High-yield Autonomics questions slide Flashcards
Cholinesterase inhibitors can be used for
atropine overdose as well as Alzheimer’s
Anti-muscarinic effects in CNS and heart also include
- sedation, delirium, amnesia
2. initial slight brady (from block of inhibitory presyn receptors) and then tachy (block of M2 receptors in SA node)
Anti-muscarinic effects on blood vessels include
- block of muscarinic vasodilation but not manifested unless muscarinic agonist is present (it blocks M3 receptors on endothelium of vessels)
The effects of tubo and mivacurium can be overcome with
acetylcholinesterase inhibitors and increased ACh at the synaptic cleft
To prevent diffusion of an NT away from the synaptic cleft, use a
vasoconstricting agent!!
To prevent BP spike from injection of tyramine, do what?
Tachyphylaxis (acute tolerance), so small cytoplasmic pool of NE is rapidly used up with repeated tyramine injections!!
Use of fenoldopam?
Hypertensive emergences (lower the blood presssure)
Alpha1 agonists like ____ can do what four things in particular?
Epi:
1. control hemorrhage 2. contain local anesthetic!!!! 3. Anaphylactic shock (can use alpha 1 and beta 2 properties) 4. Hypotension
For shock, what might you NOT want to give?
Alpha agonist (vasoconstrictor) because of risk of not getting perfusion to your organs
Side effects of alpha adrenergic agonists:
- Hypertension/headache
- Localized ischemia (alpha 1)
- Dramatic fall in BP with RAPID WITHDRAW
- Nervousness, anxiety, insomnia
___ agonists on what receptors in _____ can ____ central symp output; this will do what?
alpha2; NTS; decrease; decrease BP and treat hypertension!!!!!
The third generation non-selective beta blockers can also do WHAT?
Block alpha1 receptors allowing for vasodilation!!
Third-generation beta-selective blockers can also do what?
Block Ca channels and entry!!
What is a difference between metoprolol and propanolol in terms of bioavailability?
More dramatic differences in individual bioavailability due to first pass metabolism and plasma protein binding
Least lipid soluble beta blocker is
atenolol (not much CNS activity)
Proposed mech’s for how beta blockers treat hypertension include:
Blocking of renin release, pre-syn beta1 receptors inhibited, blocking alpha1 receptors, blocking Ca entry, opening K channels
What could be potentially used to treat a migraine besides the ergot alkaloids and the triptans?
Something like propanolol!!
What beta blockers should be used to treat CHF???
ONLY second and third gen!!!
What is a possible explanation for ____ tachycardia and ____ hypotension with prazosin than the non-selective alpha blockers?
less; postural; Because you have LESS NE RELEASE!! If you don’t block the alpha 2 receptors, which would contribute to less NE release, then you can still control NE release and also block alpha 1 receptors which would mean minimal tachy and also treating the hypertension
Prazosin can be used to treat
Raynaud’s and frost bite (peripheral vascular disease)
Who might you not want to give a beta blocker (beta2) to?
Hypoglycemic patient or a diabetic patient on insulin (decreased glycogenolysis and lipolysis in response to hypoglycemia)
Ephedrine for nasal decongestants could lead to
an increase in HR (alpha1 and vasoconstriction)
Giving someone a MAO inhibitor and then she eats fermented foods, what are you worried about?
SEVERE HYPERTENSION; because tyramine is in the fermented foods and instead of NE being metabolized by liver and other organs with MAO, it runs rampant!!
