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NURS 101 Chapter 26 Summary

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This is a comprehensive and detailed summary on;Chapter 26 - Coagulation Modifier Drugs. An Essential Study Resource just for YOU!!

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Chapter 26: Coagulation Modifier Drugs
Study online at quizlet.com/_4q823v


1. hemostasis •general term for any process that stops 9. hemophilia •rare genetic disorder
bleeding •natural coagulation and hemostasis
•coagulation is hemostasis that occurs factors are limited or absent
because of the physiologic clotting of •patients with hemophilia can bleed to
blood death if coagulation factors are not given
•complex relationship between substances
10. two types •factor VII deficiency
that promote clot formation and either
inhibit platelet •factor VIII and/or factor IX deficiency
inhibit coagulation or dissolve a formed
aggregation
clot
11. coagulation anticoagulants, antiplatelet drugs,
2. thrombus technical term for a blood clot
modifier drugs hemorheologic drugs, thrombolytic drugs,
3. embolus thrombus that moves through blood antifibrinolytic or hemostatic
vessels 12. anticoagulants •also known as antithrombotic drugs
4. thromboembolic •MI: embolus lodges in a coronary artery •inhibit the action or formation of clotting
events •stroke: embolus obstructs a brain vessel factors
•pulmonary emboli: embolus in the •prevent clot formation
pulmonary circulation •have no direct effect on a blood clot that
•deep vein thrombus (DVT): embolus goes is already formed
to a vein in the leg •prevent intravascular thrombosis by
•"cascade" decreasing blood coagulability
5. coagulation
•used prophylactically to prevent clot
system •each activated factor serves as a catalyst
formation (thrombus) and an embolus
that amplifies the next reaction
•result is fibrin, a clot-forming substance (dislodged clot)
•intrinsic pathway and extrinsic pathway 13. anticoagulants: •action: inhibit clotting factors IIa
heparins (thrombin) and Xa
6. intrinsic and
•unfractionated heparin: "heparin"
extrinsic
•low-molecular-weight heparins
pathway of
coagulation 14. unfractionated
heparin
(heparin)




7. fibrinolytic •initiates the breakdown of clots and serves
system to balance the clotting process
•fibrinolysis
•fibrin in the clot binds to a circulating •relatively large molecule that is derived
protein known as plasminogen; the binding from animal sources
•frequently laboratory monitoring for
converts plasminogen to plasmin
•plasmin is the enzymatic protein that bleeding times such as aPTT
eventually breaks down the fibrin thrombus •heparin for catheter flush (10-100
units/mL): no monitoring is needed
into fibrin degradation products; this keeps
the thrombus localized to prevent it from 15. low-molecular- •enoxaparin (Lovenox) and dalteparin
becoming an embolus weight heparins (Fragmin)
8. fibrinolysis mechanism by which formed thrombi are (LMWHs) •synthetic smaller molecular structure
•more predictable anticoagulant response
lysed to prevent excessive clot formation
and blood vessel blockage •frequent laboratory monitoring of
bleeding times using tests such as aPTT
not needed

16. coumarins •action: inhibit vitamin K-dependent
clotting factors II, VII, IX, and X
•warfarin (Coumadin)

, 17. warfarin 23. anticoagulants: •drug allergy
(Coumadin) contraindications •any acute bleeding process or high
risk for such an occurrence
•warfarin is strongly contraindicated in
pregnancy
•other anticoagulants are rated in lower
pregnancy categories (B or C)
•LMWHs are contraindicated in patients
with an indwelling epidural catheter risk
of epidural hematoma
24. anticoagulants: •bleeding: risk increases with increased
•inhibits vitamin K synthesis by bacteria in adverse effects dosages and may be localized or
the GI tract systemic
•inhibits production of vitamin K-dependent •may also cause: heparin-induced
clotting factors II, VII, IX, and X, which are thrombocytopenia, nausea, vomiting,
normally synthesized in the liver abdominal cramps, thrombocytopenia,
•final effect prevention of clot formation anemia, hematoma, dizziness, SOB,
18. Prothrombin fever, urticaria, rash, GI distress,
lethargy, muscle pain, and purples toes
Time (PT) and
INR 25. heparin-induced •gradual reduction in platelets
thrombocytopenia: •heparin therapy can generally be
type I continued
26. heparin-induced •acute fall in the number of platelets
thrombocytopenia: (more than 50% reduction from
type II baseline)
•discontinue heparin
27. heparin-induced •thrombosis that can be fatal
19. anticoagulants: •action: inhibit thrombin (factor IIa) thrombocytopenia: •treatment: thrombin inhibitors lepirudin
direct thrombin •human antithrombin III (Thrombate) clinical and argatroban
inhibitors •lepirudin (Refludan) manifestations •use of warfarin: can cause skin necrosis
•argatroban (Argatroban) and "purple toes" syndrome
•bivalirudin (Angiomax)
28. treatment: toxic •symptoms: hematuria, melena (blood
•dabigatran (Pradaxa)
effects of heparin in the stool), petechiae, ecchymoses,
20. anticoagulants: •action: inhibit factor and gum or mucous membrane
selective factor •fondaparinux (Arixtra) bleeding
Xa inhibitors •ivaroxaban (Xarelto) •stop drug immediately
•apixaban (Eliquis) •IV protamine sulfate: 1 mg of protamine
21. anticoagulants: •vary, depending on drug can reverse the effects of 100 units of
mechanism of •work on different points of the clotting heparin
action cascade
•prevent intravascular thrombosis by
decreasing blood coagulability
•do not lyse existing clots

22. anticoagulants: •used to prevent clot formation in certain
indications settings in which clot formation is likely
- MI
- unstable angina
- atrial fibrillation
- indwelling devices, such as mechanical
heart valves
- major orthopedic surgery
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