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Pharmacotherapeutics Theory 1 > Thrombosis CUE CARDS > Flashcards

Thrombosis CUE CARDS Flashcards

1
Q

What are the Treatment options of Prevention of CVD?

A

“Does the person have symptomatic CVD?”

No: Primary Prevention - preventing MI, stroke, in someone who hasn’t had one (NOT RECOMMENDED)

Yes: Secondary Prevention

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2
Q

What does the Heart Foundation recommend in individuals with no known coronary heart disease (CHD)?

A

Doesn’t recommend that people with no known CHD take low dose aspirin daily to reduce their risk of developing CHD

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3
Q

Antiplatelet Secondary Prevention:

What is drug choice based on?

What is the first choice for monotherapy?

A

> Drug choice determined by indication
May consist of mono or dual antiplatelet therapy
Aspirin is initial choice for monotherapy

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4
Q

Antiplatelet Secondary Prevention:

What is the Benefit and Risk of Dual antiplatelet Therapy

A

> Combination benefit: Greater inhibition of platelet aggregation

> Combination risk: Increased risk of bleeding (blocking platelets from sticking together)

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5
Q

Briefly describe the restrictions on clopidogrel

A

> Secondary prevention
Hx of intolerance (aspirin)
Further events while taking aspirin (haven’t responded)
GI bleeding risk

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6
Q

Discuss Antiplatelet Monitoring

A

> A number of tests have been developed for assessing platelet reactivity
None have routine clinical application
Limited evidence for relationship between assay results and clinical outcomes

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7
Q

What is a VTE?

A

VTE is a condition in which a blood clot forms most often in the deep veins of the leg, groin or arm and travels in circulation, lodging in the lungs

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8
Q

What is a DVT?

A

DVT is a blood clot that forms in a deep vein, usually leg, groin or arm

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9
Q

What is PE?

A

PE is a blood clot that occurs when a DVT clot breaks free from a vein wall and travels to the lungs, blocking some or all of the blood supply

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10
Q

How are VTE Diagnosed?

A

> Clinical probability
Lab test: elevated D-dimer
Imaging: Ultrasonography

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11
Q

What are the risk factors of VTE?

A 
> Immobility (e.g. surgery, long-distance travel, trauma, acute illness)
> Pro-thrombotic drugs (COC, HRT)
> Coagulation abnormalities
> Age
> Prior thrombosis
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12
Q

Discuss Monitoring of LMWH and Unfractionated Heparin

A

LMWH: Effect of anticoagulation is more predictable, therefore monitoring is unnecessary

Unfractionated Heparin: requires regular (~4-6hrly monitoring)

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13
Q

How are LMWH and Unfractionated Heparin Administered?

A

LMWH: Longer acting (1 or 2 d SC)

Unfractionated Heparin: Short Acting (SC or IV infusion)

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14
Q

What are non-drug options available for VTE prophylaxis?

A

> Graduated Compression Stockings

> Intermittent Pneumatic Compression

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15
Q

Non-drug options available for VTE prophylaxis: How do Graduated Compression Stockings assist?

A

> Assists venous return

> Reduces risk of stasis

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16
Q

Non-drug options available for VTE prophylaxis: How do Intermittent Pneumatic Compression assist?

A

> Bag on outside of leg

> When pumped up, puts pressure on leg - pressure change drives venous return

17
Q

What is the mechanism by which low dose aspirin exerts anti-platelet effects without causing systemic anti-inflammatory effects?

A

> Following administration of low dose aspirin, the drug is absorbed in the hepatic portal vein (here, the concentration of aspirin is relatively high)

> COX within platelets become irreversibly acetylated and the platelets are no longer able to become activated

> Any aspirin leaving the portal vein and entering the systemic circulation is significantly diluted and so the systemic concentration is very low (hence no systemic anti-inflammatory effects)

18
Q

How come the anti-platelet effect persists?

(low dose aspirin exerts anti-platelet effects without causing systemic anti-inflammatory effects)

When is this important?

A

> The reason that the antiplatelet effect persists is that the platelets are irreversibly inactivated (if it was reversible - platelet function would return when the drug concentration drops in the systemic circulation)

> Important when it comes to consider the cessation of aspirin, for example - before surgery - the effect of aspirin will only wear off once the irreversibly inactivated platelets have been replaced (takes ~ 7 days)

19
Q

The treatment objectives of VTE is to prevent what?

Patients require what?

A

> Treatment objectives are to prevent thrombus extension, PE, post-thrombotic syndrome and recurrence

> Patients require anticoagulation: duration determined by risk factors for VTE

20
Q

Why is the duration of therapy different in someone who had VTE provoked by a transient major risk factor compared to an individual who has had recurrent unprovoked VTE?

A

> VTE Provoked by a transient major risk factor: 3 months - Patient did X which led them to getting a DVT. Will acutely allow clot to dissolve and then provide patient with relatively short term anticoagulation to make sure it doesn’t come back again

> Recurrent Unprovoked VTE: indefinite - Patient has had multiple blood clots and we don’t know why. They will probably get another one if we don’t have them on anticoagulation since we don’t know the cause in the first place

21
Q

What monitoring is used for unfractionated heparin vs LMWH?

What doses do we monitor?

A

> Unfractionated Heparin: APTT, ACT
LMWH: Cannot use APTT, can measure antiXa activity (not routine)

> Prophylactic doses don’t require monitoring

22
Q

What is the Target for APTT?

How is the Target Achieved?

A

> It varies, target defined for that particular setting
Target achieved by adjusting rate of infusion (if patient above target, decrease IR but if patient below target, increase IR)

23
Q

What is Heparin Induced Thrombocytopenia and Thrombosis?

A

> Profound thrombocytopenia (major decrease in platelets) seen in patients who have had unfractionated heparin (therefore cease heparin)

> Risk of clots forming in periphery - leads to ischaemia in those area (e.g. toes) and that may lead to limb amputation and high mortality - need to anticoagulate with fondaparinux because if you don’t, you’ll have the risk of losing limbs

24
Q

How is Warfarin Monitored?

A

> INR (how long it takes for blood to clot)

> Target ranges dependant on indication - for DVT and AF: 2-3

> Initial monitoring daily then increasing intervals to 1 month once INR stabilised

25
Q

Discuss Briefly how to manage warfarin if INR is really high or really low?

A

> If INR is 10: may need to reverse effects of warfarin very quickly with vitamin K, clotting factor concentrates

> If INR is less significantly elevated: Might give vitamin K - takes time to make clotting factors

> If INR a little elevated: hold warfarin until INR comes down but investigate what caused change in INR

Pharmacotherapeutics Theory 1 (17 decks)

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