Hepatitis/Liver Flashcards

(103 cards)

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
Decrease in vitamin K causes what?
spontaneous bleeding
26
Chronic Liver disease for Hep A?
No
27
Are there vaccines for hep A & prophylaxis IGG?
Yes
28
Symptoms of Hep A
fever, malaise, anorexia, nausea, diarrhea, vomiting, abdominal pain, and jaundice
29
Management of Hep A?
Usually occurs at home unless symptoms are severe
30
Hep A Antibodies (Anti-HAV)
indicates past infection (will have for life)
31
IgM anti-HAV
indicates present acute infection
32
Transmission of Hep B
Parenteral, sexual
33
Incubation period of Hep
30-150 days
34
Hep B risk factors
IV drug use, blood transfusion, young adults,
35
Chronic liver disease for Hep B?
yes & carrier state
36
Vaccine & prophylaxis for Hep B?
Yes,& there are HBIG prophylaxis
37
S/S for Hep B
May be insidious & variable. Abdominal pain, dyspepsia (upper abdominal discomfort), generalized aching, malasie
38
Treatment goals for hep B
to prevent replication of active hep B virus (viral suppression) & reduce the effects of chronic liver inflammation
39
Lab work-HBsAG
surface antigen. If this is positive=you have the disease. Used to screen for Hep B. Can identify it before s/s appear
40
Lab work - HbeAG
An antigen that correlates with viral activity (replication) and is used to determine infectiousness of chronic carriers. Used to monitor effectiveness of treatment.
41
Lab work- Anti-HBs
Used to detect previous exposure to Hep B or to see if you need the vaccine.
42
Lab work- Anti-Hbe
Antibody present in chronic carriers but not indicative of viral replication activity
43
Lab work- Anti-HBc-IgM
An antibody to the Hb core antigen & indicates current infection. First antibody that is produced after infection
44
Hep C Transmission
Primarily parenteral
45
Hep C incubation period
15-180 days
46
Risk factors for Hep C (9)
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
Chronic liver disease for hep C?
questionable
48
Vaccines for hep c?
No
49
Leading cause of liver disease and is the primary indication for liver transplant?
Hep C
50
Occurs primarily through injection of drugs and thru transfusion of blood products prior to 1992
Hep C
51
Most patients with acute or chronic hep C are symptomatic or asymptomatic?
Asymptomatic
52
Treatment available for Hep C?
Antiviral therapy
53
Lab work -Anti-HCV
Is the antibody to hep c & is accurate in detecting chronic state of the disease
54
Hep D Trransmisson
Parenteral
55
Hep D incubation period
uncertain
56
Risk factors for hep D
Only individuals with hep B are at risk for Hep D
57
Chronic Liver Disease for Hep D?
Yes
58
Vaccine for Hep D
Hep B Vaccine
59
Syptoms of Hep D
Similar to Hep B, progress to chronic active hep &Cirrhosis
60
Hep D needs what to replicate?
Needs hepatitis surface antigen to replicate
61
Lab work - HDAg
is the marker for the delta antigen and is detectable in early infection (Hep D)
62
Lab work - Anti-HDV
is the antibody and is present during current or previous infection (Hep D)
63
Hep D Treatment
Interferon, Pegylated interferon Alfa for 12 months
64
Hep E transmission route
Fecal-oral route
65
Hep E incubation period
2-6 weeks
66
Hep E Risk Factors
Similar to hep A
67
Chronic liver disease for hep E?
No
68
Vaccines for Hep E?
None available, hep E very rare
69
Hep E most common in....
Developing countries, Asia, middle east, Overcrowded Temporary Housing after Natural Disasters, Refugee camps
70
Hep E persons at risk
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
How Hep E is diagnosed
Confirmed only by presence of Antibody to HEV RNA, clinically not distinguishable from other hepititis
72
Hep E treatment
resolves on its own, supportive treatment of symptoms
73
Hep G persons at risk
Persons with bleeding conditions, Hemophilia, any other requiring large amounts of blood, hemodialysis, needles, infected mom to newborn, sexual transmission
74
Hep G treatment
Complex and costly, DNA test, Test development underway: Problem is once antibody is present the virus itself has disappeared
75
Chronic Hepatitis results from?
Usually from HBV or HCV
76
Will Chronic Hep progress to cirrhosis?
may or may not
77
How to diagnose Chronic Hep?
liver biopsy
78
Chronic Hep symptoms
Malaise, mild fatigue, hepatomegaly (enlargement of the liver)
79
Hepatoxicity definition
The quality of a substance which makes it toxic to liver cells
80
Toxic Hepatitis
Hep produced by a hepatotoxin, carbon, tetrachloride, or any various drugs
81
Amanita phalloides
Hepatotoxin example
82
Drug-induced Hepatitis
most common cause of acute liver failure in the us, ranges from mild to fulminant liver failure
83
Leading cause of drug induced Hepatotoxity
acetaminophen
84
Other causes of drug induced Hepatotoxity
Anesthetic agents, medications for rheumatic disease, Musculoskeletal disease, antidepressants, psychotrophic medications, anticonvulsants, anti-TB agents
85
When does Hepatotoxity start?
First day of use or month later?
86
onset S/S of hepatotoxity (7)
Abrupt chills, fever, rash, pruritis, arthralgia, anorexia, nausea
87
Later S/S of hepatotoxity (4)
Jaundice, Dark urine, Enlarged & tender liver
88
What do you do if you have hepatotoxity (4)
stop medication, evaluate for liver damage, possible referral to liver transplant center, possibly a short course of High Dose of corticosteroids
89
What should the nurse know about the prevention of hepatotoxicity? (3)
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
Fulminant Hepatic Failure
liver failure
91
Causes of Fulminant Hepatic Failure
HAV,HBV,HEV, Acetaminohen overdose
92
Life expectancy for Fulminant Hepatic Failure
less than 7 days
93
Mononucleosis
Acute infectious disease of lymphatic system
94
Lymph system includes:
nodes, spleen, tonsils
95
Mononucleosis cause by what virus
Epstien-Barr Virus (EBV) herpes virus group
96
Mononucleosis transmission
oral contact, blood transfusion
97
Early symptoms of Mononucleosis
Vague, fatigue, strep throat
98
As mononucleosis progresses, s/s include:
malaise, fever, sore throat, swollen lymph nodes, anorexia, nausea, petechial rash, enlarged liver and spleen
99
Diagnosis of Mononucleosis (5)
Abnormal liver enzymes, s/s, mono spot test to determine lymphocytosis, positive heterophil agglutination test, positive EBV antibody test
100
Mononucleosis treatment
nonspecific, treat symptoms: analgesics, bed rest, warm NS gargles, avoid constipation to avoid increasing portal BP, antibiotic for strep throat,
101
Mononucleosis timelife
Disease is self limiting 1-3 wks
102
When would steroids be administered to a patient with mononucleosis?
if life threatening complications occur ie hepatic disfunction, neuro or thrombocytopenia
103
Portal Hypertension
Hepatic veins cant get into liver. Its blocked off so the vein eventually builds up with blood.(hence hypertension)