03b: Adrenergic Drugs Flashcards
List the adrenergic receptor subtypes that act by cAMP as second messenger. Star those that decrease its production.
- Alpha-2*
- Beta 1 and 2
- D1
NE is synthesized from (X) and broken down either in synaptic cleft or in terminal by (Y).
X = Tyr Y = MAO
Phenylephrine is a(n) (X)-selective (agonist/antagonist).
X = alpha1-R
Agonist
Clonidine is a(n) (X)-selective (agonist/antagonist).
X = alpha2-R
Agonist
Isoproterenol is a(n) (X)-selective (agonist/antagonist).
X = beta-R
Agonist
Dobutamine is a(n) (X)-selective (agonist/antagonist).
X = beta1-R
Agonist
Albuterol is a(n) (X)-selective (agonist/antagonist).
X = beta2-R
Agonist
Alpha receptors are more sensitive to (Epi/NE).
Epi
Alpha receptors are more sensitive to (Isoproterenol/NE).
NE
Beta receptors are more sensitive to (Isoproterenol/NE).
Isoproterenol
Alpha receptors are more sensitive to (phenylephrine/isoproterenol).
Phenylephrine
(X) agonist could be given to (increase/decrease) renin release by acting on (alpha/beta) receptor.
X = dobutamine
Increase;
Beta1
(X) agonist could cause (mydriasis/miosis) by acting on (alpha/beta) receptor.
X = phenylephrine
Mydriasis;
Alpha1
Main effect of dopamine action on D1 receptor:
Dilates renal vasculature
T/F: Epi is relatively non-selective between alpha and beta receptors.
True
NE has greatest effect on (X) receptor and least effect on (Y). List receptors in order of NE’s preference.
X = alpha1 Y = beta2
alpha1, alpha2, beta1, beta2
Dopamine activates which (alpha/beta) receptor(s)?
Beta1 (more than), alpha1
T/F: Selectivity equals specificity.
False - absolute selectivity is specificity
T/F: Epi action on beta2 and alpha1 receptors is the same (contraction)
False - relaxation via beta2
At high Epi conc, (alpha/beta) receptor effect of (X) will predominate. Why?
Alpha1;
X = contraction
There are greater number of these receptors
Under normal conditions, administration of NE will cause (increase/decrease) in BP and (increase/decrease) HR. Which receptor/messenger account for this?
Increase; decrease
Vagal reflex; ACh via M2
T/F: Admin of NE and Epi will have same effect on HR.
False - Epi increase HR since alpha1 vasoconstriction and beta2 vasodilation about equal (stable MAP, no vagal reflex)
A moderate dose of isoproterenol will (increase/decrease) MAP and BP because:
Decrease;
Beta2 vasodilation outweighs beta1 increase HR
(X) is drug found in nasal decongestants. It targets (Y) receptors to counter/minimize (Z) effect.
X = phenylephrine Y = alpha1 Z = dilation/engorgement (of nasal mucosa blood vessels)
(X) drug commonly used to extend local anesthetic action. What’s the mechanism?
X = epi
Alpha1-R (vasoconstriction) reduces drug absorption
After cardiac arrest, (X) drug used for resuscitation purposes, targeting (Y) receptors.
X = epi Y = alpha1 and beta1
Adrenergic (agonists/antagonists) are used to treat wide angle glaucoma. (X) receptors for (vasoconstriction/vasodilation). (Y) receptors to (increase/decrease) fluid secretion.
Agonists; X = alpha1 Vasoconstriction Y = alpha2 Decrease
Adrenergic (agonists/antagonists) are used to delay labor by:
Agonists;
beta2 relaxation of uterine smooth muscle
T/F: Adrenergic agonists are used to treat opioid withdrawal.
True
(Cholinergic/Adrenergic) (agonists/antagonists) used to treat ADD.
Adrenergic agonists
Acute treatment of anaphylaxis is (X). List receptors targeted and why.
X = epi
- Alpha1 (vasoconstriction to elevate BP and suppress glottal edema)
- Beta1 (increase CO to elevate BP)
- Beta2 (counteract bronchoconstriction)
T/F: Adrenergic agonists, via vasoconstriction, can reduce risk of cerebral hemorrhage.
False! Toxicity of these drugs can cause hypertensive crisis and cerebral hemorrhage
List some effects of adrenergic agonist toxicity on the heart.
- Tachycardia
- Myocardial ischemia
- Arrhythmias
Adrenergic agonist toxicity may cause (hypo/hyper)-glycemia because (X) receptor activation promotes:
Hyperglycemia;
X = beta2 (in liver and skeletal muscle)
Glycogen to glucose conversion
Indirect-acting sympathomimetics general mechanism of action.
Increase availability of endogenous adrenergic transmitters
List examples of indirect adrenergic agonists that (increase/decrease) (epi/NE) release.
Increase NE release;
- Tyramine
- Ephedrine
- Amphetamine
(X) drug present in cheese, red wine, and (small quantities) in gut. If (Y), the enzyme that degrades it, is inhibited, individual is in danger of (Z).
X = tyramine Y = MAO Z = hypertensive crisis (too much NE released from terminals)
(X) can be converted to (Y), which is a “false transmitter”. It replaces (Z) in nerve terminals and can be released, but has little action on receptors.
X = tyramine Y = octopamine Z = NE
List two examples of indirect adrenergic agonists used for ADHD meds.
- Methylphenidate
2. Dextroamphetamine
T/F: Both ephedrine and pseudoephedrine use has been FDA-restricted due to adverse effects.
False - pseudoephedrine widely used OTC decongestant
Tricyclic antidepressants fall into (X) class of drugs. They function to (increase/decrease) (Y) messengers via which mechanism?
X = indirect adrenergic agonists
Increase
Y = NE and DA
Inhibit reuptake
T/F: Cocaine and tricyclic antidepressants function via the same mechanism of action.
True (inhibit NE, DA reuptake)
(X) is example of direct neuronal blocker. It depletes NE stores by inhibiting (Y).
X = reserpine Y = vesicular monoamine transport within synapse
Phentolamine falls into which class of drugs? Which receptor targeted?
Adrenergic (alpha receptor) antagonist
Prazosin falls into which class of drugs? Which receptor targeted?
Adrenergic (alpha1 receptor) antagonist
Propranolol falls into which class of drugs? Which receptor targeted?
Adrenergic (beta receptor) antagonist
Metoprolol falls into which class of drugs? Which receptor targeted?
Adrenergic (beta1 receptor) antagonist
Carvedilol falls into which class of drugs? Which receptor targeted?
Adrenergic (alpha1 and beta receptor) antagonist
Treatment of pheochromocytoma: (X) receptors (activated/blocked) first, then (Y) receptors.
X = alpha1
Blocked
Y = beta (also blocked)
Raynaud’s disease would be treated with adrenergic (agonist/antagonist).
Antagonist (reduce digital vasoconstriction)
BPH is treated with (cholinergic/adrenergic) (agonist/antagonist).
Adrenergic antagonist
Salt/water retention and edema could be side effect of adrenergic (agonist/antagonist) drugs. Briefly explain
Antagonist (reflex beta1-R stimulation of renal RAS system)
Adrenergic alpha-R antagonists are used to treat heart failure via which mechanism?
Reduce vascular resistance
Adrenergic beta-R (agonists/antagonists) are used to treat hypertension via which mechanism?
Antagonists;
Reduce CO and inhibit renin production
(Cholinergic/adrenergic) (agonists/antagonists) targeting (X) receptors are used to treat migraine prophylaxis.
Adrenergic antagonists;
X = beta
List examples of reflex effects that arise from postural hypotension.
- Reflex tachycardia
- Myocardial ischemia (increased O2 demand from tachycardia)
- Peripheral edema
(X) (agonists/antagonists) are used to treat BPH since they (contract/relax) bladder neck.
X = alpha-1R
Antagonists;
Relax
(X) (agonists/antagonists) used to treat open-angle glaucoma.
X = betaR
Antagonists