E2: Hepatitis/LIver Disease Flashcards

1
Q

What kind of liver injury will have the highest LFTs?

A

“Shock liver” or Tylenol toxicity

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2
Q

What is steatohepatitis? What is reflected by on bloodowork?

A
  • inflammation of the liver by fat deposition

- Can be reflected by abnormal liver tests in a hepatocellular pattern

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3
Q

Does does an AST:ALT ratio of >1.5 indicate?

A

Alcoholic liver disease

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4
Q

What does an ALT>AST AST: ALT ration < 1 indicate?

A

NASH, acute or chronic hepatitis

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5
Q

What is NAFLD?

A

Hepatic steatosis without secondary causes of hepatic fat accumulation

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6
Q

What are the two subtypes of NAFLD?

A

NAFL and NASH

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7
Q

What is the difference between NAFL and NASH?

A
  • NAFL: Fatty liver without injury or fibrosis of hepatocytes on biopsy
  • NASH: fatty liver and inflammation leading to Hepatocyte injury, risk of progression to fibrosis and cirrhosis is significant
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8
Q

What are the risk factors of NAFLD?

A
  • Abdominal obesity
  • DM2
  • HLD
  • Metabolic syndrome
  • PCOS
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9
Q

What are the decision aids that can identify patients who are at risk for progression from NAFLD to NASH and advanced fibrosis?

A
  • NAFLD fibrosis score
  • Fibrosis-4 index (FIB-4)
  • Vibration-controlled transient elastography
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10
Q

What might you seen on labs in a patient with NAFLD?

A
  • Elevated ALT and AST in a Hepatocellular pattern
  • Normal albumin, bilirubin, and INR
  • Elevated ferritin (marker for inflammation)
  • Hyperlipidemia
  • ALP elevated
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11
Q

What will you se on a liver fibroscran if the patient has NAFLD?

A

> 5% liver fat on imaging or liver biopsy

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12
Q

What is the Gold standard for characterizing liver histological alternations in NAFLD?

A

Liver biopsy

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13
Q

When should you obtain a liver biopsy for a patient with NALFD?

A

If they have NAFLD with one of the following:

  • Increased risk for steatohepatitis and/or advanced fibrosis
  • metabolic syndrome and elevated LFTs
  • Competing etiologies for hepatic steatosis and inability to exclude/assess severity of coexisting CLD without biopsy
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14
Q

What are patients with NAFLD at increased risk for? How can you treat them?

A

Cardiovascular morbidity and mortality

-aggressive modification of CVD risk factors should be considered, such as statin therapy in dyslipidemia

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15
Q

What is the recommended management of NASH?

A
  • Exercise and weight loss is the cornerstone management
  • Minimize or discontinue alcohol use
  • control DM and HTN
  • Vaccinate for Hep A and B if not immune
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16
Q

What is Hereditary hemochromatosis?

A

-Hereditary disorder of iron metabolism that results from a genetic mutation that results in increased GI absorption of iron that leads to accumulation of iron in the liver, pancreas, heart, adrenals, testes, pituitary, skin, and kidney

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17
Q

What are the late manifestations of hereditary hemochromatosis?

A

-Hepatomegaly, hepatic insufficiency, cirrhosis, DM, impotence, arthralgia, bronze skin pigmentation, cardiac arrhythmia

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18
Q

What is Bronze diabetes?

A

-Triad of DM, bronze pigmentation of skin, and cirrhosis

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19
Q

What lab findings are consistent with hereditary hemochromatosis?

A
  • Elevated LFTs
  • Screen with serum Fe and TIBC, and ferritin
  • Ferritin >200 in men, >150 in women
  • transferrin >45
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20
Q

If you suspect hereditary hemochromatosis based on patients blood work, How can you confirm the diagnosis?

A

-Refer to GI for HFE mutation analysis and possible liver biopsy

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21
Q

What is the treatment of hereditary hemochromatosis?

A

-Therapeutic phlebotomy and HCC screening every 6 months
-Avoid Vitamin C, iron containing supplements, uncooked shellfish, and alcohol
-

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22
Q

What is ordered to screen for HCC?

A

US and AFP

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23
Q

What is Wilson’s disease?

A
  • A very rare hereditary disorder of copper metabolism
  • Autosomal recessive mutation that results in decreased excretion of copper in bile and accumulation of copper in the liver
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24
Q

What are the 3 hepatic presentations of Wilson’s disease?

A
  • Acute hepatitis
  • chronic liver disease
  • Acute on chronic liver failure
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25
Q

When the livers capacity for copper is exceed in Wilson’s disease, what happens?

A

The copper is released into the blood stream and begins to accumulate in the brain, cornea, joints, kidney, heart, and pancreas

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26
Q

What findings are pathognomonic for Wilson’s disease?

A

Kayser-Fleischer rings + neurologic manifestations

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27
Q

What lab finding is often low with Wilson’s disease?

A

-Serum ceruloplasmin

DX confirmed with liver biopsy with possible molecular testing

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28
Q

What is the treatment for Wilson’s disease?

A
  • Chelating agents

- Transplant in liver failure

29
Q

What is alpha-1 antitrypsin deficiency?

A

-Genetic disorder characterized by decreased levels of alpha 1 antitrypsin in circulation

30
Q

What should you be suspicious of if you have a young, non-smoker patient with emphysema or with childhood cirrhosis?

A

Alpha 1 antitrypsin deficiency

31
Q

Who should you screen for alpha 1 antitrypsin deficiency?

A
  • Emphysema in young patients, non-smokers, or predominant basilar changes on CXR
  • Adult onset asthma
  • Clinical findings or history of unexplained CLD
  • Family hx of emphysema and/or liver disease
  • Hx of panniculitis
32
Q

What lab findings are consistent with alpha 1 antitrypsin deficiency?

A
  • Mild elevation of AST/ALT
  • Serum alpha 1 antitrypsin decreased
  • test for alpha 1 antitrypsin phenotype/genotype
33
Q

What are the possible clinical presentations of autoimmune hepatitis?

A
  • Asymptomatic with elevated liver enzymes and concurrent autoimmune disease
  • Acute hepatitis
  • CLD
  • Nonspecific symptoms such as fatigue, malaise, anorexia, pruritis, abd pain, arthritis
34
Q

What is the acute disease presentation of autoimmune hepatitis?

A

Hepatomegaly and tenderness
Jaundice
Splenomegaly
Fever

35
Q

What are the serological markers you need to order to diagnose autoimmune hepatitis?

A
  • Antinuclear antibodies (ANA)
  • Smooth muscle antibodies, anti-actin (SMA)
  • Immunoglobin G (IgG)
  • Liver kidney microsomes antibody (LKMA-1)

**order livery biopsy as well

36
Q

What is the management of Autoimmune Hepatitis?

A
  • Prednisone +/- Azathioprine combination strongly recommended and continue until remission >2 years
  • monitor bone density
  • Liver transplant is treatment if fulminant liver failure
37
Q

How is Hepatitis A transmitted?

A

-Fecal - oral, person to person, contaminated food or water

38
Q

Does Hep A cause chronic infection?

A

No

39
Q

What is the clinical presentation of Hep A?

A
  • Children <6 are likely asymptomatic
  • Adults are more likely to be symptomatic with a prodrome period of “flu like” illness
  • icteric phase: jaundice, dark urine, pruritis, light colored stool
40
Q

What are the two most commonly observed abnormalities in Hepatitis A?

A

Hepatomegaly and Jaundice

41
Q

What does a positive IgM anti HAV indicate?

A

Acute infection of Hep A

42
Q

What does a positive IgG anti-HAV indicate?

A

Immunity to Hep A

43
Q

A patient presents with elevated LFTs, bilirubin, and ALP. IgM anti HAV is positive. What is their diagnosis?

A

Acute Hep A

44
Q

What is the management of Hep A?

A
  • Supportive care (fluids and rest)

- Hospitalize if elderly, multiple comorbidities, underlying liver disease, or fulminant liver failure

45
Q

What is the leading cause of cirrhosis and HCC worldwide?

A

Hep B

46
Q

How is Hep B transmitted?

A

Blood/blood derived body fluids, person to person through blood, sexual contact, parenteral contact, and peri-natal transmission

47
Q

Is Hep B chronic?

A
  • <5% of adults will become chronic, but 80-90% of infants will become chronic
48
Q

What are the clinical signs of acute Hep B?

A
  • N/V, RUQ pain, jaundice, malaise, fever
  • elevated bilirubin and ALP
  • Elevated LFTs, with ALT >15x normal
49
Q

What is the management of acute Hep B?

A
  • Supportive care as (5% of adults recover with immunity
  • possible antiviral therapy, but only in acute liver failure or protracted course
  • admit if underlying liver disease, multiple comorbidities, or signs of liver failure
50
Q

What does it mean if the Anti-HBs is positive?

A
  • Pt was previously infected with Hep B, or received Hep B vaccination
  • This the antibody to the surface antigen
51
Q

What are the common complications of Chronic Hep B?

A
  • Cirrhosis

- HCC

52
Q

When is Hep B most likely to become chronic?

A
  • If patient is immunocompromised

- if exposure was as an infant

53
Q

What are the lab findings in a chronic Hep B infection?

A
  • Hep B surface Ag positive > 6 months

- elevated LFTs

54
Q

What does a positive HBsAg indicate?

A

Active disease, either acute or chronic

** Hepatitis B surface antigen

55
Q

What does a positive IgM anti-HBC indicate?

A

-acute exposure

56
Q

What does a positive IgG anti-HBc indicate?

Positive Total anti-HBc?

A

Both indicate previous infection

57
Q

What is the first detectable marker of infection in Hep B?

A

Hepatitis B surface antigen (HBsAg)

  • Rises before the onset of symptoms
  • detectable in blood after exposure
58
Q

What is the hallmark of an active Hep B infection?

A

HBsAg

** if elevated for more than 6 months, indicates chronic infection

59
Q

Which antibody persists indefinitely after a Hep B infection?

A

IgG anti HBc

60
Q

Which antibody signifies recovery and immunity from a Hep B infection?

A

Antibody to surface antigen (anti-HBs)

61
Q

What does it mean if a patient has a positive Anti-HBd and a positive IgG anti-HBc?

A

Prior infection with resulting immunity

62
Q

What does it mean if a patient has a positive Anti-HBs, but a negative IgG Anti-HBc?

A

Prior vaccination with resulting immunity

** Anti-HBc is negative because they have never seen the virus before so the cannot make this antibody

63
Q

What is the Hepatitis B e-antigen used for?

A

Used as an index of infectivity and a marker of replication

64
Q

What is the management of Chronic Hep B?

A
  • Vaccinate for Hep A
  • Counsel of prevention precautions
  • HCC surveillance (with or without cirrhosis)
65
Q

What is the management of Hepatitis C?

A
  • Refer to GI for treatment with new oral medications

- most are treated for 8-12 weeks induration with direct acting antiviral agents

66
Q

What is required for a Hepatitis D infection?

A

Hepatitis B infection

67
Q

How do you diagnosed Hep D?

A

HDV with Abs and HDV s Ag (+) with acute liver failure

68
Q

What labs are indicative of Hep C?

A

-Elevated LFTs and bilirubin
- (-) Hep C Ab with (+) RNA viral load
OR
(+) Hep C Ab when it was previously negative