ANS Flashcards
Can we give epinephrine PO? Why or why not?
No, since it has a short half life, and since it is a catecholamine, it is degraded in the liver, meaning most of it would never enter the bloodstream if given PO
Where are MAO and COMT located?
MAO: Mostly presynaptic terminal
COMT: Mostly liver, some free
What is the difference between Catecholamines and noncatecholamines?
The half life of catecholamines is much shorter due to COMT and MAOs, so they cannot be given PO. Non-catecholamines can be given PO and can cross the BBB while catecholamines cannot. Catecholamines are reuptaken into the presynaptic cleft (MAO here, some COMT), while non-catecholamines are broken down in the liver
Which receptors does Dobutamine interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects?
B1, A1 at high doses
Inotrope - increases cardiac contractility w/o increasing HR or BP much- used in CHF
dilates coronary arteries
Synthetic catecholamine
Agonist
Which receptors does Isoproterenol interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects? What are cautions for this medication?
“Chemical pacemaker”
Synthetic catecholamine
Agonist of beta 1 and 2 equally
effects of increased HR and contractility, when combined with CAD can lead to an MI
Which receptors does Dopamine interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects? Main indication
dopaminergic, also B1 in high concentrations and B2 in even higher concentrations, in highest concentrations a1 agonist
Dose dependent actions:
low renal dose: dilation of renal, splanchnic and cerebral arteries
slightly higher dose: increased contractility without increased HR, vasodilation (and renal dose effects)
high dose: vasoconstriction (main indication is hypotension)
Which receptors does Ephedrine interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects? How is this one different?
blocks NE reuptake, A1, A2, B1,
indirect acting agonist, can cross the BBB
Which receptors do Labetalol and Carvedilol interact with? Do they agonize or antagonize these receptors? What are the major pharmacologic effects?
“Adrenergic antagonist”
B1=B2, also hits alpha receptors in large doses
Antagonist
Vasodilation, decreased HR, decreased BP, CO uneffected
Which receptors does Phentolamine interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects?
A1=A2
Antagonist
HTN emergencies – causes vasodilation, decrease BP and increased HR
Extravasation – help reverse extreme constriction if norepinephrine extravates
Which receptors does Prazosin interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects/side effects?
A1 antagonist selective
Effects: vasodilation, prostate relaxation
Orthostatic hypotension, reflex tachycardia d/t lower BP
Also treats BPH!
What are the pharmacologic effects of drugs that:
antagonize M
ACh inhibitors
antagonize and agonize Nm
M antagonists and Ach inhibitors block PSNS activity
Muscarinic antagonists to control overactive bladder
Drugs that both antagonize and agonize Nm don’t have a lot of clinical application
Drugs that antagonize Nm and their effects
rocuronium, vecuronium; prevent muscle contraction, flaccid paralysis
Which of the following drugs is an endogenous catecholamine that increases the release of norepinephrine?
a. Dopamine
b. Albuterol
c. Prazosin
d. Atropine
a- dopamine
Which beta blocker would be the best choice for a patient who suffers from asthma?
a. Albuterol
b. Nadolol
c. Betaxolol
d. Metoprolol
C, at higher doses an asthma attack is possible with metoprolol
Your patient is really on top of their medical care. They know all their medications & even take their BP, HR, and weight daily at home! For the last week or so, they’ve noticed
their HR dropping to the 40s. Thus, they stopped taking their beta blocker. What are they at greater risk of?
a. AV heart block
b. Myocardial infarction
c. Hypotension
d. Bronchoconstriction
B- MI
Normally this pt would have a much lower HR contractility and conduction bc of beta blocker. While on beta blocker, receptors upregulated, so if the beta blocker is stopped, the HR, contractility and conduction will overwhelmingly increase. The heart would then need increased O2 bc it is beating harder and faster, causing a possible MI.
Your severely asthmatic patient comes to you on their way out of clinic with concerns because the provider just prescribed them metoprolol, a beta antagonist, and they have always been told to not take a beta blocker with their asthma. What is your first course of action?
a. Have them wait in the waiting room while you consult with their provider
b. Advise them to make another appointment with a different provider for a second opinion
c. Teach them how this medication won’t affect their asthma
d. Tell them to just take their albuterol (B2 agonist) when they take their metoprolol
C - Metropol is a beta 1 blocker, the beta receptors in the lungs are beta 2
- Why is atropine (an anticholinergic) not used for hypotension?
a. There are no muscarinic receptors on vasculature
b. It causes too much constipation and urinary retention
c. The drug is too potent; effects would result in hypertension
d. The muscarinic receptors on vasculature aren’t innervated
D – nothing is dumping NTs on them anyway
