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34 Cards in this Set
- Front
- Back
Most common complications of hepatic dysfunction are?
Manifested as? Based on? |
continued bleeding , sepsis, and hepatic decompensation
Manifested as jaundice, categorized as prehepatic, intrahepatic, post hepatic Based on repeated measures of bilirubin, transaminase enzmes and alk phos |
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Caused by hemolysis, hematoma reabsorpition, bilirubin overload from whole blood
Characterized by what? |
prehepatic dysfunction
characterized by increased unconjugated bilirubin normal plasma transaminase normal alk phos |
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Caused by viral hepatitis, drug toxicity, sepsis, arterial hypoxemia, cirrhosis
characterized by what? |
Intrahepatic dysfunction
Characterized by Increased conjugated bilirubin Markedly increased plasma transaminase Normal to slightly elevated alkaline phosphatase Also known as hepatocellular dysfunction |
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Caused by retained common bile duct stone, can also be caused by sepsis.
characterized by? |
Post hepatic dysfunction
characterized by increased conjugated bilirubin normal to slightly slevated transaminase markedly increased alk phos urine contain large amounts conjugated bilirubin |
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causes difficult to confirm, liver function often returns to normal without specific treatment
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Extrahepatic dysfunction
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Inflammatory disease of hepatocytes, most often due to viral infections or ingestion of toxic drugs
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Acute hepatitis
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Causes of Viral hepatitis
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Type A, B, C, epstein Barr, cytomegalovirus
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Early symptoms of viral Hepatitis
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Dark urine, fatique, anorexia, nausea, fever, abdominal discomfort
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Lab values Viral hepatitis
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Plasma transaminases elevated 7-14 days before onset of jaundice and decline after jaundice is noticable
Bilirubin not greater 20mg/dl unless liver disease is severe or hemolysis is also present |
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Severe and potentially fatal hepatitis is suggested by what?
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plasma albumin 2.5 or markedly long prothrombin time
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Infectious hepatitis or short incubation hepatitis
highl infectious and cross contamination within families is very common Transmission by fecal-oral route What reduces severity? Does chronic carries state exist? |
Hepatitis A
Pooled gamma globulin greatly reduces severity of type A hepatitis chronic liver disease or carrier state does not develop |
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Most common form viral hepatitis
transmission via blood transfusion, percutaneous ionculation, oral to oral and sexual activity Chronic carrier? Cancer? |
Hepatitis B virus
Persistence of HBsAg longer than six months in the absence of antibodies indicates that the patient is a chronic arrier and can potentialy infect others Primary hepatocellular carcinoma is 220 times more likely to develop in chronic carriers |
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Route of transmission inoculation, liver disease often develops and chronic state is common
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Hepatitis C
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What drugs can cause hepatitis and when do clinical signs occur?
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antibiotics, antihypertensives, anticonvulsants, analgesics, tranquilizers, and anesthetics
Signs occur 2-6 weeks after starting drug therapy |
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Unresolving disease caused by a virus, drugs, inborn errors of metabolism or unkown factors.
Moslty associated with what? Divided into what? |
chronic hepatitis
Mostly associated with hepatitis B Divided into chronic active or chronic persistent hepatitis |
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Most serious form chronic hepatitis
Ultimately resulting in cirrhosis and hepatic failure widespread inflammation and destruction of hepatocytes What treated with |
chronic Active hepatitis
Treated with corticosteroids with or without azathioprine |
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Benign non progressive inflammatory disease mainly confined to portal area-type chronic hepatitis
How treat? |
chronic persistent hepatits
nutrition, avoidance of potential hepatotoxins and frequent observation is treatment |
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S/S include hepatic encephalopathy, hyperventilation, high ammonia levels, hypoglycemia, metabolic acidosis, increased CO, renal failure, thromobocytopenia, DIC, anemia
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Acute Hepatic failure
regardless of etiology, is associated with a poor prognosis plasma transaminase levels are high and parallet the extent of hepatic injury Treatment supportive, N-acetylcyseine is a antioxidant that improves oxygen content |
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the only curative therapy for patients in hepatic failure is?
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liver transplant
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Chronic disease process which destroys the hepatic parenchyma and replaces it with collagen.
Most frequent cause is? |
cirrhosis
alcohol most frequent cause |
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alcoholic cirrhois occurs in what percent of those who consume how much alcohol?
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10% of those who consume 80g of alcohol daily for ten years
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Characterized by jaundice in assocaition with elevations of the plasma transaminase enzymes,
Ascites occurs in 50% of patients Plasma albumin may be reduced below 3g/dL Prothrombin prolonged |
Acute Alcoholic Hepatitis
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Develops several years after first attack of alcoholic hepatitis
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Portal vein hypertension
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Why does ascites occur with portal vein hypertension?
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ascites is due to decreased oncotic pressure secondary to low plasma albumin, elevated resistance to blood flow through the portal vein system and increased secretion of ADH
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What are lab values with portal vein hypertension?
Hematocrit Na Bun liver |
hematocrit 30-35
hyponatremia Bun<10 bilirubin, transaminases, alk phos mildly to moderatley elevated |
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Alcoholic cirrhosis complications are?
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hyperdynamic circulation
arterial hypoxemia hypoglycemia gallstones duodenal ulcer gastroesophageal varices hepatic encephalopathy impaired immune defense |
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compensensatory neuronal excitablility and catecholamine release following abrupt d/c of alcohol
6-8 hrs after abstinence Autonomic nervous system imbalance may be reflected by HTN, tachycardia, and dysrhythmias |
minor alcohol withdrawal syndrome
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Occurs in 5% of alcoholic pts
Medical emergency onset 48-72 hrs after stop drinking Increased SNS with catecholamine release leading to diaphoresis, hyperpyrexia, htn, and tachycardia grand mal seizures can be first sign |
Severe alcohol withdrawal
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Chronic , progressive and often fatal cholestatic liver disease
Characterized by destruction of intrahepatic bile ducts, portal inflammation and scarring development of cirrhosis and liver failure |
primary biliary cirrhosis
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Excess amounts of iron are deposited in hepatocytes, leading to scarring and cirrhosis
treated by repeated phlebotomy |
hemochromatosis
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manifested by the presence of gallstones, may present as acute cholecystitis or chronic chollithiasis
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Diseases of biliary tract
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Almost always due to obstruction of the cystic duct by gallstones
Rapid onset of severe pain in the mid epigastrium which extends into the right upper abdomen, have Murphs sign |
Acute cholecytitis
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The development of fibrotic gallbladders, which are not capable of contracting to expel bile.
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Chronic cholelithiasis
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inflammation of the hepatic biliary tree which develops in response to obstruction of the biliary tract
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Chronic cholangitis
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