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NURS 313R > Exam 3: Hepatitis > Flashcards

Exam 3: Hepatitis Flashcards

1
Q

Hepatitis

A

Inflammation of the liver

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2
Q

What is the most common cause of hepatitis?

A

Acute viral infection.

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3
Q

What are the types of hepatitis?

A

A, B, C, D, E, G

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4
Q

Hepatitis A

A
  • RNA Virus

- Virus is transmitted via oral fecal route. (Ingested and leaves the body to infect someone else through feces).

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5
Q

Factors Related to Hepatitis A

A

Poor hygiene
Crowded situation
Poor sanitary conditions

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6
Q

How can you prevent hepatitis A?

A
  • Hepatitis A and immune globulin (IG) are used for prevention
  • Booster (6-12 months after primary dose)
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7
Q

How long does immune globulin give passive immunity?

A

IG give passive immunity for 6-8 weeks if given 1-2 weeks after exposure

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8
Q

Hepatitis A Immunizations on what schedule?

A

0-1-6 month schedule

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9
Q

Side Effects of Hepatitis A vaccine

A

Usually limited to soreness and redness at injection site

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10
Q

Hepatitis B

A
  • Primarily transmitted percutaneously.
  • Permucosal exposure to infectious blood, blood products or other body fluids.
  • STD
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11
Q

Hepatitis B increases the risk for developing

A

Hepatocellular carcinoma

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12
Q

Prevention of Hepatitis B includes

A
  • Vaccination
  • Recombivax HB/Energix - B given IM at 0-1-6 months
  • HBIG
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13
Q

When can HBIG be given to patients with Hep B?

A

can be given 24 hours post exposure then vaccine series can be started

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14
Q

Hepatitis C

A

Primarily transmitted percutaneously.

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15
Q

Is there a vaccination for hepatitis C?

A

NOPE

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16
Q

Major Risk Factors for Hepatitis C

A
  • Direct percutaneous exposure
  • Transfusion of infected blood products
  • Hemodialysis
  • High risk sexual behavior
  • Organ Transplant
  • Exposure to Blood products (esp. among health care workers)
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17
Q

Hepatitis D

A

Requires the helper function of HBV to replicate.
Cannot survive on its own.
Transmission via sexual activity is much less than B.

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18
Q

Patients who are diagnosed with HDV need be co-infected with

A

HBV since HDV can’t survive without HBV.

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19
Q

Hepatitis E

A

Transmitted via fecal-oral route.

No current serologic test.

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20
Q

Most common mode of transmission of hepatitis E

A

Drinking contaminated water

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21
Q

Hepatitis G Virus

A

Can be transmitted via transfusion.

Poorly characterized Parenteral and sexually transmitted virus.

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22
Q

Hepatitis: Pathophysiology

A
  1. Liver cell damage in hepatic cell necrosis. (D/t inflammation from infection)
  2. Enlargement of Kupffer cell (may block blood flow to liver -> necrosis)
  3. Inflammation may interrupt bile flow (bile will be circulated -> jaundice)
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23
Q

3 Phases of Hepatitis

A
  1. Preicteric Phase
  2. Icteric Phase
  3. Posticteric Phase
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24
Q

Preicteric Phase

A

Lasts 1-21 days.

Period of maximal infectivity for Hepatitis.

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25
Q

Icteric Phase

A

Lasts 2-4 weeks, characterized by jaundice, hepatomegaly, clay colored stools, dark urine.

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26
Q

Posticteric Phase

A

Jaundice is disappearing, however, hepatomegaly remains.

Lasts weeks to months (2-4 months)

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27
Q

Symptoms of Preicteric Phase

A

RUQ pain, anorexia, N/V, constipation, diarrhea, headache, fever, joint pain

28
Q

Fulminant Hepatitis

A

Clinical syndrome that results in severe impairment or necrosis of liver cells and potential liver failure.

29
Q

Fulminant Hepatitis is a complication of

A

HBV accompanied by infection of HDV

30
Q

Diagnostic Findings of Hepatitis

A
  • Transaminases
  • Alkaline Phosphatase (will increase)
  • Serum Protein (will decrease)
  • Serum Bilirubin (will increase)
  • Urinary Bilirubin (will increase)
  • Prothrombin Time (will increase d/t decrease in clotting factors)
31
Q

Collaborative Care/Nursing Therapeutics

A

No specific treatment of therapy for acute viral hepatitis.

Emphasis is on measure to rest the body and assist liver in regenerating.

32
Q

Treatment for Hepatitis

A
  • High caloric (helps regenerate the liver), high protein (to replace protein that has been lost), high carbohydrate and low fat diet (because the liver does not produce enough bile to digest fat)
  • Vitamin Supplement (d/t malnutrition)
  • Rest (reduces the metabolic demands on the liver and promotes cell regeneration)
  • Avoid alcohol intake and drugs (liver is responsible for detoxification therefore, avoid to decrease workload on liver)
  • Antiviral agents
33
Q

What antiviral agent is used for hepatitis?

A

Interferon

34
Q

Therapeutic Effects: Interferon

A
  • Decreases progression of hepatic damage.
  • Reduces serum hepatitis virus, decreases incidence of cirrhosis and hepatocellular cancer.
  • Has antiproliferative action against tumor cell. (Decreases incidence of cancer)
35
Q

What are possible side effects for interferon?

A

Depression.

36
Q

What are other drugs that can be used for hepatitis?

A 
Adenovirus dipivoxil (hepsera)
Vaccination
37
Q

Adefovir dipivoxil

A

Slows down the progression of chronic HBV by interfering with viral replication.

38
Q

How would you treat jaundice?

A

Monitor occurrence
Small frequent feedings (d/t anorexia)
Avoid hot/cold foods (don’t want to overstimulate the release of pepsin’s and liver enzymes)
Adequate fluid 2500-3000/day

39
Q

The greatest risk for transmission of hepatitis A occurs

A

Before clinical symptoms are apparent

40
Q

Fulminant Hepatitis

A

Clinical syndrome that results in severe impairment or necrosis of liver cells and potential liver failure.
A complication of HBV accompanied by co-infection of HDV.

41
Q

Cirrhosis

A

Chronic progressive disease of the liver characterized by extensive degeneration and destruction to the liver parenchyma cells.

42
Q

What are common causes of cirrhosis?

A
  1. Chronic hepatitis C infection

2. Alcohol induced liver disease

43
Q

Nutrition related cirrhosis is caused by

A
  • extreme dieting
  • malabsorption
  • obesity
44
Q

What are other causes of cirrhosis?

A

Environmental factors

Genetic predisposition

45
Q

Pathophysiology of Cirrhosis

A
  1. Chronic inflammation -> necrosis -> fibrosis -> cirrhosis
  2. Decreased function of the liver d/t: hypoxia, poor cellular nutrition and irregular and disorganized liver degeneration.
46
Q

What are the four types of cirrhosis?

A
  1. Alcoholic Cirrhosis
  2. Postnecrotic Cirrhosis
  3. Biliary Cirrhosis
  4. Cardiac Cirrhosis
47
Q

Alcoholic Cirrhosis

A
  • Usually associated with alcohol abuse.
  • Alcohol irritates and damages the liver, starts the process of inflammation and fibrosis making scar tissue.
  • Creates hardened patches d/t liver regeneration.
48
Q

Postnecrotic Cirrhosis

A

Complication of viral, toxic, or idiopathic hepatitis

Broad bands of scar tissue forms within the liver.

49
Q

Biliary Cirrhosis

A
  • Associated with chronic biliary obstruction and infection. (Blockage -> causes bile to backup into the liver -> liver breakdown from the bile -> scarring)
  • Diffuse fibrosis of the liver with jaundice as the main feature.
50
Q

Cardiac Cirrhosis

A
  1. Caused by HF backing up from right atrium to portal vein -> portal vein HTN -> scarring.
  2. Right sided HF also backs up into IVC = congestion = blood backs up to liver and congestion of the cell occurs = impedes its own O2 to the liver cell = damage d/t hypoxia.
51
Q

Early Symptoms of Cirrhosis

A
  • GI disturbances (d/t altered metabolism)
  • Abdominal pain (dull, heavy feeling in RUQ or epigastrum)
  • Fever & fatigue
  • Weight loss
  • Palpable liver
52
Q

Later manifestations of Cirrhosis

A
  • Jaundice (d/t decreased ability to conjugate and excrete bilirubin)
  • Skin Lesions: SPIDER ANGIOMAS, palmar erythema, lesions
  • Hematologic disorders: THROMBOCYTOPENIA, LEUKOPENIA, ANEMIA, COAGULATION DISORDERS (caused by splenomegaly and decreased production by liver)
  • Pruritus
  • Coagulation problems (d/t decreased clotting factors)
  • Endocrine disorders (liver unable to metabolize hormones)
  • Peripheral NEuropathy
53
Q

How does splenomegaly cause thrombocytopenia, anemia and leukopenia?

A

Splenomegaly results form back up of blood from portal vein into the spleen -> over activity of the enlarged spleen results in increased removal of blood cells from circulation.
Anemia d/t inadequate RBC production and survival.

54
Q

Complications of Cirrhosis

A
  1. Portal HTN
  2. Esophageal Varices
  3. Peripheral Edema
  4. Ascites
  5. Hepatic Encephalopathy
  6. Hepatorenal Syndrome
55
Q

Portal HTN

A

Characterized by increased venous pressure in the portal circulation, as well as splenomegaly, large collateral veins, ascites, systemic HTN and esophageal varices.

READ MORE LATER

56
Q

Esophageal Varices

A

A complex of tortuous veins at the lower end of the esophagus, enlarged and swollen as a result of Portal HTN.

57
Q

Large varices are more likely to

A

Bleed.
Bleeding varices are the most life-threatening complication of cirrhosis.

READ MORE LATER

58
Q

Ascites

A

Accumulation of serous fluid in the peritoneal or abdominal cavity.

READ MORE LATER

59
Q

Hepatic Encephalopathy (coma)

A

Neuropsychiatric manifestation of liver damage r/t increase in ammonia.

READ MORE LATER

60
Q

Hepatorenal Syndrome

A

Characterized by renal failure with advancing azotemia, oliguria and intractable ascites.

READ MORE LATER

61
Q

Collaborative Care/Nursing Therapeutics: Goals for Cirrhosis

A
  1. Relieve discomfort
  2. To have minimal to no complications (ascites, varices, hepatic encephalopathy)
  3. Return to as normal a lifestyle as possible
62
Q

Collaborative Care/Nursing Therapeutics for Cirrhosis

A
  • Rest (promote liver cell regeneration by decreasing metabolic demand)
  • Nutritional Therapy: high calorie (from carbs not protein), vitamin supplements, low CHON

READ MORE LATER

63
Q

Nursing Therapeutics for Ascites

A
  • Na+ restriction
  • Diuretics
  • Fluid restriction in severe ascites
  • Parcentesis (removal of fluid through needle puncture of abdominal cavity)
  • Peritovenous shunt (surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system -> goal is to increase Na and water excretion)
64
Q

Nursing therapeutics for esophageal varices

A

-Avoid alcohol, aspirin, NSAIDS and irritating foods. (May irritate distended veins - DO NOT WANT BLEEDING OR RUPTURE)
-Upper RTI should be treated promptly and coughing should be controlled (can cause rupture)
-Beta blocker (reduces portal venous pressure by decreasing cardiac output)
-Bleeding therapy (first step is to manage airway (risk for aspiration)
READ MORE LATER

65
Q

Nursing Therapeutics for Hepatic Encephalopathy

A

-Protein restriction (ammonia is byproduct of protein breakdown)
-Lactulose
-ABT/Neomycin Sulfate (reduce bacterial flora of the colon)
-Prevent ingestion of blood
READ MORE ON STUDY GUIDE

NURS 313R (18 decks)

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