Patho Unit 3-4

  1. How does ethanol contribute to the patho of alcoholic cirrhosis?
    Ethanol metabolism results in oxygen radicals, DNA damage, and acetaldehyde

    Ethanol causes fat to be deposited (fatty liver)

    Ethanol also stims inflammatory response, leading to large accumulations of collagen
  2. How does acetaldehyde contribute to the patho of alcoholic cirrhosis?
    Acetaldehyde stims hepatic fibrosis
  3. Cirrhosis is an ___-stage liver disease.
  4. Will you still see lobules in a liver with cirrhosis?
    Cirrhosis results in masses of scar tissue, nodules (islands of hepatocytes), and disruption of the architecture of the entire liver so no more lobules.
  5. What are the 2 most common causes of cirrhosis of the liver?
    Alcoholic liver disease

    Chronic hepatitic (usually HBV or HCV)

    Less common causes: episode of liver necrosis, drug/chemical effects, genetic disease, chronic bile duct obstruction
  6. Cirrhosis is progressive firbosis of the liver which results in:
    Sever disruption of blood flow (portal blood flow)

    Hepatocytes don't properly filter the blood (impaired diffusion)
  7. What are the 2 major functional disturbances that occur with cirrhosis of the liver?
    Impaired liver function (including changes from excess estrogen)

    Portal hypertension

    (may also lead to liver cancer)
  8. What is portal hypertension?
    Increased pressure in the portal system due to increased portal blood flow or increased resistance to hepatic perfusion.
  9. What causes pre hepatic portal hypertension?
    Thrombi and narrowing of a vein

    splenomegaly shunting excessive blood
  10. What is responsible for hepatic portal hypertension?
  11. What is responsible for post hepatic hypertension?
    Severe r. heart failure
  12. What are the major clinical consquences for portal hypertension?

    Shunting of blood into portal collaterals

    Hepatic encephalopathy

    Congestive splenomegaly
  13. What is ascites? What does it result in?
    High portal v. pressure causes leakage out of capillaries.

    Results in hypoalbuminemia
  14. Where is albumin produced?
  15. What is shunting of the blood in the liver? What are some common pathways?
    Portal v. collateral circulation (anastomoses) develop to bypass the obstructed liver.

    Stomach and spleen, esophageal v. (esophageal varices which freq rupture), rectal area
  16. What are 3 mophologic categories of liver failure?
    Massive hepatic necrosis: direct toxic damage to hepatocytes

    Chronic liver disease: ending in cirrhosis

    Hepatic dysfunction: without overt necrosis
  17. What results in liver failure decomopenation?
    Systemic infections

    Electrolyte imbalance

    Severe stress

    GI bleeding
  18. What are the clinical signs of liver failure?
    Jaundice (liver isn't processing bilirubin)

    Hypoalbuminemia (ascites)

    Hyperammonemia (hepatic encephalopathy)



    Susceptiple to failure of other organ systems
  19. What is hepatic encephalopathy?
    A spectrum of disturbances in consciousness ranging from subte changes in behavior to confusion, stupor, coma, or death.

    Due to shunting of blood around diseased liver, exposes brain to ammonia which would've normally been filtered through liver
  20. What is cholelithiasis?
    Formation of cholesterol stones within gallbladder that occurs to 20% of the population

    Due to deficient amount of bile salts in relationship to amount of cholesterol
  21. Describe the incidence rate of cholelithiasis
    Higher in women, women with alotta kids, women on the pill, and fat women
  22. What comoplications do gallstones cause?
    If a stone becomes lodged in the cystic duct:

    Biliary colic (severe abd. pain w. smooth m. spasm)


    Obstructive jaundice (bile back-up in liver)
  23. What are the 2 types of biliary cirrhosis?
    Primary: slowly progressive chornic inflammation and destruciton of bile ducts, autoimmune disease against bile duct epithelium, jaundice

    Secondary (obstructive): longstanding blockage of bile ducts, results in cholestasis, followed by portal tract inflammation/scarring
  24. What is cholestasis?
    Retention of bile resulting from hepatic dysfunction or biliary obstruction

    Back up in the bile ducts, icnreased pressure indces edema and inflammation

    Elevated serum alkaline phosphatase (indication of liver cell death)
  25. When does intrahepatic cholestasis occur?
    With cirrhosis of the liver or with a tumor
  26. What are primary carcinomas of the liver more common in Asian and African countries?
    Increased incridence of chronic HBV carriers
  27. Why is the liver a common site of metastatic carcinoma?
    Dual blood supply and its highly vascular
  28. What are the 3 hormones produced by the pancreas?
    Alpha: glucagon

    Beta: insulin

    Delta: Somatostatin
  29. What causes acute pancreatitis?
    Escape of pancreatic juice from its ducts into the pancreas (harmful digestive enzymes)
  30. What are the clinical signs of acute pancreatitis?
    Severe abd pain


    Has a high mortality rate
  31. What are 2 risk factors for acute pancreatitis?
    Gallbladder disease

    Exc. alcohol comsumption
  32. What is cystic fibrosis of the pancreas?
    Abnormal cholide transport across cell membranes causes mucos to become abnormally thick and tends to precipitate and obstruct pancreatic ducts.

    Causes pancreatic juice to accumulate and the cystically dilated ducts become surrounded by fibrous tissue
  33. What is maldigestion?
    failure of chemical process to digestion
  34. What is malabsoption?
    Failure of intestinal mucosa to absorb/transport digested nutrients
  35. What is pancreatic insufficiency?
    Deficient production of pancreatic digestive enzymes leading to poor digestion (esp of fats)
  36. What is lactase deficiency?
    Undigested lactose; gas formation and osmotic diarrhea
  37. What is bile salt deficiency? What vitamins are affected?
    Poor absoptionof fats and fat-soluble vitamins

    A: night blindness

    D: decreased calcium absorption, b. deminerilization

    K: blood clotting deficiency

    E: testicular atrophy and neurologic defects in children
  38. What causes bile salt deficiency?
    Advanced liver disease

    Obstruction of common bile duct

    Disease of ileum
  39. Where do carcinomas occur in the pancreas?
    In the head of the pancreas
  40. What can tumors of the pancreas cause?
    Obstruction of the bile duct resulting in obstructive jaundice
  41. What is a insulinoma?
    Benign tumor of islet cells may cause episodes of severe hypoglycemia, can result in seizures
  42. What can cause of hyperglycemia?
    Diabetes mellitus

    Chronic pancreatic disease

    Endocrine disease

    Various drugs

    Rare hereditary disease

    All result in hyperglycemia, ketoacidosis
  43. What can cause hypoglycemia in diabetics?
    Reduced intake of flood

    Increased physical activity

    Insulin overdose
  44. What results from hypoglycemia?
    Confusion, loss of consciousness, convulsions, coma, death
  45. What is common with both diabetes insipidus and mellitus?
    Polyuria and polydipsia
  46. What causes diabetes insipidus?
    Pituitary dificiency of ADH
  47. What is diabetes mellitus?
    Chronic disorders of carb, fat, and protein metabolism

    Defective insulin secretory response causes imparied carb use which results in hyperlycemia
  48. What is common feature of both types of diabetes mellitus?
  49. What is primary diabetes mellitus?
    Type I and II
  50. What is secondary diabetes mellitus?
    Caused by chronic pancreatitis. hormonal tumors, coticosteroid drugs, many many other different types of diabetes
  51. What do beta cells of the pancreatic islets do?
    Syntehsize and store insulin in granules
  52. Glucose is a strong trigger for ____ release.

    A rise in blood glucose causes immediate insulin release, is the stimulus persists, so down the active synthesis of insulin
  53. _____ enables transport of glucose to amino acids across cell membranes.
  54. How does sinulin affect the level of serum glucose?
    Insulin decreases the level of serum glucose by promoting its influx into the liver and skeletal m. where it is used as glycogen
  55. What are 3 things insulin directly stimulates?
    Influx of glucose into skeletal and cardiac m. cells

    Conversion of gluxos to triglycerides in fat cells

    Syntehsis of proteins from amino acids
  56. What does insulin binding to its receptor site on target cells stimulate?
    GLUTs (glucos transport units) to move from the golgi apparatus to the plasma membrane

    Facilitates glucose uptake by the cell
  57. Relate the differences of Type I and Type II diabetes
    Type I:

    <20 yrs, decreased blood insulin, ketoacidosis, autoimmune, 10-205

    Type 2:

    >40 yrs, obesity, insulin resistance, 80-80%
  58. What 3 mechanisms are responsibile for the destruction of islet cells?
    Genetic susceptibility


    Environmental insult
  59. Describe the automimmune effects of type I diabetes
    Chronic automimmune attack against beta cell may exist for years before disease presents itself (even if it seems abrupt)

    Signs don't show until 90% of beta cells have been destroyed
  60. What are some theories for the environmental factors that contribute to type I diabetes
    Could be immune response against virus that shares amino acid sequence with a beta cell

    or automimmunity could be triggered by damage to beta cell
  61. What is the main pathogenic factor for type II diabetes?
    Genetic factors play a large role

    Metabolic defects such as derangement of beta cell secretion of insulin or inability of peripheral tissue to respond to insulin
Card Set
Patho Unit 3-4
Slides patho of alcoholic cirrhosis through deranged beta secretion