Term
| heart as a target of toxicity |
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Definition
| blood flow to the heart brings in toxins, highly dependent on ionic flow to create action potentials that make the heart work properly |
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Term
| risk factors for cardiotoxicity |
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Definition
| age, pre-existing disease |
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Term
| antagonism of M2 receptors |
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Definition
| increases conduction at the SA and AV nodes to increase heart rate, can exacerbate angina because of the increased oxygen demand of heart when drug is administered |
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Term
| certain drugs predispose the heart to have arrhythmias |
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Definition
| drugs can set up the heart so that it is more likely to have something go wrong, drugs that fix arrhythmias can predispose heart to getting other types of arrhythmias |
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Term
| inhibition of Na/K ATPase |
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Definition
| Digitalis: increased intracellular Na will drive Na/Ca exchanger causing there to be increased intracellular Ca causing positive ionotropy (increased contractility) |
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Term
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Definition
| Verapamil and diltiazem: negative ionotropic effect due to reduce Ca-induced Ca release in sarcoplasmic reticulum, causing BRADYcardia and (AV node) heart block |
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Term
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Definition
| contributes to excitation-contraction coupling |
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Term
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Definition
| Contributes to Pacemaker potential in SA node |
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Term
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Definition
| blockade of hERG, which regulates rapid delayed rectifier current, results in prolongation of cardiac action potential (Q-T interval) producing torsades de pointes |
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Term
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Definition
| potassium channel protein/ expression-regulator gene |
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Term
| antipsychotics, antihistamines (non-drowsy), zithromax, viagra and Cialis |
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Definition
| cause blockade or alteration of hERG functions that can result in arrhythmias |
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Term
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Definition
| time required to achieve ventricular depolarization and time to the onset of repolarization and time required to complete repolarization |
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Term
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Definition
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Term
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Definition
| ventricular contraction (atrial repolarization) |
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Term
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Definition
| ventricular repolarization |
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Term
| Q-T prolongation due to hERG interference |
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Definition
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Term
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Definition
| atypical form of ventricular tachycardia initiated only in the presence of long Q-T interval and can progress to ventricular fibrilation, can lead to sudden death |
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Term
| antiarrhythmic class IA: quinidine, procainamide, disopramide |
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Definition
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Term
| Antiarrhythmic class IC: encainide, flecainide |
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Definition
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Term
| Antiarrhythmic class III: sotalol, amiodarone |
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Definition
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Term
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Definition
| reactive free radical generated during metabolism of parent molecule, often due to mitochondrial damage and disruption of ATP production (electron transport interrupted to produce ROS) |
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Term
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Definition
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Term
| Doxorubacin-induced cytotoxicity |
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Definition
| doxorubicin smiquinone radical produced forming complex with iron becoming doxorubicin-free radical complex, hydrogen peroxide dismutates complex and results in fromation of peroxynitrite which causes cardiotoxicity |
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Term
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Definition
| disruption of electron transport chain results in ROS formation and contributes to dysfunction and shut down of mitochondria and interference with calcium handling of the cells which is needed for heart action potential function |
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Term
| consequences of mitochondrial dysfunction |
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Definition
| interferance: beta oxidation, NADH synthesis, electron transport chain, proton gradient, and mitochondrial permeability transition |
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Term
| doxorubacin (oxidative stress) and carvedilol (long period of time) |
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Definition
| drugs that cause mitochondrial dysfunction |
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Term
| hypersensitivity myocarditis |
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Definition
| inflammatory and necrotic disease of myocardium with a wide range of clinical prentation leading to heart failure and arrhythmia |
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Term
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Definition
| NOT dose-dependent and within therapeutic range it can cause hypersensitivity myocarditis |
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Term
| endothelial cell properties and functions |
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Definition
| source of anticoag, prothrombic, production of extracellular matrix, modulatoin of blood flow through vasodilators and inflammation/ immunity , growth factors and oxidation of LDL |
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Term
| mechanisms of drug-induced vascular injury |
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Definition
| biochemical injury, toxicity following direct pharmacological/ chemical perturbation, injury via immune-mediated mechanisms |
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Term
| methylxanthines (caffeine and theophylline), potassium channel activators (minoxidil, diazoxide) |
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Definition
| vasodilators affecting (large/ medium) arteries...drug induced vascular injury with long-term use |
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Term
| vasopressin, angiotensin II, Epi, phynylephrine, methoxamine |
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Definition
| vasoconstrictors affecting (small) arteries and arterioles...drug induced vascular injury with long-term use |
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Term
| cholesterol and oxygenated derivatives, organophosphates, cadmium. arsenic and mercury |
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Definition
| exacerbation of pre-existing pathology (atherosclerosis)...drug induced vascular injury with long-term use |
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Term
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Definition
| heterogeneous group of disorders characterized by inflammatory destruction of both arteries and veins |
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Term
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Definition
| changes in blood vessels, induced thickening, weakening, narrowing and scarring...drug hypersensitivity that evolves into ischemia and necrosis of vessels |
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Term
| propylthiouracil and ciprofloxacin |
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Definition
| drug-induced vasculitis; binding of drug (hepten)and protein (carrier-antigen) |
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