H.

pylori products bypass liver and are not

ASSESSMENT detoxified)
• Nausea, anorexia INDIRECT BILIRUBIN (unconjugated)
• Sour taste in mouth increased
• Belching • Hemolytic anemia
• Cramping, pain • Physiologic jaundice of the newborn
IMPLEMENTATION HBs-Ag
• Watch for signs of GI bleeding (“coffee- • Earliest marker of hepatitis B
ground” vomit) Hbs-Ag
• CBC if suspected pernicious anemia • Indicates infective state (hepatitis B)
MEDICATIONS: JAUNDICE
• Antacids Skin looks yellow if serum bilirubin >
• Antihistamine (to reduce acid secretion) 2mg/dL
• Antibiotics (to eradicate H. pylori) PREHEPATIC
PEPTIC ULCER DISEASE • Hemolysis: sickle cell anemia, Hemolytic
GASTRIC ULCER anemias (antibodies against RBC’s)
• Normal or decreased acid production HEPATIC
• Decreased mucosal resistance • Hepatitis: impaired conjuction of bilirubin
• Chronic NSAID use by liver cells
• Pain gets worse after meals POSTHEPATIC
DUODENAL ULCER • Cholestasis: impaired excertion by liver
• Increased acid production cells (estrogens, some drugs), Bile duct
• Pain typically relieved by meals obstruction
ASSESSMENT DRUG INDUCED LIVER DISEASE
• Gnawing, burning epigastric pain ESTROGENS
• Vomiting CHLORPROMAZINE
• GI bleeding>anemia • Reversible cholestasis
• Diagnosis: upper GI series or endoscopy ETHANOL
test for presence of Helicobacter pylori • Fatty liver, Cirrhosis
IMPLEMENTATION ACETAMINOPHEN/ CARBON
• Watch for signs of bleeding- “coffee- TETRACHLORIDE
ground” vomit, tarry stools • Acute liver cell necrosis
• Avoid irritating food ESTROGENS
• Avoid cigarette smoking • Hepatocellular adenoma (benign)
• Avoid aspirin, NSAIDs and steroids AFLATOXIN HEPATITIS B AND C
MEDICATIONS: • Hepatocellular carcinoma
• Antihistamine ANALYSIS
• Antibiotics to eradicate H. pylori • Altered through process?
Note: gastric resection is much common • Nutritional status?
nowadays due to more effective drugs • Bleeding risk?
including the use of antibiotics to eradicate • Skin integrity?
H. pylori IMPLEMENTATION
LIVER: SIGNS & SYMPTOMS • Check skin, gums and stool for bleeding
Jaundice – diminished bilirubin secretion • Avoid aspirin
Fetor hepaticus – sulfur compounds • Monitor weight
produced by intestinal bacteria, not cleared • Monitor abdominal cicumference
by liver • If ascites interferences with breathing >
Spider angiomas palmar erythema high Fowler’s
gynecomastia – elevated estrogen levels DIET:
Ecchymoses(easy bruising) – decreased • High carbohydrate, high calorie, vitamins
synthesis of clothing factors (low protein diet if client has hepatic
Xanthomas(yellow skin plaques / nodules) encephalopathy)
– elevated cholesterol levels • Provide counseling if client abuses alcohol
Hypoglycemia – decreased liver glycogen HEPATITIS
stores, decreased liver glucose production HEPATITIS A – contaminated water/ food
Splenomegaly – portal hypertension raw, shellfish
Encephalopathy asterixis (hand-flapping • Fecal/oral
tremor) – portosystemic shunt (digestive • 2-6wks incubation
• 0% become chronic
HEPATITIS B – blood transfusion, sexual
contact
• Parental
• 2-6 months incubation
• 10% chronic
HEPATITIS C – blood trasfusion, sexual
contact
• Parental
• 1-2 months incubation
• 50% chronic
HEPATITIS D – only in patients with
hepatitis B
• Parental
HEPATITIS E
• Fecal oral
• Mainly in southeast Asia
Note: risk from blood transfusion about
1:50,000 Hepatitis C is the most serious
(high risk of chronic cirrhosis)
ISOLATION OF INFECTIOUS CLIENT:
Required if client has hepatitis A or E and
fecal incontinence
Required if client has hepatitis B or C and is
bleeding
ASSESSMENT
PREICTERIC:
• Nonspecific: fatigue, anorexia, malaise,
weakness
• Low-grade fever
ICTERIC:
• Anorexia, weakness
• Right upper abdominal pain
• Skin pruritus
• Yellow skin and sclera, Dark urine
(urobilinogen), Elevated AST, ALT, Elevated
bilirubin, Prolonged PT and PTT > increased
risk of bleeding!
ANALYSIS
• Adequate fluid and caloric intake?
• Activity intolerance
IMPLEMENTATION