Hepatitis Flashcards
Liver histology
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
Patterns of Liver Disease
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
Presenting symptoms
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
Lab work to consider
LFTs: ALT/AST, alk. phos, bilirubin, albumin, PT/INR
Hepatitis A/B/C antibodies
Autoimmune antibodies
<50 Ceruloplasmin (Wilson’s)
TSH
Iron, ferritin (hemachormatosis)
Imaging Indicated
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
Liver Biopsy
Indicated when:
Imaging not consistent with persistently elevated LFT’s
To confirm specific diagnosis:
- Autoimmune
- Wilson’s
- PBC
- Hemachromatosis
Acute vs. Chronic Hepatitis
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
Causes of hepatitis (both acute and chronic)
Viruses
Drugs
EtOH
Toxins
Autoimmune
PBC/PSC
Wilson’s/A1A/Hemochromatosis
Ischemia
Fulminant Liver Failure
(definition, etiology, sxs, labs, tx)
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
Definition of Acute Liver Failure
Any degree of encephalopathy
**Increased INR (>1.5)
In a pt without cirrhosis with an illness less than 26 weeks duration
Hepatitis A Risk Factors
Live/travel to underdeveloped areas
Exposure to infected individuals
IVDU
More likely to develop sxs when >6 y.o.
Hepatitis A Presenting Sxs
Fever
Fatigue
Anorexia/Nausea
Jaundice
Dark urine, acholic stools
Joint pain
Sxs usually last for less than 2 months
Hepatitis A Lab tests
HAV Antibody can be present for decades
Hepatitis A Tx and Immunization
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
Hepatitis B Epidemiology
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
Acute Hep B Symptoms
Fever
Fatigue
Anorexia/Nausea
Vomiting
Dark urine/acholic stools
Joint pain
Jaundice
Chronic Hep B symptoms
Asymptomatic
Can present with a broad range of sxs from chronic hepatitis to HCC
Hep B Serological Markers
There are many different markers that can help differentiate stage of disease and/or vaccination status
Hep B Treatment
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)
Chronic Hep B Phases
Active Disease: high viral level and increased LFTs
Carrier: low viral level and normal LFTs
Immune tolerant: high viral level and normal LFTs
Chronic Hep B Complications
Majority remain asymptomatic until cirrhosis develops
Chronically infected may die prematurely of cirrhosis or liver CA (15-25%)
Hepatitis C Risk Factors
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
Acute vs. Chronic Hep C.
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)
Lab Testing
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
Hepatitis C Tx
Avoid usage of alcohol
Should check with provider before using any medications
Medical treatment depends on genotype of virus
Medication Induced Hepatitis
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
Autoimmune liver diseases
Autoimmune Hepatitis
Primary Sclerosing Cholangitis (PSC)
Primary Biliary Cirrhosis (PBC)
Autoimmune Hepatitis
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
Primary Sclerosing Cholangitis
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
Primary Biliary Cirrhosis (PBC)
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
Metabolic Liver Diseases
Alpha 1 Anti-trypsin Deficiency
Wilson’s Disease
Hemochromatosis
A1A Deficiency
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
Wilson’s Disease
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
Hemochromatosis
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
Other systemic diseases that have liver involvement
Celiac disease
Sarcoidosis
Amyloidosis
Tuberculosis
