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Clin Med- P > Hepatic Disorders > Flashcards

Hepatic Disorders Flashcards

1
Q

three clinical phases of acute viral hepatitis

A

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

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2
Q

lab values for acute viral hepatitis

A

> 500 for AST and ALT

may have hyperbilirubinemia

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3
Q

definition for chronic hepatitis. which acute hepatitis can turn chronic? what two things can chronic lead to?

A

disease > 6 months duration
HBV, HCV, and HDV
chronic can lead to end stage liver disease or hepatocellular carcinoma

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4
Q

what is fulminant hepatitis? what is the MC cause in the US and other causes

A

acute liver failure in patients with hepatitis

MC US cause is tylenol toxicity, others include viral hepatitis, reye’s syndrome, drug reactions

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5
Q

how to diagnose and tx fulminant hepatitis

A

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

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6
Q

how is Hep A and E transmitted? what is the greatest prevention measure to take?

A

fecal-oral contaminated food or water (international travel)

handwashing and improved sanitation, food safety, immunization in A

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7
Q

Hep A is associated with what CP finding

A

may have spiking fever

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8
Q

markers for diagnosis of acute Hep A and E

A

Hep A: IgM anti-HAV
past exposure: IgG HAV Ab with neg IgM

Hep E: IgM anti-HEV

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9
Q

tx for Hep A and E. what is the highest mortality of Hep E due to?

A

No treatment needed (self-limited infection)

Hep E: highest mortality due to fulminant hepatitis during pregnancy

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10
Q

pre-exposure and post-exposure prophylaxis for Hep A

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

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11
Q

what does Hep D infection require?

A

current Hep B infection (causes coinfection or superimposed infection)

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12
Q

how is Hep D transmitted? how to screen for and confirm Hep D infection?

A

primarily parenteral (blood or blood products)

screen: total anti-HDV, confirm: RT-PCR assays for HDV RNA in serum
* get Hep B serologies too

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13
Q

tx and prevention of Hep D infection

A

tx: no FDA approved management, interferon alpha used in management of chronic infection, liver txp definitive
prevention: Hep B vaccine

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14
Q

what is the MC infectious cause of chronic liver dz, cirrhosis, and liver transplant in US

A

Hep C

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15
Q

how is Hep C transmitted? unique CP finding for Hep C?

A

PARENTERAL: IV drug use MC in US, needlestick injury

CP finding: clay colored stool

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16
Q

what is the screening and confirmatory test for HCV?

A

screening: HCV antibodies (become positive wiithin 6 weeks)
confirmatory: HCV RNA
HCV antibodies DO NOT imply recovery (may be negative after recovery)

17
Q

serologies for acute Hep C, resolved acute hep C, and chronic Hep C

A

acute Hep C: + HCV RNA, +/- Anti-HCV
resolved Hep C: - HCV RNA, +/- Anti-HCV
chronic Hep C: + HCV RNA, + Anti-HCV

18
Q

what are some treatment options for Hep C? how do you check for response to therapy?

A

> 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

19
Q

how could some of the newer Hep C treatments affect patients?

A

it could potentially reactivate Hep B so make sure to perform HBV testing prior to initiating therapy

20
Q

chronic Hep B and chronic (carrier) state sxs

A

chronic: persistent sxs, elevated LFTs, and increased viral load
chronic (carrier state): AS, normal LFTs, low viral load, undetectable HBeAg

21
Q

how is Hep B transmitted? what is the vaccination schedule?

A

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

22
Q

3 step method to determine acute, chronic, recovery or immune status from Hep B serologies

A

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

23
Q

how to treat acute vs chronic Hep B

A

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

24
Q

what serology is positive in Hep B window period?

A

positive core antibody (anti-HBc) IgM

25
Q

hepatocellular carcinoma: biggest RF, clinical sxs

A

primary neoplasm of the liver
RF: chronic liver disease (HBV, HCV, HDV, cirrhosis)
clinical sxs: many are AS. weight loss, jaundice, abd pain, hepatosplenomegaly

26
Q

how to dx, tx, and surveillance of hepatocellular carcinoma

A

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)

27
Q

causes of nonalcoholic fatty liver disease? how do you diagnose this? tx?

A

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

28
Q

what is SBP? what is it a complication of? MC bug?

A

spontaneous bacterial peritonitis: infection of ascitic fluid WITHOUT perforation of bowel, complication of cirrhosis
*E. coli MC bug

29
Q

clinical sxs of SBP

A

fever, chills, abdominal pain, diarrhea

PE: ascites (fluid wave, shifting dullness)

30
Q

how to diagnose and tx SBP, prophylaxis after initial occurrence

A

dx = paracentesis (PMN’s > 250 is diagnostic for tx), culture of fluid definitive
tx = cefotaxime or ceftriaxone
proph: lifelong with bactrim or norfoloxacin

31
Q

what is cirrhosis? PP behind it. MC cause and 2nd

A

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)

32
Q

common PE findings for cirrhosis

A

ascites, hepatosplenomegaly, gynecomastia, spider angioma, caput medusa, bleeding, jaundice, muscle wasting, hepatic encephalopathy (confusion, asterixis), esophageal varices

33
Q

how to manage cirrhosis (esp encephalopathy, ascites, pruritus)

A
  • 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
34
Q

what is wilson’s disease? plus PP

A

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

35
Q

Clinical sxs of wilson’s disease

A

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)

36
Q

how to dx and tx wilson’s disease?

A

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

Clin Med- P (124 decks)

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