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Hepatic PowerPoint Presentation

Hepatic

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Hepatic

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  1. Hepatic • Working knowledge of physiological changes during disease process & effects on nutrition care.

  2. Hepatic • Translate nutrition needs into menus. • Working knowledge of MNT for hepatic disease. • Calculate and define diets for common conditions.

  3. Normal Structure • Biliary ducts Fig. 18-9, Gould next

  4. Liver and gallbladder with ducts

  5. Normal liver in situ

  6. Blood Supply to Liver • Liver circulation Fig. 22-1 next

  7. Liver circulation

  8. Sinusoids • Sinusoids Fig. 13-1 next • Also see Fig. 18-11 in Gould

  9. Cut surface normal liver with vessels & bile ducts

  10. Liver sinusoids

  11. Sinusoids • Capillary-like structures • Blood from both the hepatic artery and portal vein flow in to the sinusoids • Blood collects in central vein & then to hepatic vein

  12. Kupffer cells • Cells that line the sinusoids • Phagocytic cells of the immune system

  13. Pressure in Liver • Normally very little resistance to blood flow in liver • Hepatic vein pressure 0 mm Hg • Portal vein pressure is 8 mm Hg

  14. Pressure in Liver • Portal hypertension • Pressure in hepatic vein increases above 0 mm Hg

  15. Metabolic • What are the metabolic functions of the liver?

  16. Detoxification • Kupffer cells • Toxins detoxified • Removal of ammonia & make urea

  17. Digestion • Bile synthesis • Bilirubin • product of breakdown of heme when rbc discarded • excreted in bile

  18. What happens to all of these functions in liver disease?

  19. Progression of Liver Disease • Fatty liver • Hepatitis • Cirrhosis • ESLD

  20. Fatty liver

  21. Hepatitis • Infectious mononucleosis • Toxic chemicals • Viral infection • Excessive use of alcohol

  22. Viral Hepatitis • Hepatitis A • fecal-oral route • rapid onset • 2 - 6 weeks • acute type

  23. Viral Hepatitis • Hepatitis B and C • contaminated bodily fluids • slower onset • 6 weeks to 6 months • can become chronic

  24. Hepatitis • Symptoms • jaundice can occur • pale stools • easily fatigued

  25. Hepatitis • Symptoms • nausea & anorexia • fever • liver tenderness • liver enlarged

  26. Hepatitis • Why do these clinical manifestations happen? • hypoglycemia • fluid imbalance • bleed more easily • elevated serum bilirubin > 20mg/dl

  27. Prehepatic Jaundice • Fig. 18-12 in Gould • Hemolytic jaundice • Excessive rbc break down • Unconjuaged bilirubin high • Stool dark/normal color

  28. Intrahepatic Jaundice • If unconjugated bilirubin high means liver cell damage • If conjugated bilirubin high, means blockage

  29. Posthepatic Jaundice • Conjugated bilirubin high • Light colored stool

  30. Cirrhosis • Repeated damage, necrosis to liver • What will eventually happen to the liver?

  31. Cirrhotic liver, external surface macronodular

  32. Cirrhotic liver, macronodular

  33. Cirrohtic and fatty liver, micronodular

  34. Alcohol Acetaminophen Androgenic steroids Cyclosporine Erythromycin Glucocorticoids Isoniazid Methotrexate Methyldopa NSAIDs Hepatoxic Drugs

  35. Damage Liver • Hepatitis, especially if chronic • Biliary disorders, obstruction • Hemochromatosis • Chronic use hepatotoxic drugs

  36. Portal HTN • Due to damaged liver • Pressure too high on which end?

  37. Esophageal varices with portal HTN

  38. Portal HTN & Ascites • Forces plasma out of vessels • Is Alb high or low in the blood? • Na restricted diet • Fluid restricted diet

  39. End-stage Liver Disease • Less than 25% of liver functions • Portal systemic encephalopathy (PSE)

  40. Stage 1 apathy restlessness reversal of sleep rhythm Stage 1 slowed intellect impaired computational ability impaired handwriting ESLD Stages

  41. Stage 2 lethargy drowsiness disorientation asterixis Stage 3 stupor (arousable) hyperactive reflexes extensor plantar responses ESLD Stages

  42. ESLD Stages • Stage 4 • coma • response to painful stimuli only

  43. ESLD • Excessive ammonia in blood (NH3) • Abnormal amino acid metabolism • BCAA lower • Aromatic AA higher

  44. ESLD • False neurotransmitter hypothesis by Fischer • too many Aromatic AA favored into brain • phe - hinder neuronal transmission

  45. ESLD • False neurotransmitter hypothesis by Fischer • phe & tyr - precursor of epinephrine & norepinephrine • trypothan - precurson of serotonin

  46. ESLD • False neurotransmitter hypothesis by Fischer • high level of phe result in false neurotransmitters & competes with normal neurotransmitters

  47. ESLD • Precepitating factors • GI bleed • increased dietary protein • constipation • infection • less hepatic function

  48. Subjective Global Assessment • Four elements of pt. Hx • Recent loss of body wt • Changes in usual diet • Presence of significant gastrointestinal symptoms • Patient’s functional capacity

  49. SGA • Three elements of physical exam • loss of subcutaneous fat • muscle wasting • presence of edema or ascites