<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 Prediabetes and explain in detail? [/INST] Prediabetes is a component of the metabolic syndrome and is characterized by elevated blood sugar levels that fall below the threshold to diagnose diabetes mellitus. It usually does not cause symptoms but people with prediabetes often have obesity (especially abdominal or visceral obesity), dyslipidemia with high triglycerides and/or low HDL cholesterol, and hypertension. It is also associated with increased risk for cardiovascular disease (CVD). Prediabetes is more accurately considered an early stage of diabetes as health complications associated with type 2 diabetes often occur before the diagnosis of diabetes.
Prediabetes can be diagnosed by measuring hemoglobin A1c, fasting glucose, or glucose tolerance test. Many people may be diagnosed through routine screening tests. The primary treatment approach includes lifestyle changes such as exercise and dietary adjustments. Some medications can be used to reduce the risks associated with prediabetes. There is a high rate of progression to type 2 diabetes but not everyone with prediabetes develops type 2 diabetes. Prediabetes can be a reversible condition with lifestyle changes.
For many people, prediabetes and diabetes are diagnosed through a routine screening at a check-up. However, an additional routine screening done by dentists, a new and promising concept, and not only medical doctors, can be very effective in early detection and treatment. The earlier prediabetes is diagnosed, the more likely an intervention will be successful.

Signs and symptoms
Prediabetes typically has no distinct signs or symptoms except the sole sign of high blood sugar. Patients should monitor for signs and symptoms of type 2 diabetes mellitus such as increased thirst, increased urination, and feeling tired.

Causes
The cause of prediabetes is multifactorial and is known to have contributions from lifestyle and genetic factors. Ultimately prediabetes occurs when control of insulin and blood glucose in the body becomes abnormal, also known as insulin resistance. Risk factors for prediabetes include family history of diabetes, older age, women who have a history of gestational diabetes or high birth weight babies (greater than 9 lbs.).The increasing rates of prediabetes and diabetes suggest lifestyle and/or environmental factors that contribute to prediabetes. It remains unclear which dietary components are causative and risk is likely influenced by genetic background. Lack of physical activity is a risk factor for type 2 diabetes and physical activity can reduce the risk of progressing to type 2 diabetes.

Pathophysiology
Normal glucose homeostasis is controlled by three interrelated processes. These processes include gluconeogenesis (glucose production that occurs in the liver), uptake and utilization of glucose by the peripheral tissues of the body, and insulin secretion by the pancreatic beta islet cells. The presence of glucose in the bloodstream triggers the production and release of insulin from the pancreas beta islet cells. The main function of insulin is to increase the rate of transport of glucose from the bloodstream into certain cells of the body, such as striated muscles, fibroblasts, and fat cells. It also is necessary for transport of amino acids, glycogen formation in the liver and skeletal muscles, triglyceride formation from glucose, nucleic acid synthesis, and protein synthesis. In individuals with prediabetes, a failure of pancreatic hormone release, failure of targeted tissues to respond to the insulin present or both leads to blood glucose rises to abnormally high levels.

Diagnosis
Prediabetes can be diagnosed with three different types of blood tests:
Fasting blood sugar (glucose) level of:
110 to 125 mg/dL (6.1 mmol/L to 6.9 mmol/L) – WHO criteria
100 to 125 mg/dL (5.6 mmol/L to 6.9 mmol/L) – ADA criteria
Glucose tolerance test: blood sugar level of 140 to 199 mg/dL (7.8 to 11.0 mM) 2 hours after ingesting a standardized 75 gram glucose solution
Glycated hemoglobin (HbA1c) between 5.7 and 6.4 percent, i.e. 38.9 and 46.4 mmol/molLevels above these limits would justify a diagnosis for diabetes.

Impaired fasting glucose
Impaired fasting glycemia or impaired fasting glucose (IFG) refers to a condition in which the fasting blood glucose is elevated above what is considered normal levels but is not high enough to be classified as diabetes mellitus. It is considered a pre-diabetic state, associated with insulin resistance and increased risk of cardiovascular pathology, although of lesser risk than impaired glucose tolerance (IGT). IFG sometimes progresses to type 2 diabetes mellitus.
Fasting blood glucose levels are in a continuum within a given population, with higher fasting glucose levels corresponding to a higher risk for complications caused by the high glucose levels. Some patients with impaired fasting glucose also may be diagnosed with impaired glucose tolerance, but many have normal responses to a glucose tolerance test. Fasting glucose is helpful in identifying prediabetes when positive but has a risk of false negatives.World Health Organization (WHO) criteria for impaired fasting glucose differs from the American Diabetes Association (ADA) criteria, because the normal range of glucose is defined differently by each. Fasting plasma glucose levels 100 mg/dL (5.5 mmol/L) and higher have been shown to increase complication rates significantly, however, WHO opted to keep its upper limit of normal at under 110 mg/dL for fear of causing too many people to be diagnosed as having impaired fasting glucose, whereas the ADA lowered the upper limit of normal to a fasting plasma glucose under 100 mg/dL.
WHO criteria: fasting plasma glucose level from 6.1 mmol/L (110 mg/dL) to 6.9 mmol/L (125 mg/dL)
ADA criteria: fasting plasma glucose level from 5.6 mmol/L (100 mg/dL) to 6.9 mmol/L (125 mg/dL)

Impaired glucose tolerance
Impaired glucose tolerance (IGT) is diagnosed with an oral glucose tolerance test. According to the criteria of the World Health Organization and the American Diabetes Association, impaired glucose tolerance is defined as:
two-hour glucose levels of 140 to 199 mg per dL (7.8 to 11.0 mmol/L) on the 75-g oral glucose tolerance test. A patient is said to be under the condition of IGT when he/she has an intermediately raised glucose level after 2 hours, but less than the level that would qualify for type 2 diabetes mellitus. The fasting glucose may be either normal or mildly elevated.From 10 to 15 percent of adults in the United States have impaired glucose tolerance or impaired fasting glucose.

Hemoglobin A1c
Hemoglobin A1c is a measure of the percent of red blood cells that are glycated, or have a glucose molecule attached. This can be used as an indicator of blood glucose level over a longer period of time and is often used to diagnose prediabetes as well as diabetes. HbA1c may not accurately represent blood glucose levels and should not be used in certain medical conditions such as iron-deficiency anemia, Vitamin B12 and folate deficiency, pregnancy, hemolytic anemia, an enlarged spleen, and end-stage kidney failure.

Fasting Insulin
Hyperinsulinemia due to insulin resistance may occur in individuals with normal glucose levels and therefore is not diagnosed with usual tests. Hyperinsulinemia precedes prediabetes and diabetes that are characterized by hyperglycemia. Insulin resistance can be diagnosed by measures of plasma insulin, both fasting or during a glucose tolerance test. The use of  fasting insulin to identify patients at risk has been proposed, but is currently not commonly used in clinical practice.The implications of hyperinsulinemia is the risk of comorbidities related to diabetes that may precede changes in blood glucose, including cardiovascular diseases.

Screening
Fasting plasma glucose screening should begin at age 30–45 and be repeated at least every three years. Earlier and more frequent screening should be conducted in at-risk individuals. The risk factors for which are listed below:

Family history (parent or sibling)
Dyslipidemia (triglycerides > 200 mg/dL or HDL < 35 mg/dL)
Overweight or obesity (body mass index > 25 kg/m2)
History of gestational diabetes or infant born with birth weight greater than 9 lb (4 kg)
High risk ethnic group (such as of being of African American, Hispanic, Native American, Asian American or Pacific Islander heritage)
Hypertension (systolic blood pressure >140 mmHg or diastolic blood pressure > 90 mmHg)
Prior fasting blood glucose > 99 mg/dL
Known vascular disease
Markers of insulin resistance (PCOS, acanthosis nigricans)The United States Preventative Services Task Force (USPSTF) recommends adults who are overweight/obese and aged 40–70 years old to get screened during visits to their regular physician. The American Diabetes Association (ADA) recommends normal testing repeated every three years and recommends a larger range of people get tested: anyone over the age of 45 regardless of risk; an adult of any age who is obese or overweight and has one or more risk factors, which includes hypertension, a first degree relative with diabetes, physical inactivity, high risk race/ethnicity, Asian Americans with BMI of ≥23 kg/m2, HDL < 35 mg/dL or TG > 250 mg/dL, women who have delivered child >9 lbs or with gestational diabetes, A1c ≥ 5.7%, impaired fasting glucose (IFG) or impaired glucose tolerance (IGT).In the UK, NICE guidelines suggest taking action to prevent diabetes for people with a body mass index (BMI) of 30. For people of Black African, African-Caribbean, South Asian and Chinese descent the recommendation to start prevention starts at the BMI of 27,5. A study based on a large sample of people in England suggest even lower BMIs for certain ethnic groups for the start of prevention, for example 24 in South Asian and 21 in Bangladeshi populations.

Early detection and management
Over half the people who are diagnosed with prediabetes eventually develop type 2 diabetes and once diagnosed with prediabetes, people experience a range of emotions: distress and fear; denial and downplay of risks; guilt and self-criticism; and self-compassion. While prediabetes is a reversible condition, it requires diet change and exercise, which may be more difficult for people diagnosed prediabetes because facing the risk of a chronic condition is associated with negative emotions, which further hinder the self-regulation that is required in reversing a prediabetes diagnosis. Still, without taking action, 37% of individuals with prediabetes will develop diabetes in only 4 years, and lifestyle intervention may decrease the percentage of prediabetic patients in whom diabetes develops to 20%. The National Diabetes Prevention Program (DPP) has a Center of Disease Control (CDC)-recognized lifestyle change program that showed prediabetic people following the structured program can cut their risk of developing type 2 diabetes by 58% (71% for people over 60 years old). Considering the possibility to recover from the prediabetic status but also this emotional struggle upon diagnosis, it is encouraged for higher risk patients to get tested early. Having an additional screening option in the dental setting may offset some of the emotional struggle because it is more regularly visited and therefore has the potential to initiate earlier recognition and intervention.

Prediabetes screening in a dental setting
Its been found that people will visit their dentist more regularly than their primary physician for checkups, so the dentists office becomes a very useful place for potentially checking for diabetes. For people who are unaware of their diabetes risk and fall into the non-White, obese, or ≥45 y old category, screening at the dentists would have the highest odds of getting identified as someone at risk. Studies have been done to evaluate the overall effectiveness and value of prediabetes testing in the dental setting, usually at dental schools. One study has looked at screening through dental visits followed up by intervention programs such as the commercial Weight Watchers and found it a cost-effective means to identify and treat affected people in the long term. Cost is a factor people at risk might need to consider, since, on average, people diagnosed with diabetes have approximately 2.3 times higher medical expenditure that what expenditures would be in its absence.A simple test may be instituted at the dentists office, in which an oral blood sample is taken during a normal visit to the dentists. This sample tests for glycated hemoglobin (HbA1c) levels; HbA1c gives healthcare professionals an idea of blood glucose levels and is the most reliable form of testing for diabetes in asymptomatic patients. Fasting and "acute perturbations" are not needed for HbA1c test and it reveals average glycemic control over 3-month period. HbA1c less than 5.6% is considered normal. Glucose status can also be tested through fasting blood sugar (FBS) and requires a blood sample after a patient has fasted for at least eight hours, so it might not be as convenient. Patients who have gotten oral blood samples taken say it feels as if part of a normal procedure, and dentists say it is convenient.In a study that analyzed data from 10,472 adults from 2013 to 2014 and 2015 to 2016, it was revealed that screening for risk of prediabetes in the dental setting has the potential to alert an estimated 22.36 million adults. Diabetes may be asymptomatic for a long time, but since it would be wasteful to test every patient at the dental office, utilizing known risk factors may guide who is ideal for testing. Since a history is already taken at a dental office, a few additional questions would help guide a dentist on narrowing down who the test is recommended for. For example, people with high BMI are at higher risk for diabetes. A study done by the School of Dentistry, Diabetes Research Centre, Mazandaran University of Medical Sciences in Sari, Iran found a relation between periodontitis and the prediabetic condition, and this could be another tool to help guide who might be recommended to take the test. Periodontal disease occurs when a number of anaerobic bacteria living on the tooth surface cause infections, which leads to a potentially sustained immune response. Diabetes is a type of condition in which infections are easier to get, and hyperglycemia contributes to the mechanism causing oral complications.

Prevention
The American College of Endocrinology (ACE) and the American Association of Clinical Endocrinologists (AACE) have developed lifestyle intervention guidelines for preventing the onset of type 2 diabetes:

Healthy diet (a diet with limited refined carbohydrates, added sugars, trans fats, as well as limited intake of sodium and total calories)
Physical fitness (30–45 minutes of cardiovascular exercise per day, 3–5 days a week)
Weight loss by as little as 5–10 percent may have a significant impact on overall health

Management
There is evidence that prediabetes is a curable disease state. Although some drugs can delay the onset of diabetes, lifestyle modifications play a greater role in the prevention of diabetes. Intensive weight loss and lifestyle intervention, if sustained, may improve glucose tolerance substantially and prevent progression from IGT to type 2 diabetes. The Diabetes Prevention Program (DPP) study found a 16% reduction in diabetes risk for every kilogram of weight loss. Reducing weight by 7% through a low-fat diet and performing 150 minutes of exercise a week is the goal. The ADA guidelines recommend modest weight loss (5–10% body weight), moderate-intensity exercise (30 minutes daily), and smoking cessation.There are many dietary approaches that can reduce the risk of progression to diabetes. Most involve the reduction of added sugars and fats but there remains a lack of conclusive evidence proving the best approach.For patients with severe risk factors, prescription medication may be appropriate. This may be considered in patients for whom lifestyle therapy has failed, or is not sustainable, and who are at high-risk for developing type 2 diabetes </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 Cystic kidney disease and explain in detail? [/INST] Cystic kidney disease refers to a wide range of hereditary, developmental, and acquired conditions and with the inclusion of neoplasms with cystic changes, over 40 classifications and subtypes have been identified. Depending on the disease classification, the presentation may be at birth, or much later into adult life. Cystic disease may involve one or both kidneys and may, or may not, occur in the presence of other anomalies. A higher incidence is found in males and prevalence increases with age. Renal cysts have been reported in more than 50% of patients over the age of 50. Typically, cysts grow up to 2.88 mm annually and may cause related pain and/or hemorrhage.Of the cystic kidney diseases, the most common is polycystic kidney disease with two sub-types: the less prevalent autosomal recessive and more prevalent autosomal dominant. Autosomal recessive polycystic kidney disease (ARPKD) is primarily diagnosed in infants and young children while autosomal dominant polycystic kidney disease (ADPKD) is most often diagnosed in adulthood.Another example of cystic kidney disease is Medullary sponge kidney.

Types
More Cystic Kidney Diseases
Cystic kidney disease includes various conditions related to the formation of cysts in one or both kidneys. The most common subset is polycystic kidney disease (PKD) which is a genetic anomaly with two subsets, autosomal recessive polycystic kidney disease (ARPKD) and autosomal dominant polycystic kidney disease (ADPKD). Consequently, causation can be genetic, developmental, or associated with systemic disease which can be acquired or malignant. Examples of acquired cystic kidney disease include simple cysts and medullary sponge kidney (MSK). Other types of genetic cystic kidney disease include juvenile nephronophthisis (JNPHP), medullary cystic kidney disease (MCKD), and glomerulocystic kidney disease (GCKD).

Polycystic Kidney Disease
PKD causes numerous cysts to grow in the kidneys. These cysts are filled with fluid and if they grow excessively, changing the shape of them and making them larger, leading to kidney damage. Mutations in genes PKD1 and PKD2 are responsible for autosomal dominant polycystic kidney disease (ADPKD), which is typically diagnosed in adulthood. Those genes encode for polycystic proteins and mutations regarding those genes are inherited and responsible for the disorder of autosomal dominant cystic kidney disease. In the United States, more than half a million people have PKD, making it the fourth leading cause of kidney failure. PKD affects all races and genders equally and those with PKD have a possibility of developing cysts in other organs such as liver, pancreas, spleen, ovaries, and large bowel. Usually, these latter cysts do not impose a problem. Half of patients have no manifestation of symptoms, but symptoms may include: hematuria, back or abdominal pain, or the development of hypertension. The disease is usually manifested before age 30, and 45% develop kidney failure by age 60. Mutation in the HDK1 gene is currently thought to be responsible for autosomal recessive polycystic kidney disease (ARPKD), which can be diagnosed in the womb, shortly after birth, and usually before 15 years of age.

Cause
The site of preference for cyst development is the renal tubule.  After growth of a few millimeters has occurred, the cysts detach from the parent tubule, this detachment induced by excessive proliferation of tubular epithelium or excessive fluid secretions.

Diagnosis
Diagnosis includes imaging with ultrasound, CT and/or MRI. The least expensive, non-invasive, and most reliable method is ultrasonography but smaller cysts may escape detection, while the resolution of CT and MRI will enable smaller cysts to be captured. However, the increased complexity and expense of CT and MRI is usually reserved for higher risk situations. MRI can be used to monitor the development of cysts and growth of kidneys.Genetic test can be applicable to those who have a family history of PKD but is expensive and fails to detect PKD in 15% of cases where it is present.

Antenatal scans
Many forms of cystic kidney disease can be detected in children prior to birth </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 Psoas muscle abscess 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 Bloodstream infections and explain in detail? [/INST] Bloodstream infections (BSIs),  which include bacteremias when the infections are bacterial and fungemias when the infections are fungal, are infections present in the blood. Blood is normally a sterile environment, so the detection of microbes in the blood (most commonly accomplished by blood cultures) is always abnormal. A bloodstream infection is different from sepsis, which is the host response to bacteria.Bacteria can enter the bloodstream as a severe complication of infections (like pneumonia or meningitis), during surgery (especially when involving mucous membranes such as the gastrointestinal tract), or due to catheters and other foreign bodies entering the arteries or veins (including during intravenous drug abuse). Transient bacteremia can result after dental procedures or brushing of teeth.Bacteremia can have several important health consequences. The immune response to the bacteria can cause sepsis and septic shock, which has a high mortality rate. Bacteria can also spread via the blood to other parts of the body (which is called hematogenous spread), causing infections away from the original site of infection, such as endocarditis or osteomyelitis. Treatment for bacteremia is with antibiotics, and prevention with antibiotic prophylaxis can be given in high risk situations.

Presentation
Bacteremia is typically transient and is quickly removed from the blood by the immune system.Bacteremia frequently evokes a response from the immune system called sepsis, which consists of symptoms such as fever, chills, and hypotension.  Severe immune responses to bacteremia may result in septic shock and multiple organ dysfunction syndrome, which are potentially fatal.

Causes
Bacteria can enter the bloodstream in a number of different ways.  However, for each major classification of bacteria (gram negative, gram positive, or anaerobic) there are characteristic sources or routes of entry into the bloodstream that lead to bacteremia. Causes of bacteremia can additionally be divided into healthcare-associated (acquired during the process of receiving care in a healthcare facility) or community-acquired (acquired outside of a health facility, often prior to hospitalization).

Gram positive bacteremia
Gram positive bacteria are an increasingly important cause of bacteremia.  Staphylococcus, streptococcus, and enterococcus species are the most important and most common species of gram-positive bacteria that can enter the bloodstream.  These bacteria are normally found on the skin or in the gastrointestinal tract.Staphylococcus aureus is the most common cause of healthcare-associated bacteremia in North and South America and is also an important cause of community-acquired bacteremia. Skin ulceration or wounds, respiratory tract infections, and IV drug use are the most important causes of community-acquired staph aureus bacteremia. In healthcare settings, intravenous catheters, urinary tract catheters, and surgical procedures are the most common causes of staph aureus bacteremia.There are many different types of streptococcal species that can cause bacteremia.  Group A streptococcus (GAS) typically causes bacteremia from skin and soft tissue infections.  Group B streptococcus is an important cause of bacteremia in neonates, often immediately following birth.  Viridans streptococci species are normal bacterial flora of the mouth.  Viridans strep can cause temporary bacteremia after eating, toothbrushing, or flossing.  More severe bacteremia can occur following dental procedures or in patients receiving chemotherapy.  Finally, Streptococcus bovis is a common cause of bacteremia in patients with colon cancer.Enterococci are an important cause of healthcare-associated bacteremia.  These bacteria commonly live in the gastrointestinal tract and female genital tract.  Intravenous catheters, urinary tract infections and surgical wounds are all risk factors for developing bacteremia from enterococcal species.  Resistant enterococcal species can cause bacteremia in patients who have had long hospital stays or frequent antibiotic use in the past (see antibiotic misuse).

Gram negative bacteremia
Gram negative bacterial species are responsible for approximately 24% of all cases of healthcare-associated bacteremia and 45% of all cases of community-acquired bacteremia. In general, gram negative bacteria enter the bloodstream from infections in the respiratory tract, genitourinary tract, gastrointestinal tract, or hepatobiliary system.  Gram-negative bacteremia occurs more frequently in elderly populations (65 years or older) and is associated with higher morbidity and mortality in this population.E.coli is the most common cause of community-acquired bacteremia accounting for approximately 75% of cases. E.coli bacteremia is usually the result of a urinary tract infection. Other organisms that can cause community-acquired bacteremia include Pseudomonas aeruginosa, Klebsiella pneumoniae, and Proteus mirabilis.  Salmonella infection, despite mainly only resulting in gastroenteritis in the developed world, is a common cause of bacteremia in Africa. It principally affects children who lack antibodies to Salmonella and HIV+ patients of all ages.Among healthcare-associated cases of bacteremia, gram negative organisms are an important cause of bacteremia in the ICU. Catheters in the veins, arteries, or urinary tract can all create a way for gram negative bacteria to enter the bloodstream.  Surgical procedures of the genitourinary tract, intestinal tract, or hepatobiliary tract can also lead to gram negative bacteremia.  Pseudomonas and Enterobacter species are the most important causes of gram negative bacteremia in the ICU.

Bacteremia risk factors
There are several risk factors that increase the likelihood of developing bacteremia from any type of bacteria.  These include:

HIV infection
Diabetes Mellitus
Chronic hemodialysis
Solid organ transplant
Stem cell transplant
Treatment with glucocorticoids
Liver failure
Asplenia

Mechanism
Bacteremia can travel through the blood stream to distant sites in the body and cause infection (hematogenous spread). Hematogenous spread of bacteria is part of the pathophysiology of certain infections of the heart (endocarditis), structures around the brain (meningitis), and tuberculosis of the spine (Potts disease). Hematogenous spread of bacteria is responsible for many bone infections (osteomyelitis).Prosthetic cardiac implants (for example artificial heart valves) are especially vulnerable to infection from bacteremia. Prior to widespread use of vaccines, occult bacteremia was an important consideration in febrile children that appeared otherwise well.

Diagnosis
Bacteremia is most commonly diagnosed by blood culture, in which a sample of blood drawn from the vein by needle puncture is allowed to incubate with a medium that promotes bacterial growth. If bacteria are present in the bloodstream at the time the sample is obtained, the bacteria will multiply and can thereby be detected.Any bacteria that incidentally find their way to the culture medium will also multiply. For example, if the skin is not adequately cleaned before needle puncture, contamination of the blood sample with normal bacteria that live on the surface of the skin can occur. For this reason, blood cultures must be drawn with great attention to sterile process. The presence of certain bacteria in the blood culture, such as Staphylococcus aureus, Streptococcus pneumoniae, and Escherichia coli almost never represent a contamination of the sample. On the other hand, contamination may be more highly suspected if organisms like Staphylococcus epidermidis or Cutibacterium acnes grow in the blood culture.Two blood cultures drawn from separate sites of the body are often sufficient to diagnose bacteremia. Two out of two cultures growing the same type of bacteria usually represents a real bacteremia, particularly if the organism that grows is not a common contaminant. One out of two positive cultures will usually prompt a repeat set of blood cultures to be drawn to confirm whether a contaminant or a real bacteremia is present. The patients skin is typically cleaned with an alcohol-based product prior to drawing blood to prevent contamination. Blood cultures may be repeated at intervals to determine if persistent — rather than transient — bacteremia is present.Prior to drawing blood cultures, a thorough patient history should be taken with particular regard to presence of both fevers and chills, other focal signs of infection such as in the skin or soft tissue, a state of immunosuppression, or any recent invasive procedures.Ultrasound of the heart is recommended in all those with bacteremia due to Staphylococcus aureus to rule out infectious endocarditis.

Definition
Bacteremia is the presence of bacteria in the bloodstream that are alive and capable of reproducing. It is a type of bloodstream infection. Bacteremia is defined as either a primary or secondary process. In primary bacteremia, bacteria have been directly introduced into the bloodstream.  Injection drug use may lead to primary bacteremia. In the hospital setting, use of blood vessel catheters contaminated with bacteria may also lead to primary bacteremia. Secondary bacteremia occurs when bacteria have entered the body at another site, such as the cuts in the skin, or the mucous membranes of the lungs (respiratory tract), mouth or intestines (gastrointestinal tract), bladder (urinary tract), or genitals. Bacteria that have infected the body at these sites may then spread into the lymphatic system and gain access to the bloodstream, where further spread can occur.Bacteremia may also be defined by the timing of bacteria presence in the bloodstream: transient, intermittent, or persistent. In transient bacteremia, bacteria are present in the bloodstream for minutes to a few hours before being cleared from the body, and the result is typically harmless in healthy people. This can occur after manipulation of parts of the body normally colonized by bacteria, such as the mucosal surfaces of the mouth during tooth brushing, flossing, or dental procedures, or instrumentation of the bladder or colon. Intermittent bacteremia is characterized by periodic seeding of the same bacteria into the bloodstream by an existing infection elsewhere in the body, such as an abscess, pneumonia, or bone infection, followed by clearing of that bacteria from the bloodstream. This cycle will often repeat until the existing infection is successfully treated. Persistent bacteremia is characterized by the continuous presence of bacteria in the bloodstream. It is usually the result of an infected heart valve, a central line-associated bloodstream infection (CLABSI), an infected blood clot (suppurative thrombophlebitis), or an infected blood vessel graft. Persistent bacteremia can also occur as part of the infection process of typhoid fever, brucellosis, and bacterial meningitis. Left untreated, conditions causing persistent bacteremia can be potentially fatal.Bacteremia is clinically distinct from sepsis, which is a condition where the blood stream infection is associated with an inflammatory response from the body, often causing abnormalities in body temperature, heart rate, breathing rate, blood pressure, and white blood cell count.

Treatment
The presence of bacteria in the blood almost always requires treatment with antibiotics. This is because there are high mortality rates from progression to sepsis if antibiotics are delayed.The treatment of bacteremia should begin with empiric antibiotic coverage.  Any patient presenting with signs or symptoms of bacteremia or a positive blood culture should be started on intravenous antibiotics </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 Onyongnyong virus and explain in detail? [/INST] The onyongnyong virus (ONNV) was first isolated by researchers at the Uganda Virus Research Institute in Entebbe, Uganda, during a large outbreak of a disease in 1959 that resembled dengue fever.  ONNV is a togavirus (family Togaviridae), genus Alphavirus,  is closely related to the chikungunya and Igbo Ora viruses, and is a member of the Semliki Forest antigenic complex. The name was given to the disease by the Acholi tribe during the 1959 outbreak </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 Spondylopathy 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 Myeloid leukemia 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 Underweight and explain in detail? [/INST] An underweight person is a person whose body weight is considered too low to be healthy. A person who is underweight is malnourished.

Assessment
The body mass index, a ratio of a persons weight to their height, has traditionally been used to assess the health of a person as it pertains to weight: under the cut-off point at a BMI of 18.5, a person is considered underweight. The calculation is either weight in kilograms divided by height in meters, squared, or weight in pounds times 703, divided by height in inches, squared. Another measure of underweight is through comparison to the average weight of a cohort of people of a similar age and height: people who are at least 15% to 20% below the average weight for the group are considered underweight.Body fat percentage has been suggested as another way to assess whether a person is underweight. Unlike the body mass index, which is a proxy measurement, the body fat percentage takes into account the difference in composition between adipose tissue (fat cells) and muscle tissue and their different roles in the body. The American Council on Exercise defines the amount of essential fat, below which a person is underweight, as 10–13% for women and 2–5% for men. The greater amount of essential body fat in women supports reproductive function.

Prevalence
Using the body mass index as a measure of weight-related health, with data from 2014, age-standardised global prevalence of underweight in women and men were 9.7% and 8.8%, respectively. These values were lower than what was reported for 1975 as 14.6% and 13,8%, respectively, indicating a worldwide reduction in the extent of undernutrition.

Causes
A person may be underweight due to genetics, improper metabolism of nutrients, lack of food (frequently due to poverty), drugs that affect appetite, illness (physical or mental) or the eating disorder anorexia nervosa.Being underweight is associated with certain medical conditions, including type 1 diabetes, hyperthyroidism, cancer, and tuberculosis. People with gastrointestinal or liver problems may be unable to absorb nutrients adequately. People with certain eating disorders can also be underweight due to one or more nutrient deficiencies or excessive exercise, which exacerbates nutrient deficiencies.A common belief is that healthy underweight individuals can ‘eat what they want’ and then burn it off either by high levels of activity or elevated metabolism. It has been shown however that individuals with BMI < 18.5 eat about 12% less calories than individuals with normal BMI (21.5 to 25) and they are 23% less physically active (by accelerometry).

Problems
Being underweight can be a symptom of an underlying condition, in which case it is secondary. Unexplained weight loss may require a professional medical diagnosis.Being underweight can also cause other conditions, in which case it is primary. Severely underweight individuals may have poor physical stamina and a weak immune system, leaving them open to infection. According to Robert E. Black of the Johns Hopkins School of Public Health (JHSPH), "Underweight status ... and micronutrient deficiencies also cause decreases in immune and non-immune host defenses, and should be classified as underlying causes of death if followed by infectious diseases that are the terminal associated causes."
People who are malnourished raise special concerns, as not only gross caloric intake may be inadequate, but also intake and absorption of other vital nutrients, especially essential amino acids and micronutrients such as vitamins and minerals.In women, being severely underweight, as a result of an eating disorder or due to excessive strenuous exercise, can result in amenorrhea (absence of menstruation), infertility or complications during pregnancy if gestational weight gain is too low.Malnourishment can also cause anemia and hair loss.
Being underweight is an established risk factor for osteoporosis, even for young people. This is seen in individuals suffering from relative energy deficiency in sport, formerly known as female athlete triad: when disordered eating or excessive exercise cause amenorrhea, hormone changes during ovulation leads to loss of bone mineral density. After this low bone mineral density causes the first spontaneous fractures, the damage is often irreversible.
Although being underweight has been reported to increase mortality at rates comparable to that seen in morbidly obese people, the effect is much less drastic when restricted to non-smokers with no history of disease, suggesting that smoking and disease-related weight loss are the leading causes of the observed effect.

Treatment
Diet
Underweight individuals may be advised to gain weight by increasing calorie intake </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 Ventricular fibrillation and explain in detail? [/INST] Ventricular fibrillation (V-fib or VF) is an abnormal heart rhythm in which the ventricles of the heart quiver. It is due to disorganized electrical activity. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by sudden cardiac death in the absence of treatment. Ventricular fibrillation is initially found in about 10% of people with cardiac arrest.Ventricular fibrillation can occur due to coronary heart disease, valvular heart disease, cardiomyopathy, Brugada syndrome, long QT syndrome, electric shock, or intracranial hemorrhage. Diagnosis is by an electrocardiogram (ECG) showing irregular unformed QRS complexes without any clear P waves. An important differential diagnosis is torsades de pointes.Treatment is with cardiopulmonary resuscitation (CPR) and defibrillation. Biphasic defibrillation may be better than monophasic. The medication epinephrine or amiodarone may be given if initial treatments are not effective. Rates of survival among those who are out of hospital when the arrhythmia is detected is about 17% while in hospital it is about 46%.

Signs and symptoms
Ventricular fibrillation is a cause of cardiac arrest. The ventricular muscle twitches randomly rather than contracting in a co-ordinated fashion (from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to pump blood around the body – because of this, it is classified as a cardiac arrest rhythm, and patients in V-fib should be treated with cardiopulmonary resuscitation (CPR) and prompt defibrillation. Left untreated, ventricular fibrillation is rapidly fatal as the vital organs of the body, including the heart, are starved of oxygen, and as a result patients in this rhythm will not be conscious or responsive to stimuli. Prior to cardiac arrest, patients may complain of varying symptoms depending on the underlying cause. Patients may exhibit signs of agonal breathing, which to a layperson can look like normal spontaneous breathing, but is a sign of hypoperfusion of the brainstem.It has an appearance on electrocardiography of irregular electrical activity with no discernable pattern. It may be described as coarse or fine depending on its amplitude, or as progressing from coarse to fine V-fib. Coarse V-fib may be more responsive to defibrillation, while fine V-fib can mimic the appearance of asystole on a defibrillator or cardiac monitor set to a low gain.  Some clinicians may attempt to defibrillate fine V-fib in the hope that it can be reverted to a cardiac rhythm compatible with life, whereas others will deliver CPR and sometimes drugs as described in the advanced cardiac life support protocols in an attempt to increase its amplitude and the odds of successful defibrillation.

Causes
Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" (Moe et al. 1964). A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction".Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease. Ventricular fibrillation is also seen in those with cardiomyopathy, myocarditis, and other heart pathologies. In addition, it is seen with electrolyte imbalance, overdoses of cardiotoxic drugs, and following near drowning or major trauma. It is also notable that ventricular fibrillation occurs where there is no discernible heart pathology or other evident cause, the so-called idiopathic ventricular fibrillation.Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-hospital arrest, as well as 3–9% of the cases of ventricular fibrillation unrelated to myocardial infarction, and 14% of all ventricular fibrillation resuscitations in patients under the age of 40. It follows then that, on the basis of the fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation accounts for an appreciable mortality. Recently described syndromes such as the Brugada Syndrome may give clues to the underlying mechanism of ventricular arrhythmias. In the Brugada syndrome, changes may be found in the resting ECG with evidence of right bundle branch block (RBBB) and ST elevation in the chest leads V1-V3, with an underlying propensity to sudden cardiac death.The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for the occurrence of fibrillation in the apparent "healthy" heart. It is evident that there are mechanisms at work that we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and understanding the underlying mechanisms of sudden cardiac death in these patients without pathological evidence of underlying heart disease.Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death are often the result of gene mutations that affect cellular transmembrane ion channels. For example, in Brugada Syndrome, sodium channels are affected. In certain forms of long QT syndrome, the potassium inward rectifier channel is affected.In 1899, it was also found that ventricular fibrillation was, typically, the ultimate cause of death when the electric chair was used.

Pathophysiology
Abnormal automaticity
Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a hypoxic myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry ventricular arrhythmia.Most myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential. That is, the maximum diastolic potential is less negative and therefore exists closer to the threshold potential. Cellular depolarisation can be due to a raised external concentration of potassium ions K+, a decreased intracellular concentration of sodium ions Na+, increased permeability to Na+, or a decreased permeability to K+. The ionic basic automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to –50 to –60 mV.Myocardial cells are exposed to different environments. Normal cells may be exposed to hyperkalaemia; abnormal cells may be perfused by normal environment. For example, with a healed myocardial infarction, abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with myocardial ischaemia. In conditions such as myocardial ischaemia, possible mechanism of arrhythmia generation include the resulting decreased internal K+ concentration, the increased external K+ concentration, norepinephrine release and acidosis. When myocardial cell are exposed to hyperkalemia, the maximum diastolic potential is depolarized as a result of the alteration of Ik1 potassium current, whose intensity and direction is strictly dependent on intracellular and extracellular potassium concentrations. With Ik1 suppressed, an hyperpolarizing effect is lost and therefore there can be activation of funny current even in myocardial cells (which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents). This can lead to the instauration of automaticity in ischemic tissue.

Re-entry
The role of re-entry or circus motion was demonstrated separately by G. R. Mines and W. E. Garrey. Mines created a ring of excitable tissue by cutting the atria out of the ray fish. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischemic or infarcted myocardium, or underlying scar tissue.It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance—the propagation velocity—will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the wavefront.In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.

Triggered activity
Triggered activity can occur due to the presence of afterdepolarisations. These are depolarising oscillations in the membrane voltage induced by preceding action potentials. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed afterdepolarisations (DADs). All afterdepolarisations may not reach threshold potential, but, if they do, they can trigger another afterdepolarisation, and thus self-perpetuate.

Power spectrum
The distribution of frequency and power of a waveform can be expressed as a power spectrum in which the contribution of different waveform frequencies to the waveform under analysis is measured. This can be expressed as either the dominant or peak frequency, i.e., the frequency with the greatest power or the median frequency, which divides the spectrum in two halves.Frequency analysis has many other uses in medicine and in cardiology, including analysis of heart rate variability and assessment of cardiac function, as well as in imaging and acoustics.

Histopathology
Myofibre break-up, abbreviated MFB, is associated with ventricular fibrillation leading to death. Histomorphologically, MFB is characterized by fractures of the cardiac myofibres perpendicular to their long axis, with squaring of the myofibre nuclei.

Treatment
Defibrillation is the definitive treatment of ventricular fibrillation, whereby an electrical current is applied to the ventricular mass either directly or externally through pads or paddles, with the aim of depolarising enough of the myocardium for coordinated contractions to occur again. The use of this is often dictated around the world by Advanced Cardiac Life Support or Advanced Life Support algorithms, which is taught to medical practitioners including doctors, nurses and paramedics and also advocates the use of drugs, predominantly epinephrine, after every second unsuccessful attempt at defibrillation, as well as cardiopulmonary resuscitation (CPR) between defibrillation attempts. Though ALS/ACLS algorithms encourage the use of drugs, they state first and foremost that defibrillation should not be delayed for any other intervention and that adequate cardiopulmonary resuscitation be delivered with minimal interruption.The precordial thump is a manoeuver promoted as a mechanical alternative to defibrillation. Some advanced life support algorithms advocate its use once and only in the case of witnessed and monitored V-fib arrests as the likelihood of it successfully cardioverting a patient are small and this diminishes quickly in the first minute of onset.People who survive a "V-fib arrest" and who make a good recovery are often considered for an implantable cardioverter-defibrillator, which can quickly deliver this same life-saving defibrillation should another episode of ventricular fibrillation occur outside a hospital environment.

Epidemiology
Sudden cardiac arrest is the leading cause of death in the industrialised world. It exacts a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2%. The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or "heart attack". During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

History
Lyman Brewer suggests that the first recorded account of ventricular fibrillation dates as far back as 1500 BC, and can be found in the Ebers papyrus of ancient Egypt. An extract, recorded 3500 years ago, states: "When the heart is diseased, its work is imperfectly performed: the vessels proceeding from the heart become inactive, so that you cannot feel them … if the heart trembles, has little power and sinks, the disease is advanced and death is near." A book authored by Jo Miles suggests that it may even go back farther. Tests done on frozen remains found in the Himalayas seemed fairly conclusive that the first known case of ventricular fibrillation dates back to at least 2500 BC.Whether this is a description of ventricular fibrillation is debatable. The next recorded description occurs 3000 years later and is recorded by Vesalius, who described the appearance of "worm-like" movements of the heart in animals prior to death.The significance and clinical importance of these observations and descriptions possibly of ventricular fibrillation were not recognised until John Erichsen in 1842 described ventricular fibrillation following the ligation of a coronary artery (Erichsen JE 1842). Subsequent to this in 1850, fibrillation was described by Ludwig and Hoffa when they demonstrated the provocation of ventricular fibrillation in an animal by applying a "Faradic" (electrical) current to the heart.In 1874, Edmé Félix Alfred Vulpian coined the term mouvement fibrillaire, a term that he seems to have used to describe both atrial and ventricular fibrillation. John A. MacWilliam, a physiologist who had trained under Ludwig and who subsequently became Professor of Physiology at the University of Aberdeen, gave an accurate description of the arrhythmia in 1887. This definition still holds today, and is interesting in the fact that his studies and description predate the use of electrocardiography. His description is as follows: "The ventricular muscle is thrown into a state of irregular arrhythmic contraction, whilst there is a great fall in the arterial blood pressure, the ventricles become dilated with blood as the rapid quivering movement of their walls is insufficient to expel their contents; the muscular action partakes of the nature of a rapid incoordinate twitching of the muscular tissue … The cardiac pump is thrown out of gear, and the last of its vital energy is dissipated in the violent and the prolonged turmoil of fruitless activity in the ventricular walls." MacWilliam spent many years working on ventricular fibrillation and was one of the first to show that ventricular fibrillation could be terminated by a series of induction shocks through the heart.The first electrocardiogram recording of ventricular fibrillation was by August Hoffman in a paper published in 1912. At this time, two other researchers, George Ralph Mines and Garrey, working separately, produced work demonstrating the phenomenon of circus movement and re-entry as possible substrates for the generation of arrhythmias. This work was also accompanied by Lewis, who performed further outstanding work into the concept of "circus movement."Later milestones include the work by W. J </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 Hypertensive encephalopathy and explain in detail? [/INST] Hypertensive encephalopathy (HE) is general brain dysfunction due to significantly high blood pressure. Symptoms may include headache, vomiting, trouble with balance, and confusion. Onset is generally sudden. Complications can include seizures, posterior reversible encephalopathy syndrome, and bleeding in the back of the eye.In hypertensive encephalopathy, generally the blood pressure is greater than 200/130 mmHg. Occasionally it can occur at a BP as low as 160/100 mmHg. This can occur in kidney failure, those who rapidly stop blood pressure medication, pheochromocytoma, and people on a monoamine oxidase inhibitor (MAOI) who eat foods with tyramine. When it occurs in pregnancy it is known as eclampsia. The diagnosis requires ruling out other possible causes.The condition is generally treated with medications to relatively rapidly lower the blood pressure. This may be done with labetalol or sodium nitroprusside given by injection into a vein. In those who are pregnant, magnesium sulfate may be used. Other treatments may include anti-seizure medications.Hypertensive encephalopathy is uncommon. It is believed to occur more often in those without easy access to health care. The term was first used by Oppenheimer and Fishberg in 1928. It is classified as a type of hypertensive emergency.

Signs and symptoms
Hypertensive encephalopathy is most commonly encountered in young and middle-aged people who have hypertension. Overall, the condition is rare even among people with hypertension. Studies report that from 0.5 to 15% of people with malignant hypertension develop hypertensive encephalopathy. With the development of methods for detection and treatment of hypertension, hypertensive encephalopathy has been becoming more rare.Symptoms of hypertensive encephalopathy typically start to occur 12–48 hours after a sudden and sustained increase in blood pressure. The first manifestation of these symptoms is a severe headache. Headache occurs in greater than 75% of patients. The patient becomes restless. Alterations in consciousness may follow several hours later, which include impaired judgement and memory, confusion, somnolence and stupor. If the condition is not treated, these neurological symptoms may worsen and ultimately turn into a coma. Other symptoms may include increased irritability, vomiting, diplopia, seizures, twitching and myoclonus of the limbs. Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness) are common. They occur in  4 out of 11 cases (Jellinek et al. 1964). Hemiparesis, intracerebral hemorrhage, aphasia may also occur, but they are less common.

Pathogenesis
Hypertensive encephalopathy is caused by an increase in blood pressure. Several conditions may evoke blood pressure elevation: acute nephritis, eclampsia, crises in chronic essential hypertension, sudden withdrawal of antihypertensive treatment. Additionally, hypertensive encephalopathy may occur in pheochromocytoma, Cushings syndrome, renal artery thrombosis.The impairment of cerebral blood flow that underlies hypertensive encephalopathy is still controversial. Normally, cerebral blood flow is maintained by an autoregulation mechanism that dilates arterioles in response to blood pressure decreases and constricts arterioles in response to blood pressure increases. This autoregulation falters when hypertension becomes excessive. According to the over-regulation conception, brain vessels spasm in response to acute hypertension, which results in cerebral ischemia and cytotoxic edema. According to the autoregulation breakthrough conception, cerebral arterioles are forced to dilate, leading to vasogenic edema.Cerebral edema can be generalized or focal. Brain ventricles are compressed, cortical gyri flattened.

Diagnosis
Diagnostic methods for hypertensive encephalopathy include physical examination, blood pressure measurement, blood sampling, ECG, EEG, chest X-ray, urinalysis, arterial blood gas analysis, and imaging of the head (CAT scan and/or MRI). Since decreasing blood pressure is essential, anti-hypertensive medication is administered without awaiting the results of the laboratory tests. Electroencephalographic examination detects the absence of alpha waves, signifying impaired consciousness. In people with visual disturbances, slow waves are detected in the occipital areas.

Treatment
The initial aim of treatment in hypertensive crises is to rapidly lower the diastolic pressure to about 100 to 105 mmHg; this goal should be achieved within two to six hours, with the maximum initial fall in BP not exceeding 25 percent of the presenting value. This level of BP control will allow gradual healing of the necrotizing vascular lesions. More aggressive hypotensive therapy is both unnecessary and may reduce the blood pressure below the autoregulatory range, possibly leading to ischemic events (such as stroke or coronary disease).Once the BP is controlled, the person should be switched to medication by mouth, with the diastolic pressure being gradually reduced to 85 to 90 mmHg over two to three months. The initial reduction to a diastolic pressure of approximately 100 mmHg is often associated with a modest worsening of renal function; this change, however, is typically transient as the vascular disease tends to resolve and renal perfusion improves over one to three months. Antihypertensive therapy should not be withheld in this setting unless there has been an excessive reduction in BP. A change in medication, however, is indicated if the decline in renal function is temporally related to therapy with an angiotensin (ACE) converting enzyme inhibitor or angiotensin II receptor blocker, which can interfere with renal autoregulation and produce acute kidney failure in patients with bilateral renal artery stenosis. (See "Renal effects of ACE inhibitors in hypertension".)ref
Several parenteral antihypertensive agents are most often used in the initial treatment of malignant hypertension.
Nitroprusside – an arteriolar and venous dilator, given as an intravenous infusion. Nitroprusside acts within seconds and has a duration of action of only two to five minutes. Thus, hypotension can be easily reversed by temporarily discontinuing the infusion, providing an advantage over the drugs listed below. However, the potential for cyanide toxicity limits the prolonged use of nitroprusside, particularly in patients with chronic kidney disease.
Nicardipine – an arteriolar dilator, given as an intravenous infusion.
Clevidipine – a short-acting dihydropyridine calcium channel blocker. It reduces blood pressure without affecting cardiac filling pressures or causing reflex tachycardia.
Labetalol – an alpha- and beta-adrenergic blocker, given as an intravenous bolus or infusion </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 Chills 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 Hand and explain in detail? [/INST] A hand is a prehensile, multi-fingered appendage located at the end of the forearm or forelimb of primates such as humans, chimpanzees, monkeys, and lemurs. A few other vertebrates such as the koala (which has two opposable thumbs on each "hand" and fingerprints extremely similar to human fingerprints) are often described as having "hands" instead of paws on their front limbs. The raccoon is usually described as having "hands" though opposable thumbs are lacking.Some evolutionary anatomists use the term hand to refer to the appendage of digits on the forelimb more generally—for example, in the context of whether the three digits of the bird hand involved the same homologous loss of two digits as in the dinosaur hand.The human hand usually has five digits: four fingers plus one thumb; these are often referred to collectively as five fingers, however, whereby the thumb is included as one of the fingers. It has 27 bones, not including the sesamoid bone, the number of which varies among people, 14 of which are the phalanges (proximal, intermediate and distal) of the fingers and thumb. The metacarpal bones connect the fingers and the carpal bones of the wrist. Each human hand has five metacarpals and eight carpal bones.
Fingers contain some of the densest areas of nerve endings in the body, and are the richest source of tactile feedback. They also have the greatest positioning capability of the body; thus, the sense of touch is intimately associated with hands. Like other paired organs (eyes, feet, legs) each hand is dominantly controlled by the opposing brain hemisphere, so that handedness—the preferred hand choice for single-handed activities such as writing with a pencil, reflects individual brain functioning.
Among humans, the hands play an important function in body language and sign language. Likewise, the ten digits of two hands and the twelve phalanges of four fingers (touchable by the thumb) have given rise to number systems and calculation techniques.

Structure
Many mammals and other animals have grasping appendages similar in form to a hand such as paws, claws, and talons, but these are not scientifically considered to be grasping hands. The scientific use of the term hand in this sense to distinguish the terminations of the front paws from the hind ones is an example of anthropomorphism. The only true grasping hands appear in the mammalian order of primates. Hands must also have opposable thumbs, as described later in the text.
The hand is located at the distal end of each arm. Apes and monkeys are sometimes described as having four hands, because the toes are long and the hallux is opposable and looks more like a thumb, thus enabling the feet to be used as hands.
The word "hand" is sometimes used by evolutionary anatomists to refer to the appendage of digits on the forelimb such as when researching the homology between the three digits of the bird hand and the dinosaur hand.An adult human males hand weighs about a pound.

Areas
Areas of the human hand include:

The palm (Volar), which is the central region of the anterior part of the hand, located superficially to the metacarpus. The skin in this area contains dermal papillae to increase friction, such as are also present on the fingers and used for fingerprints.
The opisthenar area (dorsal) is the corresponding area on the posterior part of the hand.
The heel of the hand is the area anteriorly to the bases of the metacarpal bones, located in the proximal part of the palm. It is the area that sustains most pressure when using the palm of the hand for support, such as in handstand.There are five digits attached to the hand, notably with a nail fixed to the end in place of the normal claw. The four fingers can be folded over the palm which allows the grasping of objects. Each finger, starting with the one closest to the thumb, has a colloquial name to distinguish it from the others:

index finger, pointer finger, forefinger, or 2nd digit
middle finger or long finger or 3rd digit
ring finger or 4th digit
little finger, pinky finger, small finger, baby finger, or 5th digitThe thumb (connected to the first metacarpal bone and trapezium) is located on one of the sides, parallel to the arm. A reliable way of identifying human hands is from the presence of opposable thumbs. Opposable thumbs are identified by the ability to be brought opposite to the fingers, a muscle action known as opposition.

Bones
The skeleton of the human hand consists of 27 bones: the eight short carpal bones of the wrist are organized into a proximal row (scaphoid, lunate, triquetral and pisiform) which articulates with the bones of the forearm, and a distal row (trapezium, trapezoid, capitate and hamate), which articulates with the bases of the five metacarpal bones of the hand. The heads of the metacarpals will each in turn articulate with the bases of the proximal phalanx of the fingers and thumb. These articulations with the fingers are the metacarpophalangeal joints known as the knuckles. At the palmar aspect of the first metacarpophalangeal joints are small, almost spherical bones called the sesamoid bones. The fourteen phalanges make up the fingers and thumb, and are numbered I-V (thumb to little finger) when the hand is viewed from an anatomical position (palm up). The four fingers each consist of three phalanx bones: proximal, middle, and distal. The thumb only consists of a proximal and distal phalanx. Together with the phalanges of the fingers and thumb these metacarpal bones form five rays or poly-articulated chains.
Because supination and pronation (rotation about the axis of the forearm) are added to the two axes of movements of the wrist, the ulna and radius are sometimes considered part of the skeleton of the hand.
There are numerous sesamoid bones in the hand, small ossified nodes embedded in tendons; the exact number varies between people: whereas a pair of sesamoid bones are found at virtually all thumb metacarpophalangeal joints, sesamoid bones are also common at the interphalangeal joint of the thumb (72.9%) and at the metacarpophalangeal joints of the little finger (82.5%) and the index finger (48%).  In rare cases, sesamoid bones have been found in all the metacarpophalangeal joints and all distal interphalangeal joints except that of the long finger.
The articulations are:

interphalangeal articulations of hand (the hinge joints between the bones of the digits)
metacarpophalangeal joints (where the digits meet the palm)
intercarpal articulations (where the palm meets the wrist)
wrist (may also be viewed as belonging to the forearm).

Arches
The fixed and mobile parts of the hand adapt to various everyday tasks by forming bony arches: longitudinal arches (the rays formed by the finger bones and their associated metacarpal bones), transverse arches (formed by the carpal bones and distal ends of the metacarpal bones), and oblique arches (between the thumb and four fingers):
Of the longitudinal arches or rays of the hand, that of the thumb is the most mobile (and the least longitudinal).  While the ray formed by the little finger and its associated metacarpal bone still offers some mobility, the remaining rays are firmly rigid.  The phalangeal joints of the index finger, however, offer some independence to its finger, due to the arrangement of its flexor and extension tendons.The carpal bones form two transversal rows, each forming an arch concave on the palmar side.  Because the proximal arch simultaneously has to adapt to the articular surface of the radius and to the distal carpal row, it is by necessity flexible.  In contrast, the capitate, the "keystone" of the distal arch, moves together with the metacarpal bones and the distal arch is therefore rigid.  The stability of these arches is more dependent of the ligaments and capsules of the wrist than of the interlocking shapes of the carpal bones, and the wrist is therefore more stable in flexion than in extension.  The distal carpal arch affects the function of the CMC joints and the hands, but not the function of the wrist or the proximal carpal arch.  The ligaments that maintain the distal carpal arches are the transverse carpal ligament and the intercarpal ligaments (also oriented transversally).  These ligaments also form the carpal tunnel and contribute to the deep and superficial palmar arches.  Several muscle tendons attaching to the TCL and the distal carpals also contribute to maintaining the carpal arch.Compared to the carpal arches, the arch formed by the distal ends of the metacarpal bones is flexible due to the mobility of the peripheral metacarpals (thumb and little finger).  As these two metacarpals approach each other, the palmar gutter deepens. The central-most metacarpal (middle finger) is the most rigid. It and its two neighbors are tied to the carpus by the interlocking shapes of the metacarpal bones.  The thumb metacarpal only articulates with the trapezium and is therefore completely independent, while the fifth metacarpal (little finger) is semi-independent with the fourth metacarpal (ring finger) which forms a transitional element to the fifth metacarpal.Together with the thumb, the four fingers form four oblique arches, of which the arch of the index finger functionally is the most important, especially for precision grip, while the arch of the little finger contribute an important locking mechanism for power grip.  The thumb is undoubtedly the "master digit" of the hand, giving value to all the other fingers.  Together with the index and middle finger, it forms the dynamic tridactyl configuration responsible for most grips not requiring force.  The ring and little fingers are more static, a reserve ready to interact with the palm when great force is needed.

Muscles
The muscles acting on the hand can be subdivided into two groups: the extrinsic and intrinsic muscle groups.  The extrinsic muscle groups are the long flexors and extensors. They are called extrinsic because the muscle belly is located on the forearm.

Intrinsic
The intrinsic muscle groups are the thenar (thumb) and hypothenar (little finger) muscles; the interosseous muscles (four dorsally and three volarly) originating between the metacarpal bones; and the lumbrical muscles arising from the deep flexor (and are special because they have no bony origin) to insert on the dorsal extensor hood mechanism.

Extrinsic
The fingers have two long flexors, located on the underside of the forearm. They insert by tendons to the phalanges of the fingers. The deep flexor attaches to the distal phalanx, and the superficial flexor attaches to the middle phalanx. The flexors allow for the actual bending of the fingers. The thumb has one long flexor and a short flexor in the thenar muscle group. The human thumb also has other muscles in the thenar group (opponens and abductor brevis muscle), moving the thumb in opposition, making grasping possible.
The extensors are located on the back of the forearm and are connected in a more complex way than the flexors to the dorsum of the fingers. The tendons unite with the interosseous and lumbrical muscles to form the extensorhood mechanism. The primary function of the extensors is to straighten out the digits. The thumb has two extensors in the forearm; the tendons of these form the anatomical snuff box. Also, the index finger and the little finger have an extra extensor used, for instance, for pointing. The extensors are situated within 6 separate compartments.

The first four compartments are located in the grooves present on the dorsum of inferior side of radius while the 5th compartment is in between radius and ulna. The 6th compartment is in the groove on the dorsum of inferior side of ulna.

Nerve supply
The hand is innervated by the radial, median, and ulnar nerves.

MotorThe radial nerve supplies the finger extensors and the thumb abductor, thus the muscles that extends at the wrist and metacarpophalangeal joints (knuckles); and that abducts and extends the thumb.
The median nerve supplies the flexors of the wrist and digits, the abductors and opponens of the thumb, the first and second lumbrical.
The ulnar nerve supplies the remaining intrinsic muscles of the hand.All muscles of the hand are innervated by the brachial plexus (C5–T1) and can be classified by innervation:
SensoryThe radial nerve supplies the skin on the back of the hand from the thumb to the ring finger and the dorsal aspects of the index, middle, and half ring fingers as far as the proximal interphalangeal joints.
The median nerve supplies the palmar side of the thumb, index, middle, and half ring fingers.  Dorsal branches innervates the distal phalanges of the index, middle, and half ring fingers.
The ulnar nerve supplies the ulnar third of the hand, both at the palm and the back of the hand, and the little and half ring fingers.There is a considerable variation to this general pattern, except for the little finger and volar surface of the index finger.  For example, in some individuals, the ulnar nerve supplies the entire ring finger and the ulnar side of the middle finger, whilst, in others, the median nerve supplies the entire ring finger.

Blood supply
The hand is supplied with blood from two arteries, the ulnar artery and the radial artery.  These arteries form three arches over the dorsal and palmar aspects of the hand, the dorsal carpal arch (across the back of the hand), the deep palmar arch, and the superficial palmar arch.  Together these three arches and their anastomoses provide oxygenated blood to the palm, the fingers, and the thumb.
The hand is drained by the dorsal venous network of the hand with deoxygenated blood leaving the hand via the cephalic vein and the basilic vein.

Skin
The glabrous (hairless) skin on the front of the hand, the palm, is relatively thick and can be bent along the hands flexure lines where the skin is tightly bound to the underlying tissue and bones. Compared to the rest of the bodys skin, the hands palms (as well as the soles of the feet) are usually lighter—and even much lighter in dark-skinned individuals, compared to the other side of the hand. Indeed, genes specifically expressed in the dermis of palmoplantar skin inhibit melanin production and thus the ability to tan, and promote the thickening of the stratum lucidum and stratum corneum layers of the epidermis. All parts of the skin involved in grasping are covered by papillary ridges (fingerprints) acting as friction pads.  In contrast, the hairy skin on the dorsal side is thin, soft, and pliable, so that the skin can recoil when the fingers are stretched.  On the dorsal side, the skin can be moved across the hand up to 3 cm (1.2 in); an important input the cutaneous mechanoreceptors.The web of the hand is a "fold of skin which connects the digits". These webs, located between each set of digits, are known as skin folds (interdigital folds or plica interdigitalis). They are defined as "one of the folds of skin, or rudimentary web, between the fingers and toes".

Variation
The ratio of the length of the index finger to the length of the ring finger in adults is affected by the level of exposure to male sex hormones of the embryo in utero. This digit ratio is below 1 for both sexes but it is lower in males than in females on average.

Clinical significance
A number of genetic disorders affect the hand. Polydactyly is the presence of more than the usual number of fingers. One of the disorders that can cause this is Catel-Manzke syndrome. The fingers may be fused in a disorder known as syndactyly. Or there may be an absence of one or more central fingers—a condition known as ectrodactyly. Additionally, some people are born without one or both hands (amelia). Hereditary multiple exostoses of the forearm—also known as hereditary multiple osteochondromas—is another cause of hand and forearm deformity in children and adults.There are several cutaneous conditions that can affect the hand including the nails.
The autoimmune disease rheumatoid arthritis can affect the hand, particularly the joints of the fingers.
Some conditions can be treated by hand surgery. These include carpal tunnel syndrome, a painful condition of the hand and fingers caused by compression of the median nerve, and Dupuytrens contracture, a condition in which fingers bend towards the palm and cannot be straightened. Similarly, injury to the ulnar nerve may result in a condition in which some of the fingers cannot be flexed.
A common fracture of the hand is a scaphoid fracture—a fracture of the scaphoid bone, one of the carpal bones. This is the commonest carpal bone fracture and can be slow to heal due to a limited blood flow to the bone. There are various types of fracture to the base of the thumb; these are known as Rolando fractures, Bennets fracture, and Gamekeepers thumb. Another common fracture, known as Boxers fracture, is to the neck of a metacarpal. One can also have a broken finger.

Evolution
The prehensile hands and feet of primates evolved from the mobile hands of semi-arboreal tree shrews that lived about 60 million years ago.  This development has been accompanied by important changes in the brain and the relocation of the eyes to the front of the face, together allowing the muscle control and stereoscopic vision necessary for controlled grasping.  This grasping, also known as power grip, is supplemented by the precision grip between the thumb and the distal finger pads made possible by the opposable thumbs.  Hominidae (great apes including humans) acquired an erect bipedal posture about 3.6 million years ago, which freed the hands from the task of locomotion and paved the way for the precision and range of motion in human hands. Functional analyses of the features unique to the hand of modern humans have shown that they are consistent with the stresses and requirements associated with the effective use of paleolithic stone tools. It is possible that the refinement of the bipedal posture in the earliest hominids evolved to facilitate the use of the trunk as leverage in accelerating the hand.While the human hand has unique anatomical features, including a longer thumb and fingers that can be controlled individually to a higher degree, the hands of other primates are anatomically similar and the dexterity of the human hand can not be explained solely on anatomical factors.  The neural machinery underlying hand movements is a major contributing factor; primates have evolved direct connections between neurons in cortical motor areas and spinal motoneurons, giving the cerebral cortex monosynaptic control over the motoneurons of the hand muscles; placing the hands "closer" to the brain </s>