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Pharmacology: NA > Hemostasis and Coagulation Modifying Drugs > Flashcards

Hemostasis and Coagulation Modifying Drugs Flashcards

1
Q

What is Hemostasis?`

A

-Balance between clot formation and clot breakdown.

Thrombus= clot

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2
Q

3 Phases of Hemostasis?

A
  • Vascular Phase
    • vessel contract

-Platelet Phase
* start adhesion
tn phase
*Clotting

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3
Q

Platelets

A

Starts clotting than escalates clotting.

Functions:

  • Formation of platelet plug (primary hemostasis)
  • Release of chemicals for clotting (activating) secondary
    hemostasis. (from granules)
  • Active contraction after clot formation.

Prostacyclin and nitric oxide are synthesized by intact endothelial cells and acts as inhibitors of platelet aggregation. (also promotes dilation)

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4
Q

Platelets: Thrombin and Thromboxane A2

A

Thrombin: An enzyme in blood plasma that causes the clotting of blood converting fibrinogen to fibrin.

Thromboxane A2: a hormone released from platelets. It induces platelet aggregation and arterial contristriction.

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5
Q

Platelet (Plug) Phase

A

Adhesion: Platelets bind to the vascular subendothelial collagen via vWF

Activation: Damaged tissue releases Tissue Factor (TF)

  1. Most powerful platelet activator, intiator of coagulation.
  2. also known a Thromboplastin and factor III

Aggregation: of platelets require ADP and thromboxane A2, platelets start to stick together.
-thromboxabe A2 and ADP help expose the fibrinogen receptors, which becomes modified to bind fibrinogen better.

Firbrin Product: requires extrinsic, intrinsic and final common pathways, final clot formation.

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6
Q

Thromboxane A2 and NSAIDs and ASA

A

Thromboxane A2 helps platelets clot.

NSAIDs and ASA disrupt hemostatsis by inhibiting TxA2 formation thereby blunting plt activation

     * they cause patients to bleed more.
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7
Q

Clot Formation

A

Trace amounts of thrombin are generated during the initiation phase of coagulation by factor Xa (FXa) via interactions between circulating FVIIa and TF (aka FIII) expressed on subendothelial pericytes and fibroblast.

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8
Q

Fibrinogen

A

Plasma glycoprotein synthesized in the liver.

Thrombin cleaves the fibrinogen molecules, producing a soluble fibrin monomer which polymerizes to form a loose network in trapping red blood cells and a clot begins to form.

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9
Q

Cofactors

A

Calcium and Phospholipids:
-Ca required in all three pathways.

Vitamin K
-Adequate amount necessary for the liver to synthesized four of the clotting factors: II, VII, IX, annd X, as well as protein C, and protein S

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10
Q

Regulators

A

Protein C:

  • Physiological anticoagulant
  • Vit K depenednt serine protease emzyme.
  • Activated by thrombin into activated protein C (APC)
    • protein C: halts further thrombin generation by inactivating (Va and VIIIA), works in conjuction w/ protein S.

Antithrombin:

  • plasma protein from the liver, inhibits the coagulation enzymes of the intrinsic and common pathways, thrombin
  • constantly active
  • Increased adhesion in presence of heparin sulfate or administration of heparin.
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11
Q

Regulators:
Tissue Factor Pathway Inhibitor
Plasmin
Prostacyclin

A

Tissue Factor Pathway Inhibitor

  • limits action of TF
  • inhibits excessive TF-mediated activationof factor VII and X

Plasmin

  • generated by proteolytic cleavage of plasminogen, catalyzed by t-PA
  • cleaves fibrin into fibrin degradation products.

Prostacylin:

  • released by endothelium
  • inhibits platelet activation
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12
Q

Drug Eluting Stent (Antiplatelet Agents)

A

Needs 12 months of thienopyridine therapy, premature discontinuing can be catastrophic.

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13
Q

Bare Metal Stent (Antiplatelet Agents)

A

Drug therapy for 6 weeks

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14
Q

Cyclooxygenase Inhibitor: Cox inhibitor

Antiplatelet Agents

A

Aspirin

Irreversibly acetylates cox = prevents formation of thromboxane A2.

Effects on platelets are irreversible and last for the life o the platelets, 7-10 days.
-platelet inhibitor

Prevents Aggregation.

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15
Q

ADP receptor Pathway Inhibitors (thienopyridines)

Antiplatelet Agents

A

Plavix
Effient

Irrversibly bind to the platelets P2Y receptor therby blocking adenosine (ADP) binding

Often coupled with Aspirin

DOA: life of the the platelet

Discontinue 7 days before surgery

Platelet transfusion may help reverse

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16
Q

GPIIb-IIIa Antagonist

Antiplatelet Agents

A
  • Repro
  • Aggrastat
  • Eptifibatide

Bind or competitively inhibits the corresponding fibrinogen receptor that is important for platelet aggregation.

Block fibrinogen binding to platelet GP IIb/IIa receptors that are a common pathway of platelet aggregation,

17
Q

Wafarin (Coumadin)

Anticoagulant

A

Competitively inhibits vit K epoxide reductase reduction o vit K

-Narrow therapeutic Index

Reversal: FFP and Vit K and PCC
-Oral or IV vit K takes a day to reverse anticoag effect

Crosses the Placenta

Test: PT and INR

18
Q

Unfractioned and Low molecular Weight Heparin (Intrinsic pathway)

(Anticoagulant)

A

-Binds to naturall occuring antithrombin
-Heparin alone has no anticoag effect
-Prevents thrombus formation and extension prophylaxis doesn’t affect clots already present.
-Prevents thrombins consumption of clotting factors.
-Activated partial thromboplastin time (aPTT)
-Anti Xa assay: instead of PTT accounts for extremes in dosing
-ACT (activated clotting time)
-Heparin induced Thrombocytopenia (HIT)
Heparin induced Thrombocytopenia w/ Thrombosis HITT
-development of heparin induced platelet IGG
antibodies to your own platelets.
-Be suspicious if thrombosis worsens/develops,
bleeding time increases, and platelet count drops.

19
Q

Protamine for Heparin Reversal

Anticoagulant

A

-Dose of protamine required to antagonize heparin is 1mg for every 100 units of circulating heparin activity.

Give slowly over course of 20 in.

Dangers of Use: IGG/complement mediated hemodynamic catastrophes

-Doesn’t neutralize LMWH

20
Q

Selective factor 10a Inhibitors

Anticoagulant

A

-Arixtra

-Alternative for patients with HIT
_prevents DVT & PE

Xarelto

  • No easy testing
    - PCCs complete reverse

Apixaban

Edoxaban : under investigation

21
Q

Direct Thrombin Inhibitor

Anticoagulant

A
  • Good for patients with HIT
  • Immunologenic: antibodies can form
  • Testing: monitored with aPTT and ACT
  • Bivalirudin
    • commonly used for cardiac interventional procedures
    • Safe with HIT
  • Argatroban
    • Prophylaxis or treatment with HIT patients undergoing PCL
      • Not renally cleared, doesn’t make antibodies.
  • Lepirudin and Deirudin
    • Analogs of hirudin, can cause bleeding and allergies.
    • Renal Clearance
    • Monitor aPTT
  • Pradaxa
    • measured with thrombin times (TT) ecarin clottingt time (ECT) and aPTT
22
Q

Antithrombin

Anticoagulant

A

Naturally occurring anticoagulant

23
Q

Thrombolytic Agents

A
  • Acts as plasminogen activators to convert the endogenous proenzyme plasminogen to the fibrinolytic enzyme plasmin that lysis clot and other proteins.
  • Reversal: FFP, cryoprecipitate, platelets, and antifibrinolytic drugs Amicar
24
Q

Streptokinase

Thrombolytic Agents

A

Made by beta hemolytic streptococci, little affinity for fibrin, preformed antibodies may inactivate it.

25
Q

Urokinase

Thrombolytic Agents

A

Has a lower affinity for fibrin, found in limited amounts in the blood, extravascular thrombolysis (inflammation) made by endothelium.

26
Q

Recombinant Tissue Plaminogen activator (t-PA)

Thrombolytic Agents

A

Binds strongly to fibrin, found in the clot, stimulated by thrombin, for intravascular thrombolysis, made in endothelium.

27
Q

Antifibrinolytics

A

EACA, Amicar and TRanexamic Acid

-Inhibits activation of plasminogen to plasmin, an enzyme that degrades fibrin clots and fibrinogen.

Decrease in bleeding, reducing the need for RBC transfusio, reducing the need for reoperation.

28
Q

Desmopressin (DDAVP)

A

Shortens the bleeding time of patients with mild form or hemophilia A or vWF disease

29
Q

Prothrombin Complex Concentrate (PCC)

A

Vit k antagonist- induced warfaring reversal

used in hemophilia

Pharmacology: NA (4 decks)

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