<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 Torsion dystonia and can you explain it in depth? [/INST] Torsion dystonia, also known as dystonia musculorum deformans, is a disease characterized by painful muscle contractions resulting in uncontrollable distortions. This specific type of dystonia is frequently found in children, with symptoms starting around the ages of 11 or 12.  It commonly begins with contractions in one general area such as an arm or a leg that continue to progress throughout the rest of the body.  It takes roughly 5 years for the symptoms to completely progress to a debilitating state.

Causes
The disease is caused by a genetic disorder which results in a defect in a protein called Torsin A. A mutation in the DYT1 gene causes the loss of an amino acid, glutamic acid, in the Torsin A protein. Torsin A is an evolutionarily conserved AAA+ ATPase. The defective protein creates a disruption in communication in neurons that control muscle movement and muscle control.  This mutation is most usually inherited from a parent, but can occur sporadically. The disease is caused by a dominant allele, meaning that the person affected needs only one copy of the mutated DYT1 gene to have symptoms.  However, only 30 to 40 percent of those that do have the gene actually have symptoms, leading researchers to believe that there are other factors involved.

Diagnosis
Classification
There are several types of torsion dystonia that affect different areas of the body.  However, it is unknown if the gene that causes Early Onset Torsion Dystonia is responsible for the other dystonias as well.

Cervical dystonia (spasmodic torticollis): A type of dystonia that affects the head, neck and spine.  It can create problems by the characteristic turning of the head and neck from side to side.
Blepharospasm:  This type of dystonia causes involuntary contraction of the eyelids.  The main concern for this dystonia is that it can cause the eyelids to close involuntarily and for indefinite periods of time.
Oromandibular dystonia: A dystonia of the jaw, lips, and/or the tongue.  It can make eating and swallowing very complicated due to the jaw being held open or shut for periods of time.
Spasmodic dysphonia: A dystonia of the vocal cords.  The complications surrounding this form of dystonia are speech related and can cause symptoms such as speech that wavers, speech that sounds like a whisper, or speech that is hesitant.
Writers cramp (occupational dystonia): A dystonia that affects the muscles of the hand and  forearm.  It is triggered by attempting to write or execute other fine-motor hand functions.
Orofacial-Buccal dystonia (Meiges or Brueghals Syndrome): A combination of blepharospasm and oromandibular dystonia.
Early-onset torsion dystonia: The most severe type of  dystonia, it begins in an arm or leg and progresses to the rest of the body until the person — in most cases, a child — is reliant on a wheelchair.

Treatment
There is no cure for torsion dystonia.  However, there are several medical approaches that can be taken in order to lessen the symptoms of the disease.  The treatment must be patient specific, taking into consideration all of the previous and current health complications.  The doctor that creates the treatment must have intimate knowledge of the patients health and create a treatment plan that covers all of the symptoms focusing on the most chronic areas.
The first step for most with the disorder begins with some form of physical therapy in order for the patient to gain more control over the affected areas.  The therapy can help patients with their posture and gain control over the areas of their body that they have the most problems with.
The second step in the treatment process is medication.  The medications focus on the chemicals released by neurotransmitters in the nervous system, which control muscle movement.  The medications on the market today are anticholinergics, benzodiazepines, baclofen, dopaminergic agents/dopamine-depleting agents, and tetrabenazine.  Each medication is started on a low dosage and gradually increased to higher doses as the disease progresses and the side effects are known for the individual.
A more site-specific treatment is the injection of botulinum toxin.  It is injected directly into the muscle and works much the same way the oral medications do—by blocking neurotransmitters.  The injections are not a treatment for the disease, but are a means to control its symptoms.
A fourth option in the treatment for the symptoms of torsion dystonia is surgery.  Surgery is performed only if the patient does not respond to the oral medications or the injections.  The type of surgery performed is specific to the type of dystonia that the patient has. A systematic review found that some patients benefit from deep brain stimulation (DBS) surgery, but the studies may have been subject to financial bias.

Prevalence
The disease is more commonly found amongst Ashkenazi Jews.  The occurrence of torsion dystonia in the Ashkenazi Jewish population as stated by the Department of Epidemiology and Public Health of Yale University School of Medicine in New Haven, Connecticut; "Reports dating to the beginning of this century describe Ashkenazi Jewish (AJ) families with multiple cases of ITD either in siblings (Schwalbe 1908; Bernstein 1912; Abrahamson 1920) or in parents and offspring (Wechsler and Brock 1922; Mankowsky and Czerny 1929; Regensberg 1930). The first comprehensive evaluation of the mode of inheritance of ITD in Jewish and non-Jewish families was described by Zeman and Dyken (1967), who concluded that the disorder was inherited as an autosomal dominant with incomplete penetrance in both populations. Although they concluded that the gene frequency was higher in the AJ population than in non-Jews, no difference in mode of inheritance or disease mechanism was construed."

Research
A 1969 study of torsion dystonia patients found an average IQ 10 points higher than controls matched for age, sex and ethnic background.

References
Further reading
https://web.archive.org/web/20060903085219/http://www.biochem.arizona.edu/classes/bioc461/Biochem499/AngelaPulsifer/dystonia1.htm
Risch, N. J.; Bressman, S. B.; Deleon, D; Brin, M </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 Piblokto and can you explain it in depth? [/INST] Piblokto, also known as pibloktoq and Arctic hysteria, is a condition most commonly appearing in Inughuit (Northwest Greenlandic Inuit) societies living within the Arctic Circle. Piblokto is a culture-specific hysterical reaction in Inuit, especially women, who may perform irrational or dangerous acts, followed by amnesia for the event. Piblokto may be linked to repression of the personality of Inuit women. The condition appears most commonly in winter. It is considered to be a form of a culture-bound syndrome, although more recent studies (see Skepticism section) question whether it exists at all. Piblokto is also part of the glossary of cultural bound syndromes found in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).

History
Piblokto was first documented in 1892 and reports by European explorers describe the phenomenon as common to all Arctic regions. Explorers were the first to record piblokto in writing. Among these, Admiral Robert Peary provided a detailed look into the disorder during an expedition to Greenland. Peary and his men found the acts they witnessed among the Inuit women entertaining, and, having sent the womens male counterparts out on missions, became sexually involved with the remaining women. Piblokto is not limited to the indigenous people; reports of stranded sailors during the 1800s exhibiting the same symptoms have been found. The disorder is said to have existed before Western contact and still occurs today. However, as discussed below, many scholars now hold that culture bound disorders may often be an artifact of colonial encounters, and contemporary discussions of piblokto in medical anthropology and cross-cultural psychiatry consider it to be an example of the suspect nature of culture bound syndromes.

Origin
Piblokto is most often found in but not confined to the Inughuit culture in the polar regions of northern Greenland. Similar symptoms have been reported in European sailors stranded in Arctic regions in the 1800s. Among the Inughuit, the attacks are not considered out of the ordinary. No native theory of the disorder is currently reported. This condition is most often seen in Inughuit women. Piblokto is most common during long Arctic nights.

Symptoms
Piblokto is an abrupt dissociative episode with four phases: social withdrawal, excitement, convulsions and stupor, and recovery. In his book Handbook of Cultural Psychiatry, Wen-Shing Tseng provides the following example adapted from Foulks:
Mrs. A is a 30-year-old woman who has had periodic episodes of "strange experiences" in the past 3 years (since her mothers death). Three years ago, in the winter, during her first episode, she was acutely assaultive and tried to harm herself. The attack lasted about 15 min and she remembered nothing about it afterward. Two years ago, she had her second attack, which lasted about half an hour, during which time she ran from her home into the snow, tearing off her clothing.

Causes
Although there is no known cause for piblokto, Western scientists have attributed the disorder to the lack of sun, the extreme cold, and the desolate state of most villages in the region. A cause for this disorder present in this culture may be the isolation of their cultural group.This culture-bound syndrome is possibly linked to vitamin A toxicity (hypervitaminosis A). The native Inughuit diet or Eskimo nutrition provides rich sources of vitamin A through the ingestion of livers, kidneys, and fat of arctic fish and mammals and is possibly the cause or a causative factor. This causative factor is through the toxicity that has been reported for males, females, adults, children, and dogs. The ingestion of organ meats, particularly the livers of some Arctic mammals, such as the polar bear and bearded seal, in whom the vitamin is stored at levels toxic to humans, can be fatal to most people.
Inughuit tradition states that it is caused by evil spirits possessing the living. Shamanism and animism are dominant themes in Inughuit traditional beliefs with the angakkuq (healer) acting as a mediator with the supernatural forces. Angakkuit use trance states to communicate with spirits and carry out faith healing. There is a view among the Inughuit that individuals entering trance states should be treated with respect, given the possibility of a new "revelation" emerging as a result. Treatment in piblokto cases usually involves allowing the episode to run its course without interference. While piblokto can often be confused with other conditions (including epilepsy), in which failure to intervene can lead to the victim coming to harm, most cases tend to be benign.

Skepticism
Although piblokto has a place in the historical record and official medical canons, a number of Arctic researchers and Arctic residents doubt its existence. The phenomenon, they suggest, may be more rooted in the experience and behavior of the early European explorers than the Inuit themselves.In 1988 Parks Canada historian Lyle Dick began a substantial challenge to the concept that piblokto exists at all. Dick examined the original records of the European Arctic explorers, and ethnographic and linguistic reports on Inughuit societies, and discovered that not only is the majority of academic speculation into piblokto based on reports of only eight cases, but the word "piblokto" / "pibloktoq" does not exist within Inuktun (the Inughuit language); possibly, Dick concluded, this may have been the result of errors in phonetic transcription. In a 1995 paper published in the journal Arctic Anthropology, and in his 2001 book Muskox land: Ellesmere Island in the Age of Contact, Dick suggests that piblokto is a "phantom phenomenon", arising more from the Inuhuit reaction to European explorers in their midst.Similarly, Hughes and Simons have described piblokto as a "catch-all rubric under which explorers lumped various Inuhuit anxiety reactions, expressions of resistance to patriarchy or sexual coercion, and shamanistic practice". Simply put, rather than understanding piblokto as a strange cultural phenomenon, some critical scholars now understand it to be an expression of trauma of colonial violence, including rape. For example, transcultural psychiatry scholar Laurence Kirmayer writes:

Most comprehensive psychiatric texts mention pibloktoq as a culture-bound syndrome characterized by sudden wild and erratic behaviour. Recently, the historian Lyle Dick collected all the published accounts of pibloktoq, of which there are only about 25. It seems that psychiatric case description transformed a situation of sexual exploitation of Inuit women by explorers into a discrete disorder worthy of a new diagnostic label. With hindsight, we can see how insensitivity to the impact of exploration on other peoples distorted the picture when vital information on social context was not included. The legacy of these colonialist blinkers is still with us ...

See also
Wendigo
Cabin fever
Kayak angst
Prairie madness
Menerik (ru) (sometimes meryachenie) – a condition similar to piblokto found in Siberia among Yakuts, Yukagirs, and Evenks. Sidorov and Davydov draw a distinction between piblokto-like menerik and latah-like meryachenie. Others use meryachenie as an umbrella term for both piblokto-like and latah-like states.
Culture-bound syndrome

Notes
References
Further reading
Landy D (1985). "Pibloktoq (hysteria) and Inuit nutrition: possible implication of hypervitaminosis A". Soc Sci Med </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 Gastric lymphoma and can you explain it in depth? [/INST] Primary gastric lymphoma (lymphoma that originates in the stomach itself) is an uncommon condition, accounting for less than 15% of gastric malignancies and about 2% of all lymphomas.  However, the stomach is a very common extranodal site for lymphomas (lymphomas originate elsewhere and metastasise to the stomach). It is also the most common source of lymphomas in the gastrointestinal tract.

Signs and symptoms
Symptoms include epigastric pain, early satiety, fatigue and weight loss. Most people affected by primary gastric lymphoma are over 60 years old.

Risk factors
Risk factors for gastric lymphoma include the following:

Helicobacter pylori
Long-term immunosuppressant drug therapy
HIV infection

Pathophysiology
The majority of gastric lymphomas are non-Hodgkins lymphoma of B-cell origin.  These tumors may range from well-differentiated, superficial involvements (MALT) to high-grade, large-cell lymphomas. Sometimes, its hard to differentiate poorly differentiated high grade B-cell gastric lymphoma from gastric adenocarcinoma clinically or radiologically, yet histopathology with immunohistochemistry is recommended to stain specific markers on the malignant cell that favor the diagnosis of lymphoma. Immunohistochemistry stains specific clusters of differentiation that are present on B-cells like CD20. Cytokeratin is also a surface marker that is presented on epithelial cells, is stained histochemically and favors the diagnosis of epithelial tumors like adenocarcinoma.
Differentiating poor gastric lymphoma from adenocarcinoma is essential because the prognosis and modalities of treatment differ significantly.
Other lymphomas involving the stomach include mantle cell lymphoma and T-cell lymphomas which may be associated with enteropathy; the latter usually occur in the small bowel but have been reported in the stomach.

Diagnosis
These lymphomas are difficult to differentiate from gastric adenocarcinoma </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 Chronic 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 Telogen effluvium and can you explain it in depth? [/INST] Telogen effluvium is a scalp disorder characterized by the thinning or shedding of hair resulting from the early entry of hair in the telogen phase (the resting phase of the hair follicle). It is in this phase that telogen hairs begin to shed at an increased rate, where normally the approximate rate of hair loss (having no effect on ones appearance) is 125 hairs per day.There are 5 potential alterations in the hair cycle that could lead to this shedding: immediate anagen release, delayed anagen release, short anagen syndrome, immediate telogen release, and delayed telogen release.
Immediate anagen release occurs when follicles leave anagen and are stimulated to enter telogen prematurely </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 Ring chromosome 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 Schnitzler syndrome and can you explain it in depth? [/INST] Schnitzler syndrome or Schnitzlers syndrome is a rare disease characterised by onset around middle age of chronic hives (urticaria) and periodic fever, bone pain and joint pain (sometimes with joint inflammation), weight loss, malaise, fatigue, swollen lymph glands and enlarged spleen and liver.Schnitzler syndrome is considered an autoinflammatory disorder and is generally treated with anakinra, which inhibits interleukin 1.  This treatment controls the condition but does not cure it. Around 15% of people develop complications, but the condition generally does not shorten life.

Classification
Schnitzler syndrome is a late-onset autoinflammatory disorder.

Signs and symptoms
The typical onset is at around 55 years old, and the symptoms are recurrent hives, mostly on the torso and limbs, often with recurring fever, joint pain, bone pain, muscle pain, headache, fatigue, and loss of weight.

Cause
As of 2017 the cause of the disease was not understood.

Diagnosis
Blood tests show a high concentration of specific gamma-globulins (monoclonal gammopathy) of the IgM type. It almost always has light chains of the κ-type. A variant in which IgG is raised has been described, which appears to be one-tenth as common. The immunoglobulins may show up in the urine as Bence Jones proteins. Signs of inflammation are often present: these include an increased white blood cell count (leukocytosis) and a raised erythrocyte sedimentation rate and C-reactive protein </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 Apparent mineralocorticoid excess syndrome and can you explain it in depth? [/INST] Apparent mineralocorticoid excess is an autosomal recessive disorder causing hypertension (high blood pressure), hypernatremia (increased blood sodium concentration) and hypokalemia (decreased blood potassium concentration). It results from mutations in the HSD11B2 gene, which encodes the kidney isozyme of 11β-hydroxysteroid dehydrogenase type 2. In an unaffected individual, this isozyme inactivates circulating cortisol to the less active metabolite cortisone. The inactivating mutation leads to elevated local concentrations of cortisol in the aldosterone sensitive tissues like the kidney. Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor due to the non-selectivity of the receptor, leading to aldosterone-like effects in the kidney. This is what causes the hypokalemia, hypertension, and hypernatremia associated with the syndrome </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 Choriovitelline placenta 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 Nasopharyngeal carcinoma and can you explain it in depth? [/INST] Nasopharyngeal carcinoma (NPC), or nasopharynx cancer, is the most common cancer originating in the nasopharynx, most commonly in the postero-lateral nasopharynx or pharyngeal recess (fossa of Rosenmüller), accounting for 50% of cases. NPC occurs in children and adults.  NPC differs significantly from other cancers of the head and neck in its occurrence, causes, clinical behavior, and treatment. It is vastly more common in certain regions of East Asia and Africa than elsewhere, with viral, dietary and genetic factors implicated in its causation. It is most common in males. It is a squamous cell carcinoma of an undifferentiated type. Squamous epithelial cells are a flat type of cell found in the skin and the membranes that line some body cavities.  Undifferentiated cells are cells that do not have their mature features or functions.

Signs and symptoms
NPC may present as a lump or a mass on both sides towards the back of the neck. These lumps usually are not tender or painful but appear as a result of the metastatic spread of the cancer to the lymph nodes, thus causing the lymph nodes to swell. Lymph nodes are defined as glands that function as part of the immune system and can be found throughout the body. Swelling of the lymph nodes in the neck is the initial presentation in many people, and the diagnosis of NPC is often made by lymph node biopsy. Signs of nasopharyngeal cancer may appear as headaches, a sore throat, and trouble hearing, breathing, or speaking. Additional symptoms of NPC include facial pain or numbness, blurred or double vision, trouble opening the mouth, or recurring ear infections. If the ear infection does not present with an upper respiratory tract infection, then an examination should be done on the nasopharynx. This is due to the fact that, in adults, ear infections are less common than in children. Signs and symptoms related to the primary tumor include trismus, pain, otitis media, nasal regurgitation due to paresis (loss of or impaired movement) of the soft palate, hearing loss and cranial nerve palsy (paralysis). Larger growths may produce nasal obstruction or bleeding and a "nasal twang". Metastatic spread may result in bone pain or organ dysfunction. Rarely, a paraneoplastic syndrome of osteoarthropathy (diseases of joints and bones) may occur with widespread disease.

Causes
NPC is caused by a combination of factors: viral, environmental influences, and heredity.  The viral influence is associated with infection with Epstein–Barr virus (EBV). The Epstein-Barr virus is one of the most common viruses. 95% of all people in the U.S. are exposed to this virus by the time they are 30–40 years old.  The World Health Organization does not have set preventative measures for this virus because it is so easily spread and is worldwide.  Very rarely does Epstein-Barr virus lead to cancer, which suggests a variety of influencing factors.  Other likely causes include genetic susceptibility, consumption of food (in particular salted fish) containing carcinogenic volatile nitrosamines. Various mutations that activate NF-κB signalling have been reported in almost half of NPC cases investigated.The association between Epstein-Barr virus and nasopharyngeal carcinoma is unequivocal in World Health Organization (WHO) types II and III tumors but less well-established for WHO type I (WHO-I) NPC, where preliminary evaluation has suggested that human papillomavirus (HPV) may be associated. EBV DNA was detectable in the blood plasma samples of 96% of patients with non-keratinizing NPC, compared with only 7% in controls. The detection of nuclear antigen associated with Epstein-Barr virus (EBNA) and viral DNA in NPC type 2 and 3, has revealed that EBV can infect epithelial cells and is associated with their transformation. The cause of NPC (particularly the endemic form) seems to follow a multi-step process, in which EBV, ethnic background, and environmental carcinogens all seem to play an important role. More importantly, EBV DNA levels appear to correlate with treatment response and may predict disease recurrence, suggesting that they may be an independent indicator of prognosis. The mechanism by which EBV alters nasopharyngeal cells is being elucidated to provide a rational therapeutic target.It is also being investigated as to whether or not chronic sinusitis could be a potential cause of cancer of the nasopharynx. It is hypothesised that this may happen in a way similar to how chronic inflammatory conditions in other parts of the body, such as esophagitis sometimes leading to Barretts esophagus because of conditions such as gastroesophageal reflux disease.

Diagnosis
Classification
The World Health Organization (WHO) has identified three subtypes of nasopharyngeal carcinoma:
type 1: squamous cell carcinoma, typically found in older adults
type 2: non-keratinizing carcinoma
type 3: undifferentiated carcinomaType 3 is most commonly found among younger children and adolescents, with a few type 2 cases. Both type 2 and 3 have been found to be associated with elevated levels of Epstein-Barr virus titers, but not type 1. Additionally, type 2 and type 3 may be followed with an influx of inflammatory cells, including lymphocytes, plasma cells, and eosinophils, generating the term lymphoepithelioma.Nasopharyngeal carcinoma, also known as nasopharyngeal cancer, is classified as a malignant neoplasm, or cancer, arising from the mucosal epithelium of the nasopharynx, most often within the lateral nasopharyngeal recess or fossa of Rosenmüller (a recess behind the entrance of the eustachian tube opening). The World Health Organization classifies nasopharyngeal carcinoma in three types, in order of frequency: Non-keratinizing squamous cell carcinoma; keratinizing squamous cell carcinoma; and basaloid squamous cell carcinoma. The tumor must show evidence of squamous differentiation, with the non-keratinizing type (also known as lymphoepithelioma) the tumor most strongly associated with Epstein–Barr virus infection of the cancerous cells.

Staging
Staging of nasopharyngeal carcinoma is based on clinical and radiologic examination.  Most patients present with Stage III or IV disease.
Stage I is a small tumor confined to nasopharynx.
Stage II is a tumor extending in the local area, or that with any evidence of limited neck (nodal) disease.
Stage III is a large tumor with or without neck disease, or a tumor with bilateral neck disease.
Stage IV is a large tumor involving intracranial or infratemporal regions, an extensive neck disease, and/or any distant metastasis.

Risk factors
Nasopharyngeal carcinoma, classified as a squamous cell cancer, has not been linked to excessive use of tobacco. However, there are certain risk factors that can predispose an individual to NPC if exposed to them. These risk factors include: having Chinese, or Asian, ancestry, exposure to Epstein- Barr virus (EBV), unknown factors that result in rare familial clusters, and heavy alcohol consumption.

EBV
Epstein- Barr virus infects and persists in more than 90% of world population. Transmission of this virus occurs through saliva and is more commonly seen in developing countries where there are living areas are more packed together and less hygienic. Replication of this virus can occur in the oropharyngeal epithelial tissue and nasopharyngeal tissue. EBV primarily targets B lymphocytes. Patients diagnosed with NPC were found to show elevated levels of the antibodies against the EBV antigen than in individuals not diagnosed with NPC.

Smoking
Individuals that are exposed to cigarette smoking have an increased risk of developing NPC by 2- to 6-fold. Approximately two-thirds of patients with type 1 NPC was attributed to smoking in the United States. However the declining rates of smoking in the US can be associated with less prevalence of type 1 NPC. In southern China and North Africa, it has been suggested that high smoking rates come from wood fires in the country rather than cigarette smoking.

Treatment
NPC can be treated by surgery, by chemotherapy, or by radiotherapy. There are different forms of radiation therapy, including 3D conformal radiation therapy, intensity-modulated radiation therapy, particle beam therapy and brachytherapy, which are commonly used in the treatments of cancers of the head and neck. The expression of EBV latent proteins within undifferentiated nasopharyngeal carcinoma can be potentially exploited for immune-based therapies. Generally, there are three different types or treatment methods that can be used for patients with nasopharyngeal carcinoma. These three treatments are radiation therapy, chemotherapy, and surgery. Although there are currently three treatment methods, there are clinical trials taking place that may develop more effective treatments for NPC. A clinical trial is research study that works to develop new treatment techniques or to gain more information about or improve current methods. If an effective treatment comes out of the clinical trial, then this method may become a new standard treatment method. During the course of, or following, treatment, tests may be done in order to determine if the treatment is working, or if treatment needs to be dropped or changed. Tests that are done after treatment to determine the condition of patient after completing treatment are called follow-up tests and tell the doctor if the patients condition has changed or if the cancer has come back.

Radiation therapy
Radiation therapy uses high energy x-rays or other types of radiation aimed to prevent cancer cells from growing or kill them altogether. This kind of therapy can be administered to the patient externally or internally. With external radiation, a machine is used to send targeted radiation to the cancer site. A mesh mask is used on the patenting order to keep their head and neck still while the machine rotates to send out beams of radiation. In undergoing this kind of treatment, healthy cells may also be damaged during the process. Therefore, there are 2 other forms of radiation therapy that decreases the likelihood of damaging nearby healthy cells: intensity-modulated radiation therapy and stereotactic radiation therapy. Intensity-modulated radiation therapy (IMRT) uses 3D images of the size and shape of the tumor to then direct thin beams of radiation at different intensities from multiple angles. In stereotactic radiation therapy, radiation is aimed directly at the tumor. in this therapy, the total amount of radiation is divided into smaller does that will be given over the course of several days.Using radiation therapy as a cancer treatment method depends on the type and stage of cancer, however, internal and external radiation therapies can be used to treat NPC. If external radiation therapies are being aimed at the thyroid, then this could affect the way the thyroid works. For that reason, blood tests are done before and after radiation to check thyroid hormone levels.

Chemotherapy
Chemotherapy works as cancer treatment by using drugs that stop the growth of cancer cells, by either killing the cells or preventing them from dividing. This kind of therapy can be administered systemically or regionally. Systemic chemotherapy is when the chemotherapy is taken orally or is injected into a vein or muscle. In this method, the drug circulates through the blood system and can reach cancer cells throughout the body. Regional chemotherapy is when chemotherapy is administered directly into the cerebrospinal fluid, an organ, or a body cavity, for example, the abdomen. In this way, the drugs will mainly affect cancer cells in that area. However, the type of chemotherapy that is administered to the patient depends on the type and stage of the cancer. Additionally, chemotherapy can be used as an adjuvant therapy after radiation to lower the risk of recurrence in the patient. If given after radiation, chemotherapy can be used to kill any cancer cells that may have remained.

Surgery
Surgery can be used as a method to determine whether there is cancer present or to remove cancer from the body </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 Korsakoff syndrome and can you explain it in depth? [/INST] Korsakoff syndrome (KS) is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation. This neurological disorder is caused by a deficiency of thiamine (vitamin B1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. Korsakoff syndrome is often accompanied by Wernicke encephalopathy; this combination is called Wernicke–Korsakoff syndrome.Korsakoff syndrome is named after Sergei Korsakoff, the Russian neuropsychiatrist who described it during the late 19th century.

Signs and symptoms
There are seven major symptoms of Korsakoff syndrome, an amnestic-confabulatory syndrome:
anterograde amnesia, memory loss for events after the onset of the syndrome
retrograde amnesia, memory loss extends back for some time before the onset of the syndrome
amnesia of fixation, also known as fixation amnesia (loss of immediate memory, a person being unable to remember events of the past few minutes)
confabulation, that is, invented memories which are then taken as true, due to gaps in memory, with such gaps sometimes associated with blackouts
minimal content in conversation
lack of insight
apathy – interest in things is quickly lost, and there is an indifference to changeBenon R. and LeHuché R. (1920) described the characteristic signs of Korsakoff syndrome with some additional features including: confabulation (false memories), fixation amnesia, paragnosia or false recognition of places, mental excitation, and euphoria.Thiamine is essential for the decarboxylation of pyruvate, and deficiency during this metabolic process is thought to cause damage to the medial thalamus and mammillary bodies of the posterior hypothalamus, as well as generalized cerebral atrophy. These brain regions are all parts of the limbic system, which is heavily involved in emotion and memory.
KS involves neuronal loss, that is, damage to neurons; gliosis, which is a result of damage to supporting cells of the central nervous system, and bleeding also occurs in mammillary bodies. Damage to the medial dorsal nucleus or anterior nuclei of the thalamus (limbic-specific nuclei) is also associated with this disorder. Cortical dysfunction may have arisen from thiamine deficiency, alcohol neurotoxicity, and/or structural damage in the diencephalon.Originally, it was thought that a lack of initiative and a flat affect were important characteristics of emotional presentation in those affected. Studies have questioned this, proposing that neither is necessarily a symptom of KS. Research suggesting that people with Korsakoff syndrome are emotionally unimpaired has made this a controversial topic. It can be argued that apathy, which is a usual characteristic, reflects a deficit of emotional expressions, without affecting the experience or perception of emotion.KS causes deficits in declarative memory in most people, but leaves implicit spatial, verbal, and procedural memory functioning intact. People with KS have deficits in the processing of contextual information. Context memories refers to the where and when of experiences, and is an essential part of recollection. The ability to store and retrieve this information, such as spatial location or temporal order information, is impaired.
Research has also suggested that people with Korsakoff syndrome have impaired executive functions, which can lead to behavioral problems and interfere with daily activities. It is unclear, however, which executive functions are affected most. Nonetheless, IQ is usually not affected by the brain damage associated with Korsakoffs syndrome.At first it was thought that those with KS used confabulation to fill in memory gaps. However, it has been found that confabulation and amnesia do not necessarily co-occur. Studies have shown that there is dissociation between provoked confabulation, spontaneous confabulation (which is unprovoked), and false memories. That is, people affected could be led to believe certain things had happened which actually had not, but so could people without Korsakoff syndrome.

Causes
Conditions resulting in thiamine deficiency and its effects include chronic alcoholism and severe malnutrition. Alcoholism may co-occur with poor nutrition, which in addition to inflammation of the stomach lining, causes thiamine deficiency. Other causes include dietary deficiencies, prolonged vomiting, eating disorders, and the effects of chemotherapy. It can also occur in pregnant women who have a form of extreme morning sickness known as hyperemesis gravidarum. Mercury poisoning can also lead to Korsakoff syndrome.  Though it does not always co-occur, this disorder can emerge frequently as a consequential result of Wernickes encephalopathy.PET scans show that there is a decrease of glucose metabolism in the frontal, parietal and cingulated regions of the brain in those with Korsakoff syndrome. This may contribute to memory loss and amnesia. Structural neuroimaging has also shown the presence of midline diencephalic lesions and cortical atrophy.Structural lesions of the central nervous system, though rare, can also contribute to symptoms of KS. Severe damage to the medial dorsal nucleus inevitably results in memory deficit. Additionally, autopsies of people who had KS have showed lesions in both the midline and anterior thalamus, and thalamic infarctions. Bilateral infarctions to the thalamus can result in Korsakoff-induced amnesia as well. These findings imply damage to anterior thalamic nuclei can result in disruptive memory.

Risk factors
A number of factors may increase a persons risk to develop Korsakoff syndrome. These factors are often related to general health and diet.
Age
Alcoholism
Chemotherapy
Dialysis
Extreme dieting
Genetic factors

Diagnosis
KS is primarily a clinical diagnosis; imaging and lab tests are not necessary.

Prevention
The most effective method of preventing AKS is to avoid thiamine deficiency. In Western nations, the most common causes of such a deficiency are alcoholism and eating disorders. Because these are behavioral-induced causes, Korsakoff syndrome is essentially considered a preventable disease. Thus, fortifying foods with thiamine, or requiring companies that sell alcoholic beverages to supplement them with B vitamins in general or thiamine in particular, could avert many cases.

Treatment
It was once assumed that anyone with KS would eventually need full-time care. This is still often the case, but rehabilitation can help regain some, albeit often limited, level of independence. Treatment involves the replacement or supplementation of thiamine by intravenous or intramuscular injection, together with proper nutrition and hydration. However, the amnesia and brain damage caused by the disease does not always respond to thiamine replacement therapy </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 Nodular vasculitis 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 Plagiocephaly and can you explain it in depth? [/INST] Plagiocephaly, also known as flat head syndrome, is a condition characterized by an asymmetrical distortion (flattening of one side) of the skull. A mild and widespread form is characterized by a flat spot on the back or one side of the head caused by remaining in a supine position for prolonged periods.Plagiocephaly is a diagonal asymmetry across the head shape. Often it is a flattening which is to one side at the back of the head and there is often some facial asymmetry. Depending on whether synostosis is involved, plagiocephaly divides into two groups: synostotic, with one or more fused cranial sutures, and non-synostotic (deformational). Surgical treatment of these groups includes the deference method; however, the treatment of deformational plagiocephaly is controversial. Brachycephaly describes a very wide head shape with a flattening across the whole back of the head.

Causes
Slight plagiocephaly is routinely diagnosed at birth and may be the result of a restrictive intrauterine environment giving a "diamond" shaped head when seen from above. If there is premature union of skull bones, this is more properly called craniosynostosis.The incidence of plagiocephaly has increased dramatically since the advent of anti-sudden infant death syndrome recommendations for parents to keep their babies on their backs.Data also suggest that the rates of plagiocephaly are higher for twins and multiple births, premature babies, babies who were positioned in the breech position or back-to-back, as well as for babies born after a prolonged labour.

Diagnosis
A developmental and physical assessment performed by a physician or a pediatric specialist is recommended. Often imaging is obtained if the diagnosis is questionable to see if the babys sutures are present or not. If the sutures are not present, craniosynostosis may be ruled into question.It is also common for an infant with positional plagiocephaly to have misaligned ears (the ear on the affected side may be pulled forward and down and be larger or protrude more than the unaffected ear).

Prevention
Prevention methods include carrying the infant and giving the infant time to play on their stomach (tummy time), which may prevent the baby from progressing into moderate or severe plagiocephaly.Letting babies crawl may also prove to be crucial in preventing plagiocephaly as it strengthens babies spine and neck muscles. Crawling also boosts gross and fine motor skills (large and refined movements), balance, hand-eye-coordination and overall strength.In addition, specialized mattresses are available to prevent plagiocephaly. The design of these mattresses is characterized by an ergonomic design that reduces pressure on the babys head. It is very important that these mattresses are certified to guarantee their effectiveness.

Treatment
The condition may improve to some extent as the baby grows, but in some cases, home treatment or physical therapy treatment can improve the shape of a baby’s head.Early interventions (based on the severity) are of importance to reduce the severity of the degree of the plagiocephaly. Diagnosis is most commonly determined through clinical examination </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 Central core disease 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 Transient ischemic attack and can you explain it in depth? [/INST] A transient ischemic attack (TIA), commonly known as a mini-stroke, is a minor stroke whose noticeable symptoms usually end in less than an hour.  TIA causes the same symptoms associated with strokes, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, or confusion.
All forms of stroke, including TIA, result from a disruption in blood flow to the central nervous system.  A TIA is caused by a temporary disruption in blood flow to the brain, or cerebral blood flow (CBF).  The primary difference between a major stroke and the TIAs minor stroke is how much tissue death (infarction) can be detected afterwards through medical imaging. While a TIA must by definition be associated with symptoms, strokes can also be symptomatic or silent. In silent stroke, also known as silent cerebral infarct (SCI), there is permanent infarction detectable on imaging, but there are no immediately observable symptoms. The same person can have major strokes, minor strokes, and silent strokes, in any order.The occurrence of a TIA is a risk factor for having a major stroke, and many people with TIA have a major stroke within 48 hours of the TIA. All forms of stroke are associated with increased risk of death or disability. Recognition that a TIA has occurred is an opportunity to start treatment, including medications and lifestyle changes, to prevent future strokes.

Signs and symptoms
Signs and symptoms of TIA are widely variable and can mimic other neurologic conditions, making the clinical context and physical exam crucial in ruling in or out the diagnosis. The most common presenting symptoms of TIA are focal neurologic deficits, which can include, but are not limited to:
Amaurosis fugax (painless, temporary loss of vision)
One-sided facial droop
One-sided motor weakness
Diplopia (double vision)
Problems with balance and spatial orientation or dizziness
Visual field deficits, such as homonymous hemianopsia or monocular blindness
Sensory deficits in one or more limbs and of the face
Loss of ability to understand or express speech (aphasia)
Difficulty with articulation of speech (dysarthria)
Unsteady gait
Difficulties with swallowing (dysphagia)Numbness or weakness generally occur on the opposite side of the body from the affected hemisphere of the brain.
A detailed neurologic exam, including a thorough cranial nerve exam, is important to identify these findings and to differentiate them from mimickers of TIA. Symptoms such as unilateral weakness, amaurosis fugax, and double vision have higher odds of representing TIA compared to memory loss, headache, and blurred vision. Below is a table of symptoms at presentation, and what percentage of the time they are seen in TIAs versus conditions that mimic TIA. In general, focal deficits make TIA more likely, but the absence of focal findings do not exclude the diagnosis and further evaluation may be warranted if clinical suspicion for TIA is high (see "Diagnosis" section below).

TIA versus mimics
Non-focal symptoms such as amnesia, confusion, incoordination of limbs, unusual cortical visual symptoms (such as isolated bilateral blindness or bilateral positive visual phenomena), headaches and transient loss of consciousness are usually not associated with TIA, however patient assessment is still needed. Public awareness on the need to seek a medical assessment for these non-focal symptoms is also low, and can result in a delay by patients to seek treatmentSymptoms of TIAs can last on the order of minutes to one–two hours, but occasionally may last for a longer period of time. TIAs used to be defined as ischemic events in the brain that last less than 24 hours, but given the variation in duration of symptoms, this definition holds less significance. A pooled study of 808 patients with TIAs from 10 hospitals showed that 60% lasted less than one hour, 71% lasted less than two hours, and 14% lasted greater than six hours. Importantly, patients with symptoms that last more than one hour are more likely to have permanent neurologic damage, making prompt diagnosis and treatment important to maximize recovery.

Cause
The most common underlying pathology leading to TIA and stroke is a cardiac condition called atrial fibrillation, where poor coordination of contraction leads to a formation of a clot in the atrial chamber that can become dislodged and travel to a cerebral artery. Unlike in stroke, the blood flow can become restored prior to infarction which leads to the resolution of neurologic symptoms. Another common culprit of TIA is an atherosclerotic plaque located in the common carotid artery, typically by the bifurcation between the internal and external carotids, that becomes an embolism to the brain vasculature similar to the clot in the prior example. A portion of the plaque can become dislodged and lead to embolic pathology in the cerebral vessels.In-situ thrombosis, an obstruction that forms directly in the cerebral vasculature unlike the remote embolism previously mentioned, is another vascular occurrence with possible presentation as TIA. Also, carotid stenosis secondary to atherosclerosis narrowing the diameter of the lumen and thus limiting blood flow is another common cause of TIA. Individuals with carotid stenosis may present with TIA symptoms, thus labeled symptomatic, while others may not experience symptoms and be asymptomatic.

Risk factors
Risk factors associated with TIA are categorized as modifiable or non-modifiable. Non-modifiable risk factors include age greater than 55, sex, family history, genetics, and race/ethnicity. Modifiable risk factors include cigarette smoking, hypertension (elevated blood pressure), diabetes, hyperlipidemia, level of carotid artery stenosis (asymptomatic or symptomatic) and activity level. The modifiable risk factors are commonly targeted in treatment options to attempt to minimize risk of TIA and stroke.

Pathogenesis
There are three major mechanisms of ischemia in the brain: embolism traveling to the brain, in situ thrombotic occlusion in the intracranial vessels supplying the parenchyma of the brain, and stenosis of vessels leading to poor perfusion secondary to flow-limiting diameter. Globally, the vessel most commonly affected is the middle cerebral artery. Embolisms can originate from multiple parts of the body.
Common mechanisms of stroke and TIA:

Diagnosis
The initial clinical evaluation of a suspected TIA involves obtaining a history and physical exam (including a neurological exam). History taking includes defining the symptoms and looking for mimicking symptoms as described above. Bystanders can be very helpful in describing the symptoms and giving details about when they started and how long they lasted. The time course (onset, duration, and resolution), precipitating events, and risk factors are particularly important.
The definition, and therefore the diagnosis, has changed over time.  TIA was classically based on duration of neurological symptoms. The current widely accepted definition is called "tissue-based" because it is based on imaging, not time. The American Heart Association and the American Stroke Association (AHA/ASA) now define TIA as a brief episode of neurological dysfunction with a vascular cause, with clinical symptoms typically lasting less than one hour, and without evidence of significant infarction on imaging.

Laboratory workup
Laboratory tests should focus on ruling out metabolic conditions that may mimic TIA (e.g. hypoglycemia causing altered mental status), in addition to further evaluating a patients risk factors for ischemic events. All patients should receive a complete blood count with platelet count, blood glucose, basic metabolic panel, prothrombin time/international normalized ratio, and activated partial thromboplastin time as part of their initial workup. These tests help with screening for bleeding or hypercoagulable conditions. Other lab tests, such as a full hypercoagulable state workup or serum drug screening, should be considered based on the clinical situation and factors, such as age of the patient and family history. A fasting lipid panel is also appropriate to thoroughly evaluate the patients risk for atherosclerotic disease and ischemic events in the future. Other lab tests may be indicated based on the history and presentation; such as obtaining inflammatory markers (erythrocyte sedimentation rate and C-reactive protein) to evaluate for giant cell arteritis (which can mimic a TIA) in those presenting with headaches and monocular blindness.

Cardiac rhythm monitoring
An electrocardiogram is necessary to rule out abnormal heart rhythms, such as atrial fibrillation, that can predispose patients to clot formation and embolic events. Hospitalized patients should be placed on heart rhythm telemetry, which is a continuous form of monitoring that can detect abnormal heart rhythms. Prolonged heart rhythm monitoring (such as with a Holter monitor or implantable heart monitoring) can be considered to rule out arrhythmias like paroxysmal atrial fibrillation that may lead to clot formation and TIAs, however this should be considered if other causes of TIA have not been found.

Imaging
According to guidelines from the American Heart Association and American Stroke Association Stroke Council, patients with TIA should have head imaging "within 24 hours of symptom onset, preferably with magnetic resonance imaging, including diffusion sequences". MRI is a better imaging modality for TIA than computed tomography (CT), as it is better able to pick up both new and old ischemic lesions than CT. CT, however, is more widely available and can be used particularly to rule out intracranial hemorrhage. Diffusion sequences can help further localize the area of ischemia and can serve as prognostic indicators. Presence of ischemic lesions on diffusion weighted imaging has been correlated with a higher risk of stroke after a TIA.Vessels in the head and neck may also be evaluated to look for atherosclerotic lesions that may benefit from interventions, such as carotid endarterectomy. The vasculature can be evaluated through the following imaging modalities: magnetic resonance angiography (MRA), CT angiography (CTA), and carotid ultrasonography/transcranial doppler ultrasonography. Carotid ultrasonography is often used to screen for carotid artery stenosis, as it is more readily available, is noninvasive, and does not expose the person being evaluated to radiation. However, all of the above imaging methods have variable sensitivities and specificities, making it important to supplement one of the imaging methods with another to help confirm the diagnosis (for example: screen for the disease with ultrasonography, and confirm with CTA). Confirming a diagnosis of carotid artery stenosis is important because the treatment for this condition, carotid endarterectomy, can pose significant risk to the patient, including heart attacks and strokes after the procedure. For this reason, the U.S. Preventive Services Task Force (USPSTF) "recommends against screening for asymptomatic carotid artery stenosis in the general adult population". This recommendation is for asymptomatic patients, so it does not necessarily apply to patients with TIAs as these may in fact be a symptom of underlying carotid artery disease (see "Causes and Pathogenesis" above). Therefore, patients who have had a TIA may opt to have a discussion with their clinician about the risks and benefits of screening for carotid artery stenosis, including the risks of surgical treatment of this condition.
Cardiac imaging can be performed if head and neck imaging do not reveal a vascular cause for the patients TIA (such as atherosclerosis of the carotid artery or other major vessels of the head and neck). Echocardiography can be performed to identify patent foramen ovale (PFO), valvular stenosis, and atherosclerosis of the aortic arch that could be sources of clots causing TIAs, with transesophageal echocardiography being more sensitive than transthoracic echocardiography in identifying these lesions.

Differential diagnosis
Prevention
Although there is a lack of robust studies demonstrating the efficacy of lifestyle changes in preventing TIA, many medical professionals recommend them. These include:

Avoiding smoking
Cutting down on fats to help reduce the amount of plaque buildup
Eating a healthy diet including plenty of fruits and vegetables
Limiting sodium in the diet, thereby reducing blood pressure
Exercising regularly
Moderating intake of alcohol, stimulants, sympathomimetics, etc.
Maintaining a healthy weightIn addition, it is important to control any underlying medical conditions that may increase the risk of stroke or TIA, including:
Hypertension
High cholesterol
Diabetes mellitus
Atrial fibrillation

Treatment
By definition, TIAs are transient, self-resolving, and do not cause permanent impairment. However, they are associated with an increased risk of subsequent ischemic strokes, which can be permanently disabling. Therefore, management centers on the prevention of future ischemic strokes and addressing any modifiable risk factors. The optimal regimen depends on the underlying cause of the TIA.

Lifestyle modification
Lifestyle changes have not been shown to reduce the risk of stroke after TIA. While no studies have looked at the optimal diet for secondary prevention of stroke, some observational studies have shown that a Mediterranean diet can reduce stroke risk in patients without cerebrovascular disease. A Mediterranean diet is rich in fruits, vegetables and whole grains, and limited in red meats and sweets. Vitamin supplementation has not been found to be useful in secondary stroke prevention.

Antiplatelet medications
The antiplatelet medications, aspirin and clopidogrel, are both recommended for secondary prevention of stroke after high-risk TIAs. The clopidogrel can generally be stopped after 10 to 21 days. An exception is TIAs due to blood clots originating from the heart, in which case anticoagulants are generally recommended. After TIA or minor stroke, aspirin therapy has been shown to reduce the short-term risk of recurrent stroke by 60–70%, and the long-term risk of stroke by 13%.The typical therapy may include aspirin alone, a combination of aspirin plus extended-release dipyridamole, or clopidogrel alone. Clopidogrel and aspirin have similar efficacies and side effect profiles. Clopidogrel is more expensive and has a slightly decreased risk of GI bleed. Another antiplatelet, ticlopidine, is rarely used due to increased side effects.

Anticoagulant medications
Anticoagulants may be started if the TIA is thought to be attributable to atrial fibrillation. Atrial fibrillation is an abnormal heart rhythm that may cause the formation of blood clots that can travel to the brain, resulting in TIAs or ischemic strokes. Atrial fibrillation increases stroke risk by five times, and is thought to cause 10-12% of all ischemic strokes in the US. Anticoagulant therapy can decrease the relative risk of ischemic stroke in those with atrial fibrillation by 67% Warfarin is a common anticoagulant used, but direct acting oral anticoagulants (DOACs), such as apixaban, have been shown to be equally effective while also conferring a lower risk of bleeding. Generally, anticoagulants and antiplatelets are not used in combination, as they result in increased bleeding risk without a decrease in stroke risk. However, combined antiplatelet and anticoagulant therapy may be warranted if the patient has symptomatic coronary artery disease in addition to atrial fibrillation.
Sometimes, myocardial infarction ("heart attack") may lead to the formation of a blood clot in one of the chambers of the heart. If this is thought to be the cause of the TIA, people may be temporarily treated with warfarin or other anticoagulant to decrease the risk of future stroke.

Blood pressure control
Blood pressure control may be indicated after TIA to reduce the risk of ischemic stroke. About 70% of patients with recent ischemic stroke are found to have hypertension, defined as systolic blood pressure (SBP) > 140 mmHg, or diastolic blood pressure (DBP) > 90 mmHg. Until the first half of the 2010s, blood pressure goals have generally been SBP < 140 mmHg and DBP < 90 mmHg. However, newer studies suggest that a goal of SBP <130 mmHg may confer even greater benefit. Blood pressure control is often achieved using diuretics or a combination of diuretics and angiotensin converter enzyme inhibitors, although the optimal treatment regimen depends on the individual.Studies that evaluated the application of Blood pressure‐lowering drugs in people who had a TIA or stroke, concluded that this type of medication helps to reduce the possibility of a recurrent stroke, of a major vascular event and dementia. The effects achieved in stroke recurrence were mainly obtained through the ingestion of angiotensin-converting enzyme (ACE) inhibitor or a diuretic.

Cholesterol control
There is inconsistent evidence regarding the effect of LDL-cholesterol levels on stroke risk after TIA. Elevated cholesterol may increase ischemic stroke risk while decreasing the risk of hemorrhagic stroke. While its role in stroke prevention is currently unclear, statin therapy has been shown to reduce all-cause mortality and may be recommended after TIA.

Diabetes control
Diabetes mellitus increases the risk of ischemic stroke by 1.5-3.7 times, and may account for at least 8% of first ischemic strokes. While intensive glucose control can prevent certain complications of diabetes such as kidney damage and retinal damage, there has previously been little evidence that it decreases the risk of stroke or death. However, data from 2017 suggests that metformin, pioglitazone and semaglutide may reduce stroke risk.

Surgery
If the TIA affects an area that is supplied by the carotid arteries, a carotid ultrasound scan may demonstrate stenosis, or narrowing, of the carotid artery. For people with extra-cranial carotid stenosis, if 70-99% of the carotid artery is clogged, carotid endarterectomy can decrease the five-year risk of ischemic stroke by approximately half. For those with extra-cranial stenosis between 50 and 69%, carotid endarterectomy decreases the 5-year risk of ischemic stroke by about 16%. For those with extra-cranial stenosis less than 50%, carotid endarterectomy does not reduce stroke risk and may, in some cases, increase it. The effectiveness of carotid endarterectomy or carotid artery stenting in reducing stroke risk in people with intra-cranial carotid artery stenosis is currently unknown.In carotid endarterectomy, a surgeon makes an incision in the neck, opens up the carotid artery, and removes the plaque occluding the blood vessel. The artery may then be repaired by adding a graft from another vessel in the body, or a woven patch. In patients who undergo carotid endarterectomy after a TIA or minor stroke, the 30-day risk of death or stroke is 7%.Carotid artery stenting is a less invasive alternative to carotid endarterectomy for people with extra-cranial carotid artery stenosis. In this procedure, the surgeon makes a small cut in the groin and threads a small flexible tube, called a catheter, into the patients carotid artery. A balloon is inflated at the site of stenosis, opening up the clogged artery to allow for increased blood flow to the brain. To keep the vessel open, a small wire mesh coil, called a stent, may be inflated along with the balloon. The stent remains in place, and the balloon is removed.
For people with symptomatic carotid stenosis, carotid endarterectomy is associated with fewer perioperative deaths or strokes than carotid artery stenting. Following the procedure, there is no difference in effectiveness if you compare carotid endarterectomy and carotid stenting procedures, however, endarterectomy is often the procedure of choice as it is a safer procedure and is often effective in the longer term for preventing recurrent stroke. For people with asymptomatic carotid stenosis, the increased risk of stroke or death during the stenting procedure compared to an endarterectomy is less certain.People who undergo carotid endarterectomy or carotid artery stenting for stroke prevention are medically managed with antiplatelets, statins, and other interventions as well.

Prognosis
Without treatment, the risk of an ischemic stroke in the three months after a TIA is about 20% with the greatest risk occurring within two days of the TIA </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 Porokeratotic eccrine ostial and dermal duct nevus 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 Ureteritis 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 Colorado tick fever and can you explain it in depth? [/INST] Colorado tick fever (CTF) is a viral infection (Coltivirus) transmitted from the bite of an infected Rocky Mountain wood tick (Dermacentor andersoni). It should not be confused with the bacterial tick-borne infection, Rocky Mountain spotted fever. Colorado tick fever is probably the same disease that American pioneers referred to as "mountain fever".Colorado tick fever virus (CTFV) infects haemopoietic cells, particularly erythrocytes, which explains how the virus is transmitted by ticks and also accounts for the incidence of transmission by blood transfusion.

Signs and symptoms
First signs or symptoms can occur about three to six days after the initial tick bite, although it can have incubation periods of up to 20 days.  Patients usually experience a two-staged fever and illness which can continue for three days, diminish, and then return for another episode of one to three days.  The virus has the ability to live in the bloodstream for up to 120 days; therefore, coming in contact without proper precautions and the donation of blood are prohibited.
Initial symptoms include fever, chills, headaches, pain behind the eyes, light sensitivity, muscle pain, generalized malaise, abdominal pain, hepatosplenomegaly, nausea and vomiting, and a flat or pimply rash.  During the second phase of the virus, a high fever can return with an increase in symptoms. CTF can be very severe in cases involving children and can even require hospitalization.  Complications with this disease have included aseptic meningitis, encephalitis, and hemorrhagic fever, but these are rare.
CTF is seasonal, mostly occurring in the Rocky Mountain region of the United States and usually in altitudes from 4,000 to 10,000 feet (1.600 to 3.000 meters).  Patients with CTF are mostly campers and young males, who most likely have been bitten because of their  activities.

Cause
Virology
The virus particle, like other coltiviruses, is about 80 nm in diameter and is generally not enveloped.  The double-stranded RNA viral genome is about 20,000 bp long and is divided into 12 segments, which are termed Seg-1 to Seg-12.  Viral replication in infected cells is associated with characteristic cytoplasmic granular matrices.  Evidence suggests the viral presence in mature erythrocytes is a result of replication of the virus in hematopoetic erythrocyte precursor cells and simultaneous maturation of the infected immature cells rather than of direct entry and replication of CTFV in mature erythrocytes.

Tick
The Rocky Mountain wood tick is usually found attached to a host, but when it is without a host, it hides in cracks and crevices, as well as soil. If for some reason the tick is not able to find a host before the winter, it will stay under groundcover until spring, when it can resume its search.  The wood tick does not typically seek hosts in the hottest summer months.  Adult ticks tend to climb to the tops of grasses or low shrubs, attaching themselves to a host wandering by. They secure the attachment by secreting a cement-like substance from their mouths, inserting it into the host.

Transmission
Colorado tick fever is acquired by tick bite. No evidence of natural person-to-person transmission has been found. However, rare cases of transmission from blood transfusions have been reported. The virus which causes Colorado tick fever may stay in the blood for as long as four months after onset of the illness.

Diagnosis
A combination of clinical signs, symptoms, and laboratory tests can confirm the likelihood of having CTF.  Some tests include complement fixation to Colorado tick virus, immunofluorescence for Colorado tick fever, and some other common laboratory findings suggestive of CTF, including leucopenia, thrombocytopenia, and mildly elevated liver enzyme levels.
Detection of viral antibodies on red blood cells is possible.

Prevention
To avoid tick bites and infection, experts advise:

Avoid tick-infested areas, especially during the warmer months.
Wear light-colored clothing so ticks can be easily seen. Wear a long sleeved shirt, hat, long pants, and tuck pant legs into socks.
Walk in the center of trails to avoid overhanging grass and brush.
Clothing and body parts should be checked every few hours for ticks when spending time outdoors in tick-infested areas. Ticks are most often found on the thigh, arms, underarms, and legs. Ticks can be very small (no bigger than a pinhead). Look carefully for new "freckles".
The use of insect repellents containing DEET on skin or permethrin on clothing can be effective. Follow the directions on the container and wash off repellents when going indoors.
Remove attached ticks immediately.Contracting the CTF virus is thought to provide long-lasting immunity against reinfection.  However, it is always wise to be on the safe side and try to prevent tick bites.

Treatment
No specific treatment for CTF is yet available.  The first action is to make sure the tick is fully removed from the skin, then acetaminophen and analgesics can be used to help relieve the fever and 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 Mucolipidosis and can you explain it in depth? [/INST] Mucolipidosis is a group of inherited metabolic disorders that affect the bodys ability to carry out the normal turnover of various materials within cells.When originally named, the mucolipidoses derived their name from the similarity in presentation to both mucopolysaccharidoses and sphingolipidoses. A biochemical understanding of these conditions has changed how they are classified. Four conditions (types I, II, III, and IV) were historically labeled as mucolipidoses. However, type I (sialidosis) is now classified as a glycoproteinosis, and type IV (Mucolipidosis type IV) is now classified as a gangliosidosis.

ML II and III
The other two types are closely related.
Mucolipidosis types II and III (ML II and ML III) result from a deficiency of the enzyme N-acetylglucosamine-1-phosphotransferase, which phosphorylates target carbohydrate residues on N-linked glycoproteins. Without this phosphorylation, the glycoproteins are not destined for lysosomes, and they escape outside the cell.

Genetics
The mucolipidoses are inherited in an autosomal recessive manner, that is, they occur only when a child inherits two copies of the defective gene, one from each parent. When both parents carry a defective gene, each of their children faces a one in four chance of developing one of the MLs </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 Alimentary toxic aleukia 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 Sparganosis and can you explain it in depth? [/INST] Sparganosis is a parasitic infection caused by the plerocercoid larvae of the genus Spirometra including S. mansoni, S. ranarum, S. mansonoides and S. erinacei. It was first described by Patrick Manson from China in 1882, and the first human case was reported by Charles Wardell Stiles from Florida in 1908. The infection is transmitted by ingestion of contaminated water, ingestion of a second intermediate host such as a frog or snake, or contact between a second intermediate host and an open wound or mucous membrane. Humans are the accidental hosts in the life cycle, while dogs, cats, and other mammals are definitive hosts. Copepods (freshwater crustaceans) are the first intermediate hosts, and various amphibians and reptiles are second intermediate hosts.Once a human becomes infected, the plerocercoid larvae migrate to a subcutaneous location, where they typically develop into a painful nodule. Migration to the brain results in cerebral sparganosis, while migration to the eyes results in ocular sparganosis. Sparganosis is most prevalent in Eastern Asia, although cases have been described in countries throughout the world. In total, approximately 300 cases have been described in the literature up to 2003. Diagnosis is typically not made until the sparganum larva has been surgically removed. Praziquantel is the drug of choice, although its efficacy is unknown and surgical removal of the sparganum is generally the best treatment. Public health interventions should focus on water and dietary sanitation, as well as education about the disease in rural areas and discouragement of the use of poultices.

Symptoms
Clinical presentation of sparganosis most often occurs after the larvae have migrated to a subcutaneous location. The destination of the larvae is often a tissue or muscle in the chest, abdominal wall, extremities, or scrotum, although other sites include the eyes, brain, urinary tract, pleura, pericardium, and spinal canal. The early stages of disease in humans are often asymptomatic, but the spargana typically cause a painful inflammatory reaction in the tissues surrounding the subcutaneous site as they grow. Discrete subcutaneous nodules develop that may appear and disappear over a period of time. The nodules usually itch, swell, turn red, and migrate, and are often accompanied by painful edema. Seizures, hemiparesis, and headaches are also common symptoms of sparganosis, especially cerebral sparganosis, and eosinophilia is a common sign.  Clinical symptoms also vary according to the location of the sparganum; possible symptoms include elephantiasis from location in the lymph channels, peritonitis from location in the intestinal perforation, and brain abscesses from location in the brain. In genital sparganosis, subcutaneous nodules are present in the groin, labia, or scrotum and may appear tumor-like.Ocular sparganosis a particularly well-described type of sparganosis. Early signs of the ocular form include eye pain, epiphora (excessive watering of the eye), and/or ptosis (drooping of the upper eyelid). Other signs include periorbital edema and/or edematous swelling that resembles Romanas sign in Chagas disease, lacrimation,  orbital cellulitis, exophthalmos (protrusion of the eyeball), and/or an exposed cornea ulcer. The most common sign at presentation is a mass lesion in the eye. If untreated, ocular sparganosis can lead to blindness.In one case of brain infestation by Spirometra erinaceieuropaei, a man sought treatment for headaches, seizures, memory flashbacks and strange smells. Magnetic resonance imaging (MRI) scans showed a cluster of rings, initially in the right medial temporal lobe, but moving over time to the other side of the brain. The cause was not determined for four years; ultimately a biopsy was performed and a 1 cm-long tapeworm was found and removed. The patient continued to have symptoms.

Transmission
The parasite is transmitted to humans in three different ways. First, humans may acquire the infection by drinking water that is contaminated with copepods housing Spirometra larvae.  Second, humans may acquire the infection by consuming the raw flesh of one of the second intermediate hosts, such as frogs or snakes.  For example, humans consume raw snakes or tadpoles for medicinal purposes in some Asian cultures; if the snakes or tadpoles are infected, the larvae may be transmitted to humans. Third, humans may acquire the infection by placing raw poultices of the second intermediate hosts on open wounds, lesions, or the eyes for medicinal or ritualistic reasons. If the poultice is infected with plerocercoid larvae, the human may become infected. According to Zunt et al., human infection most often occurs following ingestion of infected raw snake, frog, or pig, although contact with infected flesh of an intermediate host can also cause infection.  The high prevalence in Korea may be explained by the ingestion of dog meat. In the Western hemisphere, the most common cause of infection is drinking contaminated water.

Hosts, reservoirs, and vectors
Definitive hosts of Spirometra include dogs, cats, birds, and wild carnivores, while humans are accidental hosts. First intermediate hosts include copepods and other fresh-water crustaceans, while second intermediate hosts include birds, reptiles, and amphibians. The intermediate hosts are also the reservoirs of Spirometra. There are no vectors of Spirometra.

Incubation period
The incubation period of Spirometra is 20 days to 3 years.

Morphology
The sparganum larvae are white, wrinkled, and ribbon-shaped. They range from a few millimeters in length to several centimeters. The anterior end can invaginate and bears suggestions of the sucking grooves that are present in the scolex of the mature worm.  The absence of a scolex or protoscolex in Spirometra is a key difference in differentiating between Taenia solium and Spirometra.  The worms body is also characterized by a stromal network of smooth muscle.  In general, plerocercoids in the East (S. mansoni) are described as larger and more delicate than those in the West.The eggs of S. mansonoides provide an example of the general morphological characteristics of Spirometra eggs. S. mansonoides eggs resemble the eggs of D. latum, with some specific differences. S. mansonoides eggs measure 57-66 µm by 33-37 µm, which is smaller than the eggs of D. latum. The eggs of S. mansonoides are also ellipsoidal and have a conical, prominent operculum.

Life cycle
The adult Spirometra live in the small intestine of the definitive host—a dog, cat, raccoon, or other mammal—for up to 9 years, where they produce many eggs.  When the host defecates, the unembryonated eggs leave the body in the feces and hatch when they reach fresh water. The eggs are eaten by copepods (crustaceans of the genus Cyclops), which are the first intermediate hosts. In the copepods, the eggs develop into procercoid larvae that live in the body cavity. The second intermediate hosts include fish, reptiles, or amphibians that consume the copepods. The larvae penetrate the intestinal tract of the second intermediate host, where they become plerocercoid larvae and proliferate to the subcutaneous tissues and muscles. The second intermediate host is eventually eaten by a definitive host predator, such as a dog, and the cycle begins again. Humans are accidental hosts in the cycle, becoming infected with the plerocercoid larvae by contact with or ingestion of the first or second intermediate hosts. The larvae migrate to the subcutaneous tissues in humans; however, no development takes place and the human is not capable of transmitting the disease. In S. proliferum, many larvae, rather than just a few, proliferate throughout the subcutaneous tissues of humans.

Diagnosis
Sparganosis is typically diagnosed following surgical removal of the worms, although the infection may also be diagnosed by identification of eosinophilia or identification of the parasite in a tissue specimen. If such biopsy and excision procedures are not feasible, the antisparganum ELISA test may be used. In theory, a pre-operative diagnosis could be made by identification of exposure history and a painful, migratory, subcutaneous nodule. Sparganosis usually presents as a single nodule, while other cestode infections such as cysticercosis typically present as multiple nodules. Preoperative diagnosis, however, is rare.CT and MRI scans are especially useful for diagnosis of cerebral sparganosis, as they reveal lesions in the brain. Through a retrospective analysis of 25 cases of cerebral sparganosis from 2000 to 2006, Song et al. found a number of characteristic signs that could be used in the future to diagnose cerebral sparganosis without performing an excision or tissue biopsy. The most characteristic finding was the "tunnel sign" on MRI images, showing the migrating track of the worm, while the most common finding was multiple conglomerated ring-shaped enhancements, seen as bead-shaped, usually with 3 to 6 rings. These findings led Song et al. to suggest that clinical history, ELISA, and either MRI or CT scans could be sufficient to make a sparganosis diagnosis. These lesions, however, are sometimes mistaken for tuberculosis lesions. In one case cerebral sparganosis was not diagnosed for four years, during which scans showed a cluster of rings moving from the right to the left side of the brain; ultimately the worm was found on biopsy.

Prevention
Because sparganosis is a rare infection, public health strategies have not made its prevention a priority. Public health strategies focusing on providing basic access to clean water may help to reduce future sparganosis infections. In their retrospective study of 25 cases of cerebral sparganosis, Song et al. found that 12 patients (48%) had eaten raw or uncooked frog or snake that was infected with sparganum, 5 patients (20%) had applied an animals flesh as a poultice to an open wound, 4 patients had drunk contaminated water, and the cause of infection was not known for 4 patients. As a result of these findings, Song et al. conclude that health education about sparganosis and the importance of food sanitation should be implemented in all rural endemic areas. It has been recommended that water consumed in endemic areas should be boiled or treated to prevent ingestion of Cyclops or Spirometra larvae </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 Indigestion and can you explain it in depth? [/INST] Indigestion, also known as dyspepsia or upset stomach, is a condition of impaired digestion. Symptoms may include upper abdominal fullness, heartburn, nausea, belching, or upper abdominal pain. People may also experience feeling full earlier than expected when eating. Indigestion is relatively common, affecting 20% of people at some point during their life, and is frequently caused by gastroesophageal reflux disease (GERD) or gastritis.Indigestion is subcategorized as "organic" or "functional", but making the diagnosis can prove challenging for physicians. Organic indigestion is the result of an underlying disease, such as gastritis, peptic ulcer disease (an ulcer of the stomach or duodenum), or cancer. Functional indigestion (previously called nonulcer dyspepsia) is indigestion without evidence of underlying disease. Functional indigestion is estimated to affect about 15% of the general population in western countries and accounts for a majority of dyspepsia cases.In elderly patients (60 years of age or older) or with worrisome symptoms such as trouble swallowing, weight loss, or blood loss, an endoscopy (a procedure whereby a camera attached to a flexible tube is inserted down the throat and into the stomach) is recommended to further assess and find a potential cause. In patients younger than 60 years of age, testing for the bacteria H. pylori and if positive, treatment of the infection is recommended. More details about how indigestion is diagnosed and treated can be found below.

Signs and symptoms
Symptoms
Patients experiencing indigestion likely report one, a combination of, or all of the following symptoms:
upper abdominal pain or discomfort
bloating
early satiety
postprandial fullness
nausea with or without vomiting
anorexia
regurgitation
belching

Signs
There may be abdominal tenderness, but this finding is nonspecific and is not required to make a diagnosis. However, there are physical exam signs that may point to a different diagnosis and underlying cause for a patients reported discomfort. A positive Carnett sign (focal tenderness that increases with abdominal wall contraction and palpation) suggests an etiology involving the abdominal wall musculature. Cutaneous dermatomal distribution of pain may suggest a thoracic polyradiculopathy. Tenderness to palpation over the right upper quadrant, or Murphys sign, may suggest cholecystitis or gallbladder inflammation.

Alarm symptoms
Also known as Alarm features, alert features, red flags, or warning signs in gastrointestinal (GI) literature.
Alarm features are thought to be associated with serious gastroenterologic disease and include:
chronic gastrointestinal bleeding
progressive unintentional weight loss
progressive difficulty swallowing (dysphagia)
persistent vomiting
Iron deficiency anemia
Vitamin B12 deficiency (Pernicious anemia)
epigastric mass

Cause
Indigestion is a diagnosis related to a combination of symptoms that can be attributed to "organic" or "functional" causes. Organic dyspepsia should have pathological findings upon endoscopy, like an ulcer in the stomach lining in peptic ulcer disease. Functional dyspepsia is unlikely to be detected on endoscopy but can be broken down into two subtypes, epigastric pain syndrome (EPS) and post-prandial distress syndrome (PDS). In addition, indigestion could be caused by medications, food, or other disease processes.
Psychosomatic and cognitive factors are important in the evaluation of people with chronic dyspepsia. Studies have shown a high occurrence of mental disorders, notably anxiety and depression, amongst patients with dyspepsia; however, there is little evidence to prove causation.

Organic Dyspepsia
Esophagitis
Esophagitis is an inflammation of the esophagus, most commonly caused by gastroesophageal reflux disease (GERD). It is defined by the sensation of "heartburn" or a burning sensation in the chest as a result of inappropriate relaxation of the lower esophageal sphincter at the site where the esophagus connects to the stomach. It is often treated with proton pump inhibitors. If left untreated, the chronic damage to the esophageal tissues poses a risk of developing cancer. A meta-analysis showed risk factors for developing GERD included age equal to or greater than 50, smoking, the use of non-steroid anti-inflammatory medications, and obesity.

Gastritis
Common causes of gastritis include peptic ulcer disease, infection, or medications.

Peptic Ulcer Disease
Gastric and/or duodenal ulcers are the defining feature of peptic ulcer disease (PUD). PUD is most commonly caused by an infection with H. pylori or NSAID use.

Helicobacter pylori (H.pylori) infection
The role of H. pylori in functional dyspepsia is controversial, and treatment for H. pylori may not lead to complete improvement of a patients dyspepsia. However, a recent systemic review and meta-analysis of 29 studies published in 2022 suggests that successful treatment of H. pylori modestly improves indigestion symptoms.

Pancreatobiliary Disease
These include cholelithiasis, chronic pancreatitis, and pancreatic cancer.

Duodenal micro-inflammation
Duodenal micro-inflammation caused by an altered duodenal gut microbiota, reactions to foods (mainly gluten proteins) or infections may induce dyspepsia symptoms in a subset of people.

Functional Dyspepsia
Functional dyspepsia is a common cause of chronic heartburn. More than 70% of people have no obvious organic cause for their symptoms after evaluation.  Symptoms may arise from a complex interaction of increased visceral afferent sensitivity, gastric delayed emptying (gastroparesis) or impaired accommodation to food. Diagnostic criteria for functional dyspepsia categorize it into two subtypes by symptom: epigastric pain syndrome and post-prandial distress syndrome. Anxiety is also associated with functional dyspepsia. In some people, it appears before the onset of gut symptoms; in other cases, anxiety develops after onset of the disorder, which suggests that a gut-driven brain disorder may be a possible cause.  Although benign, these symptoms may be chronic and difficult to treat.

Epigastric Pain Syndrome (EPS)
Defined by stomach pain and/or burning that interferes with daily life, without any evidence of organic disease.

Post-Prandial Distress Syndrome (PDS)
Defined by post-prandial fullness or early satiation that interferes with daily life, without any evidence of organic disease.

Food, herb, or drug intolerance
Acute, self-limited dyspepsia may be caused by overeating, eating too quickly, eating high-fat foods, eating during stressful situations, or drinking too much alcohol or coffee. Many medications cause dyspepsia, including aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics (metronidazole, macrolides), bronchodilators (theophylline), diabetes drugs (acarbose, metformin, Alpha-glucosidase inhibitor, amylin analogs, GLP-1 receptor antagonists), antihypertensive medications (angiotensin converting enzyme [ACE] inhibitors, Angiotensin II receptor antagonist), cholesterol-lowering agents (niacin, fibrates), neuropsychiatric medications (cholinesterase inhibitors [donepezil, rivastigmine]), SSRIs (fluoxetine, sertraline), serotonin-norepinephrine-reuptake inhibitors (venlafaxine, duloxetine), Parkinson drugs (Dopamine agonist, monoamine oxidase [MAO]-B inhibitors), weight-loss medications (orlistat), corticosteroids, estrogens, digoxin, iron, and opioids. Common herbs have also been show to cause indigestion, like white willow berry, garlic, ginkgo, chaste tree berry, saw palmetto, and feverfew. Studies have shown that wheat and dietary fats can contribute to indigestion and suggest foods high in short-chain carbohydrates (FODMAP) may be associated with dyspepsia. This suggests reducing or consuming a gluten-free, low-fat, and/or FODMAP diet may improve symptoms. Additionally, some people may experience dyspepsia when eating certain spices or spicy food as well as foods like peppers, chocolate, citrus, and fish.

Systemic Diseases
There are a number of systemic diseases that may involve dyspepsia, including coronary disease, congestive heart failure, diabetes mellitus, hyperparathyroidism, thyroid disease, and chronic kidney disease.

Post-infectious Causes of Dyspepsia
Gastroenteritis increases the risk of developing chronic dyspepsia. Post-infectious dyspepsia is the term given when dyspepsia occurs after an acute gastroenteritis infection. It is believed that the underlying causes of post-infectious IBS and post-infectious dyspepsia may be similar and represent different aspects of the same pathophysiology.

Pathophysiology
The pathophysiology for indigestion is not well understood; however, there are many theories. For example, there are studies that suggest a gut-brain interaction, as patients who received an antibiotic saw a reduction in their indigestion symptoms. Other theories propose issues with gut motility, a hypersensitivity of gut viscera, and imbalance of the microbiome. A genetic predisposition is plausible, but there is limited evidence to support this theory.

Diagnosis
A diagnosis for indigestion is based on symptoms, with a possible need for more diagnostic tests. In younger patients (less than 60 years of age) without red flags (e.g., weight loss), it is recommended to test for H. pylori noninvasively, followed by treatment with antibiotics in those who test positively. A negative test warrants discussing additional treatments, like proton pump inhibitors, with your doctor. An upper GI endoscopy may also be recommended. In older patients (60 or older), an endoscopy is often the next step in finding out the cause of newly onset indigestion regardless of the presence of alarm symptoms. However, for all patients regardless of age, an official diagnosis requires symptoms to have started at least 6 months ago with a frequency of at least once a week over the last 3 months.

Treatment
Functional and organic dyspepsia have similar treatments. Traditional therapies used for this diagnosis include lifestyle modification (e.g., diet), antacids, proton-pump inhibitors (PPIs), H2-receptor antagonists (H2-RAs), prokinetic agents, and antiflatulents. PPIs and H2-RAs are often first-line therapies for treating dyspepsia, having shown to be better than placebo medications. Anti-depressants, notably tricyclic antidepressants, have also been shown to be effective treatments for patients who do not respond to traditional therapies.

Diet
A lifestyle change that may help with indigestion is a change in diet, such as a stable and consistent eating schedule and slowing the pace of eating. Additionally, there are studies that support a reduction in the consumption of fats may also alleviate dyspepsia. While some studies suggest a correlation between dyspepsia and celiac disease, not everyone with indigestion needs to refrain from gluten in their diet. However, a gluten-free diet can relieve the symptoms in some patients without celiac disease. Lastly, a FODMAPs diet or diet low/free from certain complex sugars and sugar alcohols has also been shown to be potentially beneficial in patients with indigestion.

Acid suppression
Proton pump inhibitors (PPIs) were found to be better than placebo in a literature review, especially when looking at long-term symptom reduction </s>