Liver Disease Flashcards

1
Q

Hepatitis

A
  • inflammation of the liver
  • caused by infectious organism that enters body or by a toxin (alcohol or medications)
  • non-infectious hepatitis may occur secondary to exposure to a chemical or medication
  • viral hepatitis can be acute or chronic
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2
Q

5 Major Categories of Viral Hepatitis

A

1) hepatitis A virus (HAV)
2) hepatitis B virus (HBV)
3) hepatitis C virus (HCV)
4) hepatitis D virus (HDV)
5) hepatitis E virus (HEV)

hepatitis F and G have been identified but are uncommon

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3
Q

Routes of Transmission for each Category

A

Hepatitis A and E: oral-fecal route (ie. ingestion of contaminated water)

Hepatitis B and C: blood (ie IV drug abuse, sexual contact, health care work)

Hepatitis D: co-infection with HBV

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4
Q

Prevention of Viral Hepatitis

A

1) Hep B vaccination prophylaxis for all health care workers
2) proper use of standard precautions
3) use of needleless system when delivering medications and parenteral solutions
4) use of PPE appropriate to type of exposure (gown, gloves, goggles)
5) report hepatitis outbreaks to health authorities
6) frequent hand hygiene (before eating, after using toilet)
7) if traveling to underdeveloped countries, drink bottled water and limit sharing of bed linens and eating utensils

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5
Q

Manifestations of Hepatitis

A

1) headache
2) fatigue
3) arthralgia (joint pain) and myalgia (muscle pain)
4) pruritis
5) low-grade fever
6) RUQ abdominal pain
7) nausea and vomiting
8) jaundice
9) dark urine

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6
Q

Laboratory Tests

A

1) enzyme-linked immunosorbent assay (ELISA) or recombinant immunoblot assay (RIBA)
2) elevated serum liver enzymes:
- alanin aminotransferase (ALT): most definitive for assessment of liver tissue damage
- aspartate aminotransferase (AST)
- alkaline phosphatase (ALP)
- serum bilirubin
3) serologic markers
- identifies presence of virus (HAV, HBsAg and Anti HBc IgM, HCV, HDV, HEV)
- serum presence of HBsAg for longer than 6 mos. indicates chronic hepatitis and/or hepatitis carrier status.
- serum presence of HBsAb indicates immunity to HVB following the recovery from hepatitis B or a successful vaccination

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7
Q

Diagnostic Procedures

A

1) abdominal x-rays
- used to visualize possible hepatomegaly, ascites, and spleen enlargment
2) liver biopsy
- most definitive
- used to identify intensity of infection and degree of tissue damage

**post liver biopsy, client will be required to lie on affected surgical side for short period of time and nurse should monitor BP and HR to detect bleeding

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8
Q

Nursing Care

A

1) enforce standard and contact precautions
2) private room or room with other clients with same infection
3) gloves and gowns worn by nurses AND visitors while in client’s room
4) limit client’s activity (bed rest, rest periods) in order to promote hepatic healing
5) provide dietary education regarding high-carb, high-calorie, low-to moderate-fat, and low-to moderate-protein diet and small, frequent meals to promote nutrition and healing
6) only necessary meds are administered in order to promote hepatic rest and regeneration of tissue.
- cautious, if any, use of acetaminophen due to potential for liver damage
7) educate client and family regarding measures to prevent transmission of disease w/ others at home (avoid sexual intercourse until hepatitis antibody testing is negative)

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9
Q

Medications Used to Treat Hepatitis

A

1) Immunoglobulin:
- may be prescribed for household members and sexual partners of clients with hepatitis A
- prophylactic injections may be given to individuals traveling to high-risk countries
2) biologic response modifiers (BMRs):
- administered to clients with chronic hepatitis B or C for several months to induce remission
3) antivirals:
- lamivudine (Epivir, adefovir (Hepsera), or ribavirini (Rebetol) may be given for clients with chronic hepatitis B to decrease incidence of cirrhosis, or clients waiting for liver transplant

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10
Q

Complications

A

1) chronic hepatitis
- results from hepatitis B, C, or D
- increases client’s risk for liver cancer
2) fulminating hepatitis
- a fatal form of hepatitis due to inability of liver cells to regenerate with progression of necrotic process
- results in hepatic encephalopathy and death
3) cirrhosis of the liver
- continued episodes of chronic hepatitis result in scarring and permanent injury to liver and are a risk factor for liver cancer
4) liver cancer
5) liver failure

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11
Q

Cirrhosis

A
  • occurs secondary to inflammation of the liver
  • functional liver tissue is replaced with fibrotic, scar tissue
  • caused by hepatitis, alcohol abuse, or inflammatory disorders
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12
Q

Risk Factors for Cirrhosis

A

1) alcohol abuse
2) chronic viral hepatitis (B, C, or D)
3) autoimmune hepatitis (destruction of liver cells by immune system)
4) steatohepatitis (fatty liver disease causing chronic inflammation)
5) damage to liver caused by drugs, toxins, and other infections
6) chronic biliary cirrhosis (bile duct obstruction, bile stasis, hepatic fibrosis)
7) cardiac cirrhosis resulting from severe right heart failure, inducing necrosis and fibrosis due to lack of blood flow
8) obesity

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13
Q

Manifestations of Cirrhosis

A

1) fatigue, weight loss, abdominal pain, and distention
2) pruritis (severe itching of skin)
3) confusion or difficulty thinking, personality and mentation changes, emotional lability, euphoria, depression
4) GI bleeding
5) ascites
6) jaundice and icterus (yellowing of the eyes)
7) petechiae (round, pinpoint, red-purple lesions), ecchymosis, nose bleeds, hematemesis, melena (black, tarry feces associated with upper GI bleeding)
8) spider angiomas
9) dependent peripheral edema of extremities and sacrum
10) asterixis–coarse tremor characterized by rapid, nonrhythmic extension and flexion of wrists and fingers
11) fetor hepaticus–fruity or musty odor to breath

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14
Q

Laboratory Tests

A

1) serum liver enzymes:
- alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are elevated initially due to hepatic inflammation and return to normal when liver cells are not longer able to create an inflammatory response.
- alkaline phosphatase (ALP) increases in cirrhosis due to intrahepatic biliary obstruction
2) serum bilirubin is elevated
3) serum proteins and serum albumin are lowered due to lack of hepatic synthesis
4) hematological tests:
- CBC, WBC, and platelets are decreased secondary to anemia
5) PT/INR is prolonged due to decreased synthesis of prothrombin
6) ammonia levels rise when hepatocellular injury (cirrhosis) prevents conversion of ammonia to urea for excretion

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15
Q

Diagnostic Procedures

A

1) abdominal films and ultrasonography
- used to visualize possible hepatomegaly, ascites, and splee enlargement
2) liver biopsy (most definitive)
- identifies progression and extent of the cirrhosis
3) esophagogastroduodenoscopy (EGD)
- performed under moderate (conscious) sedation to detect the presence of esophageal varices

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16
Q

Care of Client with Cirrhosis

A

1) monitor respiratory status and oxygen level
2) provide comfort measures by positioning client to ease respiratory effort (may be compromised by plasma volume excess and ascites)
- have client sit in a chair or elevate head of bed to 30 degrees
3) skin integrity:
- monitor client closely for skin breakdown
- implement measures to prevent pressure ulcers
4) pruritis will cause client to scratch. encourage washing with cool water and applying lotion to decrease the itching
5) monitor for signs of fluid volume excess and keep strict I&O.
- restrict fluids and sodium if prescribed and weigh daily
6) neurological status:
- monitor client for deteriorating mental status and dementia consistent with hepatic encephalopathy
7) nutritional status:
- encourage a high-calorie, high-protein (unless has hepatic encephalopathy) diet and supplemental vitamins (B complex), folic acid, and iron
8) GI status:
- in presence of ascites, measure abdominal girth daily
9) pain status:
- assess pain and administer analgesics and GI antispasmodics as needed
10) observe client of potential bleeding complications.
- may need transfusions to replace blood volume and clotting factors as prescribed by provider
11) monitor trends in Hgb and Hct levels and note coagulation studies (aPTT, PT/INR)

17
Q

Medications Used to Treat Cirrhosis

A

**general medications are administered sparingly (esp. opioids, sedatives, and barbiturates) because metabolism is dependent upon functioning liver
1) diuretics:
administered to decrease ascites
2) PPI and H2 receptor antagonist:
-administered to decrease gastric acid secretion and risk of GI bleeding
3) lactulose:
-administered to promote ammonia excretion via the stool
4) neomycin and metronidazole (Flagyl):
-administered to remove intestinal bacteria (which produces ammonia)

18
Q

Therapeutic Procedures

A

1) paracentesis
- used to relieve ascites
2) injection sclerotherapy/variceal band ligation
- esophageal varices are either sclerosed or banded endoscopically
- decreased risk of hemorrhage with banding

19
Q

Surgical Interventions

A

1) transjugular intrahepatic portosystemic shunt (TIPS)
- done to control ascites and variceal bleeding
2) surgical bypass shunting procedures
- used as last resort for clients w/ portal hypertension and esophageal varices
- ascites is shunted form abdominal cavity to the superior vena cava
3) liver transplantation
- portions of healthy livers from trauma victims or living donors may be used for transplant
- transplanted liver portion will regenerate and grow in size based on needs of the body
- clients with severe cardiac and respiratory disease, mestastic malignant liver cancer, and continued hx of alcohol/substance abuse are not candidates

20
Q

Care of Client with Cirrhosis

A

1) encourage client to abstain from alcohol and engage in alcohol recovery program
- helps prevent further scarring and fibrosis of liver
- allows healing and regeneration of liver tissue
- prevents irritation of stomach and esophagus lining
- helps decrease risk of bleeding
- helps prevent other life-threatening complications

21
Q

Dietary Guidelines for Client with Cirrhosis

A

1) high-calorie, moderate-fat diet
2) low-sodium diet (if client has excessive fluid in peritoneal cavity)
3) low-protein (if encephalopathy, elevated ammonia)
4) small, frequent, well-balanced nutritional meals
5) supplemental vitamin-enriched liquids (Ensure, Boost)

22
Q

Complications of Cirrhosis

A

1) portal systemic encephalopathy (PSE)
- clients who have a poorly functioning liver are unable to convert ammonia and other waste products to a less toxic form.
- these products are carried to the brain and cause neurological symptoms
2) esophageal varices
- portal hypertension (elevated BP in veins that carry blood from the intestines to the liver) is caused by impaired circulation of blood through the liver
- collateral circulation is subsequently developed creating varices in upper stomach and esophagus.
- varices are fragile and can bleed easily