shevyatiwari's version from 2015-04-25 02:52


Question Answer
IVIg is synthesised artificiallyF, human derived
Peak concentrations occur in 3-4 hoursF, immediate
Within 24 hours, most IVIG has been removedF, 30%
IVIG is predominantly in the intravascular spaceT, 60%, cf extravascular 40%
Crosses the placentaT
Excreted in breast milkT
Half life of 2 weeksF, 3-5 weeks
Suppresses antibody production by igG binding via Fc fragment to corresponding cellular surface receptors on T cellsF, B cells
Upregulates autoantibody productionF, downregulates
Increases half life of circulating IG'sF, reduces, by saturating the protective neonatal Fc receptor causing execrated antibody catabolism
Neutralises complement mediated effectsT
IVIg can bind to complement componentsT
Restores TH1/2 cytokine balanceT
C/I include only anaphylaxisT
Relative C/I include CCF, renal failure, IgA deficiency, RA, cryoglobulinemiaT
Pregnancy is a relative C/I to IVIGF, not a contraindication
Infusion related adverse effects tend to occur within 10 minutesF, 30-60
IgA deficiency is a RF for anaphylaxisT
Alopecia and dermatitis are S/ET
Neutropenia and haemolysis can occur in anyoneF, ABO and Rh antibodies
Aseptic meningitis is seen in 1%F, 11%
IVIG can cause thromboembolic eventsT. Higher in those who receive higher doses or rapid infusion rates
Potential infection riskT
FBP, UEC, IgA, RF, cryoglobulinemia, hep B, C, HIV should be done before treatmentT
2mg/kg/cycle divided into 3 equal doses given on each of 3 consecutive days is standard dosingF, 2GRAMS
Infusion is given monthly in very aggressive diseaseF, monthly normally, fortnightly if very aggressive disease
Blocks the fas receptor/ligand interactionT, consequently causing keratinocyte apoptosis
Affects migration of immunocompetent cells from blood to target tissueT

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