Hematology Flashcards
RBC membrane transporter
HCO3-/Cl- to sequester bicarb and transport CO2
Platelet lifespan
10 days
platelet dense granules contents
ADP (A dense P), calcium (a dense mineral)
alpha granules contents
vWF fibrinogen
vWF receptor
GpIb (von wille BRAND)
Fibrinogen receptor
GpIIb/IIIa
Macrophages MHC class
II
Dendritic cells MHC
II
T cell costim signal
CD28
MHC II associated with CD
4
MHC I associated with CD
8
Activates fibrinogen
thrombin
activates thrombin
Va using prothrombin
First step in clotting cascade
XII activation by collagen, BM, or platelets
bradykinin actions
vasodilation
permeability
pain
Major extrinsic pathway factor
VII activated by TF
Prothrombin times measures extrinsic/intrinsic
extrinsic
PTT time measures extrinsic/intrinsic
intrinsic
Vit K and coagulation
procoagulation via factor formation
warfarin inhibits this production
Protein C and coagulation
Anticoagulation; requires protein S to cleave and inactivate Va and VIIIa
tPA and coagulation
Anticoagulation; activates plasminogen to plasmin which starts fibrinolysis
Heparin and anticoagulation
Anticoagulation; activates antithrombin
Warfarin MOA
inhibits epoxide reductase (reduces vitamin K in process of making factors)
Clot formation step 1
Injury: vWF binds exposed collagen
Clot formation step 2
Adhesion: platelets bind vWF via GpIb(rand) at injury site
platelets release dense granules (ADP and Ca)
ADP increases platelet adherence via shape changes
Clot formation step 3
Activation: ADP binding causes GpIIb/IIIa (fibrinogen r) receptor expression on platelet surface
Clot formation step 4
Aggregation: fibrinogen binds and links platelets
Pro-aggregation platelet factors
TXA2
Low blood flow
Inc. aggregation
Anti-aggregation factors
PGI2 and NO (endothelium)
Inc. blood flow
Dec. platelet aggregation
Clopidogrel MOA
Inhibits GpIIb/IIIa expression by blocking ADP receptor
Abciximab MOA
GpIIb/IIIa mAb
Glanzmann’s thrombasthenia main issue
GpIIb/IIIa defect
Basophilic stippling
Little specks in round RBC
BASte the ox TAiL:
Thalassemias
Anemia chronic
lead poisoning
Bite cells
G6PD deficiency
Ringed sideroblasts
Excess iron in mitochondria (sideroblastic anemia)
Schistocyte
DIC, TTP/HUS, mechanical hemolysis
Spherocyte
hereditary spherocytosis or autoimmune hemolysis
Teardrop cell
Bone marrow infiltration forces extramedullary hematopoiesis (sheds a tear because forced out of home)
Target cell
HALT he said to the target: HbC Asplenia Liver Thalassemia
Excessive RBC membrane
Heinz bodies
Oxidation of iron causes denatured Hgb precipitation and membrane damage -> bites taken out
G6PD
Howell-Jolly bodies
Nuclear remnants in RBC
Normally removed by spleen
Hypo-/asplenia or mothball ingestion (naphthalene)
looks like olive (Olive-Olly bodies)