Liver, Gallbladder and Pancreatic Disease

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thezidane
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Liver, Gallbladder and Pancreatic Disease
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2010-12-05 14:40:15
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Liver Gallbladder pancreatic disease
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liver, gallbladder and pancreatic disease
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  1. What is one injury mechanism that the liver has that no other internal organ has?
    The ability to regenerate. 25% of a liver can regenerate to full functional size in appropriate settings
  2. What is Jaundice?
    Etiology?
    Two types?
    • Jaundice (or icterus) is yellow-green pigmentation of the skin or sclerae caused by an increase in bilirubin!
    • Excess bilirubin (breakdown product of erythrocytes) is over 2-3mg/dl.
    • Etiology: overproduction, reduced hepatocyte uptake of bilirubin and obstruction of bile flow.
    • Unconjugated: virtually insoluble (can't even urinate it out)
    • Conjugated: soluble, nontoxic.
  3. Etiology of Jaundice: explain the 4 etiologies:
    • 1. Overproduction of bilirubin caused by increased breakdown of RBC (e.g. intravascular hemolyis-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 biirubin either intrahepatic (e.g. Dubin-Johnson's Syndrome, recurrent jaundice of pregnancy) or extrahepatic (e.g. obstructive gallstones, carcinoma of head of pancreas).
  4. Hepatitis: what is it?
    etiologies?
    Viral Hepatitis: what is this/ what types?
    • inflammation of the liver
    • Many etiologies (drugs, autoimmune disease, infections, viral)
    • Viral Hepatitis: This term is reserved fro infection by a group of hepatotropic viruses, hepatitis A, B C Delta, E and G
  5. Hepatitis A:
    Chronicity?
    Type of virus?
    Transmission
    incubation?
    • Common, Self limiting infection, no carrier state or chronic disease. Acute severe sickness that resolves.
    • RNA virus, transient viremia (not long term)
    • Fecal or oral transmission
    • incubation 15-45 days.
  6. Hepititis B
    Chronicity:
    Type of virus?
    Transmission?
    Carrier State?
    Incubation?
    Risk of malignancy?
    Vaccine?
    • Chronicity: 5-10% progress to chronic hepatitis, 90% are self-limiting infection.
    • DNA virus
    • Parental/sexual spread.
    • Serology-remains in blood, chronic, cirrhosis.
    • Incubation 30-180 days
    • Some risk of malignancy (10%) become chronic hepatitis/cirrhosis.
    • Vaccine to Hep B 95% antiHB antibody response
  7. Hepatitis C
    Type of virus:
    Incubation?
    Transmission?
    Risk of malignancy? Chronicity? Hallmark feature?
    Vaccine?
    • Hep C is the worst type of Hepatitis!
    • RNA virus: majority progress to chronic hepatitis.
    • Incubation 7-8 weeks
    • Transmission: Parental, sexual spread
    • High risk of malignancy/progression to chronic hepatitis.
    • Persistent infection + chronic hepatitis = hallmark feature of Hep C (85%) (BAD)
    • No vaccine because of genomic instability/viral change
  8. Other Hepatitis Viruses
    Hep D
    Hep E
    Hep G
    • Hep D: RNA virus, associated with Hep B
    • Hep E: Rare in US. RNA virus, usually self-limited, waterborne, animal reservoirs.
    • Hep G (not hepatotropic) No increase in serum aminotransferases, replicates in bone marrow and spleen.
  9. Disease states of Hepatitis: (5)
    • Chronic Hepatitis
    • Fulminant Hepatic necrosis
    • Carrier states (varies for each type of Hepatitis)
    • Cirrhosis
    • Hepatocellular cancer
  10. Histopathology of Hepatitis:
    Acute hepatitis?
    Necrosis?
    Chronic Hepatitis?
    • Acute hepatitis: diffuse liver injury with lobular disarray.
    • Necrosis of random, isolated liver cells (Councilman bodies).
    • Chronic Hepatitis: Portal tract inflammation with interface hepatitis.
  11. Acute viral Hepatitis:
    Resolution?
    Symptom?
    Histological features?
    What does fulminant hepatitis mean?
    Progression in what types?
    • Resolution in 8 weeks (like type A and some type B)
    • Symptoms: may be asymptomatic
    • Histology: Panlobular disarray, inflammation, hepatocyte necrosis.
    • Fulminant: massive necrosis.
    • Can become chronic (Hep B and HEP C!)
  12. Chronic Hepatitis:
    Defined as what?
    Abnormal liver function for over 6 weeks.
  13. Cirrhosis: Describe what it is. What is the histopathology?
    Disorganized liver architecture, fibrosis (fibrotic bands), parenchymal nodules secondary to reorganized vascular architecture. Factors leading to hepatocyte death and inflammation.
  14. Cirrhosis etiologies (a lot of them) what's the main one?
    • Fatty liver disease (main one 60-70%) caused by too much alcohol, obsesity, Diabeties, medications, toxins, nutritional deprivation)
    • Postnecrotic cirrhosis (post viral)
    • Biliary cirrhosis
    • Hemochromatosis (excess iron)
    • Wilson's disease (excess copper)
    • Cirrhosis associated with alpha-1 anti-trypsin deficiency.
    • Cryptogenic
  15. Symptoms of cirrhosis:
    • Nonspecific symptoms = weight loss, weakness
    • Liver failure
    • Portal hypertension: Ascites, collateral venous channels, splenomegaly.
    • Neoplasm: Hepatocellular carcinoma
  16. Hemochromatosis:
    etiologic agent of what disease?
    What causes this?
    Genetic factors?
    Treatment?
    • hemochromatosis causes cirrhosis of the liver.
    • Iron overload: build up of iron in liver, pancreas and heart.
    • Genetics: homozygous recessive, chromosome 6.
    • Tx: Phlebotomy: (draining the blood)
    • Features: micronodular cirrhosis, diabetes mellitis, skin pigmentation.
  17. Wilson's Disease:
    Causes what liver problem?
    What is it?
    Genetic features?
    Morphology/histologic features.
    Tx:
    • Causes cirrhosis
    • it's the accumulation of Copper in the liver, brain, eyes.
    • Autosomal recessive.
    • Morphology: acute/chronic, steatosis, necrosis, cirrhosis.
    • Tx: Chelation D-Penicillamine: selectively binds copper and removes it from organs.
  18. Hepatic Tumors:
    What are four benign hepatic tumors?
    • 1. Focal nodular hyperplasia (vascular, reactive non-neoplastic)
    • 2. Bile duct adenomas
    • 3. Liver cell adenomas/hepatoceullar adenoma (birth control pills, steroids).
    • 4. Hemangioma: inappropriate blood vessel proliferation. Most common tumor in infants.
  19. What are some Malignant Tumors of the liver (hepatic neoplasms) 3 types:
    • 1. Hepatocellular carcinoma (HCC)
    • 2. Cholangiocarcinoma (Bile duct carcinoma)
    • 3. Hepatocholangiocarcinoma
  20. Hepatocellular Adenoma:
    benign or malignant?
    associated with what medication?
    Presentation?
    Histology?
    • Benign
    • Associated with oral contraceptives
    • Presentation: acute abdomen, intra-abdominal bleed.
    • Histology: bland hepatocytes and no bile ducts.
  21. Hepatocellular carcinoma:
    What causes it?
    what is a serum molecule indicator?
    Histological appearance?
    Prognosis?
    Clinical history/indicators?
    • Aflatoxin, cirrhosis, Hep B and HEP C
    • elevated serum alpha-fetoprotein
    • Histology: atypical hepatocytes, more than 2-3 cell plates.
    • Poor prognosis: rapidly aggressive. Strong propensity for vascular invasion.
    • Clinical history: upper abdominal pain, fatigue and weight loss, elevated serum alpha-fetoprotein from neoplastic cells.
  22. What is Fibrolamellar Carcinoma?
    • It is a variant of Hepatocellular carcinoma (HCC)
    • Occurs in younger patients 20-40.
    • Better prognosis
    • Scirrhous tumor
  23. Biliary system anatomy: What two organs share a common orifice into the duodenum 60-70% of the time?
    Pancreas and Gallbladder (bile duct and pancreatic duct)
  24. Cholethiasis: What is it?
    silent?
    associated with what?
    What are they made of?
    Complications?
    • Cholelithiasis are Gallstones.
    • 80% silent.
    • Association with inflamed gallbladder.
    • 90% cholesterol stones, 10% pigment
    • Complications: pain, inflammation, obstruction.
  25. Cholelithiasis: Stone formation
    Pathogenesis:
    what is bile made of?
    • Supersaturation of bile (bile has 3 constituents: cholesterol, bilirubin and lecithin).
    • initiation of stone formation and growth.
  26. Cholelithiasis Risk factors for
    1. Cholesterol stones:
    2. Pigment stones:
    • 1. Cholesterol stone etiology: increase in caucasians, age and females with high estrogen. Fat, fertile, forty, females = lots of gallstones. High calorie diet, obesity.
    • 2. Pigment stones: Oriental more than occidental; rural more than urban. Chronic hemolysis, alcoholic cirrhosis, biliary infection, age.
  27. Clinical consequences of Cholelithiasis (Gall stones)
    • Obstruction of the common duct
    • Biliary cholic (gall stones)
    • Predisposition to cholecystitis
  28. Cholecystitis: What is it?
    Acute vs. Chronic
    Pathology:
    • Inflammation of the gallbladder
    • Acute: 90% of cases secondary to impacted gallstone. Secondary gram negative infection. Severe pain, chemical, bacterial reflux-ischemai.
    • Chronic: vague symptoms, stones 90%, fibrosis and inflammation.
    • Pathology: enlarged gallbladder, red to purple color with acute inflammation in gallbladder wall.
  29. What is an example of a disease affecting the exocrine and endocrine pancreas?
    • Diabetes: endocrine pancreas (insulin, glucagon)
    • Pancreatitis: exocrine pancreas (digestive enzymes)
  30. What is Acute Pancreatitis:
    How is it caused?
    Inflammation of the pancreas. Sudden onset of abdominal pain associated with elevated serum pancreatic enzymes (amylase, lipase). Secondary inflammation and necrosis (parenchymal and fat necrosis) of the pancreas.
  31. What are some etiologies of acute pancreatitis?
    • Cholelithiasis (gall stones) and alcoholism are the two main ones.
    • Also, trauma, drugs, septisemia, infection (mumps), metabolic: hypercalcemic and hyperlipic states.
    • Idiopathic
    • viral infections
  32. Chronic Pancreatitis:
    What is it?
    Causes?
    Symptoms?
    • Progressive destruction of the pancreas, chronic relapsing pancreatitis is a better term.
    • causes: alcoholism, biliary tract disease, familial hereditary, cystic fibrosis.
    • Symptoms: Abdominal pain (with each relapse), sometimes no symptoms, pancreatic insufficiency, diabetes mellitus (late).
  33. Chronic pancreatitis: morphology/histology
    • reduced acini
    • Chronic inflammation
    • fibrosis
    • Obstruction of ducts
    • Spare islets
  34. Pancreatic Tumors:
    Carcinoma of the pancreas: affects exocrine or endocrine?
    etiology?
    most common part of pancreas affected?
    symptoms?
    histology?
    prognosis?
    • Carcinoma of the pancreas affecting exocrine glands.
    • Gross pathology: majority in head of pancreas.
    • symptoms: obstruction, painless jaundice.
    • histology: adenocarcinoma (glands)
    • origin from ducts
    • Very poor prognosis
  35. Endocrine Tumors of the pancreas?
    benign or malignant?
    clinical triad?
    • Endocrine tumors of the pancreas are ISLET CELL TUMORS.
    • Insulinomas: more common, most often benign glucagonomas, somatostatinomas and VIPomas also seen.
    • Clinical tiad (Insulinoma): attacks of hypoglycemia, acute confusion/stupor, relief with glucose administration/infusion.
    • Some are malignant (metastases seen).

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