1. Liver Dysfunction and Pancreatitis
Nursing 210

2. Liver Anatomy and Physiology
Largest internal organ
Weighs about 1500 grams
Located right upper quadrant
Figure p.1075

3. Anatomy and Physiology
Approximately 75% of the blood supply comes from the portal vein
Drains the GI tract and is rich in nutrients
Remainder of blood supply enters by hepatic artery
Rich in oxygen
All blood leaves the liver through hepatic vein to the inferior vena cava

4. Liver Functions Glucose metabolism
Important role in metabolism of glucose and regulation of blood glucose
Converts glucose to glycogen (storage)
Breaks down glycogen into glucose (energy)
Additional glucose is synthesized through gluconeogenesis (amino acids or lactate)

5. Liver Functions Ammonia Conversion
Ammonia (potential toxin) is byproduct of gluconeogenesis
Liver converts ammonia into urea
Also removes ammonia produced by intestinal bacteria from portal blood
Urea is excreted in urine

6. Liver Functions Protein Metabolism
Synthesizes all plasma proteins except gamma globulin
Albumin (osmotic pressure)
Alpha and beta globulins
Blood clotting factors
Specific transport proteins
Prothrombin: liver needs vitamin K

7. Liver Functions Fat Metabolism Fatty acids broken down into ketones
Provide source of energy for muscles and other tissues
Occurs when glucose is limited as in starvation or uncontrolled diabetes
Fatty acids also used for synthesis of cholesterol, lipoproteins and other complex lipids

8. Liver Functions Vitamin and Iron Storage
Vitamins A, B12, D and several B-complex vitamins stored in liver
Iron and copper

9. Liver Functions Drug Metabolism
Liver metabolism generally results in loss of activity of the medication
Certain oral meds absorbed by GI tract may be metabolized by liver to such a great extent (first-pass effect) that bioavailability is decreased

10. Liver Functions Bile Formation
Mainly water and electrolytes (potassium, calcium, bicarbonate, chloride)
Continuously made by hepatocytes and stored in gallbladder
Emptied into intestine when needed for digestion

11. Liver Functions Bilirubin Excretion
Pigment derived from breakdown of hemoglobin
Modified by hepatocytes through conjugation to be more soluble in aqueous solutions
Conjugated bilirubin is carried by bile into duodenum for excretion

12. Liver Function and Lab Tests
Blood Studies (review Brunner p. 1079)
Serum Aminotransferase
AST
ALT
Elevated levels usually indicate cellular damage to the liver
> 70% of liver cells may be damaged before LFT’s become elevated

13. Blood Studies, cont. Pigment studies
Serum bilirubin, direct
Serum bilirubin, total
Urine bilirubin
These studies measure ability of liver to conjugate and excrete bilirubin
Abnormal results are seen in liver and biliary tract disease

14. Blood Studies, cont. Serum Ammonia
Liver converts ammonia to urea. Ammonia rises in liver failure
Protein Studies
Serum albumin
Low levels seen with liver disease
Serum globulin
Elevated levels with advanced cirrhosis and chronic active hepatitis

15. Blood Studies, cont. Tumor Marker Alpha-fetoprotein (AFP)
Increased levels are seen with hepatic carcinoma
Prothrombin Time (PT)
Time required for a firm fibrin dot to form
In liver dysfunction, increase clotting time with increased risk of bleeding

16. Liver Biopsy Used to obtain a specimen of liver tissue
Done under local anesthesia
Complications:
Pneumothorax
Peritonitis
Hemorrhage

17. Manifestations of Liver Dysfunction
Jaundice
Ascites
Portal Hypertension
Esophageal Varices
Hepatic Encephalopathy
Nutritional Deficiencies

18. Jaundice
Also known as icterus, a yellow discoloration of the skin, sclerae and mucous membranes
Caused by elevated bilirubin levels in the blood
Jaundice becomes clinically evident when the serum bilirubin level exceeds 2.5mg/dL
Several types of Jaundice: Hemolytic, Hepatocellular, Obstructive, and Hereditary Hyperbilirubinemia

20. Jaundice, cont. Symptoms
Yellow discoloration of the skin, sclerae and mucous membranes
Itching (pruritus) due to deposits of bile salts on the skin
Stool becomes light in color
Urine becomes deep orange and foamy

21. Portal Hypertension Elevated pressure in the portal venous blood
Blood flow through the liver is obstructed
Vessels enlarge, collateral circulation develops to take blood back to the systemic circulation
Two major sequelae result
Ascites
Varices

22. Ascites This is the accumulation of fluid in the peritoneal cavity
Decrease albumin levels cause decreased oncotic pressure
Fluid leaves the plasma and leaks in to the peritoneal cavity and interstitial spaces
Decrease volume causes activation of the Renin-Angiotensin system – Na & H2O retained in attempt to return intravascular volume to normal– more edema and ascites

24. Portal Hypertension and Ascites
Symptoms
Portal HTN not evident unless bleeding from collateral blood vessels or ascites occurs
Ascites – increase abdominal girth, unexplained rapid weight gain
Striae and distended veins over abdomen
Fluid and electrolyte imbalances
Respiratory difficulty may occur due to pressure on the diaphragm

25. Portal Hypertension and Ascites
Treatment
Portal HTN – treat underlying cause
Ascites
Na and fluid restrictions
Diuretic agents (Aldactone, Lasix)
Albumin therapy
Paracentesis

26. Varices Esophageal, gastric, hemorrhoidal
Due to elevated pressures in veins that drain into portal system
Often source of massive hemorrhage
Potential for bleeding increased by blood clotting abnormalities seen in patients with liver disease

27. Hepatic Encephalopathy
Impaired neurological function that occurs with profound liver failure
Accumulation of ammonia and other toxic metabolites
GI bleeding, high protein diet, bacterial infections
Other factors unrelated to increased ammonia levels
Dehydration
Surgery
Medications - sedatives, tranquilizers, analgesics,non sparing potassium diuretics

28. Hepatic Encephalopathy
Symptoms
Stage one
Normal level of consciousness w/periods of lethargy and euphoria
Slowed thought process
Slight confusion
Reversal of day – night sleep pattern
Clinical signs
Asterixis (flapping tremor of hand), impaired writing, normal EEG

29. Hepatic Encephalopathy
Stage two
Disorientation
Sleeps most of time, but easily aroused
Agitation, mood swings
Clinical signs
Asterixis, fetor hepaticus (musty odor to breath), abnormal EEG
Stage three
Deep sleep, difficult to arouse
Incoherent speech
Increased deep tendon reflexes, rigidity of extremities, markedly abnormal EEG
Stage four
comatose

30. Hepatic Encephalopathy
Treatment
Restrict protein intake in early stages
Lactulose
reduce serum ammonia through bowel evacuation
Fecal flora are changed to organisms that do not produce ammonia from urea
D/C sedatives, tranquilizers, analgesics

31. Viral Hepatitis Inflammation and necrosis of hepatic cells
Bile flow is impaired
Necrosis occurs in a spotty pattern
Liver cells may regenerate during recovery period

32. Viral Hepatitis Types Hepatitis A (HAV) Hepatitis B (HBV)
Hepatitis C (HCV)
Hepatitis D (HDV)
Hepatitis E (HEV)

33. HAV Also known as “infectious hepatitis”
Mode of transmission is fecal – oral route; poor sanitation
Incubation period days
May occur with or without symptoms, flu like
Preicteric phase – headache, anorexia, fever
Icteric phase – dark urine, jaundice of skin, sclera

34. HAV 1995 FDA approved vaccine
Recommend for travelers to locations of poor sanitation, high risk groups (homosexual men,IV drug users, day care workers)
Nursing management includes
Stressing good hygiene
Environmental sanitation

35. HAV Outcome – usually mild with recovery Fatality rate less than 1%
No carrier state
No increased risk of chronic hepatitis, cirrhosis or hepatic cancer

36. HBV Also known as “serum hepatitis”
Transmission – blood and body fluids, through mucous membranes and breaks in skin
Health care workers at great risk
IV drug users and homosexual activity
Very long incubation period: 1-6 months
May occur without symptoms, may develop arthralgias, rash

37. HBV Vaccine used to provide active immunity
Recommended for all health care workers
Passive immunity is provided through hepatitis B immune globulin (HBIG)
Recommended for people exposed to HBV who have not received vaccine or have never had HBV

38. HBV
Nursing management includes: teaching patient proper nutrition, rest, prevention of spread (blood, body fluids)
Fatality 1-10%
Carrier state possible
Increase risk for cirrhosis, chronic hepatitis and hepatic cancer

39. HCV Also known as Non-A, Non-B hepatitis
Transmission through blood transfusion, exposure to blood contaminated equipment or drug paraphernalia,sexual contact
Incubation days
Clinical course similar to HBV
Chronic carrier state occurs frequently
Increase risk for chronic liver disease and cancer

40. HCV Treatment with interferon and ribavirin
HCV accounts for 30% of liver transplants in US

41. HDV Only individuals with HBV are at risk Sexual contact, IV drug use
Symptoms similar to HBV, more likely to progress to chronic active hepatitis and cirrhosis
Investigation into interferon as treatment

42. HEV Transmitted through fecal – oral route Similar to HAV
Incubation variable days
Jaundice usually always present
No chronic state

43. Toxic and Drug Induced Hepatitis
Toxic hepatitis
Inflammatory condition caused by ingestion or inhalation of certain substances
Dry cleaning fluid
Glue
Insecticides – pesticides
Poisonous mushrooms
Rat poison

44. Toxic and Drug Induced Hepatitis
Tylenol
Aspirin
Thorazine
INH
Valium

45. Toxic and Drug Induced Hepatitis
Symptoms
Similar to those of viral hepatitis
GI and flu type symptoms
Jaundice
Hepatomegaly
Depending of substance, may take days to months for symptoms to appear

46. Fulminant Hepatic Failure
Sudden and severely impaired liver function in previously healthy person
Liver failure within 8 weeks of first clinical sign
Viral hepatitis is most common cause
Other causes
Acetaminophen
Chemicals
Wilson’s disease (copper build up in liver)

47. Cirrhosis
Chronic, degenerative process, replacement of normal tissue with scar tissue
Three types
Alcoholic (most common, chronic alcoholism)
Postnecrotic (acute viral hepatitis)
Biliary (chronic biliary obstruction and infection)
Other causes:
Toxic drug or chemical reaction
Unknown cause

49. Cirrhosis Clinical manifestations Liver enlargement Ascites
Infection and Peritonitis
Varices
Edema
Vitamin deficiency
Mental deterioration

50. Cirrhosis Treatment No alcohol Well balanced diet, unless:
Hepatic Encephalopathy – restrict protein
Ascites – restrict sodium
Vitamin supplements
B-Complex
Folic acid
A,C,and K

51. Cirrhosis Complications Read Nursing Process, Brunner, p.1103-1105
Portal hypertension
Ascites
Hepatic Encephalopathy
Esophageal varices (dilated vein)
Read Nursing Process, Brunner, p

52. Esophageal Varices
Dilated veins usually found in submucosa of lower esophagus
Occurs in 1/3 of patients with cirrhosis
Mortality 45-50%
Hemorrhage occurs from muscular exertion, coughing, sneezing, vomiting, reflux of stomach content (especially alcohol)

54. Esophageal Varices: Medical Management
Non surgical management is preferable due to high rate of mortality with emergency surgery
Pharmacologic therapy (Vasopressin) may be initial mode
Constriction of arterial bed and decrease in portal pressure
Nitroglycerin used to decrease side effect of angina
Balloon Tamponade
Pressure exerted against bleeding varices

55. Esophageal Varices Medical management Endoscopic Sclerotherapy
Sclerosing agent is injected through endoscope into varices to promote thrombosis
Esophageal Banding Therapy
Provides thrombosis and mucosal necrosis of bleeding sites by band ligation
Surgical management
Surgical bypass procedures
Devascularization and Transection

56. Esophageal Varices Nursing Management Vital signs TPN
Prevention of vomiting and straining
NG tube for gastric suction
Quiet environment, help reduce anxiety