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60 Cards in this Set
- Front
- Back
*** PLEASE SEE SUPPLEMENTAL PACKET FOR PICTURES, DIAGRAMS AND STUDY QUESTIONS RELATED TO THIS LECTURE***
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Oral Anticoagulant (prototype)
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Warfarin
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Therapeutic Uses for Heparin
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DVT-deep vein thrombosis
PE-pulmonary emboli MI-myocardial infarction Prophylaxis Thrombosis |
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Contraindications for Heparin
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Hypersensitivity
Active bleeding Hemophiliacs Severe hypertension |
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Mechanism of action for Warfarin
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Inhibits the synthesis of vitamin K dependent factors (II, VII, IX, X, protein C and S)
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Pharmacokinetics of Warfarin
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Onset of action is delayed 5-7 days in order to synthesize new factors
Orally active |
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Warfarin
Drug Interactions |
Drugs which stimulate metabolism: reduce anticoagulation
-Chronic alcohol ingestion -Barbiturates -Griseofulvin |
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Platelet
(function) |
Provide initial hemostatic plug at site of vascular injury
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Dissolution of clots (#3)
--after plasmin is formed-- |
3. plasmin digests fibrin to soluble degradative products; phagocytic WBCs remove the debris
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Pharmacokinetics of Heparin
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Parenterally administered (IV or SB)
*onset is immediate IV administered in acute case phase of thromboembolic event given at hospital or with home health |
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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
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Warfarin Treatment
Monitor... |
1. PT-prothrombin time
2.INR-Internal Normalized Ratio-standard assessment developed by WHO; allows comparison of values from different labs |
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Side Effects of Warfarin
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Increased bruising and tendency towards hemorrhaging
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Therapeutic Uses of Warfarin
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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
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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 |
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Warfarin
Drugs which inhibit metabolism |
potentiate anticoagulation
-Cimetidine (TAGAMET) -Disulfiram -Metronindazole (FLAGYL) |
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Warfarin
Drugs which inhibit platelet aggregation |
potentiate anticoagulation
Asprin->b/c it is an anti-platelet drug |
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Antiplatelet Drugs
NSAIDs |
e.g. Aspirin
-Inhibit COX enzyme, thereby inhibiting synthesis of the thromboxane A2 in platelets |
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Antiplatelet Drugs
Dipyridamole |
Thought to impair adenosine metabolism
to interfere with platelet function; exact mechanism not well understood |
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Antiplatelet (antithrombotic drugs)
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Inhibit platelet function. Prevent thrombus formation in arteries
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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 |
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Thrombolytic Drugs
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All act directly or indirectly to convert plasminogen to plasmin, which in turn, cleaves fibrin to cause lysis of thrombi
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Thrombolytic Drugs
Examples |
Alteplasse (tissue-type plasminogen activator, tPA)
Streptokinase Anistreplase Urokinase |
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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 |
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Therapeutic Uses
for Altepasse |
Emergency treatment of MI
Deep vein thrombosis |
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Toxicity of Altepasse
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Bleeding (intracranial)
Allergic Reaction |
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Occupational Therapy Implications
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Be aware that anticoagulant therapy is associated with increased tendency for bleeding and bruising
May affect ADLs Thrombolytic drugs usually given in acute situations |
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Physiology of Hemostasis
SEE PICTURES OF PHYSIOLOGY ON pg. 2 |
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A clot that adheres to vessel wall
versus an intravascular clot that floats within the blood |
Thrombus
vs Embolus |
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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) |
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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
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***SEE PAGE 3 FOR DIAGRAM OF CLOTTING CASCADE***
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Plasminogen
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The inactive proenzyme that is plasmin once activated
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Dissolution of clots (#1)
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Plasminogen (inactive proenzyme) is activated and becomes plasmin by:
1. tissue plasminogen activator (tPA)-released from vascular endothelial cells following injury |
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Dissolution of clots (#2)
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2. urokinase (produced from epithelial cells as prourokinase to plasmin-to a lesser degree)
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Dissolution of clots (#4)
---after plasmin is formed--- |
4. Plasminogen and plasmin are rapidly inactivated by their respective inhibitors
Fibrin plasminogen-->plasmin | Soluble Products |
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Treating clots
THROMBOEMBOLISM |
Abnormal clot formation
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Treating clots
DEEP VEIN THROMBOSIS |
A.K.A. DVT
Abnormal clots in legs |
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Treating Clots
PULMONARY EMBOLUS |
A.K.A. PE
Abnormal clots in lungs |
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Treating Clots
Clots can block carotid arteries resulting in O2 deprevation in the CNS |
Stroke
-mental retardation and/or physical disability |
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Treating Clots
Clots can form secondary plaque in coronary arteries-compromised delieving of O2 to heart tissues |
Myocardial Infarction
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Anticoagulants
examples: Heparin Warfarin |
Treatment of overactive clotting
Control function and synthesis of clotting factors-used in venous system (venus thrombosis) |
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Thrombolytics
examples: Attepasse (tissue-type plasminogen activator, TPA) Anistrepiase Litokinase Streptokinase |
Facilitate destruction of blood clots
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Definition of Heparin
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An anticoagulant; a glycosaminoglycan found in secretory granules of mast cells (physiological function unknown)
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Mechanism of action of Heparin
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Binds, activates and potentiates the endogenous anticoagulant, Antithrombin III (AT III) to neutralize clotting factors: II, IX, X, XI, XII and kallikrein
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Sources for Heparin
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extracted from porcine intestinal mucosa or bovine lung
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Side effects of Heparin
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Hemorrhage
Thrombocytopenia (low blood platelet count) |
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Heparin Treatment
Monitor... |
1. blood components-total blood count
2. aPTT (Partial Thromboplastin Time)-Intrinsic Pathway 3. PT (Prothrombin Time)-Extrinsic Pathway |
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Heparin Toxicity
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can be reversed with protamine sulfate
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Physiology of Hemostasis
FACTS |
Impaired hemostasis leads to bleeding
While stimulated hemostasis leads to thrombus formation ***Therefore, you need balance between the 2 systems*** |
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Physiology of Hemostasis
FACTS (in stages) STAGE #1 |
1. Vascular constriction:
initial phase; reflex response that limits blood flow |
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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
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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 |
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Physiology of Hemostasis
FACTS (in stages) STAGE #4 |
4. Dissolution of clot by action of plasmin following repair
-ensures normal blood flow resumes |
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A delicate balance between procoagulant, anticoagulant and fibrinolytic processes in the body
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Normal Hemostasis
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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
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What is:
Thrombosis |
Intravascular formation of a blood clot
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Antithrombotics
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Measures that cure or prevent
thrombosis |
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Pertaining to disintegration of a
blood clot |
Thrombolytics
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Fibrinolysis
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dissolution of clot
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