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Clin Med III Exam 2 > Hepatitis/Liver Disease > Flashcards

Hepatitis/Liver Disease Flashcards

1
Q

Workup for liver disease

A

US!
CBC w/ diff & PT/INR (anemia, platelets, albumin, bilirubi, AST, ALT, ALP)
Acute Hep panel
TSH
Iron/TIBC and Ferritin (hereditary hemochromatosis)
AMA + IgM (PBC) - autoimmune destruction of bile ducts
anti-trypic & phenotype (alpha-1-antitrypsin deficiency)
TTG, IgA (celiac)
Ceruloplasmin (wilson’s) +/- 24 hr copper
ANA, ASMA, LKMA, Anti-LC1, Anti SLA/LPA, IgG (autoimmune hepatitis)
HIV, CMV, mono – in those hospitalized where everything else is normal

consider sepsis, rhabdo

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2
Q

Ceruloplasmin

A

Wilson’s disease

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3
Q

TTG, IgA

A

celiac

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4
Q

Iron, TIBC, ferritin

A

hereditary hemochromatosis

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5
Q

AMA, IgM

A

PBC

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6
Q

AST/ALT levels:

A 
Normal: <30-40
Cirrhosis: 30-100
Chronic Hep B/C: 40-150
EtOH: 100- 800
Hep A/B/C acute: 300-3,000
Shock liver or acetaminophen toxicity: >1000 - 10,000
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7
Q

Most common liver disease in US

A

NAFLD (nonalcoholic steatohepatitis 2nd)

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8
Q

Abnormal LFTs for liver disease

A

Hepatocellular pattern (<10x ULN)
Increased ALT & AST (liver transaminases)
+/- elevated ALP (NASH)

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9
Q

General guidelines for interpreting aminotransferases

A

AST: ALT > 2 = Alcoholic Liver Disease (ALD)

ALT > AST = NASH (rario usu. <1), acute or chronic viral hepatitis

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10
Q

Cholestatic pattern of LFT

A

increase in ALP/GGT

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11
Q

NAFLD aka

A

fatty liver
hepatic steatosis
Non-alcholic steatohepatitis (NASH) - fatty liver WITH inflammation of liver w/ hepatocyte injury

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12
Q

NASH

A

fatty liver w/ inflammation of liver w/ hepatocyte injury
Worse prognosis as higher risk of developing fibrosis & cirrhosis

Bx GOLD STANDARD but not often used

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13
Q

what is considered non-alcoholic

A

<20 g ETOH/day (less than 2-3 drinks/day)

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14
Q

Subtypes of NAFLD

A

Isolated Steatosis (NAFL) - w/o injury of fibrosis of hepatocytes on bx; risk of progression to cirrhosis is MINIMAL

NASH - fatty liver + inflammation = hepatocyte injury; bx +/- fibrosis; risk of PROGRESSION of fibrosis, cirrhosis is SIGNIFICANT

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15
Q

More likely to progress to cirrhosis

A

NASH

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16
Q

NAFLD/NASH are associated w/ increased death concurrent w/

A

CVD

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17
Q

Risk factors for NAFLD

A 
• Abdominal Obesity
• DM2 (insulin resistance)
• Hyperlipidemia (high TG and Low HDL) 
• Metabolic Syndrome* 
others (not important)
• Genetic Factors (PNPLA3, TM6SF2)
• Age
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18
Q

Strongest predictor of NAFLD

A

metabolic syndrome

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19
Q

Symptoms of NAFLD/NASH

A

asymptomatic
fatty infiltration of imaging
no significant ETOH hx

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20
Q

Liver bx for NAFLD/NASH

A

combo of steatosis and inflammation +/- fibrosis (rarely get– get fibroscan or MRE instead)

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21
Q

Labs for NASH

A 
hepatocellular pattern
mild ALT/AST (rarely >300)
Normal albumin, bilirubin, INR
Ferritin elevated (marker of inflammation)
HLD (lipid panel)
Glucose (elevated of dx of DM2)
ALP elevated in 1/3 (GGT elevated)
\+/- weakly positive autoimmune factor (bx to confirm)
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22
Q

Marker of inflammation

A

ferritin

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23
Q

Management for NASH

A

exclude other causes of elevated LFT

order Fibroscan/calculate FIB-4

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24
Q

Tx for NASH

A 
exercise &amp; weight loss (main tx!!!!)
Minimize ETOH and CVD risk factors
Control DM and HLD (statins ok)
Monitor LFT/Liver tests after implementation of management
Vaccinate Hep A and Hep B if not immune
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25
Q

Liver bx use for NASH

A

confirm dx (before tx w/ meds)
exclude concomitant liver disease
assess degree

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26
Q

What is hereditary hemochromatosis?

A

Genetic mutation results in increased GI absorption of iron → leads to accumulation of iron in the liver, pancreas, heart, adrenals, testes, pituitary, skin & kidney

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27
Q

Clinical findings for hereditary hemochromatosis

A

family hx or incidentally note increased AST/ALT
No specific sx (fatigue, malaise, RUQ discomfort)

Late sx (4th-5th decade): hepatomegaly, hepatic insufficeincy, cirrhosis, DM, impotence, arthralgia (2nd/3rd MCP), bronze pigment of skin, cardiomegaly w/wo CHF

Bronze DM: Triad of DM, bronze pigment of skin, cirrhosis

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28
Q

Bronze DM

A

Dm
Bronze pigment of skin
Cirrhosis

Associated w/ hereditary hemochromatosis

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29
Q

Hereditary hemochromatosis most common in

A

caucasians of Northern european origin

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30
Q

Labs for hereditary hemochromatosis

A 
elevated LFT (AST, ALT, ALP); modest
Serum Fe &amp; TIBC &amp; ferritin (Fe/TIBC = Transferrin saturation)
- TS 45+ and/or Ferritin >200 (men), >150 (women) --> proceed to GI (HFE mutation analysis)
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31
Q

Tx for hereditary hemochromatosis

A

Therapeutic phlebotomy

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32
Q

Dx of hereditary hemochromatosis

A

genetic testing +/- liver bx

after finding TS >45, or Ferrin >200 (men), >150 (female

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33
Q

Tx for hereditary hemochromatosis

A
  • Avoid Vit C and iron supplements
  • Avoid uncooked shellfish especially oysters ( w/ iron testing elevated)
  • Avoid ETOH
  • Regular phlebotomy*** (usu. managed by hematologist )
  • Risk of cirrhosis (increased with ETOH or other liver disease)
  • w/ cirrhosis screen q 6 months (US +/- AFP)
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34
Q

When to screen for hereditary hemochromatosis

A

HFE genotype & iron testing in 1st degree relatives

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35
Q

Who to screen for HH

A

Elevated Liver tests (AST/ALT) Abnormal iron studies
First degree relative dx with HH
Evidence of liver disease* Suggestive symptoms of HH

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36
Q

Wilson’s disease: what is it?

A

auto recessive mutation
Genetic defect results decreased excretion of copper into bile and accumulation of copper in liver

Once the liver’s capacity for copper is exceeded, copper is released into the bloodstream → accumulates in brain, cornea, joints, kidney, heart, and pancreas

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37
Q

Clinical findings of wilson’s disease

A

age 3-55
hepatic, neuro and psych manifestations (tremor, dysarthria, incoordination/ataxia, parkinsonism, personality/behavior changes)
KAYSER-FLEISCHER RING + neuro manifestations = PATHOGNOMONIC

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38
Q

Pathognomonic for wilson’s

A

kayser-fleischer ring + neuro sx

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39
Q

Kayser-Fleisher ring

A

Fine pigmented granular deposits in the cornea (brownish/gray-green)

Get optho exam if WD is suspected

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40
Q

Dx of WD

A 
Mild elevation of AS/ALT
ALP normal or LOW
SERUM CERULOPLASMIN (reduced in WD - copper carrying protein) <5 ug/dl
Opto eval (K-F)
24-hour urine copper (increased)

Dx confirmed w/ liver bx +/- molecular testing

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41
Q

Tx for WD

A

chelating agents

D-penicillamine and trientine

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42
Q

Severe alpha-1-antitrypsin iis considered

A

<11 micromole/L

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43
Q

Risk w/ alpha-1-antitrypsin deficiency

A

severe lung disease
chronic liver disease

  • increase w/ cigarette smoking and onset is accelerated
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44
Q

infant/children presentation w/ alpha-1-antitrypcin deficiency

A

severe liver disease

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45
Q

When to suspect Alpha-1-antitrypsin deficiency

A

non-smoker w/ emphysema <45 YO
neonatal cholestasis
childhood cirrhosis

46
Q

Who to screen for alpha-antitrypsin

A

Emphysema

  • less than 45 YO
  • non smoker/minimal smoker
  • predominant basilar changes on CXR

Adult onset asthma
Clinical findings or hx of unexplained chronic liver disease (elevated LFTS, cirrhosis)
Family hx of emphysema/liver disease
Hx of panniculitis (skin manifestation)

47
Q

Panniculitis associated w/

A

a1 anit-tryspin deficiency

48
Q

Dx for a1 anti-trypsin

A

mildly elevated AST/ALT
Serum a1-antitrypsin (decreased)
a1 antitrypsin phenotype/genotype (MM is “wildtype”= normal)

49
Q

Tx for a1 antitrypsin deficiency

A

liver transplant

50
Q

presentation of acute severe liver disease

A

hepatomegaly + tenderness
jaundice
splenomegaly
fever (Rare)

51
Q

Dx for autoimmune hepatitis

A

ANA, ASMA, LKMA (liver-kidney microsomal antibody), LKC-1 (Liver cytosol), IgG

SLA (anti-soluble liver antigen) & anti-liver pancreas antigen (LPA) – IN CHILDREN

AST, ALT 7-10x nml
elevated bili, ALP, PT/INR
albumin decreased

52
Q

Management of autoimmune hepatitis

A

Prednisone + Azathioprine (Imuran)
- continue until remission (normal LFT)
- maintain on lowest does of Imuran for continued remission (take off steroid)
- monitor DEXA (steroid use)
Liver transplant in fulminant liver failure

53
Q

Acute viral hepatitis types

A

A and E

54
Q

causes HCC

A

B

55
Q

Fecal-oral route

A

E and A

56
Q

Vaccines available

A

A

B

57
Q

always chronic

A

C

58
Q

Seen concurrently

A

B and D (dependent on B)

59
Q

Fatal in pregnancy

A

E

60
Q

HAV transmission

A

areas w/ inadequate sanitation
Asia & African
homeless
Fecal-oral route

61
Q

Presentation of Hep A

A

children <6 YO: asymptomatic
Adults: symptomatic
- flu like prodrome
- icteric phase (jaundice, dark urine, pruritus, light colored stool)
- hepatomegaly & jaundice most common

62
Q

When does jaundice occur

A

1 week after sx onset

63
Q

Incubation for hep A

A

28 days

64
Q

Labs for hep A

A 
elevated AST/ALT (>1000 or 15x ULN)
inc. bilirubin
inc. ALP
\+ IgM anti-HAV @ onset of sx (acute infection)
IgG anti-HAV = immunity
65
Q

Tx for hep A

A

supportive - fluid + rest; full recovery by 6 months

infection precautions
notify local health dept (post exposure prophylaxis)
Vaccination

66
Q

Who should be hospitalized w/ hep A

A

elderly
multiple comorbidities
underlying liver disease
fulminant liver failure

67
Q

Transmission of hep B

A

blood/blood derived body fluids
Sexual contact
parenteral contact
peri-natal

68
Q

Leads cauing of cirrhosis and hepatocellular carcinoma

A

Hep B

69
Q

S/Sx of acute hep B

A

N/V, RUQ pain, jaundice, malaise, arthralgias, fever
INCREAED BILI, ALP
significantly increased transaminases (ALT >15x)

70
Q

Chronicity of hep B

A

rare in adults

if infected as an infant - most will become chronic

71
Q

Tx for acute hep B

A

supportive- most recover w/ immunity

+/- antiviral (acute liver failure or protracted course)

72
Q

When to hospitilize those w/ acute hep B

A

underlying liver disease
multiple comorbidities
sigsn of liver failure & need to be transferred to transplant center
Older/elderly (more severe >60 YO)

73
Q

Chronic hep B sx

A

usually asymptomatic

74
Q

Labs for chronic hep B

A 
hep B surface Ag positive >6 months
Transaminases eleved (mild or normal)
75
Q

Complications of hep B

A

cirrhosis

HCC

76
Q

When does acute hep B usually become chronic

A

immunocompromised

exposed to infant or child <5 y

77
Q

Labs for hep B

A 
HBsAg: (+) active disease (acute or chronic)
anti-HBs (+) immunity (vaccine or resolved infection)
Anti-HBc: 
- IgM anti-HBc = acute exposure
- IgG anti-HBc = previous exposure
- Total anti- HBc (previous exposure)
HBeAg
anti-HBe
78
Q

HBsAg

A

(+) before onset of sx
detectable in the blood after exposure (1-9 weeks)
Hallmark of active infection (acute or chronic)
HBsAG > 6 mo = chronic

79
Q

How long do you have IgM anti-HBc

A

4 months

80
Q

IgG anti-HBc

A

persists indefinitely

81
Q

Immunity from hep B infection lab results

A

Anti-HBs (+)

Anti-Hbc IgG (+)

82
Q

Immunity from Hep B vaccine labs

A

Anti-HBs (+)

Anti-Hbc (IgG) (-)

83
Q

Use of HBeAg

A

index od disease infectivity
- marker of replication
associated w/ higher levels of HBV DNA

anti-HBe w/ HB e Ag negative = lower levels of virus

84
Q

How to monitor for cirrhosis and imaging

A

Fibroscan

MRE

85
Q

Most common cause of liver transplant

A

Hep C

86
Q

Risk factors for hep C

A 
IV Drug use, tattoos, piercing***
recipient of clotting factors (prior to 1987)
Blood transfusion (prior to 1992)
HIV infection
Hemodialysis
Known exposure (needle stick)
children born to HCV mother
Sexual contact (rare, greater in MSM)
87
Q

Usually becomes chronic

A

Hep C

88
Q

Sx of Hep C

A 
usually asymptomatic (jaundice, fever, fatigue, n/v, RUQ discomfort)
AST/ALT in 100's (< 300)
Bilirubin elevated
(-) Hep C Ab w/ (+) RNA  viral load
OR
(+) Hep C Ab prio had (-) Hep C Ab
89
Q

Dx of chronic Hep C

A

elevated LFR/liver tests (mild)

90
Q

Most common cause of hep C in your 20’s

A

IVDU

91
Q

Who to screen for Hep C

A

persons born 1945-1965 w/o prior assesment of risk **
Blood transfusion/transplant before 1992 or clotting factor before 1987
Person who injected/intra-nasal drugs
long term dialysis
born to HCV mother
Healthcare workers/public safety after exposure
Evidence of chronic liver disease
Annually in those that inject
pregos
(unregulated) tattoo/piercing
incarcerated
HIV infection
Sexually active people about to start PEP

92
Q

Dx of Hep C

A

elevated transaminases

cirrhosis: AST > ALT
acute: in 100’s

93
Q

Tx for Hep C

A 
avoid ETOH
screen for hep A and B -- vaccinate
Screen for HIV
Regular imaging for cirrhosis
Refer to GI
94
Q

Med tx for Hep C

A

oral meds (8-12 weeks in duration)
Direct-acting anit-virals (DAA)
treatable/curable in most pts

95
Q

DNA virus

A

Hep B

96
Q

RNA virus

A

Hep C

97
Q

Seen only in conjunction w/ Hep B

A

Hep D

98
Q

Dx of Hep D

A

delta virus RNA w/ +HBsAg

99
Q

Tx for hep B

A

eradicate Hep B (refer to GI/hepatology)

100
Q

Hep E transmission

A

fecal-oral

101
Q

Presentation of Hep E

A

acute hepatitis sx- similar to hep A

travel to developing countries in last 1-2 months

102
Q

Dx of Hep E

A

Hep E RNA

103
Q

Hep E fatality

A

20% of PREGNANT!

otherwise not severe

104
Q

Tx for Hep E

A

supportive

105
Q

Acute

A

A & E

B,C,D can present acutely

106
Q

Fecal-oral

A

A and E

107
Q

Vaccine

A

(ABle to get vaccine)

A and B

108
Q

Chronic

A

hep C

109
Q

dependent on Hep B

A

D

110
Q

Fatal in pregnancy

A

E

Clin Med III Exam 2 (8 decks)

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