Hepatitis Flashcards

(60 cards)

1
Q

hepatitis

A

Systemic virus that affects the liver
Inflammation of the liver

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2
Q

what are the types of hepatitis?

A

A, B, C

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3
Q

Which types of the most common?

A

B, C

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4
Q

Pathogenesis of hepatitis

A

viral infection
Immune response – inflammatory mediators
Lysis of infected cells
Edema/swelling of tissue
Tissue hypoxia
hepatocyte death

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5
Q

s/sx hepatitis

A

many cases are asymptomatic

Causes abnormal increased LFTs, but not consistent with cell damage within liver

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6
Q

Prodromal phase

A

two weeks after exposure

fatigue, anorexia, malaise, N/V, headache, hyper algesia, cough, low-grade fever

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7
Q

T/F the prodromal phase is highly transmissible

A

True

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8
Q

icteric phase

A

begins with jaundice
2 to 6 weeks, active phase

Dark urine, clay, colored stool, enlarged liver, painful to palpate, fatigue, abdominal pain, persists

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9
Q

Which phase is considered the active phase of hepatitis?

A

Icteric

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10
Q

Recovery phase

A

resolution of jaundice
6 to 8 weeks after exposure, symptoms decrease

Enlarged liver/tender

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11
Q

complications of hepatitis

A

higher mortality in elderly and comorbidities
Chronic hepatitis
Liver cirrhosis
Liver cancer
Fulminate viral hepatitis – acute liver failure

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12
Q

hepatitis A transmission

A

Fecal – oral, IV , sexual
Foodborne illness, poor sanitation

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13
Q

s/sx hepatitis A

A

Acute onset, fever, mild severity

fatigue, fever
N/V/D, pale poop
Stomach pain, no appetite
Dark urine, jaundice

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14
Q

Can hepatitis A develop into chronic hepatitis?

A

no

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15
Q

Prevention of hepatitis A

A

hand hygiene
Vaccine – high risk exposure

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16
Q

hepatitis B transmission

A

IV. Drug use, sexual

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17
Q

is hepatitis B, a acute or insidious onset?

A

Insidious onset, long incubation Period

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18
Q

prevention of hepatitis B

A

Vaccine
Safe sex
Hygiene

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19
Q

hepatitis C transmission

A

IV. Drug use, sexual, mother fetal

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20
Q

T/F hepatitis C is an acute onset

A

False, insidious onset

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21
Q

can hepatitis C become chronic

A

Yes, leads to hepatocellular carcinoma

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22
Q

prevention of hepatitis C

A

Screening blood, hygiene

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23
Q

T/F there is no vaccine for hepatitis C

A

True

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24
Q

Hep A vaccine series

A

two doses, six months apart

All children over one year, high-risk populations

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25
hep B vaccine series
Three doses, four months apart All infants beginning as newborns
26
what are disadvantages of hepatitis treatment?
Prolonged therapy Cost Lots of side effects High relapse
27
Direct acting antiviral therapy
Drug therapy for chronic hepatitis C
28
what is the max Tylenol dosage for chronic hepatitis patients?
2 g per day
29
Cirrhosis
scarring of liver, fibrotic liver disease
30
T/F cirrhosis is reversible
False it is irreversible
31
Patho of cirrhosis
not well understood Structural changes from injury – alcohol/viruses and fibrosis
32
Patho of chronic fibrosis
Obstructive biliary channels and blood flow – jaundice, portal HTN Regeneration interrupted by hypoxia, necrosis, atrophy, and liver failure
33
fibrosis
Infiltration of WBC – leukocytes Release, inflammatory mediators in response to fibrotic process
34
How long does cirrhosis occur?
Slowly over years
35
Causes of fibrosis
Alcohol/metabolites – rate depends on amount present
36
can the removal of toxins reverse fibrosis?
No, but it can slow the progression
37
causes of cirrhosis
Hepatitis B and C Excessive alcohol intake Idiopathic **
38
How does alcoholism affect liver disease?
Inhibits exports from the liver, alterations in metabolism of vitamins and minerals and induces mount nutrition
39
what is the most common type of cirrhosis?
Alcohol cirrhosis
40
alcohol fatty liver
Fatty deposits cause lipogenesis Reversible mild, asymptomatic
41
alcoholic streatohepatisis
Precursor to cirrhosis Inflammation/degeneration of hepatocytes Becomes irreversible Anorexia, jaundice
42
alcoholic cirrhosis
Fibrosis in scarring altering liver structure Irreversible
43
T/F alcoholic streatohepatitis is reversible
False
44
pathogenesis of liver disease
Liver cells destroyed Cells try to regenerate Disorganized process Abnormal growth Poor blood flow/scar tissue Hypoxia Liver failure
45
stages of liver damage
Healthy liver Fatty liver Liver fibrosis Cirrhosis
46
s/sx liver disease
G.I. disturbances– N/V, anorexia, gas, change in bowel habits Fever, weight, loss, palpable liver
47
late s/sx of liver disease
jaundice, peripheral edema Endocrine problems Hematologic problem- anemia, bleeding Decreased albumin and protein ascites, skin lesions– spider Encephalopathy Esophageal and Anorectal varices
48
portal HTN
Resistant portal blood flow – varices and ascites
49
causes of portal HTN
systemic hypotension Vascular underfilling Stimulation of RAAS system Plasma volume expansion Increase cardiac output
50
What causes portal HTN to go from asymptomatic to symptomatic?
complications variceal hemorrhage, ascites, hepatorenal syndrome, cardiomyopathy, peritonitis
51
Treatment for portal HTN
Liver transplant
52
what is the primary driver to diagnose hepatic encephalopathy?
Level of consciousness
53
what determines the severity of hepatic encephalopathy?
The grade – minimal, one, two, three, four
54
T/F ammonia levels correlate with hepatic encephalopathy
True, toxins build up in the brain
55
Cause of fulminant/acute liver failure
Most common– acetaminophen overdose
56
T/F acute liver failure is caused by cirrhosis and fibrosis
False, it is not
57
Patho of acute liver failure
edematous hepatocytes and patchy areas of necrosis Inflammatory cell infiltrates and disrupts liver tissue
58
treatment for acute liver failure
Liver transplant
59
when does acute liver failure occur?
6-8 weeks after viral, hepatitis/metabolic liver disease 5 days to 8 weeks after overdose
60
How can the acetaminophen overdose be treated?
Acetylcysteine