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Liver, hepatitis, cirrhosis

Terms in this set (49)

•4 lobes liver
-Each surrounded by connective tissue
•extends in the lobe itself and
•divides the liver into smaller units referred to as lobules.
•supported by intra-abdominal pressure & mesenteries
-connect the liver to the adjacent intestines, abdominal wall, and diaphragm.
•blood supply from hepatic artery (indirect branch of aorta)
•portal vein → blood from the intestinal tract to the liver → vascular pathways inside liver → hepatic veins → inferior vena cava → heart
•usually is not palpable
Liver Cellular A & P
•hepatocytes (hepatic parenchymal cells)
-perform most metabolic functions
•Kupffer cells
•immunologic, detoxifying, & blood-filtering
•canaliculi (smallest bile ducts)
-between the lobules of the liver
-receive secretions from the hepatocytes → larger bile ducts & hepatic duct.
•hepatic duct joins with the cystic duct from the gallbladder to form the common bile duct → small intestine
•sphincter of Oddi controls amount of bile entering duodenum
Liver Function
•Metabolizes
-glucose, proteins, and fats; drugs, chemicals, bacteria, and foreign elements
•Converts glycogen to glucose
•Regulates blood glucose
•Converts ammonia into urea
•Stores nutrients
-Vitamins A, B12, D, and some B-complex, iron and copper
•forms and excretes bile and bilirubin
•Synthesizes factors for blood coagulation
Liver functions: (3)
Metabolizes
- glucose, proteins, and fats; drugs, chemicals, bacteria, and foreign elements
• forms and excretes bile and bilirubin
• Synthesizes factors for blood coagulation
Considerations of the Elderlym Liver
•Function not significantly affected unless disease is present.
•decreases in organ weight, blood flow, and size and number of hepatocytes;
•increase in fibrous tissue; and
•changes in metabolism of medications.
•Assessment of liver function important for determining side effects due to alterations in medication metabolism and excretion
Jaundice (Icteris)
•Most common sign of liver disorder
•Results from an abnormally high concentration of the bilirubin in the blood
•Visible on the skin, oral mucous membranes sclera
Types of Jaundice
•Hemolytic jaundice, caused by excess destruction of RBCs
•Hepatocellular jaundice, caused by liver disease
•Obstructive jaundice, caused by a block in the passage of bile between the liver and intestinal tract
Hemolytic jaundice
Caused by excess destruction of RBCs
Hepatocellular jaundice
Caused by liver disease
Bilirubin Level
•Normal total bilirubin 0.2 to 1.3 mg/dL
•>2.5 mg/dL (43 fmol/L) →jaundice
•Direct can be measured
•Indirect cannot be measured\
Sources of Bilirubin
•Produced
- Liver
- Spleen
- Bone Marrow
- reticuloendothelial system
• Hemoglobin metabolism
• RBC hemolysis/destruction
Forms of Bilirubin
•Indirect (unconjugated) - cannot be measured
-Combines with protein in blood
-Usually ↑ R/T hemolysis
-= Total -Direct
•Direct (conjugated) - can measured
-Free → Liver → conjugates direct bilirubin +glucuronide → excreted in bile → intestine → bacterial enzymes → urobilinogen →
•Urobilin = brown pigment of stool
•Blood → Urine
•Liver → Bile
What is cirrhosis
Degenerative liver disorder caused by generalized cellular damage
Indirect (unconjugated) Bilirubin
Cannot be measured
- Combines with protein in blood
- Usually ↑ R/T hemolysis
- = Total -Direct
Direct (conjugated) Bilirubin
- can be measured
- Free → Liver → conjugates direct bilirubin +glucuronide → excreted in bile → intestine → bacterial enzymes → urobilinogen →
• Urobilin = brown pigment of stool
• Blood → Urine
• Liver → Bile
Abdominal Paracentesis
A needle is inserted into the peritoneal cavity and ascitic fluid is removed

indicated by resp. distress r/t compression of lungs
Abdominal Paracentesis Nursing
- Informed consent,
- Assess labs before & after (albumin, protein, glucose, amylase, BUN/Cr-; K+ if on Lasix)
- Assess allergy to local anesthetic
- Usu. done sitting
- Ensure empty bladder
- Baseline vitals esp. BP
- Wt., abd. girth
- May need to infuse albumin/ IV fluid during.
- Monitor pt. tolerance
- Freq. vitals esp. BP/resp.
- T Q4h X48 hr.
- Wt., abd. girth compare to before
- Record/characteristics amt. fluid removed & manage specimens
- Hold pressure over site then apply dressing, ▲ prn
- Urine output Q4H
- Spironolactone (Aldactone) and furosemide (Lasix) [K+]
- Fall safety
Abdominal Paracentesis Complications
• Hypovolemia r/t fluid shift caused by protein loss
- Monitor s/s
- Prescribed albumin/IV fluids
• Bladder perforation
- Hematuria, low or no urine output, suprapubic pain &/or distention, symptoms of cystitis, and fever.
- Teach pt. to report
• Peritonitis r/t perforation of bowel
- Teach pt. to report
Hepatic Encephalopathy (Hepatic Coma/(Portal Systemic Encephalopathy (PSE))
The loss of brain function when a damaged liver doesn't remove toxins from the blood.

- CNS manifestation of liver failure: coma and death; increased ammonia level
- Treatment: eliminating dietary protein, removing residual protein, depleting intestinal microorganisms
Hepatic Encephalopathy Contributors (3)
- GI bleeding
• Liver cannot handle increase protein load causeD by RBCs in gut

- Constipation
• Ammonia has greater contact time in bowel

- Azotemia -- higher-than-normal blood level of urea or other nitrogen-containing compounds (BUN)

- Increased protein intake
• Leads to increased ammonia
Treatment of Encephalopathy (2)
- Lactulose
- Neomycin
(Goal to decrease high levels of ammonia)
Lactulose
• Splits into lactic acid & acetic acid in the intestine → acidic environment →↓ bacterial growth
• Also traps ammonia & has a laxative effect that promotes expulsion of ammonia via feces
• PO/via NG/retention enema
Neomycin
• PO/rectally
• ↓bacterial flora of the colon →↓bacterial action on protein in the feces →↓ammonia formation
• Side effects -- renal toxicity and hearing impairment
Viral Hepatitis - Clinical Manifestations
• May be asymptomatic
• Prodromal (preicteric) - "flu like" signs & symptoms (headache, malaise, fatigue, anorexia, fever) last 1 -2 weeks
• Icteric (Jaundice) - Occurs in only 25% of cases, best indicator is liver tenderness, also may have dark urine/clay stool.
• Convalescent (Posticteric) - May take weeks to months, lasts until hepatic enzymes are normal
Viral Hepatitis Lab Values
• Elevated Alt, AST, Total Bili
• Normal or elevated ALP
Most definitive diagnostic approach used to identify the intensity of the infection, and the degree of liver damage
Liver Biopsy
Viral Hepatitis Nursing Care (7)
• Contact precautions if indicated.
• Limit activity in order to promote hepatic healing.
• High-carbohydrate, high-calorie, low- to moderate-fat, and low- to moderate-protein diet, and small, frequent meals to promote nutrition and healing.
• Educate the client &family regarding measures to prevent the transmission
• Avoid alcohol,
• Avoid over-the-counter medications or herbal
• Hand hygiene.
Hepatitis A Treatment
- vaccination for post-exposure protection.

- Immunoglobulin post-exposure protection > 40 yr, <12 months old, chronic liver, immunosuppressed, allergic to vaccination
Hepatitis C Treatment
- Combination therapy with peginterferon and ribavirin (Virazole)

- Simeprevir (Olysio) with interferon & ribavirin

- Sofosbuvir (Sovaldi) --maybe no other meds - 1 pill/day X 12 weeks -cures 90%

- Ledipasvir-sofosbuvir (Harvoni) - no other meds
Hepatitis B Treatment
- Acute infection -- No medications, supportive care.

- Chronic infection -- Antiviral medications: adefovir dipivoxil (Hepsera), interferon alfa-2b (Intron A), peginterferon alfa-2a (Pegasys), lamivudine (Epivir-HBV), entecavir (Baraclude), & telbivudine (Tyzeka).
Hepatitis Complications
• Chronic hepatitis
- hepatitis B, C, or D.
- Increased risk for liver cancer
• Fulminating hepatitis
- Extremely progressive -- develop symptoms of viral hepatitis, then within hours or days develop severe liver failure.
• Cirrhosis
• Liver cancer
• Liver failure
What is the prognosis based on (list 4) cirrhosis
1: Bilirubin & albumin levels
2: Ascites
3: Neurological involvement
4: Nutritional status
Consequences of damaged liver cells (list 3)
1: Affects digestion & metabolism
2: Fluid & electrolyte imbalances
3: Impaired ability to metabolize hormones & detoxify chemicals
Most common types of cirrhosis (list 3)
1: From chronic alcohol intake
2: Chronic poisoning with certain chemicals (ie: carbon tetrachloride)
3: Ingestion of hepatotoxic drugs (ie: acetaminophen)
Postnecrotic Cirrhosis (4)
• Results from destruction of liver cells
• Infection (e.g., hepatitis)
• Metabolic liver disease
• Exposure to hepatotoxins or industrial chemicals
Biliary Cirrhosis (3)
• Scarring around bile ducts in the liver
- Related to chronic biliary obstruction and infection

• Primary biliary cirrhosis refers to a progressive autoimmune disease of the liver

• Chronic inflammation causes destruction to the small intrahepatic biliary ducts, preventing the flow of bile into the small intestine → eventually, cirrhosis and liver failure
Compensated cirrhosis
Is less severe, and signs and symptoms are more vague
Decompensated cirrhosis
liver failure
Cirrhosis s/s (9)
Chronic fatigue,
clay-colored stools
spider veins,
palmar erythema (red palms)

tea-colored urine
abdominal discomfort
Shortness of breath, nosebleeds,

Icterus, ascites, bruising
Diagnosis
Most conclusive test for cirrhosis
Liver biopsy
Blood tests cirrhosis
- ↑bilirubin, enzymes (AST [SGOT], ALT [SGPT], &GGT; ↑ PT/PTT; ↑ globulin

- down RBC (large), WBC, thrombocyte count, fibrinogen; K+; down albumin,
Cirrhosis aim of therapy (5)
- Abolish underlying causes to prevent further deterioration

- Preserving remaining liver function

• NO alcohol; nonprescription drugs

• Liver transplantation if failure

• Optimal diet (may need enteral or parenteral)
Cirrhosis Optimal diet (may need enteral or parenteral) (6)
- decrease fat if steatorrhea
- High calorie
- Adequate protein to prevent muscle wasting
- Fluid restriction if decreased Na+ prevent ascites/edema/heart failure
- 2 gm Na+ if ascites to prevent heart failure
- Advanced disease: restrict protein intake; lactulose administration
Cirrhosis medications (5)
• Antacids or histamine2 (H2)-receptor antagonists may be used to reduce gastric disturbances and decrease the potential for GI bleeding
• Potassium-sparing diuretics such as spironolactone (Aldactone)[aldosterone antagonist] to treat ascites
• Ursodeoxycholic acid (Actigall) to promote bile flow from the liver
• Cholestyramine to bind bile salts & relieve pruritus
• Transfusions of platelets/PRBC
Cirrhosis Complications (3)
• Portal Hypertension
• Esophageal Varices
• Ascites
Portal Hypertension
- Blood backs up in portal system
- Congestion; pressure
- Treatment: sodium restriction, drug therapy, surgical and nonsurgical shunt
Esophageal Varices
- Result of portal hypertension
- Esophageal bleeding: treatment
- Sclerotherapy, variceal band ligation, Sengstaken-Blakemore tube
- IV fluids; blood products
Ascites
- abnormal accumulation of protein-rich fluid in the abdominal cavity →Serum protein into peritoneal cavity
- Hepatorenal syndrome -- development of renal failure in patients with advanced chronic liver disease - renal failure is usually irreversible unless liver transplant

• Studies --renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS), and the role of renal prostaglandins (PGs).
• 40%
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