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*** PLEASE SEE SUPPLEMENTAL PACKET FOR PICTURES, DIAGRAMS AND STUDY QUESTIONS RELATED TO THIS LECTURE***
.
Oral Anticoagulant (prototype)
Warfarin
Therapeutic Uses for Heparin
DVT-deep vein thrombosis
PE-pulmonary emboli
MI-myocardial infarction
Prophylaxis Thrombosis
Contraindications for Heparin
Hypersensitivity
Active bleeding
Hemophiliacs
Severe hypertension
Mechanism of action for Warfarin
Inhibits the synthesis of vitamin K dependent factors (II, VII, IX, X, protein C and S)
Pharmacokinetics of Warfarin
Onset of action is delayed 5-7 days in order to synthesize new factors

Orally active
Warfarin

Drug Interactions
Drugs which stimulate metabolism: reduce anticoagulation

-Chronic alcohol ingestion
-Barbiturates
-Griseofulvin
Platelet
(function)
Provide initial hemostatic plug at site of vascular injury
Dissolution of clots (#3)
--after plasmin is formed--
3. plasmin digests fibrin to soluble degradative products; phagocytic WBCs remove the debris
Pharmacokinetics of Heparin
Parenterally administered (IV or SB)
*onset is immediate

IV administered in acute case phase of thromboembolic event

given at hospital or with home health
Adaptations/Modification of Heparin

examples: Enoxaparin (LOVENOX)
Delteparin (FRAGMIN)
Low molecular weight heparins are derived from chemicl of natural product-now available in U.S. and are given subcutaneously
Warfarin Treatment

Monitor...
1. PT-prothrombin time
2.INR-Internal Normalized Ratio-standard assessment developed by WHO; allows comparison of values from different labs
Side Effects of Warfarin
Increased bruising and tendency towards hemorrhaging
Therapeutic Uses of Warfarin
Treatment, prevention and recurrence of thromboembolism in patients with prosthetic heart valve, chronic artrial fibrillatio, patients undergoing moderate to high risk surgical procedures and as adjunct to coronary artery occlusion
Warafin

General Info
Structurally similar to Vit. K

acts over time

O.T. handle pt carefully b/c of side effects; watch out for bleeding
Warfarin

Drugs which inhibit metabolism
potentiate anticoagulation

-Cimetidine (TAGAMET)
-Disulfiram
-Metronindazole (FLAGYL)
Warfarin

Drugs which inhibit platelet aggregation
potentiate anticoagulation

Asprin->b/c it is an anti-platelet drug
Antiplatelet Drugs

NSAIDs
e.g. Aspirin

-Inhibit COX enzyme, thereby inhibiting synthesis of the thromboxane A2 in platelets
Antiplatelet Drugs

Dipyridamole
Thought to impair adenosine metabolism
to interfere with platelet function; exact mechanism not well understood
Antiplatelet (antithrombotic drugs)
Inhibit platelet function. Prevent thrombus formation in arteries
Antiplatelet Drugs

Glycoprotein (GP) IIb-IIIa inhibitors
e.g. Ticlopidine

Antagonize GP receptor on the platelet membrane that is stimulated by fibrinogen; fibrinogen is therefore unable to bind platelet;
platelet activation is decreased to reduce platelet-induced clotting
Thrombolytic Drugs
All act directly or indirectly to convert plasminogen to plasmin, which in turn, cleaves fibrin to cause lysis of thrombi
Thrombolytic Drugs

Examples
Alteplasse (tissue-type plasminogen activator, tPA)

Streptokinase
Anistreplase
Urokinase
Function of Alteplasse

(tissue-type plasminogen activator, tPA)
-Produced by recombinant techniques
-Converts plasminogent to plasmin
-Selective for formed clots, therefore only affects fibrin in clots not in circulation

Given in acute conditions
Therapeutic Uses

for Altepasse
Emergency treatment of MI

Deep vein thrombosis
Toxicity of Altepasse
Bleeding (intracranial)

Allergic Reaction
Occupational Therapy Implications
Be aware that anticoagulant therapy is associated with increased tendency for bleeding and bruising

May affect ADLs

Thrombolytic drugs usually given in acute situations
Physiology of Hemostasis


SEE PICTURES OF PHYSIOLOGY ON pg. 2
.
A clot that adheres to vessel wall

versus

an intravascular clot that floats
within the blood
Thrombus

vs

Embolus
How are fibrin clots formed?

FACTS
The clotting (coagulation) cascade

2 semi-independent pathways lead to formation of prothrombin (factor II):

*Intrinsic pathway-all of its components are within the blood; SLOW (2-6 minutes)

*Extrinsic pathway-triggered by extravascular damage; FAST (15 seconds)
How are fibrin clots formed?

FACTS

THE FINAL COMMON PATHWAY. . .
In the final common pathway, prothrombin is activated by thromboplastin (factor Xa) to activated prothrombin (thrombin IIa). Thrombin (IIa) then converts fibrinogen to fibrin monomers, which are converted to fibrin polymers. The fibrin polymers cross-linked to form the fibrin clot
***SEE PAGE 3 FOR DIAGRAM OF CLOTTING CASCADE***
.
Plasminogen
The inactive proenzyme that is plasmin once activated
Dissolution of clots (#1)
Plasminogen (inactive proenzyme) is activated and becomes plasmin by:

1. tissue plasminogen activator (tPA)-released from vascular endothelial cells following injury
Dissolution of clots (#2)
2. urokinase (produced from epithelial cells as prourokinase to plasmin-to a lesser degree)
Dissolution of clots (#4)

---after plasmin is formed---
4. Plasminogen and plasmin are rapidly inactivated by their respective inhibitors
Fibrin
plasminogen-->plasmin |
Soluble Products
Treating clots

THROMBOEMBOLISM
Abnormal clot formation
Treating clots

DEEP VEIN THROMBOSIS
A.K.A. DVT

Abnormal clots in legs
Treating Clots

PULMONARY EMBOLUS
A.K.A. PE

Abnormal clots in lungs
Treating Clots

Clots can block carotid arteries resulting in O2 deprevation in the CNS
Stroke
-mental retardation and/or physical disability
Treating Clots

Clots can form secondary plaque in coronary arteries-compromised delieving of O2 to heart tissues
Myocardial Infarction
Anticoagulants

examples: Heparin
Warfarin
Treatment of overactive clotting

Control function and synthesis of clotting factors-used in venous system (venus thrombosis)
Thrombolytics

examples: Attepasse (tissue-type plasminogen activator, TPA)
Anistrepiase
Litokinase
Streptokinase
Facilitate destruction of blood clots
Definition of Heparin
An anticoagulant; a glycosaminoglycan found in secretory granules of mast cells (physiological function unknown)
Mechanism of action of Heparin
Binds, activates and potentiates the endogenous anticoagulant, Antithrombin III (AT III) to neutralize clotting factors: II, IX, X, XI, XII and kallikrein
Sources for Heparin
extracted from porcine intestinal mucosa or bovine lung
Side effects of Heparin
Hemorrhage
Thrombocytopenia (low blood platelet count)
Heparin Treatment

Monitor...
1. blood components-total blood count

2. aPTT (Partial Thromboplastin Time)-Intrinsic Pathway

3. PT (Prothrombin Time)-Extrinsic Pathway
Heparin Toxicity
can be reversed with protamine sulfate
Physiology of Hemostasis

FACTS
Impaired hemostasis leads to bleeding

While stimulated hemostasis leads to thrombus formation

***Therefore, you need balance between the 2 systems***
Physiology of Hemostasis
FACTS (in stages)

STAGE #1
1. Vascular constriction:

initial phase; reflex response that
limits blood flow
Physiology of Hemostasis
FACTS (in stages)

STAGE #2
2. When vessels rupture, platelets are exposed to collagen located outside the blood vessel. Exposure to collagen, platelets release ADP (adenosine diphosphate) & thromboxane which cause the sufaces of nearby platelets to become sticky and as "sticky" platelets accumulate, a 'plug' forms
Physiology of Hemostasis
FACTS (in stages)

STAGE #3
3. Formation of a fibrin mesh

-ensures stability of platelet plug. Fibrin mesh is formed via the
coagulation cascade
Physiology of Hemostasis
FACTS (in stages)

STAGE #4
4. Dissolution of clot by action of plasmin following repair

-ensures normal blood flow resumes
A delicate balance between procoagulant, anticoagulant and fibrinolytic processes in the body
Normal Hemostasis
Spontaneous arrest of bleeding from a damaged blood vessel (involves blood clotting and subsequent dissolution of clot following repair)

**NOTE: thrombosis is the most common abnormal source of this
Hemostasis=Blood Coagulation
What is:

Thrombosis
Intravascular formation of a blood clot
Antithrombotics
Measures that cure or prevent
thrombosis
Pertaining to disintegration of a
blood clot
Thrombolytics
Fibrinolysis
dissolution of clot