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Unit 2 Clin Med III > L11: Hepatitis/Liver disease > Flashcards

L11: Hepatitis/Liver disease Flashcards

1
Q

Most prevalent liver disease

A

Nonalcoholic fatty liver disease

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2
Q

Spectrum of AST or ALT values for liver disese

A

Shock liver/acetominophen (10,000) > Acute Hep A, B, C > ETOH> Chronic Hep B and C > Cirrhosis > normal (15-30)

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3
Q

Hepatocellular pattern

A

Increased liver transaminases: ALT + AST

+/- Elevated ALP

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4
Q

AST:ALT>2

A

Alcoholic liver disease

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5
Q

ALT>AST (AST:ALT<1)

A

NASH

Acute or chronic viral hepatitis

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6
Q

Cholestatic pattern

A

Elevated ALP and GGT

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7
Q

Fatty liver aka

A

hepatic steatosis

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8
Q

Non-alcoholic is defined as

A

<20 g ETOH/day (less than2-3 drinks/day)

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9
Q

Non-alcoholic steatohepatitis (NASH)

A

fatty liver with inflammation of liver with hepatocyte injury→ higher risk of fibrosis, cirrhosis→ worse prognosis, progression

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10
Q

Isolated steatohepatitis (NAFLD)

A

fatty liver without injury or fibrosis→ low risk of progression to cirrhosis (but still not considered benign)

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11
Q

Diagnosis of NASH

A

Biopsy is gold standard

but Fibroscan, MRI, MRE used more often

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12
Q

Presentation of NAFLD/NASH

A

Asymptomatic

Fatty infiltration incidentally seen on imaging→ exclude other causes, ETOH

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13
Q

NAFLD/NASH on liver biopsy

A

biopsy is not necessary, but you would see: steatosis, inflammation, +/- fibrosis

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14
Q

NAFLD/NASH labs

A 
Hepatocellular pattern
Mild Elevation ALT + AST <300 IU/ml
Ferritin elevated (53-62%) → inflammation
Hyperlipidemia
Elevated fasting glucose
ALP elevated in ⅓
GGT elevated
\+/- Weakly positive autoimmune factors→ get bx to confirm
Normal albumin, bilirubin and INR
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15
Q

NAFLD/NASH

A 
Exclude all other causes of elevation of liver tests
Order Fibroscan/calculate FIB- 4
Exercise + weight loss (DOC) 
Body weight reduction associated with histological improvement
Minimize ETOH, Modify CVD risk factors
Control diabetes and hyperlipidemia
→ compensated cirrhotic→ Statins
Monitor LFT/liver tests
Vaccinate for Hep A &amp; Hep B

Liver bx→ confirm dx (before tx w/ meds), exclude concomitant liver disease, assess degree

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16
Q

DOC for NAFLD/NASH

A

Exercise + weight loss

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17
Q

Hereditary disorder of iron metabolism→ genetic mutation → increased GI absorption of iron → accumulation of iron in the liver, pancreas, heart, adrenals, testes, pituitary, skin, kidney

A

Hereditary Hemochromatosis

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18
Q

Bronze diabetes

A

Hereditary Hemochromatosis triad:
DM
Bronze pigmentation of skin
Cirrhosis

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19
Q

Hereditary Hemochromatosis presentation

A

Family history or incidental note ↑ AST + ALT (Northern Europeans)
Initially non-specific symptoms
Fatigue, malaise, RUQ discomfort

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20
Q

Hereditary Hemochromatosis labs

A

Elevated Liver tests AST, ALT, Alk Phos
Screen→ serum Fe + TIBC and ferritin
• Fe/TIBC = TS (transferrin saturation)
• TS > 45 and/or ferritin > 200 ng/mL (men) > 150 ng/mL (women) → GI- HFE* mutation analysis

Confirmed with genetic testing +/- liver biopsy

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21
Q

Hereditary Hemochromatosis management

A

Regular phlebotomy (hematologist )

Prevent cirrhosis from iron overload

Cirrhosis screen q 6 months (US +/- AFP)

Avoid Vit C, iron supplements, ETOH

Avoid uncooked shellfish (oysters) while iron testing

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22
Q

Hereditary Hemochromatosis screening guidelines

A

Genetic screen→ HFE genotype
Iron testing

Screen  in pts with:
Elevated Liver tests (AST/ALT)
Abnormal iron studies
First degree relative history
Evidence of liver disease*
Suggestive symptoms
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23
Q

Late Hereditary Hemochromatosis

A 
4th-5th decade
Hepatomegaly
hepatic insufficiency
cirrhosis (+/-complications)
DM
impotence, arthralgia (2nd/3rd MCP joints)
bronze pigmentation of skin
Cardiomegaly with or without CHF 
Bronze Diabetes
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24
Q

Very rare hereditary disorder of copper metabolism
Autosomal recessive mutation→ decreased excretion of copper into
bile→ accumulation of copper in liver→ liver capacity for copper exceeded→ released into bloodstream→ accumulates in brain, cornea, joints, kidney, heart, pancreas

A

Wilson’s Disease

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25
Q

Wilson’s disease presentation

A

Ages 3-55
Hepatic Symptoms
Neurologic/psychiatric symptoms→ tremor, dysarthria, incoordination/ataxia, parkinsonism personality/behavioral changes
Kayser-Fleischer ring→ fine pigmented brownish/gray-green granular deposits on cornea
→ detected by naked eye or ophthalmoscope

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26
Q

Wilson’s Disease treatment

A

Refer to GI with training in Hepatology

Chelating agents:
D-penicillamine
Trientine

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27
Q

Wilson’s Disease labs

A

Mildly Elevated AST/ALT
Alk phos→ normal or low
Reduced <5 ug/dl serum ceruloplasmin (initial screen)
→ plasma copper-carrying protein
Ophthalmologist eval.
Increased 24 hour urinary copper
Confirmed with liver biopsy +/- molecular testing*
First degree relative screening→ genetic analysis

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28
Q

Pathognomonic for Wilson’s Disease

A

Kayser-Fleischer ring + neuro manifestations

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29
Q

D-penicillamine

A

Copper chelating agent

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30
Q

Trientine

A

Copper chelating agent

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31
Q

Severe alpha-1 antitrypsin deficiency

A

Severe→ < 11 umol/L

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32
Q

alpha-1 antitrypsin deficiency presentation

A

non-smoker with emphysema at a young age (<45 years)
neonatal cholestasis
childhood cirrhosis

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33
Q

alpha-1 antitrypsin deficiency screening

A

Emphysema in :
• Young patient (<45 yo)
• Non-smoker or minimal smoker
• Predominant basilar changes on CXR

Adult onset asthma
• Persistent airflow obstructive pattern on post bronchodilator spirometry testing

Clinical findings or history of unexplained chronic liver disease
• Current or prior elevation of liver tests
• Patient with cirrhosis +/- portal HTN (nodular small liver, splenomegaly, low platelets)

Family hx of emphysema and/or liver disease

History of panniculitis (skin)

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34
Q

alpha-1 antitrypsin deficiency labs

A

Mild elevation of AST/ALT
Decreased serum alpha-1 antitrypsin
Alpha-1 antitrypsin genotype (MM=wildtype)

Rule out other causes
+/- Liver biopsy

35
Q

alpha-1 antitrypsin deficiency treatment

A

Liver transplant

Genetic counseling

36
Q

Autoimmune hepatitis presentation

A

Variable
Asymptomatic w/ elevated liver enzymes
Cirrhosis
Non-specific symptoms→ Fatigue, Malaise, Anorexia, Pruritus, Abdominal Pain, Arthritis

Acute severe liver disease→ Acute hepatitis +/- liver failure (⅓)
→ Hepatosplenomegaly
→ Jaundice, Fever

37
Q

Labs for autoimmune hepatitis

A
  • Antinuclear antibodies (ANA) (10%)
  • Anti-smooth muscle antibodies (ASMA) (90%)
  • +/- Liver kidney microsomal antibody (LKMA)
  • antibody to liver cytosol (LKC-1 (30-50%)
  • Anti-soluble Liver Antigen (SLA) → children
  • Anti-liver pancreas antigen (LPA) → children
  • Elevated bilirubin
  • Elevated ALP→ 3x ULN
  • Elevated PT/INR
  • Albumin (decreased)
  • AST/ALT→ 7-10x ULD
  • High IgG titer
38
Q

Autoimmune hepatitis management

A

Refer to Gastroenterologist/ hepatologist
Depends on disease activity

Prednisone +/- Azothioprine (Imuran)
• Continue until remission (normalization of LFT)
• Watch for side effects from steroids/Imuran with labs and follow-up
• Maintain on lowest dose of Imuran for continued remission
• Monitor bone density (DEXA)

Liver transplant→ fulminant liver failure

Vaccinate for Hep A and Hep B

39
Q

Prednisone +/- Azothioprine (Imuran)

A

mainstay of tx for Autoimmune hepatitis

40
Q

Acute hepatitis

A

Hep A, E

41
Q

Fecal-oral hepatitis

A

Hep A, E

42
Q

Vaccines for hepatitis

A

Hep A, B

43
Q

Hepatitis that’s fatal in pregnancy

A

Hep E

44
Q

Hep A background/transmission

A

Inadequate sanitation/clean water
Endemic→ Asia + Africa
Recent homeless outbreaks
Fecal-oral, person to person (oral-anal sex), contaminated food or water

45
Q

Hep A presentation

A 
Acute
Children <6 years asymptomatic
Adults symptomatic
Incubation→ 15-50 days (avg 28) 
Prodrome
Flu-like→ fever, N/V/A, malaise, RUQ pain
Icteric phase 
Jaundice→ 1 week after symptom onset
*Hepatomegaly*, dark urine, pruritus, light colored stool
46
Q

Hep A labs

A

Increased AST/ALT (>1000 or 15x ULN)
Increase bilirubin + ALP

(+) IgM anti-HAV→ acute
(4 months)
(+) IgG anti-HAV→ immunity

47
Q

Hep A management

A

Supportive→ fluids, rest→ recovery in 6 months

Hospitalize→ elderly, multiple comorbidities, underlying liver disease, fulminant liver failure

Infection precautions→ hand washing, food handling, food prep/cook temp >185 F, chlorine/bleach for cleaning

Notify local health department

Non immune contacts→ HAV IgG and/or vaccination

Prevention→ vaccination

48
Q

Hep A patients who get hospitalized

A

Elderly
multiple comorbidities
underlying liver disease
fulminant liver failure

49
Q

Nonimmune contacts can get ____ as Hep A prophylaxis

A

HAV IgG

Vaccine

50
Q

Hep B transmission

A

DNA virus

Blood/blood derived body fluid, sexual, parenteral contact (needle sharing), perinatal transmission during delivery

51
Q

Hep B is a ____ virus, Hep C is a ____ virus

A

Hep B: DNA virus
Hep C: RNA virus

This means Chronic Hep C can be cured/cleared from the body because it doesn’t have DNA intermediates. Chronic Hep B has no cure.

52
Q

Hep B presentation

A 
Incubation→ 45-160 days
Symptomatic (30%)→ N/V, RUQ pain, jaundice, malaise, arthralgias, fever. 
Increased bilirubin, ALP
Increased ALT >15x  
Subclinical (70% adults, 90% children)
Chronic→ <5% adults, most infants
Fulminant hepatic failure (rare)
53
Q

Leading cause of cirrhosis + hepatocellular carcinoma

A

Chronic Hep B

54
Q

Hep B management

A

Supportive→ 95% of adults recover with immunity

+/- antiviral therapy→ acute liver failure or protracted course

55
Q

Hospitalize these patients with Hep B

A

Underlying liver disease
Multiple comorbidities
Older/Elderly→ more severe in age >60 years
Signs of liver failure→ transfer to liver transplant center (rare)

56
Q

Who most commonly gets chronic hepatitis B?

A

Children <5 years

Immunocompromised

57
Q

HBsAg

A

(+) active disease→ acute or chronic
(+) >6 months→ chronic

1st detectable marker of infection→ 1-9 weeks after exposure→ before onset of symptoms
Hallmark of active infection

58
Q

Anti-HBs/HBsAb

A

(+) immune→ vaccine or resolved infection

Appears after disappearance of HBsAG→ indicates end of acute infection phase→ recovery & immunity

Hep B vaccine→ exposure to HBsAg→ (+)

59
Q

Anti-HBc

A

(+) IgM→ acute
(+) IgG→ previous
(+) Total→ previous

IgM→ shortly after HBsAg detected, or HBsAg cleared but Anti-HBs not yet detected
Acute/recent infection→ 4 months

IgG→ prior or resolving infection→ forever

Total= IgM + IgG → prior exposure

60
Q

HBeAg

A

(+) → high viral load, actively replicating
(-) → low viral load

Marker of infection→ higher levels of HBV DNA

61
Q

Anti-HBe

A

(+) → predictor of long term clearance

(+) anti-HBe + (-) HBeAg→ lower levels of HBV DNA

62
Q

HBsAg (-)
Total anti HBc (-)
Anti-HBs (-)

A

Susceptible to HBV infection

63
Q

HBsAg (-)
Total anti HBc (+)
Anti-HBs (+)

A

Immune to HBV by natural infection

64
Q

HBsAg (+)
Total anti HBc (+)
Anti-HBs (-)
IgM anti-HBc (+)

A

Acute infection with HBV

65
Q

HBsAg (+)
Total anti HBc (+)
Anti-HBs (-)
IgM anti-HBc (-)

A

Chronic infection with HBV

66
Q

HBsAg (-)
Total anti HBc (+)
Anti-HBs (-)

A

Interpretation unclear:

  • 1. Resolved infection (most common)*
    2. False (+) anti-HBc→ susceptible
    3. Low level chronic infection
    4. Resolving acute infection
67
Q

HBsAg (-)
Total anti HBc (-)
Anti-HBs (+)

A

Immune to HBV by vaccination

68
Q

most common cause of liver transplantation with hepatocellular carcinoma

A

Hep C

69
Q

Hep C

A

RNA virus
Blood/blood derived body fluid transmission
Most develop chronic infection

Risk: 
IVDU, tattoos, piercings
Transfusion <1992
Received clotting factors <1987
Know exposure (needle stick)
Children born to HVC (+) mother (rare)
Sexual contact (rare, >MSM)
70
Q

Acute Hep C infection

A 
14-180 days post exposure 
Asymptomatic (most) 
Symptomatic→ jaundice, fatigue, fever, nausea, vomiting, RUQ discomfort (10-20%) 
AST/ALT→ elevated, <300 IU/l )
Bilirubin elevated

(-) Hep C Ab with (+) RNA viral load
OR
(+) Hep C Ab prior had (-) Hep C Ab

71
Q

Chronic Hep C

A

Most asymptomatic and diagnosed by ↑LFT/liver tests→ AST + ALT <100
+/-fatigue, wt. loss, anorexia, nausea, RUQ discomfort
Cirrhosis w/in 20-30 years (10-20%) → watch for complications
Many present in 20s due to IVDU

72
Q

Screening for Hep C

A

Born 1945-1965 w/o prior assessment of risk
Received a blood transfusion or organ transplant before July 1992 or clotting factor concentrates before 1987
Injected/intra-nasal illegal drugs
Long term dialysis
Children born to HCV positive women
Healthcare workers and public safety workers after needle sticks, sharps or mucosal exposure to HCV (+) blood
Evidence of chronic liver disease (PE or labs)
IVDU→ annually
Pregnant women
Unregulated Tattoo or body piercings
Past incarceration
HIV infection (annually if they have unprotected sex)
Sexually active persons about to start PEP (post exposure prophylaxis)

73
Q

Hep C labs

A 
Varying ALT patterns:
Normal→ Chronic
Acute→ 100s
Cirrhosis→ AST>ALT
LFTs can rise and fall
74
Q

Hep C management: lifestyle

A

Screen for HAV + HBV→ not immune→ Vaccinate
Non-infected sexual partner testing→ Sexual transmission risk low(<2%, higher MSM)
Avoid ETOH intake
Don’t donate blood, organs, share toothbrushes, nail clippers, razors
Cover open cuts on skin

75
Q

Hep C management: preventing complications/cure

A

Monitor signs/complications of cirrhosis
Check for co-infection with HBV (HBsAg and HB core Ab), other causes of liver disease, HIV
Refer to GI for treatment→ Cure of Hepatitis C does not preclude re-infection
Direct-acting antiviral agents→ oral, 8-16 weeks
Regime based on: genotype, treatment (naïve or experienced), cirrhotic and non-cirrhotic +/- viral load
Treatable and curable in most patients
Resistance Associated Variant Analysis sometimes needed prior to treatment
HVC→ no known intracellular reserves, no DNA intermediates→ impact viral replication→ clearance→ cure

76
Q

Hep C serology basics

A

Hep C Ab takes 8-12 weeks to develop

RNA viral load develops 2-4 weeks after infection

77
Q

(-) Hep C Ab with (+) RNA viral load

A

Acute Hep C infection

78
Q

(+) Hep C Ab prior had (-) Hep C Ab

A

Acute Hep C infection

79
Q

(+) Hep C ab (-) RNA viral load

A

resolved (treated) Hep C

80
Q

Hepatitis D

A

Acute hepatitis symptoms
Seen only in conjunction with Hep B→ Associated with more severe course
Always test Hep B pts
Management→ Eradicate Hepatitis B (refer to GI/hepatology)

81
Q

Hep D serology

A

Delta virus RNA with +HBsAg

Used to diagnose Hep D in Hep B pts

82
Q

Hep E

A

Transmission→ Fecal-oral
Presentation→ Acute hepatitis symptoms
similar to Hep A.
Travel to developing countries in last 1-2 months (highest in East + South Asia).

Fatal in approx 20% of infected pregnant women, <1% otherwise
More severe and greater mortality in 2nd in 3rd trimester
Management→ Supportive

83
Q

Hep E serology

A

Hepatitis E RNA

84
Q

Metabolic syndrome criteria

A 
3 of the 5:
Obesity
HTN
DM
Hyperlipidemia
Hypertriglyceridemia

big risk for NASH/NAFLD

Unit 2 Clin Med III (9 decks)

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