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Cardio Exam 3 > Anti-Angina, Anti-thrombolytics & Thrombolytics > Flashcards

Anti-Angina, Anti-thrombolytics & Thrombolytics Flashcards

1
Q

Hemostasis steps

A

1st:
cessation of bleeding from an injured blood vessel
Reflex Vasospasm
-slow down the bleeding
Exposure of TF
-platelet adhesion and activation (TXA2, ADP & 5-TH)
Platelet plug
- platelet are connected to each other by fibrinogen
-role of tPA, NO and PGs

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2
Q

Hemostasis steps

A

2nd:
Fibrin clot
- conversion of prothrombin (II) to thrombin (IIa). Thrombin converts of fibrogen (I) to fibrin (Ia; mesh)
Dissolution of the clot (fibrinolysis)
-plasminogen is converted to plasmin, the enzyme that dissolves the fibrin

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3
Q

Fibrin Clot

A

involve a number of precursor proteins and active proteases
components at each stage:
- TF, Phospholipids & Ca++
- organizing surface (platelets)
- precursor protein (zymogen –> active protease)
- protease from the preceding stage –> activate next process
- non enzymatic protein cofactors (active enhance activity of other enzymes)

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4
Q

What 3 things need to happen in order for the clotting formation to happen?

A
  1. ADP binding to P2Y12–>Gi–> decrease cAMP
  2. ADP binding to P2Y1–> Gq–> increase Ca++
  3. TxA2 binding to TxA2 receptor–> Gi–> increase Ca++
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5
Q

What is the extrinsic pathway?

A

VII–>VIIa–>X–>Xa

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6
Q

What is the intrinsic pathway?

A

Phospholipids and # of factors XII–>XIIa–>XI–>XIa–>IX–>IXa–>X–>Xa

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7
Q

What is the common pathway?

A

Xa–>II (prothrombin)–> IIa (thrombin) –> I (fibrinogen) –> Ia (fibrin) –> red clot

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8
Q

Thrombin (IIa)

A

converts fibrinogen to fibrin monomers by cleaving fibrinopeptides A & B. this allows fibrin to form a gel

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9
Q

Cofactor Va

A

V: present freely in the plasma & as a component of platelets. it is coverted to Va by thrombin, which increase by 50x’s the coagulation activity of Xa

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10
Q

Xa

A

common pathway

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11
Q

Tissue Factors (TF)

A

non-enzymatic lipoprotein cofactor that greatly increases the proteolytic efficiency of VIIa. VIIa activates X.
present in the surface of cells that do not normally contact plasma

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12
Q

Antithrombin

A

a plasma protein that inhibits aggregation factors Xa and IIa.
heparan sulfate is a proteoglycan synthesized by the endothelium cells and stimulate the activity of antithrombin.

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13
Q

Protein C & S

A

degrades cofactors Va and VIIIa, which leads to the decrease in prothrombin and factor X activation.
prostaglandins (PGI2) & NO inhibit platelet aggregation.

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14
Q

Prevent clotting

A

antiplatelet agents: Aspirin, dipyridamole, ticlopidine, abcximab, eptifibatide & prasugrel
clotting cascade modulators: heparin, lepirudin, warfarin, dabigatran, rivaroxaban

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15
Q

Promote clot breakdown

A

tissue plasminogen activator (t-PA): alteplase, strepto & urokinase

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16
Q

Activated partial thr omboplastin time (aPTT)

A

add Ca++, phospholipids, and a particular substance. analyze for clotting time.
measure intrinsic pathway by factor XII

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17
Q

Prothrombin time (PT)

A 
add thromboplastin (TF+phospholipids) & analyze for clotting time.
measure of the extrinsic/common pathway
decrease in PT time= more bleeding less coagulation
increase in PT time= less bleeding more coagulation
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18
Q

Heparin Na+ & Ca++

A

heterogeneity in composition, but similar biological activity (150 USP units/mg).
naturally occurring mixture of sulfated muccopolysaccharides produced by mast cells and basophils.

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19
Q

Heparin MOA

A

increases the rate of thrombin-antithrombin reactions by making the reactive site more accessible to the protease. thrombin inactivation

20
Q

Heparin Uses

A

prevention and treatment of embolism (post-op), deep vein thrombosis, pulmonary embolism, initial management of unstable angina or acute MI.

21
Q

Heparin Information

A

Immediate onset (30-60 mins): heparin acts on ACTIVATED factors that are already circulating in the blood.
OD: protamine sulfate (+ charges that binds ionically to heparin)
DDI: any drug that may increase the risk of bleeding (salicylates). recent trauma, peptic ulcer, etc.
AE: bleeding
heparin associated thrombocytopenia (HAT): unknown MOA, but not immune mediated
heparin induced thrombocytopenia (HIT): immune mediated

22
Q

Parental Heparin

A

Pharmacokinetics: administration can be IV or SQ outpatient basis for DVT patients. has an immediate onset; hepatic elimination and excretion, with some excreted unchanged in urine
SE: thrombocytopenia (early/late) hemorrhage
Contraindications: existing bleeding conditions or bleeding tendency
OD: administer protamine sulfate (+ binds to heparin)

23
Q

LMW Heparins

A

inhibits factor Xa, very little effect on factor IIa. less incidence of thrombocytopenia and hemorrhage. more predictable PK

24
Q

Anixtra (fondaparinux)

A

synthetic heparin that binds only to Xa
-less likely to produce HIT
used for thromboprophylaxis of pts undergoing hip or knee surgery, pulmonary embolism and deep venous thrombosis.

25
Pradaxa (dabigatran)
selective and reversible inhibitor of thrombin (IIa) both free and fibrin-bound ADR: bleeding & GI hemorrhage DDI: PgP & not metabolized by CYP 450
26
Parental direct thrombin inhibitors (IIa)
``` Lepirudin: Irreversible -recombinant derivative of hirudin Bivalirudin: Reversible -synthetic, thrombin bond cleaved Argatroban: Reversible - synthetic compound based on structure of L-Arginine that binds to catalytic site of thrombin ```
27
Xarelto (rivaroxaban) | Eliquis (apixaban)
MOA: oral factor Xa inhibitor Use: thromboprophylaxis after hip or knee replacement surgery
28
Warfarin
Mainstay for prevention of thromboembolic disease MOA: it inhibits the vitamin K epoxide reductase. decrease in production of coagulation factors VII, IX, X, II, and proteins C & S. Uses: treatment of embolism, DVT, or atrial fibrillation, patients w/prosthetic valves. combined w/heparin during the initial phase of treatment. Oral of IV= 100% BA
29
Warfarin DDI
any drug that alter the: uptake or metabolism of warfarin or vitamin K (2C9 most important) synthesis, function or clearance of any factor or cell involved in hemostasis or fibrinolysis integrity of any epithelial surface increase PT time= bleed more decrease PT time= clot more
30
Warfarin ADR
hemorrhage: internal bleeding not given in pregnancy skin necrosis: 3-10 days after treatment initiation. thrombosis of microvasculature blue-tinged discoloration of plantar surfaces: purple toe syndrome OD: reduced vitamin K
31
Warfarin summary
warfarin acts slowly because it is affecting the SYNTHESIS of factors whereas Heparin acts rapidly because it is INACTIVATING factors that are already circulating. warfarin can be taken orally while heparin is IV or SQ OD: warfarin= vitamin K, heparin= protamine sulfate Primary ADR: hemorrhage
32
Aspirin
MOA: IRREVERSIBLE COX1 inhibitor and inhibits the formation of TXA2 Clinical use: prevention of atherosclerosis, thrombosis, transient ischemic attacks; unstable angina
33
Platelet aggregation- TxA2 mediated
platelet activation: increase TxA2 synthesis and secretion via COX1. TxA2 receptor activation increases Ca++ increase ADP synthesis and secretion. decrease cAMP levels and increase Ca++
34
Aspirin ADR
GI irritation: local irritation of GI mucosa aspirin induced asthma (hypersensitivity rxn's) Contraindications: bleeding disorders, hypersensitivity and Reye's syndrome
35
Plavix (clopidogrel)
MOA: irreversible P2Y12 antagonist which is coupled to Gi. cAMP inhibits platelet glycoprotein receptors and reduces fibrinogen binding and platelet aggregation ADR: bleeding, neutropenia and thrombocytopenia (rare) Use: prevention of atherosclerosis, thrombosis, transient ischemic attacks; unstable angina
36
Ticlid (ticlopidine)
MOA: same as clopidogrel ADR: GI- N/V/D; Bleeding- mild to moderate neutropenia & fatal agranulocytosis Contraindications: bleeding disorders, sever liver disease Use: pts intolerant to apsirin, prevents thrombotic stroke
37
Effient (prasugrel)
MOA: irreversible P2Y12 antagonist, which leads to prevention of GPIIb/IIIa complex formation ADR: fatal & life-threatening bleeding DDI: NDS (alfalfa & bilberry), NSAIDs, Warfarin
38
Reversible P2Y12 antagonist
Kengreal (cangrelor): IV, t1/2= 3-6 minutes | Brillinta (ticagrelor): Oral, t1/2= 7 hours
39
Persantine (dipyridamole)
MOA: decrease the degradation of cAMP via PDE inhibition, coronary vasodilator ADR: GI distress, angina, headache, dizziness and rash Use: prosthetic heart valves, may be used as an adjunct with warfarin therapy
40
Reopro (abciximab) IV
MOA: Fab fragment that binds to platelet GPIIb/IIIa receptors and prevents binding to fibrinogen ADR: bleeding, thrombocytopenia, hypotension and bradycardia Use: percutaneous transluminal coronary angioplasty as adjunct with aspirin and heparin Contraindication: aneurysm, bleeding, recent surgery, stroke DDI: unknown
41
Integrelin (eptifibate) IV
MOA: cyclic peptide inhibitor of GPIIb/IIIa binding site Use: treat acute coronary syndrome and for angioplastic coronary intervention. given in conjunction to heparin and aspirin ADR: bleeding and thrombocytopenia
42
Aggrastat (tirofiban) IV
MOA: non-peptide inhibitor of GPIIb/IIIa binding site Use: treat acute coronary syndrome and for angioplastic coronary intervention. given in conjunction to heparin and aspirin ADR: bleeding and thrombocytopenia
43
Tissue plasminogen activator (t-PA) Activase (alteplase) Retavase (reteplase)
MOA: it is a serine protease which activates plasminogen (bound to fibrin) and increases plasmin levels. it activates bound plasminogen several hundredfold. it is effective in lysing thrombi during treatment of acute MI. longer t1/2 than native t-PA and relatively resistant to inhibition by plasma activator inhibitor-1
44
Urokinase
obtained from urine | MOA: directly activates plasminogen, isolated from human kidney, therefore less chance of evoking an allergic reaction.
45
Streptokinase
protein obtained from streptocci; anistreplase | MOA: combines with plasminogen to form an active complex that converts plasminogen to plasmin to dissolve the fibrin

Cardio Exam 3 (6 decks)

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