7775100
Beschreibung
Karteikarten von Justice Mundy, aktualisiert more than 1 year ago
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Erstellt von Justice Mundy
vor fast 8 Jahre
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| Frage | Antworten |
| Aspirin: Indications | Pain relief, prevention of stroke/MI |
| Aspirin: Pharmacodynamics/pharmacokinetics | Half life becomes longer with very large doses |
| Aspirin: Side effects | Bleeding, Peptic ulceration, Reye's Syndrome, and Angiooedema |
| Aspirin: What would you tell patient? | To avoid OTC preparations. |
| rt-PA: Indications | Acute ischaemic stroke within the first 4.5 hours of onset, myocardial infarction, and massive pulmonary embolism. |
| rt-PA: Mechanism of action | Recombinant form of tissue plasminogen activator; Catalyses conversion of plasminogen to plasmin. |
| rt-PA: Side effects | Bleeding complications: ICH, GI blood loss, retroperitoneal. Allergic reaction / angiooedema (1%) |
| rt-PA: Important pharmacodynamics/pharmacokinetics | Bolus infusion needed (not for all types of rt-PA). Pharmacodynamic interactions with other blood thinners (antiplatelets / coagulants) |
| rt-PA: What would you tell patient? | Risk benefit ratio; NNT of 3 to improve neurologic disability; 1/20 approximately will come to harm from bleeding. |
| Aspirin: Mechanism of action | Irreversible inactivation of cyclooxygenase and thus platelet thromboxane production. |
| Clopidogrel: Mechanism of action | Inhibitor of platelet activation and aggregation through the irreversible binding of its active metabolite to the P2Y12 class of ADP receptors on platelets. |
| Clopidogrel: Pharmacodynamics/Pharmacokinetics | Clopidogrel must be metabolized by CYP450 enzymes to produce the active metabolite that inhibits platelet aggregation. platelets exposed to clopidogrel's active metabolite are affected for the remainder of their lifespan (about 7 to 10 days). Platelet aggregation induced by agonists other than ADP is also inhibited by blocking the amplification of platelet activation by released ADP; Avoid use with PPI's, CYP2C19 Inhibitors, NSAIDs, Warfarin (CYP2C9 Substrates), and SSRIs And SNRIs. Clopidogrel is a prodrug and is metabolized to a pharmacologically active metabolite and inactive metabolites. |
| Clopidogrel: Indications | Acute Coronary Syndrome (ACS); Recent MI, Recent Stroke, Or Established Peripheral Arterial Disease |
| Clopidogrel: Side Effects | Bleeding, Thrombotic thrombocytopenic purpura, |
| Clopidogrel: What would you tell patient? | It can cause serious bleeding, do not take while taking omeprazole or esomeprazole. |
| Dipyridamole: Mechanism of action | It likely inhibits both adenosine deaminase and phosphodiesterase, preventing the degradation of cAMP, an inhibitor of platelet function. This elevation in cAMP blocks the release of arachidonic acid from membrane phospholipids and reduces thromboxane A2 activity. Dipyridamole also directly stimulates the release of prostacyclin, which induces adenylate cyclase activity, thereby raising the intraplatelet concentration of cAMP and further inhibiting platelet aggregation. |
| Dipyridamole: Indications | Coronary artery disease, post-operative thromboembolism, stroke |
| Dipyridamole: Side Effects | Hypotension, if it occurs, is likely to be of short duration, but a vasopressor drug may be used if necessary. |
| Dipyridamole: Important Pharmacodynamics / Pharmacokinetics | Dipyridamole, a non-nitrate coronary vasodilator that also inhibits platelet aggregation, is combined with other anticoagulant drugs, such as warfarin, to prevent thrombosis in patients with valvular or vascular disorders. Dipyridamole is also used in myocardial perfusion imaging, as an antiplatelet agent, and in combination with aspirin for stroke prophylaxis. |
| Dipyridamole: What would you tell patients? | This medication is sometimes used together with other drugs that may increase your risk of bleeding. Examples are certain "blood thinners" (such as heparin, warfarin). If you are currently taking aspirin, talk to your doctor right away and ask if you should continue taking it with this medication. Before using this medication, tell your doctor or pharmacist your medical history, especially of: other heart problems (such as severe coronary artery disease, recent heart attack), low blood pressure (hypotension), liver disease, a certain muscle problem (myasthenia gravis). |
| Ticagrelor: Mechanism of action | Ticagrelor and its major metabolite reversibly interact with the platelet P2Y12 ADP-receptor to prevent signal transduction and platelet activation. Ticagrelor and its active metabolite are approximately equipotent. |
| Ticagrelor: Indications | Cardiovascular disorder prophylaxis, stent thrombosis. |
| Ticagrelor: Side Effects | Bleeding, dyspnea |
| Ticagrelor: Important pharmacodynamics / pharmacokinetics | Ticagrelor demonstrates dose proportional pharmacokinetics, which are similar in patients and healthy volunteers. |
| Ticagrelor: What would you tell patient? | It can cause bleeding that can be serious and sometimes lead to death. In cases of serious bleeding, such as internal bleeding, the bleeding may result in the need for blood transfusions or surgery; While taking it: 1) You may bruise and bleed more easily. 2) You are more likely to have nose bleeds. 3) It will take longer than usual for any bleeding to stop. |
| Tirofibran: Mechanism of action | Tirofiban is a reversible antagonist of fibrinogen binding to the GP IIb/IIIa receptor, the major platelet surface receptor involved in platelet aggregation. Platelet aggregation inhibition is reversible following cessation of the infusion of tirofiban. |
| Tirofibran: Indications | Cardiovascular disorder prophylaxis |
| Tirofibran: Side Effects | Bleeding |
| Tirofibran: Important pharmacodynamics / pharmacokinetics | Tirofiban prevents the blood from clotting during episodes of chest pain or a heart attack, or while the patient is undergoing a procedure to treat a blocked coronary artery. It is a non-peptide antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, and inhibits platelet aggregation. When administered intravenously, tirofiban inhibits ex vivo platelet aggregation in a dose- and concentration-dependent manner. When given according to the recommended regimen, >90% inhibition is attained by the end of the 30-minute infusion. Tirofiban has been recently shown in patients with unstable angina to reduce ischemic events at 48 hours following infusion when compared to standard heparin therapy. Tirofiban has a half-life of approximately 2 hours. In healthy subjects, the plasma clearance of tirofiban ranges from 213 to 314 mL/min. |
| Tirofibran: What would you tell patient? | Advise patients to watch closely for any signs of bleeding or bruising and to report these to their health care provider when they occur. Advise patients to discuss with their health care provider their use of any other medications, including over-the-counter or herbal products prior to use. |
| Coagulation Cascade | Series of protease enzymes and their cofactors. Takes place on phospholipid surface (platelet or endothelium). Consists of extrinsic, intrinsic and common pathways. Results in formation of stable fibrin clot. |
| Warfarin: Mechanism of action | Inhibits vitamin K epoxide reductase. Prevents recycling of vitamin K to reduced form after carboxylation of coagulation factors II, VII, IX and X. |
| Warfarin: Indications | Treatment of VTE. Thromboprophylaxis in AF / metallic heart valves / cardiomyopathy. |
| Warfarin: Side Effects | Warfarin necrosis, Bleeding, Osteoporosis. |
| Warfarin: Important Pharmacokinetics / Pharmacodynamics | Numerous drug interactions / food interactions. Reversal by giving vitamin K. Polymorphisms in key metabolising enzymes (VKORC1 and CYP2C9). Needs TDM and monitored loading regimen. Monitored with INR. |
| Warfarin: What Would You Tell Patient?? | Need for compliance /attendance at visits for monitoring. Care with alcohol. Must inform doctor before starting new drugs – avoid OTC aspirin. |
| Dabigatran: Mechanism of action | Direct thrombin inhibitor |
| Dabigatran: Indications | Prophylaxis of VTE. Thromboprophylaxis in AF. |
| Dabigatran: Side Effects | Bleeding |
| Dabigatran: Important Pharmacokinetics / Pharmacodynamics | No food / few drug interactions (not metabolised via CYP 450). No need for monitoring. Less readily reversed. |
| Dabigatran: What Would You Tell Patient? | Risk of bleeding |
| Rivaroxaban: Mechanism of action | Direct thrombin inhibitor |
| Rivaroxaban: Indications | Prophylaxis and treatment of VTE. Thromboprophylaxis in AF. |
| Rivaroxaban: Side Effects | Bleeding |
| Rivaroxaban: Important Pharmacokinetics / Pharmacodynamics | Predictable drug interactions (metabolised via CYP 450, inc CYP3A4). No need for monitoring. Less readily reversed. |
| Rivaroxaban: What Would You Tell Patient? | Risk of bleeding |
| Apixaban: Mechanism of action | Direct thrombin inhibitor |
| Apixaban: Indications | Thromboprophylaxis in AF / metallic heart valves / cardiomyopathy. |
| Apixaban: Side Effects | Bleeding |
| Apixaban: Important Pharmacokinetics / Pharmacodynamics | Predictable drug interactions (metabolised via CYP 450 and substrate for p glycoprotein). No need for monitoring. Less readily reversed. |
| Apixaban: What Would You Tell Patient? | Risk of bleeding |
| Unfractionated Heparin (UFH): Mechanism of action | Enhances activity of antithrombin |
| Unfractionated Heparin (UFH): Indications | Treatment of thromboembolic diseases (induction of vitamin K antagonists), VTE prophylaxis, inc during renal dialysis, ACS treatment. |
| Unfractionated Heparin (UFH): Side Effects | Risk of bleeding, HIT |
| Unfractionated Heparin (UFH): Important Pharmacokinetics / Pharmacodynamics | Administered by continuous intravenous infusion or subcutaneous injection, Complex kinetics - non-linear relationship between dose / half-life and effect – needs TDM, Effect monitored using activated partial thromboplastin time (aPTT), Reversal with protamine |
| Unfractionated Heparin (UFH): What Would You Tell Patient? | Need for regular monitoring of blood samples, Risk of bleeding |
| Low Molecular Weight Heparin (LMWH): Mechanism of action | Enhances activity of antithrombin |
| Low Molecular Weight Heparin (LMWH): Indications | Treatment of thromboembolic diseases (induction of vitamin K antagonists), VTE prophylaxis, inc during renal dialysis, ACS treatment. |
| Low Molecular Weight Heparin (LMWH): Side Effects | Risk of bleeding, HIT- less risk than UFH, Osteoporosis. |
| Low Molecular Weight Heparin (LMWH): Important Pharmacokinetics / Pharmacodynamics | Subcutaneous injection; More predictable dose-response relationship than UFH; 2-4 times longer plasma half-life; Clearance is mostly via a renal pathway, thus the half-life can be prolonged in patients with renal failure; Regular coagulation monitoring is not required. Doesn’t affect aPTT; Less readily reversed. |
| Low Molecular Weight Heparin (LMWH): What Would You Tell Patient? | Risk of bleeding; Need injection; Will need blood check (for platelets) if prolonged therapy. |
| Fondaparinux: Mechanism of action | Enhances activity of antithrombin |
| Fondaparinux: Indications | VTE prophylaxis after major surgery; ACS treatment |
| Fondaparinux: Side Effects | Risk of bleeding |
| Fondaparinux: Important Pharmacokinetics / Pharmacodynamics | Injectable only; Long plasma half-life, which allows a once-daily regimen; Exclusively eliminated by the kidneys; Regular coagulation monitoring is not required; Less readily reversed. |
| Fondaparinux: What Would You Tell Patient? | Risk of bleeding; Need injection. |
| Heparin-induced thrombocytopenia (HIT): | The development of thrombocytopenia (a low platelet count), due to the administration of various forms of heparin; Venous thromboembolism; Arterial thrombosis; Adrenal vein thrombosis – adrenal necrosis; Skin necrosis; Anaphylactic reactions; Disseminated intravascular necrosis; Warfarin – increases risk of microthrombosis; Treated with a direct thrombin inhibitor: Argatroban or Lepirudin |
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