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37 Cards in this Set
- Front
- Back
Jaundice
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Jaundice (or icterus) is yellow-green pigmentation of the skin or sclerae caused by and increase in bilirubin.
1. Overproduction of bilirubin caused by increased breakdown of red cells, (e.g.,intravascular hemolysis-hemolytic anemia) 2. Impaired uptake of bilirubin from blood secondary to liver disease, (e.g., sepsis, drug, toxicity) 3. Decreased conjugation of bilirubin in the hepatocyte, (e.g., hepatitis, neonatal jaundice, Gilbert's syndrome) 4. Impaired secretion/excretion of bilirubin either intrahepatic (e.g. Dubin-Johnson's Syndrome, recurrent jaundice of pregnancy) or extrahepatic (e.g., obstructive gallstones, carcinoma of head of pancreas) |
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Disease states of hepatitis (5)
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a. Chronic hepatitis
b. Fulminant hepatic necrosis c. Carrier states (varies for each type of hepatitis) d. Cirrhosis e. Hepatocellular cancer |
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Acute hepatitis
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Diffuse liver injury w/ lobular disarray
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Chronic hepatitis
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Portal tract inflammation w/ interface hepatitis
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Necrosis of random, isolated liver cells
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Councilman bodies
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Benign hepatic neoplasms (4)
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- Focal nodular hyperplasia (?vascular, reactive non-neoplastic),
- Bile duct adenomas - Liver cell adenomas, (birth control pills, steroids). - Hemangioma |
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Types of malignant hepatic neoplasms (3)
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1) Hepatocellular CA
2) Cholangiocarcinoma (Bile Duct Tumor) 3) Hepatocholangiocarcinoma |
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Etiology of Hepatocellular carcinoma
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- Protracted (chronic) HBV or HCV
- Aflatoxin B1 - Cirrhosis (any cause) ** Note: Any cause for chronic cell turnover |
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USA - 2-3 cases/100,000 population; 7th decade; Males>females (2:1 up to 8:1); Cirrhosis in 80-90% cases (in Western World)
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Epidemiology of hepatocelluar CA
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Clinical Hx of hepatocelluar CA
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Upper abdominal pain, fatigue, weight loss, elevated serum alpha-fetoprotein (from neoplastic cells)
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Carcinoma of the Pancreas (exocrine)
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a. Possible Etiology - Smoking, high fat intake, benzidine, history of gastrectomy
b. Gross pathology - Majority in head of pancreas c. Symptoms - obstruction, painless jaundice d. Histology - adenocarcinoma (glands) e. Origin from ducts f. Very poor prognosis |
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Islet cell tumor (endocrine)
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- Insulinomas most common, most often benign glucagonomas, somatostatinomas and VIPomas also seen.
- Some malignant (metastases seen) - Clinical triad |
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Clinical triad (insuloma)
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1) Attacks of hypoglycemia
2) Acute confusion/stupor 3) Relief w/ glucose administration/infusion |
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Transmission: Fecal-oral
Inc. Period: 15-45 days Carrier state: None Chronicity: None |
Hep A (HAV) RNA
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Transmission: Parenteral
Inc. Period: 30-180 days Carrier state: 0.1-1% Blood donors Chronicity: Acute |
Hep B (HBV) DNA
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Transmission: Parenteral
Inc. Period: 30-50 days Carrier state: Drug addicts, homos Chronicity: ? |
Hep D or delta (HDV) RNA
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Transmission: Transfusion (parenteral)
Inc. Period: 14-180 days Carrier state: 2-3% blood donors Chronicity: ? |
Hep C (HCV) RNA
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Transmission: Water-borne
Inc. Period: 6 weeks Carrier state: None Chronicity: Rare |
HEV (calivirus) RNA
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Councilman bodies
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Necrosis of random, isolated liver cells
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Histopath of cirrhosis
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a. Disorganized liver architecture
b. Fibrosis c. Parenchymal nodules secondary to d. Reorganized vascular architecture |
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Etiologies of cirrhosis (7)
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a. Fatty liver (alcohol, obesity, DM, medications): 60 - 70 %
b. Postnecrotic cirrhosis e.g.(post-viral): 10% c. Biliary cirrhosis (Primary and secondary): 5-10% d. Cirrhosis associated with hemochromatosis (iron): 5% e. Cirrhosis associated with Wilson's disease (copper): rare f. Cirrhosis associated with alpha-1 anti- trypsin deficiency: rare g. Cryptogenic: 10 - 15% |
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20 x 106 Americans affected w/ these
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Gallstones (cholelithiasis)
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Pathogenesis of gallstones
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- Supersaturation of bile (Bile has 3 constituents - Cholesterol, Bilirubin, Lecithin)
- Initiation of stone formation. - Growth |
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Demography - Northern Europe, American Indians, Mexican Americans, probable familial disposition
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Gallstones
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Etiology of gallstones (7)
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1) Obesity
2) High calorie diet 3) Clofibrate therapy 4) Gastrointestinal disorders; ileal (e.g., Crohn's disease, resection, or bypass; cystic fibrosis with pancreatic insufficiency) 5) Female sex hormones; female preponderance after puberty; estrogenic medications; ? oral contraceptives 6) Advancing age 7) Probable but not well established; pregnancy, multiparity, diabetes |
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Etiology of pigment stones
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1) Chronic hemolysis
2) Alcoholic cirrhosis 3) Biliary infection 4) Advancing age |
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Demography; Oriental more than Occidental; rural more than urban
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Pigment stones
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Clinical consequences include obstruction of common duct, biliary cholic, predisposition to cholecystitis
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Pigment stones
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Morphology of pigment stones
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- Pure cholesterol stones
- Pigment stones - Mixed stones |
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90% of cases secondary to impacted gallstone. Secondary gram negative infection
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Cholecystitis (inflammation of the bladder)
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Pathology of cholecystitis
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Enlarged gallbladder, red to purple color with acute inflammation in gallbladder wall
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Sudden onset of abdominal pain associated with elevated serum pancreatic enzymes (amylase, lipase). Secondary inflammation and necrosis (parenchymal and fat necrosis) of pancreas
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Acute pancreatitis
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Symptoms of chronic pancreatitis (4)
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1) Abdominal pain (with each relapse)
2) No symptoms 3) Pancreatic insufficiency 4) Diabetes Mellitus (late) |
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Causes of chronic pancreatitis (4)
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- Alcoholism
- Biliary tract disease - Familial hereditary - Cystic Fibrosis |
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Conditions and etiologic agents associated w/ pancreatitis (12)
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1) Cholelithiasis
2) Alcoholism 3) Trauma 4) Extension from adjacent tissues 5) Blood-borne bacterial infection 6) Viral infections 7) Ischemia 8) Vasculitis 9) Drugs 10) Hyperlipidemia 11) Hypercalcemia 12) Hereditary/familial |
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T/F Diabetes affects endocrine pancreas while pancreatitis affects the exocrine pancreas
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True
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Carcinoma of head of pancreas can lead to what?
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Impaired secretion/excretion of bilirubin extrahepatically
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