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Clinical Med III > Exam 2 - Hepatitis/Liver Disease > Flashcards

Exam 2 - Hepatitis/Liver Disease Flashcards

1
Q

What is steatohepatitis?

A

Inflammation of the liver by fat deposition

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2
Q

What AST to ALT ratio is suggestive of alcoholic liver disease?

A

AST:ALT ratio > 1.5 (traditionally 2 or more)

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3
Q

What AST to ALT ratio is suggestive of NASH or acute/chronic viral hepatitis?

A

AST:ALT ratio < 1 (ALT>AST)

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4
Q

What is Isolated Steatosis (NAFL)?

A

Fatty liver without injury or fibrosis of hepatocytes

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5
Q

What is Non-alcoholic steatohepatitis (NASH)?

What is significant about its prognosis?

A

Fatty liver and inflammation with hepatocyte injury.

Risk of progression of fibrosis, cirrhosis is significant.

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6
Q

What are some risk factors for NAFLD?

A
  • Abdominal obesity
  • DM2
  • Hyperlipidemia
  • Metabolic syndrome
  • Polycystic ovarian syndrome
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7
Q

What risk factor is the strongest predictor for NASH?

A

Metabolic syndrome

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8
Q

What is the clinical presentation of NAFLD?

A

Usually asymptomatic with majority being an incidental finding

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9
Q

What might labs and imaging reveal in NAFLD?

A
  • Mild elevation of ALT and AST, rarely above 300
  • Ferritin elevated = marker for inflammation
  • Hyperlipidemia
  • GGT and ALP elevated
  • Fibroscan (VCTE) with 5% or more liver fat on imaging or liver biopsy
  • US notes fat
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10
Q

What clinical decision aid is commonly used for identifying patients with higher likelihood for advanced fibrosis of the liver?

A
  • NFS

- Fibrosis-4 index (FIB-4)

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11
Q

What is the gold standard for characterizing liver histological alterations in NAFLD?

A

Liver biopsy

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12
Q

What can be used to treat dyslipidemia in patients with NAFLD and NASH?

A

Statins

***should be avoided those in patients with decompensated cirrhosis

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13
Q

What is the cornerstone of management for NASH?

A

Exercise and weight loss

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14
Q

What is Hereditary Hemochromatosis and what does it lead to?

A

Hereditary disorder of iron metabolism which results in increased GI absorption of iron and accumulation of iron in differing organs.

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15
Q

What is Bronze DM and what disorder is it associated with?

A

Triad of DM, bronze pigmentation of skin, cirrhosis.

Late manifestation of Hereditary Hemochromatosis.

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16
Q

How will LFTs, transferrin saturation (Fe/TIBC), and ferritin look in a patient with Hereditary Hemochromatosis?

A
  • Elevated AST, ALT, Alk Phos
  • Transferrin saturation of 45 or greater
  • Ferritin > 200 in men, > 150 in women
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17
Q

How is the diagnosis of Hereditary Hemochromatosis confirmed?

A
  • Genetic testing (HFE) +/- liver biopsy
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18
Q

The goal of treatment for Hereditary Hemochromatosis is to prevent cirrhosis from iron overload. What can you suggest to a patient to avoid this?

A
  • Avoid Vitamin C and iron containing supplements
  • Avoid uncooked shellfish, especially oysters
  • Avoid/limit alcohol intake
  • Lab monitoring and phlebotomy (managed by hematologist)
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19
Q

What is Wilson’s disease?

A

Genetic defect which results in decreased excretion of copper into bile and accumulation of copper in liver. Once liver’s capacity is exceeded, copper is released into the blood stream and accumulates elsewhere in the body.

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20
Q

What are clinical findings of Wilson’s disease?

A
  • Neurologic/Psychiatric symptoms: confusion, dysarthria, ataxia, Parkinsonism, seizures, spasticity, personality changes
  • Kayser-Fleischer rings
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21
Q

What is pathognomonic of Wilson’s disease?

A

Kayser-Fleischer rings + neurologic manifestations

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22
Q

If Kayser-Fleischer rings are found on exam, what should you do?

A

Refer to ophthalmology for exam

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23
Q

If Wilson’s disease is suspected, what test should you order for initial screening?

A

Serum ceruloplasmin (plasma copper-carrying protein)

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24
Q

What will LFTs, serum ceruloplasmin, and 24 hour urinary copper look like in a patient with Wilson’s disease?

A
  • AST/ALT: Mildly elevated
  • Alk Phos: Normal or low
  • Serum ceruloplasmin: Low
  • 24 hour urinary copper: Increased
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25
Q

How is Wilson’s disease usually diagnosed?

A

Liver biopsy

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26
Q

What is the treatment for Wilson’s disease?

A
  • Chelating agents

- Transplant in liver failure

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27
Q

When should you suspect alpha-1 antitrypsin deficiency?

A
  • Non-smoker with emphysema at a young age (< 45 years old)
  • Neonatal cholestasis
  • Childhood cirrhosis
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28
Q

What skin manifestation can be associated with alpha-1 antitrypsin deficiency?

A

Panniculitis

29
Q

What is the role of alpha-1 antitrypsin?

Where is it produced and how does it lead to pathology?

A

Protects against tissue injury.

Liver cells make it. If it is not the right shape, it will get stuck in the liver cells and accumulate in hepatocytes.

30
Q

What labs are suggestive of alpha-1 antitrypsin deficiency?

A
  • AST/ALT: Mild elevation
  • Serum alpha-1 antitrypsin: Decreased (may be high secondary to inflammation in the body)
  • Alpha-1 antitrypsin phenotype/genotype
31
Q

If patient presents with asymptomatic or acute/chronic hepatitis + elevated liver enzymes + concurrent autoimmune disease, what should you suspect?

A

Autoimmune Hepatitis

32
Q

What are some possible clinical findings of Autoimmune Hepatitis?

A
  • Acute onset (< 30 days)
  • Hepatomegaly and tenderness
  • Jaundice
  • Splenomegaly
  • Fever
33
Q

If you suspect Autoimmune Hepatitis, what should be the first labs that you order?

A
  • Antinuclear antibodies (ANA)
  • Smooth muscle antibodies, anti-actin (SMA)
  • Immunoglobin G (IgG)
34
Q

What diagnostic study is needed for the diagnosis of Autoimmune Hepatitis?

A

Liver biopsy

35
Q

What is the management of Autoimmune Hepatitis?

A
  • GI/Hepatology
  • Prednisone +/- Azothioprine (Imuran)
  • Monitor bone density (DEXA) and check for Vitamin D deficiency while on steroids
36
Q

Which forms of hepatitis are only acute infections and do not cause chronic infection?

A

A and E

*only AcutE

37
Q

Which forms of hepatitis are due to fecal-oral transmission?

A

A and E

*fEcal-orAl

38
Q

Which form of hepatitis can be fetal in pregnancy?

A

E

*Fatal in prEgnancEEE

39
Q

Which forms of hepatitis are there vaccines for?

A

A and B

*ABle to get vaccine

40
Q

What symptoms are associated with the icteric phase of Hep. A?

A
  • Jaundice (usually one week after prodrome symptom onset)
  • Dark urine
  • Pruritis
  • Light colored stool
41
Q

What are the most commonly observed abnormalities in Hep A?

A

Hepatomegaly and Jaundice

42
Q

What does AST/ALT typically look like in Hep A?

A

Elevated often at > 1000 range or 15 x ULN

43
Q

What does a (+) IgM anti-HAV test indicate?

A

Acute Hep A infection

***remains positive for about 4 months

44
Q

What does a (+) IgG anti-HAV test indicate?

A

Implies immunity to Hep A infection

45
Q

What is the typical management for Hep A?

A

Supportive care:

  • Fluids and rest
  • Full recovery in nearly all patients by 6 months
46
Q

In what populations should you consider hospitalization for Hep A and B?

A
  • Elderly ( > 60 years old)
  • Multiple comorbidities
  • Underlying liver disease
  • Liver failure
47
Q

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

A

Hepatitis B

48
Q

How is Hep B transmitted?

A

Person-person:

  • Blood
  • Sexual contact
  • Parenteral contact
  • Peri-natal
49
Q

How long does the incubation period last for Hep B?

A

Weeks to months (45 to 160 days)

50
Q

Can Hep B become a chronic infection?

A

Rare to become chronic in adult, but will become chronic in nearly all infants infected.

51
Q

What is the management of acute HBV?

A
  • Supportive care (majority of adults recover with immunity)

- Possible antiviral therapy (only in acute liver failure or protracted course consider)

52
Q

What does a (+) HBsAg test indicate?

A

Active disease (acute or chronic infection)

***Positive > 6 months = chronic

53
Q

What does a (+) anti-HBs (HBsAb) indicate?

A

Immunity to Hep B (vaccine or resolved infection)

54
Q

What does a (+) IgM anti-HBc indicate?

A

Acute exposure/infection

55
Q

What does a (+) IgG anti-HBc indicate?

A

Previous exposure/infection

56
Q

What lab marker is a hallmark of active Hep B infection?

How can you determine if the infection is chronic?

A

Hepatitis B surface antigen (HBsAg)

(+) HBsAg > 6 months = chronic infection

57
Q

Which lab marker indicates an acute/recent Hep B infection

A

IgM anti-HBc

58
Q

Which lab marker indicates a prior or resolving Hep B infection and will persist indefinitely?

A

IgG anti-HBc

59
Q

What lab marker indicates recovery and immunity to Hep B infection?

A

anti-HBs (HBsAb)

60
Q

What do the following lab results indicate?

(+) anti-HBs
(+) anti-HBc IgG

A

Prior infection with resulting immunity

61
Q

What do the following lab results indicate?

(+) anti-HBs
(-) anti-HBc IgG

A

Prior vaccination with resulting immunity

62
Q

What does a positive versus negative HBeAg indicate?

A

Positive = Virus activity replicating (high viral load)

Negative = Low level of replication (low viral load)

63
Q

How do most patients with a Hep C infection present?

A

Asymptomatic

64
Q

What will labs look like in a patient with an acute Hep C infection (AST/ALT, Bilirubin)?

A
  • AST/ALT: Usually in the 100’s (< 300)

- Bilirubin: Elevated

65
Q

What will AST/ALT levels look like in a patient with a chronic Hep C infection?

A

AST/ALT: < 100

66
Q

What is the management for Hep C infection?

A
  • Direct-acting antiviral
  • Avoid alcohol
  • If not immune, get vaccinated for Hepatitis A/B
  • Advise against donating blood/organs
  • Cover wounds
67
Q

When is Hepatitis D seen?

A

Seen only in conjunction with Hepatitis B

68
Q

How is Hepaitis D diagnosed?

A

HDV Abs and HDV RNA with (+) HBsAg

69
Q

How can you prevent Hepatitis D?

A

Vaccinate for Hepatitis B

Clinical Med III (12 decks)

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