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ASSESSMENT INDIRECT BILIRUBIN (unconjugated)

• Nausea, anorexia increased


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

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