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X Clin Med III Exam 2 > Hepatitis and Liver Disease > Flashcards

Hepatitis and Liver Disease Flashcards

1
Q

AST/ALT levels leading to differentials

A

Toxic or ischemic injury when >1000
Acute Hep C, A, C >300-3000
EtOH
Chronic Hep B and C about 100

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2
Q

Liver disease with highest prevalence in US

A

Nonalcoholic fatty liver disease

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3
Q

Abnormal labs seen in hepatitis

A

Liver tests/LFTs: hepatocellular pattern (<10xULN)
Predominantly increased ALT and AST (liver transaminases)
Maybe elevated ALP (sometimes see in NASH)

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4
Q

What is hepatitis?

A

Inflammation of the liver

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5
Q

General guidelines to interpret increased AST/ALT

A

AST:ALT >2 (alcoholic liver disease)

ALT>AST (NASH and usually ratio is less than 1 and acute/chronic viral hepatitis)

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6
Q

What is a fatty liver?

A

Hepatic steatosis

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7
Q

What is non-alcoholic steatoheatitis (NASH)?

A

Fatty liver with inflammation of liver with hepatocyte injury (higher risk in developing fibrosis and cirrhosis)
Biopsy may show fibrosis (scarring of liver)

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8
Q

What is a non-alcoholic?

A

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

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9
Q

Subtypes of nonalcoholic fatty liver disease

A 
Isolated steatosis (NAFL)
Non alcoholic steatohepatitis (NASH)
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10
Q

What is isolated steatosis?

A

Fatty liver without injury or fibrosis of hepatocytes on bx

Minimal risk of progression to cirrhosis

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11
Q

What should be considered in all pts with NAFLD?

A

Aggressive modification of CVD risk factors (also DM)

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12
Q

Risk factors of NAFLD

A 
Abd obesity
DM2 (insulin resistance)
Hyperlipidemia (high TG and low HDL)
Metabolic syndrome
Genetic factors-PNPLA3, TM6SF2 and age (less common)
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13
Q

Strongest predictor for NASH

A

Metabolic syndrome

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14
Q

What is seen on biopsy for NAFLD/NASH?

A

Steatosis (fat accumulation)
Inflammation and maybe fibrosis
(will see fatty infiltration on imaging)
*gold standard but not necessary for dx

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15
Q

Lab features of NASH

A

Hepatocellular pattern (mild elevation ALT/AST rarely above 300)
Normal bilirubin, albumin, INR
Ferritin elevated (marker for inflammation)
Hyperlipidemia
Glucose (elevated)
ALP elevated in 1/3 and maybe GGT

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16
Q

Cornerstone of management for NASH

A

Exercise and weight loss

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17
Q

How can weight loss help NASH?

A

> 3% improves steatosis
7-10% NASH resolution
10% fibrosis regression seen

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18
Q

Other management for NASH

A

Minimize alcohol, modify CVD risk factors, control DM and HLD, monitor LFTs, vaccinate Hep A and B (check for IgG Ab etc)

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19
Q

What is hereditary hemochromatosis?

A

Hereditary disorder of iron metabolism (genetic mutation results in increased GI absorption of iron and leads to accumulation in liver/pancreas/heart/other organs)

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20
Q

Clinical findings of hereditary hemochromatosis

A

FHx or incidental note increase AST/ALT
Caucasians or northern european origin
Fatigue, malaise, RUQ discomfort

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21
Q

Late manifestations of hereditary hemochromatosis

A

(generally seen in 4th-5th decade)
Hepatomegaly, hepatic insufficiency, cirrhosis, DM, impotence, arthralgia (2nd and 3rd MCPs), bronze pigmentation of skin, cardiomegaly with/without CHF

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22
Q

Bronze diabetes

A

Triad of DM, bronze pigmentation of skin and cirrhosis

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23
Q

Labs in hereditary hemochromatosis

A 
Elevated LFTs (AST, ALT, alk phos)
Screen with serum Fe and TIBC and ferritin (Fe/TIBC equals transferrin saturation)
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24
Q

What to do if transferrin sat >45 and/or ferritin >200 ng/mL in men or >150 ng/mL in women?

A

Proceed to GI (HFE mutation and analysis)

Tx is therapeutic phlebotomy

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25
Q

How to diagnose hereditary hemochromatosis

A

Genetic testing and maybe liver biopsy

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26
Q

Tx for hereditary hemochromatosis

A

Prevent cirrhosis from iron overload
Avoid vit C and iron supplements, uncooked shellfish and EToH
Do regular phlebotomy (therapeutic)
Cirrhosis screen q 6 mos (US and AFP)

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27
Q

What to do for all 1st degree relatives in hereditary hemochromatosis?

A

Genetic screening (HFE genotype) and iron testing

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28
Q

Who do you screen for hereditary hemochromatosis in (AASLD)?

A 
Elevated liver tests (AST/ALT)
Abnormal iron studies
First degree relative dx with HH
Evidence of liver disease
Suggestive sxs of HH
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29
Q

What is Wilson’s disease?

A

Very rare hereditary disorder of copper metabolism
Autosomal recessive
Genetic defect results in decreased excretion of copper into bile and accumulation of copper in liver (when exceeds that it builds up everywhere else)

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30
Q

Findings of Wilsons disease

A

Predominantly hepatic, neuro or psychiatric findings

Neuro/psych sxs (tremor, dysarthria, incoordination, ataxia, parkinsonism, personality changes)

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31
Q

Pathognomonic for Wilsons disease

A

Kayser Fleischer ring and neuro manifestations

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32
Q

What is a Kayser Fleischer ring?

A

Fine pigmented granular deposits in the cornea (brownish or gray-green)
Get ophtho exam

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33
Q

How to diagnose Wilson’s disease?

A

Mild elevation AST/ALT and alk phos (normal or low)
Screen with serum cerulospasmin (low in most pts)– <5 is strong evidence
Can also do 24 urinary copper (increased) after ceruloplasmin
Confirm with liver biopsy adf molecular testing (rare)

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34
Q

Tx for Wilsons disease

A

Chelating agents (D-penicillamine and trientine GI)

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35
Q

Alpha 1 antitrypsin deficiency

A

Genetic disorder with decreased levels of alpha 1 antitrypsin production (protects against tissue injury in lungs or liver)

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36
Q

Severe forms of alpha 1 antitrypsin below 11 micromole/L

A

At risk for severe lung disease and chronic liver disease (increase risk with cig smoking and onset is accelerated)
Infants and kids can present with severe liver disease

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37
Q

When do you want to suspect alpha-1 antitrypsin deficiency?

A

Suspect in non-smoker with emphysema at young age (<45 yrs) or in neonatal cholestasis or childhood cirrhosis

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38
Q

Who to screen in adult population for alpha 1 antitrypsin deficiency?

A

Emphysema in young pt, non/minimal smoker or predominant basilar changes on CXR
Adult onset asthma
Clinical findings or history of unexplained chronic liver disease (LFTs or cirrhosis)
Family hx of emphysema and/or liver disease
Hx of panniculitis

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39
Q

What is panniculitis?

A

Skin manifestation of alpha-1 antitrypsin deficiency

40
Q

Labs in alpha 1 antitrypsin deficiency

A

Mild elevation of AST/ALT
Serum alpha 1 antitrypsin (decreased)–(might be false neg if increased with inflammation) and ALSO get alpha 1 antitrypsin phenotype/genotype

41
Q

Treatment of alpha 1 antitrypsin deficiency

A

Liver transplant (get genetic counseling too)

42
Q

Presentation of autoimmune hepatitis

A

Asymptomatic with elevated liver enzymes
Acute hepatitis and maybe liver failure
Cirrhosis
Non specific sxs (fatigue, malaise, anorexia, pruritus, abd pain, arthritis)

43
Q

What is the presentation of acute severe liver disease associated with autoimmune hepatitis?

A

Hepatomegaly and tenderness

Jaundice, splenomegaly, fever

44
Q

Serological markers for autoimmune hepatitis

A 
Antinuclear antibodies (ANA), anti smooth muscle antibodies (ASMA), liver kidney microsomal antibody (LKMA) or antibody to liver cytosol (LKC-1 IgG) in adults!!
Anti-soluble liver antigen (SLA) and anti-liver pancreas antigen (LPA) in kids!!
45
Q

Other clinical findings depending on severity of autoimmune hepatitis

A

Elevated bilirubin
Elevated ALP
Elevated PT/INR
Albumin (decreased)

46
Q

Important labs for acute autoimmune hepatitis

A 
AST,ALT 7-10 times ULN
ASMA positive (sometimes ANA)
IgG (high titer)
ANA
LKC and maybe LKMA
SLA/LPA (kids)
47
Q

Management for autoimmune hepatitis

A

Depends on disease activity
Prednisone and maybe azothioprine (combo!)–continue until remission (take off ASAP and on lowest dose)
Monitor DEXA
Liver transplant in liver failure

48
Q

What to remember for viral hepatitis

A 
Only AcutE (no chronic)
fEcal-orAl
ABle to get vaccine
C=Chronic (most do)
Hep D is Dependent on hep B
Hep E can be fatal in prEgnancEEEE
49
Q

When do you see acute hepatitis?

A

Areas with inadequate sanitation and limited clean water
Asia and Africa
Fecal or oral transmission (person to person or contaminated food or water)
Recent outbreaks in homeless populations

50
Q

Acute presentation of hep A

A

Children <6 more likely to be asymptomatic (incubation 15-50 days)

51
Q

Prodrome of Hep A

A

Flu like (fever, malaise, anorexa, n/v, RUQ pain)

52
Q

Icteric phase of Hep A

A

Jaundice, dark urine, pruritus, light colored stool (look yellow)
Hepatomegaly and jaundice most common seen

53
Q

Labs in Hep A

A

Increased AST/ALT (>1000 or 15x ULN), increased bilirubin and increased ALP
+IgM anti-HAV at onset

54
Q

Antibodies in hep A

A

IgM anti-HAV is for acute infection (positive for 4 mos)

IgG anti-HAV implies immunity

55
Q

Management for hep A

A

Supportive (fluids, rest, full recovery in about 6 mos)
Infection precautions (hand wash, food prep, chlorine)
Notify local health dept

56
Q

When to hospitalize with hep A

A

Elderly
Multiple comorbidities
Underlying liver disease
Fulminant liver failure

57
Q

Leading cause of cirrhosis and hepatocellular carcinoma worldwide

A

Hep B

58
Q

How to get hep B

A

Blood to blood by body fluids (DNA virus)
Sexual contact
Parenteral contact
Peri-natal transmission

59
Q

Sxs of acute hep B

A

N/v, RUQ pain, jaundice, malaise, arthralgias, fever

60
Q

Labs for acute hep B

A

Increased bilirubin and ALP

Significantly increased transaminases (>15 x)

61
Q

Who becomes chronic in hep b

A

Most infants will (only some adults will)

62
Q

Management of acute hep B

A

Supportive b/c most adults recover with immunity

Antiviral therapy if acute liver failure or protracted course

63
Q

When should you admit to hospital with acute hep B?

A

Underlying liver disease
Multiple comorbidities
Signs of liver failure need to go to liver transplant center
Older or elderly (more severe when >60 YO)

64
Q

What antibodies seen with vaccine or infection?

A

Antibody to surface antigen (anti-HBs)

65
Q

What antibodies are seen in an infection?

A

Exposed to both surface and core antigens so have anti-HBc and Anti-HBs

66
Q

What do you have in current or previous hep b infection?

A

Hep B core antibody

67
Q

Lab findings for chronic hep B

A 
Hep B surface antigen positive > 6 mos
Elevated transaminases (mild or normal)
68
Q

Complications of chronic hep B

A

Cirrhosis

Hepatocellular carcinoma can occur without cirrhosis (higher than any other liver disease)

69
Q

When does Hep B become chronic more often?

A

In immune compromised adult or if exposure as an infant of child <5 YO

70
Q

Labs for hep B

A

Hep B surface antigen (HbSAg)– active disease acute or chronic
anti-HBs–immunity so vaccine or resolved infection
IgM anti-HbC–acute exposure
IgG anti-HbC and total anti-HBc–previous exposure

71
Q

What is the first detectable marker of hep B infection?

A

Hep B surface antigen (HBsAg)- because rises before onset of sxs

72
Q

What is a hallmark of active hep B infection?

A

Hep b surface antigen

73
Q

When might IgM anti-Hbc also be seen?

A

In pt who cleared HBsAg but have not yet developed surface antibody (can persist about 4 months)

74
Q

What indicate end of acute infection phase?

A

Antibody to surface antigen

75
Q

What does hep B vaccine give you?

A

+ anti-HBs/HBsAb

76
Q

Prior infection with resulting immunity to hep B

A

Hep B surface antibody positive

Hep B core antibody IgG (anti-HBc IgG) positive

77
Q

Prior vaccination with resulting immunity to Hep B

A

Hep B surface antibody positive

Hep B core antibody IgG negative

78
Q

What is the hep B e antigen used for?

A

Index of infectivity (marker of replication)

79
Q

What does antibody to hep b e antigen with HB e Ag negative status?

A

Indicates lower levels of HBV DNA

Positive anti-HBe is a predictor of long term clearance o f HBV

80
Q

Chronic Hep B management

A

Vaccinate for hep A

HCC surveillance b/c increased risk

81
Q

Who needs monitoring for HCC?

A

All pts with cirrhosis

Pts without cirrhosis (US and AFP–African Americans?)

82
Q

Transmission of hep C

A

Blood/blood derived body fluids

83
Q

Most common cause of liver transplantation

A

Hep c

84
Q

Risk factors for hep C

A

IV drug use, tattoos and piercings at unregulated facililty
Recipient of clotting factors, blood transfusion, HIV infection, hemodialysis, known exposure, children born to HCV mother, sexual contact

85
Q

Presentation of acute hep C

A

HCV asymptomatic in most cases

Some experience jaundice, fatigue, fever, n/v, RUQ discomfort

86
Q

Labs for hep C

A

AST/ALT usually in 100s (<300)
Bilirubin elevated
- Hep C Ab with + RNA viral load OR + hep C Ab prior had - Hep C Ab

87
Q

Chronic HCV presentation

A

Most develop this and cirrhosis
Most asymptomatic and diagnosed with increased LFTs and liver tests (mild)
Fatigue, wt loss, anorexia, nausea, RUQ discomfort
IVDU!!!

88
Q

Recommendations for hep C screening

A

Persons born 1945-1965 w/o prior assessment of risk is big time!

89
Q

How to diagnose chronic hep C

A

Elevated transaminases (varying ALT patterns–AST can be greater than ALT in cirrhosis)
LFTs can rise and fall
Present late in disease course (signs of cirrhosis)

90
Q

Management for Hep C

A 
Avoid ETOH
Screen for HAV and HBV and vaccinate
Discuss non infected sexual partner testing
Cure
Screen for HIV etc
91
Q

Meds for hep C

A

New oral meds (8-12 wks usually)

Check for co-infection with HBV (meds can reactivate)

92
Q

When do you see Hep D?

A

Only in conjunction with hep B

Acute hepatitis sxs

93
Q

How to diagnose hep D

A

Delta virus RNA with +HBsAg

94
Q

How to manage hep D

A

Eradicate hep B

95
Q

Presentation of hep E

A

Acute hepatitis sxs similar to hep A (travel in last couple months)

96
Q

How to diagnose hep E

A

Hep E RNA

X Clin Med III Exam 2 (9 decks)

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