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
- Why can ephedrine (mixed indirect & direct acting alpha & beta adrenergic agonist) result in more insomnia than epinephrine (direct acting alpha & beta adrenergic agonist)?
a. Ephedrine is a noncatecholamine, thus it can cross the BBB, whereas epinephrine (a
catecholamine) cannot
b. Ephedrine, since it acts indirectly & directly, is more potent
c. Ephedrine has a higher affinity for CNS adrenergic receptors than epinephrine
d. Ephedrine doesn’t agonize alpha2, which normally would result in decreased SNS outflow from the CNS
a
Indications for epinephrine and ephedrine
bronchoconstriction d/t asthma,
acute allergic rxn,
cardiac arrest,
decreased myocardial contractility (post-cardiac surgery)
Cautions for epinephrine and ephedrine
can cause tachydysrthmias
Cautions for Norepinephrine
Risk for metabolic acidosis (not removing waste products)
A1 vasoconstriction is unopposed (since B2 is not acted on which would usually dilate skeletal muscle, lungs, coronaries)
risk for tissue necrosis if extravasion
indications for Norephinephrine
severe hypotension
Side effects of norepinephrine
decreased respiration,
decreased HR bc of barroreceptor reflex
risk for metabolic acidosis
cautions for dopamine
dangerous local vasoconstriction if IV infiltrates
effects of phenylephrine (including side effects)
vasoconstriction with no HR or contractility agonism (those would be B1), bc of barroreceptor reflex this could lead to decreased HR
Risks of clonidine/Dexmedetomidine
risk for bradycardia
Indications/difference for albuterol and terbutaline
Albuterol is preferred for asthma induced brochospasm, and is inhaled
Terbutaline is for asthma or pre-term labor and can be given PO, Sub-q or inhaled
Side effects of albuterol
tachycardia, tremors (hypokalemia in large doses)
Side Effects of Labetalol and carvedilol
orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia
Indications for Labetalol and carvedilol use
tachycardia with high grade HTN
indication for Phenoxybenzamine
pheochromocytoma
How and what receptors does Phenoxybenzamine interact with?
antagonists a1 and a2
Indications for Metroprolol, esmolol, atenolol.
asthma with tachycardia/HTN
Effects for Metroprolol, esmolol, atenolol.
decreased HR,
decreased contractility
decreased AV node conduction
Contraindications for for Metroprolol, esmolol, atenolol.
bradycardia, hypotension, heart block
What is different about atenolol.
out of Metroprolol and esmolol it is the most cardio-selective Beta blocker, making it useful for pts with CAD
contraindications of Atropine
glaucoma
indications for Atropine
severe bradycardia
small dose can cause decreased secretions
bronchodilation (less PNS involvement)
What receptors does Scopolamine act on? Agonize or antagonize?
Major pharmacologic effects
difference from other drugs in class
muscarinic antagonist
sedation???, mydriasis, sea sickness prevention
What receptors does Glycopyrrolate act on? Agonize or antagonize?
Major pharmacologic effects
difference from other drugs in class
muscarinic antagonist, does not cross BBB, so only peripheral effects (quaternary ammonium)
What receptors does Ipratropium act on? Agonize or antagonize?
difference from other drugs in class/indications
muscarinic antagonist,
used in the treatment of asthma/COPD
What is the difference between Neostigmine and Pyridostigmine?
While both are Ach inhibitors, used for myasthenia gravis, and NMB reversal, Neostigmine can also be used to increase gut motility and Pyridostigmine can be used for glaucoma.
Contraindications to Succinylcholine
ESRD (bc kidneys can’t process transient hyperkalemia)
