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PHRM844 > Anticoagulation / Antiplatelets > Flashcards

Anticoagulation / Antiplatelets Flashcards

1
Q

Hemostasis

A

Arrest of bleeding from a damaged blood vessel

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2
Q

Coagulation

A

Multi-step process to plug leaking vessel

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3
Q

Phases of hemostasis

A

Injury –> bleeding
Vasospasm
Platelet plug form –> adherence / aggregation
Fibrin clot form –> prothrombin -> thrombin
Fibrinolysis –> plasminogen -> plasmin

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4
Q

Deadly duo

A

Atherosclerosis plaque and thrombosis –>
coronary plaque rupture

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5
Q

Platelet composition

A

Presence of organelles and secretory granules, but no nucleus

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6
Q

Contact with ECM initiates platelet reactions

A

Adhesion and shape change
Secretion reaction
Aggregation

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7
Q

First step of platelet activation

A

Platelet adhesion and shape change

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8
Q

Platelet adhesion mediated by

A

GP Ia binding to collagen
GP Ib binding to von Willebrand factor

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9
Q

Shape changes facilitate receptor binding

A

Intact endothelial cells secret PGI2 to inhibit thrombogenesis

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10
Q

Second step of platelet activation

A

Platelet secretion

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11
Q

Secretion / release reaction

A

Degranulation ->
Platelet granules release ADP, TXA2, serotonin (5-HT) ->
ADP, 5-HT, TXA2 activate and recruit other platelets ->
TXA2 and 5-HT are potent vasoconstrictors

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12
Q

Third step of platelet activation

A

Platelet aggregation
Conformation of GP receptors to bind fibrinogen ->
Platelets are cross-linked ->
Form temporary hemostatic plug ->
Platelets contract ->
Form irreversibly fused mass ->
Fibrin stabilizes to anchor aggregated platelets ->
Forms surface clot

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13
Q

Antiplatelet drugs

A

COX-1 Inhibitors (aspirin)
ADP receptor inhibitors
BP IIb / IIIa receptor blockers
PDE-3 inhibitors
PAR inhibitors

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14
Q

COX-1 inhibitor (aspirin)

A

Inhibition of TXA2 synthesis -> anti-platelet activity
Irreversibly COX-1 inhibition by acetylation
Prolongs bleeding time

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15
Q

Aspirin indications

A

Prophylaxis and treatment of arterial thromboembolic disorders

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16
Q

Aspirin SEs

A

Upper GI bleeding
Acute aspirin overdose
Increased CVD risk

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17
Q

ADP receptors involved in activating platelets

A

P2Y1 and P2Y12
Activation of both is required for platelet activation by ADP

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18
Q

Direct acting P2Y12 antagonists

A

Cliostazol, ticagrelor, cangrelor

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19
Q

Pro-drug P2Y12 antagonists

A

Prasugrel, clopidogrel

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20
Q

ADP receptor inhibitor MOA

A

Irreversibly block ADP receptor on platelet and activates of GP IIb / IIIa complex

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21
Q

ADP receptor inhibitor administration

A

Taken orally
Clopidogrel has a lower toxicity profile
Action lasts for several days after dose

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22
Q

ADP receptor inhibitor uses

A

Recent MI, stroke, acute coronary syndrome

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23
Q

Thrombotic thrombocytopenic purpura

A

Spurious and excessive platelet aggregation
Can be fatal

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24
Q

Prasugrel

A

Used for: acute coronary syndrome
Taken orally
Prodrug: req esterases + CYP2A4 / 2B6
Irreversibly bind P2Y12 receptor
High bleeding risk

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25
Ticagrelor
Used for: acute coronary syndrome, PCI Taken orally Binds to allosteric site, reversible Faster onset of action High bleeding risk
26
Cangrelor
Used adjunct for: PCI Given IV Binds reversibly Fast onset of action
27
PDE-3 Inhibitors MOA
Platelet aggregation inhibitor Action related to cAMP PDE inhibition and inhibiting adenosine uptake
28
Dipyridamole use
Adjunct with warfarin to prevent embolization from prosthetic heart valves Adjunct with ASA to prevet cerebrovascular ischemia
29
Cilostazol use
Intermittent claudication (muscle cramps)
30
GP IIb / IIIa receptor inhibitors MOA
Inhibits fibrinogen crosslinking of platelets to decrease aggregation
31
Eptifibatide
Given IV bolus followed by infusion up to 72 hours Short duration of action Used: prevent thromboembolism
32
Tirofiban
Reversible inhibition Given IV in dilute solution Combined with heparin for acute coronary syndrome
33
Abciximab
Given IV bolus followed by infusion Long duration of action -> high bleeding risk Adjunct with t-PA for early tx of acute MI
34
PAR inhibitors
Thrombin activates platelets GPCRs coupled to release Ca
35
PAR inhibitors MOA
Proteolytic cleavage of PAR-1 receptors
36
Vorapaxar
Oral administration Used with aspirin or clopidogrel Effects continue for days Contra: history of stroke, TIAs, hemorrhage
37
Vorapaxar use
Prevent thrombosis if previous MI or peripheral artery disease
38
Clotting factors
Serine proteases: - Factors XII, XI, X, IX, VII, II -> cleave and activate down-stream factors - Protein C -> cleave factors Va, VIIIa to inactivate them Glycoproteins: - Factors VIII, V, III, Protein S -> cofactors for protease activation - Anti-thrombin III -> binds and inhibits thrombin
39
Fibrinogen/fibrin
Substrate protein for F IIa (thrombin) Polymerizes to form clot
40
Hemophilia A
Deficiency in factor VIII
41
Hemophilia B
Deficiency in factor IX
42
Clotting factor production
All produced in liver Except von Willebrand factor is produced in endothelium Liver disease can have unpredictable effects on coagulation
43
Coagulation via extrinsic pathway
Requires tissue facto Used when vessel is damaged and blood leaks out (thromboplastin) Rapid clot formation ~15 seconds
44
Thrombin in clotting pathways
Convergence point of intrinsic and extrinsic pathways at thrombin activation Converts fibrinogen -> fibrin
45
Coagulation via intrinsic pathway
Triggered when neg charged collagen is exposed on the wall of the blood vessel Ex. blood in test tubes clotting
46
Feedback mechs increase coagulation
Thrombin - Activates factor V, VIII - Enhances platelet activation Platelet activation - Increases factor VII, X activation - Cleaves prothrombin
47
Feedback mechs decrease coagulation
Antithrombin - Neutralizes thrombin, factor Xa, IXa - Accelerated by heparin Protein C system - Inactivates factor Va, VIIIa Factor Xa - Blocks initial activation of factor VII
48
Platelet Count test
Too high: thrombocytopenia -> bone marrow malfunctions or nutritional deficiencies
49
Prothrombin time (PT/INR) test
Plasma + thromboplastin + Ca Clots in 12-14 seconds
50
aPTT test
Plasma + phospholipid + activating agent Clots in 26-33 seconds Used to monitor heparin therapy
51
Fibrinogen test
Less common 200-400 mg/dL
52
D-dimer test
Product of fibrin breakdown
53
INR ranges
Normal: 0.8-1.2 Therapeutic: 2-3 Risk of hemorrhage: >3
54
Uses for anticoagulants
Prevent excessive clotting -> causes other issues if untreated - Stroke - Post-MI - DVT - PE
55
Oral anticoagulant drugs
Coumarin anticoags - All derivatives are water soluble lactones - Warfarin is most common
56
Warfarin MOA
Inhibits Vit K-epoxide reductase -> blocks reduction of Vit K epoxide back to active form Inhibits synthesis of clotting factor II, VII, IX, X
57
Warfarin OD
Discontinue warfarin Administer Vit K If serious can admin plasma instead
58
Warfarin necrosis
Deficiency in protein C Warfarin further decreases protein C levels so can cause initial incr in blood coag at start of therapy Often common to start pts on heparin w warfarin in parallel
59
Drug's decr warfarin's effects
Rifampin Vitamin K Pregnancy
60
Drugs incr warfarin's effects
SSRI's Broad spectrum antibiotics Anabolic steroids
61
Indirect factor IIa, Xa inhibitors
Heparin - UFH - LMWH (enoxaparin, daltaparin) Non-heparinoids - Fondaparinux
62
Heparin MOA
Accelerated AT reactions -> inactivates thrombin and factor Xa
63
Heparin clinical use
Admin IV -> immediate effect Adjust dosing based on coag tests Effects stop within hours of ending therapy
64
Heparin AEs
Latrogenic hemorrhage - Tx: protamino sulfate HIT - Type 1 and 2 Osteoporosis - Associated with extended therapy
65
HIT risk ranking
UFH > LMWH > fondaparinux
66
Fondaparinux MOA
Indirectly inhibits factor Xa by selectively binding AT
67
DOACs
Direct Xa inhibitors - Rivoroxaban - Apixaban - Edoxaban - Betrixaban Direct thrombin inhibitors (DTI) - Dabigatran
68
Factor Xa inhibitor antidote
Andexanet - approved with apixaban and rivoroxaban
69
DTI actions
Non-heparinoid parenteral agents Inhibit free and fibrin-bound thrombin

PHRM844 (16 decks)

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