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[h] Cardiovascular System Flashcards

[i] Master this session in just 5 minutes.

[q] ………. are the first-line therapy for most patients with hypercholesterolemia and works by competitively inhibit HMG CoA reductase, the enzyme responsible for the conversion of HMG CoA to mevalonate (the rate limiting step in hepatic cholesterol synthesis) –> upregulation of LDL receptors causes increased uptake of LDL from the circulation.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEhNRy1Db0EgcmVkdWN0YXNlIGluaGliaXRvcnMgKFN0YXRpbnMpLg==

[q] ………… are the most effective lipid-lowering drugs for primary and secondary prevention of cardiovascular events, regardless of baseline lipid levels.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IFN0YXRpbnMu

[q] The risk of statin myopathy is increased when ……….. are used concomitantly?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IGZpYnJhdGVzIGFuZC9vciBuaWFjaW4u[Qq]

[q] Most statins are metabolized by cytochrome P-450, with the exception of pravastatin. Concomitant administration of drugs that inhibit statin metabolism (CYP450 inhibitors) is associated with …………………?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IGluY3JlYXNlZCBpbmNpZGVuY2Ugb2Ygc3RhdGluLWluZHVjZWQgbXlvcGF0aHkgYW5kIHJoYWJkb215b2x5c2lzLg==

[q] ………….  work by binding bile acid in the gastrointestinal tract, thereby interfering with its enterohepatic circulation –> Bile acid production is increased 10-fold –> LDL is reduced as a result because hepatic cholesterol is used up for the re-synthesis of bile acids

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEJpbGUgYWNpZC1iaW5kaW5nIHJlc2lucyAoQ2hvbGVzdHlyYW1pbmUsIGNvbGVzZXZlbGFtIGFuZCBjb2xlc3RpcG9sKS4=

[q] Bile acid-binding agents increase the cholesterol content of bile, thus increasing the risk for ………….?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IGZvcm1hdGlvbiBvZiBjaG9sZXN0ZXJvbCBnYWxsc3RvbmVzLg==[Qq]

[q] Because of this tendency for bile acid-binding agents to increase serum triglyceride levels, they should not be used in ……….?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IGh5cGVyY2hvbGVzdGVyb2xlbWlhIHBhdGllbnRzIHdobyBoYXZlIGNvbmNvbWl0YW50IGh5cGVydHJpZ2x5Y2VyaWRlbWlhLg==[Qq]

[q] ………… work by activating peroxisome proliferator-activated receptor alpha (PPAR-α), which leads to decreased hepatic VLDL production and increased lipoprotein lipase activity. Used in hypertriglyceridemia and cause myopathy (↑ risk with statins) and gallstones (↑ risk with bile acid resins) as side effects.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEZpYnJhdGVzIChHZW1maWJyb3ppbCwgRmVub2ZpYnJhdGUpLg==

[q] ………. inhibits lipolysis (hormone sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis, results in –>↓ plasma VLD, ↓ plasma LDL, ↑↑ plasma HDL (↓ clearance). It causes flushing, warmth, itching (mediated by prostaglandins and can be prevented by aspirin), hyperglycemia, hyperuricemia as side effects.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IE5pY290aW5pYyBhY2lkICh2aXRhbWluIEIzKS4=

[q] ……….. works by preventing cholesterol absorption at small intestine brush border –> results in ↓ LDL and cause GIT upset as side effect.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEV6ZXRpbWliZS4=

[q] …………… works by inactivation of LDL-receptor degradation → ↑ removal of LDL from bloodstream

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IFBDU0s5IGluaGliaXRvcnMgKEFsaXJvY3VtYWIsIGV2b2xvY3VtYWIpLg==

[q] ………….. works by moderate Na channel blockade preferentially in the open or activated state “state-dependent” blockade –> ↓ slope of phase 0 depolarization. It also blocks K channel (prolongs repolarization) –> ↑ AP duration, ↑ effective refractory period (ERP) in ventricular action potential, ↑ QT interval.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IENsYXNzIDFBIE5hIGNoYW5uZWwgYmxvY2tlciAoUXVpbmlkaW5lLCBQcm9jYWluYW1pZGUsIERpc29weXJhbWlkZSku[Qq]

[q] ……….. is Class 1A antiarrhythmic drug with antimuscrinic and alpha blocking effect. It cause cinchonism (GI, tinnitus, ocular dysfunction, CNS excitation), hypotension, prolongation of QRS and ↑ QT interval associated with syncope (torsades de pointes).

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IFF1aW5pZGluZS4=[Qq]

[q] ……….. is Class 1A antiarrhythmic drug with less antimuscrinic blocking effect and no alpha blockade effect. It causes systemic lupus erythematosus (SLE) like syndrome (30% incidence) more likely with slow acetylators; hematotoxicity (thrombocytopenia, agranulocytosis); CV effects (torsades).

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]wqBQcm9jYWluYW1pZGUu[Qq]

[q] ……………… is a weak Na channel blocker and shortens the action potential (left shift). Preferentially affect hypoxic and ischemic tissues.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IENsYXNzIDFCIE5hIGNoYW5uZWwgYmxvY2tlciAoTGlkb2NhaW5lLCBNZXhpbGV0aW5lLCBQaGVueXRvaW4pLg==[Qq]

[q] …………. is a class 1B Na channel blocker that is used as IV because of its first-pass metabolism. It causes CNS toxicity (seizures) as side effect.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]wqBMaWRvY2FpbmUu[Qq]

[q] …………. is a class 1B Na channel blocker that is  similar to Lidocaine but can be taken orally.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IE1leGlsZXRpbmUu[Qq]

[q] ………. is a class 1B antiarrhythmic agent which very specifically binds rapidly depolarizing and depolarized cells, that’s why it is specific for ischemic tissue and is the agent of choice for prevention and treatment of post-myocardial infarction arrhythmias.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IExpZG9jYWluZS4=[Qq]

[q] ……….. is a strong Na channel blocker. It bind avidly to the fast sodium channels responsible for phase 0 depolarization, blocking the inward sodium current and prolonging the QRS duration with no effect on AP duration.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IENsYXNzIDFDIE5hIGNoYW5uZWwgYmxvY2tlciAoRmxlY2FpbmlkZSBhbmQgcHJvcGFmZW5vbmUpLg==[Qq]

[q] ……………. are the slowest of the class 1 agents to dissociate from the sodium channel. This results in a phenomenon known as use-dependence, in which their sodium blocking effects intensify as the heart rate increases due to less time between action potentials for the medication to dissociate from the receptor.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IENsYXNzIDFDIE5hIGNoYW5uZWwgYmxvY2tlciAoRmxlY2FpbmlkZSBhbmQgcHJvcGFmZW5vbmUpLg==[Qq]

[q] ……………. is the last resort in refractory VT. Its limited use because of proarrhythmogenic effects, leading to ↑ in sudden death post-MI and when used prophylactically in VT.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEZsZWNhaW5pZGUu

[q] ……….. decrease SA and AV nodal activity by ↓ cAMP, ↓ Ca currents. It also suppress abnormal pacemakers by ↓ slope of phase 4. Used for treatment of SVT, ventricular rate control for atrial fibrillation and atrial flutter. It causes impotence, exacerbation of COPD and asthma, cardiovascular side effects (bradycardia, AV block, HF), CNS side effects (sedation, sleep alterations).

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IM6yLWJsb2NrZXJzIChjbGFzcyBJSSBBbnRpYXJyaHl0aG1pYyBEcnVncyku[Qq]

[q] …………. works by ↓ IK (delayed rectifier current) slowing phase 3 (repolarization) of AP, ↑ AP duration, ↑ ERP, and ↑ QT interval. Used for treatment of Atrial fibrillation, atrial flutter; ventricular tachycardia (amiodarone, sotalol).

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IFBvdGFzc2l1bSBjaGFubmVsIGJsb2NrZXJzIChBbWlvZGFyb25lLCBJYnV0aWxpZGUsIERvZmV0aWxpZGUsIFNvdGFsb2wpLg==[Qq]

[q] ………… mimics classes I, II, III, and IV (blocks Na, Ca, K channels and beta adrenoreceptors). Used for treatment of almost any arrhythmias. It causes pulmonary fibrosis, thyroid dysfunction, and hepatic necrosis.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEFtaW9kYXJvbmUuIFJlbWVtYmVyIHRvIGNoZWNrIFBGVHMsIExGVHMsIGFuZCBURlRzIHdoZW4gdXNpbmcgYW1pb2Rhcm9uZS4=[Qq]

[q] …………. is the only class III antiarrhythmic with beta-adrenergic blocking abilities (causing mild bradycardia) as well as class III effects (causing the QT interval prolongation). It prolongs both the PR interval and the QT interval.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IFNvdGFsb2wu[Qq]

[q] ………….. block slow cardiac Ca channels by blocking the L-type calcium channels, thereby decreasing phase 0, phase 4 and conduction velocity in the sinoatrial and AV nodes. This leads to slowing of the sinus rate and conduction through the AV node.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IENhbGNpdW0gY2hhbm5lbCBibG9ja2VycyAoY2xhc3MgSVYpLg==[Qq]

[q] ………. is the DOC for paroxysmal supraventricular tachycardias and AV nodal arrhythmias. It acts by slowing conduction through the AV node by hyperpolarizing the nodal pacemaker (↑ K efflux) and conducting cells.  It causes dyspnea (due to bronchospasm) as side effect.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IEFkZW5vc2luZS4=[Qq]

[q] Adenosine is antagonized by ……….?

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IG1ldGh5bHhhbnRoaW5lcyAodGhlb3BoeWxsaW5lIGFuZCBjYWZmZWluZSBhcmUgYWRlbm9zaW5lIHJlY2VwdG9yIGFudGFnb25pc3RzKS4=[Qq]

[q] ……….. is used for treatment of torsades de pointes and digoxin toxicity.

[c]IFNob3cgbWUgdG hlIGFuc3dlcg==[Qq]

[f]IE1hZ25lc2l1bS4=[Qq]

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