Hepatitis Flashcards

1
Q

What is the route of transmission of Hep A and E?

A

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)

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2
Q

What is the route of transmission of Hep B and D?

A

blood, unprotected sex, mother-to-baby => Hep D only seen with Hep B (Hep D virus cannot survive without Hep B)

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3
Q

What are the risk factors for Hep B and D?

A

unprotected sex and IV drug use

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4
Q

What are the sequelae of Hep B infection?

A

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)

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5
Q

What are the risk factors for Hep C?

A

blood (unprotected sex and mother-to-baby extremely rare)

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6
Q

What are the risk groups for Hep C?

A

IV drug users, health care workers

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7
Q

What are the sequelae of Hep C infection?

A

85% will have chronic infection => risk for cirrhosis (20% in those infected 20 years or more) and hepatocellular carcinoma (2% risk/year)

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8
Q

What are the clinical manifestations of acute hepatitis?

A

=> 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

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9
Q

What are the clinical manifestations of chronic hepatitis?

A

=> may be completely asymptomatic
=> mild symptoms: fatigue, abdominal discomfort, “fullness”, anorexia
=> severe symptoms (decompensated cirrhosis): jaundice, esophageal varices, palmar erythema, spider angioma, ascites, gynecomastia

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10
Q

How is the diagnosis of cirrhosis made?

A

histologically (it is not a clinical diagnosis) - tissue will never return to normal

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11
Q

What is the cause of portal HTN with liver disease?

A

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

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12
Q

What causes ascites?

A

increase in hydrostatic pressure due to cirrhosis, coupled with a decrease in oncotic pressure (3rd space fluid shift)

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13
Q

What is ascites?

A

extra fluid in the abdomen

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14
Q

How do you test for ascites?

A

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

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15
Q

What is caput medusae?

A

dilation of collateral veins of abdomen with ascites

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16
Q

What is hepatic encephalopathy?

A

an acute complication of decompensated liver failure - liver is unable to convert ammonia to urea => ammonia accumulates in the system and causes cerebral toxicity

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17
Q

What is the work up for suspected hepatitis?

A

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

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18
Q

What does presence of IgM for Hep A (IgM anti-HAV) indicate?

A

acute liver disease - especially first 6 weeks after infection => ALT will be elevated, IgG anti-HAV steadily increases

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19
Q

What do the following lab results suggest: (+) anti-HAV IgM, (+) anti-HAV IgG?

A

acute/active disease (around 5-7 weeks after infection)

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20
Q

What do the following lab results suggest: (+) anti-HAV IgM, (-) anti-HAV IgG?

A

acute/active disease (early infection - around 1-3 weeks after infection)

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21
Q

What do the following lab results suggest: (-) anti-HAV IgM, (+) anti-HAV IgG?

A

successful HAV vaccination or natural resolution of Hep A

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22
Q

What is HBsAg?

A

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)

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23
Q

What is anti-HBs?

A

antibodies to the surface antigen of Hep B - indicates resolution of active infection/immunity/successful vaccination => NEVER appears at same time as HBsAg

24
Q

What is HBcAg?

A

Hep B core antigen - never found in the blood => triggers the production of core antibodies (IgM anti-HBc, IgG anti-HBc)

25
Q

What is IgM anti-HBc?

A

early antibodies to core Hep C antigen => indicates acute infection

26
Q

What is IgG anti-HBc?

A

late antibodies to core Hep C antigen => indicates resolution of infection

27
Q

What is HBeAg?

A

E antigen - indicates high level of infectivity (correlates with higher Hep B viral load)

28
Q

What is anti-HBe?

A

antibody to E antigen - indicates low level of infectivity

29
Q

What serology do you expect to see with acute Hep B infection?

A

HBsAg and IgM anti-HBc

30
Q

What serology do you expect to see with resolution of Hep B infection?

A

anti-HBs and IgG anti-HBc

31
Q

What serology do you expect to see with chronic Hep B infection?

A

HBsAg and IgG anti-HBc

32
Q

What do the following lab results suggest: (-) HBsAg, (-) anti-HBc, (-) anti-HBsAg?

A

susceptible to infection - never had Hep B/never vaccinated

33
Q

What do the following lab results suggest: (-) HBsAg, (+) anti-HBc, (+) anti-HBsAg?

A

no acute infection/resolved Hep B infection

34
Q

What do the following lab results suggest: (-) HBsAg, (-) anti-HBc, (+) anti-HBsAg?

A

PT successfully vaccinated against Hep B (never infected)

35
Q

What do the following lab results suggest: (+) HBsAg, (+) anti-HBc, (+) anti-HBc IgM?

A

acute/active infection (both anti-HBsAg and IgM are +)

36
Q

What do the following lab results suggest: (+) HBsAg, (+) anti-HBc, (-) anti-HBc IgM, (-) anti-HBsAg?

A

chronic active infection => antibodies to surface antigen never develop

37
Q

What does the following lab result suggest: (-) anti-HCV?

A

susceptible/never infected with Hep C

38
Q

What does the following lab result suggest: (+) anti-HCV?

A

active infection with Hep C => perform HCV RNA

39
Q

What do the following lab results suggest: (+) anti-HCV, (+) HCV RNA?

A

active infection with Hep C

40
Q

What do the following lab results suggest: (+) anti-HCV, (-) HCV RNA?

A

Hep C resolved spontaneously or successfully treated

41
Q

How is acute viral hepatitis treated (Hep A or B)?

A

supportive: anti-emetics, adequate hydration, adequate nutrition, AVOID alcohol (no level is safe), avoid steroids and high-carb/low-protein diets

42
Q

What is the treatment for chronic Hep B?

A

oral direct antiviral therapy => only PTs with HBeAg and high viral load should be treated

43
Q

What is the goal in treatment for chronic Hep B?

A

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

44
Q

What is the treatment for chronic Hep C?

A

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

45
Q

What is the goal in treatment for chronic Hep C?

A

achieve sustain viral load suppression (> 6 months) => Hep C is not inserted into the human genome and can be cured

46
Q

What is the Tx for compensated cirrhosis?

A

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)

47
Q

What is the Tx for decompensated cirrhosis?

A

=> esophageal varices - non-selective beta-blockers (propranolol)
=> acites - diuretics (spironolactone) and sodium restriction
=> hepatic encephalopathy - lactulose (acidifies stool/decreases absorption of ammonia)

48
Q

Who should be screened for Hep C (anti-HCV)?

A

=> individuals born 1945-1965, regardless of risk factors

=> individuals with risk factors: IV drug users, hemodialysis PTs, HIV-infected individuals, MSM, abnormal liver enzymes

49
Q

Who should be screened for Hep B (HBsAg, IgM anti-HBc)?

A

=> all pregnant women (every pregnancy)

=> individuals with risk factors: IV drug users, hemodialysis PTs, HIV-infected individuals, MSM, abnormal liver enzymes

50
Q

Who should receive vaccination for Hep A (2 doses)?

A

travelers to endemic areas, MSM, drug users, PTs with chronic liver disease

51
Q

Who should receive vaccination for Hep B (3 doses)?

A

IV drug users, multiple sexual partners, MSM, healthcare workers, PTs with chronic liver disease, PTs with DM ages 19 to 59 years

52
Q

What is post-exposure prophylaxis for Hep A?

A

close household contacts/sexual contacts (during outbreaks) => healthy adults < 40 YO (vaccine - 2 doses) and healthy adults >= 40 YO (HAIG, followed by vaccination)

53
Q

What is post-exposure prophylaxis for Hep B?

A

percutaneous exposure/sexual contacts => HBIG and Hep B vaccine

54
Q

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)?

A
#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)
55
Q

Which tests should be included in a viral hepatitis panel?

A

anti-HAV (IgG/IgM), HBsAg, anti-HBc (IgM), anti-HCV

56
Q

What is the next best step in management of a patient with (+) anti-HCV?

A

HCV RNA (check viral load), HCV genotype (if HCV RNA is +), screening for HIV, liver ultrasound (to assess for fibrosis)

57
Q

What is the dietary recommendation for patients with acute hepatitis A?

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])