<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 Léri–Weill dyschondrosteosis 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 Hydrometra 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 Astasia-abasia 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 Postoperative nausea and vomiting and explain in detail? [/INST] Postoperative nausea and vomiting (PONV) is the phenomenon of nausea, vomiting, or retching experienced by a patient in the postanesthesia care unit (PACU) or within 24 hours following a surgical procedure. PONV affects about 10% of the population undergoing general anaesthesia each year. PONV can be unpleasant and lead to a delay in mobilization and food, fluid, and medication intake following surgery.

Cause
Emetogenic drugs commonly used in anaesthesia include nitrous oxide, physostigmine, and opioids. The intravenous anaesthetic propofol is currently the least emetogenic general anaesthetic. These medications are thought to stimulate the chemoreceptor trigger zone. This area is on the floor of the fourth ventricle and is effectively outside of the blood-brain barrier, which makes it incredibly sensitive to toxin and pharmacological stimulation. Several neurotransmitters are known, such as histamine, dopamine, serotonin, acetylcholine, and the more recently discovered neurokinin-1 (substance P).

Risk factors
A 2008 study compared 121 Japanese patients who experienced PONV after being given the general anesthetic propofol to 790 people who were free of postoperative nausea after receiving it. Those with a G at both copies of rs1800497 were 1.6 times more likely to experience PONV within six hours of surgery compared to those with the AG or AA genotypes, but they were not significantly more likely to experience PONV more than six hours after surgery.PONV results from patient, surgical, and anesthetic factors.Surgical factors that confer increased risk for PONV include procedures of increased length and gynecological, abdominal, laparoscopic  and ENT procedures, and strabismus procedures in children.
Anesthetic risk factors include the use of volatile anesthetics, nitrous oxide (N2O), opioids, and longer duration of anesthesia.
Patient factors that confer increased risk for PONV include female gender, obesity, age less than 16 years, past history of motion sickness or chemotherapy-induced nausea, high levels of preoperative anxiety, and patients with history of PONV.
Smokers and the elderly often have a decreased risk for PONV.
A risk-stratification method created by Apfel et al has been developed to determine a patients risk for PONV. The presence of 0, 1, 2, 3, or 4 of any of the following risk factors corresponds to a PONV respective risk of 10, 20, 40, 60, and 80%.- Female gender
- Non-smoking
- History of PONV or motion sickness
- Expectant use of postoperative opioid medications

Prevention
Treatment options to prevent PONV include medications such as antiemetics (for example, ondansetron or dexamethasone) or other drugs including tropisetron, dolasetron, cyclizine, and granisetron. Droperidol may cause QT prolongation and is not frequently used. Other approaches to reduce PONV include decision on the types of anaesthetic used during surgery and intravenous (IV) dextrose solutions. Increasing the IV fluids during surgery by giving additional fluid while the person is under general anaesthesia may reduce the risk of nausea/vomiting after surgery. For minor surgical procedures, more research is needed to determine the risks and benefits of this approach.

Management
Because  currently no single antiemetic available is especially effective on its own, experts recommend a multimodal approach. Anesthetic strategies to prevent vomiting include using regional anesthesia whenever possible and avoiding medications that cause vomiting. Medications to treat and prevent PONV are limited by both cost and the adverse effects. People with risk factors likely warrant preventive medication, whereas a "wait and see" strategy is appropriate for those without risk factors.

Preoperative fasting
Fasting guidelines often restrict the intake of any oral fluid 2-6 hours preoperatively, but in a large retrospective analysis in Torbay Hospital, unrestricted clear oral fluids until transfer to theatre could significantly reduce the incidence of postoperative nausea and vomiting without an increased risk in the adverse outcomes for which such conservative guidance exists.

Medications
A multimodal approach to treating a patient with PONV can be efficacious. Numerous patient factors and medication adverse effects must be taken into consideration when selecting a treatment regimen.

Serotonin (5-HT3) receptor antagonists can be administered as a single dose at the end of surgery. Adverse effects include prolongation of the QT interval on electrocardiogram (EKG). Medications include ondansetron, granisetron, and dolasetron.
Anticholinergics can be used as a long-acting patch placed behind the patients ear. Adverse effects include dry mouth and blurry vision. Care must be taken when handling the patch, as transfer of medication to the eye can induce pupillary dilation. Avoid use in elderly patients. Medications include scopolamine.
Glucocorticoids have direct antiemetic effects and can reduce need for postoperative opioids. Adverse effects include a transient increase in serum glucose level, and poor wound healing (controversial).  Medications include dexamethasone.
Butyrophenones are typically administered as a single injection at the end of surgery. Adverse effects include prolongation of the QT interval on EKG.  Medications include droperidol and haloperidol.
Phenothiazines are particularly effective in treating opioid-induced PONV. Adverse effects are dose-dependent and include sedation and extrapyramidal symptoms.  Medications include promethazine and prochlorperazine.
Neurokinin 1 (NK1) receptor antagonists prevent an emetic signal from being transmitted.  Medications include aprepitant and rolapitant.
Histamine receptor antagonists can be administered by multiple routes, including orally, intramuscularly, or rectally. Adverse effects include dry mouth, sedation, and urinary retention.  Medications include dimenhydrinate and diphenhydramine.
Propofol, an anesthetic medication, confers its own antiemetic properties.The 2020 Cochrane Anaesthesia Review Group review of Drugs for preventing postoperative nausea and vomiting in adults
after general anaesthesia: a network meta-analysis (Review)  demonstrated that combination therapy is more effective than single anti-emetic, and that dexamethasone and ondansetron (a commonly used combination) are two of the most effective anti-emetics for PONV. The review adds robust evidence of efficacy for drugs in newer classes, such as aprepitant or fosapreitant, or newer agents in familiar classes, such as ramosetron. The review does not cover the cost effectiveness of the agents included and, despite increased efficacy for newer novel agents, this may preclude their immediate utilisation in anaesthetic practice.

Alternative medicine
In conjunction with antiemetic medications, at least one study has found that application to the pericardium meridian 6 acupressure point produced a positive effect in relieving PONV. Another study found no statistically significant difference </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 Cebocephaly and explain in detail? [/INST] Cebocephaly (from Greek kebos, "monkey" + kephale, "head") is a developmental anomaly that is part of a group of defects called holoprosencephaly </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 Galloway Mowat syndrome and explain in detail? [/INST] Galloway Mowat syndrome is a very rare autosomal recessive genetic disorder, consisting of a variety of features including hiatal hernia, microcephaly and nephrotic syndrome.

Cause
The exact genetic defect in Galloway Mowat syndrome is yet to be discovered </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 Ametropic amblyopia and explain in detail? [/INST] Ametropic amblyopia is a medical condition in which the retina cannot focus on the image of a distant object, a condition often described as reduced visual acuity. This is due to large uncorrected refractive errors in the patients optic system of the eyes. Astigmatism is one of the most frequent causes of ametropic amblyopia.

References
Further reading
Moseley, Merrick J., et al. "Effectiveness of occlusion therapy in ametropic amblyopia: a pilot study." British Journal of Ophthalmology 81.11 (1997): 956–961.
Cavazos, H.;  et al. (1993). "Ametropic Amblyopia". Strabismus. Informa Plc. 1 (2): 63–67. doi:10.3109/09273979309087719. PMID 21314500.
Abraham, S. V. "Bilateral ametropic amblyopia." J Pediatr Ophthalmol Strabismus 1 (1964): 57–61.
Werner, D. B., and W. E </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 Bronchitis and explain in detail? [/INST] Bronchitis is inflammation of the bronchi (large and medium-sized airways) in the lungs that causes coughing. Bronchitis usually begins as an infection in your nose, ears, throat, or sinuses. The infection then makes its way down to the bronchi. Symptoms include coughing up sputum, wheezing, shortness of breath, and chest pain. Bronchitis can be acute or chronic.Acute bronchitis usually has a cough that lasts around three weeks, and is also known as a chest cold. In more than 90% of cases the cause is a viral infection. These viruses may be spread through the air when people cough or by direct contact. A small number of cases are caused by a bacterial infection such as Mycoplasma pneumoniae or Bordetella pertussis. Risk factors include exposure to tobacco smoke, dust, and other air pollution. Treatment of acute bronchitis typically involves rest, paracetamol (acetaminophen), and nonsteroidal anti-inflammatory drugs (NSAIDs) to help with the fever.Chronic bronchitis is defined as a productive cough – one that produces sputum – that lasts for three months or more per year for at least two years. Many people with chronic bronchitis also have chronic obstructive pulmonary disease (COPD). Tobacco smoking is the most common cause, with a number of other factors such as air pollution and genetics playing a smaller role. Treatments include quitting smoking, vaccinations, rehabilitation, and often inhaled bronchodilators and steroids. Some people may benefit from long-term oxygen therapy.Acute bronchitis is one of the more common diseases. About 5% of adults and 6% of children have at least one episode a year. Acute bronchitis is the most common type of bronchitis. By contrast in the United States, in 2018, 9.3 million people were diagnosed with the less common chronic bronchitis.

Acute bronchitis
Acute bronchitis, also known as a chest cold, is short term inflammation of the bronchi of the lungs. The most common symptom is a cough, that may or may not produce sputum. Other symptoms may include coughing up mucus, wheezing, shortness of breath, fever, and chest discomfort. Fever when present is mild. The infection may last from a few to ten days. The cough may persist for several weeks afterwards, with the total duration of symptoms usually around three weeks. Symptoms may last for up to six weeks.

Cause
In more than 90% of cases, the cause is a viral infection. These viruses may spread through the air when people cough or by direct contact. Risk factors include exposure to tobacco smoke, dust, and other air pollutants. A small number of cases are due to bacteria such as Mycoplasma pneumoniae or Bordetella pertussis.

Diagnosis
Diagnosis is typically based on a persons signs and symptoms. The color of the sputum does not indicate if the infection is viral or bacterial. Determining the underlying organism is usually not required. Other causes of similar symptoms include asthma, pneumonia, bronchiolitis, bronchiectasis, and COPD. A chest X-ray may be useful to detect pneumonia.Another common sign of bronchitis is a cough which lasts ten days to three weeks. If the cough lasts for longer than a month, it may become chronic bronchitis. In addition, a fever may be present.  Acute bronchitis is normally caused by a viral infection. Typically, these infections are rhinovirus, parainfluenza, or influenza. No specific testing is normally needed in order to diagnose acute bronchitis.

Treatment
One form of prevention is to avoid smoking and other lung irritants. Frequent hand washing may also be protective. Treatment for acute bronchitis usually involves rest, paracetamol (acetaminophen), and NSAIDs to help with the fever. Cough medicine has little support for its use, and is not recommended in children under the age of six. There is tentative evidence that salbutamol may be useful in treating wheezing; however, it may result in nervousness and tremors. Antibiotics should generally not be used. An exception is when acute bronchitis is due to pertussis. Tentative evidence supports honey and pelargonium to help with symptoms. Getting plenty of rest and drinking enough fluids are often recommended as well. Chinese medicinal herbs are of unclear effect.

Epidemiology
Acute bronchitis is one of the most common diseases. About 5% of adults are affected, and about 6% of children have at least one episode a year. It occurs more often in the winter. More than 10 million people in the US visit a doctor each year for this condition, with about 70% receiving antibiotics which are mostly not needed. There are efforts to decrease the use of antibiotics in acute bronchitis. Acute bronchitis is the most common type of bronchitis.

Chronic bronchitis
Chronic bronchitis is a lower respiratory tract disease, defined by a productive cough that lasts for three months or more per year for at least two years. The cough is sometimes referred to as a smokers cough since it often results from smoking. When chronic bronchitis occurs together with decreased airflow it is known as chronic obstructive pulmonary disease (COPD). Many people with chronic bronchitis have COPD however, most people with COPD do not also have chronic bronchitis. Estimates of the number of people with COPD who have chronic bronchitis are 7 to 40%. Estimates of the number of people who smoke and have chronic bronchitis who also have COPD is 60%.The term "chronic bronchitis" was used in previous definitions of COPD but is no longer included in the definition. The term is still used clinically. While both chronic bronchitis and emphysema are often associated with COPD, neither is needed to make the diagnosis. A Chinese consensus commented on symptomatic types of COPD that include chronic bronchitis with frequent exacerbations.Chronic bronchitis is marked by mucus hypersecretion and mucins. The excess mucus is produced by an increased number of goblet cells, and enlarged submucosal glands in response to long-term irritation. The mucous glands in the submucosa secrete more than the goblet cells. Mucins thicken mucus, and their concentration  has been found to be high in cases of chronic bronchitis, and also to correlate with the severity of the disease. Excess mucus can narrow the airways, thereby limiting airflow and accelerating the decline in lung function, and result in COPD. Excess mucus shows itself as a chronic productive cough and its severity and volume of sputum can fluctuate in periods of acute exacerbations. In COPD, those with the chronic bronchitic phenotype with associated chronic excess mucus, experience a worse quality of life than those without.The increased secretions are initially cleared by coughing. The cough is often worse soon after awakening, and the sputum produced may have a yellow or green color and may be streaked with specks of blood. In the early stages, a cough can maintain mucus clearance. However, with continued excessive secretion mucus clearance is impaired, and when the airways become obstructed a cough becomes ineffective. Effective mucociliary clearance depends on airway hydration, ciliary beating, and the rates of mucin secretion. Each of these factors is impaired in chronic bronchitis. Chronic bronchitis can lead to a higher number of exacerbations and a faster decline in lung function. The ICD-11 lists chronic bronchitis with emphysema (emphysematous bronchitis) as a "certain specified COPD".

Cause
Most cases of chronic bronchitis are caused by tobacco smoking. Chronic bronchitis in young adults who smoke is associated with a greater chance of developing COPD. There is an association between smoking cannabis and chronic bronchitis.  In addition, chronic inhalation of air pollution, or irritating fumes or dust from hazardous exposures in occupations such as coal mining, grain handling, textile manufacturing, livestock farming, and metal moulding may also be a risk factor for the development of chronic bronchitis. Bronchitis caused in this way is often referred to as industrial bronchitis, or occupational bronchitis.  Rarely genetic factors also play a role.Air quality can also affect the respiratory system with higher levels of nitrogen dioxide and sulfur dioxide contributing to bronchial symptoms. Sulfur dioxide can cause inflammation which can aggravate chronic bronchitis and make infections more likely.Air pollution in the workplace is the cause of several non-communicable diseases (NCDs) including chronic bronchitis.

Treatment
Decline in lung function in chronic bronchitis may be slowed by stopping smoking. Chronic bronchitis may be treated with a number of medications and occasionally oxygen therapy. Pulmonary rehabilitation may also be used.A distinction has been made between exacerbations (sudden worsenings) of chronic bronchitis, and otherwise stable chronic bronchitis. Stable chronic bronchitis can be defined as the normal definition of chronic bronchitis, plus the absence of an acute exacerbation in the previous four weeks. A Cochrane review found that mucolytics in chronic bronchitis may slightly decrease the chance of developing an exacerbation. The mucolytic guaifenesin is a safe and effective treatment for stable chronic bronchitis. This has an advantage in that it is available as an extended use tablet which lasts for twelve hours. Erdosteine is a mucolytic recommended by NICE. GOLD also supports the use of some mucolytics that are advised against when inhaled corticosteroids are being used, and singles out erdosteine as having good effects regardless of corticosteroid use. Erdosteine also has antioxidant properties. Erdosteine has been shown to significantly reduce the risk of exacerbations, shorten their duration, and hospital stays. In those with the chronic bronchitic phenotype of COPD, the phosphodiesterase-4 inhibitor roflumilast may decrease significant exacerbations.

Epidemiology
Chronic bronchitis affects about 3.4% to 22% of the general population. Individuals over 45 years of age, smokers, those that live or work in areas with high air pollution, and anybody with asthma all have a higher risk of developing chronic bronchitis. This wide range is due to the different definitions of chronic bronchitis that can be diagnosed based on signs and symptoms or the clinical diagnosis of the disorder. Chronic bronchitis tends to affect men more often than women. While the primary risk factor for chronic bronchitis is smoking, there is still a 4%-22% chance that non smokers can get chronic bronchitis. This might suggest other risk factors such as the inhalation of fuels, dusts, fumes and genetic factor. In the United States, in 2016, 8.6 million people were diagnosed with chronic bronchitis, and there were 518 reported deaths. Per 100,000 of population the death rate of chronic bronchitis was 0.2.

History
The condition of bronchitis has been recognised for many centuries, in several different cultures including the Ancient Greek, Chinese, and Indian, with the presence of excess phlegm and cough noted in recognition of the same condition. Early treatments of chronic bronchitis included garlic, cinnamon and ipecac, among others. Modern treatments were developed during the second half of the 20th century.In Britain in 1808, a physician Charles Badham was the first person to describe the condition and name the acute form as acute bronchitis.  This was written of in a book entitled Inflammatory conditions of the bronchia. In this book Badham distinguished three forms of bronchitis including acute and chronic. A second edition of this book was renamed An Essay on Bronchitis and published in 1814. Bradham used the term catarrh to refer to the cardinal symptoms of chronic cough and mucus hypersecretion of chronic bronchitis, and described chronic bronchitis as a disabling disorder.In 1901 an article was published on the treatment of chronic bronchitis in the elderly. The symptoms described have remained unchanged. The cause was thought to be brought on by dampness, cold weather, and foggy conditions, and treatments were aimed towards various cough mixtures, respiratory stimulants, and tonics. It was noted that something other than the weather was thought to be at play. Exacerbations of the condition were also described at this time. Another physician Harry Campbell was referred to who had written in the British Medical Journal a week before. Campbell had suggested that the cause of chronic bronchitis was due to toxic substances, and recommended pure air, simple food, and exercise to remove them from the body.A joint research programme was undertaken in Chicago and London from 1951 to 1953 in which the clinical features of one thousand cases of chronic bronchitis were detailed. The findings were published in the Lancet in 1953. It was stated that since its introduction by Badham, chronic bronchitis had become an increasingly popular diagnosis. The study had looked at various associations such as the weather, conditions at home, and at work, age of onset, childhood illnesses, smoking habits, and breathlessness. It was concluded that chronic bronchitis invariably led to emphysema, particularly when the bronchitis had persisted for a long time.In 1957 it was noted that at the time there were many investigations being carried out into chronic bronchitis and emphysema in general, and among industrial workers exposed to dust. Excerpts were published dating from 1864 in which Charles Parsons had noted the occurring consequence of the development of emphysema from bronchitis. This was seen to be not always applicable. His findings were in association with his studies on chronic bronchitis among pottery workers.A CIBA (now Novartis) meeting in 1959, and a meeting of the American Thoracic Society in 1962, defined chronic bronchitis as a component of COPD, in the terms that have not changed.

Eosinophilic bronchitis
Eosinophilic bronchitis is a chronic dry cough, defined by the presence of an increased number of a type of white blood cell known as eosinophils. It has a normal finding on X-ray and has no airflow limitation.

Protracted bacterial bronchitis
Protracted bacterial bronchitis in children, is defined as a chronic productive cough with a positive bronchoalveolar lavage that resolves with antibiotics. Protracted bacterial bronchitis is usually caused by Streptococcus pneumoniae, non-typable Haemophilus influenzae, or Moraxella catarrhalis </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 Trichobacteriosis axillaris 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 Shock (circulatory) and explain in detail? [/INST] Shock is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system. Initial symptoms of shock may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest, as complications worsen.Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. Low volume shock, also known as hypovolemic shock, may be from bleeding, diarrhea, or vomiting. Cardiogenic shock may be due to a heart attack or cardiac contusion. Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. Distributive shock may be due to sepsis, anaphylaxis, injury to the upper spinal cord, or certain overdoses.The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation.Treatment of shock is based on the likely underlying cause. An open airway and sufficient breathing should be established. Any ongoing bleeding should be stopped, which may require surgery or embolization. Intravenous fluid, such as Ringers lactate or packed red blood cells, is often given. Efforts to maintain a normal body temperature are also important. Vasopressors may be useful in certain cases. Shock is both common and has a high risk of death. In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%.

Signs and symptoms
The presentation of shock is variable, with some people having only minimal symptoms such as confusion and weakness. While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion, these may not always be present. While a fast heart rate is common, those on β-blockers, those who are athletic, and in 30% of cases of those with shock due to intra abdominal bleeding, heart rate may be normal or slow. Specific subtypes of shock may have additional symptoms.
Dry mucous membrane, reduced skin turgor, prolonged capillary refill time, weak peripheral pulses, and cold extremities can be early signs of shock.

Low volume
Hypovolemic shock is the most common type of shock and is caused by insufficient circulating volume. The most common cause of hypovolemic shock is hemorrhage (internal or external); however, vomiting and diarrhea are more common causes in children. Other causes include burns, as well as excess urine loss due to diabetic ketoacidosis and diabetes insipidus.Signs and symptoms of hypovolemic shock include:

A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia
Cool skin due to vasoconstriction and stimulation of vasoconstriction
Rapid and shallow breathing due to sympathetic nervous system stimulation and acidosis
Hypothermia due to decreased perfusion and evaporation of sweat
Thirst and dry mouth, due to fluid depletion
Cold and mottled skin (livedo reticularis), especially extremities, due to insufficient perfusion of the skinThe severity of hemorrhagic shock can be graded on a 1–4 scale on the physical signs. The shock index (heart rate divided by systolic blood pressure) is a stronger predictor of the impact of blood loss than heart rate and blood pressure alone. This relationship has not been well established in pregnancy-related bleeding.

Cardiogenic
Cardiogenic shock is caused by the failure of the heart to pump effectively. This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart failure (CHF), myocardial contusion, or valvular heart disease problems.Symptoms of cardiogenic shock include:

Distended jugular veins due to increased jugular venous pressure
Weak or absent pulse
Abnormal heart rhythms, often a fast heart rate
Pulsus paradoxus in case of tamponade
Reduced blood pressure
Shortness of breath, due to pulmonary congestion

Obstructive
Obstructive shock is a form of shock associated with physical obstruction of the great vessels of the systemic or pulmonary circulation. Several conditions can result in this form of shock.

Cardiac tamponade in which fluid in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation.
Tension pneumothorax Through increased intrathoracic pressure, bloodflow to the heart is prevented (venous return).
Pulmonary embolism is the result of a thromboembolic incident in the blood vessels of the lungs and hinders the return of blood to the heart.
Aortic stenosis hinders circulation by obstructing the ventricular outflow tract
Hypertrophic sub-aortic stenosis is overly thick ventricular muscle that dynamically occludes the ventricular outflow tract.
Abdominal compartment syndrome defined as an increase in intra-abdominal pressure to > 20 mmHg with organ dysfunction. Increased intraabdominal pressure can be due to sepsis and severe abdominal trauma. This increased pressure reduces blood flow back to the heart, thereby reducing blood flow to the body and resulting in signs and symptoms of shock.Many of the signs of obstructive shock are similar to cardiogenic shock, however treatments differ. Symptoms of obstructive shock include:

Abnormal heart rhythms, often a fast heart rate.
Reduced blood pressure.
Cool, clammy, mottled skin, often due to low blood pressure and vasoconstriction.
Decreased urine output.

Distributive
Distributive shock is low blood pressure due to a dilation of blood vessels within the body. This can be caused by systemic infection (septic shock), a severe allergic reaction (anaphylaxis), or spinal cord injury (neurogenic shock).
Septic shock is the most common cause of distributive shock. It is caused by an overwhelming systemic infection resulting in vasodilation leading to hypotension. Septic shock can be caused by Gram negative bacteria such as (among others) Escherichia coli, Proteus species, Klebsiella pneumoniae (which have an endotoxin on their surface that produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body), other Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins. Septic shock also includes some elements of cardiogenic shock. In 1992, the ACCP/SCCM Consensus Conference Committee defined septic shock: " ... sepsis-induced hypotension (systolic blood pressure < 90 mmHg or a reduction of 40 mmHg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to: lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified. The pathophysiology behind septic shock is as follows: 1) Systemic leukocyte adhesion to endothelial cells 2) Reduced contractility of the heart 3) Activation of the coagulation pathways, resulting in disseminated intravascular coagulation 4). Increased levels of neutrophilsThe main manifestations of septic shock are due to the massive release of histamine which causes intense dilation of the blood vessels. People with septic shock will also likely be positive for SIRS criteria. The most generally accepted treatment for these patients is early recognition of symptoms, and early administration of broad spectrum and organism specific antibiotics.
Signs of septic shock include:
Abnormal heart rhythms, often a fast heart rate
Reduced blood pressure
Decreased urine output
Altered mental status
Anaphylactic shock is caused by a severe anaphylactic reaction to an allergen, antigen, drug, or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability. Signs typically occur after exposure to an allergen and may include:
Skin changes, such as hives, itching, flushing, and swelling.
Wheezing and shortness of breath.
Abdominal pain, diarrhea, and vomiting.
Lightheadedness, confusion, headaches, loss of consciousness.
High spinal injuries may cause neurogenic shock, which is commonly classified as a subset of distributive shock. The classic symptoms include a slow heart rate due to loss of cardiac sympathetic tone and warm skin due to dilation of the peripheral blood vessels. (This term can be confused with spinal shock which is a recoverable loss of function of the spinal cord after injury and does not refer to the hemodynamic instability.)

Endocrine
Although not officially classified as a subcategory of shock, many endocrinology disturbances in their severe form can result in shock.
Hypothyroidism (can be considered a form of cardiogenic shock) in people who are critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.
Thyrotoxicosis (cardiogenic shock) may induce a reversible cardiomyopathy.
Acute adrenal insufficiency (distributive shock) is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.
Relative adrenal insufficiency (distributive shock) in critically ill patients where present hormone levels are insufficient to meet the higher demands.

Cause
Shock is a common end point of many medical conditions. Shock triggered by a serious allergic reaction is known as anaphylactic shock, shock triggered by severe dehydration or blood loss is known as hypovolemic shock, shock caused by sepsis is known as septic shock, etc. Shock itself is a life-threatening condition as a result of compromised body circulation. It can be divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic, and obstructive. A few additional classifications are occasionally used, such as endocrinologic shock.

Pathophysiology
There are four stages of shock. Shock is a complex and continuous condition, and there is no sudden transition from one stage to the next. At a cellular level, shock is the process of oxygen demand becoming greater than oxygen supply.One of the key dangers of shock is that it progresses by a positive feedback loop. Poor blood supply leads to cellular damage, which results in an inflammatory response to increase blood flow to the affected area. Normally, this causes the blood supply level to match with tissue demand for nutrients. However, if there is enough increased demand in some areas, it can deprive other areas of sufficient supply, which then start demanding more. This then leads to an ever escalating cascade.
As such, shock is a runaway condition of homeostatic failure, where the usual corrective mechanisms relating to oxygenation of the body no longer function in a stable way. When it occurs, immediate treatment is critical in order to return an individuals metabolism into a stable, self-correcting trajectory. Otherwise the condition can become increasingly difficult to correct, surprisingly fast, and then progress to a fatal outcome. In the particular case of anaphylactic shock, progression to death might take just a few minutes.

Initial
During the Initial stage (Stage 1), the state of hypoperfusion causes hypoxia. Due to the lack of oxygen, the cells perform lactic acid fermentation. Since oxygen, the terminal electron acceptor in the electron transport chain, is not abundant, this slows down entry of pyruvate into the Krebs cycle, resulting in its accumulation. The accumulating pyruvate is converted to lactate (lactic acid) by lactate dehydrogenase. The accumulating lactate causes lactic acidosis.

Compensatory
The Compensatory stage (Stage 2) is characterised by the body employing physiological mechanisms, including neural, hormonal, and bio-chemical mechanisms, in an attempt to reverse the condition.  As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood, so the body attempts to return to acid–base homeostasis by removing that acidifying agent. The baroreceptors in the arteries detect the hypotension resulting from large amounts of blood being redirected to distant tissues, and cause the release of epinephrine and norepinephrine. Norepinephrine causes predominately vasoconstriction with a mild increase in heart rate, whereas epinephrine predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. The renin–angiotensin axis is activated, and arginine vasopressin (anti-diuretic hormone) is released to conserve fluid by reducing its excretion via the renal system. These hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the renin–angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock.

Progressive/decompensated
The Progressive stage (stage 3) results if the underlying cause of the shock is not successfully treated. During this stage, compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells in the body, sodium ions build up within the intracellular space while potassium ions leak out. Due to lack of oxygen, cellular respiration diminishes and anaerobic metabolism predominates. As anaerobic metabolism continues, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, will lead to leakage of fluid and protein into the surrounding tissues.  As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.  If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.

Refractory
At Refractory stage (stage 4), the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently.  One of the primary reasons that shock is irreversible at this point is that much of the cellular ATP (the basic energy source for cells) has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid. Because cells can only produce adenosine at a rate of about 2% of the cells total need per hour, even restoring oxygen is futile at this point because there is no adenosine to phosphorylate into ATP.

Diagnosis
The diagnosis of shock is commonly based on a combination of symptoms, physical examination, and laboratory tests. Many signs and symptoms are not sensitive or specific for shock, thus many clinical decision-making tools have been developed to identify shock at an early stage. A high degree of suspicion is necessary for the proper diagnosis of shock.
The first change seen in shock is increased cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and are easier to acquire. If shock progresses anaerobic metabolism will begin to occur with an increased blood lactic acid as the result. While many laboratory tests are typically performed, there is no test that either conclusively makes or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be useful to determine volume status.

Management
The best evidence exists for the treatment of septic shock in adults. However, the pathophysiology of shock in children appears to be similar so treatment methodologies have been extrapolated to children. Management may include securing the airway via intubation if necessary to decrease the work of breathing and for guarding against respiratory arrest. Oxygen supplementation, intravenous fluids, passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe. In select cases, compression devices like non-pneumatic anti-shock garments (or the deprecated military anti-shock trousers) can be used to prevent further blood loss and concentrate fluid in the bodys head and core. It is important to keep the person warm to avoid hypothermia as well as adequately manage pain and anxiety as these can increase oxygen consumption. Negative impact by shock is reversible if its recognized and treated early in time.

Fluids
Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liter normal saline bolus over 10 minutes or 20 mL/kg in a child) which is usually instituted as the person is being further evaluated. Colloids and crystalloids appear to be equally effective with respect to outcomes., Balanced crystalloids and normal saline also appear to be equally effective in critically ill patients. If the person remains in shock after initial resuscitation, packed red blood cells should be administered to keep the hemoglobin greater than 100 g/L.For those with hemorrhagic shock, the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist (known as permissive hypotension). Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70–90 mmHg, or until the patient has adequate mentation and peripheral pulses. Hypertonic fluid may also be an option in this group.

Medications
Vasopressors may be used if blood pressure does not improve with fluids. Common vasopressors used in shock include: norepinephrine, phenylephrine, dopamine, and dobutamine.
There is no evidence of substantial benefit of one vasopressor over another; however, using dopamine leads to an increased risk of arrhythmia when compared with norepinephrine. Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma but may be of use in neurogenic shock. Activated protein C (Xigris), while once aggressively promoted for the management of septic shock, has been found not to improve survival and is associated with a number of complications. Activated protein C was withdrawn from the market in 2011, and clinical trials were discontinued. The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes. If used at all it should only be considered if the blood pH is less than 7.0.People with anaphylactic shock are commonly treated with epinephrine. Antihistamines, such as Benadryl (diphenhydramine) or ranitidine are also commonly administered. Albuterol, normal saline, and steroids are also commonly given.

Mechanical support
Intra-aortic balloon pump (IABP) – a device inserted into the aorta that mechanically raises the blood pressure. Use of Intra-aortic balloon pumps is not recommended in cardiogenic shock.
Ventricular assist device (VAD) – A mechanical pump that helps pump blood throughout the body. Commonly used in short term cases of refractory primary cardiogenic shock.
Artificial heart (TAH)
Extracorporeal membrane oxygenation (ECMO) – an external device that completely replaces the work of the heart.

Treatment goals
The goal of treatment is to achieve a urine output of greater than 0.5 mL/kg/h, a central venous pressure of 8–12 mmHg and a mean arterial pressure of 65–95 mmHg. In trauma the goal is to stop the bleeding which in many cases requires surgical interventions. A good urine output indicates that the kidneys are getting enough blood flow.

Epidemiology
Septic shock (a form of distributive shock), is the most common form of shock. Shock from blood loss occurs in about 1–2% of trauma cases. Overall, up to one-third of people admitted to the intensive care unit (ICU) are in circulatory shock. Of these, cardiogenic shock accounts for approximately 20%, hypovolemic about 20%, and septic shock about 60% of cases.

Prognosis
The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Low volume, anaphylactic, and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock, especially septic shock where treatment is delayed or the antimicrobial drugs are ineffective, however has a mortality rate between 30% and 80%; cardiogenic shock has a mortality rate of up to 70% to 90%, though quick treatment with vasopressors and inotropic drugs, cardiac surgery, and the use of assistive devices can lower the mortality.

History
There is no evidence of the word shock being used in its modern-day form prior to 1743 </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 Facial symmetry and explain in detail? [/INST] Facial symmetry is one specific measure of bodily symmetry. Along with traits such as averageness and youthfulness it influences judgments of aesthetic traits of physical attractiveness and beauty. For instance, in mate selection, people have been shown to have a preference for symmetry.Facial bilateral symmetry is typically defined as fluctuating asymmetry of the face comparing random differences in facial features of the two sides of the face. The human face also has systematic, directional asymmetry: on average, the face (mouth, nose and eyes) sits systematically to the left with respect to the axis through the ears, the so-called aurofacial asymmetry.

Directional asymmetry
Directional asymmetry is a systematic asymmetry of some parts of the face across the population. A theory of directional asymmetries in the human body is the axial twist hypothesis. As predicted by this theory, the eyes, nose and mouth are, on average, located slightly to the left of the axis through the ears. This aurofacial asymmetry is very small in young adults (0.5 degree), but much larger in small children (4 degrees).

Fluctuating asymmetry
Fluctuating asymmetry is the non-systematic variation of individual facial landmarks with respect to the facial midline, i.e., the line perpendicular to the line through the eyes, which crosses the tip of the nose and the chin.
A wide variety of methods have been used to examine the claim that facial symmetry plays a role in judgments of beauty. Blending of multiple faces to create a composite and face-half mirroring have been among the techniques used.

Conclusions derived from face mirroring, however, have been called into question, because it has been shown that mirroring face-halves creates artificial features. For example, if the nose of an individual is slightly bent to the right side, then mirroring the right side of the face will lead to an over-sized nose, while mirroring the left side will lead to an unnaturally small nose.

Attractiveness
Facial symmetry has been found to increase ratings of attractiveness in human faces. More symmetrical faces are perceived as more attractive in both males and females, although facial symmetry plays a larger role in judgments of attractiveness concerning female faces.While studies employing the composite faces produced results that indicate that more symmetrical faces are perceived as more attractive, studies applying the face-half mirroring technique have indicated that humans prefer slight asymmetry. Also, studies have shown that nearly symmetrical faces are considered highly attractive as compared to asymmetrical ones. The symmetry of the nose seems to be more important than that of the lips.

Dynamic asymmetries
Highly conspicuous directional asymmetries can be temporary ones. For example, during speech, most people (76%) tend to express greater amplitude of movement on the right side of their mouth. This is most likely caused by the uneven strengths of contralateral neural connections between the left hemisphere of the brain (linguistic localization) and the right side of the face.

Facial averageness vs. symmetry
Experiments suggest that symmetry and averageness make independent contributions to attractiveness.

Aging
Facial symmetry is also a valid marker of cognitive aging. Progressive changes occurring throughout life in the soft tissues of the face will cause more prominent facial asymmetry in older faces. Therefore, symmetrical transformation of older faces generally increases their attractiveness while symmetrical transformation in young adults and children will decrease their attractiveness.

Personality and Big Five personality traits
Research indicates that facial symmetry is correlated with the big-five model of personality. The five factors are:
Openness to experience (inventive/curious vs. consistent/cautious)
Conscientiousness (efficient/organized vs. easy-going/careless)
Extraversion (outgoing/energetic vs. solitary/reserved)
Agreeableness (friendly/compassionate vs. challenging/detached)
Neuroticism (sensitive/nervous vs. secure/confident)A consistent finding is that facial symmetry is positively correlated with extraversion, indicating that individuals with more symmetric faces are also more extroverted.  More symmetrical faces are also judged to be lower on neuroticism but higher on conscientiousness and agreeableness (asymmetrical faces were rated as less agreeable than normal ones, but the more symmetrical were again rated as somewhat less agreeable than the normal).  More symmetrical faces are also more likely to have more desirable social attributes assigned to them, such as sociable, intelligent or lively.However, the relationship of facial symmetry and the big-five personality model remains somewhat unclear with regard to neuroticism, openness, agreeableness and conscientiousness </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 Upper airway resistance syndrome and explain in detail? [/INST] Upper airway resistance syndrome is a sleep disorder characterized by the narrowing of the airway that can cause disruptions to sleep. The symptoms include unrefreshing sleep, fatigue, sleepiness, chronic insomnia, and difficulty concentrating. UARS can be diagnosed by polysomnograms capable of detecting Respiratory Effort-related Arousals. It can be treated with lifestyle changes, orthodontics, surgery, or CPAP therapy. UARS is considered a variant of sleep apnea, although some scientists and doctors believe it to be a distinct disorder.

History
Upper airway resistance syndrome was first recognized at Stanford University in the late 1980s and the article that described it by name along with its relationship to OSA was published in 1992 by Dr. Christian Guilleminault et al.

Signs and symptoms
Symptoms of UARS are similar to those of obstructive sleep apnea, but not inherently overlapping. Fatigue, insomnia, daytime sleepiness, unrefreshing sleep, anxiety, and frequent awakenings during sleep are the most common symptoms. Oxygen desaturation is minimal or absent in UARS, with most having a minimum oxygen saturation >92%.Many patients experience chronic insomnia that creates both a difficulty falling asleep and staying asleep. As a result, patients typically experience frequent sleep disruptions. Most patients with UARS snore, but not all.Some patients experience hypotension, which may cause lightheadedness, and patients with UARS are also more likely to experience headaches and irritable bowel syndrome.Predisposing factors include a high and narrow hard palate, an abnormally small intermolar distance, an abnormal overjet greater than or equal to 3 millimeters, and a thin soft palatal mucosa with a short uvula. In 88% of the subjects, there is a history of early extraction or absence of wisdom teeth. There is an increased prevalence of UARS in east Asians.

Pathophysiology
Upper airway resistance syndrome is caused when the upper airway narrows without closing. Consequently, airflow is either reduced or compensated for through an increase in inspiratory efforts. This increased activity in inspiratory muscles leads to the arousals during sleep which patients may or may not be aware of.A typical UARS patient is not obese and possesses small jaws, which can result in a smaller amount of space in the nasal airway and behind the base of the tongue. Patients may have other anatomical abnormalities that can cause UARS such as deviated septum, inferior turbinate hypertrophy, a narrow hard palate that reduces nasal volume, enlarged tonsils, or nasal valve collapse. UARS affects equal numbers of males and females.Why some patients with airway obstruction present with UARS and not OSA is thought to be caused by alterations in nerves located in the palatal mucosa. UARS patients have largely intact and responsive nerves, while OSA patients show clear impairment and nerve damage. Functioning nerves in the palatal mucosa allow UARS patients to more effectively detect and respond to flow limitations before apneas and hypopneas can occur. Patients with intact nerves are able to dilate the genioglossus muscle, a key compensatory mechanism utilized in the presence of airway obstruction. What damages the nerves is not definitively known, but it is hypothesized to be caused by the long term effects of gastroesophageal reflux and/or snoring.

Diagnosis
UARS is diagnosed using the Respiratory Disturbance Index (RDI). A patient is considered to have UARS when they have an Apnea-Hypopnea Index (AHI) less than 5, but an RDI greater than or equal to 5. Unlike the Apnea-Hypopnea Index, the Respiratory Disturbance Index includes Respiratory Effort-related Arousals (RDI = AHI + RERA Index). In 2005, the definition of Sleep Apnea was changed to include patients with UARS by using RDI to determine sleep apnea severity.
The diagnosis of UARS is based on findings on a polysomnogram. On polysomnograms, a UARS patient will have very few apneas and hypopneas, but many Respiratory effort-related Arousals. RERAs are periods of increased respiratory effort lasting for more than ten seconds and ending in arousal. Whether or not an event is classified as a RERA or Hypopnea depends on the definition of Hypopnea used by the sleep technician.  The American Academy of Sleep Medicine currently recognizes two definitions. The scoring of Respiratory Effort-related Arousals is currently designated as "optional" by the AASM. Thus, many patients who receive sleep studies may receive a negative result, even if they have UARS.Based on symptoms, patients are commonly misdiagnosed with idiopathic insomnia, idiopathic hypersomnia, chronic fatigue syndrome, fibromyalgia, or a psychiatric disorder such as ADHD or depression. Studies have found that children with UARS are frequently misdiagnosed with ADHD. One study found UARS or OSA present in up to 56% of children with ADHD. Studies show that symptoms of ADHD caused by UARS significantly improve or remit with treatment in surgically treated children.

Management
Behavioral modification
Behavioral modifications include getting at least 7–8 hours of sleep and various lifestyle changes, such as positional therapy. Sleeping on ones side rather than in a supine position or using positional pillows can provide relief, but these modifications may not be sufficient to treat more severe cases. Avoiding sedatives including alcohol and narcotics can help prevent the relaxation of airway muscles, and thereby reduce the chance of their collapse. Avoiding sedatives may also help to reduce snoring.

Medications
Nasal steroids may be prescribed in order to ease nasal allergies and other obstructive nasal conditions that could cause UARS.

Positive airway pressure therapy
If left untreated, UARS can develop into obstructive sleep apnea. Treatments for OSA such as positive airway pressure therapy can be effective at stopping the progression of UARS.Positive airway pressure therapy is similar to that in obstructive sleep apnea and works by stenting the airway open with pressure, thus reducing the airway resistance. Use of a CPAP can help ease the symptoms of UARS </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 Intermediate uveitis and explain in detail? [/INST] Intermediate uveitis is a form of uveitis localized to the vitreous and peripheral retina. Primary sites of inflammation include the vitreous of which other such entities as pars planitis, posterior cyclitis, and hyalitis are encompassed. Intermediate uveitis may either be an isolated eye disease or associated with the development of a systemic disease such as multiple sclerosis or sarcoidosis. As such, intermediate uveitis may be the first expression of a systemic condition. Infectious causes of intermediate uveitis include Epstein–Barr virus infection, Lyme disease, HTLV-1 virus infection, cat scratch disease, and hepatitis C.
Permanent loss of vision is most commonly seen in patients with chronic cystoid macular edema (CME). Every effort must be made to eradicate CME when present. Other less common causes of visual loss include retinal detachment, glaucoma, band keratopathy, cataract, vitreous hemorrhage, epiretinal membrane and choroidal neovascularization.

Signs and symptoms
Clinical signs include redness of the eye, pain, blurring of vision, photophobia and floaters.
However, some individuals, particularly children, can present with few to no symptoms.

Associated conditions
Associations of the disease with such entities as multiple sclerosis, sarcoidosis, or inflammatory bowel disease suggest an autoimmune component in at least a subset of patients </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 Neonatal meningitis and explain in detail? [/INST] Neonatal meningitis is a serious medical condition in infants that is rapidly fatal if untreated. Meningitis is an inflammation of the meninges, the protective membranes of the central nervous system, is more common in the neonatal period (infants less than 44 days old) than any other time in life, and is an important cause of morbidity and mortality globally. Mortality is roughly half in developing countries and ranges from 8%-12.5% in developed countries.Symptoms seen with neonatal meningitis are often unspecific and may point to several conditions, such as sepsis (whole body inflammation). These can include fever, irritability, and dyspnea. The only method to determine if meningitis is the cause of these symptoms is lumbar puncture (an examination of the cerebrospinal fluid).The most common cause of neonatal meningitis is bacterial infection of blood, known as bacteremia. Organisms responsible are different; most commonly group B streptococci (i.e. Streptococcus agalactiae), Escherichia coli, and Listeria monocytogenes. Although there is a low mortality rate in developed countries, there is a 50% prevalence rate of neurodevelopmental disabilities after meningitis caused by E. coli and Streptococcus agalactiae, and a 79% prevalence after meningitis caused by Gram-negative rods other than E. coli. Delayed treatment of neonatal meningitis may cause cerebral palsy, blindness, deafness, seizure disorders, and learning deficiencies.

Signs and symptoms
The following is a list of common signs and symptoms of neonatal meningitis.
Fever
poor appetite
anterior fontanelle bulging
seizures
jitteriness
dyspnea
irritability
anorexia
vomiting
diarrhea
abdominal distention (increase in abdominal size)
neck rigidity
cyanosis
jaundice
sunset eyes (downward gaze of the eyes)
abnormal body temperature (hypo-or hyperthermia)
change of activity (lethargy or irritability)These symptoms are unspecific and may point to many different conditions.

Complications
Neuroimaging (X-ray imaging of the brain) is recommended to detect the complications of meningitis. Complications should be suspected when the clinical course is characterized by shock, respiratory failure, focal neurological deficits, a positive cerebrospinal fluid culture after 48 to 72 hours of appropriate antibiotic therapy, or infection with certain organisms, such as Citrobacter koseri and Cronobacter sakazakii for example. Ultrasounds are useful for early imaging to determine ventricular size and hemorrhaging. CT scans later in the therapy should be used to dictate prolonged treatment.If intracranial abscesses (collection of pus in the brain) are found, treatment consisting of a combination of surgical drainage of the abscess and antimicrobial therapy for 4 to 6 weeks is recommended. More imaging should be completed after the end of antibiotic treatment because abscesses have been found after weeks from start of treatment.Relapses have also occurred after appropriate treatment when infected by Gram-negative enteric bacilli.

Hearing Loss
Meningitis is one of the leading causes of acquired deafness. Nearly 8% of those with Meningitis will have a permanent sensorineural hearing loss. The longer meningitis is left untreated, the greater the risk of seizures and permanent neurological damage such as hearing loss, memory difficulty, learning disabilities, brain damage, gait problems, kidney failure, shock, and even death. Hearing loss in those with Meningitis can occur when the body is fighting off the infection and the cells reach the inner ear where the hair cells and nerve fibers become damaged. Hearing loss can also occur after Meningitis is resolved due to an increased risk for ossification of the cochlea. Ossification of the cochlea can make it difficult to place a Cochlear Implant for hearing losses that are treated unsuccessfully with hearing aids. Bacterial Meningitis is likely to lead to hearing loss. It is important to have a hearing test as soon as possible. It would be best to complete a hearing test before leaving the hospital or within four weeks of improvement of symptoms. Fluctuating hearing loss has been observed in a large number of patients, so it is best to have routine hearing tests to monitor the hearing loss. Viral Meningitis is less likely to cause hearing loss and it is recommended to perform a hearing test if the patient is experiencing any hearing difficulties. All hearing losses are different so there is no predictive loss for Meningitis. Children are assessed through behavioral testing (if old enough), Otoacoustic Emissions (OAEs), and Auditory Brainstem Response (ABR).Impact in Children for Communication
If hearing loss is left undetected and/or untreated, this can lead to later acquisition of language and delayed reading skills. Since untreated Meningitis can cause brain damage and learning disabilities, children with a history of Meningitis may be developmentally delayed when compared to their typically developing peers.

Laboratory features
Laboratory features that are characteristic of neonatal bacterial meningitis include:
Isolation of a bacterial pathogen from the cerebrospinal fluid by culture and/or visualization by Gram stain
Increased cerebrospinal fluid white blood cell count (typically >1000 white blood cells/μL, but may be lower, especially with Gram-positive bacteria), usually with a predominance of neutrophils
Elevated cerebrospinal fluid protein concentration (>150 mg/dL in preterm (premature birth) and >100 mg/dL in term infants)
Decreased cerebrospinal fluid glucose concentration (<20 mg/dL [1.1 mmol/L] in preterm (premature birth) and <30 mg/dL [1.7 mmol/L] in term (on time) infants)

Causes
Neonatal meningitis is caused by group B streptococci Streptococcus agalactiae (39%-48% of cases), Escherichia coli (30%-35%), other Gram-negative rods (8%-12%), Streptococcus pneumoniae (about 6%), and Listeria monocytogenes (5%-7%). Meningitis is typically caused from either a bacterial or viral infection, however, it can be caused by fungal, parasitic, or amebic infections as well.  Even more rare, Meningitis can be caused by some cancers, Lupus, specific drugs, head injuries, and brain surgeries. Most neonatal meningitis results from bacteremia (bacterial infection of the blood) with hematogenous spread to the central nervous system (CNS).

Early-onset
In early-onset neonatal meningitis, acquisition of the bacteria is from the mother either before the baby is born or during birth. The most common bacteria found in early-onset are Streptococcus agalactiae, Escherichia coli, and Listeria monocytogenes. In developing countries, Gram-negative enteric (gut) bacteria are responsible for the majority of early onset meningitis.

Late-onset
Late-onset meningitis may be caused by other Gram-negative bacteria and staphylococcal species. In developing countries, Streptococcus pneumoniae accounts for most cases of late onset.

Herpes Simplex Virus
Herpes simplex virus is a rare cause of meningitis, occurring only 0.165 in 10,000 live births in the UK and 0.2-5 in 10,000 live births in the US Both HSV-1 and HSV-2 can cause neonatal meningitis, however, HSV-2 accounts for 70% of the cases.Herpes simplex virus is transmitted to neonates mainly during delivery (when infected maternal secretions come into contact with the baby and accounting for 85% of cases), but also occur in utero (while the fetus is still in the womb, 5% of cases) or even post-delivery, receiving the infection from the community (10% of cases). The most important factors impacting the transmission of the virus is the stage of the mothers infection (symptomatic or non-symptomatic) and the damage of any maternal membranes during birth (the longer the tissue is damaged, the higher the chance of neonatal infection).

Pathogenesis
Generally, the progression of neonatal meningitis starts with bacteria colonizing the gastrointestinal tract. The bacteria then invades through the intestinal mucosa layer into the blood, causing bacteremia followed by invasion of the cerebrospinal fluid. The neonates less efficient immune system (especially the alternative complement system) lessens their defense against invading bacteria. Colonization of the mother plays an important role in transmission to the neonate, causing early-onset meningitis.

Group B Streptococcus
Neonatal Streptococcus agalactiae infection is acquired in utero or during passage through the vagina. Evidence suggests that vaginal colonization  by Streptococcus agalactiae during pregnancy increases the risk of vertical transmission and early-onset disease in neonates.

Neonatal meningitis-causing E. coli
Some strains of E. coli have a capsule, called K1, which protects the bacteria from the innate immune system and allows it to penetrate the central nervous system. The capsule contains sialic acid, which is found widely in humans and so does not set off the defenses of the body. Sialic acid also plays a role in the bacterias ability to invade through the blood-brain barrier. The capsule can be variably O-acetylated.

Diagnosis
Bacterial Infection
A lumbar puncture (spinal tap) is necessary to diagnose meningitis. Cerebrospinal fluid culture is the most important study for the diagnosis of neonatal bacterial meningitis because clinical signs are non-specific and unreliable. Blood cultures may be negative in 15-55% of cases, making them unreliable as well. However, a cerebrospinal fluid to blood glucose ratio below two-thirds has a strong relationship to bacterial meningitis. A spinal tap should be done in all neonates with suspected meningitis, with suspected or proven sepsis (whole body inflammation) and should be considered in all neonates in whom sepsis is a possibility. The role of the spinal tap in neonates who are healthy appearing but have maternal risk factors for sepsis is more controversial; its diagnostic yield in these patients may be low.Early-onset is deemed when infection is within one week of birth. Late-onset is deemed after the first week.

Viral Infection
Babies born from mothers with symptoms of Herpes simplex virus should be tested for viral infection. Liver tests, complete blood count, cerebrospinal fluid analysis, and a chest X-ray should all be completed to diagnose meningitis. Samples should be taken from skin, conjunctiva (eye), mouth and throat, rectum, urine, and the cerebrospinal fluid for viral culture and polymerase chain reaction.

Prevention
Bacterial
Prevention of neonatal meningitis is primarily intrapartum (during labor) antibiotic prophylaxis (prevention) of pregnant mothers to decrease chance of early-onset meningitis by Streptococcus agalactiae. For late-onset meningitis, prevention is passed onto the caretakers to stop the spread of infectious microorganisms. Proper hygiene habits are first and foremost, while stopping improper antibiotic use; such as over-prescriptions, use of broad spectrum antibiotics, and extended dosing times will aid prevention of late-onset neonatal meningitis. A possible prevention may be vaccination of mothers against Streptococcus agalactiae and E. coli, however, this is still under development.

Viral
The only form of prevention from viral infection of the neonate is a Caesarean section form of delivery if the mother is showing symptoms of infection.

Treatment
Treatment for meningitis is antibiotics. The particular drugs used are based on culture results that identify the infecting bacteria, but a mix of ampicillin, gentamicin, and cefotaxime is used for early-onset meningitis before their identification. A regimen of antistaphylococcal antibiotic, such as nafcillin or vancomycin, plus cefotaxime or ceftazidime with or without an aminoglycoside is recommended for late-onset neonatal meningitis. The aim for these treatments is to sterilize the cerebrospinal fluid of all pathogens. A repeat spinal tap 24 to 48 hours after treatment has been started should be done to confirm sterilization.Limited evidence suggests that adjuvant corticosteroids may reduce the short-term risk of hearing loss in newborn infants with meningitis, but it is uncertain whether corticosteroids help to reduce the risk of death or longer-term hearing loss.

Group B Streptococci
For meningitis suspected to be caused by Streptococcus agalactiae, the following treatment is recommended by the American Academy of Pediatrics: doses of penicillin up to 450 000 U/kg daily (270 mg/kg/day) divided 8 hourly if <7 days of age and divided 6 hourly if >7 days of age. For penicillin [the recommended dose is up to 300 mg/kg/daily divided 8 hourly if <7 days of age or 4–6 hourly if >7 days of age </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 Presbycusis and explain in detail? [/INST] Presbycusis (also spelled presbyacusis, from Greek πρέσβυς presbys "old" + ἄκουσις akousis "hearing"), or age-related hearing loss, is the cumulative effect of aging on hearing. It is a progressive and irreversible bilateral symmetrical age-related sensorineural hearing loss resulting from degeneration of the cochlea or associated structures of the inner ear or auditory nerves. The hearing loss is most marked at higher frequencies. Hearing loss that accumulates with age but is caused by factors other than normal aging (nosocusis and sociocusis) is not presbycusis, although differentiating the individual effects of distinct causes of hearing loss can be difficult.
The cause of presbycusis is a combination of genetics, cumulative environmental exposures and pathophysiological changes related to aging. At present there are no preventive measures known; treatment is by hearing aid or surgical implant.
Presbycusis is the most common cause of hearing loss, affecting one out of three persons by age 65, and one out of two by age 75. Presbycusis is the second most common illness next to arthritis in aged people.
Many vertebrates such as fish, birds and amphibians do not experience presbycusis in old age as they are able to regenerate their cochlear sensory cells, whereas mammals including humans have genetically lost this regenerative ability.

Presentation
Primary symptoms:

sounds or speech becoming dull, muffled or attenuated
need for increased volume on television, radio, music and other audio sources
difficulty using the telephone
loss of directionality of sound
difficulty understanding speech, especially women and children
difficulty in speech discrimination against background noise (cocktail party effect)Secondary symptoms:

hyperacusis, heightened sensitivity to certain volumes and frequencies of sound, resulting from "recruitment"
tinnitus, ringing, buzzing, hissing or other sounds in the ear when no external sound is presentUsually occurs after age 50, but deterioration in hearing has been found to start very early, from about the age of 18 years. The ISO standard 7029 shows expected threshold changes due purely to age for carefully screened populations (i.e. excluding those with ear disease, noise exposure etc.), based on a meta-analysis of published data. Age affects high frequencies more than low, and men more than women. One early consequence is that even young adults may lose the ability to hear very high frequency tones above 15 or 16 kHz. Despite this, age-related hearing loss may only become noticeable later in life. The effects of age can be exacerbated by exposure to environmental noise, whether at work or in leisure time (shooting, music, etc.). This is noise-induced hearing loss (NIHL) and is distinct from presbycusis. A second exacerbating factor is exposure to ototoxic drugs and chemicals.
Over time, the detection of high-pitched sounds becomes more difficult, and speech perception is affected, particularly of sibilants and fricatives. Patients typically express a decreased ability to understand speech. Once the loss has progressed to the 2–4 kHz range, there is increased difficulty understanding consonants. Both ears tend to be affected. The impact of presbycusis on communication depends on both the severity of the condition and the communication partner.Older adults with presbycusis often exhibit associated symptoms of social isolation, depression, anxiety, frailty and cognitive decline.
The risk of having cognitive impairment increased 7 percent for every 10 dB of hearing loss at baseline. No effect of hearing aids was seen in the Lin Baltimore study.

Causes
The aging process has three distinct components: physiologic degeneration, extrinsic damage (nosocusis), and intrinsic damage (sociocusis). These factors are superimposed on a genetic substrate, and may be overshadowed by general age-related susceptibility to diseases and disorders.
Hearing loss is only weakly correlated with age. In preindustrial and non-industrial societies, persons retain their hearing into old age. In the Framingham cohort study, only 10% of the variability of hearing with age could be explained by age-related physiologic deterioration.  Within family groups, heredity factors were dominant; across family groups, other, presumably sociocusis and nosocusis factors were dominant.

Heredity: factors like early aging of the cochlea and susceptibility of the cochlea for drug insults are genetically determined.
Oxidative stress
General inflammatory conditions

Sociocusis
Sociocusis is the condition of those who have hearing loss attributed to continuous noise exposures, unrelated to their job or occupation. This exposure to these stimuli is frequent, and are often considered common "background noises" that affect the hearing abilities of individuals. Examples of sociocusis-related stimuli are the continuous noises from traffic, home appliances, music, television, and radio. The accumulated exposure to these noises over many years can lead to a condition similar to pure presbycusis.

Nosocusis
Nosocusis factors are those that can cause hearing loss, which are not noise-based and separate from pure presbycusis. They may include:
Ototoxic drugs: Ingestion of ototoxic drugs like aspirin may hasten the process of presbycusis.
vascular degeneration
Atherosclerosis: May diminish vascularity of the cochlea, thereby reducing its oxygen supply.
Dietary habits: Increased intake of saturated fat may accelerate atherosclerotic changes in old age.
Smoking: Is postulated to accentuate atherosclerotic changes in blood vessels aggravating presbycusis.
Diabetes: May cause vasculitis and endothelial proliferation in the blood vessels of the cochlea, thereby reducing its blood supply.
Hypertension: causes potent vascular changes, like reduction in blood supply to the cochlea, thereby aggravating presbycusis.However, a recent study found that diabetes, atherosclerosis and hypertension had no correlation to presbycusis, suggesting that these are nosocusis (acquired hearing loss) factors, not intrinsic factors.

Pathophysiology
Examples of microscopic changes seen in this condition are hair cell degeneration of the cochlea and giant stereociliary degeneration.
There are four pathological phenotypes of presbycusis:

Sensory: characterised by degeneration of the organ of Corti, the sensory organ for hearing. Located within the scala media, it contains hair cells with stereocilia, which extend to the tectorial membrane. The organs outer hair cells play a significant role in the amplification of sound and is extremely sensitive to external and internal factors. If the outer hair cells are damaged, they do not regenerate. This results in a loss of sensitivity of hearing, as well as an abnormal perceived loudness in the aspect of the tonotopic spectrum that the damaged cells serve.
Neural: characterised by degeneration of cells of the spiral ganglion.
Strial/metabolic: characterised by atrophy of stria vascularis in all turns of cochlea. Located in the lateral wall of the cochlea, the stria vascularis contains sodium-potassium-ATPase pumps that are responsible for producing the endolymph resting potential. As individuals age, a loss of capillaries leads to the endolymphatic potential becoming harder to maintain, which brings a decrease in cochlear potential.
Cochlear conductive: due to stiffening of the basilar membrane thus affecting its movement.  This type of pathology has not been verified as contributing to presbycusis.In addition there are two other types:

Mixed
IndeterminateThe shape of the audiogram categorizes abrupt high-frequency loss (sensory phenotype) or flat loss (strial phenotype).
The mainstay of SNHL is strial, with only about 5% of cases being sensory. This type of presbycusis is manifested by a low-frequency hearing loss, with unimpaired speech recognition.
Classically, audiograms in neural presbycusis show a moderate downward slope into higher frequencies with a gradual worsening over time. A severe loss in speech discrimination is often described, out of proportion to the threshold loss, making amplification difficult due to poor comprehension.
The audiogram associated with sensory presbycusis is thought to show a sharply sloping high-frequency loss extending beyond the speech frequency range, and clinical evaluation reveals a slow, symmetric, and bilateral progression of hearing loss.

Diagnosis
Hearing loss is classified as mild, moderate, severe or profound. Pure-tone audiometry for air conduction thresholds at 250, 500, 1000, 2000, 4000, 6000 and 8000 Hz is traditionally used to classify the degree of hearing loss in each ear.  Normal hearing thresholds are considered to be 25 dB sensitivity, though it has been proposed that this threshold is too high, and that 15 dB (about half as loud) is more typical.  Mild hearing loss is thresholds of 25–45 dB; moderate hearing loss is thresholds of 45–65 dB; severe hearing loss is thresholds of 65–85 dB; and profound hearing loss thresholds are greater than 85 dB.
Tinnitus occurring in only one ear should prompt the clinician to initiate further evaluation for other etiologies. In addition, the presence of a pulse-synchronous rushing sound may require additional imaging to exclude vascular disorders.

Otoscopy
An examination of the external ear canal and tympanic membrane performed by a medical doctor, otolaryngologist, or audiologist using an otoscope, a visual instrument inserted into the ear. This also allows some inspection of the middle ear through the translucent tympanic membrane.

Tympanometry
A test administered by a medical doctor, otolaryngologist or audiologist of the tympanic membrane and middle ear function using a tympanometer, an air-pressure/sound wave instrument inserted into the ear canal.  The result is a tympanogram showing ear canal volume, middle ear pressure and eardrum compliance. Normal middle ear function (Type A tympanogram) with a hearing loss may suggest presbycusis. Type B and Type C tympanograms indicate an abnormality inside the ear and therefore may have an additional effect on the hearing.

Laboratory studies
This may include a blood or other sera test for inflammatory markers such as those for autoinflammatory diseases.

Audiometry
A hearing test administered by a medical doctor, otolaryngologist (ENT) or audiologist including pure tone audiometry and speech recognition may be used to determine the extent and nature of hearing loss, and distinguish presbycusis from other kinds of hearing loss. Otoacoustic emissions and evoked response testing may be used to test for audio neuropathy. The diagnosis of a sensorineural pattern hearing loss is made through audiometry, which shows a significant hearing loss without the "air-bone gap" that is characteristic of conductive hearing disturbances. In other words, air conduction is equal to bone conduction. Persons with cochlear deficits fail otoacoustic emissions testing, while persons with 8th cranial nerve (vestibulocochlear nerve) deficits fail auditory brainstem response testing.

Presbycusis audiogram
Magnetic resonance imaging (MRI)
As part of differential diagnosis, an MRI scan may be done to check for vascular anomalies, tumors, and structural problems like enlarged mastoids. MRI and other types of scan cannot directly detect or measure age-related hearing loss.

Treatment
At present, presbycusis, being primarily sensorineural in nature, cannot be prevented, ameliorated or cured.  Treatment options fall into three categories: pharmacological, surgical and management.

There are no approved or recommended pharmaceutical treatments for presbycusis.

Cochlear implant
In cases of severe or profound hearing loss, a surgical cochlear implant is possible. This is an electronic device that replaces the cochlea of the inner ear.  Electrodes are typically inserted through the round window of the cochlea, into the fluid-filled scala tympani. They stimulate the peripheral axons of the primary auditory neurons, which then send information to the brain via the auditory nerve. The cochlea is tonotopically mapped in a spiral fashion, with lower frequencies localizing at the apex of the cochlea, and high frequencies at the base of the cochlea, near the oval and round windows. With age, comes a loss in distinction of frequencies, especially higher ones. The electrodes of the implant are designed to stimulate the array of nerve fibers that previously responded to different frequencies accurately. Due to spatial constraints, the cochlear implant may not be inserted all the way into the cochlear apex. It provides a different kind of sound spectrum than natural hearing, but may enable the recipient to recognize speech and environmental sounds.

Middle ear implants
These are surgically implanted hearing aids inserted onto the middle ear. These aids work by directly vibrating the ossicles, and are cosmetically favorable due to their hidden nature.

Management
Hearing aids help improve hearing of many elderly.  Hearing aids can now be tuned to specific frequency ranges of hearing loss.
Aural rehabilitation for the affected person and their communication partners may reduce the impact on communication. Techniques such as squarely facing the affected person, enunciating, ensuring adequate light, minimizing noise in the environment, and using contextual cues are used to improve comprehension.

Research
Pharmaceuticals
Pharmacological treatment options are limited, and remain clinically unproven. Among these are the water-soluble coenzyme Q10 formulation, the prescription drug Tanakan, and combination antioxidant therapy.

In a study performed in 2010, it was found that the water-soluble formulation of coenzyme Q10 (CoQ10) caused a significant improvement in liminar tonal audiometry of the air and bone thresholds at 1000 Hz, 2000 Hz, 4000 Hz, and 8000 Hz.
Antioxidant therapy – age-related hearing loss was reduced in animal models with a combination agent comprising six antioxidant agents that target four sites within the oxidative pathway: L-cysteine-glutathione mixed disulfide, ribose-cysteine, NW-nitro-L-arginine methyl ester, vitamin B12, folate, and ascorbic acid. It is thought that these supplements attenuate the decline of cochlear structure due to prolonged oxidative stress. However, more recent studies have had conflicting results. In 2012, a study was done with CBA/J female mice. They were placed on an antioxidant-rich diet for 24 months consisting of vitamins A, C, E, L-carnitine, and α-lipoic acid. While this increased the inner ears antioxidant capacity, the actual hearing loss was unaffected. Therefore, in this study, antioxidants were shown not to improve presbycusis mechanisms.
The effects of the pharmaceutical drug Tanakan were observed when treating tympanophonia in elderly women. Tanakan was found to decrease the intensity of tympanitis and improve speech and hearing in aged patients, giving rise to the idea of recommending treatment with it to elderly patients with presbycusis or normal tonal hearing.
AM-111, an otoprotective peptide, was shown in a chinchilla study to rescue and protect against hearing loss following impulse noise trauma. AM-111 acts as a cell-permeable inhibitor of JNK-mediated apoptosis. IP injections or local injections into membrane of the round window were given, and permanent threshold shifts (PTS) were measured three weeks after impulse noise exposure. AM-111 animals had significantly lower PTS, implicating AM-111 as a possible protective agent against JNK-mediated cochlear cell death and against permanent hearing deficits after noise trauma.
The anti-inflammatory, anti-oxidant substance Ebselen was observed to reduce hearing loss in a study done in 2007. It has been previously shown that noise trauma correlates with decreases in glutathione peroxidase (GPx) activity, which has been linked to loss of the outer hair cells. GPx1, an isoform of GPx, is predominantly expressed in stria vascularis, cochlea, spiral ligament, organ of Corti, and spiral ganglion cells. The stria vascularis displayed significant decreases in GPx1 immunoreactivity and increased swelling following noise exposure in rats. There was also significant outer hair cell loss in the cochlea within five hours of noise exposure. Administration of Ebselen before and after the noise stimulus reduced stria vascularis swelling as well as cochlear outer hair cell loss. This implicates Ebselen as a supplement for GPx1 in the outer hair cell degradation mechanism of hearing loss. This treatment is currently in active clinical trials.
A γ-secretase inhibitor of Notch signaling was shown to induce new hair cells and partially recover hearing loss. Auditory hair cell loss is permanent damage due to the inability of these cells to regenerate </s>