<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 Babesiosis and can you explain it in depth? [/INST] Babesiosis or  piroplasmosis is a malaria-like parasitic disease caused by infection with a eukaryotic parasite in the order Piroplasmida, typically a Babesia or Theileria, in the phylum Apicomplexa. Human babesiosis transmission via tick bite is most common in the Northeastern and Midwestern United States and parts of Europe, and sporadic throughout the rest of the world. It occurs in warm weather.  People can get infected with Babesia parasites by the bite of an infected tick, by getting a blood transfusion from an infected donor of blood products, or by congenital transmission (an infected mother to her baby).
Ticks transmit the human strain of babesiosis, so it often presents with other tick-borne illnesses such as Lyme disease. After trypanosomes, Babesia is thought to be the second-most common blood parasite of mammals. They can have major adverse effects on the health of domestic animals in areas without severe winters.  In cattle the disease is known as Texas cattle fever or redwater.

Signs and symptoms
Half of all children and a quarter of previously healthy adults with Babesia infection are asymptomatic. When people do develop symptoms, the most common are fever and hemolytic anemia, symptoms that are similar to those of malaria. People with symptoms usually become ill 1 to 4 weeks after the bite, or 1 to 9 weeks after transfusion of contaminated blood products. A person infected with babesiosis gradually develops malaise and fatigue, followed by a fever. Hemolytic anemia, in which red blood cells are destroyed and removed from the blood, also develops. Chills, sweats, and thrombocytopenia are also common symptoms. Symptoms may last from several days to several months.Less common symptoms and physical exam findings of mild-to-moderate babesiosis:

In more severe cases, symptoms similar to malaria occur, with fevers up to 40.5 °C (105 °F), shaking chills, and severe anemia (hemolytic anemia). Organ failure may follow, including adult respiratory distress syndrome. Sepsis in people who have had a splenectomy can occur rapidly, consistent with overwhelming post-splenectomy infection. Severe cases are also more likely to occur in the very young, very old, and persons with immunodeficiency, such as HIV/AIDS patients.A reported increase in human babesiosis diagnoses in the 2000s is thought to be caused by more widespread testing and higher numbers of people with immunodeficiencies coming in contact with ticks, the disease vector. Little is known about the occurrence of Babesia species in malaria-endemic areas, where Babesia can easily be misdiagnosed as Plasmodium. Human patients with repeat babesiosis infection may exhibit premunity.

Cause
Babesia species are in the phylum Apicomplexa, which also has the protozoan parasites that cause malaria, toxoplasmosis, and cryptosporidiosis. Four clades of Babesia species infect humans. The main species in each clade are:
B. microti (<3 µm)
B.  duncani
B. divergens (cattle parasite seen mostly in Europe) and B. venatorum (roe deer parasite, formerly called EU1), most closely related to the large Babesia clade
Large Babesia (>3 µm) mostly infects ungulates, but also includes K01 strain (an isolated case observed in South Korea, see isolated cases)

Pathophysiology
Babesia parasites reproduce in red blood cells, where they can be seen as cross-shaped inclusions (four merozoites asexually budding, but attached together forming a structure looking like a "Maltese cross") and cause hemolytic anemia, quite similar to malaria.
Unlike the Plasmodium parasites that cause malaria, Babesia species lack an exoerythrocytic phase, so the liver is usually not affected.In nonhuman animals, Babesia canis rossi, Babesia bigemina, and Babesia bovis cause particularly severe forms of the disease, including a severe haemolytic anaemia, with positive erythrocyte-in-saline-agglutination test indicating an immune-mediated component to the haemolysis. Common sequelae include haemoglobinuria "red-water", disseminated intravascular coagulation, and "cerebral babesiosis" caused by sludging of erythrocytes in cerebral capillaries.In bovine species, the organism causes hemolytic anemia, so an infected animal shows pale mucous membranes initially. As the levels of bilirubin (a byproduct of red blood cell lysis) continue to increase, the visible mucous membranes become yellow in color (icterus) due to the failure of the liver to metabolize the excess bilirubin.  Hemoglobinuria is seen due to excretion of red-blood-cell lysis byproducts via the kidneys. Fever of 40.5 °C (105 °F) develops due to release of inflammatory byproducts.

Diagnosis
Only specialized laboratories can adequately diagnose Babesia infection in humans, so Babesia infections are considered highly under-reported. It develops in patients who live in or travel to an endemic area or receive a contaminated blood transfusion within the preceding 9 weeks, so this aspect of the medical history is vital. Babesiosis may be suspected when a person with such an exposure history develops persistent fevers and hemolytic anemia. The definitive diagnostic test is the identification of parasites on a Giemsa-stained thin-film blood smear.So-called "Maltese cross formations" on the blood film are diagnostic (pathognomonic) of babesiosis, since they are not seen in malaria, the primary differential diagnosis. Careful examination of multiple smears may be necessary, since Babesia may infect less than 1% of circulating red blood cells, thus be easily overlooked.Serologic testing for antibodies against Babesia (both IgG and IgM) can detect low-level infection in cases with a high clinical suspicion, but negative blood film examinations. Serology is also useful for differentiating babesiosis from malaria in cases where people are at risk for both infections. Since detectable antibody responses require about a week after infection to develop, serologic testing may be falsely negative early in the disease course.A polymerase chain reaction (PCR) test has been developed for the detection of Babesia from the peripheral blood. PCR may be at least as sensitive and specific as blood-film examination in diagnosing babesiosis, though it is also significantly more expensive. Most often, PCR testing is used in conjunction with blood film examination and possibly serologic testing.Other laboratory findings include decreased numbers of red blood cells and platelets on complete blood count.In animals, babesiosis is suspected by observation of clinical signs (hemoglobinuria and anemia) in animals in endemic areas. Diagnosis is confirmed by observation of merozoites on thin film blood smear examined at maximum magnification under oil using Romonovski stains (methylene blue and eosin). This is a routine part of the veterinary examination of dogs and ruminants in regions where babesiosis is endemic.Babesia canis and B. bigemina are "large Babesia species" that form paired merozoites in the erythrocytes, commonly described as resembling "two pears hanging together", rather than the "Maltese cross" of the "small Babesia species". Their merozoites are around twice the size of small ones.Cerebral babesiosis is suspected in vivo when neurological signs (often severe) are seen in cattle that are positive for B. bovis on blood smear, but this has yet to be proven scientifically. Outspoken red discoloration of the grey matter post mortem further strengthens suspicion of cerebral babesiosis. Diagnosis is confirmed post mortem by observation of Babesia-infected erythrocytes sludged in the cerebral cortical capillaries in a brain smear.

Treatment
Treatment of asymptomatic carriers should be considered if parasites are still detected after 3 months. In mild-to-moderate babesiosis, the treatment of choice is a combination of atovaquone and azithromycin. This regimen is preferred to clindamycin and quinine because it has fewer side effects. The standard course is 7 to 10 days, but this is extended to at least 6 weeks in people with relapsing disease. Even mild cases are recommended to be treated to decrease the chance of inadvertently transmitting the infection by donating blood. In severe babesiosis, the combination of clindamycin and quinine is preferred. In life-threatening cases, exchange transfusion is performed. In this procedure, the infected red blood cells are removed and replaced with uninfected ones.
Imizol is a drug used for treatment of babesiosis in dogs.
Extracts of the poisonous, bulbous plant Boophone disticha are used in the folk medicine of South Africa to treat equine babesiosis. B. disticha is a member of the daffodil family Amaryllidaceae and has also been used in preparations employed as arrow poisons, hallucinogens, and in embalming. The plant is rich in alkaloids, some of which display an action similar to that of scopolamine.

Epidemiology
Babesiosis is a vector-borne illness usually transmitted by Ixodes scapularis ticks. B. microti uses the same tick vector as Lyme disease, and may occur in conjunction with Lyme. The organism can also be transmitted by blood transfusion. Ticks of domestic animals, especially Rhipicephalus (Boophilus) microplus and R. (B.) decoloratus transmit several species of Babesia to livestock, causing considerable economic losses to farmers in tropical and subtropical regions.In the United States, the majority of babesiosis cases are caused by B. microti, and occur in the Northeast and northern Midwest from May through October. Areas with especially high rates include eastern Long Island, Fire Island, Nantucket Island, and Marthas Vineyard.
The Centers for Disease Control and Prevention now requires state health departments to report infections using Form OMB No. 0920-0728. In 2014, Rhode Island had an incidence of 16.3 reported infections per 100,000 people.In Europe, B. divergens is the primary cause of infectious babesiosis and is transmitted by I. ricinus.Babesiosis has emerged in Lower Hudson Valley, New York, since 2001.In Australia, one locally-acquired case of B. microti has been reported, which was fatal. A subsequent investigation found no additional evidence of human Babesiosis in over 7000 patient samples, leading the authors to conclude that Babesiosis was rare in Australia. A similar disease in cattle, commonly known as tick fever, is spread by Babesia bovis and B. bigemina in the introduced cattle tick Rhipicephalus microplus.  This disease is found in eastern and northern Australia.

Isolated cases
A table of isolated cases of babesiosis, which may be underestimated given how widely distributed the tick vectors are in temperate latitudes.

History
The disease is named for the genus of the causative organism, which was named after the Romanian bacteriologist Victor Babeș. In 1888, Victor Babeș identified the microorganisms in red blood cells as the cause of febrile hemoglobinuria in cattle. In 1893, Theobald Smith and Frederick Kilborne discovered that a tick was the vector for transmission in Texas cattle. The agent was B. bigemina. This was the first demonstration that an arthropod could act as a disease vector to transmit an infectious agent to a vertebrate host.In 1957, the first human case was documented in a splenectomized Croatian herdsman. The agent was B. divergens. In 1969, the first case was reported in an immunocompetent individual on Nantucket Island. The agent was B. microti, and the vector was the tick I. scapularis. Equine babesiosis (caused by the protozoan Theileria equi) is also known as piroplasmosis (from the Latin piro, meaning pear + Greek plasma, a thing formed).

Other animals
Veterinary treatment of babesiosis does not normally use antibiotics. In livestock and  animals, diminazen (Berenil), imidocarb, or trypan blue would be the drugs of choice for treatment of B. canis rossi (dogs in Africa), B. bovis, and B. bigemina (cattle in Southern Africa).  In acute cases in cattle, blood transfusion may be carried out.
A vaccine is effective against B. canis canis (dogs in the Mediterranean region), but is ineffective against B. c. rossi. B. imitans causes a mild form of the disease that frequently resolves without treatment (dogs in Southeast Asia).

References
External links

Center for Global Health (2019-06-25). "Babesiosis". Parasites and Health, DPDx—Laboratory Identification of Parasites of Public Health Concern. Centers for Disease Control & Prevention. Archived from the original on 2013-03-07. Retrieved 2003-10-07. Public domain source from which the first version of this article was derived.
Krause, Peter J;  et al. (27 January 2021). "Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA): 2020 Guideline on Diagnosis and Management of Babesiosis". Clinical Infectious Diseases. 72 (2): e49–e64 </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 Induced coma and can you explain it in depth? [/INST] An induced coma – also known as a medically induced coma (MIC), barbiturate-induced coma, or drug-induced coma – is a temporary coma (a deep state of unconsciousness) brought on by a controlled dose of an anesthetic drug, often a barbiturate such as pentobarbital or thiopental. Barbiturate comas are used to protect the brain during major neurosurgery, as a last line of treatment in certain cases of status epilepticus that have not responded to other treatments, and in refractory intracranial hypertension following traumatic brain injury.
Induced coma usually results in significant systemic adverse effects. The patient is likely to completely lose respiratory drive and require mechanical ventilation; gut motility is reduced; hypotension can complicate efforts to maintain cerebral perfusion pressure and often requires the use of vasopressor drugs. Hypokalemia often results. The completely immobile patient is at increased risk of bed sores as well as infection from catheters.
Induced coma is a feature of the Milwaukee protocol, a controversial method that is promoted as a means of treating rabies infection in people.

Theory
Barbiturates reduce the metabolic rate of brain tissue, as well as the cerebral blood flow </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 Barretts esophagus and can you explain it in depth? [/INST] Barretts esophagus is a condition in which there is an abnormal (metaplastic) change in the mucosal cells lining the lower portion of the esophagus, from stratified squamous epithelium to simple columnar epithelium with interspersed goblet cells that are normally present only in the small intestine and large intestine. This change is considered to be a premalignant condition because it is associated with a high incidence of further transition to esophageal adenocarcinoma, an often-deadly cancer.The main cause of Barretts esophagus is thought to be an adaptation to chronic acid exposure from reflux esophagitis. Barretts esophagus is diagnosed by endoscopy: observing the characteristic appearance of this condition by direct inspection of the lower esophagus; followed by microscopic examination of tissue from the affected area obtained from biopsy. The cells of Barretts esophagus are classified into four categories: nondysplastic, low-grade dysplasia, high-grade dysplasia, and frank carcinoma. High-grade dysplasia and early stages of adenocarcinoma may be treated by endoscopic resection or radiofrequency ablation. Later stages of adenocarcinoma may be treated with surgical resection or palliation. Those with nondysplastic or low-grade dysplasia are managed by annual observation with endoscopy, or treatment with radiofrequency ablation. In high-grade dysplasia, the risk of developing cancer might be at 10% per patient-year or greater.The incidence of esophageal adenocarcinoma has increased substantially in the Western world in recent years. The condition is found in 5–15% of patients who seek medical care for heartburn (gastroesophageal reflux disease, or GERD), although a large subgroup of patients with Barretts esophagus are asymptomatic. The condition is named after surgeon Norman Barrett (1903–1979) even though the condition was originally described by Philip Rowland Allison in 1946.

Signs and symptoms
The change from normal to premalignant cells indicate Barretts esophagus does not cause any particular symptoms. Barretts esophagus, however, is associated with these symptoms:

frequent and longstanding heartburn
trouble swallowing (dysphagia)
vomiting blood (hematemesis)
pain under the sternum where the esophagus meets the stomach
pain when swallowing (odynophagia), which can lead to unintentional weight lossThe risk of developing Barretts esophagus is increased by central obesity (vs. peripheral obesity). The exact mechanism is unclear. The difference in distribution of fat among men (more central) and women (more peripheral) may explain the increased risk in males.

Pathophysiology
Barretts esophagus occurs due to chronic inflammation.  The principal cause of chronic inflammation is gastroesophageal reflux disease, GERD (UK: GORD).  In this disease, acidic stomach, bile, and small intestine and pancreatic contents cause damage to the cells of the lower esophagus. In turn, this provokes an advantage for cells more resistant to these noxious stimuli in particular HOXA13-expressing stem cells that are characterised by distal (intestinal) characteristics and outcompete the normal squamous cells.This mechanism also explains the selection of HER2/neu (also called ERBB2) and the overexpressing (lineage-addicted) cancer cells during the process of carcinogenesis, and the efficacy of targeted therapy against the Her-2 receptor with trastuzumab (Herceptin) in the treatment of adenocarcinomas at the gastroesophageal junction.
Researchers are unable to predict who with heartburn will develop Barretts esophagus. While no relationship exists between the severity of heartburn and the development of Barretts esophagus, a relationship does exist between chronic heartburn and the development of Barretts esophagus. Sometimes, people with Barretts esophagus have no heartburn symptoms at all.
Some anecdotal evidence indicates those with the eating disorder bulimia are more likely to develop Barretts esophagus because bulimia can cause severe acid reflux, and because purging also floods the esophagus with acid. However, a link between bulimia and Barretts esophagus remains unproven.During episodes of reflux, bile acids enter the esophagus, and this may be an important factor in carcinogenesis.  Individuals with GERD and BE are exposed to high concentrations of deoxycholic acid that has cytotoxic effects and can cause DNA damage.

Diagnosis
Both macroscopic (from endoscopy) and microscopic positive findings are required to make a diagnosis. Barretts esophagus is marked by the presence of columnar epithelia in the lower esophagus, replacing the normal squamous cell epithelium—an example of metaplasia. The secretory columnar epithelium may be more able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased risk of adenocarcinoma.

Screening
Screening endoscopy is recommended among males over the age of 60 who have reflux symptoms that are of long duration and not controllable with treatment. Among those not expected to live more than 5 years screening is not recommended.The Seattle protocol is used commonly in endoscopy to obtain endoscopic biopsies for screening, taken every 1 to 2 cm from the gastroesophageal junction.
Since the COVID-19 pandemic In Scotland, the local NHS started using a swallowable sponge (Cytosponge) in hospitals to collect cell samples for diagnosis. Preliminary studies have shown this diagnostic test to be a useful tool for screening people with heartburn symptoms and improved diagnosis.

Intestinal metaplasia
The presence of goblet cells, called intestinal metaplasia, is necessary to make a diagnosis of Barretts esophagus. This frequently occurs in the presence of other metaplastic columnar cells, but only the presence of goblet cells is diagnostic. The metaplasia is grossly visible through a gastroscope, but biopsy specimens must be examined under a microscope to determine whether cells are gastric or colonic in nature. Colonic metaplasia is usually identified by finding goblet cells in the epithelium and is necessary for the true diagnosis.Many histologic mimics of Barretts esophagus are known (i.e. goblet cells occurring in the transitional epithelium of normal esophageal submucosal gland ducts, "pseudogoblet cells" in which abundant foveolar [gastric] type mucin simulates the acid mucin true goblet cells).  Assessment of relationship to submucosal glands and transitional-type epithelium with examination of multiple levels through the tissue may allow the pathologist to reliably distinguish between goblet cells of submucosal gland ducts and true Barretts esophagus (specialized columnar metaplasia). The histochemical stain Alcian blue pH 2.5 is also frequently used to distinguish true intestinal-type mucins from their histologic mimics. Recently, immunohistochemical analysis with antibodies to CDX-2 (specific for mid and hindgut intestinal derivation) has also been used to identify true intestinal-type metaplastic cells. The protein AGR2 is elevated in Barretts esophagus and can be used as a biomarker for distinguishing Barrett epithelium from normal esophageal epithelium.The presence of intestinal metaplasia in Barretts esophagus represents a marker for the progression of metaplasia towards dysplasia and eventually adenocarcinoma. This factor combined with two different immunohistochemical expression of p53, Her2 and p16 leads to two different genetic pathways that likely progress to dysplasia in Barretts esophagus. Also intestinal metaplastic cells can be positive for CK 7+/CK20-.

Epithelial dysplasia
After the initial diagnosis of Barretts esophagus is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer:  development of epithelial dysplasia (or "intraepithelial neoplasia").
Among all metaplastic lesions, around 8% were associated with dysplasia. particularly a recent study demonstrated that dysplastic lesions were located mainly in the posterior wall of the esophagus.Considerable variability is seen in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high-grade dysplasia in Barrett be confirmed by at least two fellowship-trained GI pathologists prior to definitive treatment for patients. For more accuracy and reproducibility, it is also recommended to follow international classification systems, such as the "Vienna classification" of gastrointestinal epithelial neoplasia (2000).

Management
Many people with Barretts esophagus do not have dysplasia. Medical societies recommend that if a patient has Barretts esophagus, and if the past two endoscopy and biopsy examinations have confirmed the absence of dysplasia, then the patient should not have another endoscopy within three years.Endoscopic surveillance of people with Barretts esophagus is often recommended, although little direct evidence supports this practice. Treatment options for high-grade dysplasia include surgical removal of the esophagus (esophagectomy) or endoscopic treatments such as endoscopic mucosal resection or ablation (destruction).The risk of malignancy is highest in the United States in Caucasian men over fifty years of age with more than five years of symptoms. Current recommendations include routine endoscopy and biopsy (looking for dysplastic changes). Although in the past physicians have taken a watchful waiting approach, newly published research supports consideration of intervention for Barretts esophagus. Balloon-based radiofrequency ablation, invented by Ganz, Stern, and Zelickson in 1999, is a new treatment modality for the treatment of Barretts esophagus and dysplasia and has been the subject of numerous published clinical trials. The findings demonstrate radiofrequency ablation is at least 90% effective to completely clear Barretts esophagus and dysplasia, with durability of up to five years and a favorable safety profile.Anti-reflux surgery has not been proven to prevent esophageal cancer. However, the indication is that proton pump inhibitors are effective in limiting the progression of esophageal cancer. Laser treatment is used in severe dysplasia, while overt malignancy may require surgery, radiation therapy, or systemic chemotherapy. A recent five-year random-controlled trial has shown that photodynamic therapy using photofrin is statistically more effective in eliminating dysplastic growth areas than sole use of a proton pump inhibitor.There is presently no reliable way to determine which patients with Barretts esophagus will go on to develop esophageal cancer, although a recent study found the detection of three different genetic abnormalities was associated with as much as a 79% chance of developing cancer in six years.Endoscopic mucosal resection has also been evaluated as a management technique </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 Emotional and behavioral disorders and can you explain it in depth? [/INST] Emotional and behavioral disorders (EBD; also known as behavioral and emotional disorders) refer to a disability classification used in educational settings that allows educational institutions to provide special education and related services to students who have displayed poor social and/or academic progress.The classification is often given to students after conducting a Functional Behavior Analysis. These students need individualized behavior supports such as a Behavior Intervention Plan, to receive a free and appropriate public education. Students with EBD may be eligible for an Individualized Education Plan (IEP) and/or accommodations in the classroom through a 504 Plan.

History
Early history
Before any studies were done on the subject, mental illnesses were often thought to be a form of demonic possession or witchcraft. Since much was unknown, there was little to no distinction between the different types of mental illness and developmental disorders that we refer to today. Most often, they were dealt with by performing an exorcism on the person exhibiting signs of any mental illness. In the early to mid 1800s, asylums were introduced to America and Europe. There, patients were treated cruelly and often referred to as lunatics by the doctors in the professional fields. The main focus of asylums were to shun people with mental illnesses from the public. In 1963, the Community Mental Health Centers Construction Act (Public Law 88–164), was passed by Congress and signed by John F. Kennedy, which provided federal funding to community mental health centers. This legislation changed the way that mental health services were handled and also led to the closure of many large asylums. Many laws soon followed assisting more and more people with EBDs. 1978 came with the passing of Public Law 94- 142 which required free and public education to all disabled children including those with EBDs. An extension of PL 94–142, PL 99-457, was put into act which would provide services to all disabled children from the ages of 3-5 by the 1990–91 school year. PL 94-142 has since been renamed to the Individuals with Disabilities Education Act (IDEA).

Use and development of the term
Various terms have been used to describe irregular emotional and behavioral disorders. Many of the terms such as mental illness and psychopathology were used to describe adults with such conditions. Mental illness was a label for most people with any type of disorder and it was common for people with emotional and behavioral disorders to be labeled with a mental illness. However, those terms were avoided when describing children as it seemed too stigmatizing. In the late 1900s the term "behaviorally disordered" appeared. Some professionals in the field of special education accepted the term while others felt it ignored emotional issues. In order to make a more uniformed terminology, the National Mental Health and Special Education Coalition, which consists of over thirty professional and advocacy groups, coined the term "emotional and behavioral disorders" in 1988.

Criteria
According to the Individuals with Disabilities Education Act an EBD classification is required if one or more of the following characteristics is excessively observed in a student over a significant amount of time:
Learning challenges that cannot be explained by intellectual, sensory, or health factors.
Trouble keeping up or building satisfactory relationships with peers and teachers.
Inappropriate behavior (against self or others) or emotions (shares the need to harm others or self, low self-worth) in normal conditions.
An overall attitude of unhappiness or depression.
A tendency to develop physical symptoms or fears related with individual or school issues.The term "EBD" includes students diagnosed with schizophrenia. However, it does not have any significant bearing on students who are socially maladjusted unless they also meet the above criteria.

Criticisms
Providing or failing to provide an EBD classification to a student may be controversial, as the IDEA does not clarify which children would be considered "socially maladjusted". Students with a psychiatric diagnosis of conduct disorder are not guaranteed to receive additional educational services under an EBD classification. Students with an EBD classification who meet the diagnostic criteria for various disruptive behavior disorders, including attention-deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), or conduct disorder (CD) do not have an automatic eligibility to receive an IEP or 504 Plan. Students considered "socially maladjusted", but ineligible for an EBD classification (i.e., students diagnosed with conduct disorder), often receive better educational services in special education classrooms or alternative schools with high structure, clear rules, and consistent consequences.

Student characteristics
Students with EBD are a diverse population with a wide range of intellectual and academic abilities. Males, African-Americans, and economically disadvantaged students are over-represented in the EBD population, and students with EBD are more likely to live in single-parent homes, foster homes, or other non-traditional living situations. These students also tend to have low rates of positive social interactions with peers in educational contexts. Students with EBD are often categorized as "internalizers" (e.g., have poor self-esteem, or are diagnosed with an anxiety disorder or mood disorder) or "externalizers" (e.g., disrupt classroom instruction, or are diagnosed with disruptive behavior disorders such as oppositional defiant disorder and conduct disorder). Male students may be over-represented in the EBD population because they appear to be more likely to exhibit disruptive externalizing behavior that interferes with classroom instruction. Females may be more likely to exhibit internalizing behavior that does not interfere with classroom instruction, though to what extent this perception is due to social expectations of differences in male and female behavior is unclear. In any case, it is important to note that both internalizing and externalizing behaviour can and do occur in either sex; Students with EBD are also at an increased risk for learning disabilities, school dropout, substance abuse, and juvenile delinquency.

Internalizing and externalizing behavior
A person with EBD with "internalizing" behavior may have poor self-esteem, have depression, experience loss of interest in social, academic, and other life activities, and may exhibit non-suicidal self-injury or substance abuse. Students with internalizing behavior may also have a diagnosis of separation anxiety or another anxiety disorder, post-traumatic stress disorder (PTSD), specific or social phobia, obsessive–compulsive disorder (OCD), panic disorder, and/or an eating disorder. Teachers are more likely to write referrals for students that are overly disruptive. Screening tools used to detect students with high levels of "internalizing" behavior are not sensitive and are rarely used in practice. Students with EBD with "externalizing" behavior may be aggressive, non-compliant, extroverted, or disruptive.
Students with EBD that show externalizing behavior are often diagnosed with attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), conduct disorder, and/or bipolar disorder; however, this population can also include typically developing children that have learned to exhibit externalizing behavior for various reasons (e.g., escape from academic demands or access to attention). These students often have difficulty inhibiting emotional responses resulting from anger, frustration, and disappointment. Students who "externalize" exhibit behaviors such as insulting, provoking, threatening, bullying, cursing, and fighting, along with other forms of aggression. Male students with EBD exhibit externalizing behavior more often than their female counterparts.Children and adolescents with ADD or ADHD may display different types of externalizing behavior and should be either medicated or going through behavioral treatment for their diagnosis. Adolescents with severe ADHD would likely benefit most from both medication and behavioral treatment. Younger children should go through behavioral treatment before being treated with medication. Another recommended form of treatment for children and adolescents diagnosed with ADHD would be counseling from a mental health professional. Treatment options will improve performance of children and adolescents on emotion recognition tasks, specifically response time as there is no difficulty recognizing human emotions. The degree of required treatments vary depending on the degree of ADD or ADHD the individual has.
Treatment for these types of behaviors should include the parents as it is evident that their parenting skills impact on how their child deals with their symptoms, especially when at a younger age. Parents going through a parenting skills training program were reported a decrease in internalizing and externalizing behavior in their children post-training program. The program included learning how to give positive attention, increase good behavior with small frequent rewards and specific praise as well as learning how to decrease attention when the child behaved poorly.

Effect on cognition
In recent years, many researchers have been interested in exploring the relationship between emotional disorders and cognition. Evidence has revealed that there is a relationship between the two. Strauman (1989) investigated how emotional disorders shape a persons cognitive structure, that is, the mental processes people utilize to make sense of the world around them. He recruited three groups of individuals: those with social phobias, those with depression, and controls with no emotional disorder diagnosis. He wanted to determine whether these groups had a cognitive structure showing an actual/ideal (AI) discrepancy (referring to an individual not believing that they have achieved their personal desires) or actual/own/other (AOO) discrepancy (referring to an individuals actions not living up to what their significant other believes that they need to be). He found that depressed individuals had the highest AI discrepancy and social phobics had the greatest AOO discrepancy, while the controls were lower or in between the two for both discrepancies.Specific cognitive processes (e.g., attention) may be different in those with emotional disorders. MacLeod, Mathews, and Tata (1986) tested the reaction times of 32 participants, some of whom were diagnosed with Generalized Anxiety disorder, when presented with threatening words. They found that when threatening words were presented, people with greater anxiety tended to have increased selective attention, meaning that they reacted quicker to a stimulus in an area where a threatening word was just presented (32-59ms faster). When in the control group, subjects reacted slower when there was a threatening word proceeding the stimulus (16-32ms slower).Emotional disorders can also alter the way people regulate their emotions. Joormann and Gotlib (2010) conducted a study with depressed, or previously depressed, individuals to test this. They found that, when compared to individuals who have never had a depressive episode, previously and currently depressed individuals tended to use maladaptive emotion regulation strategies (such as rumination or brooding) more. They also found that when depressed individuals displayed cognitive inhibition (slowing of response to a variable that had been previously ignored) when asked to describe a negative word (ignored variable was a positive word), they were less likely to ruminate or brood. When they displayed cognitive inhibition when asked to describe a positive word (ignored variable was a negative word), they were more likely to reflect.

Services in the United States
There are many types of services available to EBD students, referenced below. One service is one-on-one support (or an aide) who assists in everyday activities and academics. Another service is foundations offer behavior services as well as counseling support. Some services include classrooms that are dedicated to educational foundations and work on building the student up possessively. States also offer dedicated schools with multiple resources that help students with EBD excel and transition (back) into local schools.

Texas
The state of Texas has the Texas Behavior Support Initiative (TBSI) authorized by Senate Bill 1196 and Texas Administrative Code §89.1053. With its design to provide knowledge for the use of constructive behavior interventions and to aid students, including students with disabilities. TBSI meets the legislative requirements for the use of restraint and time-out, along with providing the baseline work for behavior strategies and prevention throughout each environment.

New York
The state of New York has the Foundations Behavioral Health that has been approved out of state educations and residential provider with the New York State Education Dept. Foundations offer Academic and Behavioral Health Services to students between the ages of 14–21. This program allows students educational experience to have strategic interventions to aid their social and behavioral functioning. Some of the programs highlights include Functional Behavioral Assessment (FBA), Behavioral Intervention Plan (BIP) & Community Based Instruction (CBI).

California
The state of California has Spectrum Center classrooms in Los Angeles and the San Francisco area which are providing Emotional Disabilities and Behavioral Services. They provide academic classrooms for students who are actively working to improve grade-level standards and working toward getting their high school diploma.  The main practice is the use of Positive Behavior Interventions and Supports (PBIS). PBIS instructional practices help students determine their skill level and progress, restore their skills through direct instruction, knowing the standards on their grade level and small group counseling.

Michigan
The state of Michigan has a Behavioral Education Center (BEC) in Bangor. Its purpose is to aid local schools directs with students between the ages of 5–26 years old with EBDs. Along with having students use appropriate behaviors and skills to successfully return to their local school setting </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 Benign prostatic hyperplasia and can you explain it in depth? [/INST] Benign prostatic hyperplasia (BPH), also called prostate enlargement, is a noncancerous increase in size of the prostate gland. Symptoms may include frequent urination, trouble starting to urinate, weak stream, inability to urinate, or loss of bladder control. Complications can include urinary tract infections, bladder stones, and chronic kidney problems.The cause is unclear. Risk factors include a family history, obesity, type 2 diabetes, not enough exercise, and erectile dysfunction. Medications like pseudoephedrine, anticholinergics, and calcium channel blockers may worsen symptoms. The underlying mechanism involves the prostate pressing on the urethra and thereby making it difficult to pass urine out of the bladder. Diagnosis is typically based on symptoms and examination after ruling out other possible causes.Treatment options include lifestyle changes, medications, a number of procedures, and surgery. In those with mild symptoms, weight loss, exercise, and decreasing caffeine intake are recommended, although the quality of the evidence for exercise is low. In those with more significant symptoms, medications may include alpha blockers such as terazosin or 5α-reductase inhibitors such as finasteride. Surgical removal of part of the prostate may be carried out in those who do not improve with other measures. Some herbal medicines that have been studied, such as saw palmetto, have not been shown to help. Other herbal medicines somewhat effective at improving urine flow include beta-sitosterol from Hypoxis rooperi (African star grass), pygeum (extracted from the bark of Prunus africana), pumpkin seeds (Cucurbita pepo), and stinging nettle (Urtica dioica) root.About 105 million men are affected globally. BPH typically begins after the age of 40. Half of males age 50 and over are affected. After the age of 80, that figure climbs to as high as about 90% of males affected. Although prostate specific antigen levels may be elevated in males with BPH, the condition does not increase the risk of prostate cancer.

Signs and symptoms
BPH is the most common cause of lower urinary tract symptoms (LUTS), which are divided into storage, voiding, and symptoms which occur after urination. Storage symptoms include the need to urinate frequently, waking at night to urinate, urgency (compelling need to void that cannot be deferred), involuntary urination, including involuntary urination at night, or urge incontinence (urine leak following a strong sudden need to urinate). Voiding symptoms include urinary hesitancy (a delay between trying to urinate and the flow actually beginning), intermittency (not continuous), involuntary interruption of voiding, weak urinary stream, straining to void, a sensation of incomplete emptying, and uncontrollable leaking after the end of urination. These symptoms may be accompanied by bladder pain or pain while urinating, called dysuria.Bladder outlet obstruction (BOO) can be caused by BPH. Symptoms are abdominal pain, a continuous feeling of a full bladder, frequent urination, acute urinary retention (inability to urinate), pain during urination (dysuria), problems starting urination (urinary hesitancy), slow urine flow, starting and stopping (urinary intermittency), and nocturia.BPH can be a progressive disease, especially if left untreated. Incomplete voiding results in residual urine or urinary stasis, which can lead to an increased risk of urinary tract infection.

Causes
Hormones
Most experts consider androgens (testosterone and related hormones) to play a permissive role in the development of BPH. This means that androgens must be present for BPH to occur, but do not necessarily directly cause the condition. This is supported by evidence suggesting that castrated boys do not develop BPH when they age. In an unusual study of 26 eunuchs from the palace of the Qing dynasty still living in Beijing in 1960, the prostate could not be felt in 81% of the studied eunuchs. The average time since castration was 54 years (range, 41–65 years). On the other hand, some studies suggest that administering exogenous testosterone is not associated with a significant increase in the risk of BPH symptoms, so the role of testosterone in prostate cancer and BPH is still unclear. Further randomized controlled trials with more participants are needed to quantify any risk of giving exogenous testosterone.Dihydrotestosterone (DHT), a metabolite of testosterone, is a critical mediator of prostatic growth. DHT is synthesized in the prostate from circulating testosterone by the action of the enzyme 5α-reductase, type 2. DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells. DHT is ten times more potent than testosterone because it dissociates from the androgen receptor more slowly. The importance of DHT in causing nodular hyperplasia is supported by clinical observations in which an inhibitor of 5α-reductase such as finasteride is given to men with this condition. Therapy with a 5α-reductase inhibitor markedly reduces the DHT content of the prostate and, in turn, reduces prostate volume and BPH symptoms.Testosterone promotes prostate cell proliferation, but relatively low levels of serum testosterone are found in patients with BPH. One small study has shown that medical castration lowers the serum and prostate hormone levels unevenly, having less effect on testosterone and dihydrotestosterone levels in the prostate.While there is some evidence that estrogen may play a role in the cause of BPH, this effect appears to be mediated mainly through local conversion of androgens to estrogen in the prostate tissue rather than a direct effect of estrogen itself. In canine in vivo studies castration, which significantly reduced androgen levels but left estrogen levels unchanged, caused significant atrophy of the prostate. Studies looking for a correlation between prostatic hyperplasia and serum estrogen levels in humans have generally shown none.In 2008, Gat et al. published evidence that BPH is caused by failure in the spermatic venous drainage system resulting in increased hydrostatic pressure and local testosterone levels elevated more than 100 fold above serum levels. If confirmed, this mechanism explains why serum androgen levels do not seem to correlate with BPH and why giving exogenous testosterone would not make much difference.

Diet
Studies indicate that dietary patterns may affect development of BPH, but further research is needed to clarify any important relationship. Studies from China suggest that greater protein intake may be a factor in development of BPH. Men older than 60 in rural areas had very low rates of clinical BPH, while men living in cities and consuming more animal protein had a higher incidence. On the other hand, a study in Japanese-American men in Hawaii found a strong negative association with alcohol intake, but a weak positive association with beef intake. In a large prospective cohort study in the US (the Health Professionals Follow-up Study), investigators reported modest associations between BPH (men with strong symptoms of BPH or surgically confirmed BPH) and total energy and protein, but not fat intake. There is also epidemiological evidence linking BPH with metabolic syndrome (concurrent obesity, impaired glucose metabolism and diabetes, high triglyceride levels, high levels of low-density cholesterol, and hypertension).

Degeneration
Benign prostatic hyperplasia is an age-related disease. Misrepair-accumulation aging theory suggests that development of benign prostatic hyperplasia is a consequence of fibrosis and weakening of the muscular tissue in the prostate. The muscular tissue is important in the functionality of the prostate, and provides the force for excreting the fluid produced by prostatic glands. However, repeated contractions and dilations of myofibers will unavoidably cause injuries and broken myofibers. Myofibers have a low potential for regeneration; therefore, collagen fibers need to be used to replace the broken myofibers. Such misrepairs make the muscular tissue weak in functioning, and the fluid secreted by glands cannot be excreted completely. Then, the accumulation of fluid in glands increases the resistance of muscular tissue during the movements of contractions and dilations, and more and more myofibers will be broken and replaced by collagen fibers.

Pathophysiology
As men age, the enzymes aromatase and 5-alpha reductase increase in activity. These enzymes are responsible for converting androgen hormones into estrogen and dihydrotestosterone, respectively. This metabolism of androgen hormones leads to a decrease in testosterone but increased levels of DHT and estrogen.
Both the glandular epithelial cells and the stromal cells (including muscular fibers) undergo hyperplasia in BPH. Most sources agree that of the two tissues, stromal hyperplasia predominates, but the exact ratio of the two is unclear.:694Anatomically the median and lateral lobes are usually enlarged, due to their highly glandular composition. The anterior lobe has little in the way of glandular tissue and is seldom enlarged. (Carcinoma of the prostate typically occurs in the posterior lobe – hence the ability to discern an irregular outline per rectal examination). The earliest microscopic signs of BPH usually begin between the age of 30 and 50 years old in the PUG, which is posterior to the proximal urethra.:694 In BPH, the majority of growth occurs in the transition zone (TZ) of the prostate.:694 In addition to these two classic areas, the peripheral zone (PZ) is also involved to a lesser extent.:695 Prostatic cancer typically occurs in the PZ. However, BPH nodules, usually from the TZ are often biopsied anyway to rule out cancer in the TZ.:695 BPH can be a progressive growth that in rare instances leads to exceptional enlargement. In some males, the prostate enlargement exceeds 200 to 500 grams. This condition has been defined as giant prostatic hyperplasia (GPH).

Diagnosis
The clinical diagnosis of BPH is based on a history of LUTS (lower urinary tract symptoms), a digital rectal exam, and exclusion of other causes of similar signs and symptoms. The degree of LUTS does not necessarily correspond to the size of the prostate. An enlarged prostate gland on rectal examination that is symmetric and smooth supports a diagnosis of BPH. However, if the prostate gland feels asymmetrical, firm, or nodular, this raises concern for prostate cancer.Validated questionnaires such as the American Urological Association Symptom Index (AUA-SI), the International Prostate Symptom Score (I-PSS), and more recently the UWIN score (urgency, weak stream, incomplete emptying, and nocturia) are useful aids to making the diagnosis of BPH and quantifying the severity of symptoms.

Laboratory investigations
Urinalysis is typically performed when LUTS are present and BPH is suspected to evaluate for signs of a urinary tract infection, glucose in the urine (suggestive of diabetes), or protein in the urine (suggestive of kidney disease). Bloodwork including kidney function tests and prostate specific antigen (PSA) are often ordered to evaluate for kidney damage and prostate cancer, respectively. However, checking blood PSA levels for prostate cancer screening is controversial and not necessarily indicated in every evaluation for BPH. Benign prostatic hyperplasia and prostate cancer are both capable of increasing blood PSA levels and PSA elevation is unable to differentiate these two conditions well. If PSA levels are checked and are high, then further investigation is warranted. Measures including PSA density, free PSA, rectal examination, and transrectal ultrasonography may be helpful in determining whether a PSA increase is due to BPH or prostate cancer.

Imaging and other investigations
Uroflowmetry is done to measure the rate of urine flow and total volume of urine voided when the subject is peeing.Abdominal ultrasound examination of the prostate and kidneys is often performed to rule out hydronephrosis and hydroureter. Incidentally, cysts, tumours, and stones may be found on ultrasound. Post-void residual volume of more than 100 ml may indicate significant obstruction. Prostate size of 30 cc or more indicates enlargement of the prostate.Prostatic calcification can be detected through transrectal ultrasound (TRUS). Calcification is due to solidification of prostatic secretions or calcified corpora amylacea (hyaline masses on the prostate gland). Calcification is also found in a variety of other conditions such as prostatitis, chronic pelvic pain syndrome, and prostate cancer. For those with elevated levels of PSA, TRUS guided biopsy is performed to take a sample of the prostate for investigation. Although MRI is more accurate than TRUS in determining prostate volume, TRUS is less expensive and almost as accurate as MRI. Therefore, TRUS is still preferred to measure prostate volume.

Differential diagnosis
Medical conditions
The differential diagnosis for LUTS is broad and includes various medical conditions, neurologic disorders, and other diseases of the bladder, urethra, and prostate such as bladder cancer, urinary tract infection, urethral stricture, urethral calculi (stones), chronic prostatitis, and prostate cancer. Neurogenic bladder can cause urinary retention and cause symptoms similar to those of BPH. This may occur as a result of uncoordinated contraction of the bladder muscle or impairment in the timing of bladder muscle contraction and urethral sphincter relaxation. Notable causes of neurogenic bladder include disorders of the central nervous system such as Parkinsons disease, multiple sclerosis, and spinal cord injuries as well as disorders of the peripheral nervous system such as diabetes mellitus, vitamin B12 deficiency, and alcohol-induced nerve damage. Individuals affected by heart failure often experience nighttime awakenings to urinate due to redistribution of fluid accumulated in swollen legs.

Medications
Certain medications can increase urination difficulties by increasing bladder outlet resistance due to increased smooth muscle tone at the prostate or bladder neck and contribute to LUTS. Alpha-adrenergic agonist medications, such as decongestants with pseudoephedrine can increase bladder outlet resistance. In contrast, calcium channel blockers and anticholinergic medications can worsen urinary retention by promoting bladder muscle relaxation. Diuretic medications such as loop diuretics (e.g., furosemide) or thiazides (e.g., chlorthalidone) can cause or worsen urinary frequency and nighttime awakenings to urinate.

Management
When treating and managing benign prostatic hyperplasia, the aim is to prevent complications related to the disease and improve or relieve symptoms. Approaches used include lifestyle modifications, medications, and surgery.

Lifestyle
Lifestyle alterations to address the symptoms of BPH include physical activity, decreasing fluid intake before bedtime, moderating the consumption of alcohol and caffeine-containing products and following a timed voiding schedule.
Patients can also attempt to avoid products and medications with anticholinergic properties that may exacerbate urinary retention symptoms of BPH, including antihistamines, decongestants, opioids, and tricyclic antidepressants; however, changes in medications should be done with input from a medical professional.

Physical activity
Physical activity has been recommended as a treatment for urinary tract symptoms. A 2019 Cochrane review of six studies involving 652 men assessing the effects of physical activity alone, physical activity as a part of a self-management program, among others.  However, the quality of evidence was very low and therefore it remains uncertain whether physical activity is helpful in men experiencing urinary symptoms caused by benign prostatic hyperplasia.

Voiding position
Voiding position when urinating may influence urodynamic parameters (urinary flow rate, voiding time, and post-void residual volume). A meta-analysis found no differences between the standing and sitting positions for healthy males, but that, for elderly males with lower urinary tract symptoms, voiding in the sitting position--
decreased the post void residual volume;
increased the maximum urinary flow, comparable with pharmacological intervention; and
decreased the voiding time.This urodynamic profile is associated with a lower risk of urologic complications, such as cystitis and bladder stones.

Medications
The two main medication classes for BPH management are alpha blockers and 5α-reductase inhibitors.

Alpha blockers
Selective α1-blockers are the most common choice for initial therapy. They include alfuzosin, doxazosin, silodosin, tamsulosin, terazosin, and naftopidil. They have a small to moderate benefit at improving symptoms. Selective alpha-1 blockers are similar in effectiveness but have slightly different side effect profiles. Alpha blockers relax smooth muscle in the prostate and the bladder neck, thus decreasing the blockage of urine flow. Common side effects of alpha blockers include orthostatic hypotension (a head rush or dizzy spell when standing up or stretching), ejaculation changes, erectile dysfunction, headaches, nasal congestion, and weakness. For men with LUTS due to an enlarged prostate, the effects of naftopidil, tamsulosin and silodosin on urinary symptoms and quality of life may be similar. Naftopidil and tamsulosin may have similar levels of unwanted sexual side effects but fewer unwanted side effects than silodosin.Tamsulosin and silodosin are selective α1 receptor blockers that preferentially bind to the α1A receptor in the prostate instead of the α1B receptor in the blood vessels. Less-selective α1 receptor blockers such as terazosin and doxazosin may lower blood pressure. The older, less selective α1-adrenergic blocker prazosin is not a first line choice for either high blood pressure or prostatic hyperplasia; it is a choice for patients who present with both problems at the same time. The older, broadly non-selective alpha blocker medications such as phenoxybenzamine are not recommended for control of BPH. Non-selective alpha blockers such as terazosin and doxazosin may also require slow dose adjustments as they can lower blood pressure and cause syncope (fainting) if the response to the medication is too strong.

5α-reductase inhibitors
The 5α-reductase inhibitors finasteride and dutasteride may also be used in men with BPH. These medications inhibit the 5α-reductase enzyme, which, in turn, inhibits production of DHT, a hormone responsible for enlarging the prostate. Effects may take longer to appear than alpha blockers, but they persist for many years. When used together with alpha blockers, no benefit was reported in short-term trials, but in a longer-term study (3–4 years) there was a greater reduction in BPH progression to acute urinary retention and surgery than with either agent alone, especially in people with more severe symptoms and larger prostates. Other trials have confirmed reductions in symptoms, within 6 months in one trial, an effect that was maintained after withdrawal of the alpha blocker. Side effects include decreased libido and ejaculatory or erectile dysfunction. The 5α-reductase inhibitors are contraindicated in pregnant women because of their teratogenicity due to interference with fetal testosterone metabolism, and as a precaution, pregnant women should not handle crushed or broken tablets.

Phosphodiesterase inhibitors (PDE)
A 2018 Cochrane review of studies on men over 60 with moderate to severe lower urinary tract symptoms analyzed the impacts of phosphodiesterase inhibitors (PDE) in comparison to other drugs. These drugs may improve urinary symptoms slightly and reduce urinary bother but may also cause more side effects compared to placebo. The evidence in this review found that there is probably no difference between PDE and alpha blockers, however when used in combination they may provide a greater improvement in symptoms (with more side effects). PDE also likely improves symptoms when used in combination with 5-alpha reductase inhibitors.
Several phosphodiesterase-5 inhibitors are also effective, but may require multiple doses daily to maintain adequate urine flow. Tadalafil, a phosphodiesterase-5 inhibitor, was considered then rejected by NICE in the UK for the treatment of symptoms associated with BPH. In 2011, the U.S. Food and Drug Administration approved tadalafil to treat the signs and symptoms of benign prostatic hyperplasia, and for the treatment of BPH and erectile dysfunction (ED), when the conditions occur simultaneously.

Others
Antimuscarinics such as tolterodine may also be used, especially in combination with alpha blockers. They act by decreasing acetylcholine effects on the smooth muscle of the bladder, thus helping control symptoms of an overactive bladder.

Self-catheterization
Intermittent urinary catheterization is used to relieve the bladder in people with urinary retention. Self-catheterization is an option in BPH when it is difficult or impossible to completely empty the bladder. Urinary tract infection is the most common complication of intermittent catheterization. Several techniques and types of catheter are available, including sterile (single-use) and clean (multiple use) catheters, but, based on current information, none is superior to others in reducing the incidence of urinary tract infection.

Surgery
If medical treatment is not effective, surgery may be performed. Surgical techniques used include the following:

Transurethral resection of the prostate (TURP): the gold standard. TURP is thought to be the most effective approach for improving urinary symptoms and urinary flow, however, this surgical procedure may be associated with complications in up to 20% of men </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 Benzodiazepine overdose and can you explain it in depth? [/INST] Benzodiazepine overdose describes the ingestion of one of the drugs in the benzodiazepine class in quantities greater than are recommended or generally practiced. The most common symptoms of overdose include central nervous system (CNS) depression, impaired balance, ataxia, and slurred speech. Severe symptoms include coma and respiratory depression. Supportive care is the mainstay of treatment of benzodiazepine overdose. There is an antidote, flumazenil, but its use is controversial.Deaths from single-drug benzodiazepine overdoses occur infrequently, particularly after the point of hospital admission. However, combinations of high doses of benzodiazepines with alcohol, barbiturates, opioids or tricyclic antidepressants are particularly dangerous, and may lead to severe complications such as coma or death. In 2013, benzodiazepines were involved in 31% of the estimated 22,767 deaths from prescription drug overdose in the United States. The US Food and Drug Administration (FDA) has subsequently issued a black box warning regarding concurrent use of benzodiazepines and opioids. Benzodiazepines are one of the most highly prescribed classes of drugs, and they are commonly used in self-poisoning. Over 10 years in the United Kingdom, 1512 fatal poisonings have been attributed to benzodiazepines with or without alcohol. Temazepam was shown to be more toxic than the majority of benzodiazepines. An Australian (1995) study found oxazepam less toxic and less sedative, and temazepam more toxic and more sedative, than most benzodiazepines in overdose.

Signs and symptoms
Following an acute overdose of a benzodiazepine the onset of symptoms is typically rapid with most developing symptoms within 4 hours. Patients initially present with mild to moderate impairment of central nervous system function. Initial signs and symptoms include intoxication, somnolence, diplopia, impaired balance, impaired motor function, anterograde amnesia, ataxia, and slurred speech. Most patients with pure benzodiazepine overdose will usually only exhibit these mild CNS symptoms. Paradoxical reactions such as anxiety, delirium, combativeness, hallucinations, and aggression can also occur following benzodiazepine overdose. Gastrointestinal symptoms such as nausea and vomiting have also been occasionally reported.Cases of severe overdose have been reported and symptoms displayed might include prolonged deep coma or deep cyclic coma, apnea, respiratory depression, hypoxemia, hypothermia, hypotension, bradycardia, cardiac arrest, and pulmonary aspiration, with the possibility of death. Severe consequences are rare following overdose of benzodiazepines alone but the severity of overdose is increased significantly if benzodiazepines are taken in overdose in combination with other medications. Significant toxicity may result following recreation drug misuse in conjunction with other CNS depressants such as opioids or alcohol. The duration of symptoms following overdose is usually between 12 and 36 hours in the majority of cases. The majority of drug-related deaths involve misuse of heroin or other opioids in combination with benzodiazepines or other CNS depressant drugs. In most cases of fatal overdose it is likely that lack of opioid tolerance combined with the depressant effects of benzodiazepines is the cause of death.The symptoms of an overdose such as sleepiness, agitation and ataxia occur much more frequently and severely in children. Hypotonia may also occur in severe cases.

Toxicity
Benzodiazepines have a wide therapeutic index and taken alone in overdose rarely cause severe complications or fatalities. More often than not, a patient who inadvertently takes more than the prescribed dose will simply feel drowsy and fall asleep for a few hours.  Benzodiazepines taken in overdose in combination with alcohol, barbiturates, opioids, tricyclic antidepressants, or sedating antipsychotics, anticonvulsants, or antihistamines are particularly dangerous. Additionally, emergency department visits involving benzodiazepines compared to other sedative-hypnotics have much higher odds of hospitalization, patient transfer, or death. In the case of alcohol and barbiturates, not only do they have an additive effect but they also increase the binding affinity of benzodiazepines to the benzodiazepine binding site, which results in a very significant potentiation of the CNS and respiratory depressant effects. In addition, the elderly and those with chronic illnesses are much more vulnerable to lethal overdose with benzodiazepines. Fatal overdoses can occur at relatively low doses in these individuals.

Comparability
The various benzodiazepines differ in their toxicity since they produce varying levels of sedation in overdose. A 1993 British study of deaths during the 1980s found flurazepam and temazepam more frequently involved in drug-related deaths, causing more deaths per million prescriptions than other benzodiazepines. Flurazepam, now rarely prescribed in the United Kingdom and Australia, had the highest fatal toxicity index of any benzodiazepine (15.0), followed by temazepam (11.9), versus benzodiazepines overall (5.9), taken with or without alcohol. An Australian (1995) study found oxazepam less toxic and less sedative, and temazepam more toxic and more sedative, than most benzodiazepines in overdose. An Australian study (2004) of overdose admissions between 1987 and 2002 found alprazolam, which happens to be the most prescribed benzodiazepine in Australia and the United States, to be more toxic than diazepam and other benzodiazepines. They also cited a review of the Annual Reports of the American Association of Poison Control Centers National Data Collection System, which showed alprazolam was involved in 34 fatal deliberate self-poisonings over 10 years (1992–2001), compared with 30 fatal deliberate self-poisonings involving diazepam. In a New Zealand study (2003) of 200 deaths, Zopiclone, a benzodiazepine receptor agonist, had similar overdose potential as benzodiazepines.

Pathophysiology
Benzodiazepines bind to a specific benzodiazepine receptor, thereby enhancing the effect of the neurotransmitter gamma-aminobutyric acid (GABA) and causing CNS depression. In overdose situations this pharmacological effect is extended leading to a more severe CNS depression and potentially coma  or cardiac arrest.  Benzodiazepine-overdose-related coma may be characterised by an alpha pattern with the central somatosensory conduction time (CCT) after median nerve stimulation being prolonged and the N20 to be dispersed. Brain-stem auditory evoked potentials demonstrate delayed interpeak latencies (IPLs) I-III, III-V and I-V. Toxic overdoses of benzodiazepines therefore cause prolonged CCT and IPLs.

Diagnosis
The diagnosis of benzodiazepine overdose may be difficult, but is usually made based on the clinical presentation of the patient along with a history of overdose. Obtaining a laboratory test for benzodiazepine blood concentrations can be useful in patients presenting with CNS depression or coma of unknown origin. Techniques available to measure blood concentrations include thin layer chromatography, gas liquid chromatography with or without a mass spectrometer, and radioimmunoassay. Blood benzodiazepine concentrations, however, do not appear to be related to any toxicological effect or predictive of clinical outcome. Blood concentrations are, therefore, used mainly to confirm the diagnosis rather than being useful for the clinical management of the patient.

Treatment
Medical observation and supportive care are the mainstay of treatment of benzodiazepine overdose. Although benzodiazepines are absorbed by activated charcoal, gastric decontamination with activated charcoal is not beneficial in pure benzodiazepine overdose as the risk of adverse effects would outweigh any potential benefit from the procedure. It is recommended only if benzodiazepines have been taken in combination with other drugs that may benefit from decontamination. Gastric lavage (stomach pumping) or whole bowel irrigation are also not recommended. Enhancing elimination of the drug with hemodialysis, hemoperfusion, or forced diuresis is unlikely to be beneficial as these procedures have little effect on the clearance of benzodiazepines due to their large volume of distribution and lipid solubility.

Supportive measures
Supportive measures include observation of vital signs, especially Glasgow Coma Scale and airway patency. IV access with fluid administration and maintenance of the airway with intubation and artificial ventilation may be required if respiratory depression or pulmonary aspiration occurs. Supportive measures should be put in place prior to administration of any benzodiazepine antagonist in order to protect the patient from both the withdrawal effects and possible complications arising from the benzodiazepine. A determination of possible deliberate overdose should be considered with appropriate scrutiny, and precautions taken to prevent any attempt by the patient to commit further bodily harm. Hypotension is corrected with fluid replacement, although catecholamines such as norepinephrine or dopamine may be required to increase blood pressure. Bradycardia is treated with atropine or an infusion of norepinephrine to increase coronary blood flow and heart rate.

Flumazenil
Flumazenil (Romazicon) is a competitive benzodiazepine receptor antagonist that can be used as an antidote for benzodiazepine overdose. Its use, however, is controversial as it has numerous contraindications. It is contraindicated in patients who are on long-term benzodiazepines, those who have ingested a substance that lowers the seizure threshold, or in patients who have tachycardia, widened QRS complex on ECG, anticholinergic signs, or a history of seizures. Due to these contraindications and the possibility of it causing severe adverse effects including seizures, adverse cardiac effects, and death, in the majority of cases there is no indication for the use of flumazenil in the management of benzodiazepine overdose as the risks in general outweigh any potential benefit of administration. It also has no role in the management of unknown overdoses. In addition, if full airway protection has been achieved, a good outcome is expected, and therefore flumazenil administration is unlikely to be required.Flumazenil is very effective at reversing the CNS depression associated with benzodiazepines but is less effective at reversing respiratory depression. One study found that only 10% of the patient population presenting with a benzodiazepine overdose are suitable candidates for flumazenil. In this select population who are naive to and overdose solely on a benzodiazepine, it can be considered. Due to its short half life, the duration of action of flumazenil is usually less than 1 hour, and multiple doses may be needed. When flumazenil is indicated the risks can be reduced or avoided by slow dose titration of flumazenil. Due to risks and its many contraindications, flumazenil should be administered only after discussion with a medical toxicologist.

Epidemiology
In a Swedish (2003) study benzodiazepines were implicated in 39% of suicides by drug poisoning in the elderly 1992–1996. Nitrazepam and flunitrazepam accounted for 90% of benzodiazepine implicated suicides. In cases where benzodiazepines contributed to death, but were not the sole cause, drowning, typically in the bath, was a common method used. Benzodiazepines were the predominant drug class in suicides in this review of Swedish death certificates. In 72% of the cases, benzodiazepines were the only drug consumed. Thus, many of deaths associated with benzodiazepine overdoses may not be a direct result of the toxic effects but either due to being combined with other drugs or used as a tool to kill oneself using a different method, e.g. drowning.In a Swedish retrospective study of deaths of 1987, in 159 of 1587 autopsy cases benzodiazepines were found </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 Thiamine deficiency and can you explain it in depth? [/INST] Thiamine deficiency is a medical condition of low levels of thiamine (Vitamin B1). A severe and chronic form is known as beriberi. The two main types in adults are wet beriberi and dry beriberi. Wet beriberi affects the cardiovascular system, resulting in a fast heart rate, shortness of breath, and leg swelling. Dry beriberi affects the nervous system, resulting in numbness of the hands and feet, confusion, trouble moving the legs, and pain. A form with loss of appetite and constipation may also occur. Another type, acute beriberi, found mostly in babies, presents with loss of appetite, vomiting, lactic acidosis, changes in heart rate, and enlargement of the heart.Risk factors include a diet of mostly white rice, alcoholism, dialysis, chronic diarrhea, and taking high doses of diuretics. In rare cases, it may be due to a genetic condition that results in difficulties absorbing thiamine found in food. Wernicke encephalopathy and Korsakoff syndrome are forms of dry beriberi. Diagnosis is based on symptoms, low levels of thiamine in the urine, high blood lactate, and improvement with thiamine supplementation.Treatment is by thiamine supplementation, either by mouth or by injection. With treatment, symptoms generally resolve in a few weeks. The disease may be prevented at the population level through the fortification of food.Thiamine deficiency is rare in the United States. It remains relatively common in sub-Saharan Africa. Outbreaks have been seen in refugee camps. Thiamine deficiency has been described for thousands of years in Asia, and became more common in the late 1800s with the increased processing of rice.

Signs and symptoms
Symptoms of beriberi include weight loss, emotional disturbances, impaired sensory perception, weakness and pain in the limbs, and periods of irregular heart rate. Edema (swelling of bodily tissues) is common. It may increase the amount of lactic acid and pyruvic acid within the blood. In advanced cases, the disease may cause high-output cardiac failure and death.
Symptoms may occur concurrently with those of Wernickes encephalopathy, a primarily neurological thiamine deficiency-related condition.
Beriberi is divided into four categories. The first three are historical and the fourth, gastrointestinal beriberi, was recognized in 2004:

Dry beriberi especially affects the peripheral nervous system.
Wet beriberi especially affects the cardiovascular system and other bodily systems.
Infantile beriberi affects the babies of malnourished mothers.
Gastrointestinal beriberi affects the digestive system and other bodily systems.

Dry beriberi
Dry beriberi causes wasting and partial paralysis resulting from damaged peripheral nerves.  It is also referred to as endemic neuritis. It is characterized by:

Difficulty with walking
Tingling or loss of sensation (numbness) in hands and feet
Loss of tendon reflexes
Loss of muscle function or paralysis of the lower legs
Mental confusion/speech difficulties
Pain
Involuntary eye movements (nystagmus)
VomitingA selective impairment of the large proprioceptive sensory fibers without motor impairment can occur and present as a prominent sensory ataxia, which is a loss of balance and coordination due to loss of the proprioceptive inputs from the periphery and loss of position sense.

Brain disease
Wernickes encephalopathy (WE), Korsakoff syndrome (also called alcohol amnestic disorder), and Wernicke–Korsakoff syndrome are forms of dry beriberi.Wernickes encephalopathy is the most frequently encountered manifestation of thiamine deficiency in Western society, though it may also occur in patients with impaired nutrition from other causes, such as gastrointestinal disease, those with HIV/AIDS, and with the injudicious administration of parenteral glucose or hyperalimentation without adequate B-vitamin supplementation. This is a striking neuro-psychiatric disorder characterized by paralysis of eye movements, abnormal stance and gait, and markedly deranged mental function.Korsakoff syndrome, in general, is considered to occur with deterioration of brain function in patients initially diagnosed with WE. This is an amnestic-confabulatory syndrome characterized by retrograde and anterograde amnesia, impairment of conceptual functions, and decreased spontaneity and initiative.Alcoholics may have thiamine deficiency because of:

Inadequate nutritional intake:  Alcoholics tend to intake less than the recommended amount of thiamine.
Decreased uptake of thiamine from the GI tract:  Active transport of thiamine into enterocytes is disturbed during acute alcohol exposure.
Liver thiamine stores are reduced due to hepatic steatosis or fibrosis.
Impaired thiamine utilization:  Magnesium, which is required for the binding of thiamine to thiamine-using enzymes within the cell, is also deficient due to chronic alcohol consumption.  The inefficient use of any thiamine that does reach the cells will further exacerbate the thiamine deficiency.
Ethanol per se inhibits thiamine transport in the gastrointestinal system and blocks phosphorylation of thiamine to its cofactor form (ThDP).Following improved nutrition and the removal of alcohol consumption, some impairments linked with thiamine deficiency are reversed, in particular poor brain functionality, although in more severe cases, Wernicke–Korsakoff syndrome leaves permanent damage.  (See delirium tremens.)

Wet beriberi
Wet beriberi affects the heart and circulatory system. It is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become edematous. Wet beriberi is characterized by:

Increased heart rate
Vasodilation leading to decreased systemic vascular resistance, and high-output heart failure
Elevated jugular venous pressure
Dyspnea (shortness of breath) on exertion
Paroxysmal nocturnal dyspnea
Peripheral edema (swelling of lower legs) or generalized edema (swelling throughout the body)
Dilated cardiomyopathy

Gastrointestinal beriberi
Gastrointestinal beriberi causes abdominal pain. It is characterized by:

Abdominal pain
Nausea
Vomiting
Lactic acidosis

Infants
Infantile beriberi usually occurs between two and six months of age in children whose mothers have inadequate thiamine intake. It may present as either wet or dry beriberi.In the acute form, the baby develops dyspnea and cyanosis and soon dies of heart failure. These symptoms may be described in infantile beriberi:

Hoarseness, where the child makes moves to moan, but emits no sound or just faint moans caused by nerve paralysis
Weight loss, becoming thinner and then marasmic as the disease progresses
Vomiting
Diarrhea
Pale skin
Edema
Ill temper
Alterations of the cardiovascular system, especially tachycardia (rapid heart rate)
Convulsions occasionally observed in the terminal stages

Cause
Beriberi is often caused by eating a diet with a very high proportion of calorie rich polished rice (common in Asia) or cassava root (common in sub-Saharan Africa), without much if any thiamine containing animals or vegetables.It may also be caused by shortcomings other than inadequate intake - diseases or operations on the digestive tract, alcoholism, dialysis or genetic deficiencies. All those causes mainly affect the central nervous system, and provoke the development of  Wernickes encephalopathy.
Wernickes disease is one of the most prevalent neurological or neuropsychiatric diseases. In autopsy series, features of Wernicke lesions are observed in approximately 2% of general cases. Medical record research shows that about 85% had not been diagnosed, although only 19% would be asymptomatic. In children, only 58% were diagnosed. In alcohol abusers, autopsy series showed neurological damages at rates of 12.5% or more. Mortality caused by Wernickes disease reaches 17% of diseases, which means 3.4/1000 or about 25 million contemporaries. The number of people with Wernickes disease may be even higher, considering that early stages may have dysfunctions prior to the production of observable lesions at necropsy. In addition, uncounted numbers of people can experience fetal damage and subsequent diseases.

Genetics
Genetic diseases of thiamine transport are rare but serious. Thiamine responsive megaloblastic anemia syndrome (TRMA) with diabetes mellitus and sensorineural deafness is an autosomal recessive disorder caused by mutations in the gene SLC19A2, a high affinity thiamine transporter. TRMA patients do not show signs of systemic thiamine deficiency, suggesting redundancy in the thiamine transport system. This has led to the discovery of a second high-affinity thiamine transporter, SLC19A3. Leigh disease (subacute necrotising encephalomyelopathy) is an inherited disorder that affects mostly infants in the first years of life and is invariably fatal. Pathological similarities between Leigh disease and WE led to the hypothesis that the cause was a defect in thiamine metabolism. One of the most consistent findings has been an abnormality of the activation of the pyruvate dehydrogenase complex.Mutations in the SLC19A3 gene have been linked to biotin-thiamine responsive basal ganglia disease, which is treated with pharmacological doses of thiamine and biotin, another B vitamin.
Other disorders in which a putative role for thiamine has been implicated include subacute necrotising encephalomyelopathy, opsoclonus myoclonus syndrome (a paraneoplastic syndrome), and Nigerian seasonal ataxia (or African seasonal ataxia). In addition, several inherited disorders of ThDP-dependent enzymes have been reported, which may respond to thiamine treatment.

Pathophysiology
Thiamine in the human body has a half-life of 18 days and is quickly exhausted, particularly when metabolic demands exceed intake. A derivative of thiamine, thiamine pyrophosphate (TPP), is a cofactor involved in the citric acid cycle, as well as connecting the breakdown of sugars with the citric acid cycle. The citric acid cycle is a central metabolic pathway involved in the regulation of carbohydrate, lipid, and amino acid metabolism, and its disruption due to thiamine deficiency inhibits the production of many molecules including the neurotransmitters glutamic acid and GABA. Additionally, thiamine may also be directly involved in neuromodulation.

Diagnosis
A positive diagnosis test for thiamine deficiency involves measuring the activity of the enzyme transketolase in erythrocytes (Erythrocyte transketolase activation assay). Alternatively, thiamine and its phosphorylated derivatives can directly be detected in whole blood, tissues, foods, animal feed, and pharmaceutical preparations following the conversion of thiamine to fluorescent thiochrome derivatives (thiochrome assay) and separation by high-performance liquid chromatography (HPLC). Capillary electrophoresis (CE) techniques and in-capillary enzyme reaction methods have emerged as alternative techniques in quantifying and monitoring thiamine levels in samples.
The normal thiamine concentration in EDTA-blood is about 20-100 µg/L.

Treatment
Many people with beriberi can be treated with thiamine alone. Given thiamine intravenously (and later orally), rapid and dramatic recovery occurs, generally within 24 hours.Improvements of peripheral neuropathy may require several months of thiamine treatment.

Epidemiology
Beriberi is a recurrent nutritional disease in detention houses, even in this century. In 1999, an outbreak of beriberi occurred in a detention center in Taiwan. High rates of illness and death in overcrowded Haitian jails in 2007 were traced to the traditional practice of washing rice before cooking. In the Ivory Coast, among a group of prisoners with heavy punishment, 64% were affected by beriberi. Before beginning treatment, prisoners exhibited symptoms of dry or wet beriberi with neurological signs (tingling: 41%), cardiovascular signs (dyspnoea: 42%, thoracic pain: 35%), and edemas of the lower limbs (51%). With treatment, the rate of healing was about 97%.Populations under extreme stress may be at higher risk for beriberi. Displaced populations, such as refugees from war, are susceptible to micronutritional deficiency, including beriberi. The severe nutritional deprivation caused by famine also can cause beriberis, although symptoms may be overlooked in clinical assessment or masked by other famine-related problems. An extreme weight-loss diet can, rarely, induce a famine-like state and the accompanying beriberi.

History
Earliest written descriptions of thiamine deficiency are from ancient China in the context of Chinese medicine. One of the earliest is by Ge Hong in his book Zhou hou bei ji fang (Emergency Formulas to Keep up Your Sleeve) written sometime during the third century. Hong called the illness by the name jiao qi, which can be interpreted as "foot qi". He described the symptoms to include swelling, weakness, and numbness of the feet. He also acknowledged that the illness could be deadly, and claimed that it could be cured by eating certain foods, such as fermented soybeans in wine. Better known examples of early descriptions of "foot qi" are by Chao Yuanfang (who lived during 550–630) in his book Zhu bing yuan hou lun (Sources and Symptoms of All Diseases) and by Sun Simiao (581–682) in his book Bei ji qian jin yao fang (Essential Emergency Formulas Worth a Thousand in Gold).In the late 19th century, beriberi was studied by Takaki Kanehiro, a British-trained Japanese medical doctor of the Imperial Japanese Navy. Beriberi was a serious problem in the Japanese navy; sailors fell ill an average of four times a year in the period 1878 to 1881, and 35% were cases of beriberi. In 1883, Takaki learned of a very high incidence of beriberi among cadets on a training mission from Japan to Hawaii, via New Zealand and South America. The voyage lasted more than nine months and resulted in 169 cases of sickness and 25 deaths on a ship of 376 men. With the support of the Japanese Navy, he conducted an experiment in which another ship was deployed on the same route, except that its crew was fed a diet of meat, fish, barley, rice, and beans. At the end of the voyage, this crew had only 14 cases of beriberi and no deaths. This convinced Takaki and the Japanese Navy that diet was the cause. In 1884, Takaki observed that beriberi was common among low-ranking crew who were often provided free rice, thus ate little else, but not among crews of Western navies, nor among Japanese officers who consumed a more varied diet.
In 1897, Christiaan Eijkman, a Dutch physician and pathologist, demonstrated that beriberi is caused by poor diet, and discovered that feeding unpolished rice (instead of the polished variety) to chickens helped to prevent beriberi. The following year, Sir Frederick Hopkins postulated that some foods contained "accessory factors"—in addition to proteins, carbohydrates, fats, and salt—that were necessary for the functions of the human body. In 1901, Gerrit Grijns, a Dutch physician and assistant to Christiaan Eijkman in the Netherlands, correctly interpreted beriberi as a deficiency syndrome, and between 1910 and 1913, Edward Bright Vedder established that an extract of rice bran is a treatment for beriberi. In 1929, Eijkman and Hopkins were awarded the Nobel Prize for Physiology or Medicine for their discoveries.

Etymology
Although according to the Oxford English Dictionary, the term "beriberi" comes from a Sinhalese phrase meaning "weak, weak" or "I cannot, I cannot", the word being duplicated for emphasis, the origin of the phrase is questionable. It has also been suggested to come from Hindi, Arabic, and a few other languages, with many meanings like "weakness", "sailor", and even "sheep". Such suggested origins were listed by Heinrich Botho Scheube, among others. Edward Vedder wrote in his book Beriberi (1913) that "it is impossible to definitely trace the origin of the word beriberi". Word berbere was used in writing at least as early as 1568 by Diogo do Couto, when he described the deficiency in India.Kakke, which is a Japanese synonym for thiamine deficiency, comes from the way "jiao qi" is pronounced in Japanese. "Jiao qi" is an old word used in Chinese medicine to describe beriberi. "Kakke" is supposed to have entered into the Japanese language sometime between the sixth and eighth centuries.

Other animals
Poultry
As most feedstuffs used in poultry diets contain enough quantities of vitamins to meet the requirements in this species, deficiencies in this vitamin do not occur with commercial diets. This was, at least, the opinion in the 1960s.Mature chickens show signs three weeks after being fed a deficient diet. In young chicks, it can appear before two weeks of age. Onset is sudden in young chicks, with anorexia and an unsteady gait. Later on, locomotor signs begin, with an apparent paralysis of the flexor of the toes. The characteristic position is called "stargazing", with the affected animal sitting on its hocks with its head thrown back in a posture called opisthotonos.  Response to administration of the vitamin is rather quick, occurring a few hours later.

Ruminants
Polioencephalomalacia (PEM) is the most common thiamine deficiency disorder in young ruminant and nonruminant animals.  Symptoms of PEM include a profuse, but transient, diarrhea, listlessness, circling movements, stargazing or opisthotonus (head drawn back over neck), and muscle tremors. The most common cause is high-carbohydrate feeds, leading to the overgrowth of thiaminase-producing bacteria, but dietary ingestion of thiaminase (e.g., in bracken fern), or inhibition of thiamine absorption by high sulfur intake are also possible.  Another cause of PEM is Clostridium sporogenes or Bacillus aneurinolyticus infection. These bacteria produce thiaminases that can cause an acute thiamine deficiency in the affected animal.

Snakes
Snakes that consume a diet largely composed of goldfish and feeder minnows are susceptible to developing thiamine deficiency. This is often a problem observed in captivity when keeping garter and ribbon snakes that are fed a goldfish-exclusive diet, as these fish contain thiaminase, an enzyme that breaks down thiamine.

Wild birds and fish
Thiamine deficiency has been identified as the cause of a paralytic disease affecting wild birds in the Baltic Sea area dating back to 1982. In this condition, there is difficulty in keeping the wings folded along the side of the body when resting, loss of the ability to fly and voice, with eventual paralysis of the wings and legs and death. It affects primarily 0.5–1 kg-sized birds such as the European herring gull (Larus argentatus), common starling (Sturnus vulgaris), and common eider (Somateria mollissima). Researches noted, "Because the investigated species occupy a wide range of ecological niches and positions in the food web, we are open to the possibility that other animal classes may develop thiamine deficiency, as well."p. 12006In the counties of Blekinge and Skåne (southernmost Sweden), mass deaths of several bird species, especially the European herring gull, have been observed since the early 2000s. More recently, species of other classes seems to be affected. High mortality of salmon (Salmo salar) in the river Mörrumsån is reported, and mammals such as the Eurasian elk (Alces alces) have died in unusually high numbers. Lack of thiamine is the common denominator where analysis is done. In April 2012, the County Administrative Board of Blekinge found the situation so alarming that they asked the Swedish government to set up a closer investigation.

References
Further reading
Arnold, D (2010). "British India and the beri-beri problem". Medical History. 54 (3): 295–314. doi:10.1017/S0025727300004622. PMC 2889456. PMID 20592882.
Chisholm, Hugh, ed. (1911). "Beri-Beri"  </s>