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Developed by: Dawn Johnson, RN, MSN, Ed.  Internally and externally  Prevent bleeding from wounds which could lead to shock or even death.

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Presentation on theme: "Developed by: Dawn Johnson, RN, MSN, Ed.  Internally and externally  Prevent bleeding from wounds which could lead to shock or even death."— Presentation transcript:

1 Developed by: Dawn Johnson, RN, MSN, Ed

2  Internally and externally  Prevent bleeding from wounds which could lead to shock or even death

3  Injured vessel constricts to slow blood flow  Platelets adhere to injured area and aggregate, plugging damaged vessel  Coagulation cascade occurs thus forming insoluble fibrin strands which slows blood flow more

4  Injured cells release prothrombin activator  Prothrombin activator changes prothrombin to thrombin  Thrombin changes fibrinogen to fibrin  Fibrin forms an insoluble web over injured area which stops blood flow

5  Anticoagulants  Thrombolytics  Hemostatics

6  Inhibiting specific clotting factors in the coagulation cascade  Diminishing the clotting action of platelets  Both ways increase the time to form clots

7  Dissolve life-threatening clots

8  Promote formation of clots  Inhibit removal of fibrin

9  Examples - heparin (Heplock), warfarin (Coumadin)  Mechanism of action - inhibit specific clotting factors which interfere with coagulation cascade in order to prevent formation or enlargement of clot  Primary use - thromboembolic disease; prevent formation of clots in veins  Adverse effects - abnormal bleeding

10  Example - ticlopidine (Ticlid)  Mechanism of actions  Aspirin: inhibits thromboxane2, which prevents aggregation of platelets  ADP receptor blockers: interfere with platelet plasma membrane, which prevents platelet aggregation  Glycoprotein IIb/IIIa inhibitors: glycoprotein IIb/IIIa enzyme inhibited which prevents platelet aggregation

11  Primary uses - prevent clot formation in arteries  Adverse effects - abnormal bleeding; reduce number of neutrophils

12  Example - alteplase (Activase)  Mechanism of action - convert plasminogen to plasmin which causes fibrin to degrade, then preexisting clot dissolves  Primary uses - acute MI, pulmonary embolism, acute ischemic CVA, DVT, arterial thrombosis, coronary thrombosis, clear thrombi in arteriovenous cannulas and blocked IV catheters  Adverse effects - abnormal bleeding; contraindicated in patients with active bleeding or recent trauma

13  Example - aminocaproic (Amicar)  Mechanism of action - prevent fibrin from dissolving, which enhances stability of the clot  Primary use - prevent and treat excessive bleeding from surgical sites  Adverse effects - none listed

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15  Provide essential building blocks for RBC production.  They do so by increasing hemoglobin which is necessary for oxygen transportation

16  Iron  Vitamin B12  Folic Acid

17  Used to treat the most common form of anemia-iron defieciency.  One function of iron-production of hemoglobin.  Treatment is usually 6 months  Parenteral iron therapy is used for patients who can’t absorb oral preparations, aren’t compliant with oral treatment, or have bowel d/o

18  Iron is reduced by antacids as well as foods such as coffee, tea, eggs, and milk.  Other drug interactions are: Tetracycline or any of the cycline drugs, methlydopa, ciprofloxacin, oloxacin, chloramphenicol, and pencillamine may be reduced.  Cimetidine and other histamine2-receptor antagonists may decrease GI absorption of iron.

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