Pulmo 5

Front 1

tissue factor activates what clotting factor first?

Back 1

factor VII

Front 2

what is the first protease in teh common pathway?

Back 2

factor X

Front 3

what activates the conversion of X to Xa?

Back 3

Va (a binding protein)

Front 4

is factor VIIIa a binding protein or a protease?

Back 4

binding protein

Front 5

what factor is responsible for creating cross-linked fibrin?

Back 5

XIIIa

Front 6

list the 5 endogenous ways in which termination of clotting occurs

Back 6

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

Front 7

what is cleaved from fibrinogen to form fibrin?

Back 7

4 alpha knobs of the fibrinopeptides

Front 8

vit K required for which factors?

Back 8

2 (prothrombin), VII, IX, X

Front 9

why do 2,8,9,10 need vit K?

Back 9

to catalyze the carboxylation of their glu amino acids

Front 10

once the glu aa's are carboxylated to form Gla, what is the next step

Back 10

binding of calcium; the complex them binds to the phospholipid membrane at the site of injury

Front 11

describe the thrombomodulin protein c protein s pathway

Back 11

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

Front 12

what are 3 exogenous ways to terminate clotting/

Back 12

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

Front 13

what is factor V leiden/

Back 13

mutation on factor V binding site for protein C

Front 14

what are some ways in which a malignancy can cause hypercoag?

Back 14

-results in the patient being static
-venous obstruction
-release of procoagulants by the cancer

Front 15

is estrogen (via HRT, BCP) considered a RF for coagulation?

Back 15

yes

Front 16

why will recent surgery increase risk for coagulation

Back 16

causing vascular injury (one ot the things in virchow's triangle)

Front 17

why is Tamoxifen a/w coagulation

Back 17

it is a chemotherapeutic agent containing estrogen - and estrogen is a/w coagulation

Front 18

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)

Back 18

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)

Front 19

what ist eh gold stadard for visualizing thromboses in periphery? in pulmonary vasculature?

Back 19

contrast venography
pulmonary angiography

Front 20

is MRI more effective at imaging peripheral or pulmonary emboli?

Back 20

peripheral. B/c in lung, there is poor signal/noise ratio in air filled lungs

Front 21

what is the correct order for the algorithm for PE?
-spiral CT
-MRI
-CXR
-leg doppler
-pulmonary angiography
-V/P scintigraphy (nuclear med)

Back 21

-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

Front 22

are ABGs helpful in PE?

Back 22

-not really.
-you migth see hypoxemia
-will see hypercapnia

Front 23

what is the normal INR? waht is the target INR if youre on warfarin?

Back 23

normal INR: 1
on warfarin: 2-3

Front 24

which one do you need to closely monitor SUH or LMWH? why?

Back 24

SUH b/c its highly protein bound

Front 25

what is heparin-induced thrombocytopenia?

Back 25

immune mediated- causes platelet aggregation --> thrombosis

Front 26

heparin and warfarin. which is immediate acting? which is delayed acting?

Back 26

warfarin = delayed
heparin = immediate

Front 27

can you use thrombolytics and fibrinolytics simultaneously?

Back 27

no!! too large a bleeding risk

Front 28

indications for thrombolytic therapy?

Back 28

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)

Front 29

what are teh thrombolytic agents?

Back 29

streptokinase
urokinase
tissue plasminogen activator

Front 30

waht are teh 4 major options for VTE therapy?

Back 30

1. anticoags
2. fibrinolytics
3. thrombectomy
4. caval interruption

Front 31

is surgical thrombectomy common? when would we use it?

Back 31

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)

Front 32

what is caval interruption?

Back 32

placement of filter in IVC - traps bl clots

Front 33

D2E fragments are cleared by...

Back 33

the liver

Front 34

what PTT do you want to achieve when administering heparin IV?

Back 34

1.5-2.5 x baseline PTT

Front 35

why might you see (rarely) hemoptysis with Pulm embolism? (i.e. what would it indiate?)

Back 35

lung infarct (rare b/c of dual circulation to lungs)

Front 36

what are characteristic features of ABGs and A-a gradient in pulm embolism

Back 36

PaO2 decreased (hypoxemia)
PaCO2 usually decreased (respiratory compensation by hyperventilation)
A-a gradient will be elevated

Front 37

what sided heart failure is characteristic of pulm embolism?

Back 37

RH failure

Front 38

would you expect displacement of hte interventricular septum to the R or L side of the heart in pulm embolism?

Back 38

into the left (since the pulmonary circuit is hi pressure now - RH will become hypertrophied)