Pathophys Exam 3

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Rx2013
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53555
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Pathophys Exam 3
Updated:
2010-12-05 19:06:43
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Liver
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Liver
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  1. Blood flow in the liver
    from the intestine => portal vein => hepatic vein => heart
  2. Liver lobule made up of
    sinusoids
  3. Kuppffer cell
    • eat up everything bad
    • old RBCs
    • foreign material
  4. Stellate (normal)
    stores fat soluble vitamins
  5. Hepatocyte
    produce bile
  6. Stellate (cirrhosis)
    becomes active
  7. Alanine aminotransferase (ALT) normal level
    5-60 units/L
  8. Aspartate aminotransferase normal level
    5-45 units/L
  9. Markers of inflammation or injury to liver cells
    ALT and AST
  10. Levels to check synthesis in the Liver
    • Albumin
    • prothrombin time
    • INR
  11. Normal albumin level
    3.5-5.0 g/dL
  12. Normal prothrombin time
    10-13 sec
  13. Normal INR
    1.0
  14. Markers of excretory function
    • Gamma-glutamyltransferase (GGT)
    • Alkaline Phosphatase
  15. Normal Gamma-glutamyltransferase levels
    0-60 units/L
  16. normal alkaline phosphatase levels
    30-120 units/L
  17. Level that will be elevated in alcohol disease
    GGT
  18. Level that will be elevated in obstruction
    Alkaline phosphatase
  19. Normal total bilirubin
    0.1-1.2 mg/dl
  20. normal conjugated bilirubin
    0.1-0.3 mg/dl
  21. normal free bilirubin (indirect)
    0.3-0.8 mg/dL
  22. Ways to excrete conjugated bilirubin
    • feces
    • general circulation to urine
  23. Phase I reactions
    • oxidation (cyp450)
    • reductions
    • hydroxylation
  24. Phase II reactions
    • Glucuronidation
    • Sulfation
    • Conjugation
  25. top three cyp enzymes
    • CYP3A4/5
    • CYP2D6
    • CYP2C8/9
  26. Direct hepatotoxic injury leads to
    • generation of toxic metabolites
    • acetaminophen
  27. cirrhosis effect on glucose
    • hypoglycemia
    • not making or storing glucose
  28. Lipid metabolism in the liver
    • oxidation of FFAs to ketones in starvation
    • formation of triglycerides
    • synthesis of cholesterol, phospholipids and lipoprotiens for cell wall synthesis
    • conversion of carbs to triglycerides for storage in fat
  29. Alcoholics in america
    > 10 million
  30. Deaths caused by alcoholic liver disease
    100-200,000 per year
  31. % of hospitalized pt with alcohol problems
    25-30%
  32. Metabolism of alcohol
    • absorbed from stomach and intestine
    • EtOH => aldehyde via alcohol dehydrogenase
  33. continued metabolism of alcohol leads to
    accumulation of acetaldehyde and H+ ions in the liver, intestinal lumen and pancrease
  34. Roles of Acetaldehyde
    • increased lipid synthesis and production of ketones & lactic acid due to increased ratio of NADH:NAD+
    • binds other molecules and prevents detox
    • promotes collagen synthesis and fibrogenesis
  35. Risk factors for alcoholic liver disease
    • 40-80 g/day for many years (2 wine or 6 pack of beer)
    • female > male
    • hepatitis
    • smoking (free radicals)
  36. Stages of alcoholic liver disease
    • fatty liver "steatosis"
    • Alcoholic hepatitis
    • cirrhosis
  37. All stages of alcoholic liver disease are reversible except
    cirrhosis
  38. Components of Fatty Liver "steatosis"
    • fat in hepatocytes
    • reversis with abstinence
  39. Components of alcoholic hepatitis
    • mallory bodies and neutrophils (inflammatory cells)
    • swelling and necrosis of hepatocytes
    • 2 (AST) : 1 (ALT) ratio
    • tenderness, nausea, jaundice, ascites
    • nutritional deficiencies
  40. Cirrhosis
    end stage chronic liver disease
  41. Causes of cirrhosis
    • alcoholism
    • viral hepatitis
    • drugs/chemicals (tylenol eating too much fat)
    • iron deposition (hemochromatosis)
    • copper deposition (wilson's)
  42. Pathophysiology of cirrhosis
    • can't clear toxins from body
    • fibrosis throughout liver (stellate cells)
    • nodules
    • formation of septae bands between nodules
    • obstructs blood flow
  43. increased fibrous tissue in the liver leads to
    • obstruction in blood flow
    • increased pressure in the portal vein
  44. Portal vein Hypertension
    • >12 mmHg
    • Increased NO causes vasodilation
    • collateral vessesl begin to form to relieve pressure
    • increased blood flow
  45. Complications of protal hypertension
    • caput medusae
    • hemorrhoids
    • ascites
    • splenomegaly
    • hepatic encephalopaty
  46. Splenomegaly is caused by
    shunting of blood in to the splenic vein
  47. results of splenomegaly
    • blood elements become sequestered in spleen
    • life span of rbc, platelets and wbc decrease
  48. Esophageal varcis
    • occurs with portal vein HTN
    • collateral vessels form and cause rupture of of thin walls
    • massive bleeding shown in cough, vomit and stool
  49. Esophageal varices can occur in % of cirrosis
    65%
  50. patients with esophageal varices have a % mortality rate
    50%
  51. Treatment of Esophageal varices
    • blood products and fluids
    • injection therapy
    • band ligation
    • vasoactive medications
  52. Coagulopathy
    lowered production of clotting factors5,7,9, & 10, prothrombin and fibrinogen when liver becomes fibrotic
  53. Signs/labs for coagulopathy
    • bleeding
    • bruising
    • purpura
    • increased PT and INR
  54. Hepatic encephalopathy
    • mental status changes
    • altered metabolism of AA
    • accumulation of nitrogenous substances (ammonia)
    • no conversion of NH3 to urea
  55. Cardinal sign of hepatic encephalopathy
    asterixis (arms flap down)
  56. Treatment of Hepatic Encephalopathy
    • protein restriction (20g/day)
    • Lactulose (gets rid of ammonia causes diarrhea)
  57. Ammonia level that causes confusion
    40
  58. Peripheral Edema
    • hypoalbuminemia
    • decreased plasma oncotic pressure
    • fluid leaks into muslces and tissues
    • also contributes to ascites
  59. Ascites
    collection of fluid in the peritoneal cavity
  60. Pathophysiology that leads to ascites
    cirrhosis =>portal htn => vasodilations => arterial underfilling => activation of vasoconstrictors => Na and water retention => ascites and dilutional hyponatremia
  61. dilutional hyponatremia
    normal sodium but retain much more water
  62. Serum albumin-ascitic albumin
    • <1.1 g/dL: perotonitis, cancer nephrotic syndrome
    • >1.1 g/dL: portal HTN, cirrhosis, CHF
  63. clinical manifestations of ascites
    • fluid shifting
    • percussion
    • rebound tenderness
    • abd. pain
    • guarding, sob, hypoactive bowel sounds
  64. complication of ascites
    bacterial peritonitis
  65. clinical manifestations of spontaneous bacterial peritonitis
    • similar to ascites plus
    • fever
    • leukocytosis
    • altered mental status
  66. Feminization/hypogonadism results from
    down regulation of the HPA axis
  67. signs of hypogonadism
    • gynecomastia
    • testicular atrophy
    • spider angioma
  68. cause of jaundice
    2mg/dL serum bilirubin
  69. Phases of bilirubin metabolism effected in jaundice
    all
  70. presentation of jaundice
    • clay colored stool
    • dark urine
    • increased alk phos
    • increased AST/ALT
    • pruritis
  71. 3 phases of hepatitis
    • prodromal
    • icterus
    • convalescent
  72. Prodromal phase of hepatitis
    one to two weeks before full blown signs and symptoms
  73. icterus phase of hepatitis
    • dark urine
    • light stool
    • jaundice
    • pruritis
    • increased liver enzymes and bilirubin
  74. convalescent stage of hepatitis
    • return of appetite
    • disappearance of jaundice
    • continued malaise and weakness
  75. Hep A
    • fecal/oral
    • person/sex/food
    • common adult accute disease
    • not chronic
    • vaccine
  76. Hep B
    • perenteral transmission
    • sex/IVDU/perinatal
    • common acute disease
    • adults <10%, children common
    • vaccine
  77. Hep C
    • parenteral transmission
    • IVDU/perinatal
    • uncommon accute disease
    • frequence of chronic >70%
    • no vaccine
  78. Foodborne Hepatitis type and what foods?
    • Hep A
    • shellfish
    • water
    • milk
    • veggies
  79. incubation period of Hep A
    2-6 weeks
  80. Accute illness period for Hep A
    6-8 weeks
  81. Symptoms of Hep A
    • fever
    • malaise
    • nausea/anorexia/abd pain
    • jaundice
    • increased AST/ALT and dark urine
  82. Hepatitis A is caused by
    a single stranded RNA virus which is shed in the stool before signs and symptoms develope
  83. Children less than 6 with Hep A
    won't show symptoms
  84. what do you give the patient if they have already been exposed to hep A?
    IgG
  85. IgM
    present in acute Hep A
  86. Hepatitis B is caused by
    double stranded DNA virus called a Dane particle
  87. Incubation period of Hep B
    4-26 weeks (8-12 avg)
  88. transmission of Hep B
    • infected blood/serum/body fluids
    • perinatal
  89. high risk fluids to harbor hep B
    blood and wound drainage
  90. Moderate risk of Hep B transmission
    • semen
    • vag fluid
    • saliva
  91. Low risk fluids for transmission of hep B
    • urine
    • feces
    • sweat
    • tears
  92. Dane particle contains
    DNA polymerase
  93. Risk factors for Hep B
    • sex
    • IVDU
    • Health care
    • birth
  94. Clinical presentation of Hep B
    • 30% no s/s
    • jaundice
    • fatigue
    • abd pain/anorexia/nv
  95. Surface antigen
    • HBsAg
    • 1st detectable
  96. Core antigen
    • HBcAg
    • cell damage during acute infection on biopsy
  97. E Antigen
    • HBeAg
    • Ongoing active viral replication
  98. Antisurface Antigen Antibody
    • Anti-HBs
    • protective immunity after acute infection or vaccine
  99. Anticore Antigen Antibody
    • AntiHBc
    • denotes prior infection
    • distinguishes acute and chronic
  100. hepatitis B DNA
    • HBV DNA
    • marker of active replication
  101. Susceptible to hep B (test results)
    • HBsAg: Negative
    • Anti-HBC: negative
    • Anti-HBS: negative
  102. Immune due to natural infections (test shows)
    • HBsAg: Negative
    • Anti-HBC: positive
    • Anti-HBS: positive
  103. Immune due to hepatitis B vaccine
    • HBsAg: Negative
    • Anti-HBC: negative
    • Anti-HBS: positive
  104. Acute infection shows
    • HBsAg: Positive
    • Anti-HBC: positive
    • IgM anti-HBc: positive
    • Anti-HBS: negative
  105. Chronic infection shows
    • HBsAg: positive
    • Anti-HBC: positivive
    • IgM anti-HBc: negative
    • Anti-HBS: negative
  106. Hepatitis C caused by
    ssRNA virus
  107. Hepatitis C is responsible for % of chronic hepatitis
    60-85%
  108. Hep C may lead to
    liver cancer or cirrhosis
  109. Hep C clinical presentation
    • jaundice is uncommon
    • non-specific symptoms such as malaise, weight loss, fatigue
  110. Two things appear in Hep C
    • rna virus present
    • antibody present after 3 months

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