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CV II > Anticoagulants, Antiplatelets Antifibrinolytic > Flashcards

Anticoagulants, Antiplatelets Antifibrinolytic Flashcards

1
Q

Arterial thrombosis

A

White clot
Mostly platelets in plug due to high blood flow
TREAT PLATELETS & ATHEROSCLEROSIS

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2
Q

Venous thrombosis

A

Red clot
Vascular stasis, especially around valves, more RBCs
Lots of fibrin forming a long tail
Can easily break loose and cause embolism
TREAT COAGULATION

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3
Q

Heparin

A 
(Unfractionated heparin)
Parenteral anticoagulant therapy
Heparin binds to antithrombin 3 
Inhibits thrombin Xa, IXa, XIa, XIIa 
Prolongs aPTT and thrombin time and at high doses can prolong PT
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4
Q

Heparin administration routes (2)

A

1) Continuous IV preceded by IV bolus
2) SubQ minidose for slower release
DO NOT GIVE IM OR ORAL

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5
Q

Heparin Use

A

IMMEDIATE ANTICOAGULANT
Prophylaxis of post-op thrombus
DVT and PE (large dose to inhibit established PE)
DIC

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6
Q

What if you need prolonged anticoagulation?

A

Use heparin initially and admin longer acting and longer onset warfarin or newer anticoagulants** test question

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7
Q

Heparin Toxicity

A

Bleeding from undiagnosed bleeding site!!

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8
Q

Treatment of Heparin Overdose

A

Stop heparin
Use PROTAMINE SULFATE which binds to and inactivates heparin but must be given slowly IV
Also give fresh frozen plasma to resupply the coag factors

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9
Q

Protamine Sulfate

A

Heparin antedOte that needs to be given slowly IV

NOT A WARFARIN ANTEDOTE

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10
Q

HIT 1

A

Heparin- Induced Thrombocytopenia
Transient reversible clumping of platelets >100,000
Occurs first few days
Asymptomatic and recover OK even w/o heparin withdrawal

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11
Q

HIT 2

A 
Heparin- Induced Thrombocytopenia 
Delayed onset 5-14 dyas 
Severe thrombocytopenia <100,000
Immune mediated rxn, heparin Ab complex causing significant platelet aggregation 
Consequences of peripheral thrombus severe (stroke MI skin necrosis) 
Amputation needed in 25% 
Mortality 25% 
Occurs in 3% of pt
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12
Q

Continuous monitoring of this needs to occur when on heparin

A

The aPTT time to keep w/i therapeutic range

Also watch soft tissue for signs of internal bleeding

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13
Q

LMWH Most commonly used trade name and common name

A

Enoxaparin (Lovenox)

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14
Q

What are the advantages of using LMWH over UH?

A

LMWH binds to Factor Xa better and with higher selectivity
It has a longer duration (2-5x)
Simpler kinetics as it doesn’t bind to as many endo cells/proteins/platelets
CLOTTING TEST IS NOT REQUIRED (no aPTT)
No dose dependent clearance

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15
Q

Warfarin = Coumadin

A

Oral Anticoagulant

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16
Q

Warfarin MOA

A

Inhibits Vit K dependent posttranslation modification of clotting factors: thrombin, VII, IX, X, Protein C and S
Without addition of carboxyl group the clotting factors cannot bind to Ca and phospholipid surface and cannot be inactivated
The clotting factors are present but inactive?

17
Q

Warfarin onset and duration and termination

A

All are delayed
Onset 36-72 hr bc pre-exisiting clotting factors are slowly cleared from the blood
liver and kideny metabolism

18
Q

How much of warfarin is protein bound?

A

99%, only 1% is active which can cause lots of drug/drug interaction problems

19
Q

When can you never use Warfarin?

A

PREGNANT PATIENTS

20
Q

How is warfarin administered?

A

Orally

21
Q

What test do you need to run on pt taking Warfarn?

A

INR which is an adjusted PT time, need to take often and it gets expensive
targer INR 2.0-3.0
PATIENT VARIABILITY IS HIGH

22
Q

Dabigatran

A

Orally active, direct thrombin inhibitor
Not metabolized by hepatic enzymes
Excreted mainly in urine

23
Q

Advantages of Dabigatran

A

Directly binds to thrombin both clothbound and circulating
Rapid onset of action
Does not require INR monitoring
Non-inferior efficacy and similar safety to warfarin

24
Q

Dabigatran approved use

A

Prevention of thromboembolic stroke in patients with non-valvular AF

25
Q

Direct Thrombin Inhibitors

A

Approved for use in pt with thrombosis related to HIT and during coronary angioplasty, any time when there is a lot of clot formation

26
Q

Aspirin

A

At very low does irreversibly inhibits COX1 & COX2
Cannot synthesize new enzyme so inhibits TXA2 formation and platelet aggregation for life of platelet (7-10 days)
ONLY LOW DOSES REQUIRED OR WILL BLOCK PGI2

27
Q

Aspirin Therapeutic Use

A

MYOCARDIAL INFARCTION
Primary prevention of CVD
Reduction of thromboembolic complications in general

28
Q

Clopidogrel (Plavix)

A

Irreversibly inhibits platelet ADP receptor and thus blocks the ADP mediated activation of GPIIb/IIIa complex thus inhibiting fibrinogen binding and platelet aggregation

29
Q

Abciximab (ReoPro)

A

Monoclonal Ab prevents fibrinogen binding to glycoprotein GPIIb-IIIa thus inhibiting platelet aggregation
Greater antithombus than aspirin/heparin

30
Q

Dipyridamole (Persantine)

A

Inhibits platelet aggregation and is a weak vasodilator
Secondary prevention of MI/stroke
Extended release formula used and often used in combination w/aspirin (Aggrenox)
HA a problem

31
Q

Cilostaxol (Pletal)

A

Inhibits PDE III and increases cyclic AMP
Inhibits platelet aggregation and stimulates vasodilation
Reduces Sx of PAD and intermittent claudication
Contraindicated in CHF

32
Q

What drugs destroy pathological thrombi?

A

Alteplase, reteplaes, tenectplase and streptokinase

33
Q

Indications for thrombolytic therapy

A

AMI
PE
DVT
Ischemic stroke but only after CAT/MRI scans

34
Q

rtPA, Alteplase, Activase

A

Recombinant Tissue Plasminogen Activator
tPA via genetic engineering
SERIOUS HEMORRHAGE

35
Q

Reteplase

A

Fibrinolytic drug

diffuses more freely into clot than alteplase with shorter half life

36
Q

Tenectepalse (TNKase)

A

Single bolus
As effective as alteplase w/o the severe bleeding
Easier to administer due to longer half life

37
Q

Streptokinase

A

Nonenzymatic activator of plasminogen
Loading dose saturates pre-exisiting Ab
Cheaper than rtPA
SERIOUS HEMORRHAGE TOO

CV II (5 decks)

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