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61 Cards in this Set
- Front
- Back
Annular pancreas |
Developmental malformation in which the pancreas forms a ring around the duodenum; risk of duodenal obstruction |
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Acute pancreatitis |
Inflammation and hemorrhage of the pancreas due to auto digestion of pancreatic parenchyma by pancreatic enzymes (premature activation of trypsin leads to activation of other pancreatic enzymes); results in liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the peripancreatic fat |
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Causes of acute pancreatitis |
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Clinical features of acute pancreatitis |
1. Epigastric abdo pain that radiates to back 2. Naseau and vomiting 3. Periumbilical and flank hemorrhage (necrosis spreads into periumbilical soft tissue and retroperitoneum) 4. Elevated serum lipase and amylase, lipase is more specific for pancreatic damage 5. Hypocalcemia (Ca2+ consumed during saponification in fat necrosis) |
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Complications of acute pancreatitis |
1. Shock 2. Pancreatic pseudocyst 3. Pancreatic abscess 4. DIC and ARDS |
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What causes shock in acute pancreatitis? |
Peripancreatic hemorrhage and fluid sequestration |
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Pancreatic pseudocyst as seen in acute pancreatitis |
Formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes
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Pancreatic abscess |
often due to E. coli; presents with abdo pain, high fever, and persistently elevated amylase |
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Chronic pancreatitis |
Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis; most commonly due to alcohol and CF (in children); however many cases are idiopathic |
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Clinical features of chronic pancreatitis |
1. Epigastric abdo pain that radiates to back 2. Pancreatic insufficiency 3. Secondary diabetes mellitus 4. Increased risk for pancreatic carcinoma |
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What do imaging and contrast studies reveal in chronic pancreatitis? |
Dystrophic calcification of pancreatic parenchyma on imaging; a 'chain of lakes' pattern due to dilatation of pancreatic ducts |
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Pancreatic carcinoma |
Adenocarcinoma arising from the pancreatic ducts; most commonly seen in the elderly (average age is 70) |
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Major risk factors for pancreatic carcinoma |
Smoking and chronic pancreatitis |
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Clinical features of pancreatic carcinoma |
1. Epigastric abdo pain and weight loss 2. Obstructive jaundice with pale stoles and palpable gallbladder (assoc. w/ tumors in head of pancreas) 3. Secondary DM (assoc. w/tumors in body or tail) 4. Pancreatitis 5. Migratory thrombophlebitis (Trousseau sign) |
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Serum tumor marker for pancreatic carcinoma |
CA 19-9 |
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Trousseau sign |
Presents as swelling, erythema, and tenderness in extremities (seen in 10% of patients with pancreatic carcinoma) |
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Whipple procedure |
Surgical resection to treat pancreatic carcinoma; involves en bloc removal of head and neck of pancreas, proximal duodenum, and gallbladder |
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Prognosis of pancreatic carcinoma |
Very poor; 1-year survival is < 10% |
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Biliary atresia |
Failure to form or early destruction of extra hepatic biliary tree leading to biliary obstruction within first 2 months of life; presents as jaundice and progresses to cirrhosis |
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Cholelithiasis |
Gallstones; due to precipitation of cholesterol or bilirubin in bile that arises with (1) supersaturation of cholesterol or bilirubin, (2) decreased phospholipids (e.g., lecithin) or bile acids (these normal increase solubility), or (3) stasis |
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What is the classic example of drug that increases the risk of cholesterol stones? |
Cholestryramine (it binds bile acids) |
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How does stasis increase the risk for gallbladder stones? |
Stasis may lead to an overgrowth of bacteria, which can de-conjugate bilirubin; this form of bilirubin in the bile can lead to stones |
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Cholesterol stones |
Yellow stones; most common type (90%) of stones, especially in the West; usually radiolucent though some (10%) are radiopaque due to associated calcium |
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Risk factors for cholesterol stones |
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Bilirubin stones appearance on imaging |
usually radiopaque |
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Risk factors for bilirubin stones |
Extravascular hemolysis (increased bilirubin in bile) and biliary tract infection (e.g., E coli, Ascaris lumbricoides, and Clonorchis sinensis) |
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Complications of gallstones |
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Biliary colic |
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Acute cholecystitis |
Acute inflammation of gallbladder wall due to impacted stone in cystic duct resulting in dilatation with pressure ischemia, bacterial overgrowth (E coli), and inflammation |
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How does acute cholecystitis present? |
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Chronic cholecystitis |
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How does chronic cholecystitis present? |
Vague right upper quadrant pain, especially after eating |
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Porcelain gallbladder |
Late complication of chronic cholecystitis; shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification; increased risk for carcinoma (should be removed via cholecystectomy) |
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Ascending cholangitis |
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Gallstone ileus |
Gallstone enters and obstruct small bowel due to cholecystitis with fistula formation between gallbladder and small bowel |
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Gallbladder carcinoma |
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Classic presentation of gallbladder carcinoma |
Cholecystitis in an elderly woman |
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Earliest sign of jaundice |
Scleral icterus |
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What levels do serum bilirubin have to reach in order for jaundice to occur? |
Usually above 2.5 mg/dL |
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Extravascular hemolysis or ineffective erythropoiesis |
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Physiologic jaundice of the newborn |
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Kernicterus |
Due to high levels of bilirubin: UCB is fat soluble and can deposit in the basal ganglia, leading to neurological deficits and death |
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Gilbert syndrome |
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Crigler-Najjar Syndrome |
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Dubin-Johnson syndrome |
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Biliary tract obstruction (obstructive jaundice) |
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Viral hepatitis |
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HAV and HEV mode of transmission |
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What is HEV in pregnant women associated with? |
Fulminant hepatitis (liver failure with massive liver necrosis) |
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Type of hepatitis and serum markers for HAV and HEV |
Acute hepatitis; no chronic state
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HBV mode of transmission |
Parenteral transmission (e.g., childbirth, unprotected intercourse, IV drug abuse, and needle stick) |
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HBV disease course |
Results in acute hepatitis, chronic disease occurs in 20% of cases |
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HCV mode of transmission and disease course |
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Serum markers HCV |
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HDV |
Dependent on HBV for infection; superinfection upon existing HBV is more severe than confection (infection with both at the same time) |
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Which is the first serologic marker to rise in HBV infection? |
HBsAG (presence > 6 months defines chronic state) |
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What are the markers for infection with acute HBV? |
HBsAG, HBeAG and HBV DNA, IgM |
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Which marker indicates resolved HBV infection? |
HBcAB (IgG) and HBsAB (IgG protective) |
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Other viral causes of hepatitis |
EBV, CMV |
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How does acute hepatitis present? |
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What characterizes chronic hepatitis? |
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