Download Free Medical Drugs for Circulatory Disorders PowerPoint Presentation

Drugs for Circulatory Disorders PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Anticoagulant, which is titled "Drugs for Circulatory Disorders", to know about drugs used are to maintain, preserve or restore circulation including anticoagulants and antiplatelets (antithrombotics), thrombolytics, antilipemics, and peripheral vasodilatiors.

Tags : Anticoagulant, Drugs, Circulatory Disorders, circulation, anticoagulants, antiplatelets, antithrombotics, thrombolytics, antilipemics, peripheral vasodilatiors

Published on : May 25, 2021 | Views : 1494 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Drugs for Circulatory Disorders
Slide 2-

Circulatory Disorders Drugs used are to maintain, preserve or restore circulation Anticoagulants & antiplatelets (antithrombotics), thrombolytics, antilipemics, peripheral vasodilatiors Anticoagulants - prevent formation of clots that inhibit circulation Antiplatelets - prevent platelet aggregation Thrombolytics (clot busters) - attack/dissolve formed clots Antilipemics - decrease bld. lipid concentration Peripheral vasodilators - promote dilation of vessels narrowed by vasospasm
Slide 3-

Circulatory Disorders Thrombus Formation Clot is a Thrombus formed in an arterial or venous vessel thrombophlebitis - Both inflammation and clots are present Some thrombus can be superficial but it’s the DVT that’s a concern  embolism to lungs.
Slide 4-

Circulatory Disorders Thrombus Formation Arterial formation - begins w/ platelet adhesion to arterial vessel wall  Adenosine diphosphate (ADP) released from platelets  more platelet aggregation  Bld. flow inhibited  fibrin, platelets & RBC’s surround clot  build up of size structure  occludes bld vessels  tissue ischemia The result of Arterial Thrombus is localized tissue injury from lack of perfusion
Slide 5-

Circulatory Disorders Thrombus Formation Venous Formation - Usually from slow bld flow - Can occur rapidly Stagnation of the blood flow initiate the coagulation cascade production of fibrinenmeshes RBC’s & platelets to form the thrombus. Venous thrombus has a long tail that can break off to produce an embolus. These travel to faraway sites then lodge  in lung (capillary level)  inadequate O2 & CO2 exchange occur (ie. pulmonary embolism & cerebral embolism) Oral & parenteral anticoagulants (Heparin/Warfarin) primarily act by preventing venous thrombosis Antiplatelet drugs primarily act by preventing arterial thrombosis
Slide 6-

Circulatory Disorders Thrombus Formation Hemostasis is the normal homeostatic process of blood clotting. Clotting proteins normally circulate in an inactive state & must be activated to form a fibrin clot. When there is a trigger - inc. bld viscosity from bed rest & stasis - the clotting cascade is activated. Bld vessel injured  platelets adhering to site of injury  release of ADP a platelet plug - is ex. of Intrinsic clotting path. Tissue injury (outside bld vessels) = extrinsic pathway activated
Slide 7-

Circulatory Thrombus Formation Risk Factors for Deep Vein Thrombophlebitis and Thromboembolism Three factors increasing risk 1) Stasis of venous flow, 2) damage of the endothelium(inner lining of vein), and 3) hypercoagulability of the blood. Hx. of thrombophlebitis, abdominal & pelvic surgery, Obesity, neoplasms (lung), CHF, Advanced age, A-fib, vasospasm, Prolonged immobility (bed-rest, long trip spinal cord injury, FX. hip), CVA MI PG, post partum, Estrogen TX (oral contraceptives), IV therapy, trauma, Sepsis, Venous cannulation, Drug abuse, Cigarette smoking Excessive vit E intake Hypercoagulable states (Polycythemia, severe anemias, Dehydration or malnutrition), Antithrombin III deficiency
Slide 8-

Circulatory Disorders Anticoagulants Inhibit clot formation - Do NOT dissolve clots already formed, but prophylactically prevent new clots Used in clients w/ venous/arterial disorders that put them at inc. risk of clot formation Venous = DVT & Pulmonary embolism Arterial = Coronary thrombosis (MI), artificial heart valves, CVA
Slide 9-

Circulatory Disorders Heparin A natural substance in the liver that prevents clot formation. Primary use is to prevent venous thrombosis that can lead to pulmonary embolism (PE) or stroke Combines w/ antithrombin III  inactivates thrombin and other clotting factors then the conversion of fibrinogen to fibrin doesn’t occur so the clot is prevented Poorly absorbed through GI mucosa - given SQ & IV Prolongs clotting time - partial thromboplastin time (PTT) & activated partial thromboplastin time (aPTT) - both bld tests are monitored during therapy
Slide 10-

Circulatory Disorders Heparin Use - DVT, PE, & CVA, Rx of clients w/ heart valve prosthesis, during CV surgery, post op, during hemodialysis * Low doses = prophylactically to prevent DVT * Full doses = treats a thromboembolism & promotes neutralization of activated clotting factors = prevents extension of thrombi & formation of emboli * If started shortly after formation of a thrombus - heparin will also prevent it from developing into an insoluble stable thrombus = reduced tissue damage
Slide 11-

Circulatory Disorders Heparin SE - Decreased platelet count = thrombocytopenia Hemorrhage - give protamine sulfate IV (an anticoagulant antagonist) DI - Inc. effects w/ ASA, NSAIDs, thrombolytics Dec. effect w/ NTG
Slide 12-

Circulatory - LMWH Low Molecular Weight Heparins (LMWHs) - recently introduced to prevent venous thromboembolism Binds to Antithrombin III which inhibits the synthesis of factor Xa & formation of thrombin - enoxaparin (Lovenox) & dalteparin sodium (Fragmin) - more stable dose, lower risk of bleeding, freq. lab monitoring not required
Slide 13-

Circulatory Disorders LMWHs Use - Prevention of DVT after hip & knee replacement surgery & abd. surgery Can be administered at home Administered SQ BID Available in prefilled syringes w/ attached needles Usually given in the abdomen Average Rx is 7 to 14 days Bleeding less likely to occur DI - caution client not to take antiplatelet drugs (ASA) during therapy
Slide 14-

Circulatory Disorders Warfarin (Coumadin) Action - Inhibits activity of vit. K required for the activation of clotting factors II, VII, IX, & X. Blocking these factors prevents clot formation Use - prophylactically to prevent venous thrombosis, A. fib., PE, coronary occlusion, thrombophlebitis Prolongs clotting time & is monitored by the lab bld. tests prothrombin time (PT) & International normalized ratio (INR) - usually before administering the next dose until therapeutic levels are reached. INR is 1.3 - 2.0 therapeutic levels on coumadin = 2.0 - 3.0
Slide 15-

CIRCULATORY DISORDERS Warfarin (Coumadin) INR is replacing the PT  INR more accurate. Need higher levels for prosthetic heart valves, cardiac valvular disease and recurrent emboli. PT not consistent lab to lab or reagents used. PT is 1.5 – 2 times the reference value to be therapeutic Regular monitoring is required for the duration of drug therapy Warfarin is well absorbed through the G.I. tract. Food decreases.
Slide 16-

Circulatory Disorders Warfarin (Coumadin) Has a long t1/2 & duration of action - drug accumulation poss. and can cause internal bldg. - Observe for: petechiae, ecchymosis, tarry stools, hematemesis. Monitor menstrual flow - Teach client importance of bld tests & to look out for signs of bleeding DI - LOTS!!! consult a physician before taking any over the counter medications Vit. K (phytonadione) = antagonist of Warfarin. Used for OD/ uncontrolled bleeding
Slide 17-

Intrinsic Clotting Pathway Blood or collagen contact XII XIIa (H) XI XIa (H) (W) IX IXa (H) CA++ PF 3 VIII (W) Extrinsic Clotting Pathway Tissue trauma Tissue factor (W) VII  VIIa Common Pathway (W) X Xa (H) (Next slide) The Clotting Cascade
Slide 18-

Common Pathway Xa (H) Ca++ PF 3 V (W) (W) Prothrombin Thrombin Ca++ Fibrinogen Fibrin (soluble) CA++ XIIIa XIII Fibrin (insoluble) (H) (H) (F)
Slide 19-

Circulatory Disorders Antiplatelet Drugs Aspirin, Dipyridamole (Persantine), Ticlopidine (Ticlid) abciximab (ReoPro), tirofiban (Aggrastat) Action: To prevent thrombosis in the arteries by suppressing platelet aggregation via diff. methods Use: Prevention of MI/stroke for clients w/ family hx - prevention of a repeat MI, stroke in clients having TIA’s Persantine & Ticlid = similar to ASA but more expensive ReoPro & Aggrastat = mainly for acute coronary syndromes. Route = IV
Slide 20-

Circulatory Disorders Thormbolytics Thromboembolism - Occlusion of an artery or vein caused by a thrombus or embolus - results in ischemia that causes necrosis of the tissue distal to the obstructed area. - it takes about 1 to 2 weeks for the blood clot to disintegrate by natural fibrinolytic mechanisms - if new thrombus dissolved quicker damage minimized & bld flow restored faster  purpose of therapy Thrombolytics promote fibrinolytic mechanism (convert plasminogen to plasmin & destroys the fibrin in the clot) - administering a thrombolytic drug = clot disintegrates
Slide 21-

Circulatory Disorders Thrombolytics Use = Acute MI - w/ in 4 hrs to dissolve clot & unblock artery, so decrease necrosis to myocardium & hospital stay is decreased. Other uses: Pulmonary embolism, DVT, Noncoronary arterial occlusion Streptokinase, Urokinase, Tissue plasminogen activator (t-PA), anisoylated plasminogen streptokinase activator complex (APSAC) Streptokinase & Urokinase are enzymes that act to convert plasminogen to plasmin t-PA and APSAC activate plasminogen by acting specifically on clot.
Slide 22-

Circulatory - Thrombolytics All 5 drugs induce fibrinolysis (fibrin breakdown) Side effects: hemorrhage, allergic reactions (anaphylaxis) & vascular collapse-more with Streptokinase Onset and peak are immediate and rapid, duration can be 12h. t-PA most expensive - $2500/tx, short t1/2 (5-7 min.) not associated with anaphylaxis. Aminocaproic acid (Amicar) an antithrombolytic used to stop bleeding by inhibiting plasminogen activation. Used to stop bleeding from heart surgery, trauma & abruptio placenta.
Slide 23-

Circulatory Disorders Antilipemics Used to Lower bld. lipid levels Cholesterol, triglycerides & phospholipids transported in the body bound to protein in various amounts - chylomicrons, very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), high-density lipoproteins (HDL) - more protein & less lipid (removes chol. from bld. stream & deliver it to the liver) VLDL & LDL contribute to atheroslerotic plaque in bld vessels - composed of mainly cholesterol & triglycerides
Slide 24-

Circulatory Disorders Antilipemics Nonpharmacologic = before drugs to dec. BP - Reduce saturated fats & chol intake in the diet - Exercise - Body wt. reduction - Eliminate smoking If drug therapy needs to be initiated, clients still need to make lifestyle changes Compliance an issue
Slide 25-

Circulatory Disorders Antilipemics Cholestyramine (Questran) - Powder form, Colestipol (Colestid) - a newer resin - both lower chol. Clofibrate (Atromid-S), gemfibrozil (Lopid) - fibric acid derivatives effective in reducing triglyceride & VLDL levels. - Highly protein bound. do not take w/ anticoagulants - compete - Clofibrate - many side effects - dysrhythmias, angina Nicotinic acid or niacin (vit B2) - reduces VLDL & LDL - effective in dec. chol levels, Many SE’s
Slide 26-

Circulatory Disorders Antilipemics Statin drugs inhibit enzyme HMG CoA reductase in chol biosynthesis ( HMG CoA reductase inhibitors) = Dec. the concentration of chol & dec. LDL & sl. inc. in HDL atorvastatin calcium (Lipitor), cerivastatin (Baycol), fluvastatin (Lescol), lovastatin (Mevacor) - - SE = GI disturbances, headaches, muscle cramps & tiredness (all complaints early in tx.) - monitor serum liver enzymes - Annual Eye exams d/t poss cataract formation - Useful in coronary artery disease (CAD) & mortality rate
Slide 27-

Circulatory - Antilipemics If therapy withdrawn, cholesterol levels return to pretreatment levels  lifetime commitment Lovastatin is absorbed with food. High 1st hepatic pass -50% Onset and peak occurs in hours , but takes several days to have a therapeutic effect. Duration is up to 3 weeks. NI Monitor blood lipid levels, liver functions, if GI upset occurs have client take with sufficient water or with meals. Desired Lab Values = CHOL <200; triglyceride <150; LDL < 130; HDL > 60
Slide 28-

Circulatory Disorders Peripheral Vasodilators Peripheral Vasodilators - Increase bld flow to extremities Peripheral vascular disease is a problem in the elderly - Numbness & coolness of extremities, intermittent claudication (pain/weakness of limb when walking - symptoms absent at rest), poss. leg ulcers - Primary cause is hyperlipemia from atherosclerosis & arteriosclerosis - arteries become occluded
Slide 29-

Circulatory Disorders Peripheral Vasodilators Peripheral vasodilators more effective for disorders resulting from vasospasm (Raynaud’s disease) than from vessel occlusion or arteriosclerosis Vasodilators have diff. actions but all promote vasodilation Isoxsuprine (Vasodilan) - Beta-2 adrenergic agonist - causes vasodilation on arteries w/in skeletal muscles, bronchodilation may also occur - SE = lightheadedness, dizziness, orthostatic hypotension, tachycardia, GI distress
Slide 30-

Circulatory Disorders Peripheral Vasodilators Pentoxifylline (Trental) - an antihemorrheologic agent - improves microcirculation & tissue perfusion inc. in tissue O2. Not a vasodilator, but dilates rigid arteriosclerotic bld vessels - arterioles, capillaries & venules - Use = clients w/ intermittent claudication - Take w/ food - Avoid smoking d/t nicotine increases vasoconstriction
Slide 31-

MATH The order for medication is 12 mg. The medication you have is labeled 5 mg per ml. How much do you give? 12mg X 1 ml. 5 mg = 2.4 ml You have a vial labeled 40 mg/mL. You need to give 0.1 g. How much should you give. Convert 0.1g to mg. = 100mg 100 mg X 1 mL = 40 mg 2.5 mL
Slide 32-

MATH You have an order to give 250 mcg. A dosage of 0.2 mg. per 2 ml. is what’s available. Convert 0.2 mg. to mcg. = 200 mcg. 250 mcg X 2 ml. = 200 mcg 5 X 2 ml. = 4 10 4 = 2.5 ml.