PR3154 CA Recap Flashcards
This deck covers concepts you're weaker at
what is the difference between plasma and serum
plasma has fibrinogen (sample will not clot); serum does not have fibrinogen (sample will clot)
what are granulocyte? describe how they look like.
basophil (blue, allergies, bilobed nucleus), eosinophil (red, parasitic inf, bilobed nucleus), neutrophil (bigger than rbc, most abundant wbc, usually first to arrive at site of inf)
what are agranulocytes?
monocyte and lymphocyte (M bigger than L but both bigger than RBC)
what is the fn of blood?
regulate, protect, transport
what are the components of blood
wbc, rbc, platelet, plasma
what makes up the plasma
water, soluble things, protein
what makes up the buffy coat?
wbc, platelets
what are some proteins found in plasma?
Ig, fibrinogen, albumin
define hematocrit and state the normal levels found in males and females
avg vol of rbc relative to vol of blood
males 46%
females 42%
where does erythropoiesis occur with age?
fetus: yolk sac then liver, spleen, lymph node
<5: all bone marrow
5-20: bone marrow of rib, sternum, vertebrae, prox end of long bone
>20: minus prox end of long bones
they eventually become fat
what conditions are required for erythropoiesis?
oxygen and erythropoeitin
identify some reasons for an incr in erythropoietin release?
any factors that result in more O2 needed to be generated (either incr O2 DD or decr O2 SS)
or any factors that result in more RBC needed (eg. anemia, reduced blood flow, blood donation)
explain how new RBC is made (the process of erythropoiesis)
erythroblast (ribo syn) –> late erythroblast (hb accum inside) –> normoblast (nucleus ejected) –> reticulocyte –> RBC
recall what it is called when there is too much/little rbc and wbc
too much rbc - polycythemia/erythemia
too much wbc - leukocytosis
too few wbc - leukopenia
explain the process of blood clotting
when platelet plug forms –> vwf secr by platelet binds to collagen –> GP on platelet binds to vwf –> platelet activation and platelet agonist released –>»_space;» platelet –> joined via fibrinogen (weak) –> thrombin convert fibrinogen to fibrin –> stronger cross link –> stabilised using fibrin stabilising factor, factor 13 which is activated by thrombin too
can tell that thrombin is an impt key player hence, to keep thrombin supply, PF3 is impt (factor 3) which is incr when there is platelet aggregation! also need factor 10a to convert prothrombin to thrombin
this whole thing is a +ive feedback loop