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Pharm Review CNS
Questions Review of CNS
| Questions | Answers |
|---|---|
| Major neurotransmitter released at end organ effectors of the thoracolumbar division of the autonomic nervous system: | norepinephrine |
| Neurotransmitter of preganglionic fibers | acetylcholine |
| "Fight or flight" activation of the ANS: | blood flow shifted from cutaneous beds to skeletal muscle |
| Dopamine beta hydroxylase catalyzes: | dopamine to norepinephrine |
| Most potent at beta adrenergic receptors | isoproterenol (Isuprel) |
| Powerful agonist at both alpha and beta adrenergic receptors | epinephrine |
| Predominant autonomic tone: | salivary glands: parasympathetic |
| Positive inotropic drug that at low doses specifically promotes an increase in renal blood flow: | dopamine (Intropin) |
| Preganglionic fibers terminating on adrenal medullary chromaffin cells release: | acetylcholine |
| Primary receptor type at autonomic ganglia: | cholinergic: nicotinic |
| Enzyme responsible for acetylcholine synthesis: | choline acetyltransferase |
| Cholinergic receptor type that mediates the decrease in heart rate: | muscarinic |
| Effect of atropine on the heart: | increased rate |
| Drugs activating this receptor are used in treating asthma: | beta2 adrenergic |
| Epinephrine effects on the heart: | coronary vasodilation |
| Receptor activation mainly responsible for positive inotropism: | beta1 |
| Epinephrine effects by the increased rate of the: | heart |
| Epinephrine effects on respiration: | stimulation |
| Activates alpha receptors: | phenylephrine (Neo-Synephrine |
| Orthostatic (postural) hypotension: | alpha receptor blocker |
| Norepinephrine pressor response blocked by: | prazosin (Minipress) |
| Bronchodilation | albuterol (Ventolin,Proventil),ipratropium (Atrovent) |
| Positive chronotropic effects of epinephrine: | beta1 receptor activation |
| Most likely to increase myocardial afterload: | phenylephrine (Neo-Synephrine) |
| Decreases blood pressure: | propranolol (Inderal |
| Prevents blood pressure reduction seen with isoproterenol (Isuprel): | propranolol (Inderal) |
| Beta-2 selective agonist: | (blank) |
| Physiological effects associated with isoproterenol (Isuprel): | increased blood glucose |
| Immediate biosynthetic precursor of epinephrine | norepinephrine |
| Isoproterenol (Isuprel): cardiopulmonary effects: | increases peripheral resistance |
| cardiopulmonary effects of Isoproterenol (Isuprel): | positive chronotropism |
| Drug causes pupillar dilation with no effect on accommodation: | (blank) |
| Albuterol (Ventolin,Proventil): | bronchodilation |
| sympathomimetic; at low doses: increases renal blood flow: | dopamine |
| beta-1 selective receptor blocker: | metoprolol (Lopressor) |
| Effective in reversing respiratory and cardiovascular effects of anaphylactic shock: | eprinephrine |
| Major neurotransmitter at sympathetic nerve endings: | norepinephrine, noradrenaline |
| The action of sympathomimetic drugs on the liver causes an increase in blood glucose levels by a process called: | glycogenolysis |
| Alpha receptor activation of this eye muscle causes mydriasis: | (blank) |
| Direct sympathetic effects on the heart are mediated by this receptor type: | beta repeptor |
| The dominant autonomic tone in the heart is: | parasympathetic, cholinergic, acetylcholine |
| Major neurotransmitter at autonomic ganglia: | nicotinic, acetylcholine |
| This drug increases heart rate, contributing to increase blood pressure: | Epinephrine |
| alpha-1 adrenergic receptor-mediated affecting precapillary resistance vessels of the skin, kidney, and mucosa | Vasoconstrictive effects of epinephrine |
| Rapid administration of epinephrine, with resulting significant systolic pressure elevation will cause this effect on heart rate: | decrease in heart rate |
| A decrease in diastolic pressures associated with epinephrine administration would most likely occur in which dosage? | relatively low doses |
| Renal effects relatively low epinephrine dose: | Renal effects relatively low epinephrine dose |
| Most probable BP effect of epinephrine, if epinephrine is administered after an alpha-receptor antagonist: | decreased blood-pressure response to epinephrine |
| Prominent cardiac beta-adrenergic receptor type: | beta-1 |
| Significant respiratory tract effects of epinephrine: | beta-2 receptor-mediated bronchodilation |
| Examples of epinephrine metabolic effects | free fatty acids: increased |
| Epinephrine effects on AV nodall conduction: | increased conduction velocity |
| Major adrenergic effects on skin/mucosa arteriole vascular beds: | constriction |
| beta-2 adrenergic receptor mediated effects on skeletal muscle arteriole vasculature: | dilation |
| Alpha-adrenergic effects on pulmonary arterioles: | constriction |
| Beta-adrenergic effects on pulmonary arterioles: | dilation |
| Alpha-adrenergic effects on renal arterioles: | constriction |
| beta-2 adrenergic receptor effects on systemic veins: | dilation |
| Major alpha-adrenergic receptor effect on renin secretion: | decrease |
| Decreases bronchial gland secretion: | alpha-1 adrenergic |
| Primary neurotransmitter released by postganglionic neurons of the autonomic sympathetic system: | norepinephrine |
| Decreased heart rate following norepinephrine infusion is most likely due to: | activation of the baroreceptor system causing a reflex-mediated decrease in heart rate |
| Vascular effects of norepinephrine (Levophed): | norepinephrine pressor effects blocked by prazosin (Minipress) |
| Immediate synthetic precursor of norepinephrine: | dopamine |
| CNS neurotransmitter associated with the basal ganglia and motor control: | dopamine, acetylcholine |
| Low doses, this precursor of norepinephrine causes renovascular dilation: | dopamine (Intropin) |
| Significant therapeutic use for dopamine: | treatment of cardiogenic/hypovolemic shock |
| Has limited action at alpha-adrenergic receptors: | isoproterenol (Isuprel) |
| Adverse effects associated with isoproterenol (Isuprel) administration: | arrhythmias, tachycardia, palpitations, palpitations |
| Cardiovascular characteristics of patients who might benefit from IV dopamine (Intropin) administration: | high urinary output |
| Simultaneous increases in myocardial contractility, glomerular filtration rate, sodium excretion, urine output, and renal blood flow are associated most likely with: | dopamine (Intropin) |
| IV dopamine (Intropin) properties: | causes reduced ventilatory response to arterial hypoxemia |
| Properties of dobutamine (Dobutrex): | positive inotropic effect is mediated through beta-adrenergic receptor activation |
| Examples of beta-2 selective adrenergic agonists: | albuterol (Ventolin,Proventil) |
| Primary use for alpha-2-selective adrenergic agonists: | to reduce blood pressure |
| Major mechanism of antihypertensive effects associated with alpha-2-selective adrenergic agonists: | reduced sympathetic outflow |
| Primary objective sympathomimetic drug use for management of shock: | ensure adequate CNS perfusion |
| Most likely to reduce myocardial performance in a damaged heart by increasing afterload: | phenylephrine (Neo-Synephrine) |
| Receptor system most likely responsible for improved myocardial contractility when dopamine is administered at low concentrations: | dopamine receptors (D1) |
| Beta-adrenergic receptor blockers: effects on the heart: | increased AV nodal refractory period |
| Beta-adrenergic receptor blockers are usually effective in reducing blood pressure in both " high-renin" and "low-renin" patients: | true |
| Most likely to cause dangerous bronchiolar constriction in asthmatic patients or patients with COPD | propranolol (Inderal)l |
| Mechanism(s) for propranolol-decreased amide local anesthetic clearance: | decreased hepatic blood flow |
| Choline ester most susceptible to hydrolysis by acetylcholinesterase: | acetylcholine |
| Associated with parasympathetic activation (direct effects): | decrease cardiac contractility |
| Muscarinic agent: enhances transmission through the A-V node: | atropine |
| Least likely to be used as a mydriatic because of long-duration of action: | atropine |
| Clinically-used to treat sinus bradycardia secondary to acute myocardial infarction: | atropine |
| Reflex bradycardia secondary to an abrupt increase in blood pressure may be blocked by: | atropine |
| Location(s) of cholinergic synaptic sites: | neuromuscular junction, some CNS synapses |
| Cholinergic receptor type primarily localized at skeletal muscle neuromuscular junctions: | nicotinic |
| Highly sensitive to the action of acetylcholinesterase: | acetylcholine |
| Muscarinic receptor subtype primarily associated with the heart: | M2 |
| Cardiac muscarinic Type M2-receptor mediated action(s): | Decreased atrial and ventricular contractility |
| Tends to cause fast responses: | (blank) |
| Cholinergic-mediated vasodilation involves liberation of this substance, a gas, from endothelial cells: | nitric oxide |
| Dominating autonomic tone in the ventricle: | sympathetic |
| Mydriasis without loss of accommodation | sympathomimetic |
| Management of severe bradycardia and A-V block associated with acute myocardial infarction: | atropine |
Created by:
Nerd