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OPT Liver

hepatic failure can be slow or sudden; occurs after 80-90% of liver function lost
3 patterns of hepatic failure 1. hepatic necrosis 2. chronic liver disease 3. hepatic dysfunction
fetor hepaticus musty/sweet and sour odor from undegraded GI bacteria
hepatorenal syndrome alterations in blood flow from hepatic failure that also result in renal failure
hepatopulmonary syndrome alterations in blood flow from hepatic failure that also result in pulmonary dysfunction
hepatic encephalopathy CNS alteration from shunted blood flow due to hepatic insufficiency; behavior problems, coma and death
icterus aka jaundice; yellow discoloration of skin, eyes and mucosa secondary to bilirubin accumulation
unconjugated bilirubin bilirubin bound to albumin from RBC breakdown in spleen; not water soluble and unable to excreted
conjugated bilirubin bilirubin converted by liver so can be excreted
cholestasis retention of bilirubin and other biliary components especially bile salts and cholesterols -elevated serum alkaline phosphatase -intestinal malabsorption
jaundice result of cholestasis but with additional symptoms
pruritus deposition of bile acids in peripheral tissues, especially the skin
skin xanthomas from excess cholesterol accumulation in cholestasis
cirrhosis diffuse alteration in liver of fibrous bands circling islands of hepatocytes forming nodules in liver
cryptogenic cirrhosis cause of cirrhosis is unknown
causes of death from cirrhosis: 1. progressive liver failure 2. complications of portal hypertension 3. hepatocellular carcinoma
4 main clinical syndromes associated with liver disease: 1. hepatic failure 2. jaundice and cholestasis 3. cirrhosis 4. portal hypertension
portal hypertension elevation of blood pressure in portal circulation
4 clinical consequences of portal hypertension: 1. ascites 2. portosystemic venous shunts 3. splenomegaly 4. hepatic encephalopathy
ascites collection of fluid in peritoneal cavity, can lead to hydrothorax
portosystemic venous shunts venous flow is slowed to bypass the liver
esophageal varices dilated esophageal veins to bypass portal circulation
caput medusae enlargement of fetal umbilical veins forming superficial pattern around umbilicus
splenomegaly spleen enlargement from from prolonged congestion
3 patterns of alcoholic liver disease 1. hepatic steatosis 2. alcoholic hepatitis 3. alcoholic cirrhosis
hepatic steatosis aka fatty liver; intracytoplasmic accumulation of lipid material in hepatocytes secondary to drinking, reversible
alcoholic hepatitis hepatic degeneration from alcohol consumption; ballooning degeneration and necrosis
Mallory bodies (Mallory-Denk bodies) eosinophilic cytoplasmic inclusions indicative of cell damage
alcoholic cirrhosis follows 15-20 years of alcoholic consumption; fibrosis of liver with collagenous bands surrounding hepatocyte nodules, higher risk of hepatocellular carcinoma
nonalcoholic steatohepatitis (NASH) pattern of steatosis, hepatitis and cirrhosis in non-drinkers; obesity and insulin-intolerance are predisposing factors
Reye syndrome disorder that creates fatty change in the liver and encephalopathy secondary to the loss of hepatic mitochondrial function
hepatitis A virus (HAV, epidemic/infectious hepatitis) RNA virus, acute, self-limited hepatitis; spread fecal-orally
icteric hepatitis jaundice present in hepatitis
anicteric hepatitis no jaundice present in hepatitis
hepatitis B virus (HBV, serum hepatitis) DNA virus, predisposes to hepatocellular carcinoma; has acute, chronic and carrier states -can test serum markers to determine stage of disease (Anti-HBs IgG persists for life, used for vaccine)
hepatits C virus RNA virus, mostly spread by blood, acute, chronic, and carrier states, and predisposes to hepatocellular carcinoma
hepatitis D virus (Delta agent) RNA virus, can only infect in presence of HBV
hepatitis E virus RNA virus, like hepatitis A (fecal-oral); dangerous for pregnant women
asymptomatic infection serologic evidence of infection but no symptoms, elevated transaminases
acute infection symptomatic disease shortly after incubation period
fulminant viral hepatits acute liver failure from massive liver necrosis that occurs in 2-3 weeks
chronic hepatitis symptomatic with biochemical or serological evidence of hepatic disease for more than 6 months
subacute hepatic necrosis cases of acute liver failure that develop more slowly
carrier state infection without clinical systems but still contagious
autoimmune hepatitis immune-mediated chronic liver destruction without an associated virus
hemochromatosis (pigment cirrhosis) group of genetic disorders that produce excess iron deposited in liver, creating fibrosis and predisposes to hepatocellular carcinoma
secondary iron overload acquired forms of excess iron from other sources
bronze diabetes skin and pancreatic alterations of excess iron increasing pigmentation
diagnostic triad of hemochromatosis: 1. skin pigmentation 2. diabetes mellitus 3. hepatomegaly
Wilson disease cirrhosis that develops from copper overload
cavernous hemangioma benign tumor of dilated vascular channels; can bleed if biopsied
hepatic adenoma benign tumor of encapsulated mass of hepatocytes in sheets and cords; after longterm contraceptive use
hepatocellular carcinoma (liver cell carcinoma, hepatoma) malignancy of hepatocytes, shows elevated alpha-fetoprotein
aflatoxin released by fungus Aspergillus flavus; increases cancer risk in conjunction with HBV
cholelithiasis aka gallstones; found in people who are fat, forty, female and fertile
biliary colic blocked biliary duct that results in extreme pain
cholecystitis inflammation of the gallbladder, usually associated with gallstones {calculous cholecystitis}
carcinoma of the gallbladder most common in biliary tract and associated with cholelithiasis
cholangiocarcinoma cancer that arises from epithelial lining of biliary ducts, both inside and outside the liver
pancreatitis inflammation of the pancreas
acute pancreatitis (acute pancreatic necrosis) reversible, inflammatory lesions associated with alcoholism/gallstones
acute edematous pancreatitis mild, self-limiting disorder
acute hemorrhagic pancreatitis severe, life-threatening disorder; elevated amylase and lipase
chronic pancreatitis (chronic relapsing pancreatitis) irreversible destruction of exocrine pancreas that leads to fibrosis
calcifying pancreatitis intraluminal plugs that form dystrophic calcifications
carcinoma of the pancreas carcinoma of exocrine portion, extremely deadly cancer; exhibits Trousseau sign
diabetes mellitus metabolic disorders that cause hyperglycemia due to defects in insulin secretion or action
type 1 diabetes mellitus insulin-dependent and juvenile-onset; severe lack of insulin from autoimmune attack -polyuria, polydipsia, and polyphagia -ketoacidosis
type 2 diabetes mellitus insulin-resistant and inadequate host response; genetic factors including {obesity} and {stress}
insulitis lymphocytic infiltration of islets, only in type 1
amyloid deposition amylin released in islets, only in type 2
diabetic microangiopathy thickening of basement membrane in small arterioles
diabetic nephropathy renal changes in diabetic patients
diffuse glomerulosclerosis thickening of basement membrane of glomerular capillaries
nodular glomerulosclerosis (Kimmelstiel-Wilson lesion) ball-like deposits in matrix of mesangium
retinopathy eye problems associated with diabetes mellitus
pancreatic neuroendocrine tumors islet cell tumors
insulinoma beta-cell tumor; causes hyperinsulinism and hypoglycemia
gastrinoma tumor that increases gastrin secretion, usually in duodenum or pancreas; causes {Zollinger-Ellison syndrome}- combination of pancreatic islet tumor, gastric acid, and severe peptic ulcers
Created by: Alexandra Arnold Alexandra Arnold