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29 Cards in this Set
- Front
- Back
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primary sclerosing cholangitis
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noninfx inflamma and sclerosis of bile ducts
pruritis (1st sign), RUQ pain, jaundice, cirrhosis elevated direct bilirubin elevate alkaline phosphatase high risk: IBD especially ulcerative collitis in young jewish males |
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primary biliary cirrhosis
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autoimmi destruction of intrahepatic bile ducts
pruritis-->jaundice, steatorrhea, xanthelasmas (+) AMA elevated ALP, GGT, bilirubin (later) women 35-60 more common in CREST, Sjogren's synd, Type I DM |
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uridine diphosphated glucuronosyl transferase
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converst indirect bilirubin to direct
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primary causes of jaundice
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1: hemolysis: ince indirect bilirubin (G6PD def, sickle cell, AHA)
2) def of glucuronosyl transferase: incre indirect (gilbert, briggler najjar) 3) defect in transport of bilirubin from liver to bile duct: incre direct bilirubin (viral hepatitis, mononucleosis, rotor syn, dubin johnson synd) 4)obstruction of biliary system: incre direct |
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criggler najjar
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type 2: AD, decreased uridine diphosphated glucuronosyl transferase-->chronic elevation of inderent bilirubin
type 1: AR, absent uridine diphosphated glucuronosyl transferase, no direct bilirubin, die in 1 YEAR |
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dubin johnsn
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impaired hepatocellular secretion secondary to a carrier defect
darkly pigmented liver + elevated direct bilirubin |
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hepatitis A (HAV)
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only acute
RNA virus fecal/oral transmission via contaminated feced and water actue: HAV IgM late: HAV IgG (protected due to previous infs, or vaccinated) incubation 2-6 weeks |
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Hep B (HBV)
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serum hepatitis
DNA virus HBs-Ag: indicates current infx (either acute or chronic) HBe-Ag: marker for highest infectivity period transmission: parentarraly, sexually, verticaaly incubation: 2-6 mons 10% become chronic |
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hepatitis C (HCV)
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leading infectious liver dis
episodic increases in transaminases (ALT, AST) wiht normal intervals, all other hep virus produce constant increases in ALT, AST transfusion hepatitis transmission: parenterally incubation: 1-2 months 50-70%: chronic (hepatocellular carcinoma, cirhosis) |
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HEP D (HDV)
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RNA virus
occurs only with HBV becaiuse require HBV's Ag coat for replication 2 types of infx: coinfx: HBV and HDV acquired simultaneously superinfx: hbv established then get HDV: increase mortatlity of HBV parenterally and sexually |
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HEP E
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self limited
never chronic but fulminant in prego trans: fecal/oral route via water SE asia, Middle east |
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HEp G
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trans: parentally, sexually, vertically
increase survival of HIV pts |
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HBV
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HBs-Ag: surface ag, indicates current infx, persist for about 3-4 mons, if present >6 mons=chronic, used in vaccines
Anti-HBs: antibody to HBsAg after symps disapear, indicates immnity AntiHBc; antibody to the core, indicates exposure to hep B virus (past or present infx, not made by vaccines) appears 4 weks after HBSAg, remains elevated after infx, present during WINDOW PERIOD, NOT PROTECTIVE HBeAg: appears after HBSAG and disappears before it, indicates extreme infectivity HBV DNA: in those wiht current infx, used to determine viral load after dx, higher value means higher infecivity, present in WINDOW PERIOD |
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WINDOW PERIOD
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level of HBS-Ag and anti HBS are too low to be measured even though are infected wiht HBV
negative: hbsag, and anti HBS-ag posivitve: Anti-HBc, and HBV DNA |
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HBV vaccines
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make anti HBSAg, but not antiHBCAg
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alcoholic cirrhosis (Laennec's cirrhosis)
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irreversible, most common cause of cirrhosis, end stage of alcoholic hepatitis
cause fatty liver (hepatic steatosis), focal liver necrosis, pmn infiltrate, intracytoplasmic eosinophilic hyaline inclusions (mallory bodies, alcoholic hyaline) testicular atrophy high estrogen-->spider angiomata-->gynecomastia, palmar erythema hepatocyte death-->hepatic encephalopathy (due to high ammonia) fibrosis-->portal HTN-->ascites (due to low albumin), esophageal varices, hemmorrhoids early stage alcohilic cirrhosis: micronodular late stage alcoholic cirrhosis: macronodular |
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cirrhosis due to viruses or toxins
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macronodular
methotrexate, amiodarone, HBV HCV |
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wilsons dis
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accumulate CU in brain, kidney, liver, cornea
decreased ceruloplasmin psycosis, athetosis, incordication (1st sign) high urine Cu (screening test) kayser fleisher rings cirrhosis |
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most common liver cancer
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metastatic liver cancer
primary sites: breast, lung colon |
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primary liver cancer
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hepatocellular carcinoma (hepatoma)
massive hepatomegaly at tumor site massive elevation of ALP (made by liver), minor increase in AST, ALT (most of liver is normal) AFP: tumor marker casues: chronic HBV, HCV, aflatoxin exposure |
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intussusception
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usually termical ileum into ascending colon
risk: upto 7 years old, highest risk: 5-10 months most significant risk: adenovirus infx (pharyngitis, red eye, casue peyers patcch to become huge and become a lead point) vomit, sausage shaped mass palpable at RUQ and vacant RLQ, CURRANT JELLY STOOLS |
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midgut volvuls
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duodenum and colon malrotate arounnd mesentary art-->constrinction of bowel and vessel
neonates vomitting, diarrhea, abdo distension |
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necrotizing enterocolitis
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neonates
risks: maternal NSAID used (def. blood supptly to baby gut), prematurity (immature gut), comorbid dis (icrease sympathetics-->vasoconstrict BV in gut) bowel mucosa necrosis vomit, blood in stool, lethargy, temp intability |
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stills dis
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acutely febrile, polyarthrittis, neg RF, micrognathia
occurs before 16, 75% complete remission by adults |
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psoriatic arthritis
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no RF
affects DIP-->sausage digits HLA B27 |
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Felty syndrome
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splenomegaly, polyarticular RA, neutropenia
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osteogenisis inperfecta
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disorger of collagen-->increa bone Fx, blue thin sclera
newborn type is most severe: skull is WORMIAN BONES |
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osteopetrosis (marble bone, albers-schonberg dis)
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sclerosis of vertebrla endplate-->rugger jersey vertebrae (radiologically)
very brittle bones |
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aseptic necrosis
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cut in blood supply
secondary to trauma to head of femus, tibial tuberosity or scaphoid bone osgood schlatter dis (aseptic necrosis of tibial tubeosisty) and legg calve perther dis (aseptic nec of femoral head in children w/out trauma hx casue hip pain, knee pain, self limited) |
