Hepatitis Flashcards
hepatitis
Systemic virus that affects the liver
Inflammation of the liver
what are the types of hepatitis?
A, B, C
Which types of the most common?
B, C
Pathogenesis of hepatitis
viral infection
Immune response – inflammatory mediators
Lysis of infected cells
Edema/swelling of tissue
Tissue hypoxia
hepatocyte death
s/sx hepatitis
many cases are asymptomatic
Causes abnormal increased LFTs, but not consistent with cell damage within liver
Prodromal phase
two weeks after exposure
fatigue, anorexia, malaise, N/V, headache, hyper algesia, cough, low-grade fever
T/F the prodromal phase is highly transmissible
True
icteric phase
begins with jaundice
2 to 6 weeks, active phase
Dark urine, clay, colored stool, enlarged liver, painful to palpate, fatigue, abdominal pain, persists
Which phase is considered the active phase of hepatitis?
Icteric
Recovery phase
resolution of jaundice
6 to 8 weeks after exposure, symptoms decrease
Enlarged liver/tender
complications of hepatitis
higher mortality in elderly and comorbidities
Chronic hepatitis
Liver cirrhosis
Liver cancer
Fulminate viral hepatitis – acute liver failure
hepatitis A transmission
Fecal – oral, IV , sexual
Foodborne illness, poor sanitation
s/sx hepatitis A
Acute onset, fever, mild severity
fatigue, fever
N/V/D, pale poop
Stomach pain, no appetite
Dark urine, jaundice
Can hepatitis A develop into chronic hepatitis?
no
Prevention of hepatitis A
hand hygiene
Vaccine – high risk exposure
hepatitis B transmission
IV. Drug use, sexual
is hepatitis B, a acute or insidious onset?
Insidious onset, long incubation Period
prevention of hepatitis B
Vaccine
Safe sex
Hygiene
hepatitis C transmission
IV. Drug use, sexual, mother fetal
T/F hepatitis C is an acute onset
False, insidious onset
can hepatitis C become chronic
Yes, leads to hepatocellular carcinoma
prevention of hepatitis C
Screening blood, hygiene
T/F there is no vaccine for hepatitis C
True
Hep A vaccine series
two doses, six months apart
All children over one year, high-risk populations
hep B vaccine series
Three doses, four months apart
All infants beginning as newborns
what are disadvantages of hepatitis treatment?
Prolonged therapy
Cost
Lots of side effects
High relapse
Direct acting antiviral therapy
Drug therapy for chronic hepatitis C
what is the max Tylenol dosage for chronic hepatitis patients?
2 g per day
Cirrhosis
scarring of liver, fibrotic liver disease
T/F cirrhosis is reversible
False it is irreversible
Patho of cirrhosis
not well understood
Structural changes from injury – alcohol/viruses and fibrosis
Patho of chronic fibrosis
Obstructive biliary channels and blood flow – jaundice, portal HTN
Regeneration interrupted by hypoxia, necrosis, atrophy, and liver failure
fibrosis
Infiltration of WBC – leukocytes
Release, inflammatory mediators in response to fibrotic process
How long does cirrhosis occur?
Slowly over years
Causes of fibrosis
Alcohol/metabolites – rate depends on amount present
can the removal of toxins reverse fibrosis?
No, but it can slow the progression
causes of cirrhosis
Hepatitis B and C
Excessive alcohol intake
Idiopathic **
How does alcoholism affect liver disease?
Inhibits exports from the liver, alterations in metabolism of vitamins and minerals and induces mount nutrition
what is the most common type of cirrhosis?
Alcohol cirrhosis
alcohol fatty liver
Fatty deposits cause lipogenesis
Reversible
mild, asymptomatic
alcoholic streatohepatisis
Precursor to cirrhosis
Inflammation/degeneration of hepatocytes
Becomes irreversible
Anorexia, jaundice
alcoholic cirrhosis
Fibrosis in scarring altering liver structure
Irreversible
T/F alcoholic streatohepatitis is reversible
False
pathogenesis of liver disease
Liver cells destroyed
Cells try to regenerate
Disorganized process
Abnormal growth
Poor blood flow/scar tissue
Hypoxia
Liver failure
stages of liver damage
Healthy liver
Fatty liver
Liver fibrosis
Cirrhosis
s/sx liver disease
G.I. disturbances– N/V, anorexia, gas, change in bowel habits
Fever, weight, loss, palpable liver
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
portal HTN
Resistant portal blood flow – varices and ascites
causes of portal HTN
systemic hypotension
Vascular underfilling
Stimulation of RAAS system
Plasma volume expansion
Increase cardiac output
What causes portal HTN to go from asymptomatic to symptomatic?
complications
variceal hemorrhage, ascites, hepatorenal syndrome, cardiomyopathy, peritonitis
Treatment for portal HTN
Liver transplant
what is the primary driver to diagnose hepatic encephalopathy?
Level of consciousness
what determines the severity of hepatic encephalopathy?
The grade – minimal, one, two, three, four
T/F ammonia levels correlate with hepatic encephalopathy
True, toxins build up in the brain
Cause of fulminant/acute liver failure
Most common– acetaminophen overdose
T/F acute liver failure is caused by cirrhosis and fibrosis
False, it is not
Patho of acute liver failure
edematous hepatocytes and patchy areas of necrosis
Inflammatory cell infiltrates and disrupts liver tissue
treatment for acute liver failure
Liver transplant
when does acute liver failure occur?
6-8 weeks after viral, hepatitis/metabolic liver disease
5 days to 8 weeks after overdose
How can the acetaminophen overdose be treated?
Acetylcysteine
