<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Familial Mediterranean fever and can you explain it in depth? [/INST] Familial Mediterranean fever (FMF) is a hereditary inflammatory disorder.: 149   FMF is an autoinflammatory disease caused by mutations in Mediterranean fever gene, which encodes a 781–amino acid protein called pyrin. While all ethnic groups are susceptible to FMF, it usually occurs in people of Mediterranean origin—including Sephardic Jews, Mizrahi Jews, Ashkenazi Jews, Assyrians, Armenians, Azerbaijanis, Levantines, Kurds, Greeks, Turks and Italians.The disorder has been given various names, including familial paroxysmal polyserositis, periodic peritonitis, recurrent polyserositis, benign paroxysmal peritonitis, periodic disease or periodic fever, Reimann periodic disease or Reimann syndrome, Siegal-Cattan-Mamou disease, and Wolff periodic disease. Note that "periodic fever" can also refer to any of the periodic fever syndromes.

Signs and symptoms
Attacks
There are seven types of attacks. Ninety percent of all patients have their first attack before they are 18 years old. All develop over 2–4 hours and last anywhere from 6 hours to 5 days. Most attacks involve fever.
Abdominal attacks, featuring abdominal pain, affect the whole abdomen with all signs of peritonitis (inflammation of abdominal lining), and acute abdominal pain like appendicitis. They occur in 95% of all patients and may lead to unnecessary laparotomy. Incomplete attacks, with local tenderness and normal blood tests, have been reported.
Joint attacks mainly occur in large joints, especially in the legs. Usually, only one joint is affected. 75% of all FMF patients experience joint attacks.
Chest attacks include pleuritis (inflammation of the pleura) and pericarditis (inflammation of the pericardium). Pleuritis occurs in 40% of patients and makes it difficult to breathe or lie flat, but pericarditis is rare.
Scrotal attacks due to inflammation of the tunica vaginalis are somewhat rare but may be mistaken for testicular torsion.
Myalgia (rare in isolation)
Erysipeloid rashes (a skin reaction on the legs that can mimic cellulitis, rare in isolation)

Complications
AA-amyloidosis with kidney failure is a complication and may develop without overt crises. AA amyloid protein is produced in very large quantities during attacks, and at a low rate between them, and accumulates mainly in the kidney, as well as the heart, spleen, gastrointestinal tract, and thyroid.There appears to be an increase in the risk for developing particular vasculitis-related diseases (e.g. Henoch–Schönlein purpura), spondylarthropathy, prolonged arthritis of certain joints and protracted myalgia.

Genetics
The MEFV gene is located on the short arm of chromosome 16 (16p13). Many different mutations of the MEFV gene can cause the disorder. Having one mutation is unlikely to cause the condition. Having two mutations either a copy from both parents, or two different mutations, one from each parent is the threshold for a genetic diagnosis of FMF. However, most individuals who comply with the genetic diagnosis of FMF remain asymptomatic or undiagnosed.  Whether this is due to modifier genes or environmental factors remains to be established.

Pathophysiology
Virtually all cases are due to a mutation in the Mediterranean Fever (MEFV) gene on the chromosome 16, which codes for a protein called pyrin or marenostrin. Various mutations of this gene lead to FMF, although some mutations cause a more severe picture than others. Mutations occur mainly in exons 2, 3, 5 and 10.The function of pyrin has not been completely elucidated, but in short, it is a protein that binds to the adaptor ASC and the pro form of the enzyme caspase-1 to generate multiprotein complexes called inflammasomes in response to certain infections. In healthy individuals, pyrin-mediated inflammasome assembly (which leads to the caspase 1) dependent processing and secretion of the pro-inflammatory cytokines (such as interleukin-18 (IL-18) and IL-1β) is a response to enterotoxins from certain bacteria. The gain-of-function mutations in the MEFV gene render Pyrin hyperactive, and subsequently, the formation of the inflammasomes becomes more frequent.The pathophysiology of familial Mediterranean fever has recently undergone significant advances: at basal state, pyrin is kept inactive by a chaperone protein (belonging to the family of 14.3.3 proteins) linked to pyrin through phosphorylated serine residues. The dephosphoration of pyrin is an essential prerequisite for the activation of the pyrin inflammasome. Inactivation of RhoA GTPases (by bacterial toxins, for example) leads to the inactivation of PKN1 / PKN2 kinases and dephosphoration of pyrin. In healthy subjects, the dephosphorylation step alone does not cause activation of the pyrin inflammasome. In contrast, in FMF patients, the dephosphorylation of serines is sufficient to trigger the activation of the pyrin inflammasome. This suggests that there is a two-level regulation and that the second regulatory mechanism (independent of (de)phosphorylation) is deficient in FMF patients. This deficient mechanism is probably located at the level of the B30.2 domain (exon 10) where most of the pathogenic mutations associated with FMF are located. It is probably the interaction of this domain with the cytoskeleton (microtubules) that is failing, as suggested by the efficacy of colchicine.It is not conclusively known what exactly sets off the attacks, and why overproduction of IL-1 would lead to particular symptoms in particular organs (e.g. joints or the peritoneal cavity).

Diagnosis
The diagnosis is clinically made on the basis of the history of typical attacks, especially in patients from the ethnic groups in which FMF is more highly prevalent. An acute phase response is present during attacks, with high C-reactive protein levels, an elevated white blood cell count and other markers of inflammation. In patients with a long history of attacks, monitoring the kidney function is of importance in predicting chronic kidney failure.A genetic test is also available to detect mutations in the MEFV gene.  Sequencing of exons 2, 3, 5, and 10 of this gene detects an estimated 97% of all known mutations.A specific and highly sensitive test for FMF is the "metaraminol provocative test (MPT)", whereby a single 10 mg infusion of metaraminol is administered to the patient. A positive diagnosis is made if the patient presents with a typical, albeit milder, FMF attack within 48 hours. As MPT is more specific than sensitive, it does not identify all cases of FMF, although a positive MPT can be very useful.

Treatment
Attacks are self-limiting, and require analgesia and NSAIDs (such as diclofenac). Colchicine, a drug otherwise mainly used in gout, decreases attack frequency in FMF patients. The exact way in which colchicine suppresses attacks is unclear </s>


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Abdominal pain and can you explain it in depth? [/INST] Abdominal pain, also known as a stomach ache, is a symptom associated with both non-serious and serious medical issues.
Common causes of pain in the abdomen include gastroenteritis and irritable bowel syndrome. About 15% of people have a more serious underlying condition such as appendicitis, leaking or ruptured abdominal aortic aneurysm, diverticulitis, or ectopic pregnancy. In a third of cases the exact cause is unclear.Given that a variety of diseases can cause some form of abdominal pain, a systematic approach to the examination of a person and the formulation of a differential diagnosis remains important.

Differential diagnosis
The most frequent reasons for abdominal pain are gastroenteritis (13%), irritable bowel syndrome (8%), urinary tract problems (5%), inflammation of the stomach (5%) and constipation (5%). In about 30% of cases, the cause is not determined. About 10% of cases have a more serious cause including gallbladder (gallstones or biliary dyskinesia) or pancreas problems (4%), diverticulitis (3%), appendicitis (2%) and cancer (1%). More common in those who are older, ischemic colitis, mesenteric ischemia, and abdominal aortic aneurysms are other serious causes.

Acute abdominal pain
Acute abdomen can be defined as severe, persistent abdominal pain of sudden onset that is likely to require surgical intervention to treat its cause. The pain may frequently be associated with nausea and vomiting, abdominal distention, fever and signs of shock. One of the most common conditions associated with acute abdominal pain is acute appendicitis.

Selected causes
Traumatic: blunt or perforating trauma to the stomach, bowel, spleen, liver, or kidney
Inflammatory:
Infections such as appendicitis, cholecystitis, pancreatitis, pyelonephritis, Peritonitis, pelvic inflammatory disease, hepatitis, mesenteric adenitis, or a subdiaphragmatic abscess
Perforation of a peptic ulcer, a diverticulum, or the caecum
Complications of inflammatory bowel disease such as Crohns disease or ulcerative colitis
Mechanical:
Small bowel obstruction secondary to adhesions caused by previous surgeries, intussusception, hernias, benign or malignant neoplasms
Large bowel obstruction caused by colorectal cancer, inflammatory bowel disease, volvulus, fecal impaction or hernia
Vascular: occlusive intestinal ischemia, usually caused by thromboembolism of the superior mesenteric artery

By system
A more extensive list includes the following:
Gastrointestinal
GI tract
Inflammatory: gastroenteritis, appendicitis, gastritis, esophagitis, diverticulitis, Crohns disease, ulcerative colitis, microscopic colitis
Obstruction: hernia, intussusception, volvulus, post-surgical adhesions, tumors, severe constipation, hemorrhoids
Vascular: embolism, thrombosis, hemorrhage, sickle cell disease, abdominal angina, blood vessel compression (such as celiac artery compression syndrome), superior mesenteric artery syndrome, postural orthostatic tachycardia syndrome
Digestive: peptic ulcer, lactose intolerance, celiac disease, food allergies, indigestion
Glands
Bile system
Inflammatory: cholecystitis, cholangitis
Obstruction: cholelithiasis, tumours
Liver
Inflammatory: hepatitis, liver abscess
Pancreatic
Inflammatory: pancreatitis
Renal and urological
Inflammation: pyelonephritis, bladder infection
Obstruction: kidney stones, urolithiasis, urinary retention, tumours
Vascular: left renal vein entrapment
Gynaecological or obstetric
Inflammatory: pelvic inflammatory disease
Mechanical: ovarian torsion
Endocrinological: menstruation, Mittelschmerz
Tumors: endometriosis, fibroids, ovarian cyst, ovarian cancer
Pregnancy: ruptured ectopic pregnancy, threatened abortion
Abdominal wall
muscle strain or trauma
muscular infection
neurogenic pain: herpes zoster, radiculitis in Lyme disease, abdominal cutaneous nerve entrapment syndrome (ACNES), tabes dorsalis
Referred pain
from the thorax: pneumonia, pulmonary embolism, ischemic heart disease, pericarditis
from the spine: radiculitis
from the genitals: testicular torsion
Metabolic disturbance
uremia, diabetic ketoacidosis, porphyria, C1-esterase inhibitor deficiency, adrenal insufficiency, lead poisoning, black widow spider bite, narcotic withdrawal
Blood vessels
aortic dissection, abdominal aortic aneurysm
Immune system
sarcoidosis
vasculitis
familial Mediterranean fever
Idiopathic
irritable bowel syndrome (IBS)(affecting up to 20% of the population, IBS is the most common cause of recurrent and intermittent abdominal pain)

By location
The location of abdominal pain can provide information about what may be causing the pain. The abdomen can be divided into four regions called quadrants. Locations and associated conditions include:
Diffuse
Peritonitis
Vascular: mesenteric ischemia, ischemic colitis, Henoch-Schonlein purpura, sickle cell disease, systemic lupus erythematosus, polyarteritis nodosa
Small bowel obstruction
Irritable bowel syndrome
Metabolic disorders: ketoacidosis, porphyria, familial Mediterranean fever, adrenal crisis
Epigastric
Heart: myocardial infarction, pericarditis
Stomach: gastritis, stomach ulcer, stomach cancer
Pancreas: pancreatitis, pancreatic cancer
Intestinal: duodenal ulcer, diverticulitis, appendicitis
Right upper quadrant
Liver: hepatomegaly, fatty liver, hepatitis, liver cancer, abscess
Gallbladder and biliary tract: inflammation, gallstones, worm infection, cholangitis
Colon: bowel obstruction, functional disorders, gas accumulation, spasm, inflammation, colon cancer
Other: pneumonia, Fitz-Hugh-Curtis syndrome
Left upper quadrant
Splenomegaly
Colon: bowel obstruction, functional disorders, gas accumulation, spasm, inflammation, colon cancer
Peri-umbilical (the area around the umbilicus, aka the belly button)
Appendicitis
Pancreatitis
Inferior myocardial infarction
Peptic ulcer
Diabetic ketoacidosis
Vascular: aortic dissection, aortic rupture
Bowel: mesenteric ischemia, Celiac disease, inflammation, intestinal spasm, functional disorders, small bowel obstruction
Lower abdominal pain
Diarrhea
Colitis
Crohns
Dysentery
Hernia
Right lower quadrant
Colon: intussusception, bowel obstruction, appendicitis (McBurneys point)
Renal: kidney stone (nephrolithiasis), pyelonephritis
Pelvic: cystitis, bladder stone, bladder cancer, pelvic inflammatory disease, pelvic pain syndrome
Gynecologic: endometriosis, intrauterine pregnancy, ectopic pregnancy, ovarian cyst, ovarian torsion, fibroid (leiomyoma), abscess, ovarian cancer, endometrial cancer
Left lower quadrant
Bowel: diverticulitis, sigmoid colon volvulus, bowel obstruction, gas accumulation, Toxic megacolon
Right low back pain
Liver: hepatomegaly
Kidney: kidney stone (nephrolithiasis), complicated urinary tract infection
Left low back pain
Spleen
Kidney: kidney stone (nephrolithiasis), complicated urinary tract infection
Low back pain
kidney pain (kidney stone, kidney cancer, hydronephrosis)
Ureteral stone pain

Pathophysiology
Abdominal pain can be referred to as visceral pain or peritoneal pain. The contents of the abdomen can be divided into the foregut, midgut, and hindgut. The foregut contains the pharynx, lower respiratory tract, portions of the esophagus, stomach, portions of the duodenum (proximal), liver, biliary tract (including the gallbladder and bile ducts), and the pancreas. The midgut contains portions of the duodenum (distal), cecum, appendix, ascending colon, and first half of the transverse colon. The hindgut contains the distal half of the transverse colon, descending colon, sigmoid colon, rectum, and superior anal canal.Each subsection of the gut has an associated visceral afferent nerve that transmits sensory information from the viscera to the spinal cord, traveling with the autonomic sympathetic nerves. The visceral sensory information from the gut traveling to the spinal cord, termed the visceral afferent, is non-specific and overlaps with the somatic afferent nerves, which are very specific. Therefore, visceral afferent information traveling to the spinal cord can present in the distribution of the somatic afferent nerve; this is why appendicitis initially presents with T10 periumbilical pain when it first begins and becomes T12 pain as the abdominal wall peritoneum (which is rich with somatic afferent nerves) is involved.

Diagnosis
A thorough patient history and physical examination is used to better understand the underlying cause of abdominal pain.
The process of gathering a history may include:
Identifying more information about the chief complaint by eliciting a history of present illness; i.e. a narrative of the current symptoms such as the onset, location, duration, character, aggravating or relieving factors, and temporal nature of the pain. Identifying other possible factors may aid in the diagnosis of the underlying cause of abdominal pain, such as recent travel, recent contact with other ill individuals, and for females, a thorough gynecologic history.
Learning about the patients past medical history, focusing on any prior issues or surgical procedures.
Clarifying the patients current medication regimen, including prescriptions, over-the-counter medications, and supplements.
Confirming the patients drug and food allergies.
Discussing with the patient any family history of disease processes, focusing on conditions that might resemble the patients current presentation.
Discussing with the patient any health-related behaviors (e.g. tobacco use, alcohol consumption, drug use, and sexual activity) that might make certain diagnoses more likely.
Reviewing the presence of non-abdominal symptoms (e.g., fever, chills, chest pain, shortness of breath, vaginal bleeding) that can further clarify the diagnostic picture.
Using Carnetts sign to differentiate between visceral pain and pain originating in the muscles of the abdominal wall.After gathering a thorough history, one should perform a physical exam in order to identify important physical signs that might clarify the diagnosis, including a cardiovascular exam, lung exam, thorough abdominal exam, and for females, a genitourinary exam.Additional investigations that can aid diagnosis include:
Blood tests including complete blood count, basic metabolic panel, electrolytes, liver function tests, amylase, lipase, troponin I, and for females, a serum pregnancy test.
Urinalysis
Imaging including chest and abdominal X-rays
ElectrocardiogramIf diagnosis remains unclear after history, examination, and basic investigations as above, then more advanced investigations may reveal a diagnosis. Such tests include:
Computed tomography of the abdomen/pelvis
Abdominal or pelvic ultrasound
Endoscopy and/or colonoscopy

Management
The management of abdominal pain depends on many factors, including the etiology of the pain </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Cirrhosis and can you explain it in depth? [/INST] Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, and end-stage liver disease, is the impaired liver function caused by the formation of scar tissue known as fibrosis due to damage caused by liver disease. Damage causes tissue repair and subsequent formation of scar tissue, which over time can replace normal functioning tissue, leading to the impaired liver function of cirrhosis. The disease typically develops slowly over months or years. Early symptoms may include tiredness, weakness, loss of appetite, unexplained weight loss, nausea and vomiting, and discomfort in the right upper quadrant of the abdomen. As the disease worsens, symptoms may include itchiness, swelling in the lower legs, fluid build-up in the abdomen, jaundice, bruising easily, and the development of spider-like blood vessels in the skin. The fluid build-up in the abdomen may become spontaneously infected. More serious complications include hepatic encephalopathy, bleeding from dilated veins in the esophagus, stomach, or intestines, and liver cancer.Cirrhosis is most commonly caused by alcoholic liver disease, non-alcoholic steatohepatitis (NASH – the progressive form of non-alcoholic fatty liver disease), heroin abuse, chronic hepatitis B, and chronic hepatitis C. Heavy drinking over a number of years can cause alcoholic liver disease. Liver damage has also been attributed to heroin usage over an extended period of time as well. NASH has a number of causes, including obesity, high blood pressure, abnormal levels of cholesterol, type 2 diabetes, and metabolic syndrome. Less common causes of cirrhosis include autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis that disrupts bile duct function, genetic disorders such as Wilsons disease and hereditary hemochromatosis, and chronic heart failure with liver congestion.Diagnosis is based on blood tests, medical imaging, and liver biopsy.Hepatitis B vaccine can prevent hepatitis B and the development of cirrhosis, but no vaccination against hepatitis C is available. No specific treatment for cirrhosis is known, but many of the underlying causes may be treated by a number of medications that may slow or prevent worsening of the condition. Avoiding alcohol is recommended in all cases. Hepatitis B and C may be treatable with antiviral medications. Autoimmune hepatitis may be treated with steroid medications. Ursodiol may be useful if the disease is due to blockage of the bile duct. Other medications may be useful for complications such as abdominal or leg swelling, hepatic encephalopathy, and dilated esophageal veins. If cirrhosis leads to liver failure, a liver transplant may be an option.Cirrhosis affected about 2.8 million people and resulted in 1.3 million deaths in 2015. Of these deaths, alcohol caused 348,000, hepatitis C caused 326,000, and hepatitis B caused 371,000. In the United States, more men die of cirrhosis than women. The first known description of the condition is by Hippocrates in the fifth century BCE. The term "cirrhosis" was derived in 1819 from the Greek word "kirrhos," which describes the yellowish color of a diseased liver.

Signs and symptoms
Cirrhosis can take quite a long time to develop, and symptoms may be slow to emerge. Some early symptoms include tiredness, weakness, loss of appetite, weight loss, and nausea. People may also feel discomfort in the right upper abdomen around the liver.As cirrhosis progresses, symptoms can include neurological changes. This can consist of cognitive impairments, confusion, memory loss, sleep disorders, and personality changes.Worsening cirrhosis can cause a build-up of fluid in different parts of the body such as the legs (edema) and abdomen (ascites). Other signs of advancing disease include itchy skin, bruising easily, dark urine, and yellowing of the skin.

Liver dysfunction
These features are a direct consequence of liver cells not functioning:

Spider angiomata or spider nevi happen when there is dilatation of vasculature beneath the skin surface. There is a central, red spot with reddish extensions that radiate outward. This creates a visual effect that resembles a spider. It occurs in about one-third of cases. The likely cause is an increase in estrogen. Cirrhosis causes a rise of estrogen due to increased conversion of androgens into estrogen.
Palmar erythema presents as reddish palms below the thumb and little finger. This is seen in about 23% of cirrhosis cases. This is a result of increased estrogen.
Gynecomastia, or the increase of breast size in men, is caused by increased estradiol (a potent type of estrogen). This can occur in up to two-thirds of cases.
Hypogonadism signifies a decreased functionality of the gonads. This can result in impotence, infertility, loss of sexual drive, and testicular atrophy. A swollen scrotum may also be evident.
Liver size can be enlarged, normal, or shrunken in people with cirrhosis. As the disease progresses, the liver will typically shrink due to the result of scarring.
Jaundice is the yellowing of the skin. It can additionally cause yellowing of mucous membranes notably of the white of the eyes. This phenomenon is due to increased levels of bilirubin, which may also cause the urine to be dark-colored.

Portal hypertension
Liver cirrhosis makes it hard for blood to flow in the portal venous system. This resistance creates a backup of blood and increases pressure. This results in portal hypertension. Effects of portal hypertension include:

Ascites is a build-up of fluid in the peritoneal cavity in the abdomen
An enlarged spleen in 35 to 50% of cases
Esophageal varices and gastric varices result from collateral circulation in the esophagus and stomach (a process called portacaval anastomosis). When the blood vessels in this circulation become enlarged, they are called varices. Varices are more likely to rupture at this point. Variceal rupture often leads to severe bleeding, which can be fatal.
Caput medusae are dilated paraumbilical collateral veins due to portal hypertension. Blood from the portal venous system may be forced through the paraumbilical veins and ultimately to the abdominal wall veins. The created pattern resembles the head of Medusa, hence the name.
Cruveilhier-Baumgarten bruit is bruit in the epigastric region (on examination by stethoscope). It is due to extra connections forming between the portal system and the paraumbilical veins.

Other nonspecific signs
Some signs that may be present include changes in the nails (such as Muehrckes lines, Terrys nails, and nail clubbing). Additional changes may be seen in the hands (Dupuytrens contracture) as well as the skin/bones (hypertrophic osteoarthropathy).

Advanced disease
As the disease progresses, complications may develop. In some people, these may be the first signs of the disease.

Bruising and bleeding can result from decreased production of clotting factors
Hepatic encephalopathy (HE) occurs when ammonia and related substances build up in the blood. This build-up affects brain function when they are not cleared from the blood by the liver. Symptoms can include unresponsiveness, forgetfulness, trouble concentrating, changes in sleep habits, or psychosis. One classic physical examination finding is asterixis. This is the asynchronous flapping of outstretched, dorsiflexed hands. Fetor hepaticus is a musty breath odor resulting from increased dimethyl sulfide and is a feature of HE.
Sensitivity to medication can be caused by decreased metabolism of the active compounds
Acute kidney injury (particularly hepatorenal syndrome)
Cachexia associated with muscle wasting and weakness

Causes
Cirrhosis has many possible causes, and more than one cause may be present. History taking is of importance in trying to determine the most likely cause. Globally, 57% of cirrhosis is attributable to either hepatitis B (30%) or hepatitis C (27%). Alcohol use disorder is another major cause, accounting for about 20-40% of the cases.

Common causes
Alcoholic liver disease (ALD, or alcoholic cirrhosis) develops for 10–20% of individuals who drink heavily for a decade or more. Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates. This injury happens through the formation of acetaldehyde from alcohol. Acetaldehyde is reactive and leads to the accumulation of other reactive products in the liver.  People with ALD may also have concurrent alcoholic hepatitis. Associated symptoms are fever, hepatomegaly, jaundice, and anorexia. AST and ALT blood levels are both elevated, but at less than 300 IU/liter, with an AST:ALT ratio > 2.0, a value rarely seen in other liver diseases. In the United States, 40% of cirrhosis-related deaths are due to alcohol.
In non-alcoholic fatty liver disease (NAFLD), fat builds up in the liver and eventually causes scar tissue. This type of disorder can be caused by obesity, diabetes, malnutrition, coronary artery disease, and steroids. Though similar in signs to alcoholic liver disease, no history of notable alcohol use is found. Blood tests and medical imaging are used to diagnose NAFLD and NASH, and sometimes a liver biopsy is needed.
Chronic hepatitis C, an infection with the hepatitis C virus, causes inflammation of the liver and a variable grade of damage to the organ. Over several decades, this inflammation and damage can lead to cirrhosis. Among patients with chronic hepatitis C, 20–30% develop cirrhosis. Cirrhosis caused by hepatitis C and alcoholic liver disease are the most common reasons for liver transplant. Both hepatitis C and hepatitis B-related cirrhosis can also be attributed with heroin addiction.
Chronic hepatitis B causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B and accelerates cirrhosis in co-infection.

Less common causes
In primary biliary cholangitis (previously known as primary biliary cirrhosis), the bile ducts become damaged by an autoimmune process. This leads to  liver damage. Patients may have no symptoms. While other people could present with fatigue, pruritus, or skin hyperpigmentation. The liver is typically enlarged which is referred to as hepatomegaly. Rises in alkaline phosphatase, cholesterol, and bilirubin levels occur. Patients are usually positive for anti-mitochondrial antibodies.
Primary sclerosing cholangitis is a disorder of the bile ducts that presents with pruritus, steatorrhea, fat-soluble vitamin deficiencies, and metabolic bone disease. A strong association with inflammatory bowel disease is seen, especially ulcerative colitis.
Autoimmune hepatitis is caused by an attack of the liver by lymphocytes. This causes inflammation and eventually scarring as well as cirrhosis. Findings include elevations in serum globulins, especially gamma globulins.
Hereditary hemochromatosis usually presents with skin hyperpigmentation, diabetes mellitus, pseudogout, or cardiomyopathy, All of these are due to signs of iron overload. Family history of cirrhosis is common as well.
Wilsons disease is an autosomal recessive disorder characterized by low ceruloplasmin in the blood and increased copper of the liver. Copper in the urine is also elevated. Patients may also have Kayser-Fleischer rings in the cornea and altered mental status.
Indian childhood cirrhosis is a form of neonatal cholestasis characterized by deposition of copper in the liver
Alpha-1 antitrypsin deficiency  is an autosomal co-dominant disorder of low levels of the enzyme alpha-1 antitrypsin
Cardiac cirrhosis is due to chronic right-sided heart failure, which leads to liver congestion
Galactosemia
Glycogen storage disease type IV
Cystic fibrosis
Hepatotoxic drugs or toxins, such as acetaminophen (paracetamol), methotrexate, or amiodarone

Pathophysiology
The liver plays a vital role in the synthesis of proteins (for example, albumin, clotting factors and complement), detoxification, and storage (for example, of vitamin A and glycogen). In addition, it participates in the metabolism of lipids and carbohydrates.Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are fully reversible.The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal tissue. This scar tissue blocks the portal flow of blood through the organ, raising the blood pressure and disturbing normal function. Research has shown the pivotal role of the stellate cell, that normally stores vitamin A, in the development of cirrhosis. Damage to the liver tissue from inflammation leads to the activation of stellate cells, which increases fibrosis through the production of myofibroblasts, and obstructs hepatic blood flow. In addition, stellate cells secrete TGF beta 1, which leads to a fibrotic response and proliferation of connective tissue. TGF-β1 have been implicated in the process of activating hepatic stellate cells (HSCs) with the magnitude of fibrosis being in proportion to increase in TGF β levels.  ACTA2 is associated with TGF β pathway that enhances contractile properties of HSCs leading to fibrosis. Furthermore, it secretes TIMP1 and TIMP2, naturally occurring inhibitors of matrix metalloproteinases, which prevents them from breaking down the fibrotic material in the extracellular matrix.As this cascade of processes continues, fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout. The spleen becomes congested, and enlarged, resulting in its retention of platelets, which are needed for normal blood clotting. Portal hypertension is responsible for the most severe complications of cirrhosis.

Diagnosis
The diagnosis of cirrhosis in an individual is based on multiple factors. Cirrhosis may be suspected from laboratory findings, physical exam, and patient history. Imaging is generally obtained to evaluate the liver. A liver biopsy will confirm the diagnosis; however, is generally not required.

Imaging
Ultrasound is routinely used in the evaluation of cirrhosis. It may show a small and shrunken liver in advanced disease.  On ultrasound, there is increased echogenicity with irregular appearing areas. Other suggestive findings are an enlarged caudate lobe, widening of the fissures and enlargement of the spleen. An enlarged spleen, which normally measures less than 11–12 cm in adults, may suggest underlying portal hypertension. Ultrasound may also screen for hepatocellular carcinoma and portal hypertension. This is done by assessing flow in the hepatic vein. An increased portal vein pulsatility may be seen. However, this may be a sign of elevated right atrial pressure. Portal vein pulsatility are usually measured by an pulsatility indices (PI). A number above a certain values indicates cirrhosis (see table below).

Other scans include CT of the abdomen and MRI. A CT scan is non-invasive and may be helpful in the diagnosis. Compared to the ultrasound, CT scans tend to be more expensive. MRI provides excellent evaluation; however, is a high expense.
Cirrhosis is also diagnosable through a variety of new elastography techniques. When a liver becomes cirrhotic it will generally become stiffer. Determining the stiffness through imaging can determine the location and severity of disease. Techniques include transient elastography, acoustic radiation force impulse imaging, supersonic shear imaging and magnetic resonance elastography. Transient elastography and magnetic resonance elastography can help identify the stage of fibrosis. Compared to a biopsy, elastography can sample a much larger area and is painless. It shows a reasonable correlation with the severity of cirrhosis. Other modalities have been introduced which are incorporated into ultrasonagraphy systems. These include 2-dimensional shear wave elastography and point shear wave elastography which uses acoustic radiation force impulse imaging.Rarely are diseases of the bile ducts, such as primary sclerosing cholangitis, causes of cirrhosis. Imaging of the bile ducts, such as ERCP or MRCP (MRI of biliary tract and pancreas) may aid in the diagnosis.

Lab findings
The best predictors of cirrhosis are ascites, platelet count < 160,000/mm3, spider angiomata, and a Bonacini cirrhosis discriminant score greater than 7 (as the sum of scores for platelet count, ALT/AST ratio and INR as per table).
These findings are typical in cirrhosis:

Thrombocytopenia, typically multifactorial, is due to alcoholic marrow suppression, sepsis, lack of folate, platelet sequestering in the spleen, and decreased thrombopoietin. However, this rarely results in a platelet count < 50 000/mL.
Aminotransferases  AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferase levels do not preclude cirrhosis.
Alkaline phosphatase – slightly elevated but less than 2–3 times the upper limit of normal.
Gamma-glutamyl transferase – correlates with AP levels. Typically much higher in chronic liver disease from alcohol.
Bilirubin levels are normal when compensated, but may elevate as cirrhosis progresses.
Albumin  levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver.
Prothrombin time increases, since the liver synthesizes clotting factors.
Globulins increase due to shunting of bacterial antigens away from the liver to lymphoid tissue.
Serum sodium levels fall(hyponatremia) due to inability to excrete free water resulting from high levels of ADH and aldosterone.
Leukopenia and neutropenia are due to splenomegaly with splenic margination.
Coagulation defects occur, as the liver produces most of the coagulation factors, thus coagulopathy correlates with worsening liver disease.
Glucagon is increased in cirrhosis.
Vasoactive intestinal peptide is increased as blood is shunted into the intestinal system because of portal hypertension.
Vasodilators are increased (such as nitric oxide and carbon monoxide) reducing afterload with compensatory increase in cardiac output, mixed venous oxygen saturation.
Renin is increased (as well as sodium retention in kidneys) secondary to a fall in systemic vascular resistance.FibroTest is a biomarker for fibrosis that may be used instead of a biopsy.Other laboratory studies performed in newly diagnosed cirrhosis may include:

Serology for hepatitis viruses, autoantibodies (ANA, antismooth muscle, antimitochondria, anti-LKM)
Ferritin and transferrin saturation: markers of iron overload as in hemochromatosis, copper and ceruloplasmin: markers of copper overload as in Wilsons disease
Immunoglobulin levels (IgG, IgM, IgA) – these immunoglobins are nonspecific, but may help in distinguishing various causes.
Cholesterol and glucose
Alpha 1-antitrypsinMarkers of inflammation and immune cell activation are typically elevated in cirrhotic patients, especially in the decompensated disease stage:

C-reactive protein (CRP)
Procalcitonin (PCT)
Presepsin
soluble CD14
soluble CD163
soluble CD206 (mannose receptor)
soluble TREM-1A recent study identified15 microbial biomarkers from the gut microbiota. These could potentially be used to discriminate patients with liver cirrhosis from healthy individuals.

Pathology
The gold standard for diagnosis of cirrhosis is a liver biopsy. This is usually carried out as a fine-needle approach, through the skin (percutaneous), or internal jugular vein (transjugular). Endoscopic ultrasound-guided liver biopsy (EUS), using the percutaneous or transjugular route, has become a good alternative to use. EUS can target liver areas that are widely separated, and can deliver bi-lobar biopsies. A biopsy is not necessary if the clinical, laboratory, and radiologic data suggest cirrhosis. Furthermore, a small but significant risk of complications is associated with liver biopsy, and cirrhosis itself predisposes for complications caused by liver biopsy.Once the biopsy is obtained, a pathologist will study the sample. Cirrhosis is defined by its features on microscopy: (1) the presence of regenerating nodules of hepatocytes and (2) the presence of fibrosis, or the deposition of connective tissue between these nodules. The pattern of fibrosis seen can depend on the underlying insult that led to cirrhosis. Fibrosis can also proliferate even if the underlying process that caused it has resolved or ceased. The fibrosis in cirrhosis can lead to destruction of other normal tissues in the liver: including the sinusoids, the space of Disse, and other vascular structures, which leads to altered resistance to blood flow in the liver, and portal hypertension.

As cirrhosis can be caused by many different entities which injure the liver in different ways, cause-specific abnormalities may be seen. For example, in chronic hepatitis B, there is infiltration of the liver parenchyma with lymphocytes. In congestive hepatopathy there are erythrocytes and a greater amount of fibrosis in the tissue surrounding the hepatic veins. In primary biliary cholangitis, there is fibrosis around the bile duct, the presence of granulomas and pooling of bile. Lastly in alcoholic cirrhosis, there is infiltration of the liver with neutrophils.Macroscopically, the liver is initially enlarged, but with the progression of the disease, it becomes smaller. Its surface is irregular, the consistency is firm, and if associated with steatosis the color is yellow. Depending on the size of the nodules, there are three macroscopic types: micronodular, macronodular, and mixed cirrhosis. In the micronodular form (Laennecs cirrhosis or portal cirrhosis), regenerating nodules are under 3 mm. In macronodular cirrhosis (post-necrotic cirrhosis), the nodules are larger than 3 mm. Mixed cirrhosis consists of nodules of different sizes.

Grading
The severity of cirrhosis is commonly classified with the Child–Pugh score (also known as the Child–Pugh–Turcotte score). This system was devised in 1964 by Child and Turcotte, and modified in 1973 by Pugh and others. It was first established to determine who would benefit from elective surgery for portal decompression.  This scoring system uses multiple lab values including bilirubin, albumin, and INR. The presence of ascites and severity of encephalopathy is also included in the scoring. Patients are classified into class A, B, or C. Class A has a favorable prognosis while class C is at high risk of death.

The Child-Pugh score is a validated predictor of mortality after a major surgery. For example, Child class A patients have a 10% mortality rate and Child class B patients have a 30% mortality rate while Child class C patients have a 70 to 80% mortality rate after abdominal surgery. Elective surgery is usually reserved for those in Child class A patients. There is an increased risk for child class B individuals and they may require medical optimization. Overall, it is not recommended for Child class C patients to undergo elective surgery.In the past, the Child-Pugh classification was used to determine patients who were candidates for a liver transplant. Child-Pugh class B is usually an indication for evaluation for transplant. However, there were many issues when applying this score to liver transplant eligibility. Thus, the MELD score was created.
The Model for End-Stage Liver Disease (MELD) score was later developed and approved in 2002. It was approved by the United Network for Organ Sharing (UNOS) as a way to determine the allocation of liver transplants to awaiting people in the United States. It is also used as a validated survival predictor of cirrhosis, alcoholic hepatitis, acute liver failure, and acute hepatitis. The variables included bilirubin, INR, creatinine, and dialysis frequency. In 2016, sodium was added to the variables and the score is often referred to as MELD-Na.MELD-Plus is a further risk score to assess severity of chronic liver disease. It was developed in 2017 as a result of a collaboration between Massachusetts General Hospital and IBM. Nine variables were identified as effective predictors for 90-day mortality after a discharge from a cirrhosis-related hospital admission. The variables include all Model for End-Stage Liver Disease (MELD)s components, as well as sodium, albumin, total cholesterol, white blood cell count, age, and length of stay.The hepatic venous pressure gradient (difference in venous pressure between incoming and outgoing blood to the liver) also determines the severity of cirrhosis, although it is hard to measure. A value of 16 mm or more means a greatly increased risk of death.

Prevention
Key prevention strategies for cirrhosis are population-wide interventions to reduce alcohol intake (through pricing strategies, public health campaigns, and personal counseling), programs to reduce the transmission of viral hepatitis, and screening of relatives of people with hereditary liver diseases.Little is known about factors affecting cirrhosis risk and progression. However, many studies have provided increasing evidence for the protective effects of coffee consumption against the progression of liver disease. These effects are more noticeable in liver disease that is associated with alcohol use disorder. Coffee has antioxidant and antifibrotic effects. Caffeine may not be the important component; polyphenols may be more important. Drinking two or more cups of coffee a day is associated with improvements in the liver enzymes ALT, AST, and GGT. Even in those with liver disease, coffee consumption can lower fibrosis and cirrhosis.

Treatment
Generally, liver damage from cirrhosis cannot be reversed, but treatment can stop or delay further progression and reduce complications. A healthy diet is encouraged, as cirrhosis may be an energy-consuming process. A recommended diet consists of high-protein, high-fiber diet plus supplementation with branched-chain amino acids. Close follow-up is often necessary. Antibiotics are prescribed for infections, and various medications can help with itching. Laxatives, such as lactulose, decrease the risk of constipation. Carvedilol increases survival benefit for patients with cirrhosis and portal hypertension.Alcoholic cirrhosis caused by alcohol use disorder is treated by abstaining from alcohol. Treatment for hepatitis-related cirrhosis involves medications used to treat the different types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune hepatitis.Cirrhosis caused by Wilsons disease is treated by removing the copper which builds up in organs. This is carried out using chelation therapy such as penicillamine. When the cause is an iron overload, iron is removed using a chelation agent such as deferoxamine or by bloodletting.As of 2021, there are recent studies studying drugs to prevent cirrhosis caused by non-alcoholic fatty liver disease (NAFLD or NASH). A drug called semaglutide was shown to provide greater NASH resolution versus placebo. No improvement in fibrosis was observed. A combination of cilofexor/firsocostat was studied in patients with bridging fibrosis and cirrhosis. It was observed to have led to improvements in NASH activity with a potential antifibrotic effect. Lanifibranor is also shown to prevent worsening fibrosis.

Preventing further liver damage
Regardless of the underlying cause of cirrhosis, consumption of alcohol and other potentially damaging substances are discouraged. There is no evidence that supports the avoidance or dose reduction of paracetamol in people with compensated cirrhosis; it is thus considered a safe analgesic for said individuals.Vaccination of susceptible patients should be considered for hepatitis A and hepatitis B.
Treating the cause of cirrhosis prevents further damage; for example, giving oral antivirals such as entecavir and tenofovir where cirrhosis is due to hepatitis B prevents progression of cirrhosis. Similarly, control of weight and diabetes prevents deterioration in cirrhosis due to non-alcoholic fatty liver disease.Avoid drugs that could further harm the liver. These include several drugs such as anti-depressants, certain antibiotics, and NSAIDs (like ibuprofen). These agents are hepatotoxic as they are metabolized by the liver. If medication that harms the liver is still recommended by your doctor, the dosage can be adjusted.

Lifestyle
According to a 2018 systematic review based on studies that implemented 8 to 14 week-long exercise programs, there is currently insufficient scientific evidence regarding either the beneficial or harmful effects of physical exercise in people with cirrhosis on all-cause mortality, morbidity (including both serious and non-serious adverse events), health-related quality of life, exercise capacity and anthropomorphic measures. These conclusions were based on low to very low quality research, which imposes the need to develop further research with higher quality, especially to evaluate its effects on clinical outcomes.

Transplantation
If complications cannot be controlled or when the liver ceases functioning, liver transplantation is necessary. Survival from liver transplantation has been improving over the 1990s, and the five-year survival rate is now around 80%. The survival rate depends largely on the severity of disease and other medical risk factors in the recipient. In the United States, the MELD score is used to prioritize patients for transplantation. Transplantation necessitates the use of immune suppressants (ciclosporin or tacrolimus).

Decompensated cirrhosis
Manifestations of decompensation in cirrhosis include gastrointestinal bleeding, hepatic encephalopathy, jaundice or ascites. In patients with previously stable cirrhosis, decompensation may occur due to various causes, such as constipation, infection (of any source), increased alcohol intake, medication, bleeding from esophageal varices or dehydration. It may take the form of any of the complications of cirrhosis listed below.
People with decompensated cirrhosis generally require admission to a hospital, with close monitoring of the fluid balance, mental status, and emphasis on adequate nutrition and medical treatment – often with diuretics, antibiotics, laxatives or enemas, thiamine and occasionally steroids, acetylcysteine and pentoxifylline. Administration of saline is avoided, as it would add to the already high total body sodium content that typically occurs in cirrhosis. Life expectancy without liver transplant is low, at most 3 years.

Palliative care
Palliative care is specialized medical care that focuses on providing patients with relief from the symptoms, pain, and stress of a serious illness, such as cirrhosis. The goal of palliative care is to improve quality of life for both the patient and the patients family and it is appropriate at any stage and for any type of cirrhosis.Especially in the later stages, people with cirrhosis experience significant symptoms such as abdominal swelling, itching, leg edema, and chronic abdominal pain which would be amenable for treatment through palliative care. Because the disease is not curable without a transplant, palliative care can also help with discussions regarding the persons wishes concerning health care power of attorney, do not resuscitate decisions and life support, and potentially hospice. Despite proven benefit, people with cirrhosis are rarely referred to palliative care.

Immunity
Cirrhosis is known to cause immune dysfunction in numerous ways. It impedes the immune system from working normally.

Bleeding and blood clot risk
Cirrhosis can increase the risk of bleeding. The liver produces various proteins in the coagulation cascade (coagulation factors II, VII, IX, X, V, and VI). When damaged, the liver is impaired in its production of these proteins. This will ultimately increase bleeding as clotting factors are diminished. Clotting function is estimated by lab values, mainly platelet count, prothrombin time (PT), and international normalized ratio (INR).
The American Gastroenterological Association (AGA) provided recommendations in 2021 in regards to coagulopathy management of cirrhotic patients in certain scenarios.
The AGA does not recommend for extensive pre-procedural testing, including repeated measurements of PT/INR or platelet count before patients with stable cirrhosis undergo common gastrointestinal procedures. Nor do they suggest the routine use of blood products, such as platelets, for bleeding prevention. Cirrhosis is stable when there are no changes in baseline abnormalities of coagulation lab values.
For patients with stable cirrhosis and low platelet count undergoing common low-risk procedures, the AGA does not recommend the routine use of thrombopoietin receptor agonists for bleeding prevention.
In hospitalized patients who meet standard guidelines for clot prevention, the AGA suggests standard prevention.
The AGA does not recommend in routine screening for portal vein thrombosis. If there is a portal vein thrombosis, the AGA suggests treatment by anticoagulation.
In the case of cirrhosis with atrial fibrillation, the AGA recommends using anticoagulation over no anticoagulation.

Complications
Ascites
Salt restriction is often necessary, as cirrhosis leads to accumulation of salt (sodium retention). Diuretics may be necessary to suppress ascites. Diuretic options for inpatient treatment include aldosterone antagonists (spironolactone) and loop diuretics. Aldosterone antagonists are preferred for people who can take oral medications and are not in need of an urgent volume reduction. Loop diuretics can be added as additional therapy.Where salt restriction and the use of diuretics are ineffective then paracentesis may be the preferred option. This procedure requires the insertion of a plastic tube into the peritoneal cavity. Human serum albumin solution is usually given to prevent complications from the rapid volume reduction. In addition to being more rapid than diuretics, 4–5 liters of paracentesis is more successful in comparison to diuretic therapy.

Esophageal and gastric variceal bleeding
For portal hypertension, nonselective beta blockers such as propranolol or nadolol are commonly used to lower blood pressure over the portal system. In severe complications from portal hypertension, transjugular intrahepatic portosystemic shunting (TIPS) is occasionally indicated to relieve pressure on the portal vein. As this shunting can worsen hepatic encephalopathy, it is reserved for those patients at low risk of encephalopathy. TIPS is generally regarded only as a bridge to liver transplantation or as a palliative measure. Balloon-occluded retrograde transvenous obliteration can be used to treat gastric variceal bleeding.Gastroscopy (endoscopic examination of the esophagus, stomach, and duodenum) is performed in cases of established cirrhosis. If esophageal varices are found, prophylactic local therapy may be applied such as sclerotherapy or banding, and beta blockers may be used.

Hepatic encephalopathy
Hepatic encephalopathy is a potential complication of cirrhosis. It may lead to functional neurological impairment ranging from mild confusion to coma. Goal of treatment is reducing ammonia. This can can achieved by administering lactulose or lactitol to increase potassium. Hydration and nutritional support is also provided. Protein uptake is encouraged. The underlying cause may also need to be identified and treated. Causes include alcohol use, excess protein, gastrointestinal bleeding, infection, constipation, and vomiting/diarrhea. Drugs like benzodiazepines, diuretics, or narcotics can also precipitate hepatic encephalopathy. A low protein diet is recommended with gastrointestinal bleeding. Rifaximin is administered if mental state does not improve in 48 hours. Antibiotic treatment may need to be continued for at least 3 months. The grading or severity of hepatic encephalopathy is determined by mental status.

Hepatorenal syndrome
Hepatorenal syndrome is a serious complication of end-stage cirrhosis when kidney damage is also involved.

Spontaneous bacterial peritonitis
People with ascites due to cirrhosis are at risk of spontaneous bacterial peritonitis.

Portal hypertensive gastropathy
Portal hypertensive gastropathy refers to changes in the mucosa of the stomach in people with portal hypertension, and is associated with cirrhosis severity.

Infection
Cirrhosis can cause immune system dysfunction, leading to infection. Signs and symptoms of infection may be nonspecific and are more difficult to recognize (for example, worsening encephalopathy but no fever). Moreover, infections in cirrhosis are major triggers for other complications (ascites, variceal bleading, hepatic enecphalopathy, organ failures, death).

Hepatocellular carcinoma
Hepatocellular carcinoma is the most common primary liver cancer, and the most common cause of death in people with cirrhosis. Screening using an MRI scan can detect this cancer and is often carried out for early signs which has been shown to improve outcomes.

Epidemiology
Each year, approximately one million deaths are due to complications of cirrhosis, making cirrhosis the 11th most common cause of death globally. Cirrhosis and chronic liver disease were the tenth leading cause of death for men and the twelfth for women in the United States in 2001, killing about 27,000 people each year.The cause of cirrhosis can vary; alcohol and non-alcoholic fatty liver disease are main causes in western and industrialized countries, whereas viral hepatitis is the predominant cause in low and middle-income countries. Cirrhosis is more common in men than in women </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ventricular tachycardia and can you explain it in depth? [/INST] Ventricular tachycardia (V-tach or VT) is a fast heart rate arising from the lower chambers of the heart. Although a few seconds of VT may not result in permanent problems, longer periods are dangerous; and multiple episodes over a short period of time are referred to as an electrical storm. Short periods may occur without symptoms, or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may result in ventricular fibrillation (VF) and turn into cardiac arrest. This conversion of the VT into VF is called the degeneration of the VT. It is found initially in about 7% of people in cardiac arrest.Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems, or a heart attack. Diagnosis is by an electrocardiogram (ECG) showing a rate of greater than 120 beats per minute and at least three wide QRS complexes in a row. It is classified as non-sustained versus sustained based on whether it lasts less than or more than 30 seconds. The term ventricular arrhythmia refers to the group of abnormal cardiac rhythms originating from the ventricle, which includes ventricular tachycardia, ventricular fibrillation, and torsades de pointes.In those who have normal blood pressure and strong pulse, the antiarrhythmic medication procainamide may be used. Otherwise, immediate cardioversion is recommended, preferably with a biphasic DC shock of 200 joules. In those in cardiac arrest due to ventricular tachycardia, cardiopulmonary resuscitation (CPR) and defibrillation is recommended. Biphasic defibrillation may be better than monophasic. While waiting for a defibrillator, a precordial thump may be attempted (However reserved to those who have the prior experience of doing so) in those on a heart monitor who are seen going into an unstable ventricular tachycardia. In those with cardiac arrest due to ventricular tachycardia, survival is about 45%. An implantable cardiac defibrillator or medications such as calcium channel blockers or amiodarone may be used to prevent recurrence.

Signs and symptoms
While a few seconds may not result in problems, longer periods are dangerous. Short periods may occur without symptoms or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may turn into ventricular fibrillation and can result in cardiac arrest.

Cause
Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems (e.g., low blood levels of magnesium or potassium), inherited channelopathies (e.g., long-QT syndrome), catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular dysplasia, alcohol withdrawal syndrome (typically following atrial fibrillation), or a myocardial infarction.

Pathophysiology
The morphology of the tachycardia depends on its cause and the origin of the re-entry electrical circuit in the heart.In monomorphic ventricular tachycardia, the shape of each heart beat on the ECG looks the same because the impulse is either being generated from increased automaticity of a single point in either the left or the right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is scarring of the heart muscle from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit around the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of monomorphic VT include right ventricular dysplasia, and right and left ventricular outflow tract VT.Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. QT prolongation may be congenital or acquired. Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia. Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic. Other relatively common drugs including some antibiotics and antihistamines may also be a danger, in particular in combination with one another. Problems with blood levels of potassium, magnesium and calcium may also contribute. High-dose magnesium is often used as an antidote in cardiac arrest protocols.

Diagnosis
The diagnosis of ventricular tachycardia is made based on the rhythm seen on either a 12-lead ECG or a telemetry rhythm strip. It may be very difficult to differentiate between ventricular tachycardia and a wide-complex supraventricular tachycardia in some cases. In particular, supraventricular tachycardias with aberrant conduction from a pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia. Other rarer phenomena include Ashman beats and antidromic atrioventricular re-entry tachycardias.Various diagnostic criteria have been developed to determine whether a wide complex tachycardia is ventricular tachycardia or a more benign rhythm. In addition to these diagnostic criteria, if the individual has a history of a myocardial infarction, congestive heart failure, or recent angina, the wide complex tachycardia is much more likely to be ventricular tachycardia.The proper diagnosis is important, as the misdiagnosis of supraventricular tachycardia when ventricular tachycardia is present is associated with worse prognosis. This is particularly true if calcium channel blockers, such as verapamil, are used to attempt to terminate a presumed supraventricular tachycardia. Therefore, it is wisest to assume that all wide complex tachycardia is VT until proven otherwise.ECG features of Ventricular Tachycardia in addition to the increased Heart rate are:
i) A wide QRS Complex ( Because the ectopics for the generation of the cardiac impulse originates in the Ventricular Myocyte and propagated via the intermyocyte conduction, which is a delayed conduction)
ii) A Josephsons sign where there is the notch in the downsloping of the S wave near its nadir.(Considered very specific for the VT).
iii) Capture beats (Normal QRS complex in between when the Heart pick up the  sinus rhythm from the impulses generated by the SA node), fusion beats ( due to the fusion of the Abnormal and the Normal QRS complexes) which has a unique morphology .
iv) Positive or negative concordance.
v) Extreme Axis deviation or NORTH WEST axis . ( Axis between -90 to +180 degrees)

Classification
Ventricular tachycardia can be classified based on its morphology:
Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG).
Scar-related monomorphic ventricular tachycardia is the most common type and a frequent cause of death in patients having survived a heart attack, especially if they have weak heart muscle.
Right ventricular outflow tract (RVOT) tachycardia is a type of monomorphic ventricular tachycardia originating in the right ventricular outflow tract. RVOT morphology refers to the characteristic pattern of this type of tachycardia on an ECG.
The source of the re-entry circuit can be identified by evaluating the morphology of the QRS complex in the V1 lead of a surface ECG. If the R wave is dominant (consistent with a right bundle branch block morphology), this indicates the origin of the VT is the left ventricle. Conversely, if the S wave is dominant (consistent with a left bundle branch block morphology, this is consistent with VT originating from the right ventricle or interventricular septum.
Polymorphic ventricular tachycardia, on the other hand, has beat-to-beat variations in morphology. This may appear as a cyclical progressive change in cardiac axis, previously referred to by its French name torsades de pointes ("twisting of the spikes"). However, at the current time, the term torsades de pointes is reserved for polymorphic VT occurring in the context of a prolonged resting QT interval.Another way to classify ventricular tachycardias is the duration of the episodes: Three or more beats in a row on an ECG that originate from the ventricle at a rate of more than 120 beats per minute constitute a ventricular tachycardia.
If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia.
If the rhythm lasts more than 30 seconds, it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds).A third way to classify ventricular tachycardia is on the basis of its symptoms: Pulseless VT is associated with no effective cardiac output, hence, no effective pulse, and is a cause of cardiac arrest (see also: pulseless electrical activity [PEA]). In this circumstance, it is best treated the same way as ventricular fibrillation (VF), and is recognized as one of the shockable rhythms on the cardiac arrest protocol. Some VT is associated with reasonable cardiac output and may even be asymptomatic. The heart usually tolerates this rhythm poorly in the medium to long term, and patients may certainly deteriorate to pulseless VT or to VF.Occasionally in ventricular tachycardia, supraventricular impulses are conducted to the ventricles, generating QRS complexes with normal or aberrant supraventricular morphology (ventricular capture). Or, those impulses can be merged with complexes that are originated in the ventricle and produce a summation pattern (fusion complexes).Less common is ventricular tachycardia that occurs in individuals with structurally normal hearts. This is known as idiopathic ventricular tachycardia and in the monomorphic form coincides with little or no increased risk of sudden cardiac death. In general, idiopathic ventricular tachycardia occurs in younger individuals diagnosed with VT. While the causes of idiopathic VT are not known, in general it is presumed to be congenital, and can be brought on by any number of diverse factors.

Treatment
Therapy may be directed either at terminating an episode of the abnormal heart rhythm or at reducing the risk of another VT episode. The treatment for stable VT is tailored to the specific person, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. Individuals with pulseless VT or unstable VT are hemodynamically compromised and require immediate electric cardioversion to shock them out of the VT rhythm.

Cardioversion
If a person still has a pulse, it is usually possible to terminate the episode using electric cardioversion. This should be synchronized to the heartbeat if the waveform is monomorphic if possible, in order to avoid degeneration of the rhythm to ventricular fibrillation. An initial energy of 100J is recommended </s>


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Arterial occlusion and can you explain it in depth? [/INST] Arterial occlusion is a condition involving partial or complete blockage of blood flow through an artery. Arteries are blood vessels that carry oxygenated blood to body tissues. An occlusion of arteries disrupts oxygen and blood supply to tissues, leading to ischemia. Depending on the extent of ischemia, symptoms of arterial occlusion range from simple soreness and pain that can be relieved with rest, to a lack of sensation or paralysis that could require amputation.Arterial occlusion can be classified into three types based on etiology: embolism, thrombosis, and atherosclerosis. These three types of occlusion underlie various common conditions, including coronary artery disease, peripheral artery disease, and pulmonary embolism, which may be prevented by lowering risk factors. With improper prevention or management, these diseases can progress into life-threatening complications of myocardial infarction, gangrene, ischemic stroke, and in severe cases, terminate in brain death or cardiac arrest.Arterial occlusion is diagnosed by exercise testing, ultrasonic duplex testing, and multi-detector coronary tomography angiography. Meanwhile, treatment can vary from surgical interventions such as bypass, endarterectomy, and embolectomy, to blood-thinning medication.

Signs and symptoms
Signs and symptoms of arterial occlusion depend on several factors, including the location, extent, and onset of blockage. Normally, the blockage should affect approximately 70% of the artery for symptoms to become noticeable.  Symptoms can be less severe during gradual narrowing, as this allows time for the widening of existing vessels and the formation of new ones (collateral vessels), allowing blood to still reach the area. Symptoms in this case will simply be intermittent claudication. Sudden narrowing leads to more severe consequences, given the lack of time for collateral vessels to grow. As such, coldness, numbness or even paralysis of the affected body parts may result.The commonest symptom of arterial occlusion is intermittent claudication, which consists of a painful, aching sensation in the affected muscle. This is often provoked with physical activity and relieved with rest. Pain and muscle aching may build up with walking, and accelerate with light jogging or walking uphill. Often, pain is relieved after several minutes of rest.  However, affected individuals are limited to short spurts of activity, impairing their quality of life.
For severe symptoms, the signs are usually visible and lead to ischemia. The clinical presentation of ischemia consists of the 6 Ps, including pallor, pain, paresthesia, paralysis, pulselessness, and poikilothermia. Affected individuals initially notice a paleness of the affected region and feel severe pain. As the condition worsens, the region appears bluish and numb. In extreme cases, this will give way to paralysis and poikilothermia, possibly requiring amputation of the affected limb.

Types of arterial occlusion
Commonly observed types of arterial occlusion include thrombosis, atherosclerosis, and embolism.

Embolism
An embolism involves the occlusion of blood vessels by an embolus. Arterial occlusion by an embolus is termed arterial embolism. An embolus is an agent that blocks blood flow by physically obstructing blood vessels. This includes gas bubbles, fatty deposits, amniotic fluid, blood clots, and foreign material. Arterial emboli occasionally detach from primary sites and travel via circulation to occlude secondary arteries, causing multiple ischemic sites.

Thrombosis
Thrombosis occurs when thrombi occlude vessels in the body. A thrombus, or a blood clot, is a mobilized mass of blood cells that circulates within the body. Thrombi can occlude veins (venous thrombosis) or arteries (arterial thrombosis). The etiology of thrombosis is described by Virchows Triad, which includes hemostasis, vascular wall damage, and hypercoagulability. Arterial thromboses significantly narrow or completely block arterial blood flow and oxygen delivery to tissues.

Atherosclerosis
In atherosclerosis, the inner endothelial layer of arteries is stiffened by the deposition of an atheromatous plaque. Atheromatous plaques, also called atherosclerotic plaques, are made of fats and lipid-laden macrophages. Plaque deposition both physically narrows an artery and impairs the function of endothelial cells, potentiating their production of vasoconstrictive chemicals to constrict the arterial lumen. This leads to turbulent blood flow in the arteries, affecting oxygen supply to tissues downstream.

Diseases of arterial occlusion
The pathophysiology of diseases of arterial occlusion depends on the type of occlusion, the severity of blockage, and the location of the occluded artery. Common diseases of arterial occlusion include Coronary Artery Disease, Peripheral Artery Disease, and Pulmonary Embolism.

Coronary Artery Disease
Coronary Artery Disease (CAD) results from the stenosis of coronary arteries by an atherosclerotic plaque. The coronary arteries perfuse the cardiomyocytes located within the myocardium. Cardiomyocytes require constant perfusion to aid the pumping of the heart. In CAD, atheromatous plaque formation in a coronary artery limits oxygen supply to cardiomyocytes, impairing heart contractility.
CAD severity varies based on the extent of coronary artery occlusion. At 75% luminal narrowing, patients experience symptoms associated with limited perfusion of cardiomyocytes, especially under strenuous conditions. Under physical exertion, CAD induces chest pain, termed stable angina. Stable angina may deteriorate into unstable angina, marking the initiation of Acute Coronary Syndrome, which may further deteriorate into a myocardial infarction.
Risk factors for CAD include smoking, high cholesterol, obesity, and family history of CAD. Primarily, the accumulation of cholesterol in the bloodstream from high-fat diets lead to atherosclerotic occlusion and its clinical consequences. Therefore, preventative measures for CAD mainly involve diet changes. A diet low in saturated and trans fats with an abundance of vegetables, fruits, and grains may lower the incidence of CAD.

Peripheral Artery Disease
Peripheral artery disease (PAD), or limb ischemia, affects the femoral, popliteal, or iliac arteries. PAD is caused by atherosclerotic plaques that occlude blood flow to extremities. Once blood flow is impeded, ischemic muscle cells switch from aerobic to anaerobic metabolism to cope with oxygen scarcity. Anaerobic metabolism, however, is energy-inefficient, lowering the concentration of the intracellular energy molecule, ATP, within muscles.  ATP depletion leads to a leakage of calcium into muscle cells, disrupting various muscular components and eventually causing muscle fiber necrosis.Risk factors for PAD include old age, smoking, hypertension, and high cholesterol, with smoking being the greatest contributing factor. This is because tobacco smoke contains potent chemicals that severely increase the occurrence of PAD. Thus, primary prevention of PAD is achieved with smoking cessation.

Pulmonary Embolism
Pulmonary embolism (PE) involves occlusion of a pulmonary artery by an embolus, most often a thrombus, obstructing blood flow to the lungs. Impairment of pulmonary circulation leads to severe ventilation-perfusion mismatching of the lungs, terminating in hypoxemia and respiratory failure. Most PEs are sequelae of Deep Vein Thrombosis (DVT), resulting from the breakage and propagation of a venous thrombus formed within the extremities to a pulmonary artery.As DVT commonly precedes PE, risk factors for PE overlap with risk factors for DVT. These include a sedentary lifestyle, prior surgery, trauma, history of DVT, and hypertension. A sedentary lifestyle and lack of movement are critical modifiable risk factors for PE. Immobility reduces the rate of leg muscle contraction, enhancing thrombus formation in vessels of the calves that may propagate to the lungs. Thus, physical activity is essential in preventing PE.

Complications
Diseases of arterial occlusion may progress into life-threatening conditions with improper prevention or management. Myocardial infarction, gangrene, and ischemic stroke are among the complications of severe arterial occlusion.

Myocardial Infarction
A myocardial infarction (MI), or heart attack, arises from complete occlusion of a coronary artery. The most frequent cause of MI is the rupturing of an atherosclerotic plaque formed in CAD. Plaque rupture exposes the subendothelial matrix beneath the plaque, initiating thrombus formation within the vasculature. The thrombus deposits on the ruptured plaque to completely block the coronary artery, halting oxygen supply to cardiomyocytes. Under hypoxia, cardiomyocytes perform anaerobic respiration, producing more lactate. With blocked coronary circulation, lactate clearance from cardiomyocytes is also hindered. Lactate accumulation reduces contractility and eventually necroses cardiomyocytes, releasing their troponin storage into the bloodstream. Serum troponin elevation is a characteristic biomarker of MI.Depending on the severity of ischemia, MIs are categorized as NSTEMI or STEMI. NSTEMI stands for Non-ST Elevation Myocardial Infarction, referencing the lack of ST-segment elevation in ECG traces. This is because in NSTEMI, only part of the myocardial wall is infarcted, which does not diagnostically present with ST-elevation.
NSTEMI becomes STEMI when the entire myocardial wall is infarcted. Diagnostically, STEMI displays prolonged ST-segment elevation in ECG traces, and is thus named ST-Elevation Myocardial Infarction. Minutes after STEMI, fatal cardiac arrest could occur. STEMI is life-threatening if immediate reperfusion therapy is not initiated.

Gangrene
Gangrene, specifically dry gangrene, is caused by an atherosclerotic or thromboembolic arterial occlusion. Gangrene is a complication of prolonged PAD, leading to shriveling, blackening, and infarction of peripheral tissue, commonly in the extremities. In severe cases, amputation of the affected limb is required.

Ischemic Stroke
Ischemic stroke is a thrombotic, or rarely, thromboembolic or atherosclerotic complication of arteries supplying the brain. Occlusion of brain arteries leads to rapid ischemic death of neurons, both at the infarct core and ischemic penumbra. Similar to cardiomyocytes, neurons require constant perfusion for proper function. Any interruption of blood supply causes neurons to switch to anaerobic metabolism, exhausting intracellular ATP levels. ATP depletion causes an influx of calcium cations into neurons and efflux of excess glutamate, triggering the apoptosis and necroptosis of neurons.Neuronal necrosis precipitates irreversible brain damage. Cerebral areas most susceptible to ischemic damage include the speech and motor cortices, leading to contralateral paralysis, speech, and comprehension loss. Severe or prolonged strokes may terminate in coma or brain death. Therefore, the diagnosis and treatment of ischemic stroke are time-dependent.

Diagnosis
There are several methods of diagnosing arterial occlusion, ranging from straightforward setups like exercise testing, to advanced scanning equipment such as ultrasonic duplex scanning or Multi-Detector Coronary Tomography (MDCT) angiography.

Exercise Testing
Exercise testing is a simplistic, non-invasive method of diagnosing intermittent claudication. Blood pressure measurements at the suspected area can be taken before and after exercise, as some symptoms only appear during strenuous activity. Commonly, a treadmill setting at 2 mph with a 12-degree slope is utilized. Subjects are asked to walk on the treadmill for a maximum of 5 minutes or until moderate pain is felt. The time to pain or maximal walking duration is recorded and compared with baselines.
Healthy individuals maintain systolic blood pressures at a normal range. Once exercise becomes more intense, there may be a temporary fall in systolic pressure, which quickly returns to normal with rest. However, those with intermittent claudication struggle to maintain standard values of systolic pressure, while recovery back to baseline is prolonged.

Ultrasonic Duplex Testing
Ultrasonic duplex scanning was developed to primarily determine the extent of atherosclerosis in carotid arteries. Since then, its application has widened to include arteries in the limbs. The technique utilizes high-frequency sound waves for visualization of flow direction and velocity within the arteries in an area of interest. The term duplex refers to 2 modes of ultrasound scanning being conducted. The B-mode transducer allows for an image of the vessel to be obtained, providing visual cues on the extent of occlusion. Meanwhile, the doppler probe is used to acquire data on velocity and direction of blood flow.

Multi-Detector Coronary Tomography (MDCT) Angiography
Traditionally, angiography is an invasive technique which involves inserting a flexible plastic catheter into the artery of interest. A radioactive contrast dye is then injected through the catheter and viewed on an X-ray. This contrast material does not permanently discolor any organs, but simply interacts with X-rays to produce a more precise diagnosis.Due to technological advances, clinicians have begun to use a less invasive approach called Multi-Detector Coronary Tomography (MDCT) angiography. Rather than inserting a large catheter into the artery, this technique requires a small injection of contrast dye using a standard intravenous catheter inserted into the arm, much like a regular injection. MDCT scanners then locate the contrast dye to show blockages within the arteries. MDCT angiography is more sensitive in detecting blockage and subsequent diseases such as CAD compared to invasive X-ray angiography.

Treatment
Treatment for arterial occlusion varies depending on the extent of blockage. In severe cases, surgical intervention is needed to remove the blockage from the affected artery. Currently, there are 3 types of surgical approaches, including surgical bypass, endarterectomy, and embolectomy. If surgery is not required, blood-thinning medication may be prescribed.

Surgical Bypass
A surgical bypass is a procedure performed to treat CAD. This procedure involves bypassing the blocked portion of the artery by replacing it with a healthy vessel from elsewhere in the body. The surgeon attaches one end of the new vessel right before the blockage, and the other end in the area after the affected portion </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Vaginitis and can you explain it in depth? [/INST] Vaginitis, also known as vulvovaginitis, is inflammation of the vagina and vulva. Symptoms may include itching, burning, pain, discharge, and a bad smell. Certain types of vaginitis may result in complications during pregnancy.The three main causes are infections, specifically bacterial vaginosis, vaginal yeast infection, and trichomoniasis. Other causes include allergies to substances such as spermicides or soaps or as a result of low estrogen levels during breast-feeding or after menopause. More than one cause may exist at a time. The common causes vary by age. Prepubescent girls are often at risk for development of vulvovaginitis because of low amounts of estrogen and an underdeveloped labia minora.Diagnosis generally include examination, measuring the pH, and culturing the discharge. Other causes of symptoms such as inflammation of the cervix, pelvic inflammatory disease, cancer, foreign bodies, and skin conditions should be ruled out.Treatment depends on the underlying cause. Infections should be treated. Sitz baths may help with symptoms. Soaps and feminine hygiene products such as sprays should not be used. About a third of women have vaginitis at some point in time. Women of reproductive age are most often affected.

Signs and symptoms
A woman may have vaginal irritation, itching, or burning or may notice a foul-smelling or abnormal discharge that could appear green or yellow.The following signs or symptoms may indicate the presence of infection:
Irritation or itching of the genital area
inflammation (irritation, redness, and swelling caused by the presence of extra immune cells) of the labia majora, labia minora, or perineal area
vaginal discharge
foul vaginal odor
pain/irritation with sexual intercourse

Complications
Vaginal infections left untreated can lead to further complications, especially for the pregnant woman. For bacterial vaginosis, these include "premature delivery, postpartum infections, clinically apparent and subclinical pelvic inflammatory disease, [as well as] postsurgical complications (after abortion, hysterectomy, caesarian section), increased vulnerability to HIV infection and, possibly, infertility". Studies have also linked trichomoniasis with increased likelihood of acquiring HIV; theories include that "vaginitis increases the number of immune cells at the site of infection, and HIV then infects those immune cells." Other theories suggest that trichomoniasis increases the amount of HIV genital shedding, thereby increasing the risk of transmission to sexual partners.  While the exact association between trichomoniasis infection and HIV genital shedding has not been consistently demonstrated, "there is good evidence that TV treatment reduces HIV genital shedding. Five studies were reported in the literature and, of these, four found a decrease in HIV genital shedding after TV treatment."Further, there are complications which lead to daily discomfort such as:

persistent discomfort
superficial skin infection (from scratching)
complications of the causative condition (such as gonorrhea and candida infection)

Causes
Infection
Vaginitis is often caused by an infection or the disruption of the healthy vaginal flora. The vaginal flora consists of those organisms which generally do not cause symptoms and is dominated mainly by Lactobacillus species. Disruption of the normal flora can cause a vaginal yeast infection. Vaginal yeast infection can affect women of all ages and is very common. The yeast Candida albicans is the most common cause of vaginitis. Specific forms of vaginal inflammation include the following types:
Infectious vaginitis accounts for 90% of all cases in reproductive age women:

Candidiasis: vaginitis caused by proliferation of Candida albicans, Candida tropicalis, Candida krusei
Bacterial vaginosis: vaginitis caused by increased growth of Gardnerella (a bacterium).
Aerobic vaginitisOther less common infections are caused by gonorrhea, chlamydia, Mycoplasma, herpes, Campylobacter, improper hygiene, and some parasites, notably Trichomonas vaginalis. Rare cases of amebic vaginitis have been reported, primarily in tropical, developing countries. Women who have diabetes develop infectious vaginitis more often than women who do not.Further, either a change in pH balance or introduction of foreign bacteria in the vagina can lead to infectious vaginitis. Physical factors that have been claimed to contribute to the development of infections include the following: constantly wet vulva due to tight clothing, chemicals coming in contact with the vagina via scented tampons, antibiotics, birth control pills, or a diet favoring refined sugar and yeast.

Hormonal
Hormonal vaginitis includes atrophic vaginitis usually found in postmenopausal women.

Irritation/allergy
Irritant vaginitis can be caused by allergies or reactions to vaginal sprays, douches, spermicides, soaps, detergents, or fabric softeners. It can also be caused by hot tubs, abrasion, tissue, tampons, or topical medications.
Foreign body vaginitis (most common foreign bodies are retained tampons or condoms) may cause extremely malodorous vaginal discharges. Treatment consists of removal, for which ring forceps may be useful. Further treatment is generally not necessary.

Diagnosis
Diagnosis is typically suspected based on a womens symptoms. Diagnosis is made with microscopy (mostly by vaginal wet mount) and culture of the discharge after a careful history and physical examination have been completed. The color, consistency, acidity, and other characteristics of the discharge may be predictive of the causative agent. Determining the agent is especially important because women may have more than one infection, or have symptoms that overlap those of another infection, which dictates different treatment processes to cure the infection. For example, women often self-diagnose for yeast infections but due to the 89% misdiagnosis rate, self-diagnoses of vaginal infections are highly discouraged.Another type of vaginitis, called desquamative inflammatory vaginitis (DIV) also exists. The cause behind this type is still poorly understood. DIV corresponds to the severe forms of aerobic vaginitis. About 5 to 10% of women are affected by aerobic vaginitis.The International Statistical Classification of Diseases and Related Health Problems codes for the several causes of vaginitis are:

Prevention
Prevention of candidiasis, the most common type of vaginitis, includes using loose cotton underwear. The vaginal area should be washed with water. Perfumed soaps, shower gels, and vaginal deodorants should be avoided. Douching is not recommended. The practice upsets the normal balance of yeast in the vagina and does more harm than good.Prevention of bacterial vaginosis includes healthy diets and behaviors as well as minimizing stress as all these factors can affect the pH balance of the vagina.Prevention of trichomoniasis revolves around avoiding other peoples wet towels and hot tubs, and safe-sex procedures, such as condom use.Some women consume good bacteria in food with live culture, such as yogurt, sauerkraut and kimchi, or in probiotic supplements either to try to prevent candidiasis, or to reduce the likelihood of developing bacterial vaginitis following antibiotic treatment. There is no firm evidence to suggest that eating live yogurt or taking probiotic supplements will prevent candidiasis.Studies have suggested a possible clinical role for the use of standardized oral or vaginal probiotics in the treatment of bacterial vaginosis, either in addition to or in place of the typical antibiotic regimens. However, recent articles question their efficacy in preventing recurrence compared with other means, or conclude that there is insufficient evidence for or against recommending probiotics for the treatment of bacterial vaginosis.

Treatment
The cause of the infection determines the appropriate treatment. It may include oral or topical antibiotics and/or antifungal creams, antibacterial creams, or similar medications. A cream containing cortisone may also be used to relieve some of the irritation. If an allergic reaction is involved, an antihistamine may also be prescribed. For women who have irritation and inflammation caused by low levels of estrogen (postmenopausal), a topical estrogen cream might be prescribed.
The following are typical treatments for trichomoniasis, bacterial vaginosis, and yeast infections:

Trichomoniasis: Oral treatment with either metronidazole or tinidazole. "Sexual partner(s) should be treated simultaneously. Patients should be advised to avoid sexual intercourse for at least 1 week and until they and their partner(s) have completed treatment and follow-up."
Bacterial vaginosis: The most commonly used antibiotics are metronidazole, available in both pill and gel form, and clindamycin available in both pill and cream form.
Yeast infections: Local azole, in the form of ovula and cream. All agents appear to be equally effective. These anti-fungal medications, which are available in over the counter form, are generally used to treat yeast infections. Treatment may last anywhere between one, three, or seven days.

Aerobic vaginitis
Treatment can include topical steroids to diminish the inflammation. Antibiotics to diminish the proportion of aerobic bacteria is still a matter of debate. The use of local antibiotics, preferably local non-absorbed and broad spectrum, covering enteric gram-positive and gram-negative aerobes, can be an option </s>