<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Danon disease and can you explain it in depth? [/INST] Danon disease (or glycogen storage disease Type IIb) is a metabolic disorder. Danon disease is an X-linked lysosomal and glycogen storage disorder associated with hypertrophic cardiomyopathy, skeletal muscle weakness, and intellectual disability. It is inherited in an X-linked dominant pattern.

Symptoms and signs
Males
In males the symptoms of Danon Disease are more severe. Features of Danon Disease in males are:
An early age of onset of muscle weakness and heart disease (onset in childhood or adolescence)
Some learning problems or intellectual disability can be present
Muscle weakness can be severe and can affect endurance and the ability to walk
Heart disease (cardiomyopathy) can be severe and can lead to a need for medications. It usually progress to heart failure, commonly complicated by atrial fibrillation and embolic strokes with severe neurological disability, leading to death unless heart transplant is performed.
Cardiac conduction abnormalities can occur. Wolff-Parkinson-White syndrome is a common conduction pattern in Danon disease.
Symptoms are usually gradually progressive
Some individuals may have visual disturbances, and/or retinal pigment abnormalities
Danon Disease is rare and unfamiliar to most physicians. It can be mistaken for other forms of heart disease and/or muscular dystrophies, including Pompe disease.Females
In females the symptoms of Danon Disease are less severe. Common symptoms of Danon Disease in females are:
A later age of onset of symptoms. Many females will not have obvious symptoms until late adolescence or even adulthood.
Learning problems and intellectual disability are usually absent.
Muscle weakness is often absent or subtle. Some females will tire easily with exercise
Cardiomyopathy is often absent in childhood. Some women will develop this in adulthood. Cardiomyopathy can be associated with atrial fibrillation and embolic strokes.
Cardiac conduction abnormalities can occur. Wolff-Parkinson-White syndrome is a common conduction pattern in Danon disease.
Symptoms in females progress more slowly than in males.
Some females may have visual disturbances, and/or retinal pigment abnormalities
Danon Disease is rare and unfamiliar to most physicians. The milder and more subtle symptoms in females can make it more difficult to diagnose females with Danon Disease

Causes
Although the genetic cause of Danon Disease is known, the mechanism of disease is not well understood. Danon disease involves a genetic defect (mutation) in a gene called LAMP2, which results in a change to the normal protein structure. While the function of the LAMP2 gene is not well understood, it is known that LAMP2 protein is primarily located in small structures within cells called lysosomes.

Genetics
It is associated with LAMP2. The status of this condition as a GSD has been disputed.

Diagnosis
Making a diagnosis for a genetic or rare disease can often be challenging. Healthcare professionals typically look at a persons medical history, symptoms, physical exam, and laboratory test results in order to make a diagnosis. The following resources provide information relating to diagnosis and testing for this condition </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Granulomatous prostatitis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Restrictive lung disease and can you explain it in depth? [/INST] Restrictive lung diseases  are a category of extrapulmonary, pleural, or parenchymal respiratory diseases that restrict lung expansion, resulting in a decreased lung volume, an increased work of breathing, and inadequate ventilation and/or oxygenation. Pulmonary function test demonstrates a decrease in the forced vital capacity.

Presentation
Due to the chronic nature of this disease, the leading symptom of restrictive lung disease is progressive exertional dyspnea.  For acute on chronic cases, shortness of breath, cough, and respiratory failure are some of the more common signs.

Causes
Restrictive lung diseases may be due to specific causes which can be intrinsic to the parenchyma of the lung, or extrinsic to it.

Intrinsic
Pneumoconiosis caused by long-term exposure to dusts, especially in mining. For example, Asbestosis.
Radiation fibrosis, usually from the radiation given for cancer treatment.
Certain drugs such as amiodarone, bleomycin and methotrexate.
As a consequence of another disease such as rheumatoid arthritis.
Hypersensitivity pneumonitis due to an allergic reaction to inhaled particles.
Acute respiratory distress syndrome (ARDS), a severe lung condition occurring in response to a critical illness or injury.
Infant respiratory distress syndrome due to a deficiency of surfactant in the lungs of a baby born prematurely.
TuberculosisMany cases of restrictive lung disease are idiopathic (have no known cause). Still, there is generally pulmonary fibrosis. Examples are:

Idiopathic pulmonary fibrosis
Idiopathic interstitial pneumonia, of which there are several types
Sarcoidosis
Eosinophilic pneumonia
Lymphangioleiomyomatosis
Pulmonary Langerhans cell histiocytosis
Pulmonary alveolar proteinosisConditions specifically affecting the interstitium are called interstitial lung diseases.

Extrinsic
Nonmuscular diseases of the upper thorax such as kyphosis, pectus carinatum and pectus excavatum.
Diseases restricting lower thoracic/abdominal volume (e.g. obesity, diaphragmatic hernia, or the presence of ascites).
Pleural thickening.

Pathophysiology
In normal respiratory function, the air flows in through the upper airway, down through the bronchi and into the lung parenchyma (the bronchioles down to the alveoli) where gas exchange of carbon dioxide and oxygen occurs </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Urolagnia and can you explain it in depth? [/INST] Urolagnia (also urophilia, and, more colloquially, a golden shower or watersports) associates sexual excitement with the sight or thought of urine or urination, and may also refer to such behaviours or acts. It is a paraphilia.The term has origins in the Greek language (from ouron, "urine", and lagneia, "lust").Golden shower is slang for the practice of urinating on another person for sexual pleasure.

Overview
Urolagnia is an inclination to derive sexual satisfaction from the vision or idea of urination. It is a paraphilia. During the activity, urine may be consumed or the person may bathe in it. Other variations include arousal from wetting or seeing someone else urinate in their pants or underclothes, or wetting the bed. Other forms of urolagnia may involve a tendency to be sexually aroused by smelling urine-soaked clothing or body parts. In many cases, a strong correlation or conditioning arises between urine smell or sight, and the sexual act. For some individuals the phenomenon may include a diaper fetish and/or arousal from infantilism.
Urolagnia is sometimes associated with, or confused with the Japanese practice of omorashi, arousal from having a full bladder or a sexual attraction to someone else experiencing the discomfort or pain of a full bladder, possibly a sadomasochistic inclination.

Common variations
Golden shower: A shower or stream of urine is directed onto another person or persons.
Clothes wetting: The person is sexually aroused by wetting ones clothing or observing another person doing so. Usually that person prefers to stage the wetting so that his/her legs (or other body parts) become soaked with urine. The warm sensation felt when urine trickles on the body seems to give very relaxing and pleasurable feelings to the person. In many cases, that person is also aroused by smelling body parts that have a urine scent. Others get aroused by telling some people about when they lost control and wet themselves. Some prefer a particular type of clothing to urinate.
Exhibitionism: Becoming noticeably desperate or wetting oneself with the express purpose of being seen by strangers. Practitioners have described going to public places such as a mall or a park. Some intend to create situations where others can see their wet clothing.
Human urinal: Within the BDSM community, some individuals desire to be used as a human urinal and some desire to use a human urinal.  The submissive  is usually strictly forbidden from placing their lips directly on the body of the dominant so the practice routinely involves them receiving much of the spray all over their face, hair and body; however, another way of doing this that applies mostly to male dominants, is to place the mouth on the head of the penis and drink the urine as it is released. One other, less common variation of this kink involves the dominant partner urinating inside the submissive partners vagina or anus, which is usually followed up by the submissive partner ejecting the urine from their orifice(s).
Omorashi: The act of holding ones own urine until the need to urinate is urgent, making another hold in their urine, or watching another person with an urgent need to urinate. This fetish sometimes originates from childhood memories of needing, or of seeing another needing, to urinate. Arousal may be triggered by seeing the body movements or facial expressions of that person. It can also be heightened by the person saying that they have to urinate. The arousal from being desperate comes from the sensation of having a full bladder.
Voyeurism: Seeing another urinate without the persons knowledge either through video taping by a hidden camera, or by lurking in locations where people are urinating or are likely to have an urge to urinate.

Frequency
Jennifer Eve Rehor of San Francisco State University points out that such data as exists on what she calls "unconventional" or "kink" sexual behavior is generally problematic because of the way that it has been collected, through criminal and clinical case studies. Behavior that appears neither in criminal trials nor in clinical studies (for example, because the individuals concerned do not commonly seek professional help) is therefore under-reported. Rehor therefore surveyed 1,764 female participants in "kink" behavior (mostly association with BDSM) in 2010–11, receiving 1,580 valid responses </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Uterine hypoplasia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Nasal concha and can you explain it in depth? [/INST] In anatomy, a nasal concha (), plural conchae (), also called a nasal turbinate or turbinal, is a long, narrow, curled shelf of bone that protrudes into the breathing passage of the nose in humans and various animals. The conchae are shaped like an elongated seashell, which gave them their name (Latin concha from Greek κόγχη). A concha is any of the scrolled spongy bones of the nasal passages in vertebrates.In humans, the conchae divide the nasal airway into four groove-like air passages, and are responsible for forcing inhaled air to flow in a steady, regular pattern around the largest possible surface area of nasal mucosa. As a ciliated mucous membrane with shallow blood supply, the nasal mucosa cleans and warms the inhaled air in preparation for the lungs.
A rapidly dilating arteriolar circulation to these bones may lead to a sharp increase in the pressure within, in response to acute cooling of the body core. The pain from this pressure is often referred to as "brain freeze", and is frequently associated with the rapid consumption of ice cream. The shallowness of the venous blood supply of the mucosa contributes to the ease with which nosebleed can occur.

Structure
Conchae are composed of pseudostratified columnar, ciliated respiratory epithelium with a thick, vascular, and erectile glandular tissue layer. The conchae are located laterally in the nasal cavities, curling medially and downward into the nasal airway. Each pair is composed of one concha in either side of the nasal cavity, divided by the septum.The superior conchae are smaller structures, connected to the middle conchae by nerve-endings, and serve to protect the olfactory bulb.  The openings to the posterior ethmoidal sinuses exist under the superior meatus.The middle conchae are smaller. In humans, they are usually as long as the little finger. They project downwards over the openings of the maxillary and anterior and middle ethmoid sinuses, and act as buffers to protect the sinuses from coming in direct contact with pressurized nasal airflow. Most inhaled airflow travels between the inferior concha and the middle meatus.The inferior conchae are the largest, and can be as long as the index finger in humans, and are responsible for the majority of airflow direction, humidification, heating, and filtering of air inhaled through the nose.The inferior conchae are graded 1–4 based on the inferior concha classification system (known as the inferior turbinate classification system) in which the total amount of the airway space that the inferior concha takes up is estimated. Grade 1 is 0–25% of the airway, grade 2 is 26–50% of the airway, grade 3 is 51–75% of the airway and grade 4 is 76–100% of the airway.There is sometimes a pair of supreme conchae superior to the superior conchae. When present, these usually take the form of a small crest.

Function
The conchae comprise most of the mucosal tissue of the nose and are required for functional respiration. They are enriched with airflow pressure and temperature-sensing nerve receptors (linked to the trigeminal nerve route, the fifth cranial nerve), allowing for tremendous erectile capabilities of nasal congestion and decongestion, in response to the weather conditions and changing needs of the body. In addition, the erectile tissue undergoes an often unnoticed cycle of partial congestion and decongestion called the nasal cycle. The flow of blood to the nasal mucosa in particular the venous plexus of the conchae is regulated by the pterygopalatine ganglion and heats or cools the air in the nose.
The nasopulmonary and nasothoracic reflexes regulate the mechanism of breathing through deepening of inhalation. Triggered by the flow of the air, the pressure of the air in the nose, and the quality of the air, impulses from the nasal mucosa are transmitted by the trigeminal nerve to the breathing centres in the brainstem, and the generated response is transmitted to the bronchi, the intercostal muscles, and the diaphragm.
The conchae are also responsible for filtration, heating, and humidification of air inhaled through the nose. Of these three, filtration is achieved mostly by other more effective means such as mucous and cilia. As air passes over the conchae, it is heated to 32–34 °C (89–93 °F), humidified (up to 98% water saturation) and filtered.

Immunological role
The respiratory epithelium that covers the erectile tissue (or lamina propria) of the conchae plays a major role in the bodys first line of immunological defense. The respiratory epithelium is partially composed of mucus-producing goblet cells. This secreted mucus covers the nasal cavities, and serves as a filter, by trapping air-borne particles larger than 2 to 3 micrometers. The respiratory epithelium also serves as a means of access for the lymphatic system, which protects the body from being infected by viruses or bacteria.

Smell
The conchae provide, first and foremost, the humidity needed to preserve the delicate olfactory epithelium, which in turn is needed to keep the olfactory receptors healthy and alert. If the epithelial layer gets dry or irritated, it may cease to function. This is usually a temporary condition but, over time, may lead to chronic anosmia. The turbinates also increase the surface area of the inside of the nose, and, by directing and deflecting airflow across the maximum mucosal surface of the inner nose, they are able to propel the inspired air. This, coupled with the humidity and filtration provided by the conchae, helps to carry more scent molecules towards the higher, and very narrow regions of the nasal airways, where olfaction nerve receptors are located.The superior conchae completely cover and protect the nerve axons piercing through the cribriform plate (a porous bone plate that separates the nose from the brain) into the nose. Some areas of the middle conchae are also innervated by the olfactory bulb. All three pairs of conchae are innervated by pain and temperature receptors, via the trigeminal nerve (or, the fifth cranial nerve). Research has shown that there is a strong connection between these nerve endings and activation of the olfactory receptors, but science has yet to fully explain this interaction.

Clinical significance
Dysfunction
Large, swollen conchae, often referred to clinically as turbinates, may lead to blockage of nasal breathing. Allergies, exposure to environmental irritants, or a persistent inflammation within the sinuses can lead to turbinate swelling. Deformity of the nasal septum can also result in enlarged turbinates.Treatment of the underlying allergy or irritant may reduce turbinate swelling. In cases that do not resolve, or for treatment of deviated septum, turbinate surgery may be required.

Surgery
Turbinectomy is a surgery for the reduction or removal of the turbinates. There are different techniques, including bipolar radiofrequency ablation, also known as somnoplasty;  reduction by the use of pure heat;  and turbinate sectioning.
In the case of sectioning, only small amounts of turbinate tissue are removed because the turbinates are essential for respiration. Risks of reduction of the inferior or middle turbinates include empty nose syndrome. Dr. Houser: "this is especially true in cases of anterior inferior turbinate (IT) resection because of its important role in the internal nasal valve."Concha bullosa is an abnormal pneumatization of the middle turbinate, which may interfere with normal ventilation of the sinus ostia and can result in recurrent sinusitis.

Other animals
Generally, in animals, nasal conchae are convoluted structures of thin bone or cartilage located in the nasal cavity. These are lined with mucous membranes that can perform two functions. They can improve the sense of smell by increasing the area available to absorb airborne chemicals, and they can warm and moisten inhaled air, and extract heat and moisture from exhaled air to prevent desiccation of the lungs. Olfactory turbinates are found in all living tetrapods, and respiratory turbinates are found in most mammals and birds.
Animals with respiratory turbinates can breathe faster without drying out their lungs, and consequently can have a faster metabolism. For example, when the emu exhales, its nasal turbinates condense moisture from the air and absorbs it for reuse. Dogs and other canids possess well-developed nasal turbinates. These turbinates allow for heat exchange between small arteries and veins on their maxilloturbinate (turbinates positioned on maxilla bone) surfaces in a counter-current heat-exchange system. Dogs are capable of prolonged chases, in contrast to the ambush predation of cats, and these complex turbinates play an important role in enabling this (cats only possess a much smaller and less-developed set of nasal turbinates). This same complex turbinate structure help conserve water in arid environments. The water conservation and thermoregulatory capabilities of these well-developed turbinates in dogs may have been crucial adaptations that allowed dogs (including both domestic dogs and their wild prehistoric gray wolf ancestors) to survive in the harsh Arctic environment and other cold areas of northern Eurasia and North America, which are both very dry and very cold.Reptiles and more primitive synapsids have olfactory turbinates that are involved in sensing smell rather than preventing desiccation.  While the maxilloturbinates of mammals are located in the path of airflow to collect moisture, sensory turbinates in both mammals and reptiles are positioned farther back and above the nasal passage, away from the flow of air. Glanosuchus has ridges positioned low in the nasal cavity, indicating that it had maxilloturbinates that were in the direct path of airflow. The maxilloturbinates may not have been preserved because they were either very thin or cartilaginous. The possibility has also been raised that these ridges are associated with an olfactory epithelium rather than turbinates. Nonetheless, the possible presence of maxilloturbinates suggests that Glanosuchus may have been able to rapidly breathe without drying out the nasal passage, and therefore could have been an endotherm.The bones of nasal turbinates are very fragile and seldom survive as fossils. In particular none have been found in fossil birds </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Left anterior fascicular block and can you explain it in depth? [/INST] Left anterior fascicular block (LAFB) is an abnormal condition of the left ventricle of the heart, related to, but distinguished from, left bundle branch block (LBBB).
It is caused by only the left anterior fascicle – one half of the left bundle branch being defective. It is manifested on the ECG by left axis deviation </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sudden arrhythmic death syndrome and can you explain it in depth? [/INST] Sudden arrhythmic death syndrome (SADS) is a sudden unexpected death of adolescents and adults, mainly during sleep. One relatively common type is known as Brugada syndrome.The syndrome is rare in most areas around the world but occurs in populations that are culturally and genetically distinct. It was first noted in 1977 among southeast Asian Hmong refugees in the United States and Canada. The syndrome was again noted in Singapore when a retrospective survey of records showed that 230 otherwise healthy Thai foreign workers living in Singapore died suddenly of unexplained causes between 1982 and 1990.

Causes
A sudden death in a young person can be caused by heart disease (including cardiomyopathy, congenital heart disease, myocarditis, genetic connective tissue disorders) or conduction disease (WPW syndrome, etc.), medication-related causes or other causes. Rare diseases called ion channelopathies may play a role such as long QT syndrome (LQTS), Brugada syndrome (BrS), CPVT (catecholaminergic polymorphic ventricular tachycardia), PCCD (progressive cardiac conduction defect), early repolarization syndrome, mixed sodium channel disease, and short QT syndrome. In 20% of cases, no cause of death can be found, even after extensive examination.In young people with type 1 diabetes, unexplained deaths could be attributed to night time hypoglycemia triggering abnormal heart rhythms or cardiac autonomic neuropathy, a damage to nerves that control the function of the heart.Medical examiners have taken into account various factors, such as nutrition, toxicology, heart disease, metabolism, and genetics. Although there is no real known definite cause, extensive research showed people 18 years or older were found to have had a hypertrophic cardiomyopathy, a condition in which the heart muscle becomes oddly thickened without any obvious cause. This was the most commonly identified abnormality in sudden death of young adults. In the instances where people experience sudden death, it is most commonly found that they had had CAD (coronary artery disease) or ASCAD (atherosclerotic coronary artery disease), or any level of stress. However, studies reveal that people experienced early symptoms within the week before the terminal event such as chest pain at ~52% of patients, dyspnea at ~22%, syncope at ~7% and ~19% who experienced no symptoms. Scientists have also associated this syndrome with the gene SCN5A that is mutated and affects the function of the heart. However, all autopsies done on those who had this syndrome came back negative.In the Philippines, bangungot (or in their term, sudden adult death syndrome) is mainly caused by the Brugada syndrome.

Diagnosis
Diagnosis occurs post-mortem.

Treatment
The only proven way to prevent SADS is with an implantable cardioverter-defibrillator. Oral beta-blockers such as propranolol are ineffective.

Epidemiology
In 1980, a reported pattern of sudden deaths was brought to the attention of the Centers for Disease Control. The first reported sudden death occurred in 1948 when there were 81 similar deaths of Filipino men in Oahu County, Hawaii. However, it did not become relevant because there was no associated pattern. This syndrome continued to become more significant as years went on. By 1981–1982, the annual rate in the United States was high with 92/100,000 among Laotians-Hmong, 82/100,000 among other Laotian ethnic groups, and 59/100,000 among Cambodians.In a 2008 study it was found that over half of SADS deaths could be attributed to inherited heart disease: unexplained premature sudden deaths in family, long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy and others.A national SADS study in England, funded by the British Heart Foundation, reported results in a 2007 journal article published in Health. The study surveyed 117 coroners jurisdictions in England. Researchers found that deaths from SADS reported by these coroners occurred "predominantly in young males". There were 500 cases a year in England, which is 8 times more than was previously estimated. Families are more at risk of SADS if they have a genetic cardiac disease. The study recommended that affected families should undergo "specialised cardiological evaluation".

Asia
Southeast Asian immigrants, who were mostly fleeing the Vietnam War, most often had this syndrome, marking Southeast Asia as the area containing the most people with this fatal syndrome. There are other Asian populations that were affected, such as Filipinos and Chinese Filipinos, Japanese in Japan, and natives of Guam in the United States and Guam. The immigrants with  this syndrome were about 33 years old and seemingly healthy, and all but one of the Laotian Hmong refugees were men. The condition appears to primarily affect young Hmong men from Laos (median age 33) and Northeastern Thailand (where the population is mainly of Laotian descent).

History
Laotian Hmongs were chosen for the study because they had one of the highest sudden death rates in the United States while sleeping. They were originally from Southern China and the highlands of North Vietnam, Laos, and Thailand. The location that was picked for this study was in Ban Vinai in the Loei Province, which is approximately 15 kilometers from the Lao border. This study took place between October 1982 and June 1983 as this syndrome became more of a pressing issue. Ban Vinai was the location chosen because it had 33,000 refugees in 1982, and the largest number of recorded SADS deaths. Because this syndrome was occurring most commonly in those particular men, researchers found it most beneficial and effective to study the populations they migrated from instead of studying victims and populations in the U.S. Because of local religious practices, the Hmong men in Ban Vinai did not receive autopsies. Therefore, the only results and research obtained were relating to deaths outside of the local religion or geographical area.An interview was arranged with the next of kin who lived with them, witnessed the death, or found the body. The interviews were open ended and allowed the person who was next of kin to describe what they witnessed and what preceding events they thought were relevant to the victims death. The interviewers also collected information such as illness history, the circumstances of the death, demographic background, and history of any sleep disturbances. A genealogy was then created which included all the relatives and their vital status and/or circumstances of death.

Society and culture
During the 1970s and 1980s, when an outbreak of this syndrome began, many Southeast Asians were not able to worship properly due to the Laotian Civil War. Hmong people believe that when they do not worship properly, do not perform religious rituals properly or forget to sacrifice, the ancestor spirits or the village spirits do not protect them, thus allowing evil spirit to reach them. These attacks induce a nightmare that leads to sleep paralysis, in which the victim is conscious and experiencing pressure on the chest. It is also common to have a REM state that is out of sequence, where there is a mix of brain states that are normally held separate. After the war, the United States government scattered the Hmong refugees across the U.S. in 53 different cities. Once these nightmare visitations began, a shaman was recommended for psychic protection from the spirits of their sleep. However, scattered across 53 different cities, these victims had no access to a shaman who could protect them.
Hmong people believed that rejecting the role of becoming a shaman, they are taken into the spirit world.The study author suggested that the Hmong who died were killed by their own beliefs in the spiritual world, otherwise known as Nocturnal pressing spirit attacks. In Indonesia it is called digeuton, which translates to "pressed on" in English </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Median raphe cyst and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Neurofibromatosis type II and can you explain it in depth? [/INST] Neurofibromatosis type II (also known as MISME syndrome – multiple inherited schwannomas, meningiomas, and ependymomas) is a genetic condition that may be inherited or may arise spontaneously, and causes benign tumors of the brain, spinal cord, and peripheral nerves. The types of tumors frequently associated with NF2 include vestibular schwannomas, meningiomas, and ependymomas. The main manifestation of the condition is the development of bilateral benign brain tumors in the nerve sheath of the cranial nerve VIII, which is the "auditory-vestibular nerve" that transmits sensory information from the inner ear to the brain. Besides, other benign brain and spinal tumors occur. Symptoms depend on the presence, localisation and growth of the tumor(s), in which multiple cranial nerves can be involved. Many people with this condition also experience vision problems. Neurofibromatosis type II (NF2 or NF II) is caused by mutations of the "Merlin" gene, which seems to influence the form and movement of cells. The principal treatments consist of neurosurgical removal of the tumors and surgical treatment of the eye lesions. Historically the underlying disorder has not had any therapy due to the cell function caused by the genetic mutation.

Classification
NF2 is an inheritable disorder with an autosomal dominant mode of transmission.There are two forms of the NF2:
The Wishart-phenotype form is characterized by multiple cerebral and spinal lesions in people younger than 20 years and with rapid progression of the tumours.
People with NF2 who develop single central tumours with slow progression after the age of 20 are thought to have the Feiling–Gardner phenotype.

Symptoms and signs
Symptoms can occur at any age, typically in adolescence and early adulthood, and rarely seen in children, and severity depend on the location of the tumors. Symptoms include but are not limited to:
Tinnitus
Loss/problems of balance
Glaucoma
Seizures
Hearing loss
Vision impairment
Numbness or weakness in arms and legs

Hearing loss
Because hearing loss in those with NF2 almost always occurs after acquisition of verbal language skills, people with NF2 do not always integrate well into Deaf culture and are more likely to resort to auditory assistive technology.
One of these devices is the cochlear implant, which can sometimes restore a high level of auditory function even when natural hearing is totally lost. However, the amount of destruction to the cochlear nerve caused by the typical NF2 schwannoma often precludes the use of such an implant. In these cases, an auditory brainstem implant (ABI) can restore some level of hearing, supplemented by lip reading.

Cause
NF2 is caused by inactivating mutations in the NF2 gene located at 22q12.2 of chromosome 22, type of mutations vary and include protein-truncating alterations (frameshift deletions/insertions and nonsense mutations), splice-site mutations, missense mutations and others. Deletions, too, in the NH2-terminal domain of merlin proteins have been associated with early tumor onset and poor prognosis in people with NF2. Protein truncating mutations correlate with more severe phenotype.  There is a broad clinical spectrum known, but all people with the condition who have been checked have been found to have some mutation of the same gene on chromosome 22. Through statistics, it is suspected that one-half of cases are inherited, and one-half are the result of new,  de novo mutations.

Cause loss of hearing
The hearing loss caused by NF2 is gradual and results from the presences of bilateral cochleovestibular schwannomas, also known as acoustic neuromas, which damage to cochlear nerve causing hearing loss. Hearing loss may also result from benign tumors that grow on the vestibular and auditory nerves, which lead to the inner ear.

Pathogenesis
NF2 is caused by a defect in the gene that normally gives rise to a product called Merlin or Schwannomin, located on chromosome 22 band q11-13.1. Merlin was first discovered as a structural protein functioning as an actin cytoskeleton regulator. Later merlins tumour suppressant role was described. Merlin regulates multiple proliferative signalling cascades such as receptor tyrosine kinase signalling, p21-activated kinase signalling, Ras signalling, MEK-ERK cascade, MST-YAP cascade. In a normal cell, the concentrations of active (dephosphorylated) merlin are controlled by processes such as cell adhesion (which would indicate the need to restrain cell division). It has been shown that Merlin inhibits Rac1 which is crucial for cell motility and tumour invasion. Also, merlins interaction with cyclin D was described. It is known that Merlins deficiency can result in unmediated progression through the cell cycle due to the lack of contact-mediated tumour suppression, mainly because of the cell:cell junction disruption, sufficient to result in the tumors characteristic of Neurofibromatosis type II. Recent studies showed that besides its cytoskeletal and cytoplasmic functions Merlin also translocates to the nucleus and suppresses proliferation by inhibiting E3 ubiquitin ligase CRL4(DCAF1). Finally, most recent studies indicated that Merlin also plays important role in energy metabolism regulation. Mutations of NF2 is presumed to result in either a failure to synthesize Merlin or the production of a defective peptide that lacks the normal tumor-suppressive effect. The Schwannomin-peptide consists of 595 amino acids. Comparison of Schwannomin with other proteins shows similarities to proteins that connect the cytoskeleton to the cell membrane. Mutations in the Schwannomin-gene are thought to alter the movement and shape of affected cells with loss of contact inhibition.
Ependymomas are tumors arising from the ependyma, an epithelium-like tissue of the central nervous system. In people with NF2 and ependymomas, the tumor suppressant function of Merlin may be compromised. Loss of function mutations occurring in chromosome 22q, where Merlin proteins are coded, can promote tumorigenesis, or the creation of new tumorous cells. Deletions, too, in the NH2-terminal domain of merlin proteins have been associated with early tumor onset and poor prognosis in affected people.

Pathology
The so-called acoustic neuroma of NF2 is in fact a schwannoma of the nervus vestibularis, or vestibular schwannoma. The misnomer of acoustic neuroma is still often used. The vestibular schwannomas grow slowly at the inner entrance of the internal auditory meatus (meatus acousticus internus). They derive from the nerve sheaths of the upper part of the nervus vestibularis in the region between the central and peripheral myelin (Obersteiner-Redlich-Zone) within the area of the porus acousticus, 1 cm from the brainstem.

Genotype–phenotype correlation
Many people with NF2 were included in studies that were designed to compare disease type and progression with exact determination of the associated mutation. The goal of such comparisons of genotype and phenotype is to determine whether specific mutations cause respective combinations of symptoms. This would be extremely valuable for the prediction of disease progression and the planning of therapy starting at a young age. The results of such studies are the following:
In most cases the mutation in the NF2 gene causes shortened peptides.
There are no mutational hot spots.
People with frameshift mutations or nonsense mutations have poor prognosis.
People with missense mutations have a better prognosis.
In cases with mutations in the splice-acceptor-region, there is no good correlation to determine.
Point mutations may have only minor effects.
Cases are published in which exactly the same mutation is associated with clearly different outcomes.These results suggest that other factors (environment, other mutations) will probably determine the clinical outcome.

Diagnosis
NF2 is a genetically transmitted condition. Diagnosis is most common in early adulthood (20–30 years); however, it can be diagnosed earlier. NF2 can be diagnosed due to the presence of a bilateral vestibular schwannoma, or an acoustic neuroma, which causes a hearing loss that may begin unilaterally. If a patient does not meet this criterion of diagnosis, they must have a family history of NF2, and present with a unilateral vestibular schwannoma and other associated tumors (cranial meningioma, cranial nerve schwannoma, spinal meningioma, spinal ependymomas, peripheral nerve tumor, spinal schwannoma, subcutaneous tumor, skin plaque). This being said, more than half of all patients diagnosed with NF2 do not have a family history of the condition. Although it has yet to be included into clinical classification, peripheral neuropathy, or damage to the peripheral nerves, which often causes weakness, numbness and pain in the hands and feet, may also lead to a diagnosis of NF2. In children, NF2 can present with similar symptoms, but generally causes "visual disturbances (cataracts, hamartomas), skin tumors, mononeuropathhy (facial paresis, drop foot), symptomatic spinal cord tumors, or non-vestibular intracranial tumors".

Prenatal
Bilateral vestibular schwannomas are diagnostic of NF2.

Postnatal
Ferner et al.  give three sets of diagnostic criteria for NF2:

Bilateral vestibular schwannoma (VS) or family history of NF2 plus Unilateral VS or any two of: meningioma, glioma, neurofibroma, schwannoma, posterior subcapsular lenticular opacities
Unilateral VS plus any two of meningioma, glioma, neurofibroma, schwannoma, posterior subcapsular lenticular opacities
Two or more meningioma plus unilateral VS or any two of glioma, schwannoma and cataract.Another set of diagnostic criteria is the following:
Detection of bilateral acoustic neuroma by imaging-procedures
First degree relative with NF2 and the occurrence of neurofibroma, meningiomas, glioma, or Schwannoma
First degree relative with NF2 and the occurrence of juvenile posterior subcapsular cataract.The criteria have varied over time.
The last revision of the NF2 criteria was done by M.J. Smith in 2017. This included the consideration of a LZTR1 mutation (schwannomatosis) instead of NF2 and excluded bilateral vestibular schwannomas that occur after 70 years of age.

Treatment
Surgery
There are several different surgical techniques for the removal of acoustic neuroma. The choice of approach is determined by size of the tumour, hearing capability, and general clinical condition of the person.

The retrosigmoid approach offers some opportunity for the retention of hearing.
The translabyrinthine approach will sacrifice hearing on that side, but will usually spare the facial nerve. Post-operative cerebrospinal fluid leaks are more common.
The middle fossa approach is preferred for small tumors and offers the highest probability of retention of hearing and vestibular function.
Less invasive endoscopic techniques have been done outside of the United States for some time. Recovery times are reported to be faster. However, this technique is not yet mainstream among surgeons in the US.Larger tumors can be treated by either the translabyrinthine approach or the retrosigmoid approach, depending upon the experience of the surgical team. With large tumors, the chance of hearing preservation is small with any approach. When hearing is already poor, the translabyrinthine approach may be used for even small tumors. Small, lateralized tumours in people with NF2 with good hearing should have the middle fossa approach. When the location of the tumour is more medial a retrosigmoid approach may be better.
Auditory canal decompression is another surgical technique that can prolong usable hearing when a vestibular schwannoma has grown too large to remove without damage to the cochlear nerve. In the IAC (internal auditory canal) decompression, a middle fossa approach is employed to expose the bony roof of the IAC without any attempt to remove the tumor. The bone overlying the acoustic nerve is removed, allowing the tumour to expand upward into the middle cranial fossa. In this way, pressure on the cochlear nerve is relieved, reducing the risk of further hearing loss from direct compression or obstruction of vascular supply to the nerve.
Radiosurgery is a conservative alternative to cranial base or other intracranial surgery. With conformal radiosurgical techniques, therapeutic radiation focused on the tumour, sparing exposure to surrounding normal tissues. Although radiosurgery can seldom completely destroy a tumor, it can often arrest its growth or reduce its size. While radiation is less immediately damaging than conventional surgery, it incurs a higher risk of subsequent malignant change in the irradiated tissues, and this risk is higher in NF2 than in sporadic (non-NF2) lesions.

Medications
There are no prescription medicines currently indicated for reduction in tumor burden for NF2 patients, although in patient studies Bevacizumab has resulted in reduction in tumor growth rates and hearing improvements in some patients.

Treatment hearing loss
As hearing loss in individuals with NF2 is generally gradual, eventually profound and sensorineural, the best options for treatment for hearing loss are cochlear implants and auditory brainstem implants (ABIs), as well as supplementing hearing with lip-reading, cued speech or sign language.

Cochlear Implants
A cochlear implant is an electronic device that is surgically implants to stimulate the cochlear nerve. Cochlear implants will work only when the cochleovestibular nerve (8th nerve) and the cochlea are still functioning. In a study done with open-set speech perception testing and closed-set speech perception testing by Neff et al., they discovered that the use of cochlear implants with NF2 patients allowed significant improvement of hearing abilities. In testing of recognition of sentences of everyday speech, five out of six patients scored within the 90–100% range, and in testing of hearing in noise setting, four of six of the patients scored within the 83–96%. Additionally, all testing was done without lip-reading.

Auditory Brainstem Implants (ABIs)
Auditory Brainsteam Implants, or ABIs, are used when the cochlea or any portion of the cochleovestibular nerve are not functioning due to damage to those areas or anatomic abnormalities. The procedure is done by implanting a device that send an electrical signal directly to the cochlear nucleus, allowing sound to bypass the peripheral auditory system and straight into the brain stem.

Prognosis
NF2 is a life limiting condition. It is a rare genetic disorder that involves noncancerous tumors of the nerves that transmit balance and sound impulses from the inner ear to the brain. The prognosis is affected by early age onset, a higher number of meningiomas and schwannomas and having a decrease in mutation.An early diagnosis is the best way to ensure improvement in management. Although, even with an early diagnosis, some patients still die very young.Meningiomas and schwannomas occur in around half of patients with NF2. Meningiomas are tumors that are both intracranial and intraspinal. Schwannomas are tumors that are often centered on the internal auditory canal. Patients with NF2 who have meningiomas have a higher risk of mortality, and the treatment can be very challenging. Individuals who develop schwannomas frequently develop hearing loss and deafness. These individuals may also develop tinnitus after being presented with unilateral hearing loss </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Somatization disorder and can you explain it in depth? [/INST] Somatization disorder is a mental and behavioral disorder characterized by recurring, multiple, and current, clinically significant complaints about somatic symptoms. It was recognized in the DSM-IV-TR classification system, but in the latest version DSM-5, it was combined with undifferentiated somatoform disorder to become somatic symptom disorder, a diagnosis which no longer requires a specific number of somatic symptoms. ICD-10, the latest version of the International Statistical Classification of Diseases and Related Health Problems, still includes somatization syndrome.

Criteria
DSM-5
In the DSM-5 the disorder has been renamed somatic symptom disorder (SSD), and includes SSD with predominantly somatic complaints (previously referred to as somatization disorder), and SSD with pain features (previously known as pain disorder).

DSM-IV-TR
The DSM-IV-TR diagnostic criteria are:
A history of somatic complaints over several years, starting prior to the age of 30.
Such symptoms cannot be fully explained by a general medical condition or substance use or, when there is an associated medical condition, the impairments due to the somatic symptoms are more severe than generally expected.
Complaints are not feigned as in malingering or factitious disorder.The symptoms do not all have to occur at the same time, but may occur over the course of the disorder. A somatization disorder itself is chronic but fluctuating that rarely remits completely. A thorough physical examination of the specified areas of complaint is critical for somatization disorder diagnosis. Medical examination would provide object evidence of subjective complaints of the individual.Diagnosis of somatization disorder is difficult because it is hard to determine to what degree psychological factors are exacerbating subjective feelings of pain. For instance, chronic pain is common in 30% of the U.S. population, making it difficult to determine whether or not the pain is due to predominantly psychological factors.

ICD-10
In ICD-10, the latest version of the International Statistical Classification of Diseases and Related Health Problems, somatization syndrome is described as:
"The main features are multiple, recurrent and frequently changing physical symptoms of at least two years duration. Most patients have a long and complicated history of contact with both primary and specialist medical care services, during which many negative investigations or fruitless exploratory operations may have been carried out. Symptoms may be referred to any part or system of the body. The course of the disorder is chronic and fluctuating, and is often associated with disruption of social, interpersonal, and family behaviour."
ICD-10 also includes the following subgroups of somatization syndrome:
Undifferentiated somatoform disorder.
Hypochondriasis.
Somatoform autonomic dysfunction.
Persistent somatoform pain disorder.
Other somatoform disorders, such ones predominated by dysmenorrhoea, dysphagia, pruritus and torticollis.
Somatoform disorder, unspecified.

Cause
Although somatization disorder has been studied and diagnosed for more than a century, there is debate and uncertainty regarding its pathophysiology. Most current explanations focus on the concept of a misconnection between the mind and the body. Genetics probably contributes a very small amount to development of the disorder.One of the oldest explanations for somatization disorder advances the theory that it is a result of the bodys attempt to cope with emotional and psychological stress. The theory states that the body has a finite capacity to cope with psychological, emotional, and social distress, and that beyond a certain point symptoms are experienced as physical, principally affecting the digestive, nervous, and reproductive systems. There are many different feedback systems where the mind affects the body; for instance, headaches are known to be associated with psychological factors, and stress and the hormone cortisol are known to have a negative impact on immune functions. This might explain why somatization disorders are more likely in people with irritable bowel syndrome, and why patients with SSD are more likely to have a mood or anxiety disorder. There is also a much increased incidence of SSD in people with a history of physical, emotional or sexual abuse.Another hypothesis for the cause of somatization disorder is that people with the disorder have heightened sensitivity to internal physical sensations and pain.  A biological sensitivity to somatic feelings could predispose a person to developing SSD. It is also possible that a persons body might develop increased sensitivity of nerves associated with pain and those responsible for pain perception, as a result of chronic exposure to stressors.Cognitive theories explain somatization disorder as arising from negative, distorted, and catastrophic thoughts and reinforcement of these cognitions. Catastrophic thinking could lead a person to believe that slight ailments, such as mild muscle pain or shortness of breath, are evidence of a serious illness such as cancer or a tumor. These thoughts can then be reinforced by supportive social connections. A spouse who responds more to his or her partners pain cues makes it more likely that he or she will express greater pain. Children of parents who are preoccupied or overly attentive to the somatic complaints of their children are more likely to develop somatic symptoms. Severe cognitive distortions can make a person with SSD limit the behaviors he or she engages in, and cause increased disability and impaired functioning.

Neuroimaging evidence
A recent review of the cognitive–affective neuroscience of somatization disorder suggested that catastrophization in patients with somatization disorders tends to present a greater vulnerability to pain </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Body dysmorphic disorder and can you explain it in depth? [/INST] Body dysmorphic disorder (BDD), occasionally still called dysmorphophobia, is a mental disorder characterized by the obsessive idea that some aspect of ones own body part or appearance is severely flawed and therefore warrants exceptional measures to hide or fix it.  In BDDs delusional variant, the flaw is imagined.  If the flaw is actual, its importance is severely exaggerated.  Either way, thoughts about it are pervasive and intrusive, and may occupy several hours a day, causing severe distress and impairing ones otherwise normal activities. BDD is classified as a somatoform disorder, and the DSM-5 categorizes BDD in the obsessive–compulsive spectrum, and distinguishes it from anorexia nervosa.
BDD is estimated to affect from 0.7% to 2.4% of the population. It usually starts during adolescence and affects both men and women. The BDD subtype muscle dysmorphia, perceiving the body as too small, affects mostly males.  Besides thinking about it, one repetitively checks and compares the perceived flaw, and can adopt unusual routines to avoid social contact that exposes it.  Fearing the stigma of vanity, one usually hides the preoccupation. Commonly unsuspected even by psychiatrists, BDD has been underdiagnosed. Severely impairing quality of life via educational and occupational dysfunction and social isolation, BDD has high rates of suicidal thoughts and attempts at suicide.

History
In 1886, Enrico Morselli reported a disorder that he termed dysmorphophobia, which described the disorder as a feeling of being ugly even though there does not appear to be anything wrong with the persons appearance.  In 1980, the American Psychiatric Association recognized the disorder, while categorizing it as an atypical somatoform disorder, in the third edition of its Diagnostic and Statistical Manual of Mental Disorders (DSM).  Classifying it as a distinct somatoform disorder, the DSM-IIIs 1987 revision switched the term to body dysmorphic disorder.Published in 1994, DSM-IV defines BDD as a preoccupation with an imagined or trivial defect in appearance, a preoccupation causing social or occupational dysfunction, and not better explained as another disorder, such as anorexia nervosa.  Published in 2013, the DSM-5 shifts BDD to a new category (obsessive–compulsive spectrum), adds operational criteria (such as repetitive behaviors or intrusive thoughts), and notes the subtype muscle dysmorphia (preoccupation that ones body is too small or insufficiently muscular or lean).The term "dysmorphic" is derived from the Greek word, dismorfia - meaning abnormal or apart, and morpho meaning shape. Morselli described people who felt a subjective feeling of ugliness as people who were tormented by a physical deficit. Sigmund Freud (1856-1939), the Austrian founder of psychoanalysis, once described his patients as a "Wolf Man," as he was experiencing classical symptoms of BDD. The person he was referring to was a wealthy Russian aristocrat named Sergei Pankejeff (1886-1979).

Signs and symptoms
Dislike of ones appearance is common, but individuals with BDD have extreme misperceptions about their physical appearance. Whereas vanity involves a quest to aggrandize the appearance, BDD is experienced as a quest to normalize the appearance merely.  Although delusional in about one of three cases, the appearance concern is usually non-delusional, an overvalued idea.The bodily area of focus can be nearly any and is commonly face, hair, and skin. In addition, multiple areas can be focused on simultaneously. A subtype of body dysmorphic disorder is bigorexia (anorexia reverse or muscle dysphoria). In muscular dysphoria, patients perceive their body as excessively thin despite being muscular and trained. Many seek dermatological treatment or cosmetic surgery, which typically does not resolve the distress.  On the other hand, attempts at self-treatment, as by skin picking, can create lesions where none previously existed.BDD is an obsessive-compulsive disorder but involves more depression and social avoidance despite DOC.  BDD often associates with social anxiety disorder.  Some experience delusions that others are covertly pointing out their flaws.  Cognitive testing and neuroimaging suggest both a bias toward detailed visual analysis and a tendency toward emotional hyper-arousal.Most generally, one experiencing BDD ruminates over the perceived bodily defect several hours daily or longer, uses either social avoidance or camouflaging with cosmetics or apparel, repetitively checks the appearance, compares it to that of other people, and might often seek verbal reassurances.  One might sometimes avoid mirrors, repetitively change outfits, groom excessively, or restrict eating.BDDs severity can wax and wane, and flareups tend to yield absences from school, work, or socializing, sometimes leading to protracted social isolation, with some becoming housebound for extended periods.  Social impairment is usually greatest, sometimes approaching avoidance of all social activities.  Poor concentration and motivation impair academic and occupational performance.  The distress of BDD tends to exceed that of either major depressive disorder or diabetes, and rates of suicidal ideation and attempts are especially high.

Causal factors
As with most mental disorders, BDDs cause is likely intricate, altogether biopsychosocial, through an interaction of multiple factors, including genetic, developmental, psychological, social, and cultural.  BDD usually develops during early adolescence, although many patients note earlier trauma, abuse, neglect, teasing, or bullying. In many cases, social anxiety earlier in life precedes BDD. Though twin studies on BDD are few, one estimated its heritability at 43%. Yet other factors may be introversion, negative body image, perfectionism, heightened aesthetic sensitivity, and childhood abuse and neglect.

Social media
Constant use of social media and "selfie taking" may translate into low self-esteem and body dysmorphic tendencies. The sociocultural theory of self-esteem states that the messages given by media and peers about the importance of appearance are internalized by individuals who adopt others standards of beauty as their own. Due to excessive social media use and selfie taking, individuals may become preoccupied about presenting an ideal photograph for the public. Specifically, females mental health has been the most affected by persistent exposure to social media. Girls with BDD present symptoms of low self-esteem and negative self-evaluation. Researchers in Istanbul Bilgi University and Bogazici University in Turkey found that individuals who have low self-esteem participate more often in trends of taking selfies along with using social media to mediate their interpersonal interaction in order to fulfill their self-esteem needs. The self-verification theory, explains how individuals use selfies to gain verification from others through likes and comments. Social media may therefore trigger ones misconception about their physical look. Similar to those with body dysmorphic tendencies, such behavior may lead to constant seeking of approval, self-evaluation and even depression.In 2019 systematic review using Web of Science, PsycINFO, and PubMed databases was used to identify social networking site patterns. In particular appearance focused social media use was found to be significantly associated with greater body image dissatisfaction. It is highlighted that comparisons appear between body image dissatisfaction and BDD symptomatology. They concluded that heavy social media use may mediate the onset of sub-threshold BDD.Individuals with BDD tend to engage in heavy plastic surgery use. In 2018, the term "Snapchat Dysmorphia" was brought to life after several plastic surgeons reported that some of their patients were seeking plastic surgeries to mimic "filtered" pictures. Filtered photos, such as those on Instagram and Snapchat, often present unrealistic and unattainable looks that may be a causal factor in triggering BDD.

A Socio-Cultural Perspective
Historically, Body Dysmorphic Disorder (BDD) was originally coined “Dysmorphophobia”, a term which was widely applied in research literature among the Japanese, Russians, and Europeans. However, in American literature, the appearance of BDD was still overlooked in the 1980’s. It was introduced in the DSM-III by the APA, and the diagnostic criteria was not properly defined, as the non-delusional and delusional factors were not separated. This was later resolved with the revision of the DSM-III, which aided many by providing appropriate treatment for patients. BDD was initially considered non-delusional in European research, and was grouped with ‘monosymptomatic hypochondriacal psychoses’ – delusional paranoia disorders, before being introduced in the DSM-III.
In 1991, the demographics of individuals who experience BDD were primarily single women aged 19 or older. This statistic has not changed over the decades, women are still considered the predominant gender to experience BDD. With the rise of social media platforms, individuals are easily able to seek validation and openly compare their physical appearance to online influences, finding more flaws and defects in their own appearance. This leads to attempts to conceal the defect such as seeking out surgeons to resolve the issue of ugliness.Universally, it is evident that different cultures place much emphasis on correcting the human body aesthetic, and that this preoccupation with body image is not exclusive to just one society; one example is the binding of women’s feet in Chinese culture.Whilst physically editing the body is not unique to any one culture, research suggests that it is more common throughout Western society and is on the rise.  On close observation of contemporary Western societies, there has been an increase in disorders such as Body dysmorphic disorder, arising from ideals around the aesthetic of the human body. Scholars such as Nancy Scheper-Hughes have suggested such demand placed upon Western bodies has been around since the beginning of the 19th century, and that it has been driven by sexuality. Research also shows that BDD is linked to high comorbidity and suicidality rates. Furthermore, it appears that Caucasian women show higher rates of body dissatisfaction than women of different ethnic backgrounds and societies.Socio-cultural models depict and emphasise the way thinness is valued, and beauty is obsessed over in Western culture, where advertising, marketing and social media play a large role in manicuring the ‘perfect’ body shape, size and look. The billions of dollars spent to sell products become causal factors of image conscious societies. Advertising also supports a specific ideal body image and creates a social capital in how individuals can acquire this ideal.However, personal attitudes towards the body do vary cross-culturally. Some of this variability can be accounted for due to factors such as food insecurity, poverty, climate, and fertility management. Cultural groups who experience food insecurity generally prefer larger-bodied women, however, many societies that have abundant access to food also value moderate to larger bodies. This is evident in a comparative study of body image, body perception, body satisfaction, body-related self-esteem and overall self-esteem of German, Guatemalan Q’eqchi’ and Colombian women. Unlike the German and Colombian women, the Q’eqchi’ women in this study live in the jungles of Guatemala and remain relatively removed from modern technology and secure food resources. The study found that the Q’eqchi’ women did not have notably higher body satisfaction when compared to the German or Colombian women.
Nevertheless, the Q’eqchi’ women also showed the greatest distortion in their own body perception, estimating their physique to be slimmer than it actually was. It is thought this could be due to a lack of access to body monitoring tools such as mirrors, scales, technology, and clothing choices, but in this instance, body distortion does not seem to influence body satisfaction. This has also been shown in groups of lower-income African American women, where the acceptance of larger bodies is not necessarily equivalent to positive body image.Similar studies have noted a high prevalence of BDD in East Asian societies, where facial dissatisfaction is especially common, indicating that this is not just a Western phenomenon.

Diagnosis
Estimates of prevalence and gender distribution have varied widely via discrepancies in diagnosis and reporting.  In American psychiatry, BDD gained diagnostic criteria in the DSM-IV, having been historically unrecognized, only making its first appearance in the DSM in 1987, but clinicians knowledge of it, especially among general practitioners, is constricted </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Guttate psoriasis and can you explain it in depth? [/INST] Guttate psoriasis (also known as eruptive psoriasis) is a type of psoriasis that presents as small (0.5–1.5 cm in diameter) lesions over the upper trunk and proximal extremities; it is found frequently in young adults.: 410 : 194 The term "guttate" is used to describe the drop-like appearance of skin lesions. Guttate psoriasis is classically triggered by a bacterial infection, usually an upper respiratory tract infection.: 726

Signs and symptoms
Typically, guttate psoriasis erupts after a throat infection, or strep throat. Initially, when the throat infection has cleared up, the person can feel fine for several weeks before noticing the appearance of red spots. They appear small at first, like a dry red spot which is slightly itchy. When scratched or picked, the top layer of dry skin is removed, leaving dry, red skin beneath with white, dry areas marking where flakes of dry skin stop and start. In the weeks that follow, the spots can grow to as much as an inch in diameter. Some of the larger ones may form a pale area in the center which is slightly yellow.
Guttate psoriasis can occur on any part of the body, particularly the legs, arms, torso, eyelids, back, bottom, bikini line, and neck. The number of lesions can range from 5 to over 100 </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Calcium deficiency and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Andermann syndrome and can you explain it in depth? [/INST] Andermann syndrome, also known as agenesis of corpus callosum with neuronopathy (ACCPN) and Charlevoix disease, among other names, is a very rare neurodegenerative genetic disorder that damages the nerves used to control muscles and related to sensation and is often associated with agenesis of the corpus collosum.It was first described by Eva Andermann et al. in 1972.

Symptoms and signs
Symptoms begin in infancy and include:
hypotonia
areflexia
amyotrophy
variable degrees of dysgenesis of the corpus callosum
mild to severe intellectual and developmental delay
psychiatric problems including paranoid delusions, depression, hallucinations and autistic-like behavior

Genetics
The inheritance pattern is autosomal recessive. Several genes have been associated with the disorder, including SLC12A6.

Neuropathology
Autopsy examination of 8 cases has shown both developmental and degenerative neuropathologic features in this disease, consistent with clinical duality as both a neurodevelopmental and neurodegenerative disorder.In the central nervous system, accompanying the hypotonia at birth is hypoplasia of the corticospinal tracts. Another developmental feature is seen in the corpus callosum, which varies from absent to hypoplastic. The anterior commissure is almost always absent, but occasionally hypoplastic </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Multiple endocrine neoplasia type 1 and can you explain it in depth? [/INST] Multiple endocrine neoplasia type 1 (MEN-1) is one of a group of disorders, the multiple endocrine neoplasias, that affect the endocrine system through development of neoplastic lesions in pituitary, parathyroid gland and pancreas.
It was first described by Paul Wermer in 1954.

Signs and symptoms
Parathyroid
Hyperparathyroidism is present in ≥ 90% of patients. Asymptomatic hypercalcemia is the most common manifestation: about 25% of patients have evidence of nephrolithiasis or nephrocalcinosis. In contrast to sporadic cases of hyperparathyroidism, diffuse hyperplasia or multiple adenomas are more common than solitary adenomas.

Pancreas
Pancreatic islet cell tumors are today the major cause of death in persons with MEN-1. Tumors occur in 60-80% of persons with MEN-1 and they are usually multicentric. Multiple adenomas or diffuse islet cell hyperplasia commonly occurs. About 30% of tumors are malignant and have local or distant metastases. About 10-15% of islet cell tumors originate from a β-cell, secrete insulin (insulinoma), and can cause fasting hypoglycemia. β-cell tumors are more common in patients < 40 years of age.
Most islet cell tumors secrete pancreatic polypeptide, the clinical significance of which is unknown. Gastrin is secreted by many non–β-cell tumors (increased gastrin secretion in MEN 1 also often originates from the duodenum). Increased gastrin secretion increases gastric acid, which may inactivate pancreatic lipase, leading to diarrhea and steatorrhea. Increased gastrin secretion also leads to peptic ulcers in > 50% of MEN 1 patients. Usually the ulcers are multiple or atypical in location, and often bleed, perforate, or become obstructed. Peptic ulcer disease may be intractable and complicated. Among patients presenting with Zollinger-Ellison syndrome, 20 to 60% have MEN 1.
A severe secretory diarrhea can develop and cause fluid and electrolyte depletion with non–β-cell tumors. This complex, referred to as the watery diarrhea, hypokalemia and achlorhydria syndrome (VIPoma) has been ascribed to vasoactive intestinal polypeptide, although other intestinal hormones or secretagogues (including prostaglandins) may contribute. Hypersecretion of glucagon, somatostatin, chromogranin, or calcitonin, ectopic secretion of ACTH resulting in Cushings syndrome, and hypersecretion of somatotropin–releasing hormone (causing acromegaly) sometimes occur in non–β-cell tumors. All of these are rare in MEN 1.Nonfunctioning pancreatic tumors also occur in patients with MEN 1 and may be the most common type of pancreatoduodenal tumor in MEN 1. The size of the nonfunctioning tumor correlates with risk of metastasis and death.

Pituitary
Pituitary tumors occur in 15 to 42% of MEN 1 patients. From 25 to 90% are prolactinomas. About 25% of pituitary tumors secrete growth hormone or growth hormone and prolactin. Excess prolactin may cause galactorrhea, and excess growth hormone causes acromegaly clinically indistinguishable from sporadically occurring acromegaly. About 3% of tumors secrete ACTH, producing Cushings disease. Most of the remainder are nonfunctional. Local tumor expansion may cause visual disturbance, headache, and hypopituitarism. Pituitary tumors in MEN 1 patients appear to be larger and behave more aggressively than sporadic pituitary tumors.

Other manifestations
Adenomas of adrenal glands occurs occasionally in MEN 1 patients. Hormone secretion is rarely altered as a result, and the significance of these abnormalities is uncertain. Carcinoid tumors, particularly those derived from the embryologic foregut (lungs, thymus), occur in isolated cases. Multiple subcutaneous and visceral lipomas, angiofibromas, and collagenomas may also occur.

Genetic
People with multiple endocrine neoplasia type 1 are born with one mutated copy of the MEN1 gene in each cell. Then, during their lifetime, the other copy of the gene is mutated in a small number of cells. These genetic changes result in no functional copies of the MEN1 gene in selected cells, allowing the cells to divide with little control and form tumors. This is known as Knudsons two-hit hypothesis and is a common feature seen with inherited defects in tumor suppressor genes. Oncogenes can become neoplastic with only one activating mutation, but tumor suppressors inherited from both mother and father must be damaged before they lose their effectiveness. The exception to the "two-hit hypothesis" occurs when suppressor genes exhibit dose-response, such as ATR. The exact function of MEN1 and the protein, menin, produced by this gene is not known, but following the inheritance rules of the "two-hit hypothesis" indicates that it acts as a tumor suppressor.

Diagnosis
In a diagnostic workup individuals with a combination of endocrine neoplasias suggestive of the MEN1 syndrome are recommended to have a mutational analysis of the MEN1 gene if additional diagnostic criteria are sufficiently met, mainly including:
age <40 years
positive family history
multifocal or recurrent neoplasia
two or more organ systems affected

Types
Multiple endocrine neoplasia or MEN is part of a group of disorders that affect the bodys network of hormone-producing glands (the endocrine system). Hormones are chemical messengers that travel through the bloodstream and regulate the function of cells and tissues throughout the body. Multiple endocrine neoplasia involves tumors in at least two endocrine glands; tumors can also develop in other organs and tissues. These growths can be noncancerous (benign) or cancerous (malignant). If the tumors become cancerous, some cases can be life-threatening.

The two major forms of multiple endocrine neoplasia are called type 1 and type 2. These two types are often confused because of their similar names. However, type 1 and type 2 are distinguished by the genes involved, the types of hormones made, and the characteristic signs and symptoms.
These disorders greatly increase the risk of developing multiple cancerous and noncancerous tumors in glands such as the parathyroid, pituitary, and pancreas. Multiple endocrine neoplasia occurs when tumors are found in at least two of the three main endocrine glands (parathyroid, pituitary, and pancreatico-duodenum). Tumors can also develop in organs and tissues other than endocrine glands. If the tumors become cancerous, some cases can be life-threatening. The disorder affects 1 in 30,000 people.
Although many different types of hormone-producing tumors are associated with multiple endocrine neoplasia, tumors of the parathyroid gland, pituitary gland, and pancreas are most frequent in multiple endocrine neoplasia type 1. MEN1-associated overactivity of these three endocrine organs are briefly described here:

Overactivity of the parathyroid gland (hyperparathyroidism) is the most common sign of this disorder. Hyperparathyroidism disrupts the normal balance of calcium in the blood, which can lead to kidney stones, thinning of the bones (osteoporosis), high blood pressure (hypertension), loss of appetite, nausea, weakness, fatigue, and depression.
Neoplasia in the pituitary gland can manifest as prolactinomas whereby too much prolactin is secreted, suppressing the release of gonadotropins, causing a decrease in sex hormones such as testosterone. Pituitary tumor in MEN1 can be large and cause signs by compressing adjacent tissues.
Pancreatic tumors associated with MEN-1 usually form in the beta cells of the islets of Langerhans, causing over-secretion of insulin, resulting in low blood glucose levels (hypoglycemia) </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Congenital hypoplastic anemia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Alternobaric vertigo and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Xeroderma and can you explain it in depth? [/INST] Xeroderma, xerosis or xerosis cutis, or simply dry skin, is a skin condition characterized by excessively dry skin.The medical term xeroderma, meaning "dry skin", derives from modern Latin, xero- dry + Greek derma skin.
In most cases, dry skin can safely be treated with emollients or moisturizers. Xeroderma occurs most commonly on the scalp, lower legs, arms, hands, the knuckles, the sides of the abdomen, and thighs. Symptoms most associated with xeroderma are such skin conditions as scaling (the visible peeling of the outer skin layer), itching, and skin fissures (cracked skin).

Causes
Xeroderma is a very common condition. It happens more often in the winter when the cold air outside and the hot air inside creates a low relative humidity. This causes the skin to lose moisture and it may crack and peel. Bathing or hand washing too frequently, especially if one is using harsh soaps, can contribute to xeroderma. Xeroderma can be caused by a deficiency of vitamin A, vitamin D, zinc, systemic illness, severe sunburn, or some medication </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is De Quervain syndrome and can you explain it in depth? [/INST] De Quervain syndrome is mucoid degeneration of two tendons that control movement of the thumb and their tendon sheath. This results in pain and tenderness on the thumb side of the wrist. Radial abduction of the thumb is painful. On occasion, there is uneven movement or triggering the thumb with radial abduction. Symptoms can come on gradually or be noted suddenly.There is speculation that the problem is related to use of the hand, but this is not supported by experimental evidence. Humans tend to misinterpret painful activities as causing the problem to get worse and this misinterpretation is associated with greater pain intensity. For this reason, its better not to blame activity without strong scientific support.
The diagnosis is generally based on symptoms and physical examination. Diagnosis is supported if pain increases when the wrist is bent inwards while a person is grabbing their thumb within a fist.There is some evidence that the natural history of de Quervain tendinopathy is resolution over a period of about 1 year. Symptomatic alleviation (palliative treatment) is provided mainly by splinting the thumb and wrist. Pain medications such as NSAIDs can also be considered. Steroid injections are commonly used, but are not proved to alter the natural history of the condition. Surgery to release the first dorsal component is an option. It may be most common in middle age.

Signs and symptoms
Symptoms are pain and tenderness at the radial side of the wrist, fullness or thickening over the thumb side of the wrist, and difficulty gripping with the affected side of the hand. The onset is often gradual. Pain is made worse by movement of the thumb and wrist, and may radiate to the thumb or the forearm.

Causes
The cause of de Quervains disease is not established. Evidence regarding a possible relation with activity and occupation is debated. A systematic review of potential risk factors discussed in the literature did not find any evidence of a causal relationship with activity or occupation. However, researchers in France found personal and work-related factors were associated with de Quervains disease in the working population; wrist bending and movements associated with the twisting or driving of screws were the most significant of the work-related factors. Proponents of the view that De Quervain syndrome is a repetitive strain injury consider postures where the thumb is held in abduction and extension to be predisposing factors. Workers who perform rapid repetitive activities involving pinching, grasping, pulling or pushing have been considered at increased risk. These movements are associated with many types of repetitive housework such as chopping vegetables, stirring and scrubbing pots, vacuuming, cleaning surfaces, drying dishes, pegging out washing, mending clothes, gardening, harvesting and weeding. Specific activities that have been postulated as potential risk factors include intensive computer mouse use, trackball use, and typing, as well as some pastimes, including bowling, golf, fly-fishing, piano-playing, sewing, and knitting.Women are diagnosed more often than men. The syndrome commonly occurs during and, even more so, after pregnancy. Contributory factors may include hormonal changes, fluid retention and—again, more debatably and potentially harmfully—increased housework and lifting.

Pathophysiology
De Quervain syndrome involves noninflammatory thickening of the tendons and the synovial sheaths that the tendons run through. The two tendons concerned are those of the extensor pollicis brevis and abductor pollicis longus muscles. These two muscles run side by side and function to bring the thumb away from the hand; the extensor pollicis brevis brings the thumb outwards radially, and the abductor pollicis longus brings the thumb forward away from the palm. De Quervain tendinopathy affects the tendons of these muscles as they pass from the forearm into the hand via a fibro-osseous tunnel (the first dorsal compartment).
Evaluation of histopathological specimens shows a thickening and myxoid degeneration consistent with a chronic degenerative process, as opposed to inflammation. The pathology is identical in de Quervain seen in new mothers.

Diagnosis
De Quervain syndrome is diagnosed clinically, based on history and physical examination, though diagnostic imaging such as X-ray may be used to rule out fracture, arthritis, or other causes, based on the persons history and presentation. The modified Eichoff maneuver, commonly called the Finkelsteins test, is a physical exam maneuver used to diagnose de Quervain syndrome. To perform the test, the examiner grasps and ulnar deviates the hand when the person has their thumb held within their fist. If sharp pain occurs along the distal radius (top of forearm, about an inch below the wrist), de Quervains syndrome is likely. While a positive Finkelsteins test is often considered pathognomonic for de Quervain syndrome, the maneuver can also cause pain in those with osteoarthritis at the base of the thumb.

Differential diagnosis
Differential diagnoses include:

Osteoarthritis of the trapezio-metacarpal joint
Intersection syndrome—pain will be more towards the middle of the back of the forearm and about 2–3 inches below the wrist, usually with associated crepitus.
Wartenbergs syndrome: The primary symptom is paresthesia (numbness/tingling).

Treatment
As with many musculoskeletal conditions, the management of de Quervains disease is determined more by convention than scientific data. A systematic review and meta-analysis published in 2013 found that corticosteroid injection seems to be an effective form of conservative management of de Quervains syndrome in approximately 50% of patients, although more research is needed regarding the extent of any clinical benefits. Efficacy data are relatively sparse and it is not clear whether benefits affect the overall natural history of the illness. One of the most common causes of corticosteroid injection failure are subcompartments of the extensor pollicis brevis tendon.Most tendinoses are self-limiting and the same is likely to be true of de Quervains although further study is needed.Palliative treatments include a splint that immobilized the wrist and the thumb to the interphalangeal joint and anti-inflammatory medication or acetaminophen. Systematic review and meta-analysis do not support the use of splinting over steroid injections.Surgery (in which the sheath of the first dorsal compartment is opened longitudinally) is documented to provide relief in most patients. The most important risk is to the radial sensory nerve. A small incision is made and the dorsal extensor retinaculum is identified. Once it has been identified the release is performed longitudinally along the tendon. This is done to prevent potential subluxation of the 1st compartment tendons </s>