Primary Biliary Cholangitis, Primary Sclerosing Cholangitis, and Viral Hepatitis Flashcards Preview

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Flashcards in Primary Biliary Cholangitis, Primary Sclerosing Cholangitis, and Viral Hepatitis Deck (16)
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1
Q

Path and CM of PBC

A

AI destruction…B and T cells…anti-mito ABs against E2 subunit or pyruvate dehydroganse

Most are asx but can get hepatomegaly….with dz progression, can get comps including hyperpgi, xanthelasms, and vit D malapsorption

Most common initial is alk phos elevation with maybe elevate transmaminases….about half will get hypercholesteroelmai

Ass with other AI dzs

2
Q

Dx and managmeent of PBC

A

Elevated alk phos without ev od extrahepatic obstruction - middle aged women with mos of pruritis, fatigue and jaundice…elevated alk phos should have US

If alk phos and inc and US normal, get antimito AB measured

Can get liver biopsy as well - patchy destruciton of bile ducts in portal tracts…tracts surrounded by lymphocytic inflammatio nto form grandulomatous rxn centered on bile duct

Initial managmenet is therapy to delay destruction - ursodeoxycholic acid reduces secretion of cholesterol in bile and improves cholestasis

3
Q

PSC path

A

Mediated injury to the bile ducts

Inflamm surrounds large bile ducts with neutros and lymphos

INflmaed areas result in fibrosis and strictures…will alternate between dilation and stricture

4
Q

PSC CM/dx/comps/mg

A

Most asx but can get constitution sx

Most common presnetation is elevation in alk phos with or without elevation of milirubin

Dx - suspect in pts with IBD with elevated alk phos…get MRCP or ERCP….string or pearlys

Comps - Vit def, cholangiocarcinoma

Rapid pregression….ursodeoxycholic acid can dec secretion of cholesterol in bile….can get endoscopic dilation

Annual screening with US or MRCP to look for cholangiocarcinoma

5
Q

Hep A, Hep B, Hep C, D, and E

A

A - single strand RNA, naked, fecal-oral, 2-6 incubation, no chornic

B - dsDNA, enveloped, parenteral/sexual contact, 2-26 week incubation, some chornic

C - single strand RNA, enveloped, parenteral, 4-26 week incubation, most chronic

D - single strand RNA, enveloped (Hep B), parenteral, same as HBV, vairable

E - ssRNA, naked, fecal oral, 4-5 week incubation, no chronic

6
Q

Pathof hep

A

Viruses enter cells but do not destroy…CD4 T cells initiate immune response…CN8s play most role in clearing cells and pathogenesis

Lymphoplasmocytic mediated by CD4 is mostly in hepatic parenchyma with destruction of infection cells - spotty necrosis…portal tract is spared and developd scant infiltates…..ballooning degeneraion will occur with apoptotic cells….collagen framework collapses leading to cholestasis

Chonic - dense mononuclear infiltrate centered on portal tracts…fibrosis around portal tracts and septa form….B - ground glass and C shows scattered hepaticyte

7
Q

Acute asx with recovery

Acute sx infection

A

Cold-like sx and hepatic infection never recognized…Hep A and B during chilhood…Hep C almost always asx

Prodromal illness that can be variable…more fever with A and E….cons sx improve in a week or 2 with GI sx….elevation of AST and ALT with bilirubin later

8
Q

Acute fulminant hep

Chronic hep

A

Small percentage get hepatic fialure due to massive hpatic necoriss

Chronic more with hep C

9
Q

Hep A CM

A

Occassional morbidity and rare moretality

Mildly sx and self-limited

In children - subclinial,
Adult - more likely to get sx

Jaundice peaks in 2 weeks….as illness progresses, dark urine, acholic stools and jaundice

Dx from anti-HAV IgM ABs in the stool

10
Q

Hep B - repliaction

A

After host enters hepatocyte, DNA moves to nucleus where ti forms closed circular DNA….uses RNA polymerase of host…viral RNA transferred to cytoplasm where RNA is encapsulte into a viral core….mRNA forms template for DNA synthesases and get a neg DNA strand…using reverse transcriptase and neg strand template, a pos strand crrated….DNA core buds into intracellular membrane

11
Q

Hep B dx

A

HBs - heb B surface antigen formed by envelops GPs
HBc - hep B nucelocpasid core protein
HBe - associated with active viral rep

HBsAG appears prior to onset of sx, ABs do not develop until after the acute infection

HBe rises soon after HBs and sinifies active rep….if continued production, then will become chronic

HBc - remains within hepatocytes and is not detectable in the blood…BUT the anti-HBc IgM is detectable shortly after onset of sx….if gap between HBsAg disppearace and anti0HBs AB, anti-HBc IgM may be onley detectable sign

HBc - regardless of severity or chornicity

12
Q

Mg of He B

Tenofovir
Entecavir
IFN alpha
Lamivudine 
Adefovir
Telbivudine
A

Most with acute - conservatively

If worse - antivirla

Tenp - RT inhibt…1st line with rare resistance…contra if renal probs….effective if HIV

Ent - nucleoSIDE RT inhib….DOC with renal impairment

IFN - nhibit viral rep…atach of polyeth glycol reduces renal clearance….contraind if decomp

Lami - nucleoside RT inhib…exclusively if co-infected with HIV

Ade - TIDE RT inhibi - rarely used

Telbivudine - SIDE RT inhibt

13
Q

Hep C CM and dx

A

Chronic - asx with fluctuating levels of ALT

Screening - pts on chronic hemodialysis, clotting factors before 1987, organ transplant befroe 1992

anti-HCV antibody can indicate past exposure or ongoing infection….followed by HCV RNA PCR

In acute, ABs only presenti n 50% so if acute get both PCR and ABs

14
Q

Mg of Hep C

A

Type 1 - ledipasivr 9NS5A inhib and sofosbuvir (NS5B NA poly inhib) - 1st line
Also omvitasvir-pariaprevir and ritonavir (NS5A inhib-protease inhib with dasabuvir (NS5B RNA poly inhib)
Simepravir (protease) and sofosbuvir (RS5B RNA poly inhibt)

Type 2 and 3 - Sofosbuvir (NS5B RNA poly) and velpatasvir (NS5A inhibt)

15
Q

Hep D

A

Only a neg ssRNA that does not encode surgface proteins

Needs HBV and HBsAg to envelope virus for dissemintation

Indistinguihsable from HBV alone

16
Q

Hep E

A

Self-limited acute infection with more severe than type A….prolonged cholestatis

Fulminant hep occurs more frequently

Testing for anti-HEV Abs and HEV RNA PCR is availbale through CDC