Term
| What are the 4 main ways drugs can relax vascular smooth muscle? |
|
Definition
| Increase cGMP, decrease intracellular Ca+, stabilize or prevent depol of membrane, increase cAMP |
|
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Term
|
Definition
| Releases NO in smooth muscle, which activates guanylyl cyclase and increases cGMP. |
|
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Term
|
Definition
| Smooth muscle relaxation, esp in vessels. Vasodilation decreases venous return and heart size. May increase coronary flow in some areas and in variant angina. |
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Term
| NTG - Clinical applications? |
|
Definition
| Angina, SL for acute, oral and TD for prophylaxis, IV for ACS |
|
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Term
| NTG - Pharmacokinetics, toxicities, interactions? |
|
Definition
| high first pass effect, high lipid solubility, rapid absorption, ortho hypotension, tachy, HA, synergistic HTN with PDE5 inhibitors |
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Term
| How does isosorbide dinitrate differ from NTG? |
|
Definition
| very similar, slightly longer DOA |
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|
Term
| How does isosorbide mononitrate differ from NTG? |
|
Definition
| It's an active metabolite of the dinitrate, used orally for prophylaxis |
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Term
|
Definition
| nonselective competitive antagonist at B adrenoreceptors |
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Term
|
Definition
| Decreased HR, CO, BP, decreases myocardial O2 demand |
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|
Term
| Propranolol - Clinical applications? |
|
Definition
| prophylaxis of angina, others described in other chapters |
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|
Term
| Propranolol - pharmacokinetics, tox, interactions? |
|
Definition
| oral and parenteral, 4-6 hr DOA, asthma, AV block, acute HF, sedation, additive with all cardiac depressants |
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|
Term
| How do atenolol, metoprolol and others differ from propranolol? |
|
Definition
| B1- selective, less risk of bronchospasm but still significant |
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Term
| Verapamil and diltiazem - MOA? |
|
Definition
| Nonselective block of L-type Ca channels in vessels and heart |
|
|
Term
| Verapamil and diltiazem - effects? |
|
Definition
| Reduced vascular resistance, HR, cardiac force, decreased O2 demand |
|
|
Term
| Verapamil and diltiazem - Clinical applications? |
|
Definition
| Prophylaxis of angina, HTN, others |
|
|
Term
| Verapamil and diltiazem - Pharmacokinetics, tox, interactions? |
|
Definition
| Oral and IV, 4-8 hr DOA, AV block, acute HF, constipation, edema, additive with other cardiac depressants and hypotensive drugs |
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Term
|
Definition
| Block of vascular L-type Ca channels > cardiac channels |
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Term
|
Definition
| Like verapamil and diltiazem but less cardiac effect |
|
|
Term
| Nifedipine - clinical applications? |
|
Definition
| prophylaxis of angina, HTN |
|
|
Term
| Nifedipine - pharmacokinetics, tox, interactions? |
|
Definition
| oral, 4-6 hr DOA, excessive hypotension, additive with other vasodilators |
|
|
Term
| How do other dihydropyridines differ from nifedipine? |
|
Definition
| slower onset, longer DOA - up to 12 h or more |
|
|
Term
|
Definition
| inhibits late Na current in heart, also may modify FA oxidation |
|
|
Term
|
Definition
| Reduces cardiac O2 demand, FA oxidation may improve efficiency of cardiac O2 utilization |
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|
Term
| Ranolazine - clinical applications? |
|
Definition
|
|
Term
| Ranolazine - pharmacokinetics, tox, interactions? |
|
Definition
| oral, 6-8 hr DOA, QT prolongation, nausea, constipation, dizzyness, inhibitors of CYP3A increase concentration and DOA |
|
|
Term
| What types of drugs should be used at the onset of unstable angina (ACS)? |
|
Definition
| Anti-platelet agents - eptifibitide, tirofiban - GP IIb/IIIa inhibitors |
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Term
| At high concentrations, nitrites can cause _______, which is helpful in _______. |
|
Definition
| methemoglobinemia (convert ferrous iron to ferric form), cyanide poisoning |
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|
Term
| Nimodipine is a member of which family? What is it approved for? |
|
Definition
| dihydropyridines, management of stroke assoc with subarachnoid hemorrhage |
|
|
Term
| How does Bepridil compare to verapamil? |
|
Definition
| Similar in structure, longer DOA but more cardio tox than other CCBs |
|
|
Term
| CCBs relax ______s and to a lesser extent the... |
|
Definition
| BVs, uterus, bronchi, gut |
|
|
Term
|
Definition
| torsades de pointes and other arrthymias |
|
|
Term
| What are the detrimental effects of B-blockers for angina? |
|
Definition
| Increased heart size, longer ejection period |
|
|
Term
| Should you use B-blockers during an acute attack? |
|
Definition
| No, they have no value for acute attacks |
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