Coagulation Flashcards
factors in the intrinsic pathway (PTT, test system)
XII
XI
IX
VIII
factors in the extrinsic pathway (PT)
tissue factor
VII
factors in the common pathway
X
V
prothrombin
fibrinogen
XIII
converts XII to XIIa
kallikrein
regulates thrombin
thrombomodulin
ATIII
converts fibrinogen to fibrin
thrombin
stabilizes fibrin clot by crosslinking D molecules
XIII
fibrin degradation product
sign of pathologic clotting
D-dimer
↑ FDP
fibrin degradation products
sign of pathologic clotting
function of plasminogen
plasminogen → plasmin
fibrinolysis
convert plasminogen → plasmin
TPA
UPA
normal PT
12-15 s
normal PTT
25-35 s
normal bleeding time
< 10 min
PFA only involves ———– hemostasis
primary
platelet plug
no factors involved
explain primary hemostasis
vessel break → collagen exposure, TF released
GPIB on plt + vWF + exposed collagen
GPIIB on plt + fibrinogen + GPIIB (aggregation)
Bernard-Soulier
GPIB deficiency
platelet function problem
Glanzmann’s thrombasthenia
GPIIB deficiency
platelet function problem
abnormal PFA + ↑ PTT
vonWillebrand disease
↓ wWF, ↓ VIII
vWD panel
vWF Ag test (quantitative)
ristocetin cofactor assay (functional)
for PFA, patient must be off aspirin for…
7 days
VIII deficiency
hemophilia A
IX deficiency
hemophilia B
XI deficiency
hemophilia C
thrombolytic drug
converts plasminogen → plasmin
streptokinase
drug therapy that can give coag results like a multi-factor deficiency
thrombolytic agents
factor deficiency that causes clotting, not bleeding
XII
distinguish coag factor inhibitor from deficiency
mixing study
corrects —deficiency
does not correct —inhibitor
distinguish which factor deficiency a patient has
single factor assays
pt plasma + plasmas each deficient in one factor
remains abnormal —deficiency of that factor
coag problem causing superficial bleeding vs deep bleeding
superficial —plt problem
deeper —hemophilia
Christmas disease
hemophilia B
IX deficiency
normal fibrinogen
200-400
why is pregnancy a risk factor for DIC?
placenta can release large amounds of TF
triggers of DIC
sepsis
pregnancy
venoms
APML
trauma, burns
acute hemolytic trxn
malnutrition effect on coag pathway
↓ vitamin K
↓ functional prothrombin group factors (prothrombin, VII, IX, X)
first factor that ↓ in liver disease or vitamin K def.
VII
shortest half life
PT affected first
how can ↓ GI flora cause ↑ PT?
vitamin K deficiency
function of coumadin
inhibits vitamin K - dependent factors
function of heparin
enhances the effects of ATIII
PIVKAs
proteins affected by vitamin K deficiency
prothrombin, VII, IX, X
coag pathway inhibitors that are vitamin K-dependent
proteins C & S
functions of proteins C & S
inhibit factor V
S is cofactor for C
V not susceptible to protein C
clotting tendency
factor V leiden mutation
too much thrombin
clotting tendency
prothrombin mutation
buildup of homocysteine
clotting tendency
MTHFR mutation
normal INR
usually 2-3
sodium citrate tube ratio
9:1
bridge for multiple coag factors, tenase, PL surface
Ca
activates plts
inhibited by aspirin
arachidonic acid system
test for XIII deficiency based on clot stability
5M urea test
tests fibrinogen → fibrin step
used to detect heparin contamination
thrombin time
tests fibrinogen → fibrin step
not affected by heparin contamination
reptilase time
PTT prolonged
bleeding tendency
time & temp dependent
hemophiliacs
factor VIII inhibitor (Ab)
PTT prolonged
clotting tendency
anti-phospholipid
lupus anticoagulant
PTT with ↓ phospholipid, prolonged by LAC
PTT with ↑ phospholipid, more normal with LAC
Lupus anticoagulant
DRVVT
StaClot test
