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Pharm II Unit II > Drugs Affecting Coagulation > Flashcards

Drugs Affecting Coagulation Flashcards

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1
Q

Hemostasis is achieved in what three ways?

A

Vascular contraction (vasospasm)

Platelet adhesion, activation, aggregation

Fibrin formation and reinforcement of the platelet plug (coagulation)

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2
Q

What is the common point in the coagulation cascade, where the intrinsic and extrinsic pathways meet?

A

Factor Xa

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3
Q

Which factors are in the intrinsic pathway?

A

XII—>XIIa

XI —> XIa

IX —> IXa

X —> Xa (with VIIIa)

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4
Q

Which factors are in the extrinsic pathway?

A

III (TF) —> IIIa

VII —> VIIa-TF

X —> Xa

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5
Q

Heterogeneous mix of sulfates mucopolysaccharides (large negatively charged molecule)

A

Heparin

Action from a unique pentasaccharide

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6
Q

MOA for heparin

A

Activity is dependent on ANTITHROMBIN III

Mainly affects Xa and thrombin

Affects factors IXa, XIa and XIIa as well

Catalyst —> accelerates ATIII activity (x1000)

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7
Q

________ competes for binding to heparin and has immediate effect

A

Protamine sulfate

Works b/c it’s a large positive molecule (helps it bind to heparin’s large negative molecule)

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8
Q

What are the indications for Heparin use?

A

Anticoagulant for operations or IV catheters

Prophylaxis against thrombosis (DVT/PE)

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9
Q

***How is unfractionated heparin administered

A

Exclusively IV

Not IM —> hematoma

Onset of action is IMMEDIATE

Therapeutic target is PTT 2-2.5x normal

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10
Q

What are the adverse effects of Heparin?

A

HEMORRHAGE (true of all anticoagulants)

Allergic reactions

Mild decrease in platelets

HEPARIN-INDUCED THROMBOCYTOPENIA (HIT)

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11
Q

What is the reversal agent for Heparin

A

Protamine sulfate (think heParin)

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12
Q

Contraindications for heparin use

A

RENAL OR HEPATIC DYSFUNCTION

Don’t use in patients who are:
• Actively bleeding
• Hemophilia or other clotting disorders
• Hypersensitve
• During or after surgery of the brain, spinal cord, or eye
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13
Q

What are the names for the Low Molecular Weight Heparins?

A

Enoxaprin

Fondaparinux (a synthetic pentasaccharide)

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14
Q

***LMW Heparin is similar to UFH except…

A

Main inhibitory action is on factor Xa (not much effect on thrombin

Can be injected subcutaneously***

Lower incidence of HIT

Protamine sulfate does not completely reverse LMWH and has NO EFFECT on fondaparinux***

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15
Q

Bivalirudin is a recombinant form of hirudin, a natural anticoagulant from …

A

Leeches

Highly specific direct inhibitor of thrombin (no AT III)

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16
Q

What drug is given as an alternative anticoagulant in patients with HIT?

A

Bivalirudin (IV only)

Can cause hypersensitivity (40%)

Use caution in liver patients

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17
Q

Direct inhibitor of thrombin given as an alternative in patients with HIT

A

Argatroban (think “thro(M)Ban”)

Cleared by the liver and given by continuous IV infusion

Use caution in patients with poor liver function

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18
Q

***ORAL direct inhibitor of thrombin

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A

Dabigatran (Pradaxa)***

Used to prevent stroke in patients with non-valvular a fib

19
Q

***Direct thrombin inhibitor with predictable anticoagulant effects (so not monitored by PTT)

Study These Flashcards
A

Dabigatran***

20
Q

Why does Dabigatran (Pradaxa) have a black box warning?

Study These Flashcards
A

Avoid abrupt d/c without adequate alternative anticoagulant —> increased risk of thrombotic events

21
Q

What is the antidote for Dabigatran (Pradaxa)

Study These Flashcards
A

Idarucizumab (Praxbind)

22
Q

What are the “XaBans”?

Study These Flashcards
A

Direct inhibitors of Factor Xa

Rivaroxaban, Apixaban, Edoxaban, Betrixaban

ORAL

Used for DVT, PE, and future clots (prophylaxis)

23
Q

Rivaroxaban and Apixaban can be used in _______ patients, the other XaBans are for use in _______.

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A

R/A —> any patients (been around longer, so more studies)

Other XaBans —> patients with non-valvular afib or critically ill

24
Q

Avoid XaBans in patients with…

Study These Flashcards
A

Liver Disease

Renal Failure

25
***What is the antidote for Direct Inhibitors of Factor Xa (XaBans)?
Factor Xa decoy (Andexxa)***
26
***What it’s the MOA for Warfarin
Inhibits reduction of vitamin K —> interferes with synthesis of factors II, VII, IX, X, and Proteins C & S*** Protein C&S have shorter 1/2 life so you start to see effect because of these factors first
27
***Why do you have to start Warfarin in combo with heparin?
Because it takes 4-5 days to take full effect because it works by inhibiting clotting factor synthesis*** Peak effect after 48 hours, monitored by INR (2-3)
28
Indications for Warfarin use
Prevent development of emboli —> DVT, thromboembolism No effect on already formed thrombi Given chronically*** (oral)
29
**********ADVERSE EFFECTS OF WARFARIN************
Hemorrhage, esp into the bowel ***Reversal of action is with VITAMIN K (takes time to work) or FRESH FROZEN PLASMA Quickly reduces levels of Protein C (short half-life) —> increased chance for warfarin-induced thrombosis —> CUTANEOUS NECROSIS AND INFARCTION Must co-administer with heparin for first 5 days
30
Contraindications for Warfarin****
Pregnancy - Category X (crosses placenta, teratogenic) Drug interactions (lots!)
31
What are the four steps in Fibrinolysis?
1) tPA released from healthy endothelium 2) Circulating tPA is inactivated by PAI 3) If not bound, tPA cleaves plasminogen into plasmin 4) Plasmin degrades the fibrin threads of the clot into soluble degradation products and removes the clot
32
What is the MOA for Fibrinolytic Agents?
Convert plasminogen to plasmin (lyses thrombus from within) Given IV or intra-arterially for the lysis of clots, in MI, PE, DVT, or arterial thrombosis Can cause serious bleeding (if so, give aminocaproic acid)
33
****What are the Thrombolytics drugs?
Alteplase (Tissue plasminogen activator or t-PA) Tenecteplase These guys are CLOT-SELECTIVE
34
How is Tenecteplase different from Alteplase?
Multiple point mutant of tPA (longer plasma half-life) More fibrin specific and resistant to PAI-1 than standard tPA Becoming the fibrinolytic agent of choice
35
________ drugs directly activate plasminogen but are not clot-fibrin specific (so they do generalized systemic fibrinolysis
Urokinase drugs Streptokinase and Anistreplase OFF-MARKET****
36
What drugs are useful in bleeding disorders AND reversal of fibrinolytic therapy?
Antifibrinolytics: Aminocaproic Acid, Tranexamic Acid Completely inhibit plasminogen activation DO NOT USE IN PATIENTS WITH DIC or GU BLEEDING
37
****What is the MOA for Aspirin
IRREVERSIBLE INHIBITION of COX enzyme —> reduced prostaglandin synthesis (TXA2) —> reduced platelet aggregation Lasts the life of the platelet (7-10 days)
38
****Indications for Aspirin use
A single dose may prolong bleeding time for DAYS May be useful in patients at risk for embolisms SECONDARY PREVENTION OF CV EVENTS in patients with established CVD
39
****What is the MOA for Clopidigrel, Ticlopidine, and Prasugrel?
IRREVERSIBLY BLOCKS THE ADP RECEPTOR ON PLATELETS —> reduced platelet aggregation
40
How are Clopidigrel, Ticlopidine, and Prasugrel used?
***In patients who are allergic to aspirin (less GI bleeding) To reduce thrombotic events following MI/stroke **********DOC for preventing thrombosis in patients undergoing placement of coronary stents
41
Clopidigrel is metabolized in its active form by CYP2C19, so use with caution when...
Using drugs that impair CYP2C19 function like OMEPRAZOLE
42
***What is the MOA for Abciximab, Eptifibatide, Tirofiban?
Inhibitors of GPIIb/IIIa receptor —> reduced platelet aggregation*** Abciximab is an antibody*** Eptifibatide and Tirofiban is an analog of carboxy end of fibrinogen
43
*****Indications for GPIIb/IIIa receptor inhibitors
Combined with heparin for percutaneous coronary intervention Given IV in patients undergoing ANGIOPLASTY, ATHERECTOMY, AND STENT PLACEMENT
44
What is Vorapaxar?
Antagonist of the protease-activated receptor-1, the major thrombin receptor on human platelets Potently inhibits thrombin-related platelet aggregation, used in prophylaxis in patients with previous MI or PAD Given orally, long 1/2 life Contraindicated in patients with Hx of stroke/TIA

Pharm II Unit II (8 decks)

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