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Gastroenterology > Hepatitis > Flashcards

Hepatitis Flashcards

1
Q

Liver histology

A

Hepatocytes (do all the work)

  • synthesize serum proteins (albumin, coagulation factors, hormonal and growth factors)
  • produce bile
  • regulate nutrients (glucose, glycogen, lipids, cholesterol, amino acids)

Also: Kupffer cells

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2
Q

Patterns of Liver Disease

A

Hepatocellular

  • Viral hepatitis, alcohol induced liver disease
  • Livery injury and inflammation

Cholestatic (obstructive)

  • Obstruction, primary biliary cirrhosis, primary sclerosing cholangitis, drug induced
  • Inhibition of flow is primary issue

Mixed: features of both

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3
Q

Presenting symptoms

A

scleral icterus, jaundice

fatigue and malaise

itching (b/c high bilirubin)

RUQ pain

abdominal distention

N/V

lack of appetite

acholic stools (clay colored b/c bile deficiency), steatorrhea

drark urine

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4
Q

Lab work to consider

A

LFTs: ALT/AST, alk. phos, bilirubin, albumin, PT/INR

Hepatitis A/B/C antibodies

Autoimmune antibodies

<50 Ceruloplasmin (Wilson’s)

TSH

Iron, ferritin (hemachormatosis)

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5
Q

Imaging Indicated

A

Perform US first

Can add dopler if concerned for portal vein thrombosis

CT if concerned about pancreas

MRI can be more helpful when evaluating liver masses

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6
Q

Liver Biopsy

A

Indicated when:

Imaging not consistent with persistently elevated LFT’s

To confirm specific diagnosis:

  • Autoimmune
  • Wilson’s
  • PBC
  • Hemachromatosis
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7
Q

Acute vs. Chronic Hepatitis

A

Acute

  • <6 months
  • Jaundice present
  • Sx: anorexia, malaise, dark urine, fever, abdominal pain

Chronic:

  • Often no sxs. Sometimes see sxs of cirrhosis
  • At risk of cirrhosis, HCC
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8
Q

Causes of hepatitis (both acute and chronic)

A

Viruses

Drugs

EtOH

Toxins

Autoimmune

PBC/PSC

Wilson’s/A1A/Hemochromatosis

Ischemia

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9
Q

Fulminant Liver Failure

(definition, etiology, sxs, labs, tx)

A

The presence of acute liver failure within 8 weeks of the onset of jaundice in a pt without previous liver dz

MC causes: acetominophen, idiopathic, idiosyncratic drug rxn, viral, ischemia

Symptoms: malaise, nausea, jaundice

Labs: Very high AST/ALT, elevated bilirubin and INR

Tx: Transplant

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10
Q

Definition of Acute Liver Failure

A

Any degree of encephalopathy

**Increased INR (>1.5)

In a pt without cirrhosis with an illness less than 26 weeks duration

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11
Q

Hepatitis A Risk Factors

A

Live/travel to underdeveloped areas

Exposure to infected individuals

IVDU

More likely to develop sxs when >6 y.o.

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12
Q

Hepatitis A Presenting Sxs

A

Fever

Fatigue

Anorexia/Nausea

Jaundice

Dark urine, acholic stools

Joint pain

Sxs usually last for less than 2 months

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13
Q

Hepatitis A Lab tests

A

HAV Antibody can be present for decades

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14
Q

Hepatitis A Tx and Immunization

A

Treatment: support, self limited infecction

Immunization for: IVDU, pts with chronic liver dz, travelers, health care workers, immunosuppressed

*incidence of hep A has substantially decreased due to vaccine

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15
Q

Hepatitis B Epidemiology

A

New infections have declined substantially because universal vaccination campaigns

Common becomes chronic viral hepatitis.More common to become chornic infection in children.

Mortality due to complications secondary to disease.

Common in Asia and Africa where transmited vertically

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16
Q

Acute Hep B Symptoms

A

Fever

Fatigue

Anorexia/Nausea

Vomiting

Dark urine/acholic stools

Joint pain

Jaundice

17
Q

Chronic Hep B symptoms

A

Asymptomatic

Can present with a broad range of sxs from chronic hepatitis to HCC

18
Q

Hep B Serological Markers

A

There are many different markers that can help differentiate stage of disease and/or vaccination status

19
Q

Hep B Treatment

A

Acute: supportive

Chronic: depends on LFTs, serologies, and fibrosis level of the liver

Monitoring Chronic Hep B: AFP and Liver US every 6 months (for specific populations)

20
Q

Chronic Hep B Phases

A

Active Disease: high viral level and increased LFTs

Carrier: low viral level and normal LFTs

Immune tolerant: high viral level and normal LFTs

21
Q

Chronic Hep B Complications

A

Majority remain asymptomatic until cirrhosis develops

Chronically infected may die prematurely of cirrhosis or liver CA (15-25%)

22
Q

Hepatitis C Risk Factors

A

Those born 1945-1965 (Baby Boomers)

Blood transfusion prior to 1992 when anti-HCV was introduced

Tattoos and body piercing

IVDU/Nasal DU

HIV +

Usually do not see vertical transmission

23
Q

Acute vs. Chronic Hep C.

A

Don’t often see pts with acute infections because they will usually clear virus without seeing any symptoms

75-85% of pts progress to chornic Hep C (chronic liver disease, cirrhosis, or HCC can develop)

24
Q

Lab Testing

A

HCV RNA by PCR most sensitive

Can first be detected 10 weeks after exposure

Also get HCV genotype:

  • 1a, 1b: MC, but most difficult to tx
  • 2, 3: easier to tx
25
Q

Hepatitis C Tx

A

Avoid usage of alcohol

Should check with provider before using any medications

Medical treatment depends on genotype of virus

26
Q

Medication Induced Hepatitis

A

Usually cholestatic pattern of injury

Ingestion of drug may be weeks before sxs, adn can take months to resolve (3-12mo)

Need liver biopsy to confirm dx

Some example drugs: doxy, minocycline, augmentin, amiodarone, and tylenol

27
Q

Autoimmune liver diseases

A

Autoimmune Hepatitis

Primary Sclerosing Cholangitis (PSC)

Primary Biliary Cirrhosis (PBC)

28
Q

Autoimmune Hepatitis

A

MC middle aged women

Usually associated with other autoimmune diseases

Sxs: Can vary from only fatigue to fulminant hepatitis. Jaundice, RUQ pain, joint aches

Labs: High IgG, ANA, smooth muscle antibody (autoimmune markers), and elevated total protein

Liver bx needed to make dx

29
Q

Primary Sclerosing Cholangitis

A

MC in ~40 y.o. men with diffuse inflammation and fibrosis of biliary tree

Associated with UC

Sxs: fatigue, pruritis. Rarely RUQ discomfort

Labs: Alk phos 3-4X normal; may see elevated bilirubin

Imaging: MRCP, if not conclusive do ERCP

30
Q

Primary Biliary Cirrhosis (PBC)

A

MC 30-50y.o. women

Causes destruction of interlobular and septal bile ducts

Unknown etiology

Sxs: fatigue, pruritis, jaundice

PE: excoriations, xathelasmas on eyelids, xanthomas on extensor surfaces

Labs: Alk. phos 3-4X normal, ALT/AST mild to moderately elevated, elevated IgM, elevated cholesterol and HDL

31
Q

Metabolic Liver Diseases

A

Alpha 1 Anti-trypsin Deficiency

Wilson’s Disease

Hemochromatosis

32
Q

A1A Deficiency

A

A1A is a liver enzyme that helps break down trypsin adn other proteases. In its absence, proteins are deposited into liver

Causes pulmonary dysfunction first, and pts usually have FHx of emphysema. **Refer to pulmonologist

No tx once develop liver complications. Can consider transplant

33
Q

Wilson’s Disease

A

Autosomal recessive disorder that leads to excessive copper deposition in liver, eyes, kidneys, joints, and RBCs

MC presents as cirrhosis or neuro deficits (Also tremor, Kayser-Fleischer rings, arthropathy, hemolytic anemia)

Rare disease, exclusively diagnosed before age 40.

Decreased ceruloplasmin (Cu carrying protein in blood), inc’d urine copper, inc’d copper on liver bx

Tx: Depends on type, but Cu Chelation or transplant

34
Q

Hemochromatosis

A

Autosomal recessive

Abnormal iron storage==> iron builds up in liver, heart, pancreas, and pituitary gland

Sxs: fatigue, malaise, arthrlagias

Women present later due to menses

Dx: elevated iron saturation, ferritin; genetic testing; Gold Standard is liver bx

Tx: phlebotomy

35
Q

Other systemic diseases that have liver involvement

A

Celiac disease

Sarcoidosis

Amyloidosis

Tuberculosis

Gastroenterology (20 decks)

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