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37 Cards in this Set

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Jaundice
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)
Disease states of hepatitis (5)
a. Chronic hepatitis
b. Fulminant hepatic necrosis
c. Carrier states (varies for each type of hepatitis)
d. Cirrhosis
e. Hepatocellular cancer
Acute hepatitis
Diffuse liver injury w/ lobular disarray
Chronic hepatitis
Portal tract inflammation w/ interface hepatitis
Necrosis of random, isolated liver cells
Councilman bodies
Benign hepatic neoplasms (4)
- Focal nodular hyperplasia (?vascular, reactive non-neoplastic),
- Bile duct adenomas
- Liver cell adenomas, (birth control pills, steroids).
- Hemangioma
Types of malignant hepatic neoplasms (3)
1) Hepatocellular CA
2) Cholangiocarcinoma (Bile Duct Tumor)
3) Hepatocholangiocarcinoma
Etiology of Hepatocellular carcinoma
- Protracted (chronic) HBV or HCV
- Aflatoxin B1
- Cirrhosis (any cause)
** Note: Any cause for chronic cell turnover
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)
Epidemiology of hepatocelluar CA
Clinical Hx of hepatocelluar CA
Upper abdominal pain, fatigue, weight loss, elevated serum alpha-fetoprotein (from neoplastic cells)
Carcinoma of the Pancreas (exocrine)
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
Islet cell tumor (endocrine)
- Insulinomas most common, most often benign glucagonomas, somatostatinomas and VIPomas also seen.
- Some malignant (metastases seen)
- Clinical triad
Clinical triad (insuloma)
1) Attacks of hypoglycemia
2) Acute confusion/stupor
3) Relief w/ glucose administration/infusion
Transmission: Fecal-oral
Inc. Period: 15-45 days
Carrier state: None
Chronicity: None
Hep A (HAV) RNA
Transmission: Parenteral
Inc. Period: 30-180 days
Carrier state: 0.1-1% Blood donors
Chronicity: Acute
Hep B (HBV) DNA
Transmission: Parenteral
Inc. Period: 30-50 days
Carrier state: Drug addicts, homos
Chronicity: ?
Hep D or delta (HDV) RNA
Transmission: Transfusion (parenteral)
Inc. Period: 14-180 days
Carrier state: 2-3% blood donors
Chronicity: ?
Hep C (HCV) RNA
Transmission: Water-borne
Inc. Period: 6 weeks
Carrier state: None
Chronicity: Rare
HEV (calivirus) RNA
Councilman bodies
Necrosis of random, isolated liver cells
Histopath of cirrhosis
a. Disorganized liver architecture
b. Fibrosis
c. Parenchymal nodules secondary to
d. Reorganized vascular architecture
Etiologies of cirrhosis (7)
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%
20 x 106 Americans affected w/ these
Gallstones (cholelithiasis)
Pathogenesis of gallstones
- Supersaturation of bile (Bile has 3 constituents - Cholesterol, Bilirubin, Lecithin)
- Initiation of stone formation.
- Growth
Demography - Northern Europe, American Indians, Mexican Americans, probable familial disposition
Gallstones
Etiology of gallstones (7)
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
Etiology of pigment stones
1) Chronic hemolysis
2) Alcoholic cirrhosis
3) Biliary infection
4) Advancing age
Demography; Oriental more than Occidental; rural more than urban
Pigment stones
Clinical consequences include obstruction of common duct, biliary cholic, predisposition to cholecystitis
Pigment stones
Morphology of pigment stones
- Pure cholesterol stones
- Pigment stones
- Mixed stones
90% of cases secondary to impacted gallstone. Secondary gram negative infection
Cholecystitis (inflammation of the bladder)
Pathology of cholecystitis
Enlarged gallbladder, red to purple color with acute inflammation in gallbladder wall
Sudden onset of abdominal pain associated with elevated serum pancreatic enzymes (amylase, lipase). Secondary inflammation and necrosis (parenchymal and fat necrosis) of pancreas
Acute pancreatitis
Symptoms of chronic pancreatitis (4)
1) Abdominal pain (with each relapse)
2) No symptoms
3) Pancreatic insufficiency
4) Diabetes Mellitus (late)
Causes of chronic pancreatitis (4)
- Alcoholism
- Biliary tract disease
- Familial hereditary
- Cystic Fibrosis
Conditions and etiologic agents associated w/ pancreatitis (12)
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
T/F Diabetes affects endocrine pancreas while pancreatitis affects the exocrine pancreas
True
Carcinoma of head of pancreas can lead to what?
Impaired secretion/excretion of bilirubin extrahepatically