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Clin Med III Unit 2 > 4 Hepatitis and Liver Disease > Flashcards

4 Hepatitis and Liver Disease Flashcards

1
Q

AST/ALT 15-32 U/L

A

Normal

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2
Q

AST/ALT 28-75 U/L

A

Cirrhosis

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3
Q

AST/ALT 40-150

A

Hepatitis B/C (chronic)

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4
Q

AST/ALT 150-500 U/L

A

EtOH hepatitis

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5
Q

AST/ALT 300-3000 U/L

A

Hepatitis C, A, and B (acute)

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6
Q

AST/ALT 500-10,000 U/L

A

“Shock Liver” or Acetaminophen toxicity

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7
Q

Most common types of liver disease in the US

A

Non alcoholic fatty liver disease (17-33%)

Non alcoholic steatohepatitis (NASH) (5.7-17%)

Chronic Hep C (1.3%)

Alcoholic Liver Disease (0.8-1.3%)

Hemochromatosis (0.5%)

Chronic Hep B (0.4%)

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8
Q

Hepatitis is a general term for …

A

Inflammation of the liver

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9
Q

Hepatitis is reflected by …

A

Abnormal liver tests

Hepatocellular pattern (<10 x ULN)

Predominantly elevated ALT/AST (liver transaminases)

+/- elevated ALP (1/3 present with elevated ALP in NASH)

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10
Q

AST:ALT ratio of >2 is suggestive of…

A

Alcoholic Liver Disease

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11
Q

ALT>AST is suggestive of…

A

NASH (AST:ALT ratio usually <1)

Acute or chronic viral hepatitis

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12
Q

Liver Diseases and associated liver enzyme elevation:

Hepatocellular Diseases (ALT/AST elevation predominates)

A 
Nonalcoholic fatty liver disease
Genetic hemochromatosis
Wilson’s Disease
Alpha 1 Antitrypsin Deficiency
Autoimmune hepatitis 
Chronic/acute viral hepatitis
Alcoholic Liver Disease
Drug toxicity
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13
Q

Liver Diseases and associated liver enzyme elevation:

Cholestatic Diseases (ALP/GGT elevation predominates)

A 
PBC
PSC
Autoimmune Cholangiopathy
Sarcoidosis
Biliary Atresia
Biliary Obstruction 
Drug Hepatotoxicity
Drug Toxicity
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14
Q

Non-Alcoholic Steatohepatitis (NASH) indicates fatty liver with ______ of liver w/ hepatocyte injury

A

Inflammation

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15
Q

NASH has a worse prognosis than Fatty Liver because

A

Higher risk in developing fibrosis and cirrhosis

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16
Q

Liver disease is considered non-alcoholic if …

A

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

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17
Q

What are the two subtypes of NonAlcoholic Fatty Liver Disease?

A

Isolated Steatosis (NAFL) - fatty liver without injury or fibrosis of hepatocytes on bx

Non-Alcoholic Steatohepatitis (NASH) - fatty liver + inflammation = hepatocyte injury; bx +/- fibrosis

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18
Q

Which type of non alcoholic fatty liver disease is more likely to progress to fibrosis/cirrhosis?

A

NASH - 34-42% will progress, sometimes rapidly (<2 years)

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19
Q

Risk factors for nonalcoholic fatty liver disease

A 
Abdominal obesity
DM2
HLD (High TG and Low HDL)
Metabolic Syndrome*** (strongest predictor)
Genetic factors (PNPLA3, TM6SF2)
Age
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20
Q

Strongest predictive risk factor for NAFLD

A

Metabolic Syndrome

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21
Q

How does NAFLD/NASH present?

A

Generally asymptomatic

Fatty infiltration incidentally seen on imaging

Exclusion of other causes and no significant EtOH Hx

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22
Q

If obtained, a liver bx in a patient with NAFLD/NASH would show…

A

Steatosis (fat accumulation)

Inflammation +/- fibrosis

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23
Q

Lab findings in NASH

A

Hepatocellular pattern
• Mild elevation ALT/AST rarely above 300 IU/Ml

Normal albumin, bilirubin, INR

Ferritin elevated = marker for inflammation

HLD

Glucose elevated (or dx of DM)

ALP elevated in 1/3, GGT frequently elevated too

+/- weakly positive autoimmune factors

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24
Q

What is the main goal in managing NASH patients?

A

STOP PROGRESSION of cirrhosis

Exercise and weight loss are the cornerstones of management

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25
Q

How is body weight reduction associated with histological improvement in NASH?

A

> 3% improves steatosis in 35-100% pts

7-10% NASH resolution (64-90% of patients)

≥10% Fibrosis regression seen (45% of patients)

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26
Q

In addition to weight loss and exercise, what else do you do to manage NASH?

A

Minimize EtOH and modify CVD risk factors

Control DM and HLD (statins OK in compensated cirrhosis)

Monitor LFT after implementation

Vaccinate for Hep A and Hep B if not immune

Liver bx

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27
Q

Is it ok to use statins in patients with NASH?

A

Yes, so long as they aren’t in decompensated state

Ok to use in compensated cirrhosis

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28
Q

Hereditary disorder of iron metabolism —> accumulation of iron in the liver, pancreas, heart, adrenals, testes, pituitary, skin, and kidney

A

Hereditary Hemochromatosis

Due to genetic mutation that results in increased GI absorption of iron

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29
Q

How is hereditary hemochromatosis typically found?

A

Family history or incidentally noted increase in AST/ALT

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30
Q

What ethnic group has the highest incidence of hereditary hemochromatosis?

A

Caucasians of Northern European Origin

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31
Q

Clinical presentation of hereditary hemochromatosis

A

Initially non-specific symptoms - fatigue, malaise, RUQ discomfort

Late manifestations (4th-5th decade of life) - hepatomegaly, hepatic insufficiency, cirrhosis, DM, impotence, arthralgia, bronze pigmentation of skin, cardiomegaly w/ or w/o CHF

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32
Q

What is bronze diabetes?

A

Triad of DM, bronze pigmentation of skin, cirrhosis

Associated with hereditary hemochromatosis

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33
Q

Lab findings for hereditary hemochromatosis

A

Modest elevation of AST, ALT, Alk Phos

Screen with a serum Fe and TIBC and ferritin

If transferrin sat ≥45 and/or ferritin >200ng/mL for men or >150 ng/mL in women, proceed to GI (HFE mutation analysis)

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34
Q

What is the treatment for hereditary hemochromatosis?

A

Therapeutic phlebotomy

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35
Q

How is hereditary hemochromatosis diagnosed?

A

Lab findings confirmed with genetic testing +/- liver biopsy

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36
Q

What is the goal of treatment for hereditary hemochromatosis?

A

To prevent cirrhosis from iron overload

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37
Q

What patient ed should you give in hereditary hemochromatosis?

A

Avoid Vit C and iron supplements

Avoid uncooked shellfish esp oysters

Avoid EtOH

Regular phlebotomy (managed by hematologist)

Risk of cirrhosis —> cirrhosis screen q6 months (US +/- AFP)

Genetic screening and iron testing advised for all 1st degree relatives

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38
Q

Who should be screened for hereditary hemochromatosis?

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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39
Q

Autosomal recessive mutation —> very rare hereditary disorder of copper metabolism

A

Wilson’s Disease

Results in decreased excretion of copper into bile and accumulation of copper in liver

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40
Q

In Wilson’s disease, once the liver’s capacity for copper is exceeded, what happens?

A

Copper is released into the bloodstream —> accumulates in brain, cornea, joints, kidney, heart, and pancreas

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41
Q

Clinical presentation of Wilson’s disease

A

Usually presents between ages 3-55

Predominantly hepatic, neurologic, and/or psychiatric Sx
• Tremor, dysarthria, incoordination/ataxia, Parkinsonism, personality/behavior changes

Kayser-Fleischer ring + neurologic manifestations is PATHOGNOMONIC

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42
Q

Fine pigmented (brownish or gray green) granular deposits in the cornea, detected either by naked eye or ophthalmoscope

A

Kayser-Fleischer rings

Together with neurologic manifestions, is pathognomonic for Wilson’s Disease

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43
Q

How is Wilson’s Disease diagnosed?

A

Mildly elevated AST/ALT with normal/low Alk Phos

Initial screen with serum ceruloplasmin (reduced in 85% of WD)

Opthal eval (for K-F rings)

24 hour urinary copper (increased)

Dx usually confirmed with liver biopsy +/- molecular testing

1st degree relative screening recommended

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44
Q

Treatment for Wilson’s Disease

A

Chelation with D-penicillamine and Trientine

Done by GI with specialized training in hepatology

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45
Q

What should you suspect in a non-smoker with emphysema at a young age (<45) or in neonatal cholestasis or childhood cirrhosis?

A

Alpha-1 antitrypsin deficiency

Genetic disorder characterized by decreased levels of alpha-1 antitrypsin production

46
Q

What is alpha-1 antitrypsin?

A

Protects against tissue injury in the lungs and liver, and less often in the skin

47
Q

Adults with alpha-1 antitrypsin deficiency are at risk for…

A

Severe lung disease and chronic liver disease

Increased risk with cigarette smoking and onset is accelerated

48
Q

Infants and children with alpha-1 antitrypsin deficiency are more likely to present with…

A

Severe liver disease

49
Q

Who should be screened for alpha-1 antitrypsin deficiency?

A

Emphysema in a young (<45) non smoker, esp if predominantly basilar changes on CXR

Adult-onset asthma

Clinical findings or hx of unexplained chronic liver disease
• Current or prior elevation of liver tests
• Patient with cirrhosis +/- portal HTN

Family Hx of emphysema and/or liver disease

Hx of panniculitis (skin manifestation)

50
Q

How do you diagnose alpha-1 antitrypsin deficiency?

A

Mild elevation of AST/ALT
Serum alpha-1 antitrypsin decreased
AND
Alpha-1 antitrypsin phenotype/genotype

Rule out other causes +/- liver bx

51
Q

What is the treatment for alpha-1 antitrypsin deficiency

A

Ultimately, liver transplant

Also, genetic counseling to explain likelihood of disease passing on to children

52
Q

Clinical presentation of autoimmune hepatitis

A

Asymptomatic w/ elevated liver enzymes

Acute hepatitis +/- liver failure

Cirrhosis

Non-specific Sx:
Fatigue, malaise, anorexia, pruritis, abdominal pain, arthritis

53
Q

1/3 of patients with autoimmune hepatitis present with…

A

Severe liver disease

Hepatomegaly/tenderness
Jaundice
Splenomegaly
Fever (low grade)

54
Q

Serological markers for autoimmune hepatitis

A 
More common in adults:
Antinuclear antibodies (ANA)
Anti-smooth muscle antibodies (ASMA)
Liver kidney microsomal antibody (LKMA)
Antibody to liver cytoskeleton (LKC-1), IgG

More common in children:
Anti-soluble liver antigen (SLA)
Anti-liver pancreas antigen (LPA)

55
Q

Lab findings other than serological markers for autoimmune hepatitis

A

Elevated bilirubin

Elevated ALP

Elevated PT/INR

Albumin (decreased)

56
Q

AST/ALT levels in acute autoimmune hepatitis are typically …

A

7-10x ULN

57
Q

How is autoimmune hepatitis diagnosed?

A

Serological markers w/ exclusion of viral/other causes and histologic findings on bx

58
Q

Management of autoimmune hepatitis depends on…

A

Disease activity

Start with Prednisone +/- Azothioprine (Imuran) combination

59
Q

Hep A is common in areas with…

A

Inadequate sanitation and limited access to clean water

High endemic areas include Asia and Africa

60
Q

Route of transmission for Hep A

A

Fecal-Oral

Can be either person to person (lol rim jobs) or contaminated food/water

61
Q

Does Hep A cause chronic infection?

A

Nope

62
Q

How does Hep A present?

A

Children <6 more likely to be asymptomatic

Incubation period 15-50 days (avg 28 days)

Prodrome period (“flu-like”) - fever, malaise, anorexia, N/V, RUQ pain

Icteric Phase - jaundice, dark urine, pruritis, light colored stool (feels better but looks like shit)

Jaundice is usually one week after Sx begin

63
Q

Most commonly observed abnormalities with Hep A

A

Hepatomegaly and Jaundice

64
Q

What do your labs look like for Hep A

A

AST/ALT often >1000 or 15x ULN

Increased bilirubin

Increased ALP

+ IgM anti-HAV (Hep A antibody IgM) at onset of Sx

IgM (+) = acute infection
IgG (+) = implied immunity

65
Q

Management of Hep A is usually…

A

Supportive Care

Fluids/rest, full recovery in nearly all patients by 6 months

66
Q

Who should be hospitalized for Hep A?

A

Elderly
Multiple comorbidities
Underlying liver disease
Fulminant liver failure

67
Q

How do you prevent Hep A?

A

Hand washing
Food handling precautions
Food prep/cooking with temps >185F
Chlorine is effective for inactivation of HAV

Notify local health dept and suggest vaccination of non-immune close contacts

Vaccine available

68
Q

How is Hep B transmitted?

A

Blood/blood derived body fluids

Sharing razors, toothbrushes, etc
Contact with blood/open sores
Sex with infected partner
Parenteral contact (needles)
Peri-natal transmission (mother to child)
69
Q

Hep B is the leading cause of _____ and ________ worldwide

A

Cirrhosis and Hepatocellular carcinoma

70
Q

What is the incubation period for Hep B?

A

45-160 days

71
Q

SSx of Hep B

A

N/V, RUQ pain, jaundice, malaise, arthralgias, fever
Increased bilirubin and alk phos
Significantly increased transaminases (>15xULN)

72
Q

____% of adults but _____% of infants become chronic with Hep B

A

<5%

80-90%

73
Q

How do you manage Hep B?

A

Supportive care - 95% of adults recover with immunity

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

74
Q

Who should be hospitalized for Hep B?

A

Underlying liver disease
Multiple comorbidities
Signs of liver failure —> transplant center (<1%)
Older/elderly (disease more severe in age >60)

75
Q

If you are vaccinated for Hep B, what antigens will you have?

A

anti-HBs (surface antigens)

76
Q

If you’ve been infected with Hep B (current or previous infection), what antigens will you have?

A

Both anti-HBs (surface) and anti-HBc (core)

77
Q

When will you see HepB e antigen?

A

Really high levels indicate current acute infection

78
Q

How does Chronic Hep B present?

A

Most patients asymptomatic

Hep B surface antigen positive if >6 months

Transaminases elevated (very mild or normal)

79
Q

Complications of chronic Hep B

A

Cirrhosis

Hepatocellular Carcinoma (HCC) can occur w/o cirrhosis

80
Q

When does acute Hep B become chronic?

A

In immune compromised adults or if exposure as an infant or child <5 years

81
Q

What labs you gonna get for Hep B?

A

HepB surface antigen (HBsAg)
Antibody to surface antigen (anti-HBs)
Antibody to Hep B core antigen (anti-HBc)
Hep B envelope antigen (HBeAg)
Antibody to Hep B envelope antigen (anti-HBe)

82
Q

(+) HBsAg

A

Indicates active disease (acute or chronic)

83
Q

(+) anti-HBs

A

Indicates immunity (from either vaccine or resolved infection)

84
Q

(+) IgM anti-HBc

A

Indicates acute exposure to Hep B

85
Q

(+) IgG anti-HBc

A

Indicates previous exposure to Hep B

86
Q

(+) total anti-HBc

A

Indicates previous exposure

87
Q

First detectable marker of Hep B infection

A

Hep B surface antigen (HBsAg)

Detectable in the blood 1-9 weeks after exposure

Hallmark of active infection (acute or chronic)

HBsAg (+) >6 months

88
Q

HBsAg (+) >6 months

A

Chronic Hep B infection

89
Q

_____ appears shortly after HBsAg detected

A

IgM anti-HBc

It’s the antibody to hep B core antigen

Indicates acute or recent infection

90
Q

IgM anti-HBc can persist for …

A

~4 months

91
Q

IgG anti-HBc indicates…

A

Prior or resolving infection

Persists indefinitely

92
Q

Hep B vaccine results in positive …

A

Anti-HBs/HBsAb

The body makes antibody to surface antigen after exposed to surface antigen artificially

93
Q

Which lab is used as an index of Hep B infectivity?

A

Hep B e-antigen (HBeAg)

It’s a marker for replication, associated with higher levels of HBV DNA

94
Q

Antibody to Hep B e-antigen (anti-HBe) with HBeAg negative status indicates…

A

Lower levels of HBV DNA

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

95
Q

How is chronic Hep B managed?

A

GI will treat select patients with tenofovir/entecavir

Vaccinate for Hep A

Counsel on prevention precautions

HCC surveillance**
• All patients with or w/o cirrhosis

96
Q

_____% of Hep C patients will develop chronic infection

A

75-85%

97
Q

Most common cause of liver transplant with HCC

A

Hep C

Most common overall is NASH

98
Q

Risk factors for Hep C infection

A

IVDU**, tattoos, piercings at unregulated facility

Recipient of clotting factors prior to 1987

Blood transfusion prior to 1992

HIV infection

Hemodialysis

Known exposure (needle stick)

Children born to HCV infected mothers (rare)

Sexual contact (rare but greater in MSM)

99
Q

How does acute HCV infection present?

A

Usually 14-180 days from exposure

Asymptomatic in 70-85% of cases

10-20% —> jaundice, fatigue, fever, N/V, RUQ discomfort
• AST/ALT usually in 100s (but <300) - A/B much higher
• Bilirubin elevated
• (-) Hep C Ab w/ (+) RNA viral load OR (+) Heb C Ab with prior (-)

100
Q

_____% of Chronic Hep C patients will develop cirrhosis within 20-30 years

A

10-20%

Most are asymptomatic and diagnosed via mildly elevated LFTs

101
Q

Who should be screened for Hep C?

A

Persons born 1945-1965 w/o prior assessment of risk

Persons who received blood transfusion or transplant before July 1992 or clotting factor concentrates before 1987

Persons who have ever used injected or intranasal illegal drugs

Persons on long term dialysis

Children born to HCV positive women

Healthcare workers and public safety workers after needle sticks, sharps, or mucosal exposure to HCV positive blood

102
Q

Diagnosis of Chronic Hep C

A

Elevated transaminases - will see varying ALT patterns
• Can be normal
• In cirrhosis AST can be greater than ALT
• In acute infection, will be in the 100s

LFTs can rise and fall

Most patients present in late stage disease, already with signs of cirrhosis

103
Q

How do yo manage Hep C?

A

Avoid EtOH

Screen for Hep A/B and vaccinate if not immune

Discuss non-infected sexual partner testing

Discuss cure of Hep C does not preclude reinfection

Screen for HIV and other causes of liver disease and refer to GI for Tx

104
Q

Patients with Hep C should receive regular _____ screen

A

HCC - +/- AFP regularly even after cure

105
Q

How is Hep C treated now?

A

Direct Acting Anti-virals (DAA) x 8-12 weeks

Regime based on genotype, previous treatment, cirrhotic vs non-cirrhotic, viral load

106
Q

Hep D is only seen in conjunction with…

A

Hep B - associated with more severe course

Presents with acute hepatitis symptoms

107
Q

How is Hep D diagnosed?

A

Presence of Delta virus RNA with (+) HBsAg

Test for Hep D in all Hep B patients

108
Q

How is Hep D treated?

A

Eradicate Hep B (refer to GI/hepatology

109
Q

How is Hep E transmitted?

A

Fecal-oral

110
Q

How does Hep E present?

A

Acute hepatitis symptoms similar to Hep A

Travel Hx to developing countries in last 1-2 months

Dx: Hep E RNA present

111
Q

______ is fatal in approx 20% of infected pregnant women, otherwise, mostly benign

A

Hep E

More severe and greater mortality in 2nd and 3rd trimester

Clin Med III Unit 2 (6 decks)

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