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GI #2 > Hepatitis > Flashcards

Hepatitis Flashcards

1
Q

genetic disorder where intestinal iron absorption is unregulated, causing excess iron; mostly in white ppl

A

Hemachromatosis (HH)

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2
Q

4 ways we typically lose iron

A

sweat, skin cells, GI tract, periods

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3
Q

stages of HH in total body iron (in grams) before age 20, 20-30 and above 40 yo.

A

hepatic iron is above normal before the age of 20.
from 20-30 is typically when it gets diagnosed; can progress to tissue injury (~25g)
around 40yo, can be 35g of iron, causing cirrhosis & organ failure.

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4
Q

7 clinical features of HH

A
  • LFT abnormalities
  • hepatomegaly
  • fatigue
  • skin bronzing
  • DM
  • early onset impotence
  • arthralgia
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5
Q

who are your target pop. for HH?

A
  • unexplained liver dz
  • sx of HH
  • first degree relative w/ confirmed HH
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6
Q

4 measurements useful in diagnosing HH

A

ferritin– over 300
serum iron– over 180
transferrin saturation– over 50
TIBC– under 300

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7
Q

what is transferrin saturation

A

serum iron divided by TIBC; higher in males

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8
Q

initial screening test for HH? (1) interpret the results (2)

A

TS + ferritin
if TS under 45% + normal ferritin= no further eval.
if TS over 45% and/or elevated ferritin= genetic testing w/ HFE genotype PCR testing

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9
Q

how is HH treated? initial vs maintenance

A
  • phlebotomy before cirrhosis or DM to improve mortality
  • 1-2x a week initial
  • 3-12x/yr maintenance; can start this after ferritin drops
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10
Q

what is the single most important determinant of patient outcome in HH?

A

cirrhosis development

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11
Q

does phlebotomy affect risk of hepatocellular carcinoma in HH?

A

no– still a threat

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12
Q

2 most common cause of death in HH

A

complications from portal HTN & HCC

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13
Q

general prognosis for noncirrhotic HH patient

A

almost the same as general population if treated– which is why early detection is important

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14
Q

for hep A-E tell me
- acute or chronic or both
- route of transmission

A
  • A: acute, fecal oral
  • B: Both, bodily fluids
  • C:both, blood
  • D: chronic only, only with D
  • E: acute, fecal-oral,
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15
Q

which viral hepatitis is gotten via fecal-oral route? which is associated with worst outcome if pregnant?

A
  • A & E are fecal-oral
  • E is associated with increased risk of fulminant hepatitis if pregnant
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16
Q

which 3 viral hepatitis can be chronic? which one is chronic only & only exists with B?

A

B,C,D can be chronic
D can only be chronic & only with B

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17
Q

which hep is gotten via blood? via bodily fluids?

A

Hep C: blood
Hep B: bodily fluids

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18
Q

what is the condition?diagnosis?tx?

  • self-limting sx of fatigue, fever, N/V, jaundice, dark urine, itching
A

hep A
Labs– IgM,IgG
Tx: supportive

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19
Q
  • DNA virus found in blood, semen, vaginal fluids
  • can survive outside the body for 7 days
  • highest in asian countries
  • higher risk of needlestick transmission than HIV & HCV
A

HBV

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20
Q

two ways of transmitting HBV in high endemic areas vs low endemic areas

A
  • high: vertical or horizontal transmission; kids
  • low: percutaneous or sexual; adults
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21
Q

list some groups that should be screened for HBV

A
  • pregnant people & kids of infected moms
  • from or has parent from high endemic area
  • sexual, household and family of infected
  • those at risk of exposure to blood–healthcare workers, hemodialysis ppl
  • gay men
  • ppl w/ HIV or hep C
  • elevated ALT of unknown etiology
22
Q

how does age at initial infection predict likelihood of resolution of acute infxn

A

the younger you are when you get it, the higher the chance is that it will become chronic (90%)

23
Q

in regards to Hep B serology,

if this protein is positive, you are definitely infected.. what protein is this?

A

HBsAg– surface antigen

24
Q

in regards to Hep B serology,

if this protein is positive, you have immunity acquired either through prior infection or vaccination

A

anti-HBs or HBsAb– antibody to surface antigen

25
Q

in regards to Hep B serology,

if this is positive, its either current or past infection & this will be positive forever

A

Anti-HBc or HBcAb– total antibody to core antigen

26
Q

in regards to Hep B serology,

this is only positive during acute infection or acute flares of chronic infection

A

IgM anti-HBc– IgM class of antibody to core antigen; early phase Ig to core protein

27
Q

interpret this Hep B serology report

  • HBsAg: +
  • Anti-HBs: -
  • anti-HBc: -
A

early acute infection

28
Q

interpret this Hep B serology report

  • HBsAg: +
  • Anti-HBs: -
  • anti-HBc: +
A

early or chronic infection

29
Q

interpret this Hep B serology report

  • HBsAg: -
  • Anti-HBs: +
  • anti-HBc: +
A

cleared HBV infection- immune

30
Q

interpret this Hep B serology report

  • HBsAg: -
  • Anti-HBs: +
  • anti-HBc: -
A

HBV vaccinated!

31
Q

test to see likelihood of viral transmission
< 2K IU/mL = inactive infection

A

HBV DNA viral load measurement

32
Q

tx of acute HBV (2)

A
  • mostly resolves on its own w/ supportive care
  • monitor LFT and serology for conversion
33
Q

chronic HBV tx goals are achieved by.. (2)

A
  • reduced HBV DNA, HBeAg
  • normalized ALT & resolution of inflammation and fibrosis

NOTE: treatment is not curative

34
Q

two types of chronic HBV tx & their duration. which has more side effects? drug resistance? more viral reactivation after stopping?

A
  • interferon injections x 48 wks– more SE, no resistance, uncommon for reactivation to happen
  • years or life long Oral antivirals (ends in -vudine or -vir)
35
Q

2 ways to prevent hep B. which is active? which lasts longer?

A
  • HBIG: passive, single dose for immediate protection for few months
  • Vaccine: active 3 doses for protection over 20 years.
36
Q

who is recommended to get HBIG? (3)

A

infants of HBV+ moms
needlestick injury
postliver transplant

37
Q

can those with chronic HBV kiss and share food w/ others

A

yes

38
Q

RNA virus that only exists with Hep B; superinfection or coinfection increases risk of severe complication

A

HDV

39
Q

what are 3 things that can happen from superinfection/coinfection?

A

liver failure w/ acute infection
hepatocellular carcinoma
progression to cirrhosis

40
Q
  • single stranded RNA virus
  • most will progress to stable chronic infection.
  • mostly in younger native american males and IDU
A

HCV

41
Q

who gets screened for HCV

A
  • everyone born btwn 1945 to 1965
  • otherwise, then ppl w/ risk factors (IVDU, HIV, abnormal ALT, hemodialysis, transfusion before 1992, known exposure)
42
Q

if you do HCV antibody test and its positive, now what?

A

do HCV RNA test– if positive then current HCV if not then no current HCV infection

43
Q

how is HCV treated? is it curative?

A

direct-acting antivirals (DAA) x 8-12 wks- curative
name of meds: glecaprevir/pibretasvir, sofosbuvir/velpatasvir, ledipasvir/sofosbuvir

44
Q

what is this? how is it screened? Treated (2)?

hereditary disorder of copper metabolism in young adults that can present with acute or chronic hepatitis
- Sx: dysarthria, ataxia, chorea, depression, arthralgia
- brown or green rings in descent membrane of cornea (kayser-fleischer ring)

A

hepatolenticular degeneration/wilson’s disease
Screen: serum & urine copper high; serum ceruloplasmin low
tx: Copper chelation w/ Penicillamine & Trientine; liver transplant is curative

45
Q

what is this and how is it treated?

  • often sx of fatigue, joint ache, jaundice, abd pain in female 15-40 yo
  • AST/ALT predominance (esp ALT)
  • Dx: (+) ANA w/ elevated IgG, smooth muscle Ig & liver biopsy
A

auto-immune hepatitis
immune suppression w/ steroids and azathioprine

46
Q

what is this? labs (2)? treatment (2)?

  • autoimmune destruction of intralobular bile ducts in middle-aged women
  • dry mouth, dry eyes, fatigue, itching, arthralgias
  • portal HTN predominates
  • hypercholesterolemia
A

primary biliary cholangitis/cirrhosis (PBC)
Labs: (+)AMA, high ALP & GGT
tx: Ursodiol, obetacolic acid

47
Q

what is this? labs (2)? treatment (2)?

  • autoimmune dz of intra & extra-hepatic bile ducts mostly in men in their 30s
  • associated with ulcerative colitis
  • portal HTN predominates
A

primary sclerosing cholangitis (PSC)
labs: high ALP, GGT + high AST/ALT
tx: supportive + surveillance for cholangiocarcinoma +/- colon cancer

48
Q

according to PPP, which condition has the key histologic feature of “onion skin” fibrosis around the bile ducts?

A

PSC

49
Q

for which two hepatitis, are there vaccines?

A

hep A (2 shots), hep B (3 shots)

50
Q

which condition has a beaded appearance on ERCP?

A

PSC

GI #2 (9 decks)

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