Medical Pharmacology Practice Questions: Autonomic, adrenergic drugs and Management of Hypertension

Major mechanism of antihypertensive effects associated with alpha-2-selective adrenergic agonists:
1. competitive inhibition of vascular alpha receptors
2. reduced sympathetic outflow
Alpha-2-selective adrenergic agonists: examples
1. isoproterenol (Isuprel)
2. metaraminol (Aramine)
3. dopamine (Intropin)
4. dobutamine (Dobutrex)
5. guanabenz (Wytensin)
Adverse effects associated with clonidine (Catapres):
1. dry mouth
2. sedation
3. sexual dysfunction
4. all of the above
Clinical uses for sympathomimetic drugs:
1. hypovolemic shock caused by dehydration or blood loss
2. cardiogenic shock (pump failure)
3. cardiac output obstruction
4. loss of peripheral vascular tone
5. all of the above
Primary objective sympathomimetic drug use for management of shock:
1. increase myocardial contractility
2. decreased peripheral resistance
3. promote better renal perfusion
4. ensure adequate CNS perfusion
5. improve coronary perfusion
Most likely to reduce myocardial performance in a damaged heart by increasing afterload:
1. isoproterenol (Isuprel)
2. phenylephrine (Neo-Synephrine)
3. low-dose dopamine (Intropin)
4. low-dose epinephrine
Receptor system most likely responsible for improved myocardial contractility when dopamine is administered at low concentrations:
1. muscarinic cholinergic receptors
2. alpha adrenergic receptors
3. beta adrenergic receptors
4. dopamine receptors (D1)
5. leukotriene receptors
Reasonable intervention(s) to reverse cardiogenic shock caused by acute myocardial infarction
1. supplemental oxygen
2. IV nitroglycerin
3. intra-aortic balloon pump
4. revascularization
5. all of the above
Phosphodiesterase inhibitor(s) which have positive inotropic actions; might be used in management of cardiogenic shock
1. phentolamine (Regitine)
2. nitroglycerin
3. amrinone (Inocor)
4. clonidine (Catapres)
5. caffeine
Mechanism by a which methoxamine might terminate paroxysmal supraventricular tachycardia:
1. direct action at the AV node
2. increases SA nodal rates -- overdrives the ectopic focus
3. blocks beta-1-receptors
4. causes increased vagal tone through reflex activation -- secondary to increase blood pressure
5. directly inhibit sodium channel conductance