Hepatitis Flashcards
What is the route of transmission of Hep A and E?
oral-fecal/traveling to endemic areas (A = ate and E = eat) => both are always acute infections (E and A go away, B and C stay with me)
What is the route of transmission of Hep B and D?
blood, unprotected sex, mother-to-baby => Hep D only seen with Hep B (Hep D virus cannot survive without Hep B)
What are the risk factors for Hep B and D?
unprotected sex and IV drug use
What are the sequelae of Hep B infection?
can be acute (mild) or chronic (depends on age at which Hep B acquired) => risk for cirrhosis (20% in those infected 20 years or more) and hepatocellular carcinoma (2% risk/year)
What are the risk factors for Hep C?
blood (unprotected sex and mother-to-baby extremely rare)
What are the risk groups for Hep C?
IV drug users, health care workers
What are the sequelae of Hep C infection?
85% will have chronic infection => risk for cirrhosis (20% in those infected 20 years or more) and hepatocellular carcinoma (2% risk/year)
What are the clinical manifestations of acute hepatitis?
=> may be completely asymptomatic
=> in severe cases: fatigue, anorexia, weight loss, nausea/vomiting, abdominal discomfort, low grade fever, arthralgia
=> signs: jaundice, scleral icterus, dark urine, pale stool (bile duct unable to drain bilirubin), liver tenderness, hepatomegaly
What are the clinical manifestations of chronic hepatitis?
=> may be completely asymptomatic
=> mild symptoms: fatigue, abdominal discomfort, “fullness”, anorexia
=> severe symptoms (decompensated cirrhosis): jaundice, esophageal varices, palmar erythema, spider angioma, ascites, gynecomastia
How is the diagnosis of cirrhosis made?
histologically (it is not a clinical diagnosis) - tissue will never return to normal
What is the cause of portal HTN with liver disease?
cirrhosis causes resistance to blood flow (scarring makes the liver hard), which increases hydrostatic pressure in the portal vein and an increase in fluids in the abdomen
What causes ascites?
increase in hydrostatic pressure due to cirrhosis, coupled with a decrease in oncotic pressure (3rd space fluid shift)
What is ascites?
extra fluid in the abdomen
How do you test for ascites?
PT seated - will note bulging of lower abdomen (inspection), fluid wave (with palpation), shifting dullness at lower abdomen and tympany above (on percussion) => with PT on side, dullness shifts with gravity
What is caput medusae?
dilation of collateral veins of abdomen with ascites
What is hepatic encephalopathy?
an acute complication of decompensated liver failure - liver is unable to convert ammonia to urea => ammonia accumulates in the system and causes cerebral toxicity
What is the work up for suspected hepatitis?
travel Hx, review risk factors, alcohol consumption, review medications, Hx of diabetes/obesity/hyperlipidemia, LFTs, bilirubin, hepatitis serology (A/B/C), CMV serology, Epstein-Barr serology
What does presence of IgM for Hep A (IgM anti-HAV) indicate?
acute liver disease - especially first 6 weeks after infection => ALT will be elevated, IgG anti-HAV steadily increases
What do the following lab results suggest: (+) anti-HAV IgM, (+) anti-HAV IgG?
acute/active disease (around 5-7 weeks after infection)
What do the following lab results suggest: (+) anti-HAV IgM, (-) anti-HAV IgG?
acute/active disease (early infection - around 1-3 weeks after infection)
What do the following lab results suggest: (-) anti-HAV IgM, (+) anti-HAV IgG?
successful HAV vaccination or natural resolution of Hep A
What is HBsAg?
Hep B surface antigen (protein) - it is the first type of serology detected in the blood after infection => ALWAYS indicates active infection and NEVER found at the same time as surface antibodies (anti-HBs)
What is anti-HBs?
antibodies to the surface antigen of Hep B - indicates resolution of active infection/immunity/successful vaccination => NEVER appears at same time as HBsAg
What is HBcAg?
Hep B core antigen - never found in the blood => triggers the production of core antibodies (IgM anti-HBc, IgG anti-HBc)
What is IgM anti-HBc?
early antibodies to core Hep C antigen => indicates acute infection
What is IgG anti-HBc?
late antibodies to core Hep C antigen => indicates resolution of infection
What is HBeAg?
E antigen - indicates high level of infectivity (correlates with higher Hep B viral load)
What is anti-HBe?
antibody to E antigen - indicates low level of infectivity
What serology do you expect to see with acute Hep B infection?
HBsAg and IgM anti-HBc
What serology do you expect to see with resolution of Hep B infection?
anti-HBs and IgG anti-HBc
What serology do you expect to see with chronic Hep B infection?
HBsAg and IgG anti-HBc
What do the following lab results suggest: (-) HBsAg, (-) anti-HBc, (-) anti-HBsAg?
susceptible to infection - never had Hep B/never vaccinated
What do the following lab results suggest: (-) HBsAg, (+) anti-HBc, (+) anti-HBsAg?
no acute infection/resolved Hep B infection
What do the following lab results suggest: (-) HBsAg, (-) anti-HBc, (+) anti-HBsAg?
PT successfully vaccinated against Hep B (never infected)
What do the following lab results suggest: (+) HBsAg, (+) anti-HBc, (+) anti-HBc IgM?
acute/active infection (both anti-HBsAg and IgM are +)
What do the following lab results suggest: (+) HBsAg, (+) anti-HBc, (-) anti-HBc IgM, (-) anti-HBsAg?
chronic active infection => antibodies to surface antigen never develop
What does the following lab result suggest: (-) anti-HCV?
susceptible/never infected with Hep C
What does the following lab result suggest: (+) anti-HCV?
active infection with Hep C => perform HCV RNA
What do the following lab results suggest: (+) anti-HCV, (+) HCV RNA?
active infection with Hep C
What do the following lab results suggest: (+) anti-HCV, (-) HCV RNA?
Hep C resolved spontaneously or successfully treated
How is acute viral hepatitis treated (Hep A or B)?
supportive: anti-emetics, adequate hydration, adequate nutrition, AVOID alcohol (no level is safe), avoid steroids and high-carb/low-protein diets
What is the treatment for chronic Hep B?
oral direct antiviral therapy => only PTs with HBeAg and high viral load should be treated
What is the goal in treatment for chronic Hep B?
suppression of Hep B viral replication (low Hep B viral load and HBeAg seroconversion) => Hep B is inserted into the human genome and can never be eradicated - Tx can take 4-5 years
What is the treatment for chronic Hep C?
oral direct antiviral therapy - treatment and duration based on Hep C genotype => all PTs with active Hep C infection can benefit, except those with life expectancy < 12 months
What is the goal in treatment for chronic Hep C?
achieve sustain viral load suppression (> 6 months) => Hep C is not inserted into the human genome and can be cured
What is the Tx for compensated cirrhosis?
surveillance for HCC every 6-12 months (via ultrasound), screen for esophageal varices, avoidance of alcohol (no safe level), immunizations (Hep A/B, pneumococcal, influenza), acetaminophen < 2 g/day, high-caloric/small meals => avoid aspirin and other NSAIDs (risk for bleeding and renal failure)
What is the Tx for decompensated cirrhosis?
=> esophageal varices - non-selective beta-blockers (propranolol)
=> acites - diuretics (spironolactone) and sodium restriction
=> hepatic encephalopathy - lactulose (acidifies stool/decreases absorption of ammonia)
Who should be screened for Hep C (anti-HCV)?
=> individuals born 1945-1965, regardless of risk factors
=> individuals with risk factors: IV drug users, hemodialysis PTs, HIV-infected individuals, MSM, abnormal liver enzymes
Who should be screened for Hep B (HBsAg, IgM anti-HBc)?
=> all pregnant women (every pregnancy)
=> individuals with risk factors: IV drug users, hemodialysis PTs, HIV-infected individuals, MSM, abnormal liver enzymes
Who should receive vaccination for Hep A (2 doses)?
travelers to endemic areas, MSM, drug users, PTs with chronic liver disease
Who should receive vaccination for Hep B (3 doses)?
IV drug users, multiple sexual partners, MSM, healthcare workers, PTs with chronic liver disease, PTs with DM ages 19 to 59 years
What is post-exposure prophylaxis for Hep A?
close household contacts/sexual contacts (during outbreaks) => healthy adults < 40 YO (vaccine - 2 doses) and healthy adults >= 40 YO (HAIG, followed by vaccination)
What is post-exposure prophylaxis for Hep B?
percutaneous exposure/sexual contacts => HBIG and Hep B vaccine
What should be the next step in management of a patient with elevated liver enzymes (ALT/AST more elevated than alkaline phosphatase and ALT more elevated than AST)?
#1 - more detailed Hx #2 - repeat LFTs (ALT/AST can be elevated in healthy individuals) #3 - viral hepatitis panel #4 - albumin, coagulation studies (to check liver function)
Which tests should be included in a viral hepatitis panel?
anti-HAV (IgG/IgM), HBsAg, anti-HBc (IgM), anti-HCV
What is the next best step in management of a patient with (+) anti-HCV?
HCV RNA (check viral load), HCV genotype (if HCV RNA is +), screening for HIV, liver ultrasound (to assess for fibrosis)
What is the dietary recommendation for patients with acute hepatitis A?
frequent, small, high-calorie meals - PTs typically have poor oral intake (due to nausea - may need to provide anti-emetics) and high catabolic rate => low-protein diet should be discouraged (due to decreased protein production [inflamed liver produces less protein] and increased protein demands [for liver regeneration and antibody production])
