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Drugs for Coagulation Disorders

presentacion de farmacologia

Eimi Balleste

on 17 January 2013

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Transcript of Drugs for Coagulation Disorders

Drugs for Coagulation Disorders Talia Maldonado
William Rivera
Eimi Balleste Hemostasis Stopping of blood flow, is an essential mechanism that protects the body form both external and internal injury. Diseases and conditions that affect hemostasis
MI, CVA, venous or arterial thrombosis, valvular heart disease and indwelling catheters Coagulation Cascade Clotting factors are activated in sequence intrinsic pathway - in response to injury extrinsic pathway - when blood leaks out of a vessel and enters tissue spaces Both pathways result in prothrombinase converting prothrombin into the enzyme thrombin thrombin then converts fibrinogen (plasma protein) into fribrin strands fibrin strands form an insoluble web over the injured area to stop blood loss *normal blood clotting occurs in aprox. 6 minutes Fibrinolysis process of clot removal initiated 24 to 48 hours after clot formation and continues until it is dissolved At formation of fibrin clot nearby cells secrete the enzyme tissue plasminogen activator (TPA) converts the inactive protein plasminogen to active enzymatic form of plasmin plasmin digests the fibrin strands and removes the clot in normal function the body regulates fibrinolysis, removing only unwanted fibrin clots and allowing those present in wounds to remain in order to maintain hemostasis Diagnosing a bleeding disorder prothrombin time thrombin time activated partial thromboplastin time bleeding time platelet count Disorders Thromboembolic disorders (formation of undesirable clots) thrombus (stationary clot) arterial, may deprive an area of of adequate blood flow = tissue ischemia may result in infarction or tissue death as in the case of MI or CVA embolus (travelling clot) pieces of thrombus breaks off and travels through the bloodstream from the right atrium will cause a pulmonary emboli from the left atrium will cause a CVA or arterial infarction elsewhere Patient Susceptibility Deep Vein Thrombosis due to sluggish blood flow in the venous system usually in the veins of the legs Following surgical procedures Arterial punctures such as an angiography Patients with indwelling catheters and mechanical heart valves Bleeding disorders (abnormal clot formation) Thrombocytopenia non-hereditary platelet deficiency which results from any condition that suppresses bone marrow function can also be caused by immunosuppressant drugs and most of the medications used for cancer Hemophilia (genetic deficiencies in certain clotting factors) A - lack of clotting factor VIII (80%) B - deficiency of factor IX (20%) von Willebrand's Disease - most common inherited bleeding disease Coagulation Modification Anticoagulants Thrombolytics Hemostatics -inhibition of specific clotting factors -clot is dissolved by the drug -inhibition of fibrin destruction impart a negative charge to the surface of the platelet and inhibits the aggregation of the cells lengthen clotting time, preventing thrombi from forming and growing larger anticoagulant is given orally, intravenously or subcutaneously used primarily to prevent thrombosis in veins Parenteral Heparin - enhances the actions of Antithrombin III
- antagonist: Protamine sulfate
- S/E: abnormal bleeding
- contrindicated in bleeding disorders, high BP, recent trauma Low-molecular-weight heparins (LMWHs) - inhibits active factor X
- effects lasts two to four times longer than Heparin
- response is more stable
- less likely to cause thrombocytopenia Thrombin Inhibitors - bind to active sites of thrombin
- infused until a therapeutic aPTT value is obtained
- limited therapeutic uses bivalirudin (Angiomax) in combination with aspirin for patients undergoing angioplasty
argatroban (Acova, Novastan) and lepirudin are indicated for the prevention of thrombocytopenia induced by heparin therapy
desirudin (Iprivask) is given 15 minutes before hip replacement surgery for prophylaxis of DVT Antithrombin (ATryn) recombinant human antithrombin approved in 2009 to treat patients with congenital deficiencies of antithrombin III
obtained from genetically-engineered goats
prevention of peri-operative and peri-partum thromboembolic events Oral warfarin (Coumadin) inhibits the hepatic synthesis of coagulation factors II, VII, IX, and X
often used after condition has stabilized with heparin administered concurrently for 2 to 3 days since the optimal effect of warfarin takes several days to achieve Antagonist: Vitamin K Pregnancy category X
S/E: abnormal bleeding pentoxifylline (Trental) reduces the viscosity of red blood cells and increases their flexibility Prevention of clot formation Antiplatelets -inhibition of platelet actions Removal of existing clot Promotion of clot formation effects of a single dose may last up to a week ADP receptor blockers - alter the plasma membrane of platelets Interfere with platelet aggregation
Primarily used to prevent clot formation in arteries to prevent thrombi formation in patients with recent thromboembolic events such as a stroke or MI ticlopidine (Ticlid) - may cause neutropenia and agranulocytosis
clopidogrel (Plavix) - adverse effects similar to aspirin
prasugrel (Effient) - indicated for patients with acute coronary syndromes who undergo PCI Aspirin - inhibits the formation of thromboxane A2 Glycoprotein IIb/IIIa receptor antagonist Glycoprotein IIb/IIIa is an enzyme necessary for platelet aggregation
used to prevent thrombi in patients that experienced a recent stroke, MI or percutaneuos transluminal coronary angioplasty (PTCA)
considered most effective antiplatelet agents expensive
only given by IV route Agents for intermittent claudication IC is caused by lack of sufficient blood flow to skeletal muscles in lower limbs ischemia of skeletal muscles causes severe pain on walking pentoxifylline (Trental) - reduce viscosity and increase flexibility of RBCs
cilostazol (Pletal) - inhibit platelet aggregation and promotes vasodilation promote fibrinolysis (clot destruction) by converting plasminogen to plasmin
administered for disorders in which an intravascular clot has already formed acute MI, pulmonary embolism, acute ischemic CVA and DVT narrow margin of safety between dissolving "normal" and "abnormal" clots
rapidly destroyed in bloodstream streptokinase - first thrombolytic discovered
tenecteplase (TNKase) rapid onset
longer duration
fewer side effects TPA (Activase) - drug of choice in clearing thrombosed central intravenous lines before urokinase (obtained from pooled human donors) was used, but was later removed from the market due to risk of virus contamination also known as antifibrinolytics shorten bleeding time
used after surgical procedures oral form of tranexamic acid (Lysteda) approved in 2009 for heavy menstrual bleeding none are commonly prescribed and have very specific indications for use aminocaproic acid (Amicar) adverse effects: allergic skin reactions, headache aprotinin (Trasylol) adverse effects: anaphylaxis, thrombosis, bronchospasm, nephrotoxicity Hemostasis Basic Steps of Hemostasis * may cause HIT (Heparin-induced thrombocytopenia) Applying information... In Clinical Settings Nursing Diagnostics for Patients Receiving Anticoagulant Therapy Potential Nursing Diagnostic - Ineffective Peripheral Tissue Perfusion 00204 (related to decreased circulation in affected area) Interventions - Thrombolytic Therapy Management 4270
- Bleeding Precautions 4010
- Circulatory Precautions 4070 Nursing Diagnostics for Patients Receiving Antiplatelets Therapy Potential Nursing Diagnostic - Impaired Skin Integrity 00046 (in lower extremities related to ineffective tissue perfusion) Interventions - Lower Extremety Monitoring 3480
- Skin Surveillance 3590 NCLEX Review Questions The nurse's understanding of the clotting mechanismis important in administering anticoagulant drugs. The nurse understands that which of the following clotting factors are formed after injury to the vessels? 1. Fibrin, vitamin K
2. Thromboplastin, fibrinogen
3. Prothrombin, thrombin
4. Thrombin, fibrin Nursing interventions for a patient receiving enoxaparin (Lovenox) may include: (select all that apply.) 1. teaching the patient or family to give subcutaneous injections at home.
2. teaching the patient or family not to take any OTC drugs without first consulting with the health care provider.
3. teaching the patient to observe for unexplained bleeding such as pink, red, or dark brown urine or bloody gums.
4. teaching the patient to monitor for the development of DVT.
5. teaching the importance of drinking grapefruit juice daily. A patient is receiving a thrombolytic agent, an alteplase (Activase), following an acute myocardial infarction. Which condition is most likely attributed to thrombolytic therapy with this agent? 1. Skin rash with urticaria
2. Wheezing with labored respirations
3. Bruising and epistaxis
4. Temperature elevation of 100.8 F Answer : 4

Rationale : Prothrombinase converts prothrombin to thrombin. Thrombin then converts fibrinogen to long strands of fibrin, which provide a framework for the clot. Thrombin and fibrin are formed only after the injury occurs. Fibrin strands form an insoluble web over the injured area to stop blood loss. Answer: 1, 2, 3, 4

Rationale: Enoxaparin is a low-molecular-weight heparin (LMWH). This class of drugs has fewer side effects, including being less likely to cause thrombocytopenia. Patients and family can be taught to give subcutaneous injections at home. Teaching should include not taking any other medications without first consulting the health care provider and recognizing the signs and symptoms of bleeding. Enoxaparin is given to prevent development of DVT. Patients should be taught signs and symptoms of DVT to observe for and should contact their health care provider immediately if these develop. Answer: 3

Rationale: Thrombolytic agents dissolve existing clots rapidly and continue to have effects for 2 to 4 days. All forms of bleeding must be monitored and reported immediately. Skin rash with urticaria, wheezing with labored respirations, and temperature elevation 100.8 F are not symptoms of adverse effects directly attributed to thrombolytic therapy. 1. Adams, M., Holland, L. N., & Bostwick, P. M. (2008). Pharmacology for nurses: a pathophysiologic approach (2nd ed.). Upper Saddle River, N.J.: Pearson / Prentice Hall.
2. Herdman, T. H. (2008). NANDA-I nursing diagnoses: definitions & classification, 2009-2011 (New ed.). Oxford: Wiley-Blackwell.
3. Bulechek, G. M., Butcher, H. K., & Dochterman, J. M. (2008). Nursing Interventions Classification (NIC) (5th ed.). St. Louis, Mo.: Mosby/Elsevier.
4. Hemostasis Mechanism -stopping bleeding - YouTube. (n.d.). YouTube. Retrieved December 8, 2012, from http://www.youtube.com/watch?v=_HgTRoesu8M. Hemostasis Mechanism Coagulation Cascade (YouTube, 2012) (London Health Sciences Centre, 2012) (.docstoc.com, 2012) (Pharmacology Corner, 2012) (tube.medchrome.com, 2010) (Craven & Hirnle, 2008) References
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