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Liver Dysfunction and Pancreatitis

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Presentation on theme: "Liver Dysfunction and Pancreatitis"— Presentation transcript:

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

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