GI_Final_Session 5

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Anonymous
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GI_Final_Session 5
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2011-03-04 23:48:40
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GI gastrointestinal system
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GI final session 5 westernU 2011
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  1. (A)What is the most common cuase of gallstone in the US?
    (B)What are risk factors of gallstone?
    • (A) excess cholesterol to bile salts & lecithin
    • (B) fat (obesity), fertile (high estrogen), female of forty (age)
  2. what are important factors in the progression of cholecystitis to cholangitis?
    Predisposing factor: Billiary obstruction -->calculi, tumor or stricture

    • Bacterial infection:
    • E coli, klebsiella, Pseudomonas, enterobacter and
    • Enterococcus species
    • anaerobic infection like bacteroides
    • ascend from duodenum to billiary tract and then enter portal circulation to cause septicemia.
  3. Person presents with fever, RUQ pain, jaundice. What is that called?
    Charcoat's triad
  4. What are the clinical manifestations of acute cholangitis? if they become septic?
    • charcoat's triad
    • *clay colored stool, dark colored urine, & pruritis occurs in all obstruction

    if pt becomes septic: +confusion, HoTN --> now called Reynod's Pentad
  5. Explain the studies needed to determine acute cholangitis.
    • Labs:
    • LFTs show cholestatic pattern: high conj.Bili, AlkPhos may be elevated
    • Culture: bile
    • Image:
    • US (may see dilated common bile duct before stone) or CT
    • ERCP (endoscopic retrograde cholangiopancreatography): will show stones
    • MRCP only if ERCP unsuccessful or post-cholecystectomy pt b/c ERCP is high risk with them
  6. Exp. Tx for Cholangitis
    • Abiotics:
    • -amp-sublactam or piperacillin-tazobactem or carbapenem
    • -OR metronidazole + (ceftriaxone or FQs)

    • Drainage:
    • -endoscopic sphincterotomy w/stone extraction &/or stent insertion Tx of choice for biliary drainage in acute cholangitis

    • Sugery indiated in:
    • -persistent abd pain
    • -HoTN despite adequate resuscitation
    • -Fever >39C (102F)
    • -Mental confusion (predicts poor outcome)
  7. What is the route of spread of HepA?
    fecal-oral
  8. what are the risk factors for HepA?
    • international travel (mexico, Asia, South Am., etc)
    • homosexual activity
    • employee of daycare center
    • household contact of hepA pt
  9. What is the “disconnect” between the HAV viral genome and its antigenicity?
    • +ssRNA means it is similar to mRNA and THUS can be immediately translated into protein (in comparison, HIV, although +, will never immediately translate).
    • Eventhough HepA (HAV) is a +ssRNA, there is only one serotype & therefore infection or vaccine can give long-term immunity.
  10. What is important about the structure of HAV as it relates to its ability to infect humans?
    • HAV is a Heparnavirus in the Picornaviridae family
    • it is naked (NON-enveloped) THU can survive in environment longer (water/sea water for >months)
  11. What is the cause of the pathology associated with HAV?
    • The virus replicates in hepatocytes and are shed from those cells and are released in the stool. HAV can also be found in saliva and serum NOT urine.
    • The damage associated with HAV is not directly due to the virus since it happens to be “non-cytolytic” virus and instead, much is due to the immune response against the virus.
  12. What are the histological features of a HAV infection?
    • may see large pink cells undergoing "ballooning degeneration", later they will shrink to form an eosinophilic "councilman body"
    • mononuclear inflammatory cell infiltrate extends from the portal areas
  13. What are the clinical features of HAV?
    • *mostly dz is aSxic/benign & self limiting but, AFTER incubation of at least 30d can see:
    • --Prodromal Phase: fatigue, malaise, N/V, anorexia, fever, RUQ pain
    • --Icteric phase a few days later: jaundice, dark urine, acholic stool (light colored stool).
  14. how to dx HAV?
    • serology (ELISA) looking for presence of AB vs virus.
    • IgM during acute infection--usually present 5-10d before onset Sxs & undetectable after 6mo's ([virus] in stool decreases after jaundice appears...~2wks)
    • IgG upon recovery (IgG rises much later!)
  15. explain the timeline of HAV infection
  16. what are the complications of HAV infection?
    fulminant hepatitis-->requires liver transplant
  17. what are pre-exposure porphylaxis recommendations for HAV?
    • routine vaccine for kids 12-23mo's
    • international travelers
    • MSM, frequent blood/plamsa recipients, chronic liver dz (including HepB & C)
  18. what do you Rx for active immunization? for travel?
    • for active: 2doses of vaccine 6mo apart
    • for travel: vaccine of >2wks before travel & healthy; Ig if person is immunocompromised
  19. what are the post-exposure prophylaxis for HAV?
    Hep A vaccine alone for healthy <41yo

    • all others receiving passive immunization: pooled Ig
    • (for kids <12mo, immuno compromised, pts w/chronic liver dz or have vaccine contraindications.)
  20. Explain reasons for AST:ALT >2:1
    • alcohol-related liver dz
    • non hepatic: strenuous exercise, hemolysis, myopathy, thyroid dz, macro-AST
  21. explain risk factors for alcoholic liver dz
    • quantity: 1 beer, 4oz wine, 1oz80proof all have ~12gEtOH; M >60-80g/d or F>20-40g/d x10yrs
    • gender: F>M
    • HepC
    • obesity
    • genetics: homozygous for ALDH*2 unable to oxidize acetaldehyde & don't tolerate EtOH
  22. describe the pathogenesis fo alcoholic liver dz (image)
  23. describe the pathogenesis of alcoholic liver dz.
    • short-term ingestion of <80gEtOH (6beers) over 1-2d produces mild, reversible hepatic steatosis.
    • daily intake of >80 = risk of injury
    • daily intake >160g/d x10-20 yrs -->severe injury
    • **however only 10-15% of alcoholics develop cirrhosis
    • OTHER FACTORS:
    • gender - F>M; estrogen increases gut permeability to endotoxins --> increase LPS receptor CD14 in Kupffer cells --> predisposes to increased production of pro-inflammatory cytokines & chemokines.
    • ethnicity - rate cirrohsis AfAm > white
    • genetics - homozygous ALDH*2
    • comorbid conditions: Fe overload & infections w/ HCV/HBV increase severity of alcoholic liver dz
  24. describe the detrimental effects of alcohol on hepatocellular fn.
    exposure --> steatosis, dysfn of mito & cellular membranes, hypoxia, oxidative stress
  25. what causes hepatocellular steatosis specifically?
    • shunting of nL substrates away from catabolism & toward lipid biosynthesis due to generation of excess NADH + H+ (reduced form)
    • impaired assembly & secretion of lipoproteins
    • increased peripheral catabolism of fat
  26. describe the factors in the pathogenesis of alcoholic hepatitis.
    • acetaldehyde: the major intermediate metabolite of EtOH, induces peroxidation & acetaldehyde-protein adduct formation, further disrupting cytoskeletal & membrane fn.
    • cP450 produces reactive O2 species (ROS) that react w/ cellular proteins, damage membranes & alter hepatocellular fn.
    • alcohol-induced impaired metabolism of methionine --> decreased intrahepatic glutathione levels, thus sensitizing liver to oxidative injury
    • induction of CYP2E1 & other cP450's increases alcohol catabolism in the ER and enhances the conversion of other drugs to toxic metabolites
  27. how does alcohol specifically play a role in the inflammation in alcoholic hepatitis?
    • causes release of bacterial endotoxin from the gut into portal circulation --> inflamatory responses in the liver
    • -->activation of NF-kB, release of TNF, IL-6, TGF-a
    • stimulatese the release of endothelins from sinusoidal endothelial cells --> vasoconstriction & contraction of activated sellate cells (myofibroblasts) --> decreased hepatic sinusoidal perfusion
  28. what are signs of "fatty liver"?
    tender hepatomegaly w/ mild elevation of serum bili & AlkPhos.
  29. describe this image:
    • globular red hyaline material w/in hepatocytes = Mallory's hyaline aka "alcoholic" hyaline. they are aggregates of intermediate filaments in cytoplasm from hepatocyte injury.
    • **can also see the eosinophilic Mallory bodies in hepatocytes in Masson stain (stains fibrous tissue blue)
    • will also have swelling of hepatocytes, necrosis & PMN's
  30. what are some clinical signs of alcoholic hepatitis?
    • fever
    • spider nevi
    • jaundice
    • abd pain stimulating an acute abd
    • **majority are aSxic
  31. what are diagnostic features of alcoholic liver dz?
    • LFTs:
    • -AST:ALT rise 2-7x AND >2:1
    • -AST<300units
    • -mild increase in bili & AlkPhos

    • US liver:
    • -determine fatty infiltration of liver
    • -size of liver
  32. what is the prognosis of alcoholic liver disease? signs/complications?
    30d mortality rates >50%

    • Signs/complications of severe alcoholic hepatitis:
    • -coagulopathy (PTT >5s)
    • -anemia
    • -serum albulin [ ]s <2.5mg/dL
    • -serum bili >8mg/dL
    • -renal failure
    • -ascites
  33. Tx for alcoholic hepatitis
    • 1st alcohol abstinence & nutritional suport
    • then, discriminant fn >/=32 (w/o comorbidity)
    • Prefer: Prednisolone 32mg POd x4wks, then taper4wks
    • Alternate: Pentoxifylline 400mg POtid x 4wks
  34. how is HBV transmitted?
    • sex contact & IV drug use
    • body piercing/tattooing
    • perinatal transmission
    • *more efficient transmission than HIV-1!
  35. describe HBV and what makes it unique.
    • an enveloped virion that produces a reverse transcriptase: replicates via an RNA-intermediate
    • partially dsDNA, circulizes in host cell
    • viral genome surrounded by the hepatitis B core antigens (HBcAg & HBeAg) which is surrounded by the envelope that has the hepatitis B surface antigen (HBsAg)
    • complete virus called the Daneparticle
    • family: hepadnaviridae
  36. explain HBV replication
    • HBsAg allows attachment to liver cells
    • virus is non-cytolytic
    • viral genome can integrate into host chromosome --> make mRNA --> reverse transcriptase makes into DNA
  37. one mechanism HBV evades immune response? what can result from this?
    • mass produced non-infectious viral proteins (HBsAg) may be antigenic “decoys” inhibits neutralizing Abs
    • immune complexes can form causing type III hypersensitivity reactions ( activation of compliment cascade & PMN's i.e. inflammation -->vasculitis,rash, renal damage)
  38. what is polyarteritis nodosa and what is its relation to HBV?
    • it is a redish inflammation of small-medium sized arteries seen as slight hypermelanosis
    • there is a deposition of fibrinoid material & destruction of external & internal elastic lamae
    • there are PMN's & eosinophils, leukocytes
    • -->hemorrhage
  39. what are the clinical manifestations of acute HBV disease?
    • Acute HBV:
    • -most aSxic

    • -if have Sxs:
    • --fatigue
    • --RUQ pain
    • --N/V/fever, arthralgias
    • --jaundice
  40. what are the clinical manifestations of chronic HBV disease?
    • Chronic HBV: usually no Sx until onset end-stage liver dz
    • --ascites,coagulopathy,jaundice,hepatomegaly,splenomegaly
    • --variceal bleeding
    • --encephalopathy

    • other:
    • --PAN
    • --glomerulonephritis
    • --vasculitis
  41. how do you dx HBV dz?
    • LFTs show AST and ALT >100U/L
    • liver biopsy needed to determine the grade & stage of chronic HBV disease
  42. describe the images:
    • B/C: show hepatocytes w/diffuse granular cytoplasm "ground glass hepatocytes"
    • D: immunoperoxidase stain for HBsAg
  43. describe the timeline for acute HBV
    • window period = after disappearance of HBsAg & before HBsAb appear, where only HBcAb-IgM is + can suggest infection
  44. describe the meaning of associated ag/ab's for HBV serology.
    • Associated Ag's:
    • HBsAg (surface ag) = acute infection or chronic "carrier state"
    • HBeAg = pt is infectious

    • Associated Ab's:
    • HBsAb (surface ab) = past exposure or immune from vaccine
    • HBcAb (core)
    • -IgG = exposure, not protective
    • -IgM = acute infection
    • HBeAb (E ab) = low risk of infection
  45. what differs acute vs chronic HBV?
    chronic: inflammation >6mo, HBeAg or HBsAg will stay +
  46. describe timeline of progression to chronic HBV.
  47. describe serology for the following states of HBV:
    acute, inactive carrier, chronic, prior exposure, prior vaccine.
  48. what is the tx for ACUTE HBV
    • no tx
    • can use hepB Ig to prevent/lessen Sx's w/in 1wk of exposure, esp infants to HBsAg + moms
  49. tx for CHRONIC HBV?
    • recommend antiviral Tx for:
    • -active HBV replication (+HBeAg or HBV DNA >100,000copies/mL)
    • -liver dz (ALT > 2x upper limit nL or modl liver dz &/or fibrosis on biopsy)

    • reverse transcriptase inhibitors (e.g.lamivudine)
    • nucleoside analogues (e.g. famcicovir)
    • interferon alpha
  50. what are complications of HBV infection?
    hepatocellular carcinoma (HCC)

    • 1. screen via US, repeat every 6-12mo to detect development
    • 2. consider serum AFP but poor sens/spec: need to confirm results w/US.
  51. how can you prevent HBV infections?
    • vaccinate vs HAV
    • HBsAg is used in vaccine

    • who to vaccinate?
    • -all HIV
    • -all HCV infected
    • -dialysis
    • -post-exposure

    **development of ab response can prevent initial infection of liver cells
  52. describe family genus, genome, transmission, & chronicity of HepA, B, C, D, E.

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