Liver, Pancreas and Biliary Disorders

1. Liver, Pancreas and Biliary Disorders Dr. L. Saarmann, RN

3. Question • Which of the following is not a cause of jaundice? • Excessive destruction of red blood cells • Impaired uptake of bilirubin by the liver cells • Ingestion of iron supplements • Decreased conjugation of bilirubin • Obstruction of bile flow in the canaliculi of the hepatic lobules or in the intrahepatic or extrahepatic bile ducts

4. Answer • Excessive destruction of red blood cells • Impaired uptake of bilirubin by the liver cells • Ingestion of iron supplements: Iron supplements do not affect the metabolism of RBCs • Decreased conjugation of bilirubin • Obstruction of bile flow in the canaliculi of the hepatic lobules or in the intrahepatic or extrahepatic bile ducts

7. Cirrhosis • Chronic • Inflammation • Fibrosis • Nodules and scar tissue, parenchymal cells destroyed and replaced by nodules of scar tissue, decrease amt. of functioning liver tissue • Types • Laennec’s = alcoholic, most common in US • Postnecrotic- most common in rest of world, hepatitis or hepatotoxic drug (acetaminophen, • Biliary

8. Cirrhosis – types con’t • Post necrotic • Follows viral hepatitis • Hepatotoxins • Metabolic disorders • Wilson disease – body deposits copper in liver • Hemochromatosis -deposit iron in body and liver • Both cause cirrhosis

9. Cirrhosis – types con’t • Biliary - Stasis of bile • Intrahepatic = primary • Autoimmune, build up antibodies against own liver, bad prognosis • Extrahepatic = seconday • Prolonged obstruction- ca of bile ducts, unresolved stones, better prognosis because obstruction can be removed surgically

10. Alcoholic Cirrhosis • Alcohol • Toxic to hepatocytes • Metabolites = • Acetaldehyde • Free radicals • Alcohol dehydrogenase (in whites) = enzyme that metabolized ETOH, Asian decent alcohol …. • Depressed by testosterone, women don’t have testosterone to dampen down metabolites (also damage liver)- double whammy- alcohol and metabolites damaging to liver, men excrete some alcohol as is while women metabolize all alcohol • Depressed by low protein diet- can’t metabolize alcohol efficiently

11. Cirrhosis • Stages: • 1. Fatty liver • Increased lipogenesis, alcohol increases fat • Decreased oxidation of fatty acids • Mobilization of fat stores, from periphery into liver which affects liver function and can cause inflammation (NASH- non-alcoholic…) • Also high fat diet and sedentary lifestyle can cause fatty liver • Reversible at this stage • Hepatitis • Inflammation & necrosis of liver cells • Cirrhosis • Liver shrunk, hard- little tissue left- liver failure because not enough functioning cells

12. Manifestations (most types) • Early- usually vague, many don’t notice change because gradual change • Fatigue, weakness • Anorexia, wt loss • Change in bowel habits • Dull heavy sensation in RUQ

13. Manifestations (most types) • Late – due to hepatocellular failure and portal hypertension

14. Manifestations (most types) Manifestation Cause Impaired metabolism of sex hormones Increased circulating estrogen • Female • Menstrual disorders- amenorrhea (post- menopausal: return of period) • Male • Testicular atrophy, • Gynecomastia • Impotence; loss of libido • Loss of pectoral, axillary & pubic hair • Vascular spiders- spider angiomas • Palmarerythema

15. Manifestations (most types) Manifestion Cause Impaired synthesis of plasma proteins- decreased oncotic pressure Inc. portal pressure- blood cant move through liver and backs up hyperaldosterone • Edema & ascites (third spacing- fluid between peritoneum and abd. Wall)

16. Manifestations (most types) Manifestation Cause Dec. synthesis of clotting factors & Vit K absorption Splenomegaly- back up of portal pressure, spleen enlarges and holds onto plt., decreased plts in circulation Blood loss, dietary deficiency ETOH toxic to bone marrow (and brain)- wont make as many RBCs • Bleeding- gums with brushing teeth, epitaxis, bruise easily • Thrombocytopenia • Anemia

17. Manifestations (most types) Manifestations Cause Failure to conjugate & remove bilirubin Accumulation of bile salts in skin Unable to convert bilirubin to bile which gives stool color (stool- white/ gray) and urine is rust color • Jaundice • Pruritus- itching • Dark urine, clay colored stool

18. Darker people appear more gray than yellow, but conjuctiva are yellow despite coloring

20. Manifestations (most types) Manifestation Cause Impaired bile synthesis Inability to store vitamins • Malabsorption of fats & fat soluble vitamins- Vit A, D, E and K • Vit B complex deficiency- liver is where h20 soluble vit. Stored so you excrete them

21. Manifestations (most types) Manifestation Cause Impaired gluconeogenesis & glycogenolysis (breakdown sugar stored to be used by body) Vit deficiency Decreased ability to convert ammonia to urea, build up ammonia level (toxic to brain) • Hypoglycemia • Peripheral neuropathy • Elevated blood ammonia levels

22. Manifestations (most types) Manifestation Cause Unknown Decreased hepatic metabolism of methionine • Hepatorenal syndrome • Fetor hepaticus- musty breath odor

26. Portal hypertension • Due to obstruction of normal blood flow through the portal vascular system • Results in: • Hepatic encephalopathy aka portal-systemic encephalopathy (PSE) • Collateral circulation [esophageal varices]- build up new blood vessels to decrease pressure but weak vessels because on lack of proteins from liver, • Ascites • After ascites or bleeding esophageal varices- less than 5 years to live

27. PSE • Patho • Elevated ammonia levels • Ammonia is cerebral toxin, break down of protein makes ammonia • Can get portal-systemic anastomoses – shunting of blood around liver- makes worse because more ammonia avoids liver completely (liver changes ammonia to urea, if not functioning, goes to blood and to the brain) • Allows ammonia to bypass liver • Want low protein diet, neomycin kills bacteria in gut- ( bacteria can’t breakdown protein to ammonia) or given med to induce diarrhea to make quick exit of protein • Brought on by • Hypokalemia • Can be brought on by diuretics, (try to get rid of ascites fluid, makes hard to breathe). Constipation, GI bleeding, narcotic and sedative use, asotemia (nitogenous waste in blood), all cause increase of ammonia breakdown

28. PSE • Constipation • Infection • GI bleeding • Narcotic and sedative use • Azotemia • Anesthesia • Hypoxia

29. PSE Manifestations • Subtle personality changes • Memory loss • Irritability • Lethargy • Sleep disturbances • Confusion • Asterixis- flapping tremor of hand • Convulsions • coma

31. Collateral Circulation • Attempt to reduce portal pressure • Collateral vessels • In esophagus- varicose veins in esophagus • In rectum- hemrroids • Fragile vessels – bleed easily, can bleed out very quickly, varices increase with drinking • Caput Medusae • Around umbilicus, dilate veins

32. Collateral Circulation • Esophageal varices • Risk of bleeding increases: • Intra-abdominal pressure- sneezing, coughing, valsalva, teach to blow one nostril at a time to decrease pressure • Acid regurgitation- acids eat away at varices • Poorly chewed food, food with sharp edges • Irritation for ETOH, et al. • ASA (aspirin)- anticoagulant • Manifestations • Hematemesis- vomit blood • Melena- black tarry stool

33. Esophageal Varices • Complications: • Encephalopathy worsens, more blood in gut- more ammonia • Hypovolemic shock • Electrolyte imbalance • Metabolic acidosis, lost k+ • Respiratory alkalosis, breath rapidly and shallowly because of ascites • Treatment: Balloon tamponade of esophageal varices or cauterize bleeders

35. Ascites- 3rd spacing • Causes: • Decreased albumin • Increased portal pressure • Increased serum aldosterone • Manifestations: • Abdominal distention • Everted umbilicus • Wt gain • Dyspnea • Percussion dull in bases- because fluid pushing up on the lungs

36. Anatomy of the Biliary System Some forms of Hep. are caused by viruses insertion, but not all.

37. Hepatitis • Inflammation of liver • Types: • Viral • HAV, HBV, HBD, HBE • Toxic • From drug or chemicals • Alcoholic • autoimmune

38. Viral Hepatitis Don’t need to know incubation periods, Know how spread and what can be done • HAV – fecal/oral, contaminated food • Susceptibility: kids & young adults • Immunization: 2 shots 6 months apart • Unlikely to have it twice • HBV – parenteral/sex, rarely in feces • Susceptibility: all age groups, transfusions, injecting drug abuse, sexual contact, health care workers • Immunization: 3 shots – 0, 1, & 6 months Possible to get HAV from sex, or HBV from feces- but very rarely

39. Viral Hepatitis • HCV - parenteral – sometimes unknown- some transmission not known yet?, acute or chronic • Susceptibility: all age groups, injecting drug abuse, blood transfusions, long-term kidney dialysis, health care workers, unprotected sex with infected person, Injecting drug abuser, received a tattoo or acupuncture with contaminated instruments, solid organs from a donor who has hepatitis C, Share personal items such as toothbrushes and razors with someone who has hepatitis C (less common), born to a hepatitis C-infected mother • No vaccine • Tx with interferon, makes you feel like you have the flu, works a lot of the time • Can be deadly • Hep E only get if you have Hep B

40. Viral Hepatitis • Patho = inflammation, degeneration, regeneration of liver cells • Stages: • Pre-icteric (prodromal) - Vague sx’s, but very infectious- a lot of shedding of virus with no precaution because not dx • Fatigue, malaise • Low grade fever • Irritability, HA • RUQ pain, tenderness • Anorexia, wt loss, NVD, dyspepsia • Arthralgia • Aversion to cigarettes, even if chain smoker

41. Viral Hepatitis • Stages: • Icteric, lasts 4-6 weeks • Jaundice • Pruritis • Dark urine, clay colored stool • Splenomegaly • Post cervical lymph node enlargement • May have continuation of sx of pre-icteric stage • Recovery • Jaundice disappears • Feel well but easily fatigued, gradually decreases

42. Lab abnormalities c any liver disease • Increased AST, ALT, LDH, alkaline phosphate • Decreased total serum PRO & albumin • Increased prothrombin time (PT) • Decreased Hct & Hgb • Hyperbilirubinemia • Increased urine bilirubin & excess urobilinogen • Hypoglycemia • Steatorrhea • EEG may show generalized slowing • Thrombocytopenia, leukopenia • Hypokalemia, Hyponatremia

43. Biliary System • Cholelithiasis ‑ presence of stones in the gallbladder. • Cholecystitis ‑ acute or chronic inflammation of the gallbladder usually caused by gallstones obstructing the cystic duct. • Choledocholithiasis ‑ stones in the common bile duct • Cholangitis ‑ inflamed bile ducts secondary to obstruction or bacterial invasion

44. Risk Factors • Female, pregnancy, multiparous women • Estrogen therapy/oral contraceptives • Obesity • Age over 40 • Diabetes Mellitus • Hyperlipidemia • Sedentary life style • Native American

45. Manifestations • Biliary Colic • Murphy’s sign • GI – NV; intolerance for fatty food; bloating, flatulence, dyspepsia • Fever/chills/leukocytosis • Jaundice • Clay colored stools/ dark urine • steatorrhea

47. Pancreatitis • Acute or chronic inflammation – may disrupt endocrine and exocrine function, produces insulin and pepcid and other enzymes for digestion • Edema • Necrosis • hemorrhage

48. Pancreatitis • Acute pancreatitis • Inflammation & autodigestion • Obstruction of pancreatic ducts • Reflux of bile or duodenal contents • Toxic effects of ETOH

49. Acute pancreatitis • Types • Edematous interstitial- mild inflammation • Necrotizing- ischemic, fatty necrosis throughout, 50% mortality rate • Hemorrhagic necrotizing- eaten away major blood vessels which causes hemorrhaging

50. Acute pancreatitis • Etiology • ETOH- mostly men, causes obstruction and increases secretion production • Cholelithiasis- female more susceptible • Infections- mumps, viral Hepatitis • ABD trauma • Metabolic conditions- hyperlipidemia • PUD • Idiopathic • Drugs- diuretics, corticosteroids • ERCP (endoscopic retrograde cholangiopancreatography)- diagnostic and treatment for stones but cause trauma to pancreas and swelling resulting in blockage