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antiplate/coag pt 1
pharm exam 2
| Question | Answer |
|---|---|
| thrombin is the link between? | tissue injury, coagulation, and platelet response. |
| antiplatelets interfere with? | platelet activation and aggregation |
| platelet aggregation | platelets clump |
| fibrinolytics | clot busters-> break down fibrin which is the backbone of clotting |
| critical mediator in coagulation | thrombin |
| what does thrombin elicit | multiple responses in platelets and other cells |
| steps of platelet adhesion, activation, and aggregation | resting platelet, plaque ruptures and platelet adheres->agonists releases-> platelet activation and GP IIb-IIIa expression-> fibrinogen-> platelet aggregation |
| what produces the factors that clot and prevent clotting? | the liver |
| where do a lot of the coagulation factors converge? | Xa |
| intrinsic pathway of the coagulation cascade | contact factor pathway, platelet factors |
| extrinsic pathway of the coagulation cascade | tissue damage pathway, tissue factors |
| immobile clot | thrombus |
| drifting blood clot | embolus |
| blockage due to embolus | embolism |
| where can a thrombosis occur? | in any artery, vein, heart chamber, heart valve, etc |
| what can thrombosis lead to? | deep vein thrombosis, (DVT), pulmonary embolism (PE), myocardial infarction (MI), cerebrovascular accident (CVA) |
| where does warfarin work in the coagulation cascade? | inhibits plasma clotting cascade |
| how does warfarin work at the plasma clotting cascade? | interferes with clotting factors 2,7,9,10 (key vitamin K factors) |
| oral antiplatelets | Aspirin (ASA) P2Y12 inhibitors Phosphodiesterase type-3 (PDE-3) inhibitors |
| P2Y12 inhibitors | Clopidogrel (Plavix®) Prasugrel (Effient®) Ticagrelor (Brilinta®) |
| Phosphodiesterase type-3 (PDE-3) inhibitors | Cilostazol (Pletal®) Dipyridamole (Persantine®) Dipyridamole/ASA (Aggrenox®) |
| parenteral antiplatelets | IV P2Y12 inhibitor, Glycoprotein IIb/IIIa inhibitors |
| IV P2Y12 inhibitor | Cangrelor (Kengreal®) |
| Glycoprotein IIb/IIIa inhibitors | Eptifibatide (Integrilin®) Tirofiban (Aggrastat®) |
| indications for antiplatelets | ASCVD (i.e., CAD and PAD) -Secondary prevention (prevent recurrent event) -Primary prevention (prevent first event) Acute coronary syndromes (ACS) (i.e., acute myocardial infarction) Percutaneous coronary intervention (PCI) Acute ischemic stroke |
| aspirin mechanism | Inhibits COX-1 enzyme leading to less thromboxane A2 (TXA2)-mediated platelet activation |
| aspiring indications: treatment | Coronary artery disease (CAD) Peripheral arterial disease (PAD) Acute coronary syndrome (ACS) Percutaneous coronary intervention (PCI) Acute ischemic stroke |
| aspirin adverse events/monitoring | Bleeding Rash GI events |
| What can you do for a patient that is having GI events after receiving aspirin? | slow absorption such as giving it as IR or ER so it absorbs in the stomach instead of the gut |
| P2Y12 inhibitors examples | Clopidogrel, Prasugrel, Ticagrelor, Cangrelor |
| P2Y12 inhibitors mechanism | Inhibits ADP from binding to P2Y12 receptor leading to antiplatelet effect |
| P2Y12 inhibitors indications | Cardiovascular (i.e., ACS and PCI), neurovascular (i.e., acute ischemic stroke and stents), and peripheral vascular (i.e., stents) |
| P2Y12 inhibitors adverse events/monitoring | Bleeding - Prasugrel and ticagrelor are more potent than clopidogrel |
| P2Y12 inhibitors adverse events/monitoring: ticagrelor | dyspnea, bradycardia |
| oral anticoagulants | Warfarin (Coumadin®) Direct thrombin inhibitors Selective factor Xa inhibitors |
| Direct thrombin inhibitors | Dabigatran (Pradaxa®) |
| Selective factor Xa inhibitors: | Rivaroxaban (Xarelto®) Apixaban (Eliquis®) Edoxaban (Savaysa®) |
| DOACs | Direct thrombin inhibitors: Selective factor Xa inhibitors: |
| Direct oral anticoagulants dont require? | cofactor to bind to it first |
| parenteral anticoagulants | Heparins Low-molecular-weight heparins (LMWH) Selective factor Xa inhibitors Direct thrombin inhibitors |
| Heparins example | Unfractionated heparin (UFH) |
| low-molecular-weight heparins examples | Enoxaparin (Lovenox®) Dalteparin (Fragmin®) |
| Selective factor Xa inhibitors examples | Fondaparinux (Arixtra®) |
| Direct thrombin inhibitors examples | Argatroban Bivalirudin (Angiomax®) |
| when are you likely to see direct thrombin inhibitors? | if patient can't take heparin |
| indications for anticoagulation | prevention and treatment of thromboembolism ex: VTE- DVT, Pulmonary embolism ACS Severe left ventricular systolic dysfunction Intra-cardiac thrombus Heart valve replacement Atrial arrhythmias Afib Atrial flutter Thrombophilia Malignancy |
| mechanical heart valve triggers? | clotting cascade |
| Afib puts patients at risk for? | stroke-> need lifelong anticoagulants if tolerated |
| thrombophilia | clotting disorder, F5 mutation, need lifelong anticoagulants |
| what does heparin bind to? | antithrombin before inhibiting factor 10 and 2 |
| warfarin mechanism | Vitamin K antagonist (VKA) Inhibits VKORC1 (protein target in the liver), which is responsible for activation of vitamin K-dependent clotting factors (II, VII, IX, X) and protein C and S |
| warfarin adverse events/monitoring | Bleeding (PT/INR) Skin necrosis Purple toe syndrome |
| when warfarin is first administered what should patients be on? | IV or subQ anticoagulant for several days |
| protein C and S | anticoagulants inhibited by warfarin-> don't want blocked because can lead to clotting (might have to lower dose) |
| therapeutic index of warfarin | very narrow |
| INR in healthy individual not on warfarin? | 1 sec |
| what should INR be in patients on warfarin? | 2-3 seconds |
| warfarin drug-drug interactions | Antibiotics NSAIDs Vitamin K Steroids Alcohol Vitamin E Anticonvulsants Immunosuppressants Proton pump inhibitors Statins |
| Why do we have to monitor vitamin K when taking warfarin? | increased vitamin K makes warfarin less effective |
| warfarin monitoring indications INR 2-3 | Tx of DVT and pulmonary embolism Prevention of systemic embolism (e.g., stroke) - bioprosthetic heart valves – short-term - acute MI, LV dysfunction, intracardiac thrombus - afib/atrial flutter |
| warfarin monitoring indication INR 2.5-3.5 | Mechanical prosthetic valves (mitral) |
| warfarin monitoring indication INR 2-3 | Mechanical prosthetic valve (aortic) |
| warfarin patient counseling | Adverse effects Unusual bleeding/bruising Signs/symptoms of clotting INR monitoring and dosage changes Diet: consistent intake of dietary vitamin K Common drug interactions Tablet identification |
| unusual bleeding when taking warfarin | blood in urine/stool, coughing up blood |
| if patient on warfarin fell and hit their head we should? | scan and check for hemorrhage |
| warfarin onset of effect | slow, typically 4-5 days on average, therefore, requiring parenteral anticoagulant for “bridging” |
| when should we as nurses monitor our patients INR when administering warfarin? | daily until therapeutic for ≥ 2 days, then 2 to 3 times weekly, then less often |
| most common medication associated with bleeding complications | warfarin |
| when is warfarin often held? | for procedures or line placements (i.e., until INR < 2 but can vary) |
| when is warfarin generally administered? | in the evening per institutional recommendations (standard administration time) |
| warfarin- reversal | Discontinue/hold warfarin Vitamin K1 (phytonadione) Fresh frozen plasma (FFP) Prothrombin complex concentrates - 3-factor (Profilnine®) or 4-factor (Kcentra®) Recombinant factor VIIa (Novoseven®) |
| what do prothrombin complex concentrates give back? | factors 2,7,9,10 |
| when to give a patient prothrombin complex concentrates? | 3-factor (Profilnine®) or 4-factor (Kcentra®) |
| why are DOACs preferred to warfarin for most patients? | based on their superior safety profile and at least equivalent efficacy (i.e., stroke prevention for Afib, VTE treatment and prevention) |
| what populations should DOACs not be used for? | patients with a mechanical heart valve, severe mitral stenosis, advanced kidney disease, hypercoagulable states |
| do DOACs require hematologic monitoring? | no |
| major barrier of DOACs | cost |