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IHO Week 6 > Anti Coag Drugs > Flashcards

Anti Coag Drugs Flashcards

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1
Q

First phase of hemostasis

A

Vascular constriction limits the flow of blood to the area of injury

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2
Q

Second phase of hemostasis

A

Platelets become activated and aggregate at the site of injury, forming a temporary, loose platelet plug (primary)

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3
Q

Third phase of hemostasis

A

Fibrin mesh (clot) forms and entraps the plug (secondary)

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4
Q

Fourth phase of hemostasis

A

The clot is dissolved in order for normal blood flow to resume following tissue repair

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5
Q

What is primarily responsible for stimulating platelet clump?

A

Fibrinogen

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6
Q

Platelets clump by binding to collagen that becomes exposed following…

A

rupture of the endothelial lining of vessels

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7
Q

Upon activation, platelets release

A

ADP and TXA2 (activate additional platelets), 5HT, phospholipids, lipoproteins etc.

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8
Q

White thrombus

A

plug contains only platelets

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9
Q

Red thrombus

A

plug contains red cells as well

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10
Q

The dissolution of a clot occurs through the action of this protein

A

plasmin

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11
Q

3 classes of drugs to reduce clotting -

A
  1. Antiplatelet drugs
  2. Anticoagulant drugs
  3. Fibrinolytic drugs
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12
Q

4 types of antiplatelet drugs

A

COX inhibitors
ADP Receptor Antagonists
GPIIb/IIIa Receptor inhibitors
Adenosine reuptake inhibitors

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13
Q

COX inhibitor used in anti-clotting therapy

A

Aspirin (irreversible)

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14
Q

ADP Receptor Antagonists

A

Clopidogrel
Ticlopidine
Prasugrel

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15
Q

GPIIb/IIIa Receptor Inhibitors

A

Abciximab
Eptifibatide
Tirofiban

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16
Q

Adenosine Reuptake Inhibitor

A

Dipyridamole

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17
Q

Antiplatelets act at

A

phase 2 - platelet plug formation

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18
Q

Anticoagulants act at

A

Phase 3 - secondary hemostasis

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19
Q

Fibrinolytic drugs

A

Phase 4

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20
Q

4 types of anticoagulants

A
  1. indirect thrombin inhibitors
  2. direct thrombin inhibitors
  3. Vitamin K analog
  4. Factor Xa Inhibitor
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21
Q

Indirect thrombin inhibitors

A

Heparin
LMW heparin
Fondaparinux

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22
Q

Reverse Heparin

A

Protamine

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23
Q

Direct thrombin inhibitors

A

Bivalirudin
Argatroban
Dabigatran etexilate (oral)

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24
Q

Vitamin K analog

A

Warfarin

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25
Reverse Warfarin
Vitamin K (phytonadione)
26
Factor Xa Inhibitor
Rivaroxaban
27
Fibrinolytic drugs - Tissue plasminogen activators
Alteplase Reteplase Tenecteplase
28
List some therapeutic uses for anti-coags
Venous thromboembolism, Unstable angina, Acute MI, Stroke, Prevent thrombosis during angioplasty and cariopulmonary bypass, A. fib
29
Aspirin - things to know
Acetylsalicylate COX1 in platelets AE: Bleeding, GI dist., tinnitus
30
Low dose vs high dose aspirin
Low dose - effect platelet | High dose - anti inflammation
31
ADP receptor Antagonists
Irreversible, last as long as platelet Oral, days duration Stenting and patients who don't tolerate aspirin
32
AE of ADP receptor antagonists
Bleeding, nausea, diarrhea, rash, leukopenia | TTP - rarely with ticlopidine
33
Clopidogrel and Prasugrel have _____ than Ticlopidine
Fewer side effects
34
Clopidogrel may require activation via
CYP2C19 | Omeprazole - use with caution
35
Are ADP receptor antagonists reversible?
No, last lifetime of platelets
36
GPIIb/IIa Receptor Inhibitors MOA
Prevent binding of adhesive glycoproteins such as fibrinogen and vWF to activated platelets
37
AE of GPIIb/IIa Receptor Inhibitors
Bleeding | Thrombocytopenia (chronic use)
38
Dipyridamole MOA
- Increases cAMP and inhibits platelet activation - phosphodiesterase 3 inhibitor (increases cAMP by preventing breakdown to 5 AMP by phosphodiesterase) - Inhibits platelet uptake of adenosine and thus increases the adenosine interaction with A2 receptor - increase cAMP
39
Dipyridamole is also a
Vasodilator
40
AE of dipyridamole
Headache (vasodilation)
41
Is dipyridamole effective alone?
No, must be used in combination with aspirin or warfarin
42
Thrombin inhibitors
Parenteral anticoagulant heparin and derivatives
43
Indirect thrombin inhibitors
Unfractionated heparin LMW heparin Fondaparinux
44
Direct thrombin inhibitors
Bivalirudin Argatroban Dabigatran Etexylate (oral, new)
45
Indirect thrombin inhibitors MOA
Bind to antithrombin
46
Antithromin normally
inactivates thrombin and factor Xa
47
When indirect thrombin inhibitors bind to antithrombin
antithrombin does a better job
48
Basically.. heparin makes antithrombin...
Work REALLY WELL
49
Heparin is highly variable anticoag because
binds all over (plasma proteins, platelets, macrophages, endothelial cells)
50
HMW heparin
works on both thrombin and Xa so they don't work
51
LMW
works on thrombin and Xa
52
Fonduparidonox
Xa only
53
Protamine
highly basic pos. charged peptide that combines negatively charged heparin to form a stable complex that lacks anti-coag activity.
54
Protamine only binds
long heparin
55
Does HMW heparin have a short or long half life?
Short
56
Protamine and LMWH
incomplete reversal
57
Protamine and Fondaparinux
Won't do anything
58
Heparin monitored with
PTT
59
AE of Heparin, LMWH, Fondaparinux
Bleeding, heparin induced thrombocytopenia
60
Heparin induced thrombocytopenia
Thrombotic complications may precede 2x more likely in women IgG ab against heparin/factor 4
61
Direct thrombin inhibitors
bind directly to thrombin to inhibit enzyme
62
Warfarin
Blocks synthesis of Vitamin K dependent clotting factors | Tricky drug that requires monitoring (PT) and has tons of drug interactions
63
Direct Factor Xa
Rivaroxaban no antidote or monitoring rapid onset and short half life
64
Warfarin MOA
- inhibits Vitamin K dependent exposite reductase VKORC1 | - Inhibits vitamin K dependent gamma carboxylation of factors II, VII, IX, X and protein C
65
Warfarin inhibits
Vitamin K dependent gamma carboxylation of factors II, VII, IX and X. Protein C
66
Warfarin onset
Need to bridge, won't work initially but protein C will stop - could result in initial clotting.
67
AE Warfarin
``` Bleeding Drug Interactions (like, everything) Flatulence and diarrhea cutaneous necrosis chondrodysplasia punctata ```
68
Warfarin enantiomers
S more active | R and S metabolized differently (liver, cytochromes)
69
Polymorphism in CYP2C9
30% are slower metabolizers
70
Polymorphism in C1 subunit of VKORC1
influences warfarin interaction - dosage may need to be adjusted
71
Pharmacokinetics
ADME
72
For oral anticoagulants, pharmacokinetic drug interactions are due to
enzyme induction enzyme inhibition Decreased PBP
73
Pharmacokinetics
Biochemical and physiological effect of drug and MOA
74
for oral anticoags, pharmacodynamic drug ineractions due to
reduced clotting factor synthesis competitive antagonism with vitamin K hereditary resistance
75
Too much warfarin - what do you do?
- Stop the drug | - Add vitamin K ( or phytonadione, prothrombin complex concentrates, recombinant factor VIIa)
76
Streptokinase
rarely used clinically, complexes with plasminogen so facilitates formation of plasmin
77
Urokinase
- Kidney enzyme that directly converts plasminogen to plasmin - promotes extravascular fibrinolysis
78
Fibrinolytic Drugs
tPAs - tissue plasminogen activators -preferentially activate plasminogen that is bound to fibrin which confines it to the thrombus rather than systemic activation
79
Fibrinolytic Drugs - name 3
Alteplase Reteplase Tenecteplase
80
Common features of Fibrinolytic Drugs
Dissolves existing life-threatening thrombi Activate plasminogen Given IV Narrow spectrum
81
AE fibrinolytic drugs
Bleeding and cost
82
MOA of fibrinolytic drugs
Selective activation of fibrin bound plasminogen | only thrombolytics approved for use in stroke
83
Aminocaproic acid
``` Potent inhibitor of fibrinolysis Blocks interaction of plasmin with fibrin Minor use (prostatic sugery, tooth surgery in hemophiliacs) ```

IHO Week 6 (7 decks)

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