<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Cannabis use disorder and explain in detail? [/INST] Cannabis use disorder (CUD), also known as cannabis addiction or marijuana addiction, is defined in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and ICD-10 as the continued use of cannabis despite clinically significant impairment.

Signs and symptoms
Cannabis use is associated with comorbid mental health problems, such as mood and anxiety disorders, and discontinuing cannabis use is difficult for some users. Psychiatric comorbidities are often present in dependent cannabis users including a range of personality disorders.Based on annual survey data, some high school seniors who report smoking daily (nearly 7%, according to one study) may function at a lower rate in school than students that do not. The sedating and anxiolytic properties of tetrahydrocannabinol (THC) in some users might make the use of cannabis an attempt to self-medicate personality or psychiatric disorders.

Dependency
Prolonged cannabis use produces both pharmacokinetic changes (how the drug is absorbed, distributed, metabolized, and excreted) and pharmacodynamic changes (how the drug interacts with target cells) to the body. These changes require the user to consume higher doses of the drug to achieve a common desirable effect (known as a higher tolerance), reinforcing the bodys metabolic systems for eliminating the drug more efficiently and further down-regulating cannabinoid receptors in the brain.Cannabis users have shown decreased reactivity to dopamine, suggesting a possible link to a dampening of the reward system of the brain and an increase in negative emotion and addiction severity.Cannabis users can develop tolerance to the effects of THC. Tolerance to the behavioral and psychological effects of THC has been demonstrated in adolescent humans and animals. The mechanisms that create this tolerance to THC are thought to involve changes in cannabinoid receptor function.One study has shown that between 2001–2002 and 2012–2013, the use of marijuana in the US doubled.Cannabis dependence develops in about 9% of users, significantly less than that of heroin, cocaine, alcohol, and prescribed anxiolytics, but slightly higher than that for psilocybin, mescaline, or LSD. Of those who use cannabis daily, 10–20% develop dependence.

Withdrawal
Cannabis withdrawal symptoms occur in one-half of people in treatment for cannabis use disorders. Symptoms may include dysphoria (anxiety, irritability, depression, restlessness), disturbed sleep, gastrointestinal symptoms, and decreased appetite. It is often paired with rhythmic movement disorder. Most symptoms begin during the first week of abstinence and resolve after a few weeks. About 12% of heavy cannabis users showed cannabis withdrawal as defined by the DSM-5, and this was associated with significant disability as well as mood, anxiety and personality disorders.

Cause
Cannabis addiction is often due to prolonged and increasing use of the drug. Increasing the strength of the cannabis taken and an increasing use of more effective methods of delivery often increase the progression of cannabis dependency. It can also be caused by being prone to becoming addicted to substances, which can either be genetically or environmentally acquired.

Risk factors
Certain factors are considered to heighten the risk of developing cannabis dependence and longitudinal studies over a number of years have enabled researchers to track aspects of social and psychological development concurrently with cannabis use. Increasing evidence is being shown for the elevation of associated problems by the frequency and age at which cannabis is used, with young and frequent users being at most risk.The main factors in Australia, for example, related to a heightened risk for developing problems with cannabis use include frequent use at a young age; personal maladjustment; emotional distress; poor parenting; school drop-out; affiliation with drug-using peers; moving away from home at an early age; daily cigarette smoking; and ready access to cannabis. The researchers concluded there is emerging evidence that positive experiences to early cannabis use are a significant predictor of late dependence and that genetic predisposition plays a role in the development of problematic use.

High risk groups
A number of groups have been identified as being at greater risk of developing cannabis dependence and, in Australia, for example, have been found to include adolescent populations, Aboriginal and Torres Strait Islanders and people with mental health conditions.

Adolescents
The endocannabinoid system is directly involved in adolescent brain development. Adolescent cannabis users are therefore particularly vulnerable to the potential adverse effects of cannabis use. Adolescent cannabis use is associated with increased cannabis misuse as an adult, issues with memory and concentration, long-term cognitive complications, and poor psychiatric outcomes including social anxiety, suicidality and addiction.There are a lot of reasons why adolescents start a smoking habit. According to a study completed by Bill Sanders, influence from friends, difficult household problems, and experimentation are some of the reasons why this population starts to smoke marijuana. This segment of population seems to be one of the most influenceable group there is. They want to follow the group and look "cool", "hip" and accepted by their friends. This fear of rejection plays a big role in their decision to smoke pot. However it does not seem to be the most important factor. According to a study from Canada, the lack of knowledge about cannabis seems to be the main reason why adolescents start to smoke. The authors observed a high correlation between adolescents that knew about the mental and physical harms of cannabis and their consumption. Of the 1045 young participants in the study, those who could name the least number of negative effects about this drug were usually the ones who were consuming it. They were not isolated cases either. Actually, the study showed that the proportion of teenagers who saw cannabis as a high-risk drug and the ones who thought the contrary was about the same.

Pregnancy
There is an association between smoking cannabis during pregnancy and low birth weight. Smoking cannabis during pregnancy can lower the amount of oxygen delivered to the developing fetus, which can restrict fetal growth. The active ingredient in cannabis (D9-tetrahydrocannabinol, THC) is fat soluble and can enter into breastmilk during lactation. THC in breastmilk can then subsequently be taken up by a breastfeeding infant, as shown by the presence of THC in the infants feces. However, the evidence for long-term effects of exposure to THC through breastmilk is unclear.

Diagnosis
Cannabis use disorder is recognized in the fifth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), which also added cannabis withdrawal as a new condition.In the 2013 revision for the DSM-5, DSM-IV abuse and dependence were combined into cannabis use disorder. The legal problems criterion (from cannabis abuse) has been removed, and the craving criterion was newly added, resulting in a total of eleven criteria: hazardous use, social/interpersonal problems, neglected major roles, withdrawal, tolerance, used larger amounts/longer, repeated attempts to quit/control use, much time spent using, physical/psychological problems related to use, activities given up and craving. For a diagnosis of DSM-5 cannabis use disorder, at least two of these criteria need to be present in the last twelve-month period. Additionally, three severity levels have been defined: mild (two or three criteria), moderate (four or five criteria) and severe (six or more criteria) cannabis use disorder.Cannabis use disorder is also recognized in the eleventh revision of the International Classification of Diseases (ICD-11), adding more subdivisions including time intervals of pattern of use (episodic, continuous, or unspecified) and dependence (current, early full remission, sustained partial remission, sustained full remission, or unspecified) compared to the 10th revision.A 2019 meta-analysis found that 34% of people with cannabis-induced psychosis transitioned to schizophrenia. This was found to be comparatively higher than hallucinogens (26%) and amphetamines (22%).To screen for cannabis-related problems, several methods are used. Scales specific to cannabis, which provides the benefit of being cost efficient compared to extensive diagnostic interviews, include the Cannabis Abuse Screening Test (CAST), Cannabis Use Identification Test (CUDIT), and Cannabis Use Problems Identification Test (CUPIT). Scales for general drug use disorders are also used, including the Severity Dependence Scale (SDS), Drug Use Disorder Identification Test (DUDIT), and Alcohol, Smoking, and Substance Involvement Screening Test (ASSIST). However, there are no gold standard and both older and newer scales are still in use. To quantify cannabis use, methods such as Timeline Follow-Back (TLFB) and Cannabis Use Daily (CUD) are used. These methods measure general consumption and not grams of psychoactive substance as the concentration of THC may vary among drug users.

Treatment
Clinicians differentiate between casual users who have difficulty with drug screens, and daily heavy users, to a chronic user who uses multiple times a day. In the US, as of 2013, cannabis is the most commonly identified illicit substance used by people admitted to treatment facilities. Demand for treatment for cannabis use disorder increased internationally between 1995 and 2002. In the United States, the average adult who seeks treatment has consumed cannabis for over 10 years almost daily and has attempted to quit six or more times.Treatment options for cannabis dependence are far fewer than for opiate or alcohol dependence. Most treatment falls into the categories of psychological or psychotherapeutic, intervention, pharmacological intervention or treatment through peer support and environmental approaches. No medications have been found effective for cannabis dependence, but psychotherapeutic models hold promise. Screening and brief intervention sessions can be given in a variety of settings, particularly at doctors offices, which is of importance as most cannabis users seeking help will do so from their general practitioner rather than a drug treatment service agency.The most commonly accessed forms of treatment in Australia are 12-step programmes, physicians, rehabilitation programmes, and detox services, with inpatient and outpatient services equally accessed. In the EU approximately 20% of all primary admissions and 29% of all new drug clients in 2005, had primary cannabis problems. And in all countries that reported data between 1999 and 2005 the number of people seeking treatment for cannabis use increased.

Psychological
Psychological intervention includes cognitive behavioral therapy (CBT), motivational enhancement therapy (MET), contingency management (CM), supportive-expressive psychotherapy (SEP), family and systems interventions, and twelve-step programs.Evaluations of Marijuana Anonymous programs, modelled on the 12-step lines of Alcoholics Anonymous and Narcotics Anonymous, have shown small beneficial effects for general drug use reduction. In 2006, the Wisconsin Initiative to Promote Healthy Lifestyles implemented a program that helps primary care physicians identify and address marijuana use problems in patients.

Medication
As of 2020, there is no single medication that has been proven effective for treating cannabis use disorder; research is focused on three treatment approaches: agonist substitution, antagonist, and modulation of other neurotransmitter systems. More broadly, the goal of medication therapy for cannabis use disorder centers around targeting the stages of the addiction: acute intoxication/binge, withdrawal/negative affect, and preoccupation/anticipation.For the treatment of the withdrawal/negative affect symptom domain of cannabis use disorder, medications may work by alleviating restlessness, irritable or depressed mood, anxiety, and insomnia. Bupropion, which is a norepinephrine–dopamine reuptake inhibitor, has been studied for the treatment of withdrawal with largely poor results. Atomoxetine has also shown poor results, and is as a norepinephrine reuptake inhibitor, though it does increase the release of dopamine through downstream effects in the prefrontal cortex (an area of the brain responsible for planning complex tasks and behavior). Venlafaxine, a serotonin–norepinephrine reuptake inhibitor, has also been studied for cannabis use disorder, with the thought that the serotonergic component may be useful for the depressed mood or anxious dimensions of the withdrawal symptom domain. While venlafaxine has been shown to improve mood for people with cannabis use disorder, a clinical trial in this population actually found worse cannabis abstinence rates compared to placebo. It is worth noting that venlafaxine is sometimes poorly tolerated, and infrequent use or abrupt discontinuation of its use can lead to withdrawal symptoms from the medication itself, including irritability, dysphoria, and insomnia. It is possible that venlafaxine use actually exacerbated cannabis withdrawal symptoms, leading people to use more cannabis than placebo to alleviate their discomfort. Mirtazapine, which increases serotonin and norepinephrine, has also failed to improve abstinence rates in people with cannabis use disorder.People sometimes use cannabis to cope with their anxiety, and cannabis withdrawal can lead to symptoms of anxiety. Buspirone, a serotonin 1A receptor (5-HT1A) agonist, has shown limited efficacy for treating anxiety in people with cannabis use disorder, though there may be better efficacy in males than in females. Fluoxetine, a selective serotonin reuptake inhibitor, has failed to show efficacy in adolescents with both cannabis use disorder and depression. SSRIs are a class of antidepressant drugs that are also used for the treatment of anxiety disorders, such as generalized anxiety disorder. Vilazodone, which has both SSRI and 5-HT1A agonism properties, also failed to increase abstinence rates in people with cannabis use disorder.Studies of divalproex have found no significant benefit, though some studies have found mixed results. Baclofen, a GABA-B receptor agonist and antispasmodic medication, has been found to reduce cravings but without a significant benefit towards preventing relapse or improving sleep. Zolpidem, a GABA-A receptor agonist and "Z-hypnotic" medication, has shown some efficacy in treating insomnia due to cannabis withdrawal, though there is a potential for misuse. Entacapone was well tolerated and decreased cannabis cravings in a trial on a small number of patients. Topiramate, an antiepileptic drug, has shown mixed results in adolescents, reducing the volume of cannabis consumption without significantly increasing abstinence, with somewhat poor tolerability. Gabapentin, an indirect GABA modulator, has shown some preliminary benefit for reducing cravings and cannabis use.The agonist substitution approach is one that draws upon the analogy of the success of nicotine replacement therapy for nicotine addiction. Dronabinol, which is synthetic THC, has shown benefit in reducing cravings and other symptoms of withdrawal, though without preventing relapse or promoting abstinence. Combination therapy with dronabinol and the alpha 2 adrenergic receptor agonist lofexidine have shown mixed results, with possible benefits towards reducing withdrawal symptoms. However, overall, the combination of dronabinol and lofexidine is likely not effective for the treatment of cannabis use disorder. Nabilone, a synthetic THC analogue, has shown benefits in reducing symptoms of withdrawal such as difficulty sleeping, and decreased overall cannabis use. Despite its psychoactive effects, the slower onset of action and longer duration of action of nabilone make it less likely to be abused than cannabis itself, which makes nabilone a promising harm reduction strategy for the treatment of cannabis use disorder. The combination of nabilone and zolpidem has been shown to decrease sleep-related and mood-related symptoms of cannabis withdrawal, in addition to decreasing cannabis use. Nabiximols, a combined THC and cannabidiol (CBD) product that is formulated as an oral (buccal) spray, has been shown to improve withdrawal symptoms without improving abstinence rates. Oral CBD has not shown efficacy in reducing the signs or symptoms of cannabis use, and likely has no benefit in cannabis use withdrawal symptoms. The CB-1 receptor antagonist rimonabant has shown efficacy in reducing the effects of cannabis in users, but with a risk for serious psychiatric side effects.Naltrexone, a mu opioid receptor antagonist, has shown mixed results for cannabis use disorder—both increasing the subjective effects of cannabis when given acutely, but potentially decreasing the overall use of cannabis with chronic administration. N-acetylcysteine (NAC) has shown some limited benefit in decreasing cannabis use in adolescents, though not with adults. Lithium, a mood stabilizer, has shown mixed results for treating symptoms of cannabis withdrawal, but is likely ineffective. Quetiapine, a second-generation antipsychotic, has been shown to treat cannabis withdrawal related insomnia and decreased appetite at the expense of exacerbating cravings. Oxytocin, a neuropeptide that the body produces, has shown some benefit in reducing the use of cannabis when administered intranasally in combination with motivational enhancement therapy sessions, though the treatment effect did not persist between sessions.Finally, CB1 antagonists such as rimonabant have been tested for utility in CUD. These drugs are effective at blocking the subjective effects of cannabis intoxication as well as the somatic components. This is accomplished by preventing THC binding to the CB1 receptor, effectively eliminating the ability to get high. This is similar to how naloxone and naltrexone are used for opiates </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Koebner phenomenon and explain in detail? [/INST] The Koebner phenomenon or Köbner phenomenon (UK: , US: ), also called the Koebner response or the isomorphic response, attributed to Heinrich Köbner, is the appearance of skin lesions on lines of trauma.  The Koebner phenomenon may result from either a linear exposure or irritation.  Conditions demonstrating linear lesions after a linear exposure to a causative agent include: molluscum contagiosum, warts and toxicodendron dermatitis (a dermatitis caused by a genus of plants including poison ivy).  Warts and molluscum contagiosum lesions can be spread in linear patterns by self-scratching ("auto-inoculation").  Toxicodendron dermatitis lesions are often linear from brushing up against the plant.  Causes of the Koebner phenomenon that are secondary to scratching rather than an infective or chemical cause include vitiligo, psoriasis, lichen planus, lichen nitidus, pityriasis rubra pilaris, and keratosis follicularis (Darier disease).

Definition
The Koebner phenomenon describes skin lesions which appear at the site of injury. It is seen in:
Psoriasis
Pityriasis rubra pilaris
Lichen planus
Flat warts
Lichen nitidus
Vitiligo
Lichen sclerosus
Elastosis perforans serpiginosa
Kaposi sarcoma
Necrobiosis lipoidica
Lupus
Juvenile Idiopathic Arthritis
Still disease
Cutaneous leishmaniasis
Post kala azar dermal leishmaniasisA similar response occurs in pyoderma gangrenosum and Behcets syndrome, and is referred to as pathergy.Rarely Koebner phenomenon has been reported as a mechanism of acute myeloid leukemia dissemination.Warts and molluscum contagiosum are often listed as causing a Koebner reaction, but this is by direct inoculation of viral particles.The linear arrangement of skin lesions in the Koebner phenomenon can be contrasted to both lines of Blaschko and dermatomal distributions </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Congenital syphilis and explain in detail? [/INST] Congenital syphilis is syphilis present in utero and at birth, and occurs when a child is born to a mother with syphilis. Untreated early syphilis infections results in a high risk of poor pregnancy outcomes, including saddle nose, lower extremity abnormalities, miscarriages, premature births, stillbirths, or death in newborns. Some infants with congenital syphilis have symptoms at birth, but many develop symptoms later. Symptoms may include rash, fever, an enlarged liver and spleen, and skeletal abnormalities. Newborns will typically not develop a primary syphilitic chancre but may present with signs of secondary syphilis (i.e. generalized body rash). Often these babies will develop syphilitic rhinitis ("snuffles"), the mucus from which is laden with the T. pallidum bacterium, and therefore highly infectious. If a baby with congenital syphilis is not treated early, damage to the bones, teeth, eyes, ears, and brain can occur.

Classification
Early
This is a subset of cases of congenital syphilis. Newborns may be asymptomatic and are only identified on routine prenatal screening. If not identified and treated, these newborns develop poor feeding and runny nose. By definition, early congenital syphilis occurs in children between 0 and 2 years old </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Glomus tumor and explain in detail? [/INST] Glomus tumor was also the name formerly (and incorrectly) used for a tumor now called a paraganglioma.A glomus tumor (also known as a "solitary glomus tumor," "solid glomus tumor,") is a rare neoplasm arising from the glomus body and mainly found under the nail, on the fingertip or in the foot.: 670   They account for less than 2% of all soft tissue tumors. The majority of glomus tumors are benign, but they can also show malignant features. Glomus tumors were first described by Hoyer in 1877 while the first complete clinical description was given by Masson in 1924.Histologically, glomus tumors are made up of an afferent arteriole, anastomotic vessel, and collecting venule. Glomus tumors are modified smooth muscle cells that control the thermoregulatory function of dermal glomus bodies. As stated above, these lesions should not be confused with paragangliomas, which were formerly also called glomus tumors in now-antiquated clinical usage. Glomus tumors do not arise from glomus cells, but paragangliomas do.
Familial glomangiomas have been associated with a variety of deletions in the GLMN (glomulin) gene, and are inherited in an autosomal dominant manner, with incomplete penetrance.

Signs and symptoms
Glomus tumors are usually solitary and small lesions. The vast majority are found in the hand, wrist, foot, and under the fingernails.They are often painful, and the pain is reproduced when the lesion is placed in cold water. Multiple tumors are less likely to be painful.
These tumors tend to have a bluish discoloration, although a whitish appearance may also be noted. Elevation of the nail bed can occur.
In rare cases, the tumors may present in other body areas, such as the gastric antrum or glans penis </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Nummular dermatitis and explain in detail? [/INST] Nummular dermatitis is one of the many forms of dermatitis. it is characterized by round or oval-shaped itchy lesions. The name comes from the Latin word "nummus," which means "coin."

Signs and symptoms
Nummular dermatitis is characterized by chronic or relapsing itchy coin-sized ovoid-shaped red plaques. They can occur on the trunk, limbs, face, and hands.

Causes
Many contact sensitizers or irritants are known to cause contact dermatitis superimposed on nummular dermatitis. Studies have implicated nickel, cobalt, chromate, and fragrance as likely culprits. Xerosis, or dehydration of skin is also a likely cause. Infection with Staphylococcus aureus bacteria or Candida albicans may also play a role.

Diagnosis
Diagnosis of nummular dermatitis is largely via clinical observation </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Achilles tendinitis and explain in detail? [/INST] Achilles tendinitis, also known as achilles tendinopathy, occurs when the Achilles tendon, found at the back of the ankle, becomes sore. Achilles tendinopathy is accompanied by alterations in the tendons structure and mechanical properties. The most common symptoms are pain and swelling around the affected tendon. The pain is typically worse at the start of exercise and decreases thereafter. Stiffness of the ankle may also be present. Onset is generally gradual.It commonly occurs as a result of overuse such as running. Other risk factors include trauma, a lifestyle that includes little exercise, high-heel shoes, rheumatoid arthritis, and medications of the fluoroquinolone or steroid class. Diagnosis is generally based on symptoms and examination.There are several simple actions that individuals can take to prevent or reduce tendinitis. Though commonly used, some of these actions have limited or no scientific evidence to support them, namely pre-exercise stretching. Strengthening calf muscles, avoiding over-training, and selecting more appropriate footwear are more well-regarded options. Running mechanics can be improved with simple exercises that will help runners avoid achilles injury. Treatment typically involves rest, ice, non-steroidal antiinflammatory agents (NSAIDs), and physical therapy. In those whose symptoms last more than six months despite other treatments, surgery may be considered. Achilles tendinitis is relatively common.

Signs and symptoms
Symptoms can vary from an ache or pain and swelling to the local area of the ankles, or a burning that surrounds the whole joint. With this condition, the pain is usually worse during and after activity, and the tendon and joint area can become stiffer the following day as swelling impinges on the movement of the tendon. Many patients report stressful situations in their lives in correlation with the beginnings of pain which may contribute to the symptoms.Achilles tendon injuries can be separated into insertional tendinopathy (20%–25% of the injuries), midportion tendinopathy (55%–65%), and proximal musculotendinous junction (9%–25%) injuries, according to the location of pain.

Cause
Achilles tendinitis is a common injury, particularly in sports that involve lunging and jumping. It is also a known side effect of fluoroquinolone antibiotics such as ciprofloxacin, as are other types of tendinitis.Swelling in a region of micro-damage or partial tear can be detected visually or by touch.  Increased water content and disorganized collagen matrix in tendon lesions may be detected by ultrasonography or magnetic resonance imaging.Achilles tendinitis is thought to have physiological, mechanical, or extrinsic (i.e. footwear or training) causes. Physiologically, the Achilles tendon is subject to poor blood supply through the synovial sheaths that surround it. This lack of blood supply can lead to the degradation of collagen fibers and inflammation. Tightness in the calf muscles has also been known to be involved in the onset of Achilles tendinitis.During the loading phase of the running and walking cycle, the ankle and foot naturally pronate and supinate by approximately 5 degrees. Excessive pronation of the foot (over 5 degrees) in the subtalar joint is a type of mechanical mechanism that can lead to tendinitis.An overuse injury refers to repeated stress and strain, which is likely the case in endurance runners. Overuse can simply mean an increase in running, jumping or plyometric exercise intensity too soon.  Another consideration would be the use of improper or worn-down footwear, which lack the necessary support to maintain the foot in the natural/normal pronation.

Pathophysiology
The Achilles tendon is the extension of the calf muscle and attaches to the heel bone. It causes the foot to extend (plantar flexion) when those muscles contract.The Achilles tendon does not have good blood supply or cell activity, so this injury can be slow to heal. The tendon receives nutrients from the tendon sheath or paratendon. When an injury occurs to the tendon, cells from surrounding structures migrate into the tendon to assist in repair. Some of these cells come from blood vessels that enter the tendon to provide direct blood flow to increase healing. With the blood vessels come nerve fibers. Researchers including Alfredson and his team in Sweden  believe these nerve fibers to be the cause of the pain - they injected local anaesthetic around the vessels and this decreased significantly the pain from the Achilles tendon.

Diagnosis
Achilles tendinitis is usually diagnosed from a medical history, and  physical examination of the tendon. Projectional radiography shows calcification deposits within the tendon at its calcaneal insertion in approximately 60 percent of cases. Magnetic resonance imaging (MRI) can determine the extent of tendon degeneration, and may show differential diagnoses such as bursitis.

Prevention
Performing consistent physical activity will improve the elasticity and strength of the tendon, which will assist in resisting the forces that are applied.While stretching before beginning an exercise session is often recommended evidence to support this practice is limited. Prevention of recurrence includes following appropriate exercise habits and wearing low-heeled shoes. In the case of incorrect foot alignment, orthotics can be used to properly position the feet. Footwear that is specialized to provide shock-absorption can be utilized to defend the longevity of the tendon. Achilles tendon injuries can be the result of exceeding the tendons capabilities for loading, therefore it is important to gradually adapt to exercise if someone is inexperienced, sedentary, or is an athlete who is not progressing at a steady rate.Eccentric strengthening exercises of the gastrocnemius and soleus muscles are utilized to improve the tensile strength of the tendon and lengthen the musculotendinous junction, decreasing the amount of strain experienced with ankle joint movements. This eccentric training method is especially important for individuals with chronic Achilles tendinosis which is classified as the degeneration of collagen fibers </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Vesicoureteral reflux and explain in detail? [/INST] Vesicoureteral reflux (VUR), also known as vesicoureteric reflux, is a condition in which urine flows retrograde, or backward, from the bladder into one or both ureters and then to the renal calyx or kidneys. Urine normally travels in one direction (forward, or anterograde) from the kidneys to the bladder via the ureters, with a 1-way valve at the vesicoureteral (ureteral-bladder) junction preventing backflow.  The valve is formed by oblique tunneling of the distal ureter through the wall of the bladder, creating a short length of ureter (1–2 cm) that can be compressed as the bladder fills.  Reflux occurs if the ureter enters the bladder without sufficient tunneling, i.e., too "end-on".

Signs and symptoms
Most children with vesicoureteral reflux are asymptomatic.  Vesicoureteral reflux may be diagnosed as a result of further evaluation of dilation of the kidney or ureters draining urine from the kidney while in utero as well as when a sibling has VUR (though routine testing in either circumstance is controversial).  Reflux also increases risk of acute bladder and kidney infections, so testing for reflux may be performed after a child has one or more infections.
In infants, the signs and symptoms of a urinary tract infection may include only fever and lethargy, with poor appetite and sometimes foul-smelling urine, while older children typically present with discomfort or pain with urination and frequent urination.

Causes
In healthy individuals the ureters enter the urinary bladder obliquely and run submucosally for some distance. This, in addition to the ureters muscular attachments, helps secure and support them posteriorly. Together these features produce a valvelike effect that occludes the ureteric opening during storage and voiding of urine. In people with VUR, failure of this mechanism occurs, with resultant backward (retrograde) flow of urine.

Primary VUR
Insufficient submucosal length of the ureter relative to its diameter causes inadequacy of the valvular mechanism. This is precipitated by a congenital defect or lack of longitudinal muscle of the portion of the ureter within the bladder resulting in an ureterovesicular junction (UVJ) abnormality.

Secondary VUR
In this category the ureters valvular mechanism is initially intact and healthy but becomes overwhelmed by increased bladder pressures associated with obstruction, which distorts the ureterovesicular junction. The obstructions may be anatomical or functional. Secondary VUR can be further divided into anatomical and functional groups.

Anatomical
Posterior urethral valves; urethral or meatal stenosis. These causes are treated surgically when possible.

Functional
Bladder instability, neurogenic bladder and non-neurogenic bladder. Bladder infections may cause reflux due to the elevated pressures associated with inflammation.Resolution of functional VUR will usually occur if the precipitating cause is treated and resolved. Medical and/or surgical treatment may be indicated.

Diagnosis
The following procedures may be used to diagnose VUR:

Cystography
Fluoroscopic voiding cystourethrogram (VCUG)
Abdominal ultrasound
Technetium-99m Dimercaptosuccunic Acid (DMSA) ScintigraphyAn abdominal ultrasound might suggest the presence of VUR if ureteral dilatation is present; however, in many circumstances of VUR of low to moderate, even high severity, the sonogram may be completely normal, thus providing insufficient utility as a single diagnostic test in the evaluation of children suspected of having VUR, such as those presenting with prenatal hydronephrosis or urinary tract infection (UTI).VCUG is the method of choice for grading and initial workup, while RNC is preferred for subsequent evaluations as there is less exposure to radiation. A high index of suspicion should be attached to any case where a child presents with a urinary tract infection, and anatomical causes should be excluded. A VCUG and abdominal ultrasound should be performed in these cases
DMSA scintigraphy is used for the evaluation of the parenchymal damage, which is seen as cortical scars. After the first febrile UTI, the diagnostic role of an initial scintigraphy for detecting the damage before the VCUG was investigated and it was suggested that VCUG can be omitted in children who has no cortical scars and urinary tract dilatation.Early diagnosis in children is crucial as studies have shown that the children with VUR who present with a UTI and associated acute pyelonephritis are more likely to develop permanent renal cortical scarring than those children without VUR, with an odds ratio of 2.8. Thus VUR not only increases the frequency of UTIs, but also the risk of damage to upper urinary structures and end-stage renal disease.

Severity
Vesicoureteral reflux (VUR) is graded according to severity.
Grade I – reflux into non-dilated ureter
Grade II – reflux into the renal pelvis and calyces without dilatation
Grade III – mild/moderate dilatation of the ureter, renal pelvis and calyces with minimal blunting of the fornices
Grade IV – dilation of the renal pelvis and calyces with moderate ureteral tortuosity
Grade V – gross dilatation of the ureter, pelvis and calyces; ureteral tortuosity; loss of papillary impressionsThe younger the patient and the lower the grade at presentation the higher the chance of spontaneous resolution. Approximately 85% of grade I & II VUR cases will resolve spontaneously. Approximately 50% of grade III cases and a lower percentage of higher grades will also resolve spontaneously.

Treatment
The goal of treatment is to minimize infections, as it is infections that cause renal scarring and not the vesicoureteral reflux.   Minimizing infections is primarily done by prophylactic antibiotics in newborns and infants who are not potty trained.  However, in children who are older, physicians and parents should focus on bowel and bladder management.  Children who hold their bladder or who are constipated have a greater number of infections than children who void on a regular schedule.  When medical management fails to prevent recurrent urinary tract infections, or if the kidneys show progressive renal scarring then surgical interventions may be necessary. Medical management is recommended in children with Grade I-III VUR as most cases will resolve spontaneously. A trial of medical treatment is indicated in patients with Grade IV VUR especially in younger patients or those with unilateral disease. Of the patients with Grade V VUR only infants are trialled on a medical approach before surgery is indicated, in older patients surgery is the only option.

Endoscopic injection
Endoscopic injection involves applying a gel around the ureteral opening to create a valve function and stop urine from flowing back up the ureter. The gel consists of two types of sugar-based molecules called dextranomer and hyaluronic acid. Trade names for this combination include Deflux and Zuidex. Both constituents are well known from previous uses in medicine. They are also biocompatible, which means that they do not cause significant reactions within the body. In fact, hyaluronic acid is produced and found naturally within the body.

Medical treatment
Medical treatment entails low dose antibiotic prophylaxis until resolution of VUR occurs. Antibiotics are administered nightly at half the normal therapeutic dose. The specific antibiotics used differ with the age of the patient and include:

Amoxicillin or ampicillin – infants younger than 6 weeks
Trimethoprim-sulfamethoxazole (co-trimoxazole) – 6 weeks to 2 monthsAfter 2 months the following antibiotics are suitable:

Nitrofurantoin {5–7 mg/kg/24hrs}
Nalidixic acid
Bactrim
Trimethoprim
CephalosporinsUrine cultures are performed 3 monthly to exclude breakthrough infection. Annual radiological investigations are likewise indicated. Good perineal hygiene, and timed and double voiding are also important aspects of medical treatment </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Cellulitis and explain in detail? [/INST] Cellulitis is a bacterial infection involving the inner layers of the skin. It specifically affects the dermis and subcutaneous fat. Signs and symptoms include an area of redness which increases in size over a few days. The borders of the area of redness are generally not sharp and the skin may be swollen. While the redness often turns white when pressure is applied, this is not always the case. The area of infection is usually painful. Lymphatic vessels may occasionally be involved, and the person may have a fever and feel tired.The legs and face are the most common sites involved, although cellulitis can occur on any part of the body. The leg is typically affected following a break in the skin. Other risk factors include obesity, leg swelling, and old age. For facial infections, a break in the skin beforehand is not usually the case. The bacteria most commonly involved are streptococci and Staphylococcus aureus. In contrast to cellulitis, erysipelas is a bacterial infection involving the more superficial layers of the skin, present with an area of redness with well-defined edges, and more often is associated with a fever. The diagnosis is usually based on the presenting signs and symptoms, while a cell culture is rarely possible. Before making a diagnosis, more serious infections such as an underlying bone infection or necrotizing fasciitis should be ruled out.Treatment is typically with antibiotics taken by mouth, such as cephalexin, amoxicillin or cloxacillin. Those who are allergic to penicillin may be prescribed erythromycin or clindamycin instead. When methicillin-resistant S. aureus (MRSA) is a concern, doxycycline or trimethoprim/sulfamethoxazole may, in addition, be recommended. There is concern related to the presence of pus or previous MRSA infections. Elevating the infected area may be useful, as may pain killers.Potential complications include abscess formation. Around 95% of people are better after 7 to 10 days of treatment. Those with diabetes, however, often have worse outcomes. Cellulitis occurred in about 21.2 million people in 2015. In the United States about 2 of every 1,000 people per year have a case affecting the lower leg. Cellulitis in 2015 resulted in about 16,900 deaths worldwide. In the United Kingdom, cellulitis was the reason for 1.6% of admissions to a hospital.

Signs and symptoms
The typical signs and symptoms of cellulitis are an area that is red, hot, and painful. The photos shown here are of mild to moderate cases and are not representative of the earlier stages of the condition.

Complications
Potential complications may include abscess formation, fasciitis, and sepsis.

Causes
Cellulitis is caused by bacteria that enter and infect the tissue through breaks in the skin. Group A Streptococcus and Staphylococcus are the most common causes of the infection and may be found on the skin as normal flora in healthy individuals.About 80% of cases of Ludwigs angina, or cellulitis of the submandibular space, are caused by dental infections. Mixed infections, due to both aerobes and anaerobes, are commonly associated with this type of cellulitis. Typically, this includes alpha-hemolytic streptococci, staphylococci, and bacteroides groups.Predisposing conditions for cellulitis include an insect or spider bite, blistering, an animal bite, tattoos, pruritic (itchy) skin rash, recent surgery, athletes foot, dry skin, eczema, injecting drugs (especially subcutaneous or intramuscular injection or where an attempted intravenous injection "misses" or blows the vein), pregnancy, diabetes, and obesity, which can affect circulation, as well as burns and boils, although debate exists as to whether minor foot lesions contribute. Occurrences of cellulitis may also be associated with the rare condition hidradenitis suppurativa or dissecting cellulitis.The appearance of the skin assists a doctor in determining a diagnosis. A doctor may also suggest blood tests, a wound culture, or other tests to help rule out a blood clot deep in the veins of the legs. Cellulitis in the lower leg is characterized by signs and symptoms similar to those of a deep vein thrombosis, such as warmth, pain, and swelling (inflammation).
Reddened skin or rash may signal a deeper, more serious infection of the inner layers of skin. Once below the skin, the bacteria can spread rapidly, entering the lymph nodes and the bloodstream and spreading throughout the body. This can result in influenza-like symptoms with a high temperature and sweating or feeling very cold with shaking, as the affected person cannot get warm.In rare cases, the infection can spread to the deep layer of tissue called the fascial lining. Necrotizing fasciitis, also called by the media "flesh-eating bacteria", is an example of a deep-layer infection. It is a medical emergency.

Risk factors
The elderly and those with a weakened immune system are especially vulnerable to contracting cellulitis. Diabetics are more susceptible to cellulitis than the general population because of impairment of the immune system; they are especially prone to cellulitis in the feet, because the disease causes impairment of blood circulation in the legs, leading to diabetic foot or foot ulcers. Poor control of blood glucose levels allows bacteria to grow more rapidly in the affected tissue and facilitates rapid progression if the infection enters the bloodstream. Neural degeneration in diabetes means these ulcers may not be painful, thus often become infected. Those who have had poliomyelitis are also prone because of circulatory problems, especially in the legs.Immunosuppressive drugs, and other illnesses or infections that weaken the immune system, are also factors that make infection more likely. Chickenpox and shingles often result in blisters that break open, providing a gap in the skin through which bacteria can enter. Lymphedema, which causes swelling on the arms and/or legs, can also put an individual at risk.
Diseases that affect blood circulation in the legs and feet, such as chronic venous insufficiency and varicose veins, are also risk factors for cellulitis.Cellulitis is also common among dense populations sharing hygiene facilities and common living quarters, such as military installations, college dormitories, nursing homes, oil platforms, and homeless shelters.

Diagnosis
Cellulitis is most often a clinical diagnosis, readily identified in many people by history and physical examination alone, with rapidly spreading areas of cutaneous swelling, redness, and heat, occasionally associated with inflammation of regional lymph nodes. While classically distinguished as a separate entity from erysipelas by spreading more deeply to involve the subcutaneous tissues, many clinicians may classify erysipelas as cellulitis.  Both are often treated similarly, but cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S. aureus, which may affect treatment decisions, especially antibiotic selection. Skin aspiration of nonpurulent cellulitis, usually caused by streptococcal organisms, is rarely helpful for diagnosis, and blood cultures are positive in fewer than 5% of all cases.It is important to evaluate for co-existent abscess, as this finding usually requires surgical drainage as opposed to antibiotic therapy alone.  Physicians clinical assessment for abscess may be limited, especially in cases with extensive overlying induration, but use of bedside ultrasonography performed by an experienced practitioner readily discriminates between abscess and cellulitis and may change management in up to 56% of cases. Use of ultrasound for abscess identification may also be indicated in cases of antibiotic failure.  Cellulitis has a characteristic "cobblestoned" appearance indicative of subcutaneous edema without a defined hypoechoic, heterogeneous fluid collection that would indicate abscess.

Differential diagnosis
Other conditions that may mimic cellulitis include deep vein thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis dermatitis, which is inflammation of the skin from poor blood flow. Signs of a more severe infection such as necrotizing fasciitis or gas gangrene that would require prompt surgical intervention include purple bullae, skin sloughing, subcutaneous edema, and systemic toxicity. Misdiagnosis can occur in up to 30% of people with suspected lower-extremity cellulitis, leading to 50,000 to 130,000 unnecessary hospitalization and $195 to $515 million in avoidable healthcare spending annually in the United States. Evaluation by dermatologists for cases of suspected cellulitis has been shown to reduce misdiagnosis rates and improve patient outcomes.Associated musculoskeletal findings are sometimes reported. When it occurs with acne conglobata, hidradenitis suppurativa, and pilonidal cysts, the syndrome is referred to as the follicular occlusion triad or tetrad.Lyme disease can be misdiagnosed as cellulitis. The characteristic bullseye rash does not always appear in Lyme disease (the rash may not have a central or ring-like clearing, or not appear at all). Factors supportive of Lyme include recent outdoor activities where Lyme is common and rash at an unusual site for cellulitis, such as armpit, groin, or behind the knee. Lyme can also result in long-term neurologic complications. The standard treatment for cellulitis, cephalexin, is not useful in Lyme disease. When it is unclear which one is present, the IDSA recommends treatment with cefuroxime axetil or amoxicillin/clavulanic acid, as these are effective against both infections.

Prevention
In those who have previously had cellulitis, the use of antibiotics may help prevent future episodes. This is recommended by CREST for those who have had more than two episodes. A 2017 meta-analysis found a benefit of preventative antibiotics for recurrent cellulitis in the lower limbs, but the preventative effects appear to diminish after stopping antibiotic therapy.

Treatment
Antibiotics are usually prescribed, with the agent selected based on suspected organism and presence or absence of purulence, although the best treatment choice is unclear.  If an abscess is also present, surgical drainage is usually indicated, with antibiotics often prescribed for co-existent cellulitis, especially if extensive.  Pain relief is also often prescribed, but excessive pain should always be investigated, as it is a symptom of necrotizing fasciitis.  Elevation of the affected area is often recommended.Steroids may speed recovery in those on antibiotics.

Antibiotics
Antibiotics choices depend on regional availability, but a penicillinase-resistant semisynthetic penicillin or a first-generation cephalosporin is currently recommended for cellulitis without abscess. A course of antibiotics is not effective in between 6 and 37% of cases.

Epidemiology
Cellulitis in 2015 resulted in about 16,900 deaths worldwide, up from 12,600 in 2005.Cellulitis is a common global health burden, with more than 650,000 admissions per year in the United States alone. In the United States, an estimated 14.5 million cases annually of cellulitis account for $3.7 billion in ambulatory care costs alone. The majority of cases of cellulitis are nonculturable and therefore the causative bacteria are unknown. In the 15% of cellulitis cases in which organisms are identified, most are due to β-hemolytic Streptococcus and Staphylococcus aureus.

Other animals
Horses may acquire cellulitis, usually secondarily to a wound (which can be extremely small and superficial) or to a deep-tissue infection, such as an abscess or infected bone, tendon sheath or joint. Cellulitis from a superficial wound usually creates less lameness (grade 1–2 of 5) than that caused by septic arthritis (grade 4–5). The horse exhibits inflammatory edema, which is hot, painful swelling. This swelling differs from stocking up in that the horse does not display symmetrical swelling in two or four legs, but in only one leg. This swelling begins near the source of infection, but eventually continues down the leg </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Neuromyotonia and explain in detail? [/INST] Neuromyotonia (NMT) is a form of peripheral nerve hyperexcitability that causes spontaneous muscular activity resulting from repetitive motor unit action potentials of peripheral origin. NMT along with Morvans syndrome are the most severe types in the Peripheral Nerve Hyperexciteability spectrum. Example of two more common and less severe syndromes in the spectrum are Cramp Fasciculation Syndrome and Benign Fasciculation Syndrome.  NMT can have both hereditary and acquired (non- inherited) forms. The prevalence of NMT is unknown.

Signs and symptoms
NMT is a diverse disorder. As a result of muscular hyperactivity, patients may present with muscle cramps, stiffness, myotonia-like symptoms (slow relaxation), associated walking difficulties, hyperhidrosis (excessive sweating), myokymia (quivering of a muscle), fasciculations (muscle twitching), fatigue, exercise intolerance, myoclonic jerks and other related symptoms. The symptoms (especially the stiffness and fasciculations) are most prominent in the calves, legs, trunk, and sometimes the face and neck, but can also affect other body parts. NMT symptoms may fluctuate in severity and frequency. Symptoms range from mere inconvenience to debilitating. At least a third of people also experience sensory symptoms.

Causes
The three causes of NMT are:
Acquired
Paraneoplastic
HereditaryThe acquired form is the most common, accounting for up to 80 percent of all cases and is suspected to be autoimmune-mediated, which is usually caused by antibodies against the neuromuscular junction.
The exact cause is unknown. However, autoreactive antibodies can be detected in a variety of peripheral (e.g. myasthenia gravis, Lambert-Eaton myasthenic syndrome) and central nervous system (e.g. paraneoplastic cerebellar degeneration, paraneoplastic limbic encephalitis) disorders. Their causative role has been established in some of these diseases but not all. Neuromyotonia is considered to be one of these with accumulating evidence for autoimmune origin over the last few years. Autoimmune neuromyotonia is typically caused by antibodies that bind to potassium channels on the motor nerve resulting in continuous/hyper-excitability.  Onset is typically seen between the ages of 15–60, with most experiencing symptoms before the age of 40. Some neuromyotonia cases do not only improve after plasma exchange but they may also have antibodies in their serum samples against voltage-gated potassium channels. Moreover, these antibodies have been demonstrated to reduce potassium channel function in neuronal cell lines.

Diagnosis
Diagnosis is clinical and initially consists of ruling out more common conditions, disorders, and diseases, and usually begins at the general practitioner level. A doctor may conduct a basic neurological exam, including coordination, strength, reflexes, sensation, etc. A doctor may also run a series of tests that include blood work and MRIs.
From there, a patient is likely to be referred to a neurologist or a neuromuscular specialist. The neurologist or specialist may run a series of more specialized tests, including needle electromyography EMG/ and nerve conduction studies (NCS) (these are the most important tests), chest CT (to rule out paraneoplastic) and specific blood work looking for voltage-gated potassium channel antibodies, acetylcholine receptor antibody, and serum immunofixation, TSH, ANA ESR, EEG etc. Neuromyotonia is characterized electromyographically by doublet, triplet or multiplet single unit discharges that have a high, irregular intraburst frequency.  Fibrillation potentials and fasciculations are often also present with electromyography.Because the condition is so rare, it can often be years before a correct diagnosis is made.
NMT is not fatal and many of the symptoms can be controlled. However, because NMT mimics some symptoms of motor neuron disease (ALS) and other more severe diseases, which may be fatal, there can often be significant anxiety until a diagnosis is made. In some rare cases, acquired neuromyotonia has been misdiagnosed as amyotrophic lateral sclerosis (ALS) particularly if fasciculations may be evident in the absence of other clinical features of ALS. However, fasciculations are rarely the first sign of ALS as the hallmark sign is weakness. Similarly, multiple sclerosis has been the initial misdiagnosis in some NMT patients. In order to get an accurate diagnosis see a trained neuromuscular specialist.
People diagnosed with Benign Fasciculation Syndrome or Enhanced Physiological Tremor may experience similar symptoms as NMT, although it is unclear today whether BFS or EPT are weak forms of NMT.

Types
There are three main types of NMT:
Chronic
Monophasic (symptoms that resolve within several years of onset; postinfection, postallergic)
Relapsing Remitting

Peripheral nerve hyperexcitability
Neuromyotonia is a type of peripheral nerve hyperexcitability. Peripheral nerve hyperexcitability is an umbrella diagnosis that includes (in order of severity of symptoms from least severe to most severe) benign fasciculation syndrome, cramp fasciculation syndrome, neuromyotonia and morvans syndrome. Some doctors will only give the diagnosis of peripheral nerve hyperexcitability as the differences between the three are largely a matter of the severity of the symptoms and can be subjective. However, some objective EMG criteria have been established to help distinguish between the three.
Moreover, the generic use of the term peripheral nerve hyperexcitability syndromes to describe the aforementioned conditions is recommended and endorsed by several prominent researchers and practitioners in the field.

Treatments
There is no known cure for neuromyotonia, but the condition is treatable. Anticonvulsants, including phenytoin and carbamazepine, usually provide significant relief from the stiffness, muscle spasms, and pain associated with neuromyotonia. Plasma exchange and IVIg treatment may provide short-term relief for patients with some forms of the acquired disorder. It is speculated that the plasma exchange causes an interference with the function of the voltage-dependent potassium channels, one of the underlying issues of hyper-excitability in autoimmune neuromyotonia. Botox injections also provide short-term relief </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Developmental verbal dyspraxia and explain in detail? [/INST] Developmental verbal dyspraxia (DVD), also known as childhood apraxia of speech (CAS) and developmental apraxia of speech (DAS), is a condition in which children have problems saying sounds, syllables and words. This is not because of muscle weakness or paralysis. The brain has problems planning to move the body parts (e.g., lips, jaw, tongue) needed for speech. The child knows what they want to say, but their brain has difficulty coordinating the muscle movements necessary to say those words.The exact cause of this disorder is usually unknown. Many observations suggest a genetic cause of DVD, as many with the disorder have a family history of communication disorders. The gene FOXP2 has been implicated in many studies of the condition, and when this is the cause, the condition is inherited in an autosomal dominant manner, however roughly 75% of these cases are de novo.There is no cure for DVD, but with appropriate, intensive intervention, people with this motor speech disorder can improve significantly.

Presentation
"Childhood apraxia of speech (CAS) is a neurological childhood (pediatric) speech sound disorder in which the precision and consistency of movements underlying speech are impaired in the absence of neuromuscular deficits (e.g., abnormal reflexes, abnormal tone). CAS may occur as a result of known neurological impairment, in association with complex neurobehavioral disorders of known or unknown origin, or as an idiopathic neurogenic speech sound disorder. The core impairment in planning and/or programming spatiotemporal parameters of movement sequences results in errors in speech sound production and prosody." American Speech-Language-Hearing Association (ASHA) Ad Hoc Committee on Apraxia of Speech in Children (2007)
There are three significant features that differentiate DVD/CAS from other childhood speech sound disorders. These features are:

"Inconsistent errors on consonants and vowels in repeated productions of syllables and words
Lengthened coarticulatory transitions between sounds and syllables
Inappropriate prosody, especially in the realization of lexical or phrasal stress"Even though DVD/CAS is a developmental disorder, it will not simply disappear when children grow older. Children with this disorder do not follow typical patterns of language acquisition and will need treatment in order to make progress.

Causes
DVD/CAS is a motor disorder, which means that the problem is located in the brain and its signals, and not in the mouth. In most cases, the cause is unknown. Possible causes include genetic syndromes and disorders.Recent research has focused on the significance of the FOXP2 gene in both species and individual development. Research regarding the KE family, where half the members of the extended family, over three generations, exhibited heritable developmental verbal dyspraxia, were found to have a defective copy of the FOXP2 gene. and further studies suggest that the FOXP2 gene as well as other genetic issues could explain DVD/CAS. including 16p11.2 microdeletion syndrome.New research suggests a role for the sodium channel SCN3A in the development of the perisylvian areas, which maintain key language circuits- Broca and Wernicke Area. Patients with mutations in SCN3A had oral-motor speech disorders.Birth/prenatal injuries, as well as stroke, can also be causes of DVD/CAS. Furthermore, DVD/CAS can occur as a secondary characteristic to a variety of other conditions. These include autism, some forms of epilepsy, fragile X syndrome, galactosemia and chromosome translocations involving duplications or deletions.

Diagnosis
Developmental verbal dyspraxia can be diagnosed by a speech language pathologist (SLP) through specific exams that measure oral mechanisms of speech. The oral mechanisms exam involves tasks such as pursing lips, blowing, licking lips, elevating the tongue, and also involves an examination of the mouth. A complete exam also involves observation of the patient eating and talking. Tests such as the Kaufman Speech Praxis test, a more formal examination, are also used in diagnosis.
A differential diagnosis of DVD/CAS is often not possible for children under the age of two years old. Even when children are between 2–3 years, a clear diagnosis cannot always occur, because at this age, they may still be unable to focus on, or cooperate with, diagnostic testing.

Management
There is no cure for DVD/CAS, but with appropriate, intensive intervention, people with the disorder can improve significantly.DVD/CAS requires various forms of therapy which varies with the individual needs of the patient. Typically, treatment involves one-on-one therapy with a speech language pathologist (SLP). In children with DVD/CAS, consistency is a key element in treatment. Consistency in the form of communication, as well as the development and use of oral communication are extremely important in aiding a childs speech learning process.Many therapy approaches are not supported by thorough evidence; however, the aspects of treatment that do seem to be agreed upon are the following:

Treatment needs to be intense and highly individualized, with about 3–5 therapy sessions each week
A maximum of 30 minutes per session is best for young children
Principles of motor learning theory and intense speech-motor practice seem to be the most effective
Non-speech oral motor therapy is not necessary or sufficient
A multi-sensory approach to therapy may be beneficial: using sign language, pictures, tactile cues, visual prompts, and augmentative and alternative communication (AAC) can be helpful.Although these aspects of treatment are supported by much clinical documentation, they lack evidence from systematic research studies. In ASHAs position statement on DVD/CAS, ASHA states there is a critical need for collaborative, interdisciplinary, and programmatic research on the neural substrates, behavioral correlates, and treatment options for DVD/CAS.

Integral stimulation
One technique that is frequently used to treat DVD/CAS is integral stimulation. Integral stimulation is based on cognitive motor learning, focusing on the cognitive motor planning needed for the complex motor task of speech </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Gastroenteritis and explain in detail? [/INST] Gastroenteritis, also known as infectious diarrhea and gastro, is inflammation of the gastrointestinal tract including the stomach and intestine. Symptoms may include diarrhea, vomiting, and abdominal pain. Fever, lack of energy, and dehydration may also occur. This typically lasts less than two weeks. It is not related to influenza, even though in the U.S. it is sometimes called the "stomach flu".Gastroenteritis is usually caused by viruses, gut bacteria, parasites, and fungi can also cause gastroenteritis. In children, rotavirus is the most common cause of severe disease. In adults, norovirus and Campylobacter are common causes. Eating improperly prepared food, drinking contaminated water or close contact with a person who is infected can spread the disease. Treatment is generally the same with or without a definitive diagnosis, so testing to confirm is usually not needed.For young children in impoverished countries, prevention includes hand washing with soap, drinking clean water, breastfeeding babies instead of using formula, and proper disposal of human waste. The rotavirus vaccine is recommended as a prevention for children. Treatment involves getting enough fluids. For mild or moderate cases, this can typically be achieved by drinking oral rehydration solution (a combination of water, salts and sugar). In those who are breastfed, continued breastfeeding is recommended. For more severe cases, intravenous fluids may be needed. Fluids may also be given by a nasogastric tube. Zinc supplementation is recommended in children. Antibiotics are generally not needed. However, antibiotics are recommended for young children with a fever and bloody diarrhea.In 2015, there were two billion cases of gastroenteritis, resulting in 1.3 million deaths globally. Children and those in the developing world are affected the most. In 2011, there were about 1.7 billion cases, resulting in about 700,000 deaths of children under the age of five. In the developing world, children less than two years of age frequently get six or more infections a year. It is less common in adults, partly due to the development of immunity.

Signs and symptoms
Gastroenteritis usually involves both diarrhea and vomiting. Sometimes, only one or the other is present. This may be accompanied by abdominal cramps. Signs and symptoms usually begin 12–72 hours after contracting the infectious agent. If due to a virus, the condition usually resolves within one week. Some viral infections also involve fever, fatigue, headache and muscle pain. If the stool is bloody, the cause is less likely to be viral and more likely to be bacterial. Some bacterial infections cause severe abdominal pain and may persist for several weeks.Children infected with rotavirus usually make a full recovery within three to eight days. However, in poor countries treatment for severe infections is often out of reach and persistent diarrhea is common.  Dehydration is a common complication of diarrhea. Severe dehydration in children may be recognized if the skin color and position returns slowly when pressed. This is called "prolonged capillary refill" and "poor skin turgor". Abnormal breathing is another sign of severe dehydration. Repeat infections are typically seen in areas with poor sanitation, and malnutrition. Stunted growth and long-term cognitive delays can result.Reactive arthritis occurs in 1% of people following infections with Campylobacter species. Guillain–Barré syndrome occurs in 0.1%. Hemolytic uremic syndrome (HUS) may occur due to infection with Shiga toxin-producing Escherichia coli or Shigella species. HUS causes low platelet counts, poor kidney function, and low red blood cell count (due to their breakdown). Children are more predisposed to getting HUS than adults. Some viral infections may produce benign infantile seizures.

Cause
Viruses (particularly rotavirus (in children) and norovirus (in adults)) and the bacteria Escherichia coli and Campylobacter species are the primary causes of gastroenteritis. There are, however, many other infectious agents that can cause this syndrome including parasites and fungus. Non-infectious causes are seen on occasion, but they are less likely than a viral or bacterial cause. Risk of infection is higher in children due to their lack of immunity. Children are also at higher risk because they are less likely to practice good hygiene habits. Children living in areas without easy access to water and soap are especially vulnerable.

Viral
Rotaviruses, noroviruses, adenoviruses, and astroviruses are known to cause viral gastroenteritis. Rotavirus is the most common cause of gastroenteritis in children, and produces similar rates in both the developed and developing world. Viruses cause about 70% of episodes of infectious diarrhea in the pediatric age group. Rotavirus is a less common cause in adults due to acquired immunity. Norovirus is the cause in about 18% of all cases. Generally speaking, viral gastroenteritis accounts for 21–40% of the cases of infectious diarrhea in developed countries.Norovirus is the leading cause of gastroenteritis among adults in America accounting for about 90% of viral gastroenteritis outbreaks. These localized epidemics typically occur when groups of people spend time proximate to each other, such as on cruise ships, in hospitals, or in restaurants. People may remain infectious even after their diarrhea has ended. Norovirus is the cause of about 10% of cases in children.

Bacterial
In some countries, Campylobacter jejuni is the primary cause of bacterial gastroenteritis, with half of these cases associated with exposure to poultry. In children, bacteria are the cause in about 15% of cases, with the most common types being Escherichia coli, Salmonella, Shigella, and Campylobacter species. If food becomes contaminated with bacteria and remains at room temperature for a period of several hours, the bacteria multiply and increase the risk of infection in those who consume the food. Some foods commonly associated with illness include raw or undercooked meat, poultry, seafood, and eggs; raw sprouts; unpasteurized milk and soft cheeses; and fruit and vegetable juices. In the developing world, especially sub-Saharan Africa and Asia, cholera is a common cause of gastroenteritis. This infection is usually transmitted by contaminated water or food.Toxigenic Clostridium difficile is an important cause of diarrhea that occurs more often in the elderly. Infants can carry these bacteria without developing symptoms. It is a common cause of diarrhea in those who are hospitalized and is frequently associated with antibiotic use. Staphylococcus aureus infectious diarrhea may also occur in those who have used antibiotics. Acute "travelers diarrhea" is usually a type of bacterial gastroenteritis, while the persistent form is usually parasitic. Acid-suppressing medication appears to increase the risk of significant infection after exposure to a number of organisms, including Clostridium difficile, Salmonella, and Campylobacter species. The risk is greater in those taking proton pump inhibitors than with H2 antagonists.

Parasitic
A number of parasites can cause gastroenteritis. Giardia lamblia is most common, but Entamoeba histolytica, Cryptosporidium spp., and other species have also been implicated. As a group, these agents comprise about 10% of cases in children. Giardia occurs more commonly in the developing world, but this type of illness can occur nearly everywhere. It occurs more commonly in persons who have traveled to areas with high prevalence, children who attend day care, men who have sex with men, and following disasters.

Transmission
Transmission may occur from drinking contaminated water or when people share personal objects. Water quality typically worsens during the rainy season and outbreaks are more common at this time. In areas with four seasons, infections are more common in the winter. Worldwide, bottle-feeding of babies with improperly sanitized bottles is a significant cause. Transmission rates are also related to poor hygiene, (especially among children), in crowded households, and in those with poor nutritional status. Adults who have developed immunities might still carry certain organisms without exhibiting symptoms. Thus, adults can become natural reservoirs of certain diseases. While some agents (such as Shigella) only occur in primates, others (such as Giardia) may occur in a wide variety of animals.

Non-infectious
There are a number of non-infectious causes of inflammation of the gastrointestinal tract. Some of the more common include medications (like NSAIDs), certain foods such as lactose (in those who are intolerant), and gluten (in those with celiac disease). Crohns disease is also a non-infectious source of (often severe) gastroenteritis. Disease secondary to toxins may also occur. Some food-related conditions associated with nausea, vomiting, and diarrhea include: ciguatera poisoning due to consumption of contaminated predatory fish, scombroid associated with the consumption of certain types of spoiled fish, tetrodotoxin poisoning from the consumption of puffer fish among others, and botulism typically due to improperly preserved food.In the United States, rates of emergency department use for noninfectious gastroenteritis dropped 30% from 2006 until 2011. Of the twenty most common conditions seen in the emergency department, rates of noninfectious gastroenteritis had the largest decrease in visits in that time period.

Pathophysiology
Gastroenteritis is defined as vomiting or diarrhea due to inflammation of the small or large bowel, often due to infection. The changes in the small bowel are typically noninflammatory, while the ones in the large bowel are inflammatory. The number of pathogens required to cause an infection varies from as few as one (for Cryptosporidium) to as many as 108 (for Vibrio cholerae).

Diagnosis
Gastroenteritis is typically diagnosed clinically, based on a persons signs and symptoms. Determining the exact cause is usually not needed as it does not alter the management of the condition.However, stool cultures should be performed in those with blood in the stool, those who might have been exposed to food poisoning, and those who have recently traveled to the developing world. It may also be appropriate in children younger than 5, old people, and those with poor immune function. Diagnostic testing may also be done for surveillance. As hypoglycemia occurs in approximately 10% of infants and young children, measuring serum glucose in this population is recommended. Electrolytes and kidney function should also be checked when there is a concern about severe dehydration.

Dehydration
A determination of whether or not the person has dehydration is an important part of the assessment, with dehydration typically divided into mild (3–5%), moderate (6–9%), and severe (≥10%) cases. In children, the most accurate signs of moderate or severe dehydration are a prolonged capillary refill, poor skin turgor, and abnormal breathing. Other useful findings (when used in combination) include sunken eyes, decreased activity, a lack of tears, and a dry mouth. A normal urinary output and oral fluid intake is reassuring. Laboratory testing is of little clinical benefit in determining the degree of dehydration. Thus the use of urine testing or ultrasounds is generally not needed.

Differential diagnosis
Other potential causes of signs and symptoms that mimic those seen in gastroenteritis that need to be ruled out include appendicitis, volvulus, inflammatory bowel disease, urinary tract infections, and diabetes mellitus. Pancreatic insufficiency, short bowel syndrome, Whipples disease, coeliac disease, and laxative abuse should also be considered. The differential diagnosis can be complicated somewhat if the person exhibits only vomiting or diarrhea (rather than both).Appendicitis may present with vomiting, abdominal pain, and a small amount of diarrhea in up to 33% of cases. This is in contrast to the large amount of diarrhea that is typical of gastroenteritis. Infections of the lungs or urinary tract in children may also cause vomiting or diarrhea. Classical diabetic ketoacidosis (DKA) presents with abdominal pain, nausea, and vomiting, but without diarrhea. One study found that 17% of children with DKA were initially diagnosed as having gastroenteritis.

Prevention
Water, sanitation, hygiene
A supply of easily accessible uncontaminated water and good sanitation practices are important for reducing rates of infection and clinically significant gastroenteritis. Personal hygiene measures (such as hand washing with soap) have been found to decrease rates of gastroenteritis in both the developing and developed world by as much as 30%. Alcohol-based gels may also be effective. Food or drink that is thought to be contaminated should be avoided.Breastfeeding is important, especially in places with poor hygiene, as is improvement of hygiene generally. Breast milk reduces both the frequency of infections and their duration.

Vaccination
Due to both its effectiveness and safety, in 2009 the World Health Organization recommended that the rotavirus vaccine be offered to all children globally. Two commercial rotavirus vaccines exist and several more are in development. In Africa and Asia these vaccines reduced severe disease among infants and countries that have put in place national immunization programs have seen a decline in the rates and severity of disease. This vaccine may also prevent illness in non-vaccinated children by reducing the number of circulating infections. Since 2000, the implementation of a rotavirus vaccination program in the United States has substantially decreased the number of cases of diarrhea by as much as 80 percent. The first dose of vaccine should be given to infants between 6 and 15 weeks of age. The oral cholera vaccine has been found to be 50–60% effective over two years.There are a number of vaccines against gastroenteritis in development. For example, vaccines against Shigella and enterotoxigenic Escherichia coli (ETEC), which are two of the leading bacterial causes of gastroenteritis worldwide.

Management
Gastroenteritis is usually an acute and self-limiting disease that does not require medication. The preferred treatment in those with mild to moderate dehydration is oral rehydration therapy (ORT). For children at risk of dehydration from vomiting, taking a single dose of the anti vomiting medication metoclopramide or ondansetron, may be helpful, and butylscopolamine is useful in treating abdominal pain.

Rehydration
The primary treatment of gastroenteritis in both children and adults is rehydration. This is preferably achieved by drinking rehydration solution, although intravenous delivery may be required if there is a decreased level of consciousness or if dehydration is severe. Drinking replacement therapy products made with complex carbohydrates (i.e. those made from wheat or rice) may be superior to those based on simple sugars. Drinks especially high in simple sugars, such as soft drinks and fruit juices, are not recommended in children under five years of age as they may increase diarrhea. Plain water may be used if more specific ORT preparations are unavailable or the person is not willing to drink them. A nasogastric tube can be used in young children to administer fluids if warranted. In those who require intravenous fluids, one to four hours worth is often sufficient.

Dietary
It is recommended that breast-fed infants continue to be nursed in the usual fashion,  and that formula-fed infants continue their formula immediately after rehydration with ORT. Lactose-free or lactose-reduced formulas usually are not necessary. Children should continue their usual diet during episodes of diarrhea with the exception that foods high in simple sugars should be avoided. The BRAT diet (bananas, rice, applesauce, toast and tea) is no longer recommended, as it contains insufficient nutrients and has no benefit over normal feeding.A Cochrane Review from 2020 concludes that probiotics make little or no difference to people who have diarrhea lasting 2 days or longer and that there is no proof that they reduce its duration. They may be useful in preventing and treating antibiotic associated diarrhea. Fermented milk products (such as yogurt) are similarly beneficial. Zinc supplementation appears to be effective in both treating and preventing diarrhea among children in the developing world.

Antiemetics
Antiemetic medications may be helpful for treating vomiting in children. Ondansetron has some utility, with a single dose being associated with less need for intravenous fluids, fewer hospitalizations, and decreased vomiting. Metoclopramide might also be helpful. However, the use of ondansetron might possibly be linked to an increased rate of return to hospital in children. The intravenous preparation of ondansetron may be given orally if clinical judgment warrants. Dimenhydrinate, while reducing vomiting, does not appear to have a significant clinical benefit.

Antibiotics
Antibiotics are not usually used for gastroenteritis, although they are sometimes recommended if symptoms are particularly severe or if a susceptible bacterial cause is isolated or suspected. If antibiotics are to be employed, a macrolide (such as azithromycin) is preferred over a fluoroquinolone due to higher rates of resistance to the latter. Pseudomembranous colitis, usually caused by antibiotic use, is managed by discontinuing the causative agent and treating it with either metronidazole or vancomycin. Bacteria and protozoans that are amenable to treatment include Shigella Salmonella typhi, and Giardia species. In those with Giardia species or Entamoeba histolytica, tinidazole treatment is recommended and superior to metronidazole. The World Health Organization (WHO) recommends the use of antibiotics in young children who have both bloody diarrhea and fever.

Antimotility agents
Antimotility medication has a theoretical risk of causing complications, and although clinical experience has shown this to be unlikely, these drugs are discouraged in people with bloody diarrhea or diarrhea that is complicated by fever. Loperamide, an opioid analogue, is commonly used for the symptomatic treatment of diarrhea. Loperamide is not recommended in children, however, as it may cross the immature blood–brain barrier and cause toxicity. Bismuth subsalicylate, an insoluble complex of trivalent bismuth and salicylate, can be used in mild to moderate cases, but salicylate toxicity is theoretically possible.

Epidemiology
It is estimated that there were two billion cases of gastroenteritis that resulted in 1.3 million deaths globally in 2015. Children and those in the developing world are most commonly affected. As of 2011, in those younger than five, there were about 1.7 billion cases resulting in 0.7 million deaths, with most of these occurring in the worlds poorest nations. More than 450,000 of these fatalities are due to rotavirus in children under five years of age. Cholera causes about three to five million cases of disease and kills approximately 100,000 people yearly. In the developing world, children less than two years of age frequently get six or more infections a year that result in significant gastroenteritis. It is less common in adults, partly due to the development of acquired immunity.In 1980, gastroenteritis from all causes caused 4.6 million deaths in children, with the majority occurring in the developing world. Death rates were reduced significantly (to approximately 1.5 million deaths annually) by 2000, largely due to the introduction and widespread use of oral rehydration therapy. In the US, infections causing gastroenteritis are the second most common infection (after the common cold), and they result in between 200 and 375 million cases of acute diarrhea and approximately ten thousand deaths annually, with 150 to 300 of these deaths in children less than five years of age.

Society and culture
Gastroenteritis is associated with many colloquial names, including "Montezumas revenge", "Delhi belly", "la turista", and "back door sprint", among others. It has played a role in many military campaigns and is believed to be the origin of the term "no guts no glory".Gastroenteritis is the main reason for 3.7 million visits to physicians a year in the United States and 3 million visits in France. In the United States gastroenteritis as a whole is believed to result in costs of US$23 billion per year with that due to rotavirus alone resulting in estimated costs of US$1 billion a year.

Terminology
The first usage of "gastroenteritis" was in 1825. Before this time it was commonly known as typhoid fever or "cholera morbus", among others, or less specifically as "griping of the guts", "surfeit", "flux", "colic", "bowel complaint", or any one of a number of other archaic names for acute diarrhea. Cholera morbus is a historical term that was used to refer to gastroenteritis rather than specifically cholera.

Other animals
Many of the same agents cause gastroenteritis in cats and dogs as in humans. The most common organisms are Campylobacter, Clostridium difficile, Clostridium perfringens, and Salmonella. A large number of toxic plants may also cause symptoms.Some agents are more specific to a certain species. Transmissible gastroenteritis coronavirus (TGEV) occurs in pigs resulting in vomiting, diarrhea, and dehydration </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sialolithiasis and explain in detail? [/INST] Sialolithiasis (also termed salivary calculi, or salivary stones) is a crystallopathy where a calcified mass or sialolith forms within a salivary gland, usually in the duct of the submandibular gland (also termed "Whartons duct"). Less commonly the parotid gland or rarely the sublingual gland or a minor salivary gland may develop salivary stones.
The usual symptoms are pain and swelling of the affected salivary gland, both of which get worse when salivary flow is stimulated, e.g. with the sight, thought, smell or taste of food, or with hunger or chewing. This is often termed "mealtime syndrome". Inflammation or infection of the gland may develop as a result. Sialolithiasis may also develop because of the presence of existing chronic infection of the glands, dehydration (e.g. use of phenothiazines), Sjögrens syndrome and/or increased local levels of calcium, but in many instances the cause is idiopathic (unknown).
The condition is usually managed by removing the stone, and several different techniques are available. Rarely, removal of the submandibular gland may become necessary in cases of recurrent stone formation. Sialolithiasis is common, accounting for about 50% of all disease occurring in the major salivary glands and causing symptoms in about 0.45% of the general population. Persons aged 30–60 and males are more likely to develop sialolithiasis.

Classification
The term is derived from the Greek words sialon (saliva) and lithos (stone), and the Greek -iasis meaning "process" or "morbid condition". A calculus (plural calculi) is a hard, stone-like concretion that forms within an organ or duct inside the body. They are usually made from mineral salts, and other types of calculi include tonsiloliths (tonsil stones) and renal calculi (kidney stones). Sialolithiasis refers to the formation of calculi within a salivary gland. If a calculus forms in the duct that drains the saliva from a salivary gland into the mouth, then saliva will be trapped in the gland. This may cause painful swelling and inflammation of the gland. Inflammation of a salivary gland is termed sialadenitis. Inflammation associated with blockage of the duct is sometimes termed "obstructive sialadenitis". Because saliva is stimulated to flow more with the thought, sight or smell of food, or with chewing, pain and swelling will often get suddenly worse just before and during a meal ("peri-prandial"), and then slowly decrease after eating, this is termed meal time syndrome. However, calculi are not the only reasons that a salivary gland may become blocked and give rise to the meal time syndrome. Obstructive salivary gland disease, or obstructive sialadenitis, may also occur due to fibromucinous plugs, duct stenosis, foreign bodies, anatomic variations, or malformations of the duct system leading to a mechanical obstruction associated with stasis of saliva in the duct.Salivary stones may be divided according to which gland they form in. About 85% of stones occur in the submandibular gland, and 5–10% occur in the parotid gland. In about 0–5% of cases, the sublingual gland or a minor salivary gland is affected. When minor glands are rarely involved, caliculi are more likely in the minor glands of the buccal mucosa and the maxillary labial mucosa. Submandibular stones are further classified as anterior or posterior in relation to an imaginary transverse line drawn between the mandibular first molar teeth. Stones may be radiopaque, i.e. they will show up on conventional radiographs, or radiolucent, where they not be visible on radiographs (although some of their effects on the gland may still be visible). They may also symptomatic or asymptomatic, according to whether they cause any problems or not.

Signs and symptoms
Signs and symptoms are variable and depend largely upon whether the obstruction of the duct is complete or partial, and how much resultant pressure is created within the gland. The development of infection in the gland also influences the signs and symptoms.

Pain, which is intermittent, and may suddenly get worse before mealtimes, and then slowly get better (partial obstruction).
Swelling of the gland, also usually intermittent, often suddenly appearing or increasing before mealtimes, and then slowly going down (partial obstruction).
Tenderness of the involved gland.
Palpable hard lump, if the stone is located near the end of the duct. If the stone is near the submandibular duct orifice, the lump may be felt under the tongue.
Lack of saliva coming from the duct (total obstruction).
Erythema (redness) of the floor of the mouth (infection).
Pus discharging from the duct (infection).
Cervical lymphadenitis (infection).
Bad breath.Rarely, when stones form in the minor salivary glands, there is usually only slight local swelling in the form of a small nodule and tenderness.

Causes
There are thought to be a series of stages that lead to the formation of a calculus (lithogenesis). Initially, factors such as abnormalities in calcium metabolism, dehydration, reduced salivary flow rate, altered acidity (pH) of saliva caused by oropharyngeal infections, and altered solubility of crystalloids, leading to precipitation of mineral salts, are involved. Other sources state that no systemic abnormality of calcium or phosphate metabolism is responsible.The next stage involves the formation of a nidus which is successively layered with organic and inorganic material, eventually forming a calcified mass. In about 15-20% of cases the sialolith will not be sufficiently calcified to appear radiopaque on a radiograph, and will therefore be difficult to detect.
Other sources suggest a retrograde theory of lithogenesis, where food debris, bacteria or foreign bodies from the mouth enter the ducts of a salivary gland and are trapped by abnormalities in the sphincter mechanism of the duct opening (the papilla), which are reported in 90% of cases. Fragments of bacteria from salivary calculi were reported to be Streptococci species which are part of the normal oral microbiota and are present in dental plaque.Stone formation occurs most commonly in the submandibular gland for several reasons. The concentration of calcium in saliva produced by the submandibular gland is twice that of the saliva produced by the parotid gland. The submandibular gland saliva is also relatively alkaline and mucous. The submandibular duct (Whartons duct) is long, meaning that saliva secretions must travel further before being discharged into the mouth. The duct possesses two bends, the first at the posterior border of the mylohyoid muscle and the second near the duct orifice. The flow of saliva from the submandibular gland is often against gravity due to variations in the location of the duct orifice </s>