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Gastroenterology > Acute and Chronic Hepatitis > Flashcards

Acute and Chronic Hepatitis Flashcards

1
Q

This metabolizes carbohydrates and fatty acids and produces serum proteins – including factors involved in coagulation cascade and lipids.

A

Liver

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2
Q

This organ synthesizes fat-soluble vitamins (ADEK), functions in bile transport, and detoxifies blood from the gut.

A

Liver

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3
Q

This type of liver disease happens within a couple weeks and can induce encephalopathy within 2 weeks of the onset of jaundice.

A

Fulminant Hepatic Failure

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4
Q

This type of liver disease happens within a couple months and can induce encephalopathy after 2 weeks but less than three months of the onset of jaundice.

A

Subfulminant Hepatic Failure

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5
Q

This type of liver disease happens within a couple weeks and can induce encephalopathy more than 6 months after the onset of jaundice.

A

Chronic Liver Cirrhosis

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6
Q

Look at Causes of Acute and Chronic Hepatitis from the slides

A

:D

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7
Q

How would a patient present with Acute Hepatitis?

A
  1. Jaundice
  2. Anorexia/NV
  3. Abd. Pain
  4. Fever
  5. Changes in urine/stool
  6. Fatigue/arthalgia/myalgia/rash/diarrhea/headache – these signs suggest it is a viral cause
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8
Q

How would a patient present with Chronic Hepatitis?

A
  1. Asymptomatic elevation of transaminases
  2. Chronic Fatigue
  3. RUQ pain
  4. Dz specific (Arthritis, Wt gain, Change in skin color or rash)
  5. Ascites, Edema, Easy bruising, melena, hematemesis, encephalopathy – spec. indicative of cirrhosis and portal HTN
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9
Q

LOOK AT A PATIENTS HISTORY!!! What are factors that can contribute to acute or chronic hepatitis?

A
  1. Vasculature
  2. Drugs and Toxins
  3. Viral
  4. EtOH
  5. NAFLD
  6. Autoimmune
  7. Genetic

** Look at slide for details **

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10
Q

Chronic Hepatitis would be which strains of Hep?

A

B, C, and D

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11
Q

Which strains of Hepatitis is transmitted through feces?

A

A and E

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12
Q

Which type of Hepatitis has the highest mortality rate per year?

A

Hep C

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13
Q

This strain of Hep was common in South America, and is usually a co-infection with C and HIV

A

Hep E

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14
Q

If a patient is being seen for the first time with Hepatitis, which strain would you not test for? Why?

A

Hep D. Because Hep D only comes after Hep B.

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15
Q

The incubation rate for Hep A is roughly ________.

A

15-50 days, mean: 28 days.

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16
Q

After an acute Hep B infection, how many adults recover (%)?

A

95%

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17
Q

If 5% of the acutely infected Hep B population develop chronic hep B, how many will develop cirrhosis?

A

12-20%

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18
Q

After developing liver cirrhosis from Hep B infection, which are you more likely to get?

A. Decompensated Cirrhosis
B. Hepatocellular Carcinoma

A

A. Decompensated Cirrhosis occurs in 20-23%

***H. Carcinoma in 6-15%

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19
Q

The incubation rate for Hep B is roughly ________.

A

60-180 days, mean = 120 days

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20
Q

People with a chronic infection of Hep B can either have an active or inactive form. When looking at labs from Inactive HBsAg Carrier State, what would we see on labs?

A 
HBsAg +  (neg)
Normal ALT
HBeAg -
Anti-HBe +
HBV DNA -
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21
Q

People with a chronic infection of Hep B can either have an active or inactive form. When looking at labs from active chronic hepatitis State, what would we see on labs?

A 
HBsAg +
Elevated ALT
HBeAg +
Anti-HBe-
HBV DNA +
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22
Q

When checking ALTs on LFTs for Chronic Hep B, what would a value less than 2x normal indicate?

A

Consider Biopsy and tx if fibrosis

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23
Q

When checking ALTs on LFTs for Chronic Hep B, what would a value greater than 2x normal indicate?

A

Consider tx

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24
Q

With Hep B, if the pt is a candidate for interferon therapy, what would you try?

A

PEG-Interferon

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25
Q

If the Chronic Hep B patient is not a candidate for interferon candidate, what can we give them?

A

Tenofovir and/or Entecavir

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26
Q

What do we need to do if administering Tenofovir?

A

Follow HBeAg/HBeAb, HBV DNA. If there are two consecutive seroconversions after 12 months, consider stopping!

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27
Q

When should patients get the Hep A Vaccine?

A
  1. Travelers to endemic areas
  2. Pts with Chronic Liver Dz
  3. Children in communities with high rates
  4. Illicit IV drug users
  5. Researchers working with Hep A Virus
  6. Food handlers and day care workers
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28
Q

When should patients get the Hep B Vaccine?

A
  1. Household of spouse contacts of HBV carriers
  2. Alaskan natives, Pacific Islanders
  3. Healthcare workers (includes first responders)
  4. Injecting drug users
  5. Homosexual/bisexual men (pretty sure this means anal sex…so it’s not just them, but you know #culturallysensitive #murikah)
  6. Individuals with multiple sexual partners
  7. Maintenance hemodialysis
  8. Inmates
  9. Chronic liver disease
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29
Q

Hepatitis C’s biggest risk factor is?

A

Hemophiliacs (74-90%)

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30
Q

What is the likelihood of the general population getting Hep C?

A

1.8% (Sounds small but that’s still 130-170 million people.)

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31
Q

About how many patients with Acute Hep C infection will develop Chronic Hepatitis?

A

85% (womp womp womp)

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32
Q

Of the people with chronic Hep C infection/hepatitis, how many will get cirrhosis?

A

20%

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33
Q

How many people with Chronic Hepatitis from Hep C will die or get transplanted?

A

3.6%

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34
Q

Does Hep C or Hep B cause a greater chance of decompensated hepatitis or hepatocellular carcinoma?

A

B!

C = Decomp 6%; HCC 4%

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35
Q

Stage this Fibrosis!
Fibrous expansion of most portal areas with occasional portal to portal bridging

(Look at the images for the exam)

A

Stage 3

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36
Q

Stage this Fibrosis!
Pink BEAUTIFUL tissue

(Look at the images for the exam)

A

No fibrosis (no staging?) Normal

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37
Q

Stage this Fibrosis!
Cirrhosis (probable or defined)

(Look at the images for the exam)

A

Stage 5 & 6

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38
Q

Stage this Fibrosis!
Fibrous expansion of portal areas with marked bridging (portal to portal AND portal to central)

(Look at the images for the exam)

A

Stage 4

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39
Q

Which Hep infection would we indicate to a patient to NOT use EtOH?

A

Hep C

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40
Q

What’s the best therapy for Hep A?

A
  1. Support
  2. Immunoprophylaxis to household and intimate contacts within 2 weeks of exposure
  3. VACCINATE! The high risk populations, yo.
41
Q

What’s the best therapy for Hep B?

A
  1. Pegylated interferon, Entecavir, Tenofovir

2. Vaccinate the sexual contacts

42
Q

What’s the best therapy for Hep C?

A
  1. Pegylated Interferon, Ribavirin, DAA

2. Avoid EtOH

43
Q

What are the three types of Autoimmune Based Liver Diseases

A
  1. Autoimmune Hepatitis
  2. Primary Biliary Cirrhosis (PBC)
  3. Primary Sclerosing Cholangitis (PSC)
44
Q

Autoimmune Hepatitis is most commonly ________ but in about 1/3 of patients with this, it can also be _________.

A

Chronic; Acute

45
Q

How common is the presence of another autoimmune disorder in a patient with Autoimmune Hepatitis?

46
Q

In a patient with Autoimmune Hepatitis, Serum Protein Electrophoresis (SPEP) will show?

A

Hypergammaglobulinemia

47
Q

There are two types of Autoimmune Hepatitis. Which test would indicate Type I?

A

+ Antinuclear Antibody (ANA)

- Antimitochondrial Antibody (AMA)

48
Q

There are two types of Autoimmune Hepatitis. Which test would indicate Type II?

A

+ AntiLiver/Kidney/Microsome Antibody (LKM-Ab)

49
Q

What happens if you get the antibodies back indicated either type of Autoimmune Hepatitis?

A

Liver Biopsy

50
Q

How would you treat Autoimmune Hepatitis?

A

Steroids and Azathioprine (rapid reversal of symptoms and increased survival)

51
Q

This is a chronic cholestatic liver disease that is common in middle-aged women more than men. Commonly presenting with fatigue, pruritis, and jaundice.

A

Primary Biliary Cirrhosis (Remember this is an autoimmune dz)

52
Q

When looking at antibodies in a patient with Primary Biliary Cirrhosis, what would you see?

A

Antimitochondrial Antibody (AMA):
Positive in 95%
Negative in 5%

53
Q

When looking at immunoglobulins in a patient with Primary Biliary Cirrhosis, what would you see?

A

Elevated IgM

54
Q

What will a lung biopsy show on a patient with PBC (Primary Biliary Cirrhosis)?

A

Interlobular bile duct destruction (often granulomatous) with a preponderance of eosinophils.

55
Q

Is it possible to have PBC with Autoimmune Hepatitis?

A

Yes, you fool. 10-12% have both.

56
Q

What medication decreases the rate of progression of Primary Biliary Cirrhosis?

57
Q

What can Primary Biliary Cirrhosis cause to the rest of the body?

A

Pruritis
Vitamin ADEK Deficiency
Osteoporosis
Orthotopic Liver Transplant

58
Q

What is a Orthotopic Liver Transplant, you ask?

A

The native liver is removed and replaced by the donor organ in the same anatomic location as the original liver. And how is this different than any other type of Transplant – I have no idea.

59
Q

Look at the pathology slide for PBC

A

It’s apparently of the Florid Duct Lesion which is classic for PBC

60
Q

This is a chronic cholestatic liver disease involving the entire biliary tree. It is commonly associated with ulcerative cholitis and cholangiocarcinoma.

A

Primary Sclerosing Cholangitis (PSC)

61
Q

T/F: It is rare to have patients with ulcerative cholitis (UC) and Primary Sclerosing Cholangitis (PSC).

A

FALSE. 70% of PSC pts have UC.

62
Q

How do you establish a diagnosis in a patient with suspected PSC?

A

ERCP will show a “beaded appearance.”

HOWEVER, there is such a thing as secondary sclerosising cholangitis. So rule these out first.

63
Q

What can cause Secondary Sclerosing Cholangitis?

A

HIV Cholangiopathy, Bilary Neoplasm, Surgery/Trauma, Choledocholithiasis, and Congenital Abnormalities of the Biliary Tract.

64
Q

Do you do a lung biopsy with PSC?

A

Sure, why not!? But really, it’s most useful with a suspicion based on cholangiogram.

65
Q

How do you treat PSC?

A

Ursodiol (arguably) – improves symptoms

Orthotopic Lung Transplant is only an option in advance dz. 85-88% 5 year survival rate.

66
Q

What systemic effects does PSC have on the body?

A 
Pruritis
Vitamin ADEK Deficiency
Osteoporosis
Hyperlipidemia
Steatorrhea
Dominant Strictures/Cholangitis
Cholangiocarcinoma
67
Q

Which autoimmune dz’s cause interfere with Ca2+ absorption in the body?

A

PBC and PSC

68
Q

What are the three hereditary Liver Dzs?

A
  1. Wilson’s
  2. Hereditary Hemochromatosis
  3. Alpha-1 Antitrypsin Deficiency
69
Q

This is an autosomal recessive genetic disease that causes a defect in biliary copper excretion. This is most commonly seen in patients younger than 30 years old with neuropsychiatric signs and symptoms and non-immune hemolytic anemia.

A

Wilson’s Dz

70
Q

How will a person with Wilson’s Dz present?

A
  1. Movement disorders such as termors, poor coordination, and loss of fine motor control.
  2. Spastic Dystonic disorders like masklike facies, rigidity, and gait disturbance
  3. Pseudobulbar involvement – dysarthria, drooling, and swallowing difficulty
  4. Intellect is NOT impaired
71
Q

What condition usually predated neuropsych disorders in a patient with Wilson’s Dz?

A

Hepatitis!

AST > ALTs

72
Q

Serum Uric Acid in a patient with Wilson’s Disease will be?

A

Low due to renal tubular defect

73
Q

What are you looking for when checking for Wilson’s Dz via a slit-lamp exam?

A

Corneal Kayser-Fleischer rings (50% with hepatic presentation but 98% with neuro)

74
Q

What would a serum ceruloplasmin show in a patient with Wilson’s Dz?

A

Reduced levels in 8% (<20 microg/dL) BUT 15% are normal

75
Q

What would you see on a 24 hours urinary copper test in a patient with Wilson Dz?

A

> 100 mcg/day

76
Q

What would you see in a serum copper test in a patient with Wilson’s Dz?

A

< 80 mcg/dl which is LOW

77
Q

Would you do a Liver Biopsy in a patient with suspected Wilson’s Dz? Why or why not?

A

Yes! To confirm and quatitate >250 mcg/g of dry weight

78
Q

What are the 4 treatments for Wilson’s Dz and what do they do?

A
  1. Penicillamine (Chelator)
  2. Trientine (Chelator)
  3. Zinc (dec Intestinal Copper Absorption)
  4. BAL (Chelator)
79
Q

This is a common autosomal recessive genetic liver dz linked to the HFE gene.

A

Hereditary Hemochromatosis (HH)

80
Q

What would you see in a blood test with a person with Hereditary Hemochromatosis?

A

Transferrin Saturation >45%

Ferritin (High) >400 ng/ml in men, >300 ng/L in females.

81
Q

What is the purpose of a Liver Biopsy in a patient with Hereditary Hemochromatosis?

A

To calculate hepatic iron index and to detect the degree of fibrosis for prognosis.

An HII >1.9 is confirmatory in distinguishing from secondary causes of Fe overload

82
Q

Genetic testing is done to confirm Hereditary Hemochromatosis

83
Q

How do you treat Hereditary Hemochromatosis?

A
  1. BLEED THEM! (Phlebotomy)

2. Deforaxime

84
Q

What cells are commonly affected by Hereditary Hemochromatosis?

A

Periportal Hepatocytes

85
Q

Periportal pattern of fibrosis correlated with severity of ____________.

A

Hepatocellular siderosis

86
Q

This is a genetic disease (autosomal co-dominant alleles) that is most commonly considered with patients with emphysema at a young age or out of proportion with smoking history.

A

Alpha-1 Antitrypsin Deficienc

87
Q

How common is liver dz in patients with AAT Deficiency?

A

More common in young adults and children. Though this isn’t porgressive.

88
Q

How do you diagnose AAT Deficiency?

A

Low serum levels of AAT

Abnormal migration in serum phenotype analysis

89
Q

A liver biopsy of someone with AAT Deficiency would show

A

Characteristic PAS+ diastase resistant deposits of AT

90
Q

How do you treat liver dz assc with AAT Deficiency?

A

Orthotopic Liver Transplant

90% have a 1 year survival, 80% 5 year

91
Q

What are the two metabolic causes of liver dz?

A
  1. Alcoholic Liver Dz

2. Non-alcoholic fatty liver dz (NAFLD)

92
Q

How does Alcoholic Liver Dz commonly present?

A

Acute hepatitis and jaundice

93
Q

What will you see on LFTs for a patient with ALD (Alcoholic Liver Dz)?

A

AST/ALT Ratio: 2-3:1

94
Q

How will you treat Alcoholic Liver Dz?

A
  1. Stop EtOH or refer to rehab program
  2. EtOH hep not an indication for orthotopic liver transplant
    • Severe: Steroids!
      3. Pentoxifylline
95
Q

This is a metabolic condition that resembles alcohol-induced liver dz but occurs in patients who are not heavy drinkers. It is usually strongly associated with obesity, dyslipidemia, hyperinsulinemia and insulin resistance, and overt type II DM

96
Q

What would LFTs of a patient with NAFLD usually show?

A

AST/ALT ration of <1

97
Q

What would you see on an imaging study of a patient with NAFLD?

A

Fatty infiltration seen on US, CT, or MRI

98
Q

What must you do when trying to identify NAFLD?

A

Exclused EtOH, Hep B and C and Hereditary Hemochromatosis

**Diagnosis of Exclusion

99
Q

How do you treat NAFLD?

A

Nothing good out there.
Vitamin E will be helpful in steatohepatitis
Advise patients on treating DM or losing weight.

Gastroenterology (12 decks)

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