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AdvantageousCarnelian858

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Texas Woman's University

Farah Villanueva

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coagulation blood clotting medical presentation healthcare

Summary

This document is a presentation on coagulation modifiers, covering topics such as hemostasis, coagulation lab values, and different types of coagulation modifiers and their uses. It is likely part of a lecture or educational material for a student in a healthcare program.

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COAGULATION MODIFIERS FARAH VILLANUEVA, MSN, APRN, FNP-C TEXAS WOMAN'S UNIVERSITY NURS 3813 HEMOSTASIS • Goal: maintain integrity of the vascular compartment • Prevent blood loss • Primary hemostasis • Activation of platelets = platelet plug formation • Secondary hemostasis • Coagulation cascade =...

COAGULATION MODIFIERS FARAH VILLANUEVA, MSN, APRN, FNP-C TEXAS WOMAN'S UNIVERSITY NURS 3813 HEMOSTASIS • Goal: maintain integrity of the vascular compartment • Prevent blood loss • Primary hemostasis • Activation of platelets = platelet plug formation • Secondary hemostasis • Coagulation cascade = fibrin clot • Clot lysis • Activation of plasmin = fibrinolysis HEMOSTASIS CONTINUED • Endothelial cells • Vasocontricts to minimize blood loss and releases clotting factors • Can also prevent thrombosis by producing anticoagulant factors • Platelets • Activate and aggregate at site of injury • Lifespan is 7-10 days and removed by spleen • Coagulation cascade • Clotting factors are normally present in blood and tissues as inactive percussors • Activation • Intrinsic pathway • Occurs in the vascular system • Extrinsic pathway • Occurs in the tissues COAGULATION LAB VALUES PRIMARY HEMOSTASIS Platelet count 130,000 – 400,000 uL SECONDARY HEMOSTASIS Prothrombin time (PT) (tissue = extrinsic) 10 – 13 sec Activated partial thrombin time (aPTT) (contact = intrinsic) 28 – 38 sec Fibrinogen (clot) 175 - 400 mg/dL D-dimer (fibrin breakdown ) <500 mg/ml ETIOLOGY & PATHOPHYSIOLOGY ARTERIAL THROMBUS VENOUS THROMBUS Caused by damage to arterial endothelium which activate platelets • Atherosclerotic plaque • HTN • Turbulent blood flow Associated with slow blood flow which allows thrombin/other procoagulants to concentrate and initiate coagulation cascade • Inactivity/prolonged bed rest • Atrial fibrillation Clinical Manifestations Clinical Manifestations Obstructs blood flow • Ischemia = decreases blood flow • Infarction = tissue death Local congestion • Edema, inflammation Embolism • Easily detaches • S&S depend on location it obstructs GENERAL CONSIDERATIONS TO PREVENT BLOOD CLOTS ARTERIAL THROMBUS VENOUS THROMBUS To help prevent blood clots in the arteries, reduce risk factors that contribute to cardiovascular disease To help prevent blood clots in the veins, avoid or minimize situations that slow blood circulation Interventions: • Low-fat, low-cholesterol diet: • Total cholesterol < 200 mg/dL • LDL < 130 mg/dL • Weight reduction • Control BP • Avoid smoking • Reduce stress • Regular exercise Interventions: • Avoid tight clothing • Avoid crossing your legs at the knees • Minimize prolonged sitting or standing • Bed rest • Perform ROM exercises • Wear compression stockings or SCDs • Road trips/ traveling on a plane • Exercise your feet and legs • Walk around when you can COAGULATION MODIFIERS 4. ANTIFIBRINOLYTICS VESSEL INJURY PLATELET PLUG COAGULATIO N CASCADE 1. ANTIPLATELETS 2. ANTICOAGULANTS BLOOD CLOT 3. THROMBOLYTICS VESSEL INJURY PLATELET PLUG COAGULATION CASCADE BLOOD CLOT ANTIPLATELETS 1. NSAID (ASA) 2. Adenosine diphosphate (ADP) receptor antagonist Other antiplatelet drugs • Glycoprotein IIb/IIIa receptor antagonists • Phosphodiesterase-3 enzyme inhibitor NSAID (ASA) • Prototype: aspirin • Action • Inhibits the synthesis of prostaglandins that cause platelet aggregation • Inhibition lasts for the lifespan of the platelet (7-10 days) • Use • Long term prevention of MI and CVA • Prosthetic valves • Immediate treatment with suspected or actual acute MI, TIA, CVA (~85% thrombotic) NSAID (ASA) • SE • Uncommon with small dose • Increased risk for bleeding, stomach ulcers, tinnitus • No antidote • If severe bleeding, transfusion may be required • Contraindications • Ulcers • Active bleeding • Pregnancy • Children under 16 years of age (Reye's syndrome) ADENOSINE DIPHOSPHATE (ADP) RECEPTOR ANTAGONIST • Prototype: clopidogrel (Plavix) • prasugrel (Effient) • ticagrelor (Brilinta) • Action • Irreversibly blocks the ADP receptor on the platelet • Prevents platelet aggregation • Inhibition lasts for the lifespan of the platelet (7-10 days) • Use • Prophylaxis • Reduction of MI, stroke, vascular death with atherosclerosis • Post coronary stent placement • A fib (unable to take vitamin K antagonist) ADP RECEPTOR ANTAGONIST • SE • Increase risk of bleeding • Pruritus, rash, purpura, and diarrhea • BLACK BOX WARNING • Genetic variations of CYP2C19 function • "Poor metabolizers" (~2-14%) remain at risk for MI, CVA, and death • Genomic testing not routinely recommended • Nursing implications • Dual antiplatelet therapy (ADP + ASA) shown to be beneficial post PCI • Recommended for at least 12 months • 18 months if tolerated PATIENT EDUCATION FOR ANTIPLATELETS • Regular medical supervision and periodic blood tests required • Hemoglobin • <7 • Platelets • < 150,000 • < 50,000 • Inform health care providers (including dentists) before any invasive diagnostic testing or treatments • Medication should be withheld 5-7 days prior • Take ASA with food or after meals along with 8 oz of water to decrease stomach irritation • Don't crush or chew coated tablets Hgb < 7 Plt < 150,000 Plt < 50,000 PATIENT SCENARIO Aaron Phib is a 58-year-old male who was admitted for chest pain. An angiogram was performed and it revealed 85% occlusion of the right coronary artery. A PCI was performed with stent (x1) placement. Complete the Initial Visit section on the Google Form and do not click Next. Wait till after our discussion to click Next. VESSEL INJURY PLATELET PLUG COAGULATION CASCADE BLOOD CLOT ANTICOAGULANTS 1. Heparins 2. Vitamin K antagonists 3. Direct-acting oral anticoagulants • Direct thrombin inhibitors • Factor Xa inhibitors HEPARINS • Prototype: heparin • Action • Combines with antithrombin III to inactivate clotting factors (IX, X, XI, and XII) • Inhibit the conversion of prothrombin to thrombin • Prevent thrombus formation • Inhibit additional coagulation • Pharmacokinetics • GI tract does not absorb the drug • IV or SubQ • IV: acts immediately • SubQ: within 20-30 minutes HEPARINS • Use • Short-term • Prophylactically • Prevent DVT/PE • Post-op/ bed rest > 5 days • Therapeutically • Major illness (acute MI) • Acute thromboembolic disorders • DVT, thrombophlebitis, PE • Disseminated intravascular coagulation (DIC) • Life-threatening condition • Widespread clotting = depletes blood of coagulation factors = widespread bleeding • Goal: prevent blood coagulation long enough for clotting factors to be replenished HEPARINS • Side/Adverse effects • Hemorrhage • Local irritation • Erythema and mild pain • Heparin-induced thrombocytopenia (HIT) • Potentially life-threatening complication • Immune mediated reaction (~1-3% ) • Decreases platelet count • Management: discontinue heparin and manage anticoagulation with DTI (ex. argatroban) • Contraindications • Active bleeding (GI ulcerations, intracranial bleeding) • Recent surgery of the eye, spinal cord, or brain • Severe hypertension • Dissecting aortic aneurysm • Severe kidney or liver disease HEPARINS • Nursing implications • 2 major limitations 1. Narrow therapeutic window 2. Highly variable individual-dose response • Monitor labs • Therapeutic PTT: 45-70 seconds • Lab draws • Continuous infusion: anytime • Intermittent administration: 1 hour before scheduled dose • Not necessary with low dose or LMWHs • Double check dosage with another nurse • High aPTT or active bleeding • Stop heparin • Antidote: protamine sulfate PTT: 45-70 sec LOW-MOLECULAR-WEIGHT HEPARIN (LMWH) • Prototype: enoxaparin (Lovenox) • Suffix: -parin • Action • Synthetic heparins with smaller molecular structures • Specific to active factor X • Advantages • More predictable response • No need to monitor blood coagulation • Simplifies outpatient therapy and safety • Pharmacokinetics • SubQ = slightly delayed onset of action • Longer duration of action = difficult to rapidly stop therapy • Nursing implications • Educate patients on how to administer medication • Antidote: protamine sulfate VITAMIN K ANTAGONIST • Prototype: warfarin (Coumadin) • Action • Acts in the liver to prevent synthesis of vitamin K-dependent clotting factors (factors II, VII, IX, and X) • Competitive antagonist to hepatic use of vitamin K • Pharmacokinetics • Anticoagulant effects do not occur for 3-5 days • May be given with heparin • Transition from IV heparin to oral warfarin • Given together for 2-3 days • Use • Long-term prevention or management of venous thromboembolic disorders • DVT, PE, A fib, prosthetic valves VITAMIN K ANTAGONIST • Nursing implications • Monitor labs • Narrow therapeutic window • Highly variable dose-response • Daily evaluation of INR until a stable dose is reached • PT: 18 seconds • INR: 2-3 • INR checked every 2-4 weeks for the duration of anticoagulant drug therapy • Medication administration • Institutions will have protocols for therapeutic ranges • Hold dose if INR is > 3 and notify health care provider VITAMIN K ANTAGONIST • Nursing implications continued • Preventing interactions • Medications • ASA, NSAIDs, certain antibiotics, several antidepressants • Foods high in vitamin K • Consistent intake or in moderation • Do not change intake of foods that are high in vitamin K • Antidote • phytonadione (vitamin K) • Administered if INR level > 5 and signs of bleeding are present • Works slowly ~6 hours • Prothrombin complex concentrate [PCC human] (Kcentra) • Urgent reversal for major or life-threatening hemorrhage DIRECT-ACTING ORAL ANTICOAGULANTS (DOACs) • Non-vitamin K oral anticoagulants • New/Novel oral anticoagulants (NOACs) • Examples • Direct thrombin inhibitors (DTIs) • Factor Xa inhibitors • Advantages • Less variability in drug effect • No lab monitoring • May become first choice for oral anticoagulants DIRECT-ACTING ORAL ANTICOAGULANTS (DOACs) • Direct thrombin inhibitors (DTIs) • Prototype: dabigatran etexilate (Pradaxa) • Action • Directly and reversibly inhibits thrombin • Key enzyme in the coagulation cascade • Indirectly inhibits thrombin induced platelet aggregation • Use • Treatment and prevention of DVT and PE • Stroke prevention in nonvalvular atrial fibrillation • Antidote: idarucizumab (Praxbind) DIRECT-ACTING ORAL ANTICOAGULANTS (DOACs) • Factor Xa inhibitors • Prototype: rivaroxaban (Xarelto) • apixaban (Eliquis) • Suffix: -xaban • Action • Inhibiting factor Xa in both pathways • Indirectly inhibits thrombin induced platelet aggregation • Use • Treatment or prevention of venous thromboembolism • Stroke prevention in nonvalvular atrial fibrillation • Following knee or hip surgery • Antidote: andexanet (Andexxa) PATIENT EDUCATION FOR ALL BLOOD THINNERS • All increases the risk for bleeding • Implement safety precautions to prevent injury • Avoid walking barefoot • Avoid contact sports • Use an electric razor • Avoid injections if possible • Carry an identification card/necklace/bracelet • Report any signs of bleeding • Excessive bleeding, bruising, blood in urine/stool • Superficial bleeding • Apply direct pressure for 3-5 minutes or longer if necessary • Take medication as directed • Too little: increases risk for blood clot formation • Too much: can cause bleeding • Avoid taking other drugs or supplements without consulting provider PATIENT SCENARIO It's been several months since Mr. Phib was discharged after his PCI. Today he presents to the ER with pain and swelling in his left leg. He states that he just returned home from flying an international flight. Complete the ER Visit and Re-hospitalization sections on the Google Form and do not click Next. Wait till after our discussion to click Next. VESSEL INJURY PLATELET PLUG COAGULATION CASCADE BLOOD CLOT THROMBOLYTICS THROMBOLYTICS • Prototype: alteplase (rtPA) • Action • Breaks unwanted blood clot • Changes plasminogen to plasmin to dissolve fibrin clot • Use • Reestablish blood flow to prevent or limit tissue damage • MI • PE • CVA THROMBOLYTICS • Adverse effects • Bleeding • Minimize risk • Select recipients carefully • Use caution > 65-80-year old • Taking anticoagulants • HTN (if >180, treat first) • Avoid invasive procedures when possible • Brain hemorrhage (6-8% risk; 3% mortality rate) • Contraindications • Aneurysms • Known coagulopathy or internal bleeding • Intraspinal surgery or trauma • Recent major surgery • Past time frame THROMBOLYTICS • Nursing implications • Treatment with tPA within 3-4.5 hours after onset of symptoms • Within 90 minutes is best • Narrow margin of safety • Only experienced personnel should perform thrombolytic therapy • Minimize injections • Can cause bleeding, bruising, or hematomas • Monitor • Cardiac monitor • VS every 15-30 minutes • S&S of bleeding • Labs • aPTT • Bleeding time • INR PATIENT SCENARIO Complete the remaining sections on the Google Form. We will discuss the rest of the case when you are finished. ANTIFIBRINOLYTICS VESSEL INJURY PLATELET PLUG COAGULATION CASCADE BLOOD CLOT ANTIFIBRINOLYTICS • Prototype: aminocaproic acid (Amicar) • Action • Prevents lysis of fibrin by plasminogen • Promotes clot formation • Use • Prevent and treat excessive bleeding from surgery • Nursing implications • Caution: may cause hypotension and bradycardia when given IV • Need cardiac monitor and frequent VS REFERENCES • Frandsen, G & Pennington, S.S. (2021). Abrams’ clinical drug therapy: Rationales for nursing practice (12th ed.). Philadelphia, PA: Wolters Kluwer. Helpful videos: Pharmacology - Anticoagulants & Antiplatelets (MADE EASY) THANK YOU WHAT QUESTIONS DO YOU HAVE?

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