungs. It leads to impaired gas exchange and may cause hypoxemia and respiratory failure. It is due to either failure of the left ventricle of the heart to remove oxygenated blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung tissue directly or blood vessels of the lung (non-cardiogenic pulmonary edema).Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly preventing further damage and assuring full recovery to the lung. Pulmonary edema, especially when sudden (acute), can lead to respiratory failure or cardiac arrest due to hypoxia. It is a cardinal feature of congestive heart failure. The term edema is from the Greek οἴδημα (oidēma, "swelling"), from οἰδέω (oidéō, "(I) swell").

Types
Classically it is cardiogenic (left ventricular) but fluid may also accumulate due to damage to the lung. This damage may be from direct external injuries or injuries mediated by high pressures within the pulmonary circulation. When directly or indirectly caused by increased left ventricular pressure, pulmonary edema may form when mean pulmonary pressure rises from the normal average of 15 mmHg to above 25 mmHg, where pulmonary fluid may form. Broadly, the causes of pulmonary edema can be divided into cardiogenic and non-cardiogenic. By convention, cardiogenic specifically refers to left ventricular causes.

Cardiogenic
Congestive heart failure which is due to the hearts inability to pump the blood out of the pulmonary circulation at a sufficient rate resulting in elevation in pulmonary wedge pressure and edema – this usually is due to left ventricular failure, but may also be from arrhythmias, or fluid overload, (e.g. from kidney failure or intravenous therapy).
Hypertensive crisis can cause pulmonary edema as the elevation in blood pressure and increased afterload on the left ventricle hinders forward flow in blood vessels and causes the elevation in wedge pressure and subsequent pulmonary edema.

Non-cardiogenic
Negative pressure pulmonary edema in which a significant negative (internal) pressure in the chest (such as from an inhalation against an upper airway obstruction) ruptures capillaries and floods the alveoli with blood. Negative pressure pulmonary edema has an incidence in the range of 0.05-0.1% in cases of general anesthesia. The negative pressure causes a significant increase in preload, thereby increasing pulmonary blood volume.  There is also a significant increase in left ventricular afterload, which causes a decreased cardiac output.  The increase in pulmonary blood volume and pressure along with a decrease in cardiac output to the lungs will increase the pulmonary transudative pressures and the risk of pulmonary edema. With all this occurring, pulmonary vascular resistance increases causing a shift of the intraventricular septum.  The ventricular septal shift to the left causes a left ventricular diastolic dysfunction, which further increases pulmonary hydrostatic pressures and the risk.
Neurogenic causes  (seizures, head trauma, strangulation, electrocution).
Pulmonary embolismAcute lung injury may also cause pulmonary edema directly through injury to the vasculature and parenchyma of the lung. It includes acute lung injury and acute respiratory distress syndrome. (ALI-ARDS) cover many of these causes, but they may also include:

Inhalation of hot or toxic gases
Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents)
Aspiration, e.g., gastric fluid
Reexpansion, i.e. post large volume thoracocentesis, resolution of pneumothorax, post decortication, removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema.
Reperfusion injury, i.e., postpulmonary thromboendartectomy or lung transplantation
Swimming induced pulmonary edema also known as immersion pulmonary edema
Transfusion Associated Circulatory Overload occurs when multiple blood transfusions or blood-products (plasma, platelets, etc.) are transfused over a short period of time.
Transfusion associated Acute Lung Injury is a specific type of blood-product transfusion injury that occurs when the donors plasma contained antibodies against the recipient, such as anti-HLA or anti-neutrophil antibodies.
Severe infection or inflammation which may be local or systemic. This is the classical form of acute lung injury-adult respiratory distress syndrome.Some causes of pulmonary edema are less well characterised and arguably represent specific instances of the broader classifications above.

Arteriovenous malformation
Hantavirus pulmonary syndrome
High altitude pulmonary edema (HAPE)
Envenomation, such as with the venom of Atrax robustus

Signs and symptoms
The most common symptom of pulmonary edema is difficulty breathing (dyspnea), but may include other symptoms such as coughing up blood (classically seen as pink or red, frothy sputum), excessive sweating, anxiety, and pale skin. Shortness of breath can manifest as orthopnea (inability to breath sufficiently when lying down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic and cardiogenic pulmonary edema due to left ventricular failure. The development of pulmonary edema may be associated with symptoms and signs of "fluid overload" in the lungs; this is a non-specific term to describe the manifestations of right ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon due to fluid), raised jugular venous pressure and hepatomegaly, where the liver is excessively enlarged and may be tender or even pulsatile. Other signs include end-inspiratory crackles (crackling sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound.

Flash pulmonary edema
Flash pulmonary edema (FPE), is rapid onset acute pulmonary edema. It is most often precipitated by acute myocardial infarction or mitral regurgitation, but can be also caused by aortic regurgitation, heart failure, or almost any cause leading to elevated left ventricular filling pressures. Treatment of FPE should be directed at the underlying cause, but the mainstays are nitroglycerin, ensuring adequate oxygenation with non-invasive ventilation, and decrease of pulmonary circulation pressures while FPE stays.Recurrence of FPE is thought to be associated with hypertension and may signify renal artery stenosis. Prevention of recurrence is based on managing or preventing hypertension, coronary artery disease, renovascular hypertension, and heart failure.

Diagnosis
There is no single test for confirming that breathlessness is caused by pulmonary edema – there are many causes of shortness of breath; but there are methods to suggest a high probability of an edema.
Low oxygen saturation in blood and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. A chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (biased blood flow to the superior parts instead of inferior parts of the lung), and possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edemaLung ultrasounds, employed by a healthcare provider at the point of care, is also a useful tool to diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water, track changes over time, and differentiate between cardiogenic and non-cardiogenic edema.Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous pressures and high pulmonary artery pressures leading to pulmonary edema.
Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT) are also typically requested as further diagnosis. B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Fecal impaction and explain in detail? [/INST] A fecal impaction is a solid, immobile bulk of feces that can develop in the rectum as a result of chronic constipation.
A related term is fecal loading which refers to a large volume of stool in the rectum of any consistency. Fecal impaction is a common result of neurogenic bowel dysfunction and causes immense discomfort and pain. Treatment of fecal impaction includes laxatives, enema, and pulsed irrigation evacuation (PIE).

Signs and symptoms
Symptoms include chronic constipation. There can be fecal incontinence and paradoxical overflow diarrhea (encopresis) as liquid stool passes around the obstruction. Complications may include necrosis and ulcers of the rectal tissue. Abdominal pain and bloating could also be present depending on the severity of the condition. Loss of appetite can also occur.

Causes
There are many possible causes; for example, physical inactivity, not eating enough fiber, dehydration, and holding in bowel movements.
Medications such as opioid pain relievers (fentanyl, buprenorphine, methadone, codeine, oxycodone, hydrocodone, morphine, hydromorphone, etc.) and certain sedatives that reduce intestinal movement may cause fecal matter to become too large, hard and/or dry to expel.
Specific conditions, such as irritable bowel syndrome, certain neurological disorders, paralytic ileus, gastroparesis, diabetes, dehydration, enlarged prostate gland, distended colon, ingested foreign object, inflammatory bowel diseases such as Crohns disease and colitis,  and autoimmune diseases such as amyloidosis, celiac disease, lupus, and scleroderma can cause constipation. Hypothyroidism can cause chronic constipation because of sluggish, slower, or weaker colon contractions. Iron supplements or increased blood calcium levels are also potential causes. Spinal cord injury is a common cause of constipation, due to ileus.
Manual removal of a fecal impaction is often required with obese patients in traction, after a barium enema, and in poorly hydrated older adults.

Prevention
Reducing opiate-based medication (when possible, tolerable, and safe; prescription medication changes should be done under the supervision of a physician), and adequate intake of liquids (water) and dietary fiber and daily exercise.

Treatment
The treatment of fecal impaction requires both the remedy of the impaction and treatment to prevent recurrences. Decreased motility of the colon results in dry, hard stools that in the case of fecal impaction become compacted into a large, hard mass of stool that cannot be expelled from the rectum.
Various methods of treatment attempt to remove the impaction by softening the stool, lubricating the stool, or breaking it into pieces small enough for removal. Enemas and osmotic laxatives can be used to soften the stool by increasing the water content until it is soft enough to be expelled. Osmotic laxatives such as magnesium citrate work within minutes - eight hours for onset of action, and even then they may not be sufficient to expel the stool.
Osmotic laxatives can cause cramping and even severe pain as the patients attempts to evacuate the contents of the rectum are blocked by the fecal mass. Polyethylene glycol (PEG 3350) may be used to increase the water content of the stool without cramping. This may take 24 to 48 hours for it to take effect, and it is not well suited to cases where the impaction needs to be removed immediately due to risk of complications or severe pain. Enemas (such as hyperosmotic saline) and suppositories (such as glycerine suppositories) work by increasing water content and stimulating peristalsis to aid in expulsion, and both work much more quickly than oral laxatives.
Because enemas work in 2–15 minutes, they do not allow sufficient time for a large fecal mass to soften. Even if the enema is successful at dislodging the impacted stool, the impacted stool may remain too large to be expelled through the anal canal. Mineral oil enemas can assist by lubricating the stool for easier passage. In cases where enemas fail to remove the impaction, polyethylene glycol can be used to attempt to soften the mass over 24–48 hours, or if immediate removal of the mass is needed, manual disimpaction may be used. Manual disimpaction may be performed by lubricating the anus and using one gloved finger with a scoop-like motion to break up the fecal mass. Most often manual disimpaction is performed without general anaesthesia, although sedation may be used. In more involved procedures, general anaesthesia may be used, although the use of general anaesthesia increases the risk of damage to the anal sphincter. If all other treatments fail, surgery may be necessary.
An easier, more comfortable, and more efficient method to enema and manual disimpaction is to use pulsed irrigation evacuation (PIE). This method implemented with PIE MED allows for patients to rest in bed as the procedure takes place. By using pulsating water to enter into the colon to soften and break down the dense mass, PIE effectively treats fecal impaction. Research studies have shown that by the success of the PIE MED treatment prevented patient hospitalization for fecal impaction.Individuals who have had one fecal impaction are at high risk of future impactions. Therefore, preventive treatment should be instituted in patients following the removal of the mass. Increasing dietary fiber, increasing fluid intake, exercising daily, and attempting regularly to defecate every morning after eating should be promoted in all patients.Often underlying medical conditions cause fecal impactions; these conditions should be treated to reduce the risk of future impactions. Many types of medications (most notably opioid pain medications, such as codeine) reduce motility of the colon, increasing the likelihood of fecal impactions. If possible, alternate medications should be prescribed that avoid the side effect of constipation.Given that all opioids can cause constipation, it is recommended that any patient placed on opioid pain medications be given medications to prevent constipation before it occurs. Daily medications can also be used to promote normal motility of the colon and soften stools. Daily use of laxatives or enemas should be avoided by most individuals as it can cause the loss of normal colon motility. However, for patients with chronic complications, daily medication under the direction of a physician may be needed.
Polyethylene glycol 3350 can be taken daily to soften the stools without the significant risk of adverse effects that are common with other laxatives. In particular, stimulant laxatives should not be used frequently because they can cause dependence in which an individual loses normal colon function and is unable to defecate without taking a laxative. Frequent use of osmotic laxatives should be avoided as well as they can cause electrolyte imbalances.
Research shows that pulsed irrigation evacuation with the PIE MED device is successful in all tested patients in studies, making pulsed irrigation evacuation the most effective and reliable form of fecal impaction treatment.

Fecaloma
A fecaloma is a more extreme form of fecal impaction, giving the accumulation an appearance of a tumor.A fecaloma can develop as the fecal matter gradually stagnates and accumulates in the intestine and increases in volume until the intestine becomes deformed. It may occur in chronic obstruction of stool transit, as in megacolon and chronic constipation. Some diseases, such as Chagas disease, Hirschsprungs disease and others damage the autonomic nervous system in the colons mucosa (Auerbachs plexus) and may cause extremely large or "giant" fecalomas, which must be surgically removed (disimpaction). Rarely, a fecalith will form around a hairball (Trichobezoar), or other hygroscopic or desiccant nucleus.
It can be diagnosed by:

CT scan
Projectional radiography
UltrasoundDistal or sigmoid, fecalomas can often be disimpacted digitally or by a catheter which carries a flow of disimpaction fluid (water or other solvent or lubricant). Surgical intervention in the form of sigmoid colectomy or proctocolectomy and ileostomy may be required only when all conservative measures of evacuation fail. Attempts at removal can have severe and even lethal effects, such as the rupture of the colon wall by catheter or an acute angle of the fecaloma (stercoral perforation), followed by sepsis. It may also lead to stercoral perforation, a condition characterized by bowel perforation due to pressure necrosis from a fecal mass or fecaloma.

See also
Aerosol impaction
Colon
Dental impaction
Impaction (animals)

References
Further reading
Wrenn K (September 1989). "Fecal impaction". The New England Journal of Medicine. 321 (10): 658–62. doi:10.1056/NEJM198909073211007 </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sterility and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Porphyria cutanea tarda and explain in detail? [/INST] Porphyria cutanea tarda is the most common subtype of porphyria. The disease is named because it is a porphyria that often presents with skin manifestations later in life. The disorder results from low levels of the enzyme responsible for the fifth step in heme production. Heme is a vital molecule for all of the bodys organs. It is a component of hemoglobin, the molecule that carries oxygen in the blood.
Hepatoerythropoietic porphyria has been described as a homozygous form of porphyria cutanea tarda, although it can also be caused if two different mutations occur at the same locus.

Symptoms and signs
Porphyria cutanea tarda (PCT) is recognized as the most prevalent subtype of porphyritic diseases.PCT is characterized by onycholysis and blistering of the skin in areas that receive higher levels of exposure to sunlight.  The primary cause is a deficiency of uroporphyrinogen decarboxylase (UROD), a cytosolic enzyme that is a step in the enzymatic pathway that leads to the synthesis of heme. Behind the direct cause there are a number of genetic and environmental risk factors.Patients who are diagnosed with PCT typically seek treatment following the development of photosensitivities causing blisters and erosions on exposed areas of the skin. This is usually observed in the face, hands, forearms, and lower legs. Healing is slow and leaves scarring. Though blisters are the most common skin manifestations of PCT, other skin manifestations include hyperpigmentation (similar to a tan) and hypertrichosis (mainly on the cheeks) also occur. PCT is a chronic condition, with external symptoms often subsiding and recurring as a result of multiple factors.  In addition to the skin lesions, chronic liver disease is very common in patients with sporadic PCT.  This involves hepatic fibrosis (scarring of the liver), and inflammation. However, liver problems are less common in patients with the inherited form of the disease. Additionally, patients will often void a wine-red color urine with an increased concentration of uroporphyrin I due to their enzymatic deficiency.

Vitamin, mineral, and enzyme deficiencies
Certain vitamin and minerals deficiencies are common in people with porphyria cutanea tarda.  The most common deficiencies are beta-Carotene, retinol, vitamin A and vitamin C.  Beta-Carotene is required to synthesize vitamin A and vitamin A is needed to synthesize retinol.  A lack of retinol-binding protein is due to a lack of retinol which is required to trigger its production.Porphyrins interact with iron, absorbing photons to create reactive oxygen species is the mechanism of action causing the itchy, painful blisters of PCT.  The reactive oxygen species consume the skin antioxidants beta-carotene, vitamin E, and vitamin C.  Supplementation of these three vitamins reduces the oxidation and potentially diminishes the severity of blister formation.  No single one of the three vitamins can inhibit the damaging effects of oxidized porphyrins, specifically uroporphyrins and coproporphyrins, but all three working together synergistically are capable of neutralizing their damaging effects.

Genetics
Inherited mutations in the UROD gene cause about 20% of cases (the other 80% of cases do not have mutations in UROD, and are classified as sporadic). UROD makes an enzyme called uroporphyrinogen III decarboxylase, which is critical to the chemical process that leads to heme production. The activity of this enzyme is usually reduced by 50% in all tissues in people with the inherited form of the condition.Nongenetic factors such as excess iron or partially genetic factors such as alcohol use disorder and others listed above can increase the demand for heme and the enzymes required to make heme. The combination of this increased demand and reduced activity of uroporphyrinogen decarboxylase disrupts heme production and allows byproducts of the process to accumulate in the body, triggering the signs and symptoms of porphyria cutanea tarda.The HFE gene makes a protein that helps cells regulate the absorption of iron from the digestive tract and into the cells of the body. Certain mutations in the HFE gene cause hemochromatosis (an iron overload disorder). People who have these mutations are also at an increased risk of developing porphyria cutanea tarda.In the 20% of cases where porphyria cutanea tarda is inherited, it is inherited in an autosomal dominant pattern, which means one copy of the altered gene is sufficient to decrease enzyme activity and cause the signs and symptoms of the disorder.

Other
While inherited deficiencies in uroporphyrinogen decarboxylase often lead to the development of PCT, there are a number of risk factors that can both cause and exacerbate the symptoms of this disease. One of the most common risk factors observed is infection with the Hepatitis C virus.  One review of a collection of PCT studies noted Hepatitis C infection in 50% of documented cases of PCT. Additional risk factors include alcohol use disorder, excess iron (from iron supplements as well as cooking on cast iron skillets), and exposure to chlorinated cyclic hydrocarbons and Agent Orange.It can be a paraneoplastic phenomenon.

Exacerbating factors
Alcohol
Estrogen
Iron
Hepatitis C virus

Pathogenesis
Porphyria cutanea tarda is primarily caused by uroporphyrinogen decarboxylase deficiency (UROD).  Uroporphyrinogen decarboxylase occurs in nature as a homodimer of two subunits.  It participates in the fifth step in heme synthesis pathway, and is active in the cytosol.  This enzymatic conversion results in coproporphyrinogen III as the primary product.  This is accomplished by the clockwise removal of the four carboxyl groups present in the cyclic uroporphyrinogen III molecule. Therefore, a deficiency in this enzyme causes the aforementioned buildup of uroporphyrinogen and hepta-carboxylic porphyrinogen, and to a lesser extent hexa-carboxylic porphyrinogen, and penta-carboxylic porphyrinogen in the urine, which can be helpful in the diagnosis of this disorder.The dermatological symptoms of PCT that include blistering and lesions on sun-exposed areas of the skin are caused by a buildup of porphyrin compounds (specifically uroporphyrinogen) close to the surface of the skin that have been oxidized by free radicals or sunlight. The oxidized porphyrins initiate degranulation of dermal mast cells, which release proteases that catabolize the surrounding proteins.  This begins a cell-mediated positive feedback loop which matches the description of a type 4 delayed hypersensitivity reaction.  The resulting blisters, therefore, do not appear immediately but begin to show up 2–3 days after sun exposure.  Due to the highly conjugated structure of porphyrins involving alternating single and double carbon bonds, these compounds exhibit a deep purple color, resulting in the discoloration observed in the skin. Excess alcohol intake decreases hepcidin production which leads to increased iron absorption from the gut and an increase in oxidative stress. This oxidative stress then leads to inhibition of uroporphyrinogen decarboxylase, creating an excess of uroporphyrinogen III which is oxidized from the relatively harmless porphyrinogens into their oxidized porphyrins form.  Concentrated instances of oxidative stress (alcohol, physical trauma, psychological stress, etc.) cause the liver to hemorrhage these porphyrins into the blood stream where they are then susceptible to oxidation.The strong association of PCT with Hepatitis C virus infection is not entirely understood. Studies have suggested that the cytopathic effect of the virus on hepatocytes can lead to the release of free iron.  This iron can disrupt the activity of cytochrome p450, releasing activated oxygen species.  These can oxidize the UROD substrate uroporphyrinogen, which can result in the inhibition of UROD and lead to deficient activity of this key enzyme.Excess alcohol use is frequently associated with both inducing PCT and aggravating a preexisting diagnosis of the disorder.  It is thought to do so by causing oxidative damage to liver cells, resulting in oxidized species of uroporphyrinogen that inhibit the activity of hepatic UROD.  It is also felt to increase the uptake of iron in liver cells, leading to further oxidation of uroporphyrinogen by the release of activated oxygen species. Additionally, exposure to chlorinated cyclic hydrocarbons can lead to a deficiency in the activity of uroporphyrinogen decarboxylase, causing the buildup of excess uroporphyrinogen. Additionally, alcohol has been shown to increase the activity of the delta-aminolevulinic acid synthetase (ALA synthetase), the rate-limiting enzymatic step in heme synthesis in the mitochondria, in rats. Therefore, alcohol consumption may increase the production of uroporphyrinogen, exacerbating symptoms in individuals with porphyria cutanea tarda.

Diagnosis
While the most common symptom of PCT is the appearance of skin lesions and blistering, their appearance is not conclusive. Laboratory testing commonly reveals high levels of uroporphyrinogen in the urine, clinically referred to as uroporphyrinogenuria.  Additionally, testing for common risk factors such as hepatitis C and hemochromatosis is strongly suggested, as their high prevalence in patients with PCT may require additional treatment.  If clinical appearance of PCT is present, but laboratories are negative, the diagnosis of pseudoporphyria should be seriously considered.

Classification
Some sources divide PCT into two types: sporadic and familial. Other sources include a third type, but this is less common.

One study used 74% as the cutoff for UROD activity, with those patients under that number being classified as type II, and those above classified as type III if there was a family history, and type I if there was not.Genetic variants associated with hemochromatosis have been observed in PCT patients, which may help explain inherited PCT not associated with UROD.

Treatment
Since PCT is a chronic condition, a comprehensive management of the disease is the most effective means of treatment.  Primarily, it is key that patients diagnosed with PCT avoid alcohol consumption, iron supplements, excess exposure to sunlight (especially in the summer), as well as estrogen and chlorinated cyclic hydrocarbons, all of which can potentially exacerbate the disorder.  Additionally, the management of excess iron (due to the commonality of hemochromatosis in PCT patients) can be achieved through phlebotomy, whereby blood is systematically drained from the patient. A borderline iron deficiency has been found to have a protective effect by limiting heme synthesis.  In the absence of iron, which is to be incorporated in the porphyrin formed in the last step of the synthesis, the mRNA of erythroid 5-aminolevulinate synthase (ALAS-2) is blocked by attachment of an iron-responsive element (IRE) binding cytosolic protein, and transcription of this key enzyme is inhibited.Low doses of antimalarials can be used. Orally ingested chloroquine is completely absorbed in the gut and is preferentially concentrated in the liver, spleen, and kidneys. They work by removing excess porphyrins from the liver via increasing the excretion rate by forming a coordination complex with the iron center of the porphyrin as well as an intramolecular hydrogen bond between a propionate side chain of the porphyrin and the protonated quinuclidine nitrogen atom of either alkaloid. Due to the presence of the chlorine atom, the entire complex is more water-soluble allowing the kidneys to preferentially remove it from the blood stream and expel it through urination. Chloroquine treatment can induce porphyria attacks within the first couple of months of treatment due to the mass mobilization of porphyrins from the liver into the blood stream. Complete remission can be seen within 6–12 months as each dose of antimalarial can only remove a finite amount of porphyrins and there are generally decades of accumulation to be cleared </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pyoderma and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Dopamine dysregulation syndrome and explain in detail? [/INST] Dopamine dysregulation syndrome (DDS) is a dysfunction of the reward system observed in some individuals taking dopaminergic medications for an extended length of time. It typically occurs in people with Parkinsons disease (PD) who have taken dopamine agonist medications for an extended period of time. It is characterized by self-control problems such as addiction to medication, gambling, or sexual behavior.

Signs and symptoms
The most common symptom is craving for dopaminergic medication. However other behavioral symptoms can appear independently of craving or co-occur with it. Craving is an intense impulse of the subject to obtain medication even in the absence of symptoms that indicate its intake. To fulfill this need the person will self-administer extra doses. When self-administration is not possible, aggressive outbursts or the use of strategies such as symptom simulation or bribery to access additional medication can also appear.Hypomania, manifesting with feelings of euphoria, omnipotence, or grandiosity, are prone to appear in those moments when medication effects are maximum;  dysphoria, characterized by sadness, psychomotor slowing, fatigue or apathy are typical with dopamine replacement therapy (DRT) withdrawal. Different impulse control disorders have been described including gambling, compulsive shopping, eating disorders and hypersexuality. Behavioral disturbances, most commonly aggressive tendencies, are the norm. Psychosis is also common.

Causes
Parkinsons disease is a common neurological disorder characterized by a degeneration of dopamine neurons in the substantia nigra and a loss of dopamine in the putamen. It is described as a motor disease, but it also produces cognitive and behavioral symptoms. The most common treatment is dopamine replacement therapy, which consists in the administration of levodopa (L-Dopa) or dopamine agonists (such as pramipexole or ropinirole) to patients. Dopamine replacement therapy is well known to improve motor symptoms but its effects in cognitive and behavioral symptoms are more complex. Dopamine has been related to the normal learning of stimuli with behavioral and motivational significance, attention, and most importantly the reward system. In accordance with the role of dopamine in reward processing, addictive drugs stimulate dopamine release. Although the exact mechanism has yet to be elucidated, the role of dopamine in the reward system and addiction has been proposed as the origin of DDS. Models of addiction have been used to explain how dopamine replacement therapy produces DDS. One of these models of addiction proposes that over the usage course of a drug there is a habituation to the rewarding effects that it produces at the initial stages. This habituation is thought to be dopamine mediated. With long-term administration of L-dopa the reward system gets used to it and needs higher quantities. As the user increases drug intake there is a loss of dopaminergic receptors in the striatum which acts in addition to an impairment in goal-direction mental functions to produce an enhancement of sensitization to dopamine therapy. The behavioral and mood symptoms of the syndrome are produced by the dopamine overdose.

Diagnosis
Diagnosis of the syndrome is clinical since there are no laboratory tests to confirm it. For diagnosis a person with documented responsiveness to medication has to increase medication intake beyond dosage needed to relieve their parkinsonian symptoms in a pathological addiction-like pattern. A current mood disorder (depression, anxiety, hypomanic state or euphoria), behavioral disorder (excessive gambling, shopping or sexual tendency, aggression, or social isolation) or an altered perception about the effect of medication also have to be present. A questionnaire on the typical symptoms of DDS has also been developed and can help in the diagnosis process.

Prevention
The main prevention measure proposed is the prescription of the lowest possible dose of dopamine replacement therapy to individuals at risk. The minimization of the use of dopamine agonists, and of short duration formulations of L-Dopa can also decrease risk of the syndrome.

Management
First choice management measure consists in the enforcement of a dopaminergic drug dosage reduction. If this decrease is maintained, dysregulation syndrome features soon decrease. Cessation of dopamine agonists therapy may also be of use </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Skin condition and explain in detail? [/INST] A skin condition, also known as cutaneous condition, is any medical condition that affects the integumentary system—the organ system that encloses the body and includes skin, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment.Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying causes and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), cause (skin conditions resulting from physical factors), and so on.Clinically, the diagnosis of any particular skin condition begins by gathering pertinent information of the presenting skin lesion(s), including: location (arms, head, legs); symptoms (pruritus, pain); duration (acute or chronic); arrangement (solitary, generalized, annular, linear); morphology (macules, papules, vesicles); and color (red). Some diagnoses may also require a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data. The introduction of cutaneous ultrasound has allowed the detection of cutaneous tumors, inflammatory processes, and skin diseases.

Layer of skin involved
The skin weighs an average of 4 kg (8.8 lb), covers an area of 2 m2 (22 sq ft), and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are glabrous skin, the nonhairy skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type,  hairs in structures called pilosebaceous units have a hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands are from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

Epidermis
The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers via diffusion from the dermis, since the epidermis is without direct blood supply.  The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95% of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

Dermis
The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis interdigitates with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance also called extra fibrillar matrix. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

Subcutaneous tissue
The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Diseases of the skin
Diseases of the skin include skin infections and skin neoplasms (including skin cancer).

History
In 1572, Geronimo Mercuriali of Forlì, Italy, completed De morbis cutaneis (On the diseases of the skin). It is considered the first scientific work dedicated to dermatology.

Diagnoses
The physical examination of the skin and its appendages, as well as the mucous membranes, forms the cornerstone of an accurate diagnosis of cutaneous conditions. Most of these conditions present with cutaneous surface changes termed "lesions," which have more or less distinct characteristics. Often proper examination will lead the physician to obtain appropriate historical information and/or laboratory tests that are able to confirm the diagnosis. Upon examination, the important clinical observations are the (1) morphology, (2) configuration, and (3) distribution of the lesion(s). With regard to morphology, the initial lesion that characterizes a condition is known as the "primary lesion", and identification of such a lesions is the most important aspect of the cutaneous examination. Over time, these primary lesions may continue to develop or be modified by regression or trauma, producing "secondary lesions". However, with that being stated, the lack of standardization of basic dermatologic terminology has been one of the principal barriers to successful communication among physicians in describing cutaneous findings. Nevertheless, there are some commonly accepted terms used to describe the macroscopic morphology, configuration, and distribution of skin lesions, which are listed below.

Lesions
Primary lesions
Macule: A macule is a change in surface color, without elevation or depression, so nonpalpable, well or ill-defined, variously sized, but generally considered less than either 5 or 10 mm in diameter at the widest point.
Patch: A patch is a large macule equal to or greater than either 5 or 10 mm across, depending on ones definition of a macule. Patches may have some subtle surface change, such as a fine scale or wrinkling, but although the consistency of the surface is changed, the lesion itself is not palpable.
Papule: A papule is a circumscribed, solid elevation of skin, varying in size from less than either 5 or 10 mm in diameter at the widest point.
Plaque: A plaque has been described as a broad papule, or confluence of papules equal to or greater than 10 mm, or alternatively as an elevated, plateau-like lesion that is greater in its diameter than in its depth.
Nodule: A nodule is morphologically similar to a papule in that it is also a palpable spherical lesion less than 10 mm in diameter </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Cognitive deficit and explain in detail? [/INST] Cognitive deficit is an inclusive term to describe any characteristic that acts as a barrier to the cognition process.The term may describe

deficits in overall intelligence (as with intellectual disabilities),
specific and restricted deficits in cognitive abilities (such as in learning disorders like dyslexia),
neuropsychological deficits (such as in attention, working memory or executive function),
or it may describe drug-induced impairment in cognition and memory (such as that seen with alcohol, glucocorticoids, and the benzodiazepines.)

Cause
It usually refers to a durable characteristic, as opposed to altered level of consciousness, which may be acute and reversible. Cognitive deficits may be inborn or caused by environmental factors such as brain injuries, neurological disorders, or mental illness.

Screening
Screening for cognitive impairment in those over the age of 65 without symptoms is of unclear benefit versus harm as of 2020. In a large population-based cohort study included 579,710 66-year-old adults who were followed for a total of 3,870,293 person-years (average 6.68 ± 1.33 years per person), subjective cognitive decline was significantly associated with an increased risk of subsequent dementia.

Treatment
Older people with cognitive impairment appear to improve somewhat with light therapy.

Other findings
Although one would expect cognitive decline to have major effects on job performance, it seems that there is little to no correlation of health with job performance.  With the exception of cognitive-dependent jobs such as air-traffic controller, professional athlete, or other elite jobs, age does not seem to impact ones job performance. This obviously conflicts with cognitive tests given, so the matter has been researched further.
One possible reason for this conclusion is the rare need for a person to perform at their maximum. There is a difference between typical functioning, that is – the normal level of functioning for daily life, and maximal functioning, that is – what cognitive tests observe as our maximum level of functioning. As the maximum cognitive ability that we are able to achieve decreases, it may not actually affect our daily lives, which only require the normal level.Some studies have indicated that childhood hunger might have a protective effect on cognitive decline. One possible explanation is that the onset of age-related changes in the body can be delayed by calorie restriction. Another possible explanation is the selective survival effect, as the study participants who had a childhood with hunger tend to be the healthiest of their era.

See also
PASS Theory of Intelligence
Fluid and crystallized intelligence

References
Further reading
Das, J.P.; Naglieri, J.A.; Kirby, J.R. (1994). Assessment of Cognitive Processes. Needham Heights, MA: Allyn & Bacon. ISBN 0-205-14164-1.
Das, J.P. (2002). A better look at intelligence. Current Directions in Psychology, 11, 28–32.
Goldstein, Gerald; Beers, Susan, eds (2004). Comprehensive Handbook of Psychological Assessment: Volume I: Intellectual and Neurological Assessment. Hoboken, NJ: John Wiley & Sons.
Kaufman, Alan S. (2000). "Chapter 20: Tests of Intelligence".  In Sternberg, Robert J. (ed.). Handbook of Intelligence. Cambridge: Cambridge University Press. pp. 445–476. ISBN 978-0-521-59648-0.
Naglieri, Jack A.; Otero, Tulio M. (2012). "Chapter 15: The Cognitive Assessment System: From Theory to Practice".  In Flanagan, Dawn P.; Harrison, Patti L. (eds.). Contemporary Intellectual Assessment: Theories, tests, and issues (Third ed.). New York: Guilford Press. pp. 376–399. ISBN 978-1-60918-995-2. ERIC ED530599.
Sattler, Jerome M. (2008). Assessment of Children: Cognitive Foundations. La Mesa (CA): Jerome M. Sattler, Publisher.
Urbina, Susana (2004) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Blood type and explain in detail? [/INST] A blood type (also known as a blood group) is  a classification of blood, based on the presence and absence of antibodies and inherited antigenic substances on the surface of red blood cells (RBCs). These antigens may be proteins, carbohydrates, glycoproteins, or glycolipids, depending on the blood group system. Some of these antigens are also present on the surface of other types of cells of various tissues. Several of these red blood cell surface antigens can stem from one allele (or an alternative version of a gene) and collectively form a blood group system.Blood types are inherited and represent contributions from both parents of an individual. As of 2021, a total of 43 human blood group systems are recognized by the International Society of Blood Transfusion (ISBT). The two most important blood group systems are ABO and Rh; they determine someones blood type (A, B, AB, and O, with + or − denoting RhD status) for suitability in blood transfusion.

Blood group systems
A complete blood type would describe each of the 43 blood groups, and an individuals blood type is one of many possible combinations of blood-group antigens. Almost always, an individual has the same blood group for life, but very rarely an individuals blood type changes through addition or suppression of an antigen in infection, malignancy, or autoimmune disease. Another more common cause of blood type change is a bone marrow transplant. Bone-marrow transplants are performed for many leukemias and lymphomas, among other diseases. If a person receives bone marrow from someone of a different ABO type (e.g., a type A patient receives a type O bone marrow), the patients blood type should eventually become the donors type, as the patients hematopoietic stem cells (HSCs) are destroyed, either by ablation of the bone marrow or by the donors T-cells. Once all the patients original red blood cells have died, they will have been fully replaced by new cells derived from the donor HSCs. Provided the donor had a different ABO type, the new cells surface antigens will be different from those on the surface of the patients original red blood cells.Some blood types are associated with inheritance of other diseases; for example, the Kell antigen is sometimes associated with McLeod syndrome. Certain blood types may affect susceptibility to infections, an example being the resistance to specific malaria species seen in individuals lacking the Duffy antigen. The Duffy antigen, presumably as a result of natural selection, is less common in population groups from areas having a high incidence of malaria.

ABO blood group system
The ABO blood group system involves two antigens and two antibodies found in human blood. The two antigens are antigen A and antigen B. The two antibodies are antibody A and antibody B. The antigens are present on the red blood cells and the antibodies in the serum. Regarding the antigen property of the blood all human beings can be classified into four groups, those with antigen A (group A), those with antigen B (group B), those with both antigen A and B (group AB) and those with neither antigen (group O). The antibodies present together with the antigens are found as follows:
Antigen A with antibody B
Antigen B with antibody A
Antigen AB with neither antibody A nor B
Antigen null (group O) with both antibody A and BThere is an agglutination reaction between similar antigen and antibody (for example, antigen A agglutinates the antibody A and antigen B agglutinates the antibody B). Thus, transfusion can be considered safe as long as the serum of the recipient does not contain antibodies for the blood cell antigens of the donor.The ABO system is the most important blood-group system in human-blood transfusion. The associated anti-A and anti-B antibodies are usually immunoglobulin M, abbreviated IgM, antibodies. It has been hypothesized that ABO IgM antibodies are produced in the first years of life by sensitization to environmental substances such as food, bacteria, and viruses, although blood group compatibility rules are applied to newborn and infants as a matter of practice. The original terminology used by Karl Landsteiner in 1901 for the classification was A/B/C; in later publications "C" became "O". Type O is often called 0 (zero, or null) in other languages.

Rh blood group system
The Rh system (Rh meaning Rhesus) is the second most significant blood-group system in human-blood transfusion with currently 50 antigens. The most significant Rh antigen is the D antigen, because it is the most likely to provoke an immune system response of the five main Rh antigens. It is common for D-negative individuals not to have any anti-D IgG or IgM antibodies, because anti-D antibodies are not usually produced by sensitization against environmental substances. However, D-negative individuals can produce IgG anti-D antibodies following a sensitizing event: possibly a fetomaternal transfusion of blood from a fetus in pregnancy or occasionally a blood transfusion with D positive RBCs. Rh disease can develop in these cases. Rh negative blood types are much less common in Asian populations (0.3%) than they are in European populations (15%).The presence or absence of the Rh(D) antigen is signified by the + or − sign, so that, for example, the A− group is ABO type A and does not have the Rh (D) antigen.

ABO and Rh distribution by country
As with many other genetic traits, the distribution of ABO and Rh blood groups varies significantly between populations.

Other blood group systems
As of 2021, 41 blood-group systems have been identified by the International Society for Blood Transfusion in addition to the ABO and Rh systems. Thus, in addition to the ABO antigens and Rh antigens, many other antigens are expressed on the RBC surface membrane. For example, an individual can be AB, D positive, and at the same time M and N positive (MNS system), K positive (Kell system), Lea or Leb negative (Lewis system), and so on, being positive or negative for each blood group system antigen. Many of the blood group systems were named after the patients in whom the corresponding antibodies were initially encountered. Blood group systems other than ABO and Rh pose a potential, yet relatively low, risk of complications upon mixing of blood from different people.Following is a comparison of clinically relevant characteristics of antibodies against the main human blood group systems:

Clinical significance
Blood transfusion
Transfusion medicine is a specialized branch of hematology that is concerned with the study of blood groups, along with the work of a blood bank to provide a transfusion service for blood and other blood products. Across the world, blood products must be prescribed by a medical doctor (licensed physician or surgeon) in a similar way as medicines.

Much of the routine work of a blood bank involves testing blood from both donors and recipients to ensure that every individual recipient is given blood that is compatible and is as safe as possible. If a unit of incompatible blood is transfused between a donor and recipient, a severe acute hemolytic reaction with hemolysis (RBC destruction), kidney failure and shock is likely to occur, and death is a possibility. Antibodies can be highly active and can attack RBCs and bind components of the complement system to cause massive hemolysis of the transfused blood.Patients should ideally receive their own blood or type-specific blood products to minimize the chance of a transfusion reaction. It is also possible to use the patients own blood for transfusion. This is called autologous blood transfusion, which is always compatible with the patient. The procedure of washing a patients own red blood cells goes as follows: The patients lost blood is collected and washed with a saline solution. The washing procedure yields concentrated washed red blood cells. The last step is reinfusing the packed red blood cells into the patient. There are multiple ways to wash red blood cells. The two main ways are centrifugation and filtration methods. This procedure can be performed with microfiltration devices like the Hemoclear filter. Risks can be further reduced by cross-matching blood, but this may be skipped when blood is required for an emergency. Cross-matching involves mixing a sample of the recipients serum with a sample of the donors red blood cells and checking if the mixture agglutinates, or forms clumps. If agglutination is not obvious by direct vision, blood bank technologist usually check for agglutination with a microscope. If agglutination occurs, that particular donors blood cannot be transfused to that particular recipient.  In a blood bank it is vital that all blood specimens are correctly identified, so labelling has been standardized using a barcode system known as ISBT 128.
The blood group may be included on identification tags or on tattoos worn by military personnel, in case they should need an emergency blood transfusion. Frontline German Waffen-SS had blood group tattoos during World War II.
Rare blood types can cause supply problems for blood banks and hospitals. For example, Duffy-negative blood occurs much more frequently in people of African origin, and the rarity of this blood type in the rest of the population can result in a shortage of Duffy-negative blood for these patients.  Similarly, for RhD negative people there is a risk associated with travelling to parts of the world where supplies of RhD negative blood are rare, particularly East Asia, where blood services may endeavor to encourage Westerners to donate blood.

Hemolytic disease of the newborn (HDN)
A pregnant woman may carry a fetus with a blood type which is different from her own. Typically, this is an issue if a Rh- mother has a child with a Rh+ father, and the fetus ends up being Rh+ like the father. In those cases, the mother can make IgG blood group antibodies. This can happen if some of the fetus blood cells pass into the mothers blood circulation (e.g. a small fetomaternal hemorrhage at the time of childbirth or obstetric intervention), or sometimes after a therapeutic blood transfusion.  This can cause Rh disease or other forms of hemolytic disease of the newborn (HDN) in the current pregnancy and/or subsequent pregnancies.  Sometimes this is lethal for the fetus; in these cases it is called hydrops fetalis. If a pregnant woman is known to have anti-D antibodies, the Rh blood type of a fetus can be tested by analysis of fetal DNA in maternal plasma to assess the risk to the fetus of Rh disease. One of the major advances of twentieth century medicine was to prevent this disease by stopping the formation of Anti-D antibodies by D negative mothers with an injectable medication called Rho(D) immune globulin. Antibodies associated with some blood groups can cause severe HDN, others can only cause mild HDN and others are not known to cause HDN.

Blood products
To provide maximum benefit from each blood donation and to extend shelf-life, blood banks fractionate some whole blood into several products. The most common of these products are packed RBCs, plasma, platelets, cryoprecipitate, and fresh frozen plasma (FFP).  FFP is quick-frozen to retain the labile clotting factors V and VIII, which are usually administered to patients who have a potentially fatal clotting problem caused by a condition such as advanced liver disease, overdose of anticoagulant, or disseminated intravascular coagulation (DIC).Units of packed red cells are made by removing as much of the plasma as possible from whole blood units.
Clotting factors synthesized by modern recombinant methods are now in routine clinical use for hemophilia, as the risks of infection transmission that occur with pooled blood products are avoided.

Red blood cell compatibility
Blood group AB  individuals have both A and B antigens on the surface of their RBCs, and their blood plasma does not contain any antibodies against either A or B antigen. Therefore, an individual with type AB blood can receive blood from any group (with AB being preferable), but cannot donate blood to any group other than AB.  They are known as universal recipients.
Blood group A  individuals have the A antigen on the surface of their RBCs, and blood serum containing IgM antibodies against the B antigen. Therefore, a group A individual can receive blood only from individuals of groups A or O (with A being preferable), and can donate blood to individuals with type A or AB.
Blood group B  individuals have the B antigen on the surface of their RBCs, and blood serum containing IgM antibodies against the A antigen. Therefore, a group B individual can receive blood only from individuals of groups B or O (with B being preferable), and can donate blood to individuals with type B or AB.
Blood group O (or blood group zero in some countries) individuals do not have either A or B antigens on the surface of their RBCs, and their blood serum contains IgM anti-A and anti-B antibodies. Therefore, a group O individual can receive blood only from a group O individual, but can donate blood to individuals of any ABO blood group (i.e., A, B, O or AB). If a patient needs an urgent blood transfusion, and if the time taken to process the recipients blood would cause a detrimental delay, O negative blood can be issued. Because it is compatible with anyone, O negative blood is often overused and consequently is always in short supply. According to the American Association of Blood Banks and the British Chief Medical Officers National Blood Transfusion Committee, the use of group O RhD negative red cells should be restricted to persons with O negative blood, women who might be pregnant, and emergency cases in which blood-group testing is genuinely impracticable.

Table note
1. Assumes absence of atypical antibodies that would cause an incompatibility between donor and recipient blood, as is usual for blood selected by cross matching.

An Rh D-negative patient who does not have any anti-D antibodies (never being previously sensitized to D-positive RBCs) can receive a transfusion of D-positive blood once, but this would cause sensitization to the D antigen, and a female patient would become at risk for hemolytic disease of the newborn.  If a D-negative patient has developed anti-D antibodies, a subsequent exposure to D-positive blood would lead to a potentially dangerous transfusion reaction. Rh D-positive blood should never be given to D-negative women of child-bearing age or to patients with D antibodies, so blood banks must conserve Rh-negative blood for these patients. In extreme circumstances, such as for a major bleed when stocks of D-negative blood units are very low at the blood bank, D-positive blood might be given to D-negative females above child-bearing age or to Rh-negative males, providing that they did not have anti-D antibodies, to conserve D-negative blood stock in the blood bank. The converse is not true; Rh D-positive patients do not react to D negative blood.
This same matching is done for other antigens of the Rh system as C, c, E and e and for other blood group systems with a known risk for immunization such as the Kell system in particular for females of child-bearing age or patients with known need for many transfusions.

Plasma compatibility
Blood plasma compatibility is the inverse of red blood cell compatibility. Type AB plasma carries neither anti-A nor anti-B antibodies and can be transfused to individuals of any blood group; but type AB patients can only receive type AB plasma. Type O carries both antibodies, so individuals of blood group O can receive plasma from any blood group, but type O plasma can be used only by type O recipients.

Table note
1. Assuming absence of strong atypical antibodies in donor plasma

Rh D antibodies are uncommon, so generally neither D negative nor D positive blood contain anti-D antibodies.  If a potential donor is found to have anti-D antibodies or any strong atypical blood group antibody by antibody screening in the blood bank, they would not be accepted as a donor (or in some blood banks the blood would be drawn but the product would need to be appropriately labeled); therefore, donor blood plasma issued by a blood bank can be selected to be free of D antibodies and free of other atypical antibodies, and such donor plasma issued from a blood bank would be suitable for a recipient who may be D positive or D negative, as long as blood plasma and the recipient are ABO compatible.

Universal donors and universal recipients
In transfusions of packed red blood cells, individuals with type O Rh D negative blood are often called universal donors. Those with type AB Rh D positive blood are called universal recipients. However, these terms are only generally true with respect to possible reactions of the recipients anti-A and anti-B antibodies to transfused red blood cells, and also possible sensitization to Rh D antigens. One exception is individuals with hh antigen system (also known as the Bombay phenotype) who can only receive blood safely from other hh donors, because they form antibodies against the H antigen present on all red blood cells.Blood donors with exceptionally strong anti-A, anti-B or any atypical blood group antibody may be excluded from blood donation. In general, while the plasma fraction of a blood transfusion may carry donor antibodies not found in the recipient, a significant reaction is unlikely because of dilution.
Additionally, red blood cell surface antigens other than A, B and Rh D, might cause adverse reactions and sensitization, if they can bind to the corresponding antibodies to generate an immune response.  Transfusions are further complicated because platelets and white blood cells (WBCs) have their own systems of surface antigens, and sensitization to platelet or WBC antigens can occur as a result of transfusion.
For transfusions of plasma, this situation is reversed.  Type O plasma, containing both anti-A and anti-B antibodies, can only be given to O recipients.  The antibodies will attack the antigens on any other blood type.  Conversely, AB plasma can be given to patients of any ABO blood group, because it does not contain any anti-A or anti-B antibodies.

Blood typing
Typically, blood type tests are performed through addition of a blood sample to a solution containing antibodies corresponding to each antigen. The presence of an antigen on the surface of the blood cells is indicated by agglutination. In these tests, rather than agglutination, a positive result is indicated by decolorization as red blood cells which bind to the nanoparticles are pulled toward a magnet and removed from solution.

Blood group genotyping
In addition to the current practice of serologic testing of blood types, the progress in molecular diagnostics allows the increasing use of blood group genotyping. In contrast to serologic tests reporting a direct blood type phenotype, genotyping allows the prediction of a phenotype based on the knowledge of the molecular basis of the currently known antigens. This allows a more detailed determination of the blood type and therefore a better match for transfusion, which can be crucial in particular for patients with needs for many transfusions to prevent allo-immunization.

History
Blood types were first discovered by an Austrian physician, Karl Landsteiner, working at the Pathological-Anatomical Institute of the University of Vienna (now Medical University of Vienna). In 1900, he found that blood sera from different persons would clump together (agglutinate) when mixed in test tubes, and not only that, some human blood also agglutinated with animal blood. He wrote a two-sentence footnote:

The serum of healthy human beings not only agglutinates animal red cells, but also often those of human origin, from other individuals. It remains to be seen whether this appearance is related to inborn differences between individuals or it is the result of some damage of bacterial kind.
This was the first evidence that blood variation exists in humans. The next year, in 1901, he made a definitive observation that blood serum of an individual would agglutinate with only those of certain individuals. Based on this he classified human bloods into three groups, namely group A, group B, and group C. He defined that group A blood agglutinates with group B, but never with its own type. Similarly, group B blood agglutinates with group A. Group C blood is different in that it agglutinates with both A and B. This was the discovery of blood groups for which Landsteiner was awarded the Nobel Prize in Physiology or Medicine in 1930. (C was later renamed to O after the German Ohne, meaning without, or zero, or null.) Another group (later named AB) was discovered a year later by Landsteiners students Adriano Sturli and Alfred von Decastello without designating the name (simply referring it to as "no particular type"). Thus, after Landsteiner, three blood types were initially recognised, namely A, B, and C.Czech serologist Jan Janský was the first to recognise and designate four blood types in 1907 that he published in a local journal, using the Roman numerical I, II, III, and IV (corresponding to modern O, A, B, and AB respectively). Unknown to Janský, an American physician William L. Moss introduced almost identical classification in 1910; but his I and IV corresponding Janskýs IV and I. Moss came across Janskýs paper as his was being printed, mentioned it in a footnote. Thus the existence of two systems immediately created confusion and potential danger in medical practice. Mosss system was adopted in Britain, France, and the US, while Janskýs was preferred in most other European countries and some parts of the US. It was reported that "The practically universal use of the Moss classification at that time was completely and purposely cast aside. Therefore in place of bringing order out of chaos, chaos was increased in the larger cities." To resolve the confusion, the American Association of Immunologists, the Society of American Bacteriologists, and the Association of Pathologists and Bacteriologists made a joint recommendation in 1921 that the Jansky classification be adopted based on priority. But it was not followed particularly where Mosss system had been used.In 1927, Landsteiner, who had moved to the Rockefeller Institute for Medical Research in New York, and as a member of a committee of the National Research Council concerned with blood grouping suggested to substitute Janskýs and Mosss systems with the letters O, A, B, and AB. There was another confusion on the use of O which was introduced by Polish physicians Ludwik Hirszfeld and German physician Emil von Dungern in 1910. It was never clear whether it was meant for the figure 0, German null for zero or the upper case letter O for ohne, meaning without; Landsteiner chose the latter.
In 1928 the Permanent Commission on Biological Standardization adopted Landsteiners proposal and stated:The Commission learns with satisfaction that, on the initiative of the Health Organization of the League of Nations, the nomenclature proposed by von Dungern and Hirszfeld for the classification of blood groups has been generally accepted, and recommends that this nomenclature shall be adopted for international use as follows: 0 A B AB. To facilitate the change from the nomenclature hitherto employed the following is suggested:
Jansky ....0(I) A(II) B(III) AB(IV)
Moss ... O(IV) A(II) B(III) AB(I)This classification became widely accepted and after the early 1950s it was universally followed.Hirszfeld and Dungern discovered the inheritance of blood types as Mendelian genetics in 1910 and the existence of sub-types of A in 1911. In 1927, Landsteiner, with Philip Levine, discovered the MN blood group system, and the P system. Development of the Coombs test in 1945, the advent of transfusion medicine, and the understanding of ABO hemolytic disease of the newborn led to discovery of more blood groups. As of 2020, the International Society of Blood Transfusion (ISBT) recognizes 41 blood groups.

Society and culture
A popular pseudoscientific belief in Eastern Asian countries (especially in Japan and South Korea) known as 血液型 ketsuekigata / hyeoraekhyeong is that a persons ABO blood type is predictive of their personality, character, and compatibility with others. Researchers have established no scientific basis exists for blood type personality categorization, and studies have found no "significant relationship between personality and blood type, rendering the theory "obsolete" and concluding that no basis exists to assume that personality is anything more than randomly associated with blood type."

See also
Blood type (non-human)
Human leukocyte antigen
hh blood group

References
Further reading
Dean, Laura (2005). Blood Groups and Red Cell Antigens, a guide to the differences in our blood types that complicate blood transfusions and pregnancy. Bethesda MD: National Center for Biotechnology Information. ISBN 1-932811-05-2. NBK2261.
Mollison PL, Engelfriet CP, Contreras M (1997). Blood Transfusion in Clinical Medicine (10th ed.). Oxford UK: Blackwell Science. ISBN 0-86542-881-6.

External links

BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH has details of genes and proteins, and variations thereof, that are responsible for blood types
Online Mendelian Inheritance in Man (OMIM): ABO Glycosyltransferase; ABO - 110300
Online Mendelian Inheritance in Man (OMIM): Rhesus Blood Group, D Antigen; RHD - 111680
"Blood group test". Gentest.ch GmbH. Archived from the original on 2017-03-24. Retrieved 2017-03-23.
"Blood Facts – Rare Traits". LifeShare Blood Centers. Archived from the original on September 26, 2006 </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Vaginal lubrication and explain in detail? [/INST] Vaginal lubrication is a naturally produced fluid that lubricates a
vagina. Vaginal lubrication is always present, but production increases significantly near ovulation and during sexual arousal in anticipation of sexual intercourse. Vaginal dryness is the condition in which this lubrication is insufficient, and sometimes artificial lubricants are used to augment it. Without sufficient lubrication, sexual intercourse can be painful. The vaginal lining has no glands, and therefore the vagina must rely on other methods of lubrication. Plasma from vaginal walls due to vascular engorgement is considered to be the chief lubrication source, and the Bartholins glands, located slightly below and to the left and right of the introitus (vaginal opening), also secrete mucus to augment vaginal-wall secretions. Near ovulation, cervical mucus provides additional lubrication.

Vaginal discharge
Composition
The lubricating fluid can vary in consistency, texture, taste, color, and odor, depending on sexual arousal, the phase of the menstrual cycle, the presence of an infection, certain drugs, genetic factors, and diet.Vaginal fluid is slightly acidic and can become more acidic with certain sexually transmitted diseases. The normal pH of vaginal fluid is between 3.8 and 4.5, contrasting with male semen which is typically between 7.2 and 7.8 (neutral pH is 7.0).During arousal, vaginal lubrication, also sometimes called "arousal fluid", is produced. This is clear, thin, and slippery. It typically only lasts up to an hour. Colloquially, this is referred to as "getting wet".

Production
The human vagina is serviced by nerves that respond to vasoactive intestinal polypeptide (VIP). As a result, VIP induces an increase in vaginal blood flow accompanied by an increase in vaginal lubrication. The findings suggest that VIP may participate in the control of the local physiological changes observed during sexual arousal: genital vasodilation and increase in vaginal lubrication.

Vaginal dryness
Insufficient lubrication or vaginal dryness can cause dyspareunia, which is a type of sexual pain disorder. While vaginal dryness is considered an indicator for sexual arousal disorder, vaginal dryness may also result from insufficient excitement and stimulation or from hormonal changes caused by menopause (potentially causing atrophic vaginitis), pregnancy, or breast-feeding </s>