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pathoma
NC anemia w intravascular hemolysis
| Question | Answer |
|---|---|
| paroxysmal noctural hemoglobinuria is d/t what deficiency? | myeloid stem cells have deficiency in GPI which is an anchoring protein for DAF- which protects RBCs WBCs and platelets from destruction by complement, by inhibiting C3 convertase. |
| why does complement mediated lysis occur at night? | bc at night we breathe shallowly- retain Co2= respiratory acidosis. acidosis causes activation of complement. this causes the cells to be lysed and can cuase hemoglobinemia or uria (d/t intravascular hemolysis). hemosideruria after a few days |
| what test is used to screen for PNH? | sucrose test. it activates complement |
| whats the confirmatory test for PNH? | clow cytometry to detect a lack in CD55 (DAF) on blood cells |
| what is the main cause of death in PNH pts? | thrombosis- hepatic, portal or cerebral veins. bc destroyed platelets will release factors that activate complement |
| complications of PNH? | AML (acute MYELOID leukemia) and IDA (d/t chronic loss of hb in urine) |
| how does G6PD deficiency cause intravascular hemolysis? | G6PD def= dec in HALF LIFE of G6PD= DEC in NADPH = DEC in reduced glutithione = oxidative stress causes intravascular hemolysis with h2o2. (cant protect RBCs against oxidative stresses) |
| there are 2 variants of G6PD deficiency, what is the difference? | african variant has a mild decrease in g6pd half life to cause mild intravascular hemolysis in the presence of oxidative stress while the meditteranean variant has marked decrease in g6pd half life to cause marked intravascular hemolysis |
| what do both variants of g6pd defiency have in common/ | both protective against falciparium malaria |
| what do you see on a blood smear of a g6pd pt under oxidative stress/ | heinz bodies (oxidative stress precipitates hb as heinz bodies) and bite cells- from macrophages to remove the heinz bodies |
| what is the screen for g6pd deficiency? | heinz preparation- (preciptated hb can be seen w special heinz stain). |
| what confirms the dx of g6pd deficiency? | enzyme tests (has to be done weeks after an acute episode) |
| what is IHA immune hemolytic anemia? | its IgG or IgM mediated ab destruction of the RBC membrane |
| what is IgG mediated IHA? | it binds to RBC membrane in warm temps. and causes destruction of membrane by spleen macrophages= spherocytes. |
| what is IgG mediated IHA associated w? | SLE, CLL, and drugs- penicillins and cephalosporins |
| how can drugs induce igG mediated IHA? | drugs can bind to membrane of RBC and IgG then binds to drug-membrane complex. or drugs can cause production of autoantibodies that bind to self ag on RBCs. |
| tx of IgG mediated IHA? | steroids (slow ab production), IVIG (get spleen to attack Ig instead of RBCs), remove offending drug or splenectomy |
| what kind of hemolysis is seen in IgM mediated IHA? what happens? | intravascular hemolysis. IgM binds to RBC in cold temperatures and fixes complement |
| how do you diagnose IHA? | direct and indirect coombs test. direct- determines presence of ab on RBC (anti-IgG is added to pt serum, agglutination= +). indirect- determines presence of ab in pt serum. |
| microangiopathic hemolytic anemia is d/t what type of hemolysis? | intravascular hemolysis from vascular pathology- RBCs are destroyed as they pass through circulation. |
| malaria is an infection of RBCs and the liver by ________ species, transmitted by a female ________ _________ | plasmodium species; transmitted by female Anopheles mosquito |
| what is the difference btw P. falciparum and P. vivax and ovale when it comes to fever they cause | falciparium causes a daily fever where vivax and ovale cause a fever every other day |
| malaria is what type of hemolysis then? | intravascular- RBCs rupture as a result of falciparium life cycle. (spleen also consumes somes infected RBCs- results in extravascular hemolysis with splenomegaly) |
| decreased RBCs in the bone marrow with a low corrected recticulocyte count is called what? | anemia d/t decreased production |
| what are some causes of anemia d/t decreased production? | macrocytic or microcytic anemia. renal failure (decreased EPO production by peritubular cells). or damage to the bone marrow precursor cells |
Created by:
afrank1