Hepatitis - GI Flashcards
Etiologies of hepatitis
1) Viral Hepatitis
A, B, C, D, E viruses, rarely: CMV, HSV, EBV
2) Alcoholic hepatitis
3) Drug-Induced or toxic hepatitis
Acetaminophen, Isoniazid, Chlorpromazine, Erythromycin…
4) Ischemic hepatitis (shock liver)
5) Autoimmune
Pathophysiology
-Hepat-itis (inflammation of the liver)
-Hep(A,C,D,E)Viruses are RNA viruses
-Hepatitis B Virus-DNA virus
-Cell mediated immune response is damaging
-Hepatocellular necrosis, scarring
-Inflammatory process may damage liver parenchyma, bile canaliculi
-Hepatocellular regeneration within 48 hours
Progressive liver inflammation & necrosis ->
Fibrosis of liver cells -> Nodular appearance->
Disruption of hepatic blood flow leading to ascites, varices, and GI bleeding->
Loss of detoxifying function of liver leading to hepatic encephalopathy and coagulopathies
Four Phases
INCUBATION—See Chart
PRODROMAL (preicteric)2 weeks after exposure
ICTERIC (jaundice)2-6 weeks
Hepatocellular destruction ensues
RECOVERY 6-8 weeks after exposure
Resolving jaundice, liver enlargement may persist
ACUTE hepatitis - signs and sxs
- Asymptomatic
- Elevated serum aminotransferase levels (LFTs): Usually greater than 500-1000
- Fever, fatigue
- Abdominal pain-RUQ
- Nausea, vomiting
- Loss of appetite
- Clay-colored stools, darker urine
- Joint pain
- Jaundice, rash & pruritus
- Fulminant acute hepatitis: Systemic
Fulminant Acute Hepatitis
- Systemic inflammatory process mostly involving liver
- May damage liver parenchyma, bile canaliculi, or rarely massive hepatic necrosis
May also lead to:
- Obstructive jaundice
- Liver failure
- Intestinal bleeding, cardiorespiratory insufficiency, and renal failure
- Hepatic encephalopathy (Ammonia levels)
- Confusion, stupor, coma
Chronic Liver Disease/hepatitis- Signs and sxs
-Asymptomatic
-Spectrum of illness (chronic)
Hepatitis-> chronic inflammation -> cirrhosis->Hepatocellular carcinoma (HCC)
-Cirrhosis or fatty liver disease
-Gynecomastia
-Hepatorenal Syndrome
-Temporal or proximal muscle wasting
-Spider nevi, caput medusae, esophageal varices
-Palmar erythema, Depuytren’s contractures
-Jugular venous distension: sign of right heart failure and suggests hepatic congestion
-Ascites: Cirrhosis, CHF, nephrosis, cancer
Hepatitis A
-Transmission: Fecal-oral route
-Risk Factors: daycare, group home, foreign travel to endemic areas, MSM, contaminated water sources/ food
-Presentation
Ages < 6 yo, more likely to be asymptomatic
Ages > 50 yo likely to have more complications
Diagnosis
-Serum IgM anti HAV antibodies (detectable 4-6 months), exam, ALT/AST usually > 500
Course
-Generally self limiting, no chronicity
-10-15% may relapse after 6 months after acute illness is resolved
Management
-Supportive, mostly outpatient
-Contact isolation, viral shedding 1 wk post sxs onset
-Avoid EtOH, fatty foods, Meds (ASA)
-Rare few require hospitalization
-Report to health department, MDH
Hep A - Follow-Up
Patient Goals
-Hygiene, STI prevention, Hep B vaccination, ensure contacts vaccinated, EtOH assessment, med use (APAP combined products)
Monitoring
-Minimal– Sxs, hydration, LFTs, IgM to IgG conversion (+/-)
-Vaccine (series of 2 at 6 months apart)
-Immunize after age 1
-92% decline since vaccines in 1995
-Vaccinate those with other hepatitis infections or liver disease
Hepatitis B
Transmission
-Contact with infected corporal fluids via IV drug use, needlesticks, intercourse, infants born to infected mothers-Not breastmilk
Risk Factors
-Asian & Pacific islanders (1/12), household contacts to infected person, hemodialysis patients, MSM, other STIs
-Diagnosis: Hepatitis B surface Antigen (HBsAg) is positive in acute and chronic infections
Course: 25-50% kids 1-5 yo develop chronic HBV & >90% infants, 30-50% over 5 yo develop chronic disease, 15-25% of chronically infected develop progressive liver disease
-Management acutely: Supportive, IVF, pain medications, consult with hepatologist, patient education, report to MDH, close contacts to be notified by patient
HBV therapies
- Recommended that therapy be initiated and monitored by hepatologist. Avoid RESISTANCE!
- Not recommended in children, may induce resistance and not generally effective
- Lamivudine
- Decreases HBV activity and ongoing liver inflammation
- Adefovir
- Resistance to adefovir is less likely compared to lamivudine
- Entecavir
- More potent than lamivudine and adefovir. Resistance uncommon
Hep B Serology
Hep B surface antibody (HBsAb)
- If (+) then immunity established
- If (-) and not infected-IMMUNIZE!
Hep B core antibody (HBcAb)
-If (+)resolved infection, immune, cannot pass on to others or false +
Hep B surface antigen (HBsAg)
- If (+) hep B infection (chronic vs acute TBD)
- If (-) No active HBV infection, not a carrier
HBV carriers
- Hepatologist Referral to establish care
- Annual monitoring by PCP or specialist
- usually asymptomatic
- Liver ultrasound
- Alpha fetoprotein (tumor marker)
- LFTs
- HBV PCR DNA to assess viral load (millions may consider tx)
- LFTs throughout year PRN for symptoms
- If symptoms redevelop: LFTs, Bilirubin, Coags, consider U/S, HBV DNA PCR
Hepatitis C
Risk factors
-IVD, intranasal cocaine use, tattoos, sex with multiple partners, other STDs, or sex with trauma, HIV infection, Baby boomers (Born 1945-1965)
Transmission
-IV drug use, blood
-Controversy over transmission via intercourse
Presentation
-Diagnosis: Positive HCV antibody (serology), then order HCV RNA PCR (Viral load)
-If virus present=Infected
-If viral load not detectable=Resolved infection OR false positive antibody test
-Course: 75-80% develop chronic hepatitis
-20-30% will have sxs of acute hepatitis
-Management: Referral to hepatologist, supportive, antiviral medications based on course of illness
HCV follow-up
- Patient Goals: EtOH/substance assessment prn, engage in pt ed
- Monitoring of treatment/disease
- 25% develop cirrhosis/liver disease
- Leading cause of HCC and need for liver transplant
- 41% of PCPs weren’t clear on interpreting results of viral hepatitides
- No vaccination available
Hepatitis D
Pathophysiology
-HDV is a single stranded RNA virus-needs HBV DNA for replication, incubation ~ 90 days
-Epidemiology: 10 million worldwide
Transmission
-Permucosal, percutaneous, injecting drug users, sexual transmission less common, perinatal transmission is rare
Risk Factors
-IVD, hemophiliacs, HBV infected, multiple sexual partners, MSM, HHC of infected persons, infants born to infected mothers, other STIs
-Presentation—Indistinguishable from HBV infection
-Superinfection: HDV acquired by person with chronic HBV
-Usually development of chronic HDV
-Co-infection: simultaneously acquired, severe acute dz, low risk chronic infection
-Diagnosis: HDV Ag or HDV RNA PCR
-Course: Cannot produce infection in absence of HBsAg, needs HBV DNA for replication
-Management: Supportive, manage HBV infection. Increased risk of liver complications
