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100

difference between acute and chronic PE

acute = free floating

chronic = contiguous with vessel wall

100

what is done if PE is unprovoked

hypercoaguable work up

100

name 4 possible sources of emboli

thrombus

air

Amniotic fluid

Fat (from bone     marrow after a fracture)

Foreign bodies

Parasites

Infection (septic     emboli)

Tumor cells

100

what are high risk medications to cause PE

estrogen-containing contraception

post-menopausal estrogen replacement therapy

selective estrogen receptor modulators (like tamoxifen)

cancer therapies

100

name 1 LMWH and list 2 reasons why LMWH might be preferred over UFH

Enoxaparin (Lovenox), Dalteparin (Fragmin), Tinzaparin (Inohep)

Decreased risk of HIT

Can be used at home (bc it is IM injection)

200
where do saddle emboli lodge

at the main pulmonary artery bifurcation

200

why must IVC filters be removed at some point

they double risk of DVT in first 2 years

200

where are thrombi most and least likely to come from?

most likely- femoral veins/lower extremity

least likely- upper extremities or calves (below the knee)

200

purpose of anticoagulants?

PREVENT new clots, not dissolve current clots

200

what is heparin reversal?

Which type of heparin is fully reversed and what kind of heparin is partially reversed?

protamine sulfate

UFH fully reversed, LMWH partially reversed

300

name the 3 parts of virchow's triad and give an example of each one

venous stasis (ex. bed bound after surgery, polycythemia, pregnancy, travel)

vessel wall injury (ex. hypertension, damage from surgery, smoking)

hypercoaguability (ex inherited- factor V leiden or accquired- antiphospholipid syndrome)

300

when is IVC filter used for PE

Used when anticoagulation is contraindicated or if VTE recurs despite oral anticoagulants

300

reversal for dabigatran

Idarucizumab 

300

when are thrombolytics/fibrinolytics indicated? 

name 1 thrombolytics/fibrinolytic

name 1 absolute contraindication to thrombolytics/fibrinolyritics


high-risk PE, acute myocardial infarction, and acute ischemic stroke

Alteplase (tPA) and Tenecteplase

previous intracranial hemorrhage, active internal bleeding, recent ischemic stroke or head trauma within the past 3 months

400

biggest risk factor for PE?

a previous PE

400

what is the most accurate diagnostic method for PE?

why is it less preferred than the gold standard?

Pulmonary Angiography

It is invasive

400

what is primary reversal of warfarin, and what is used if primary reversal agent(s) cannot be used?

Why is the alternative less preferred (aka what side effects can happen from the alternative)?

4-Factor PCC (Kcentra) + IV vitamin K = primary

Plasma / FFP + vitamin K

Plasma / FFP + vitamin K is less preferred because it is slower, larger volume is required, and Risk of fluid overload / transfusion reactions

400

when do you need to initiate dabigatran in relation to parental therapy

parental therapy = 5-7 days

Initiate dabigatran < 2 hours prior to time of next scheduled dose of parental anticoagulation

400

name all medications that need to be monitored while patient is taking by either PT/INR or aPTT/PTT

warfarin (PT/INR)

UFH (aPTT/PTT)

500

gold standard for diagnosing a PE and what is used if the gold standard cannot be used

CTA is gold standard, V/Q scan used when CTA is contraindicated

500

name 3 things that can indicate PE on CXR

Palla's sign (enlarged right descending pulmonary artery)

Westermark’s sign (hyperlucency)

Hampton’s hump (wedge-shaped opacity representing pulmonary infarct)

500

why does warfarin require bridging therapy?

Because Protein C and S are depleted rapidly, initiating warfarin creates a temporary pro-thrombotic state

500

what is general MOA of HIT

Body forms antibodies to heparin, antibodies cause platelet sequestration and paradoxical thrombosis

500

what is parental therapy that is NOT UFH or LMWH?

what is its MOA?

name reversal agent

Pentasaccharides (Fondaparinux)

indirect inhibition of factor Xa via antithrombin III

no reversal agent

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