Hepatic Disorders Flashcards
three clinical phases of acute viral hepatitis
1) . prodromal phase: malaise, fatigue, URI sxs, athralgia, decreased desire to smoke, abd pain, loss of appetite
2) . icteric phase: jaundice (most don’t develop this phase)
3) . fulminant phase: encephalopathy, coagulopathy, hepatomegaly, jaundice, ascites, asterixis
lab values for acute viral hepatitis
> 500 for AST and ALT
may have hyperbilirubinemia
definition for chronic hepatitis. which acute hepatitis can turn chronic? what two things can chronic lead to?
disease > 6 months duration
HBV, HCV, and HDV
chronic can lead to end stage liver disease or hepatocellular carcinoma
what is fulminant hepatitis? what is the MC cause in the US and other causes
acute liver failure in patients with hepatitis
MC US cause is tylenol toxicity, others include viral hepatitis, reye’s syndrome, drug reactions
how to diagnose and tx fulminant hepatitis
dx: sxs, encephalopathy, abnormal LFTs, increased INR, hypoglycemia, elevated ammonia
* look for tylenol or hep levels
tx: supportive by IV fluids/electrolytes, mannitol if ICP elevation, Blood products if active bleeding, lactulose for encephalopathy
* liver transplant definitive
how is Hep A and E transmitted? what is the greatest prevention measure to take?
fecal-oral contaminated food or water (international travel)
handwashing and improved sanitation, food safety, immunization in A
Hep A is associated with what CP finding
may have spiking fever
markers for diagnosis of acute Hep A and E
Hep A: IgM anti-HAV
past exposure: IgG HAV Ab with neg IgM
Hep E: IgM anti-HEV
tx for Hep A and E. what is the highest mortality of Hep E due to?
No treatment needed (self-limited infection)
Hep E: highest mortality due to fulminant hepatitis during pregnancy
pre-exposure and post-exposure prophylaxis for Hep A
pre-exposure: give vaccine 2 doses, 6 months apart for ppl with increased risk of transmission or international travelers aged 6 mo or older
post-exposure:
-healthy aged 1-40 yo: HAV vaccine
-healthy > 40 yo: HAV vaccine +/- immunoglobulin
-immunocompromised or chronic liver dz: HAV vaccine plus HAV immunoglobulin
*all given within two weeks of exposure
what does Hep D infection require?
current Hep B infection (causes coinfection or superimposed infection)
how is Hep D transmitted? how to screen for and confirm Hep D infection?
primarily parenteral (blood or blood products)
screen: total anti-HDV, confirm: RT-PCR assays for HDV RNA in serum
* get Hep B serologies too
tx and prevention of Hep D infection
tx: no FDA approved management, interferon alpha used in management of chronic infection, liver txp definitive
prevention: Hep B vaccine
what is the MC infectious cause of chronic liver dz, cirrhosis, and liver transplant in US
Hep C
how is Hep C transmitted? unique CP finding for Hep C?
PARENTERAL: IV drug use MC in US, needlestick injury
CP finding: clay colored stool
what is the screening and confirmatory test for HCV?
screening: HCV antibodies (become positive wiithin 6 weeks)
confirmatory: HCV RNA
HCV antibodies DO NOT imply recovery (may be negative after recovery)
serologies for acute Hep C, resolved acute hep C, and chronic Hep C
acute Hep C: + HCV RNA, +/- Anti-HCV
resolved Hep C: - HCV RNA, +/- Anti-HCV
chronic Hep C: + HCV RNA, + Anti-HCV
what are some treatment options for Hep C? how do you check for response to therapy?
> 95% cure rate with 12 wks of newer oral therapy
newer: Harvoni, elbasvir/grazoprevir
older: interferon alpha-2b + ribavirin
* response to therapy is determined by PCR-RNA viral load at 12 and 24 weeks after therapy
how could some of the newer Hep C treatments affect patients?
it could potentially reactivate Hep B so make sure to perform HBV testing prior to initiating therapy
chronic Hep B and chronic (carrier) state sxs
chronic: persistent sxs, elevated LFTs, and increased viral load
chronic (carrier state): AS, normal LFTs, low viral load, undetectable HBeAg
how is Hep B transmitted? what is the vaccination schedule?
parenteral, percutaneous, sexual
*can’t have vaccine with baker’s yeast allergy
Infant: birth, 1-2 mo, 6 mo
adult: 1st dose, 2nd 1 mo later, 3rd 6 mo after initial
3 step method to determine acute, chronic, recovery or immune status from Hep B serologies
1). Look at SURFACE antigen (HbsAg): if positive then it is acute or chronic infection
2). Continue on to look at CORE antibody (anti-HBc): if IgM then acute, If IgG then chronic
(positive HbeAg means chronic Hep B is replicative)
3). Go to step three from step 1 if HbsAg is negative: look at SURFACE ab (anti-HBs)
*if surface Ab is only thing positive: vaccination
if surface Ab is positive and core antibody (anti-HBc) is IgG: recovered
how to treat acute vs chronic Hep B
acute: only supportive tx needed
chronic: antiviral therapy only if severe, persistent sxs, marked jaundice, inflammation on liver biopsy (Entecavir, tenofavir)
* can stop chronic tx if two tests 4 weeks apart have negative HbsAg
what serology is positive in Hep B window period?
positive core antibody (anti-HBc) IgM
hepatocellular carcinoma: biggest RF, clinical sxs
primary neoplasm of the liver
RF: chronic liver disease (HBV, HCV, HDV, cirrhosis)
clinical sxs: many are AS. weight loss, jaundice, abd pain, hepatosplenomegaly
how to dx, tx, and surveillance of hepatocellular carcinoma
dx: contrast enhanced CT, liver biopsy
tx: surgical resection if confined to lobe and not associated with cirrhosis
surveillance: US every 6 months (+/- alpha-fetoprotein) in high risk pts (active Hep B infection, high viral load)
causes of nonalcoholic fatty liver disease? how do you diagnose this? tx?
causes: obesity, HLD, glucocorticoid use, DM
Dx = biopsy which shows microvesicular fatty deposits similar to alcoholic liver disease WITHOUT hx of heavy alcohol use
Tx = managing underlying cause
what is SBP? what is it a complication of? MC bug?
spontaneous bacterial peritonitis: infection of ascitic fluid WITHOUT perforation of bowel, complication of cirrhosis
*E. coli MC bug
clinical sxs of SBP
fever, chills, abdominal pain, diarrhea
PE: ascites (fluid wave, shifting dullness)
how to diagnose and tx SBP, prophylaxis after initial occurrence
dx = paracentesis (PMN’s > 250 is diagnostic for tx), culture of fluid definitive
tx = cefotaxime or ceftriaxone
proph: lifelong with bactrim or norfoloxacin
what is cirrhosis? PP behind it. MC cause and 2nd
irreversible liver fibrosis with nodular regeneration secondary to chronic liver disease
PP: nodules cause increased portal pressure (macronodules associated with higher risk of hepatocellular carcinoma)
-Chronic Hep C is MC cause, alcohol next (also nonalcoholic fatty LD)
common PE findings for cirrhosis
ascites, hepatosplenomegaly, gynecomastia, spider angioma, caput medusa, bleeding, jaundice, muscle wasting, hepatic encephalopathy (confusion, asterixis), esophageal varices
how to manage cirrhosis (esp encephalopathy, ascites, pruritus)
- avoid alcohol and hepatotoxic meds, vaccines, weight reduction, tx any underlying cause, txp is definitive
- encephalopathy: lactulose or rifaximin
- ascites: sodium restriction, diuretics (spironolactone, lasix)
- pruritus: cholestyramine
what is wilson’s disease? plus PP
autosomal recessive leading to copper accumulation in the body (liver, brain, kidney, joints, kidney)
*defect in copper transporting protein (ceruloplasmin) which leads to decreased biliary copper excretion
Clinical sxs of wilson’s disease
liver: hepatitis, hepatosplenomegaly, cirrhosis, liver failure
CNS: dysarthria (MC), dystonia, parkinson like sxs
psych: psychosis, delusions, personality changes
joints: arthralgias from copper deposition
eyes: “kayser-fleischer” rings (brown or green rings due to copper deposition on cornea)
how to dx and tx wilson’s disease?
dx: decreased serum ceruloplasmin 1st, inc 24 hr urinary copper excretion (useful for monitoring tx), liver biopsy is definitive (increased hepatic copper)
tx: copper chelating agents (trientine or D-Penicillamine + B6, zinc supplementation (interferes with intestinal copper absorption
