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Nursing II > Hepatitis/Liver > Flashcards

Hepatitis/Liver Flashcards

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1
Q

Liver Functions (8)

A

PDSM (People Drink SO Much)
1. Produces: ABC (Albumin, Bile & coag factors) 2. Detoxes 3.Stores glycogen 4.Metabolizes. Aluminum is a biproduct of food that is metabolized and leaves in urine
It also Maintains blood osmotic pressure (BP)

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2
Q

Where is the liver located?

A

RUQ, has 4 lobes

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3
Q

What is the liver made of?

A

Hepatocytes- liver cells

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4
Q

What makes the liver special?

A

It has a dual blood supply. It receives blood from the hepatic portal vein and the hepatic artery. It therefor has venous & arterial blood.

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5
Q

Jaundice

A

caused by the livers inability to secrete & metabolize bilirubin.

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6
Q

Complications of Portal hypertension?

A

Ascites & gastroesophageal varices

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7
Q

Ascites

A

Third space fluid in abdomen

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8
Q

Gastroesophageal Varices

A

Veins in esophagus expand. varicose veins in esophagus

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9
Q

symptoms of Ascites

A

Increased abdominal girth, weight gain, swelling of the lower extremities

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10
Q

Ascites Treatment

A

Sodium restriction, diuretics, transjugular intraphepatic portosystemic shunt (TIPS), or paracentesis (only temporary removal of fliud)

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11
Q

Ascites pathway

A

cirrhosis of liver

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12
Q

Hepatitis definition

A

inflammation of the liver.

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13
Q

Severe hepatitis can cause?

A

Cirrhosis

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14
Q

3 phases of Jaundice?

A

Preicteric Phase, Icteric Phase, Postictric Phase

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15
Q

Preicteric Phase

A

Occurs prior to onset of jaundice, flulike symptoms, GI upset, n/v, diarrhea, anorexia, pain, h/a, muscle aches, polyarthritis

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16
Q

Icteric Phase

A

Onset of jaundice, pruritis, light colored stools, brown urine, decrease in preicteric symptoms

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17
Q

Postichtric Phase

A

Serum bilirubin & enzymes return to normal, increase in energy, pain subsides, GI symptoms subsides

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18
Q

Hep A transmission

A

fecal-oral

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19
Q

Hep A Incubation period

A

15-45 days

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20
Q

Hep A Risk factors

A

day care, employee/prisions/dd facilities, travel to foreign contries, young adults, person with clotting factor disorders, persons with chronic liver disease

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21
Q

Types of Liver tests

A

Liver scan, liver biopsy, serum anti-body testing, enzyme levels (LDH, ALP etc. when enzymes are elevated this indicates that there is liver cell damage)

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22
Q

Causes of inflammation of the liver

A

Alcohol, toxins, cholestasis, viral infections,

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23
Q

Decrease in Vitamin A causes what?

A

night blindness & skin and eye changes

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24
Q

Decrease in riboflavin causes what?

A

skin & mucus lesions

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25
Q

Decrease in vitamin K causes what?

A

spontaneous bleeding

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26
Q

Chronic Liver disease for Hep A?

A

No

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27
Q

Are there vaccines for hep A & prophylaxis IGG?

A

Yes

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28
Q

Symptoms of Hep A

A

fever, malaise, anorexia, nausea, diarrhea, vomiting, abdominal pain, and jaundice

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29
Q

Management of Hep A?

A

Usually occurs at home unless symptoms are severe

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30
Q

Hep A Antibodies (Anti-HAV)

A

indicates past infection (will have for life)

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31
Q

IgM anti-HAV

A

indicates present acute infection

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32
Q

Transmission of Hep B

A

Parenteral, sexual

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33
Q

Incubation period of Hep

A

30-150 days

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34
Q

Hep B risk factors

A

IV drug use, blood transfusion, young adults,

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35
Q

Chronic liver disease for Hep B?

A

yes & carrier state

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36
Q

Vaccine & prophylaxis for Hep B?

A

Yes,& there are HBIG prophylaxis

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37
Q

S/S for Hep B

A

May be insidious & variable. Abdominal pain, dyspepsia (upper abdominal discomfort), generalized aching, malasie

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38
Q

Treatment goals for hep B

A

to prevent replication of active hep B virus (viral suppression) & reduce the effects of chronic liver inflammation

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39
Q

Lab work-HBsAG

A

surface antigen. If this is positive=you have the disease. Used to screen for Hep B. Can identify it before s/s appear

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40
Q

Lab work - HbeAG

A

An antigen that correlates with viral activity (replication) and is used to determine infectiousness of chronic carriers. Used to monitor effectiveness of treatment.

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41
Q

Lab work- Anti-HBs

A

Used to detect previous exposure to Hep B or to see if you need the vaccine.

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42
Q

Lab work- Anti-Hbe

A

Antibody present in chronic carriers but not indicative of viral replication activity

43
Q

Lab work- Anti-HBc-IgM

A

An antibody to the Hb core antigen & indicates current infection. First antibody that is produced after infection

44
Q

Hep C Transmission

A

Primarily parenteral

45
Q

Hep C incubation period

A

15-180 days

46
Q

Risk factors for Hep C (9)

A

IV drug use, Blood transfusions, multiple sex partners, hemodialysis, Receiving blood products or organ transplant before 1992, receiving clotting factor before 1987, a child born to a mother infected with HCV, past Rx of chronic hemodialysis

47
Q

Chronic liver disease for hep C?

A

questionable

48
Q

Vaccines for hep c?

A

No

49
Q

Leading cause of liver disease and is the primary indication for liver transplant?

A

Hep C

50
Q

Occurs primarily through injection of drugs and thru transfusion of blood products prior to 1992

A

Hep C

51
Q

Most patients with acute or chronic hep C are symptomatic or asymptomatic?

A

Asymptomatic

52
Q

Treatment available for Hep C?

A

Antiviral therapy

53
Q

Lab work -Anti-HCV

A

Is the antibody to hep c & is accurate in detecting chronic state of the disease

54
Q

Hep D Trransmisson

A

Parenteral

55
Q

Hep D incubation period

A

uncertain

56
Q

Risk factors for hep D

A

Only individuals with hep B are at risk for Hep D

57
Q

Chronic Liver Disease for Hep D?

A

Yes

58
Q

Vaccine for Hep D

A

Hep B Vaccine

59
Q

Syptoms of Hep D

A

Similar to Hep B, progress to chronic active hep &Cirrhosis

60
Q

Hep D needs what to replicate?

A

Needs hepatitis surface antigen to replicate

61
Q

Lab work - HDAg

A

is the marker for the delta antigen and is detectable in early infection (Hep D)

62
Q

Lab work - Anti-HDV

A

is the antibody and is present during current or previous infection (Hep D)

63
Q

Hep D Treatment

A

Interferon, Pegylated interferon Alfa for 12 months

64
Q

Hep E transmission route

A

Fecal-oral route

65
Q

Hep E incubation period

A

2-6 weeks

66
Q

Hep E Risk Factors

A

Similar to hep A

67
Q

Chronic liver disease for hep E?

A

No

68
Q

Vaccines for Hep E?

A

None available, hep E very rare

69
Q

Hep E most common in….

A

Developing countries, Asia, middle east, Overcrowded Temporary Housing after Natural Disasters, Refugee camps

70
Q

Hep E persons at risk

A

Older Adolescents, young adults, children infected have mild or no s/s, pregnant women have severe illness: Fulminant hep or dealth, older men in developed countries

71
Q

How Hep E is diagnosed

A

Confirmed only by presence of Antibody to HEV RNA, clinically not distinguishable from other hepititis

72
Q

Hep E treatment

A

resolves on its own, supportive treatment of symptoms

73
Q

Hep G persons at risk

A

Persons with bleeding conditions, Hemophilia, any other requiring large amounts of blood, hemodialysis, needles, infected mom to newborn, sexual transmission

74
Q

Hep G treatment

A

Complex and costly, DNA test, Test development underway: Problem is once antibody is present the virus itself has disappeared

75
Q

Chronic Hepatitis results from?

A

Usually from HBV or HCV

76
Q

Will Chronic Hep progress to cirrhosis?

A

may or may not

77
Q

How to diagnose Chronic Hep?

A

liver biopsy

78
Q

Chronic Hep symptoms

A

Malaise, mild fatigue, hepatomegaly (enlargement of the liver)

79
Q

Hepatoxicity definition

A

The quality of a substance which makes it toxic to liver cells

80
Q

Toxic Hepatitis

A

Hep produced by a hepatotoxin, carbon, tetrachloride, or any various drugs

81
Q

Amanita phalloides

A

Hepatotoxin example

82
Q

Drug-induced Hepatitis

A

most common cause of acute liver failure in the us, ranges from mild to fulminant liver failure

83
Q

Leading cause of drug induced Hepatotoxity

A

acetaminophen

84
Q

Other causes of drug induced Hepatotoxity

A

Anesthetic agents, medications for rheumatic disease, Musculoskeletal disease, antidepressants, psychotrophic medications, anticonvulsants, anti-TB agents

85
Q

When does Hepatotoxity start?

A

First day of use or month later?

86
Q

onset S/S of hepatotoxity (7)

A

Abrupt chills, fever, rash, pruritis, arthralgia, anorexia, nausea

87
Q

Later S/S of hepatotoxity (4)

A

Jaundice, Dark urine, Enlarged & tender liver

88
Q

What do you do if you have hepatotoxity (4)

A

stop medication, evaluate for liver damage, possible referral to liver transplant center, possibly a short course of High Dose of corticosteroids

89
Q

What should the nurse know about the prevention of hepatotoxicity? (3)

A

understand the clearance of medications & observe patients for signs of further deterioration. Must know what meds have a high “first pass effect” thus use meds that are injectable

90
Q

Fulminant Hepatic Failure

A

liver failure

91
Q

Causes of Fulminant Hepatic Failure

A

HAV,HBV,HEV, Acetaminohen overdose

92
Q

Life expectancy for Fulminant Hepatic Failure

A

less than 7 days

93
Q

Mononucleosis

A

Acute infectious disease of lymphatic system

94
Q

Lymph system includes:

A

nodes, spleen, tonsils

95
Q

Mononucleosis cause by what virus

A

Epstien-Barr Virus (EBV) herpes virus group

96
Q

Mononucleosis transmission

A

oral contact, blood transfusion

97
Q

Early symptoms of Mononucleosis

A

Vague, fatigue, strep throat

98
Q

As mononucleosis progresses, s/s include:

A

malaise, fever, sore throat, swollen lymph nodes, anorexia, nausea, petechial rash, enlarged liver and spleen

99
Q

Diagnosis of Mononucleosis (5)

A

Abnormal liver enzymes, s/s, mono spot test to determine lymphocytosis, positive heterophil agglutination test, positive EBV antibody test

100
Q

Mononucleosis treatment

A

nonspecific, treat symptoms: analgesics, bed rest, warm NS gargles, avoid constipation to avoid increasing portal BP, antibiotic for strep throat,

101
Q

Mononucleosis timelife

A

Disease is self limiting 1-3 wks

102
Q

When would steroids be administered to a patient with mononucleosis?

A

if life threatening complications occur ie hepatic disfunction, neuro or thrombocytopenia

103
Q

Portal Hypertension

A

Hepatic veins cant get into liver. Its blocked off so the vein eventually builds up with blood.(hence hypertension)

Nursing II (16 decks)

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