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HIGH YIELD HEME

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laracrystalo's version from 2016-07-17 21:13

onc

Question Answer
t(8;14)Burkitt (c-myc --> increase cell growth)
t(14;18)follicular lymphoma (BCL2 --> inhibits apoptosis)
t(11;14)mantle cells (cyclin D1 --> G1 to S progression)
CD5+mantle cell
t(12;21)ALL
t(15;17)AML M3 (PML)
ATRA treatment AML M3
DIC is common presentationAML (Promyelocytic)
Auer rods AML
myeloperoxidase +AML
down syndrome ALL, AML
t(9;22)CML (BCR-ABL --> oncogene that increases TK activity)
differentiate with leukemoid rxnCML (low LAP)
TRAP +hairy cell
dry tap on aspirationhairy cell
smudge cells CLL, SLL
CD20+ and CD5+SLL, CLL
rouleaux formation IgIgG
RBC agglutination formation IgIgM
reed-sternberg cells + lacunar cellsnodular sclerosing HL
noncleaved B cellburkitt's
starry skyburkitt's
small cleaved B cell with irregular nucleifollicular
BCL2follicular
c-mycburkitt
precursor to CLLSLL
precursor to ALLlymphoblastic lymphoma
waxing and waning painless lymphadenopathyfollicular
CD5+CLL
cerebriform nucleimycosis fungoides
associated with downsALL
thymic massALL
CD10+ALL
Tdt+ALL
treatment for CLLchlorambucil
treatment for hairy cellcladribine and pentostatin
MPO aggregatesAML auer rods
basophiliaCML
treatment for CMLimatinib
large megakaryocytesEssential thrombocytosis
old ageCLL
middle ageAML
young ageALL
treatment for hairy cell2CD
no lymphadenopathyhairy cell
hypogammaglobulinemiaCLL
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bleeding/coagulation disorders

Question Answer
lots of megakaryocytic in bone marrowITP
anti GpIIB/IIIA antibodiesITP
no platelet clumpingglanzmann
agglutination with riscocetin testglanzmann, vWF disease
no agglutination in riscocetin testbernard solier
large plateletsbernard solier
decreased platelet to vWF bindingbenard soulier
decreased gpIbbernard soulier
decreased gpIIbglanzmann
decreased adamts 13TTP
schistocytes and LDHTTP
increased bleeding time with decreased platelet countbernard solier, ITP, TTP
increased bleeding time aloneglanzmann
associated with HIVTTP
headaches, fever, hemolytic anemia, acute renal failure, shockTTP
too much vWFTTP
too much platelet aggregationTTP
treatment for TTPplasmapheresis
lupus thrombocytopeniaITP
hemarthrosishemophilia
hemophilia treatmentdesmopressin (induces vWF to work better)
infant bleeding from umbilical stump but normal bleeding tests?factor XIII deficiency
hereditary DVTs?factor V leiden
deficiency that causes thrombosis AND hemorrhage?factor XII deficiency (hagemen)
increased bleeding time AND increased PTT?vWF disease
low agglutination with riscocetin testvWF disease
decreased fibrinogen levelsDIC
white renal cortex ?DIC causes hemorrhage of whole kidney but cortex first
consumption of platelets with schistocytesTTP
impaired platelet adhesionvWF, bernard soulier
liver disease vs vitamin K problem?inject vitamin K and see what happens!
what in amniotic fluid can cause DIC in mom?tissue factor
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RBC

Question Answer
aniscocytosisvarying sizes (increased RDW)
poilocytosisvarying shapes
main source of energy for RBC?glucose (glycolysis), then HMP shunt
total O2 content of bloodPaO2 + SaO2 (Hb)
affect SaO2cyanide, methemoglobinemia
microcytic anemiasthalassemia, chronic disease, iron deficiency, lead poisoning, sickle cell, sideroblastic
high RDW anemiairon deficiency
causes of sideroblastic anemiaB6 deficiency (isoniazid use), alcoholics, porphyria, lead poisoning
port-wine urine after exposure to light? acute intermittent porphyria
associated with HCVporphyria cutaneous tarda
defect of porphobilinogen deaminaseacute intermittent porphyria
defect of uroporphyrinogen I synthaseacute intermittent porphyria
defect of hydroxymethylbilane synthaseacute intermittent porphyria
what builds up in AIP?porphobilinogen and ALA
what builds up in porphyria cutaneous trade?uroporphyrinogen III
instant wine-red urineporphyria cutanea tarda
HbH electrophoresis3 alpha genes of alpha thalasemia
HbBart electorphoresis4 alpha genes of alpha thalassemia
anemia at 6 months with higher HbFbeta thalassemia
low HbA, high HbA2, high HbFbeta thalassemia
basophilic stipplingbeta thalassemia
target cellsthalassemia, asplenia, liver disease,
howell-jolly bodiesasplenia (sickle) nuclear remnants of young RBC
amino acid substitution of b globinsickle cell
insufficient production of b globinbeta thalassemia
necator americanusiron deficiency anemia
diphyllobothrium latumB12 deficiency megaloblastic anemia
spur cellssevere cirrhosis macrocytic anemia (due to decreased cholesterol in RBCs)
massive splenomegalyCML, myelofibrosis, mono CMV and EBV
decreased myeloid/erythroid ratio?reticulocytosis! seen in hemolytic anemias
universal RBC donorO
universal plasma recipientO
universal RBC recipientAB
universal plasma donorAB
jaundice in 1st 24 hours after birth?ABO incompatibility
spherocytes in cord blood smear?ABO incompatibility
ABO incompatibilitytype O mom passes antiA or AntiB IgG antibodies to non type O fetus. + direct coombs test on fetal cord blood
+ direct coombs test on fetal cord bloodABO incompatibility
intrauterine Rh incompatibilityhydrops fetalis
neonate Rh incompatibilitykernicterus and hepatosplenomegaly
increased MCHCspherocytosis
decreased leukocyte alk phosparoxysmal nocturnal hemoglobinuria
screen test for PNHham's acidified serum test
diagnostic test for PNHflow cytometry for CD 55 and CD 59
heinz bodiesG6PD deficiency
bite cellsG6PD deficiency --> heinz bodies that have been chewed by splenic macrophage
how to differentiate between G6PD deficiency and pyruvate kinase deficiency hemolytic anemia?check for NADPH--> if there is NADPH, then it's pyruvate kinase deficiency
blue skin in cyanosisdeoxyhemoglobin causes this (even seen in polycythemia bc hb not well saturated)
labs in polycythemia veraincreased hct, increased plasma volume, normal O2 sat, splenomegaly, normal or decreased EPO
polycythemia associated complicationsclots leading to things like amarosis fugax and budd chiari
dehydration causes what kind of polycythemia?relative polycythemia due to the decreased ECF --> relative increase in hot
hypercalcemia in multiple myeloma mechanism?B cells secrete IL1 that works to activate osteoclasts --> lytic bone lesions
how does waldenstrom's macroglobulinemia differ from multiple myeloma?W has IgM production (instead of IgG), so there is RBC agglutination (rather than rouleaux). This causes hyperviscocity and primary amyloid
what enzyme does lead block?Aminolevulinate dehydratase and ferrokelitase
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pharm

Question Answer
what do thrombolytics do?convert plasminogen to plasmin
how to monitor thrombolytics?D dimer
warfarin mechanisminhibits epoxide reductase (decreases gamma carboxylation of II, VII, IX, X, C, S)
warfarin adminoral
warfarin solubilitylipid --> so binds to albumin and can easily get displaced by other drugs!
monitor warfarinPT and ESR
what happens when you first administer warfarin?initially, there is pro-coagulant bc of C and S action --> therefore give heparin with it at first
heparin actionincreases antithrombin III and blocks factor II mainly
monitor heparin?PTT
kinetics of heparin?0-order
heparin administration?IV
monitor LMWHXa levels
LMWH admin?subcutaneous
LMWH namesenoxaparin and dalteparin
antithrombin III analogueslepirudin, bivalirudin, argatroban
what do antithrombin III analogues treat?HIT
aspirinirreversible nonselective COX inhibitor --> decreases TXA2 --> decreased platelet aggregation
dipyridamoledecreases platelet adhesion
Clopidogrelblocks ADP
ticlodipineblocks ADP
side effect of neutropeniaticlodipine
block IIbIIIaabciximab, tirofiban, ebtifibitide
antidote for warfarinvitamin K or fresh frozen plasma
antidote for heparinprotamine sulfate
antidote for tPAaminocaproic acid
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