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2700 - Week 2
Anticoagulants and Antiplatelets
| Term | Definition |
|---|---|
| What is hemostasis and what are the 4 aspects of the physiological process? | Process that prevents blood loss 1. Vasoconstriction 2. Platelet plug formation 3. Coagulation 4. Clot stabilization |
| Describe the coagulation cascade | Fibrinogen turned to fibrin Activated through the intrinsic or extrinsic pathway Results in fibrin clot formation |
| What is the cause and the driver of arterial thrombosis? What is the treatment focus? | Vessel wall injury or atherosclerotic plaque rupture. Driver: platelets Treatment: antiplatelets |
| What is the cause and the driver of venous thrombosis? What is the treatment focus? | Slow or stagnant blood flow Driver - coagulation factors Treatment - anticoagulents |
| Class: Anticoagulants | Prevent formation of fibrin-rich clots |
| Class: Antiplatelets | Prevent platelet activation & aggregation |
| Class: Thrombolytics | Dissolve existing clots |
| Class: Reversal Agents | Counteract anticoagulants/thrombolytics |
| Class: Hemostatic Agents | Promote clotting (usually in dressings) |
| What is the normal control range for aPTT? | 25–35 seconds |
| What is the therapeutic range for aPTT during heparin therapy? | 44–70 seconds or 1.5–2.5× baseline |
| When is aPTT drawn for continuous IV heparin? | Anytime |
| When is aPTT drawn for intermittent IV heparin? | About 1 hour before the dose |
| What is the normal control range for PT? | 11–13 seconds |
| What is the therapeutic PT range for warfarin therapy? | ~18 seconds or 1.5× control |
| What are the INR therapeutic ranges? | - Normal: 0.8–1.2 - Warfarin: 2–3 - Mechanical valve/high-risk: 2.5–3.5 |
| What is the purpose of anticoagulants? | Prevent the formation or extension of clots but DO NOT breakdown existing clots |
| What are some subclasses of anticoagulants | Heparins Vitamin K antagonists DOACs/NOACs |
| Contraindications for anticoagulants | - Acute bleeding - trauma, stroke, ulceration - Warfarin - pregnancy Can be given 2 hours after removal of epidural |
| What are the side effects of anticoagulants | - Bleeding - Spinal/epidural hematoma - Nausea, vomiting, cramps |
| What are some ways that you can assess for bleeding? | - Skin, oral mucous membranes, gums, urine, and stool - Easy bruising - Excessive bleeding from shaving or toothbrushing - Unexpected epistaxis |
| What are some ways to prevent bleeding? | - Fall minimizing - electric razor - soft bristled toothbrush - minimize lab draws, Iv,subQ, and IM routes |
| What should the nurse educate the patient on if they are receiving anticoagulants? | * regular lab testing * Signs of abnormal bleeding * Prevention of bleeding * Medic alert bracelet * Avoid high Vit. K foods |
| Heparins | Anticoagulant - reduces thrombin and thus fibrin production |
| What is the route and what unit is Heparin usually prescribed in? | IV or SubQ only, and prescribed in units |
| How does the route of administration differ between Low Molecular Weight Heparin (LMWH) and Unfractionated Heparin (UFH)? | LMWH is given SubQ only UFH can be given SubQ or IV |
| Which type of heparin requires aPTT monitoring and regular blood work? | Unfractionated Heparin |
| What condition must LMWH doses be adjusted in patients? | Chronic kidney disease Monitored in: - renal impairment - pregnancy -obesity |
| What is the onset for LMWH vs. UFH | LMWh - 3-5 hours UFH - Immediate (IV) or 20-60min (sub q) |
| What are some examples of LMWH | - Enoxaparin - Dalteparin |
| What are some examples of UFH | Heparin sodium Heparin Leo |
| What is the 0.9%NS mL equivalent to a heparin flush? | 20mL |
| Why have many institutions replaced heparin flushes with 0.9% normal saline for IV ports? | Due to the risk of heparin-induced thrombocytopenia (HIT), most institutions now use 0.9% normal saline for flushing heparin-lock IV ports |
| What are the clot-related conditions where heparin infusions are indicated? | Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) |
| In which cardiac emergencies is heparin used? | Acute Coronary Syndromes (NSTEMI, STEMI, unstable angina) |
| When is heparin used for patients with atrial fibrillation? | When stroke risk is high and the patient is transitioning to oral anticoagulants (e.g., warfarin) |
| What is aPTT, why is it monitored with heparin use, and what is the target range? | Assesses the intrinsic pathway, it is drawn to make sure that heparin is at a therapeutic not toxic level The target range - 1.5-2.5x normal (45-70 seconds) |
| What route requires aPPT lab monitoring for heparin? | Continuous infusions and intermittent doses |
| How is the dosing for LMWH calculated | By weight |
| What are the signs of toxicity for heparin? | Hematuria Melena Petechiae Ecchymoses membrane bleeding |
| What is the antidote for heparin? | Protamine sulphate (1mg of PS inactivates 100 units of heparin) |
| What is Heparin-Induced Thrombocytopenia? | Immune reaction to heparin, the body forms antibodies against a complex of heparin. These antibodies activate platelets, which leads to: - Thrombocytopenia (platelet drop) - Paradoxical hypercoagulability (the body forms clots everywhere) |
| When do you suspect Heparin-Induced Thrombocytopenia? | When platelet drop >50% from baseline Onset 5-14 days after beginning med |
| What are some things to remember when administering heparin? | - Double check with nurse - SubQ not intramuscularly - areas of deep fat - Not given within 5 cm of umbilicus - Don't aspirate or massage the injection site |
| What is the nurse’s response when asked how Heparin works? A. It converts plasminogen to plasmin to dissolve clots B. suppresses coagulation by helping antithrombin C. blocks vitamin K–dependent clotting factors D. inhibits platelet‑activating enzymes | B |
| The baseline activated partial thromboplastin time (aPTT) is 40 seconds. Which aPTT value indicates that a therapeutic dose has been achieved? A. 110 B. 50 C. 70 D. 90 | C (1.5 to 2 times the baseline) |
| What are the 2 pathways to inhibit clotting factors? | Blocking vitamin K - which will block synthesis factors that produce fibrin 2. Direct oral anticoagulants - inhibits the factors directly to stop clotting. |
| Warfarin | Oral anticoagulant |
| What does Warfarin do? | Inhibits the synthesis of vit. K clotting factors - prevents clot formation |
| What monitoring needs to occur for a patient taking warfarin? | Close INR monitoring |
| What are is the normal INR levels vs the therapeutic INR for warfarin | Normal - 0.8-1.2 With warfarin - 2-3.5 (narrow index - high risk med) |
| What is the black box warning for warfarin? | Risk of major or fetal bleeding |
| What are the pharmacokinetics for warfarin? | O- 8-12 hours P- 3-5 days D - 2-5 days The existing clotting factors have to degrade first |
| What are some indications for warfarin? | - Long term thrombosis prevention: Prosthetic heart valves, VTE, PE, and atrial fibrillation (Amiodarone & warfarin) - Recurrent stroke and TIA prevention |
| What are some contraindications for warfarin? | Active bleeding recent eye, brain or spinal surgery Planned lumbar puncture Pregnancy Liver disease or alcoholism |
| What are the mechanisms by which drugs increase warfarin's effects? | - Displacement from plasma albumin - Inhibition of hepatic enzymes that degrade warfarin - Decreased synthesis of clotting factors |
| Which drugs increase warfarin's effects? | - Aspirin - Sulfonamides - Acetaminophen - Amiodarone - Trimethoprim-sulfamethoxazole (Septra) |
| What are the mechanisms by which drugs promote bleeding with warfarin? | - Inhibition of platelet aggregation - Inhibition of clotting factors - Generation of GI ulcers |
| Which drugs promote bleeding when combined with warfarin? | - Aspirin and other salicylates - Clopidogrel - Apixaban - Heparins - Glucocorticoids |
| What are the mechanisms by which drugs decrease warfarin's effects? | - Induction of hepatic drug-metabolizing enzymes - Increased synthesis of clotting factors - Inhibition of warfarin absorption |
| Which drugs decrease warfarin's effects? | - Phenytoin - Oral contraceptives - Vitamin K - Cholestyramine |
| What are some examples of food that are high in Vitamin K? | Kale Spinach Collard greens Tomatoes |
| What are some drinks that can effect warfarin's effects? | Grapefruit juice Cranberry juice Green tea |
| What do toxic effects of warfarin cause? | Bleeding, lethargy, muscle pain, purple toes |
| How is warfarin reversed? | 1. Discontinue med 2. Vit. K reverses effects |
| How long does it take for warfarin effects to be reversed? | 36-42 hours |
| Dabigatran (Pradaxa) | Direct thrombin inhibitor |
| What is the mechanism of action of direct thrombin inhibitors? | Block thrombin, preventing the conversion of fibrinogen to fibrin |
| What is the antidote for dabigatran? | Idarucizumab (Praxbind) |
| What are the clinical uses of dabigatran? | - Stroke prevention in atrial fibrillation - Treatment and prevention of DVT/PE |
| Rivaroxaban (Xarelto) | Direct Factor Xa inhibitor |
| What is the mechanism of action of direct Factor Xa inhibitors? | They block Factor Xa, preventing thrombin formation. |
| What is the antidote for Factor Xa inhibitors? | Andexanet alfa (Andexxa) |
| What are the clinical uses of Factor Xa inhibitors? | - DVT/PE treatment and prevention - Stroke prevention in atrial fibrillation |
| What are three advantages of new oral anticoagulants over warfarin? | - Short duration of action - Fewer food-drug interactions - No need for routine INR monitoring |
| What are some side effects for dabigatran? | Bleeding Gi symptoms |
| What do antiplatelets do? | To prevent platelet adhesion and reduce clot formation. |
| What are the four major groups of antiplatelet drugs? | - Aspirin - P2Y₁₂ ADP receptor antagonists - PAR-1 antagonists - GP IIb/IIIa receptor antagonists |
| How does aspirin work as an antiplatelet agent? | It irreversibly inhibits COX enzymes, reducing thromboxane A₂ and platelet aggregation. |
| What is the mechanism of PAR-1 antagonists? | block thrombin-mediated platelet activation. |
| What do GP IIb/IIIa receptor antagonists prevent? | Fibrinogen binding and platelet cross-linking. |
| What are common adverse effects of antiplatelet drugs? | Bleeding risks, which vary by drug. |
| What is the drug class of aspirin? | Antiplatelet (COX-1 inhibitor) and NSAID. |
| What is aspirin’s mechanism of action? | Irreversibly inhibits COX-1 in platelets → ↓ thromboxane A₂ → ↓ platelet activation & aggregation. |
| How long does aspirin’s antiplatelet effect last? | For the lifespan of the platelet (~7 days). |
| What are the therapeutic uses of aspirin at different doses? | - Low-dose: stroke & MI prevention - Moderate dose: antipyretic & analgesic - High dose: anti-inflammatory |
| What is the most common adverse effect of aspirin? | GI irritation and bleeding. |
| What increases bleeding risk when taking aspirin? | Combining with other antiplatelets or anticoagulants. |
| Clopidogrel | P2Y12 Adenosine Diphosphate (ADP) Receptor Antagonist |
| What is the primary use of Clopidogrel? | To prevent blockage of coronary artery stents and reduce thrombotic events (MI, ischemic stroke, vascular death) |
| What is the most serious adverse effect of Clopidogrel? | Bleeding |
| What are common side effects of Clopidogrel? | Abdominal pain, dyspepsia, diarrhea, rash |
| When should Clopidogrel be discontinued before elective surgery? | 5 days |
| What is Thrombotic Thrombocytopenic Purpura (TTP)? | A rare but fatal emergency causing clotting in small vessels, thrombocytopenia, fever, hemolytic anemia, renal/neurologic dysfunction |
| When is TTP most likely to occur during Clopidogrel therapy? | within first 2 weeks |
| Prasugrel | P2Y12 ADP Receptor Antagonist |
| When is Prasugrel indicated? | After PCI/stent placement to prevent stent thrombosis |
| Who benefits from Prasugrel over Clopidogrel? | Patients with poor response to Clopidogrel |
| What are some contraindications for prasugrel? | Patients with prior stroke or TIA, active bleeding Adults ≥75 years due to increased bleeding risk |
| Ticagrelor | P2Y12 ADP Receptor Antagonis |
| What is Ticagrelor indicated for? | Acute Coronary Syndrome ± Percutaneous Coronary Intervention |
| Why should aspirin doses >100 mg/day be avoided with Ticagrelor? | Higher doses reduce Ticagrelor’s effectiveness |
| What are 3 adverse effects of Ticagrelor | Bleeding Dyspnea (common) Bradyarrhythmias |
Created by:
ahgecas25