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25 Cards in this Set

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Important elements of patient hx when venous thromboembolism (VTE) is suspect?
1. Previous thrombotic events? Objectively documented?

2. Family hx of thrombotic events?

3. Age at presentation of first thrombotic event?

4. Presence or absence of known genetic or acquired risk factors?

5. Unusual location (hepatic/portal/mesenteric vein/cerebral sinus) or frequency of thrombosis?
Possible PE findings with VTE?
- localized pain, tenderness, swelling
- discoloration of affected limp

- asymptomatic
- may exhibit DOE, pleuritic chest pain, rarely hemoptysis
- CXR is usually normal
- Massive PE -- syncope, hypotension, marked hypoxemia, right ventricular dysfxn
How do we test for DVT?
1. duplex doppler ultrasonography
-- test of choice for screening
-- not sensitive for thrombi below the knee

2. contrast venography
-- sensitive to both calf and thigh DVT
-- useful in recurrent DVT w/ persistent abnormalities of the deep venous system
How do we test for PE?
1. spiral CT
-- relative sensitivity compared to V/Q may depend on the size of vessel involved
-- imporved specificity over V/Q and thus useful in pts w/ abnormal CXR prior to pursuing pulmonary angiography

2. Ventilation-perfusion scan (V/Q scan)
-- normal scan essentially rules out PE
-- mismatch defects (ventilation w/o perfusion) suggest PE
-- pts w/ matched defects and abnormal CSR are difficult to interpret and frequently read as intermediate probability or indeterminate

3. Pulmonary angiography
-- GOLD standard
-- avoid in pts w/ evidence of pulm HTN
VTE Lab assessment?
1. D-dimer
2. Eval for hypercoag state
Explain D-dimer values and VTEs.
sensitive D-Dimer assays have a very high predictive value of a negative test when used to eval suspected VTE
What do we look for when evaluating for hypercoag state?
1. activated protein C resistance (clotting assay)
2. factor V leiden mutation (PCR)
3. prothrombin G20210A (PCR)
4. Antithrombin fxnal assay
5. protein C fxnal assay
6. protein S fxnal assay
7. lupus anticoag
-- screening w/ PTT, dilute Russel viper venom time (dRVVT)
-- 1:1 mix to demonstrate inhibitor pattern
-- confirmatory test in presence of excess lipid (neutralized inhibitor)
8. serologic tests for antiphospholipid antibodies (i.e. cardiolipin)
9. plasma homocysteine
Caveats in testing for hypercoag states.
Due to presence of an inflamm state and consumption by the thrombus, measurement of protein fxn and Ag levels is NOT reliable during an acute episode of thrombus
-- testing not recommended during acute event

Antithrombic therapy can affect these measurements

In general, testing for thrombophilia should be done 4-6wks after the pt has completed their course of oral anticoags
Anticoagulant agents?
1. unfractionated heparin (UH)
2. Low molecular weight heparin (LMWH)
3. Warfarin
4. Hirudin (Refludan)
5. Argatroban
6. Fondaparinux
7. other novel agents
Unfractionated heparin
Primary drug for treatment of acute thrombosis, both arterial and venous

Chemically: heterogenous mix of highy sulfated CHO polymers which BIND ANTITHROMBIN WITH HIGH AFFINITY

Action: accelerates inhibition of coagulaton proteases-- factor Xa and thrombin-- by antithrombin
-- May have antithrombin independent effects

Admin IV and effective w/in minutes

Half-life: Approx 1 1/2 hours

Target: prolong PTT to 1.5-2.0 times control values

Major complications: bleeding, HIT, and accelerated osteoporosis
Low molecular weight heparin
Heparin prep depleted of high molec wt polymers
-- predom anti-factor Xa activity

Dosed by weight (w/o monitoring coag times) and causes minimal or no PTT prolongation

Antithrombotic effects equivalent to UH for prophylaxis/trtmt of DVT/PE

More predictable pharmacodynamics making wt-based dosing w/o monitoring

Lower incidence of HIT, possibly less incidenc of osteoporosis
PRIMARY ORAL DRUG for anticoag

Mech: interferes w/ VitK dependent γ-carboxylation of coag proteases
-- gradual decline of factors VII, IX, X, and prothrombin) in order of their respective half lives

PT prolings w/in 2 days but pt not considered therapeutic until several more days (all factors reach steady state)

Adjust to INR of 2.0-3.0

Complications: bleeding, warfarin-induced skin necrosis (rare), drug interactions

INR needs to be carefully monitored following any med changes
Recombinant version of leach anticoag protein

Low molecular weight DIRECT thrombin inhibitor

Admin IV and monitored by PTT w/ target of 1.5 to 2.5

FDA approved drug for TREATMENT OF HIT

Complications: increased risk of bleeding relative to haparin

Cleared: kidneys
Synthetic compound containing arginine

Binds serine active site in thrombin, competitively inhibiting its fxn

FDA approved drug for TREATMENT of HIT

Complications: increased risk of bleeding relative to heparin

Cleared: liver
Pentasaccharide that binds to ATIII caysing inhibition of factor Xa

Given s.q.
List antiplatelet agents.
1. ASA
2. Clopidogrel
3. GpIIb/IIIa inhibitors (ReoPro)
irreversibly inhibits platelet cyclooxygenase, blocking production of thromboxane A2, an important mediator of platelet activation

Cheap, effective tx for number of clinical syndromes:
- asymptomatic males and females 50yo
- silent MI
- stable/unstable angina
- acute MI
- aortocoronary bypass surgery
- acute occlusion following coronary angioplasty
- peripheral vascular disease
- transient cerebral ischemia
- placental insufficiency
- atrial fib
- prosthetic heart valves
thienopyridine derivative

Inhib ADP-dep platelet aggregation

Requires hepatic metabolism; relatively long half-life

**More effective than ASA in preventing ischemic stroke, MI or vascular death in pts at high risk

Can be used in combo w/ ASA
GpIIb/IIIa inhibitors (ReoPro)
Fab fragment of monoclonal Ab directed against the fibrin(ogen) receptor on platelets (GpIIb/IIIa)

Major risks: hemorrhage, thrombocytopenia

Reduced risk of death, MI or urgent CABG following coronay angioplasty
Fibrinolytic agents?
1. TPA
2. Urokinase
3. Streptokinase
MOA of fibrinolytic agents?
Activate plasminogen to PLASMIN which degrades the fibrin thrombus

Systemic fibrinolytic state often seen w/ decreased fibrinogen, factor V, and factor VIII levels

Broader use of fibrinolytics is primarily limited by ~0.5-1% incidence of cerebral hemorrhage noted in large MI trials
Indications for fibrinolysis?
1. most commonly used in setting of acute MI

2. acute periph arterial obstruction (limb salvage)

3. recent use in ischemic stroke; tradeoff is relatively high since incidence of intracerebral bleed is 6-22%

4. massive PE with hemodynamic compromise
Standard treatment of VTE?
1. Uncomplicated DVT/PE
- at least 5 days of heparin (UH or LMWH) overlapping w/ warfarin to achieve target INR 2-3

Duration: 3-6 mos for first event

2. "Idiopathic DVT" occurring in absence of precip clinical factors
-- duration of tx should be longer

Vena caval filters -- used to prevent PE in pts w/ absolute contraindications to anticoag, or for recurrent events on therapeutic anticoag
Anticoag for mechanical and prosthetic heart valves?
Mechanical valves
-- lifelong risk
-- target INR 2.5-3.5

Tissue (porcine) valves
-- increased risk 1st 3 months
-- target INR 2-3
Anticoag for atrial fib?
Chronic Afib is assoc w/ signif increased risk of thromboembolic stroke
-- warfarin superior to ASA for prevention
-- may do equally well on ASA if no valvular heart disease or left ventric dysfxn