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1. Clin Med III > 2- Hepatic/liver Disease > Flashcards

2- Hepatic/liver Disease Flashcards

1
Q

An AST/ ALT > 1.5 (but traditionally ≥ 2) indicates what condition?

A

Alcoholic liver disease

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2
Q

An AST/ ALT < 1.0 indicates what condition?

A

NASH (often acute or chonic viral hepatitis)

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3
Q

An AST/ ALT > 10 indicates what condition?

A

Cirrhosis

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4
Q

An ALT/ AST < 1.0 indicates what condition?

A

Fatty liver

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5
Q

What conditions are indicative of low to high ALT values? (ranging from ~40 to 10,000)

A

Hepatitis B + C chronic → EtOH → Hepatitis C, A + B acute → “shock liver” or acetaminophen toxicity

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6
Q

What is defined as inflammation of the liver by fat deposition?

A

Steatohepatitis

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7
Q

Predominantly elevated ALT and AST (liver transaminases) indicate what?

A

Hepatocellular pattern

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8
Q

What is the spectrum of diseases included as part of NAFLD (non- alcoholic fatty liver disease)?

A

NAFL → NASH → NASH cirrhosis

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9
Q

How is NAFL (aka isolated steatosis) defined?

A

Fatty liver without injury or fibrosis of hepatocytes on bx

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10
Q

How is NASH defined?

A

Fatty liver + inflammation = hepatocyte injury

Risk of progression of fibrosis, cirrhosis is significant

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11
Q

The following are RFs for what condition?

Abd obesity, DMT2, hyperlipidemia, metabolic syndrome, PCOS

A

NAFLD

(metabolic syndrome = strongest predictor)

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12
Q

How does NAFLD typically present clinically?

A

Asx, often incidental finding

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13
Q

What tools are used to aid in identifying those with NAFLD that are at risk for advanced fibrosis?

A

NAFLD fibrosis score, fibrosis-4 index, vibration-controlled transient elastography (VCTE)

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14
Q

On fibroscan (VCTE) you note ≥ 5% liver fat on imaging or liver bx, US notes fat present on the liver, labs show hepatocellular pattern with elevated ferritin, lipids, and glucose. What are you concerned for?

A

NAFLD

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15
Q

When is it recommended to obtain a liver biopsy in pts with NAFLD?

A

Increased risk for advanced fibrosis, metabolic syndrome/ elevated LFTs, need to r/o competing etiologies

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16
Q

What conditions must be r/o when evaluating suspected NAFLD?

A

Significant alcohol consumption, competing etiologies for hepatic steatosis, coexisting causes of chronic liver disease (CLD)

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17
Q

Pts with NAFLD are at a high risk for what?

A

CV morbidity/ mortality

(aggressive modification of CVD RFs should be considered)

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18
Q

What is used in the treatment of dyslipidemia in patients with NAFLD and NASH, and when should this treatment be avoided?

A

Statins; avoided in pts with decompensated cirrhosis

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19
Q

What is considered the “cornerstone” of NASH management?

A

Exercise and weight loss

(should also minimize EtOH, control underlying conditions, vaccinate)

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20
Q

What is the relationship between body weight reduction and histological improvement of NASH?

A

>3% improves steatosis

7-10% NASH resolution

≥10% fibrosis regression

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21
Q

What are the hereditary liver disorders? (3)

A

Hereditary hemochromatosis, alpha-1 antitrypsin deficiency, Wilson’s disease

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22
Q

What is hereditary hemochromatosis?

A

Hereditary disorder of iron metabolism

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23
Q

What is the pathophysiology of hereditary hemochromatosis?

A

Genetic mutation → increased GI absorption of iron → accumulation of iron in tissues

(liver, pancreas, heart, adrenals, testes, pituitary, skin, kidney)

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24
Q

How does hereditary hemochromatosis present clinically (early stages)?

A

FH or incidentally noted increased AST and ALT

Initially non-specific sxs (fatigue, malaise, RUQ discomfort)

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25
Q

The following are complications of what disease?

Hepatomegaly, hepatic insufficiency, cirrhosis, DM, impotence, arthralgia, bronze pigmentation of skin, cardiomegaly +/- CHF, cardiac arrhythmia

A

Hereditary hemochromatosis

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26
Q

What is the triad a/w Bronze Diabetes (rare) and what condition can it be seen with?

A

Can be seen with hereditary hemochromatosis

Triad: DM, bronze pigmentation of skin, cirrhosis

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27
Q

Early diagnosis of hereditary hemochromatosis is important. What lab studies should be ordered?

A

Abd chem panel, iron studies and screening if (+) FH

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28
Q

Pt with concern for liver disease shows elevated liver tests/ LFTs, along with transferrin sat ≥ 45 and/ or ferritin > 200 (men) OR > 150 (women). What condition should you be concerned for?

A

Hereditary hemochromatosis

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29
Q

How is a diagnosis of hereditary hemochromatoma confirmed?

A

Genetic testing (GI mutation analysis) +/- liver bx

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30
Q

What is the goal of treatment for hereditary hemochromatosis and how is this done?

A

Goal is to prevent cirrhosis from iron load → therapeutic phlebotomy and q 6 months HCC screening w/ cirrhosis

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31
Q

What lifestly recommendations should be made for a pt with hereditary hemochromatosis to prevent cirrhosis from iron overload?

A

Avoid vit C, iron containing supplements, uncooked shellfish, EtOH

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32
Q

What is recommended for all 1st degree relatives of a pt with hereditary hemochromatosis?

A

HFE genotype and iron testing

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33
Q

According to AASLD guidelines, who should be screened for hereditary hemochromatosis?

A

Elevated liver tests, abd iron studies, 1st degree relative dx, evidence of liver disease, suggestive sxs

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34
Q

What condition is a very rare hereditary disorder of copper metabolism that leads to decreased excretion of copper into bile and accumulation of copper in the liver?

A

Wilson’s disease

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35
Q

Hepatic presentation of Wilson’s disease includes what?

A

Acute hepatitis, chronic liver disease, acute or chronic liver failure

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36
Q

In Wilson’s disease, once the liver’s capacity for copper is exceeded, copper is released into the bloodstream and starts to accumulate where?

A

Brain, cornea, joints, kidney, heart, pancreas

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37
Q

What are the common clinical manifestations of Wilson’s disease? (systems)

A

Hepatic, neurologic, psychiatric

(neuro/ psych: confusion, dysarthria, incoordination/ ataxia, Parkinsonism, seizures, dystonia, spasticity, personality/ behavior changes)

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38
Q

What is pathognomonic for Wilson’s disease?

A

Kayser-Fleischer ring + neuro manifestations

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39
Q

Pt presents with a brownish or gray-green color to their eye and you note neurologic manifestations as well. What are you concerned for and what should you do?

A

Wilson’s disease/ Kayser-Fleisher ring

Get ophthamology exam

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40
Q

What lab diagnostics should be ordered with suspicion of Wilson’s disease?

A

Serum ceruloplasmin (low, <5 = strong evidence), 24 hr urinary copper (inc), liver bx +/- molecular testing (dx confirmation), AST/ ALT (N/ low)

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41
Q

If available, what is recommended for 1st degree relatives of pts with Wilson’s disease?

A

Screening w/ genetic analysis

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42
Q

What is the treatment for Wilson’s disease?

A

Chelating agents and transplant if liver failure

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43
Q

Alpha-1 antitrypsin deficiency is a genetic disorder characterized by decreased levels of alpha-1 antitrypsin in circulation. What is the pathophysiology of this condition?

A

Liver cells make alpha-1 antitrypsin → abn shape get stuck in liver cells → accumulation in hepatocytes

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44
Q

What is the role of alpha-1 antitrypsin in the body?

A

Protects against tissue injury

45
Q

What levels of alpha-1 antitrypsin in circulation indicate severe disease?

A

< 11 micromole/ L

46
Q

Adults with an alpha-1 antitrypsin deficiency are at risk for what?

A

Severe lung disease and chronic liver disease

47
Q

Who are at an increased risk for alpha-1 antitrypsin def and who is more likely to present with severe liver disease?

A

Increased risk w/ cigarette smoking (and accelerated onset)
Infants and children more likely to present w/ severe liver disease

48
Q

What disease might you suspect in a non-smoker with emphysema at a young age (< 45 yo), emphysema with predominant basilar changes on CXR, or in neonatal cholestasis/ childhood cirrhosis?

A

Alpha-1 antitrypsin def

49
Q

Who should be screened for alpha-1 antitrypsin def?

A

Emphysema in abn population, adult onset asthma, clinical findings/ hx or unexplained chronic liver disease, FH of emphysema/ liver disease, hx of panniculitis

50
Q

What skin manifestations can be a/w alpha-1 antitrypsin def?

A

Panniculitis

51
Q

What lab diagnostics should be ordered if suspicion for alpha-1 antitrypsin def?

A

AST/ ALT (mild elevation) serum alpha-1 antitrypsin (dec), alpha-1 antitrypsin phenotype/ genotype, +/- liver bx

52
Q

What is the tx for alpha-1 antitrypsin def?

A

Tx of liver disease = liver transplant

Genetic counseling (risk of passing to children)

53
Q

What disease can manifest with variable presentation ranging from asx → acute/ chronic liver inflammation → acute liver failure +/- hx of autoimmune related disease?

A

Autoimmune hepatitis (AIH)

54
Q

How will hutoimmune hepatitis (AIH) present with acute onset (<30 days)? (4)

A

Hepatomegaly/ tenderness, jaundice, splenomegaly, fever

55
Q

What labs should be ordered first in the dx of autoimmune hepatitis (AIH)?

A

ANA, SMA, IgG, LKMA-1, liver bx

(LMKA = liver kidney microsomal antibody, order for children initially and to secure dx in adults)

(other tests: LC-1, anti-SLA, LKMA-3, pANCA, IAIHG scoring system)

56
Q

How is autoimmune hepatitis (AIH) diagnosed?

A

Serological markers w/ exclusion of viral/ other causes and histologic features (interface hepatitis) on bx

57
Q

What is the management for autoimmune hepatitis (AIH)?

A
  • Refer to gastroenterologist/ hepatologist
  • Prednisone +/- Azothioprine @ lowest dose ≥ 2 yrs (continue until remission)
  • Liver transplant if liver failure
  • Monitor DEXA (give calcium + vit D)
  • Vaccinate
  • Screen for autoimmune conditions
58
Q

What types of viral hepatitis are only acute?

A

A and E

(although B, C and D can present acutely)

*only AcutE

59
Q

What types of viral hepatitis are transmitted via fecal-oral routes?

A

E and A

*Eat Ass

60
Q

For which types of viral hepatits can you get a vaccine?

A

A and B

ABle to get vaccine

61
Q

What type of viral hepatitis typically presents chronically?

A

C

62
Q

Hep D is depdenent on what?

A

Hep B

63
Q

In what population can Hep E be fatal in?

A

Pregnancy

64
Q

In what areas is HAV common in due to transmission via fecal-oral routes from person to person or contaminated food or water?

A

Areas with inadequate sanitation

(can also be seen w/ homeless- outbreaks in USA)

65
Q

What population is more likely to be sx/ asx with Hep A?

A

Children < 6 yo - asx

Adults- sx

66
Q

Pt presents with jaundice, dark urine, pruritus, and light colored stool. Hx of fever, malaise, anorexia, N/V, RUQ pain. On PE you note hepatomegaly. What are you concerned for?

A

Hep A (icteric phase)

67
Q

In addition to elevated LFTs, what antibodies will be positive with Hep A?

A

IgM anti-HAV (+) = acute infection (sx onset)

IgG anti-HAV (+) = immunity

68
Q

What is the typical management for Hep A?

A

Fluids and rest (most recovered by 6 mos)

69
Q

Who should be hospitalized with Hep A?

A

Elderly, multiple comorbidites, underlying liver disease, fulminant liver failure

70
Q

What is included in the management of Hep A aside from supportive care?

A

Infection precautions, notify local health dept, post-exposure prophylaxis for non-immune close contacts, prevention with vaccine

71
Q

How is Hep B transmitted?

A

Person to person via: blood, sexual contact, parenteral contact, peri-natal transmission

72
Q

What type of hepatitis is a leading cause of cirrhosis and hepatocellular carcinoma worldwide?

A

HBV

73
Q

Is acute hep B typially sx or asx?

A

Asx

(if sx: N/V, RUQ pain, jaundice, malaise, arthralgias, fever)

74
Q

What lab findings are a/w acute hep B?

A

Elevated bilirubin, ALP, and transaminases

(ALT > 15x)

75
Q

What % of pts with acute hep B develop chronic disease?

A

<5% of adults will become chronic, 80-90% of infants will become chronic

76
Q

Although rare, what complication is a/w acute hep B?

A

Fulminant hepatic failure

(severe and sudden)

77
Q

What is the management for hep B?

A

Supportive care (majority recover w/ immunity)

+/- antiviral therapy if acute liver failure/ prolonged disease

78
Q

When should pts with hep B be admitted to the hospital?

A

Underlying liver disease, mulitple comorbidities, signs of liver failure, older/ elderly (more severe if > 60 yo)

79
Q

Hep B vaccine results in presence of what antibody?

A

Anti-HBs (surface)

(core antibody will be negative)

80
Q

Hep B infection (current or previous) results in presence of what antibody?

A

Anti-HBc and anti-HCs (surface and core)

81
Q

What lab findings are a/w chronic hep B?

A

HepB surface Ag (HBsAg) > 6 months, elevated transaminases

82
Q

What are the complications of chronic hep B?

A

Cirrhosis, HCC (hepatocellular carcinoma) (can occur w/o cirrhosis)

83
Q

Acute hep B most often becomes chronic in what pt populations?

A

IMC adult or if exposure as an infant or child < 5 yo

84
Q

If lab work shows + IgM anti-HBc, what does this indicate?

A

Acute hep B infection

85
Q

If lab work shows + IgG anti-HBc or total anti-HBc, what does this indicate?

A

Previous infection

86
Q

What is used as an index of infectivity and marker of replication for Hep B?

A

HepB e-antigen (HBeAg), a/w higher levels of HBV DNA

87
Q

Antibody to hep B e-antigen (anti-HBe) w/ HB e Ag negative status indicates what?

A

Lower levels of HBV DNA, predictor of long term clearance of HBV

88
Q

If interpretation of Hep B serologic test results are unclear (HBsAg (-), total anti-HBc (+), anti-HBs (-))… this indicates 4 possibilies: resolved infection, false +, low level chronic infection, resolving acute infection. What is the management?

A

Diagnose and refer to GI

89
Q

What is the general management for a pt acutely infected with Hep B?

A

Monitor and ensure immunity developed

90
Q

What is the management for chronic Hep B?

A
  • HCC surveillance (increased risk)- all pts with cirrhosis, and q 6 months for pts w/o cirrhosis
  • Vaccinate for Hep A
  • Counsel on prevention precations
91
Q

IV drug use, intra-nasal drug use, tattoos and piercings are RFs for what type of hepatitis?

(others: recipient of clotting factors, blood transfusion, HIV infection, hemodialysis, incarceration, known exposure, children born to infected mother, sexual contact)

A

Hep C

92
Q

Is acute HCV typically sx or asx?

A

Asx

(if sx: jaundice, fatigue, fever, nausea, vomiting, RUQ discomfort)

93
Q

Aside from AST/ ALT in 100s (usually < 300) and elevated bilirubin, what other lab values will be found for Hep C? (serology)

A

(-) Hep C Ab w/ (+) RNA viral load

OR

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

94
Q

When evaluating for chronc Hep C, if HCV Ab and HCV RNA are negative, what should you do?

A

Repeat HCV RNA w/ + RF in > 3 weeks

95
Q

When evaluating for chronc Hep C, if HCV Ab and HCV RNA are positive, what should you do?

A

DAA (direct acting antiviral), do not await spontaneous resolution

96
Q

What is recommended due to many new cases of chronic HCV in 20’s age group due to IVDU?

A

1 time testing for all 18 yo or older

97
Q

When do most pts with chronic Hep C present?

A

Late in disease course, signs of cirrhosis

98
Q

What is included in the management of Hep C?

A

Avoid EtOH intake, screen for HAV/ HBV/ HIV, vaccinate, non-infected sexual partner testing, check for pregnancy

99
Q

If after “cure” of Hep C with direct acting antiviral (DAA), ALT/ AST is elevated w/o cause, what should you do?

Cure does not prevent re-infection

A

Refer to GI for tx with DAA x 8-12 weeks

100
Q

Due to the risk for HCC in a pt with Hep C, what is routine management?

A

Regular imaging + AFP for HCC screening, monitor for cirrhosis

101
Q

Oral regimens for DAA prescribed after GI referral is based on what? (4)

A

Genotype/ previous tx, +/- cirrhosis, +/- compensation, +/- co-infection with HBV before tx

102
Q

Is DAA (direct acting antiviral) approved for treatment during pregnancy?

A

NO

103
Q

HDV Abs and HDV RNA with + HBsAg is associated with what?

A

More severe Hep D

104
Q

How is Hep D prevented?

A

Hep B vaccination

105
Q

What is the tx for Hep D?

A

Interferon (IFN) alfa/ weekly x 1 year +/- tx for Hep B

(no specific tx for acute Hep D- defer tx to liver transplant facility)

106
Q

How does Hep E present?

A

Acute hepatitis sxs

107
Q

How is Hep E diagnosed?

A

Hep E RNA

108
Q

In what population can Hep E be fatal?

A

Pregnant women (more severe/ greater mortality in 2nd and 3rd trimester)

109
Q

What is the management of Hep E?

A

Supportive

1. Clin Med III (29 decks)

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