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
name the factors involved in the ext and int pathway
also name the factors involved in the common pathway
ext: 3 - 7 - 10 - thrombin - fibrin - meshwork
int: 12 - 11 - 9 - 10 - thrombin - fibrin - meshwork
common: 10 - fibrin - meshwork
factor 3 is not usually found in blood and is only pr when there damaged tissue hence it belongs to (and starts) ext pathway
what coagulation pathways (what factors) does each OAC work on
apix rivarox edoxaban - 10 (common)
enoxaparin - 10 (common)
warfarin - 2 7 9 10 (int and ext)
heparin - 2 10 (common)
recall ext path 3 7 10 and int path 12 11 9 10
what kind of inhibitors are dabi and riva
competitive and reversible
compare dabi to riva
riva has shorter t1/2 (effect reverse more quick)
riva need to be wary of cyp3a4 and pgp inhib/inducer
dabi has low bioF (give enteric coated)
dabi will cause more GI sx
what is an adv the -teplases have over urokinase/streptokinase?
teplases are better because they BIND PREFERENTIALLY TO CLOT ASSOCIATED PLASMINOGEN hence activating plasmin in clots
what should not be taken with fibrinolytics?
NO (may decr alteplase conc)
other apt/oac
what is the dose to be used for dabi and edoxaban for VTET
dabi - 150mg bd
edox - 60mg od
which pt population should not be started on edoxaban?
crcl > 95; high likelihood of tx failure
what are the 3 sides of the virchows triad
blood stasis
hypercoagulability
vasc injury
how does afib cause stroke?
uncontrolled contraction at left atrium - blood pool and conc of clotting factors at left atrium - clot break off and go to left vent then aorta then cerebral circ blocked
what is mcha2ds2vasc
used to determine is oac shld be started
cong HF; HTN; =>75; DM; hx of stroke; vasc disease; 65-74
what are some impt counselling points for sdm with pts when starting oac for spaf
- highlight stroke risk using mchadsvasc
- describe what can happen if not anticoaged
- talk about se of oac and bleed risk, then look at HASBLED to see if modifiable bleed risk
- compare between doacs and vka to do sdm
recall SPAF dosing
apix 5 bd 2.5 bd (ABS)
riva 20 od 15 od (crcl)
dabi 150 bd 110 bd (age)
edox 60 od 30 od (crcl & bw)
list the ddi with doacs
dual inhib of 3a4 and pgp
- rito, azole, clarith
dual inducer of 3a4 and pgp
- rifam, sjw
antiseizures
- valpro, cbz, pht
list the ddi with warfarin
2c9 inhib
- amiodarone, bactrim, flucanazole, metronidazole, erythromycin
2c9 inducer
- rifam, sjw, cbz
no need dose adj
- amox clav, doxy, macrolides
explain how different lifestyle factors might derange inr
inhib 2c9, decr met, incr warf, incr inr = alc binding
induce 2c9, incr met, decr warf, decr inr = chronic alc, smoke, sudden incr exercise
provide impt warfarin counselling points
maintain diet, missed dose, when to go a&e, interchanging of meds, let dr/dentist know of warf tx
recall ami dosing
load asp 100mg 300mg
load tica / clopi 180mg 600mg
tica 90 bd (12m) acs
clopi 75 od (6m) ccs
but if high bleed risk –> 3m
when can thrombolytics be used in ais/ami
ami: when pci cnt be done
ais: within 4.5h, bp < 185/110 BG > 2.8, change in CT, disabling stroke
describe the components of abcd2 for tia risk
age - 60-64 (0) vs 65 abv (1)
bp - htn (1) vs normal (0)
clinical sx - unilat weak (2), speech (1), others (0)
duration of tia - 60min abv (2), 10-59 (1), <10 (0)
dm - yes (1) vs no (0)
high risk tia is 4 and abv
