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77 Cards in this Set
- Front
- Back
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evan's syndrome
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ITP and autoimmune hemolytic anemia, can cause warm agglutanin ds
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extravascular hemolytic anemias
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sickle cell ds, G6PD def, and hereditary spherocytosis
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do you see jaundice in intravascular hemolytic anemias
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no
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causes of non hemolytic, normocytic anemias
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AOCD, kidney ds (no epo), aplastic anemia
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what is the TIBC in AOCD (low, nl, or high)
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low (because iron stores are high)
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what type of ig is associated with cold ab ds
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igm
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what two infections are associated with cold ab ds
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mono and mycoplasma
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what are the defective proteins in hereditary spherocytosis
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spectrin and ankyrin
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what abnl cell do you see on a smear with warm agglut ds
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spherocytes
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is warm agglut ds intra or extravascular hemolysis
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extravascular (rbc's phagocytosed by macrophages, no complement fixing because IgG)
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is cold agglut ds intra or extravascular hemolysis
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intravascular (IgM-->fix complement) and can also be extravascular (phagocytosis by liver macrophages)
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what are some clinical findings with thal mj
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1. splenomegaly
2. skeletal deformaties (frontal bossing and other) 3. iron overload (due to transfusions) |
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what is the transferrin saturation in AOCD (high, low, nl)
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nl (trans sat = serum iron/TIBC)
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what is glanzmann's thrombasthenia
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defect in plt plug formation by dec gp2b/3a (plt to fibrinogen to plt)
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what is bernard-souli ds
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defect in plt plug formation by dec gp1b (plt to collagen)
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is the plt count increased, decreased or nl with glanzmann's
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nl
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is the plt count increased, decreased or nl with bernard-souli
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decreased
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what would a BM aspirate show in ITP
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increased megakaryocytes
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what is the defect in ITP
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anti-gp2b/3a (leads to peripheral plt destruction)
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dx for TTP
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low plts and shistocytes required. others:neuro, renal, fever
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what is the txt for VWD
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DDVAP (it releases stored VWF)
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is the PTT nl, high or low in VWD
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high because vwf carries factor VIII
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is the PTT nl, high or low in DIC
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high because using up all coag factors
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is the PT nl, high or low in DIC
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high because using up all coag factors
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P vera: epo up, down or nl
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epo down (-feedback)
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what is a major toxic effect of heparin therapy
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heperin induced thrombocytopenia (HIT)
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what is the pathophys of HIT
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stimulates antibodies against plts--> leads to plt activation--> can get thrombosis with thrombocytopenia
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do thalasemias have micro or macrocytosis
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micro
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do corticosteroids increase or decrease circulating PMNs levels
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increase because the demarginate PMNs so there are more in circulation
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when do you see basophilia
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myeloproliferative disorders
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what is the pathophys of G6PD def
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without G6PD, oxidative agents convert hgb to methgb which gets denatured and ppts as heinz bodies. spleen macrophages pinch off the heinz bodies creating bite or blister cells-->hemolysis
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what kinds of drugs cause neutropenia
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antipsychotics, antiepileptics, antithyroid and some abx
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what do sulfa drugs do to PMN count
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cause agranulocytosis (also levamisol contaminated coccaine and others)
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how do you treat TTP
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PLEX (not plts- they fuel the fire!)
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what does TF/FVIIa activate
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X (direct) and IX (indirect)
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what does thrombin activate
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plts, 5,8,11,13
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what is the most sensitive test for monitoring heparin
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TT>PTT>PT (note TT is too sensitive so use PTT)
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what is the lupus inhibitor
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anti-phopholipid (can't correct PTT with 1:1)
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monocytosis- which conditions
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myelodysplastic syndromes, infx, ibd, leukemia
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when do you do a 1:1 mixing test
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when you have an abnl PTT to determine if the have a deficiency or inhibitor (a deficiency will be corrected, and inhibitor won't be)
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splenic enlargment will lead to what
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decreased plts
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what does protein c inactivate
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Va and VIIIa
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antithrombin III inactivates...
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2,9,10,11
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what do deficiencies in anticoag proteins do to PT, PTT, TT
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all are nl
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what is the PTT change with VWD
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increased because vwf carries factor VIII
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what does DDVAP do
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increases release of factor VIII and vwf
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prothrombin 20210 is what kind of mutation
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gain of function point mutation codes for increased factor II levels (prothrombin)
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are arterial thromboses platelet or fibrin rich
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platelet (white thrombosis)
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does factor V leiden have high, low or nl PTT
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nl (same time to clot, but stays around longer because can't inactivate factor V well)
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what are some clinical and lab findings with anti-phopholipid antibody syndrome
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thrombosis, recurrent miscarriage and persistant anti-PL ab (lupus inhibitor and/or anticardiolipin ab). Also have prolonged PTTs
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characteristic labs in DIC
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decreased plts, fibrinogen; increased FDPs, PT, PTT, TT
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what is purpura fulminans
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a syndrome of DIC with skin necrosis and secondary hemorrhage. indicates high grade DIC. causes include sepsis or homozygous def in protein c or s
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what factors does heparin inactivate
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II (thrombin) and X
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what factors does LMWH inactivate
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X only (not thrombin)
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what kind of thrombosis does aspirin help prevent
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arterial only
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what kind of thrombosis does heparin help prevent
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arterial and venous
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what kind of thrombosis does warfarin help prevent
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arterial an venous
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when is a pRBC transfusion indicated
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when you need to increase O2 carrying capacity such as with symptomatic anemia (tachycardia>100, mental change, heart ischemia, angina, SOB)
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what type of plasma can an O recipient receive
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O, A, B, or AB (O has all the antibodies that these have)
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how does heparin effect antithrombin
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it causes antithrombin to rapidly inactivate factors IIa and Xa
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what type of hemolysis (intra or extravascular) can Rh mismatch cause
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extravascular (rbc's phagocytosed by macrophages, no complement fixing because IgG)
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what type of hemolysis (intra or extravascular) can ABO mismatch cause
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intravascular (complement fixing because IgM)
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what is the number 1 cause of fatalities with blood transfusions
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human error
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what antigens to plts have
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ABO and HLA (although consider Rh when giving a plt transfusion because trace amts of RBCs are found in plts)
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what is in fresh frozen plasma
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clotting factors, fibrinogen (and citrate as an anticoag)
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when is a plasma transfusion indicated
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DIC, liver ds, trauma, massive transfusion, Pt/PTT>1.5x nl, and warfarin reversal if no time for vit K
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when is cryoprecipitate indicated
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when you need lots of fibrinogen in a small volume (it also has VIII, vwf, and XIII)
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what is TRALI
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transfusion related acute lung injury from donor antiHLA or anti-PMN attacking recipient WBCs.. new lung injury within 6 hrs of transfusion. bilat chest infiltrates, hypoxemia, not PE risk factors, usually fever chills and hypotension
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how do you prevent transfusion associated GVHD
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irradiate the blood (indicated for severe immunodef pts)
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is transfusion assoc GVHD an acute or delayed transfusion rxn
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delayed ( sx 8-10 days s/p tx)
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p vera labs
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increased rbcs, may have high plts, basophilia, high hgb/hct, may have high wbcs, decreased epo, +Jak2, and teardrops on smear
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what syndromes can manifest with a Jak2 mutation
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p vera (97%), ET (50%), and myelofibrosis (50%)
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what is the major complication of ET
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thrombosis
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what BM cell type is effected in myelofibrosis
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megakaryocytes
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txt for p vera
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phlebotomy, hydroxyurea, p32, low dose aspirin to decrease thrombosis risk, ifn alpha
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myelodysplastic syndrome labs (smear, bm, genetics)
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smear: macrocytosis, lg plts, monocytosis, marrow:ringed sideroblasts and sm megakaryocytes, genetics: monosomy 5,7,8
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what is the ANC for agranulocytosis
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ANC<200
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