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38 Cards in this Set

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  • Back
tissue factor activates what clotting factor first?
factor VII
what is the first protease in teh common pathway?
factor X
what activates the conversion of X to Xa?
Va (a binding protein)
is factor VIIIa a binding protein or a protease?
binding protein
what factor is responsible for creating cross-linked fibrin?
XIIIa
list the 5 endogenous ways in which termination of clotting occurs
1. dilution of factors in flowing blood
2. trapping of proteases in the clot
3. plasma protease inhibitors such as antithrombin
4. thrombomodulin - protein S - protein C cascade
5. plasminogen activation by tPa (tissue type factor), streptokinase, uPA (urokinase) to form plasmin which cleaves triple helix of fibrin
what is cleaved from fibrinogen to form fibrin?
4 alpha knobs of the fibrinopeptides
vit K required for which factors?
2 (prothrombin), VII, IX, X
why do 2,8,9,10 need vit K?
to catalyze the carboxylation of their glu amino acids
once the glu aa's are carboxylated to form Gla, what is the next step
binding of calcium; the complex them binds to the phospholipid membrane at the site of injury
describe the thrombomodulin protein c protein s pathway
essentially thrombomodulin is made by teh endothelial cell membrane and convets throbin from a procoagulant to an anti-coagulant. it does this by activating protein C and protein S. These proteins are going to inactivate factors Va and VIIIa
what are 3 exogenous ways to terminate clotting/
1. warfarin - competitive antag with K; prevents carboxylation of glu
2. heparin - speeds up rxn of AT and thrombin
3. metal chelators such as citrate - strip calcium from Gla proteins
what is factor V leiden/
mutation on factor V binding site for protein C
what are some ways in which a malignancy can cause hypercoag?
-results in the patient being static
-venous obstruction
-release of procoagulants by the cancer
is estrogen (via HRT, BCP) considered a RF for coagulation?
yes
why will recent surgery increase risk for coagulation
causing vascular injury (one ot the things in virchow's triangle)
why is Tamoxifen a/w coagulation
it is a chemotherapeutic agent containing estrogen - and estrogen is a/w coagulation
how does the V/Q ratio differ in pulm embolism vs. in other disease stages that cause regional defects in lung perfusino (e.g. emphysema, pulmonary atresia)
in PE, you have V/Q mismatching. Other pulmonary conditions such as COPD, asthma, pneumonia and pulmonary edema tend to cause both decreased V and Q (matched V/Q defect)
what ist eh gold stadard for visualizing thromboses in periphery? in pulmonary vasculature?
contrast venography
pulmonary angiography
is MRI more effective at imaging peripheral or pulmonary emboli?
peripheral. B/c in lung, there is poor signal/noise ratio in air filled lungs
what is the correct order for the algorithm for PE?
-spiral CT
-MRI
-CXR
-leg doppler
-pulmonary angiography
-V/P scintigraphy (nuclear med)
-CXR (frequently normal; do this to rule out DDx like atelectasis)
-Spiral CT - poor sensitivity as we go through distal branches, good specificity
-Leg doppler
-V/P scintigraphy - if normal, can rule out PE
-pulmonary angiography - GOLD STANDARD - but a/w morbidity & mort
are ABGs helpful in PE?
-not really.
-you migth see hypoxemia
-will see hypercapnia
what is the normal INR? waht is the target INR if youre on warfarin?
normal INR: 1
on warfarin: 2-3
which one do you need to closely monitor SUH or LMWH? why?
SUH b/c its highly protein bound
what is heparin-induced thrombocytopenia?
immune mediated- causes platelet aggregation --> thrombosis
heparin and warfarin. which is immediate acting? which is delayed acting?
warfarin = delayed
heparin = immediate
can you use thrombolytics and fibrinolytics simultaneously?
no!! too large a bleeding risk
indications for thrombolytic therapy?
1. major PE (i.e. a/w hypotension, RH failure, severe hypoxemia)

2. submassive PE - if pt has previous heart/pulm condition

3. proximal vein thrombosis (certain cases)
what are teh thrombolytic agents?
streptokinase
urokinase
tissue plasminogen activator
waht are teh 4 major options for VTE therapy?
1. anticoags
2. fibrinolytics
3. thrombectomy
4. caval interruption
is surgical thrombectomy common? when would we use it?
not common at all
would use it if there way acute recurrence of an embolus (e.g. if a vein was de-endothelialized it owuld be highly thrombogenic)
what is caval interruption?
placement of filter in IVC - traps bl clots
D2E fragments are cleared by...
the liver
what PTT do you want to achieve when administering heparin IV?
1.5-2.5 x baseline PTT
why might you see (rarely) hemoptysis with Pulm embolism? (i.e. what would it indiate?)
lung infarct (rare b/c of dual circulation to lungs)
what are characteristic features of ABGs and A-a gradient in pulm embolism
PaO2 decreased (hypoxemia)
PaCO2 usually decreased (respiratory compensation by hyperventilation)
A-a gradient will be elevated
what sided heart failure is characteristic of pulm embolism?
RH failure
would you expect displacement of hte interventricular septum to the R or L side of the heart in pulm embolism?
into the left (since the pulmonary circuit is hi pressure now - RH will become hypertrophied)