Misc Sweatman Pharm Flashcards
Did these quickly as I studied, sorry if some are bizzarre half-thoughts
Effects of beta-1 and -2 receptor activation?
accelerates SA node, increases contractility, accelerates ectopic pacemakers IN HEART
Effects of alpha-1 receptor activation?
contract vessels by increasing DAG and IP3, which results in an increase of Ca++
What receptors act via NE?
alpha 1, alpha 2, beta 1
What receptors act via epi?
alpha 1, alpha 2, beta 1, beta 2
What receptor would you block to treat BPH?
alpha 1
What class of drugs cause 1st dose orthostatic hypotension? What specific drug is the most prominent?
alpha blockers
prazosin
Effects of alpha 2 receptors?
decrease cAMP production, which blocks further release of NE (feedback inhibition)
Effects of alpha-1 antagonists?
antagonist circulating NE and epi, which prevents vasoconstriction
Effects of alpha-2 antagonists?
block feedback inhibition, which increases NE release
increases CO, “tempering” BP lowering
Treatment for pheochromocytoma?
phenoxybenzamine
phentolamine
(alpha blocker)
Why does phenoxybenzamine cause nasal congestion and drowsiness?
minor action = blocking histamine, serotonin and ACh
What treats hypertensive emergency?
phentolamine
What is the difference between a small versus a large dose of alpha 2 antagonist?
small: increases BP
large: decrease BP (due to periph vasodil)
What limits the use of phentolamine in essential HTN?
postural hypotension, reflex tach ppt arrhythmias
Epi causes (increased/decreased) BP); treatment with an alpha blocker will.... Treatment with a beta blocker will...
increased BP
decrease BP
no effect
NE causes (increased/decreased) BP; treatment with an alpha blocker will.... Treatment with a beta blocker will...
increased BP
slight decrease in BP
no effect
What drug class affects renin release?
B1 agonists (on JG cells)
Intrinsic sympathomimetic activity?
pure: propranolol
partial:
pindolol
Drugs with membrane stabilizing ability?
propranolol
cervedilol
class 1 antiarrhythmics
How do drugs stabilize membranes?
bind/block fast Na channels which are responsible for rapid depol (decrease phase 0 slope)
What is intrinsic sympathomimetic activity?
activate receptors in the absence of catecholamines
What is inverse sympathomimetic activity?
selectively bind to inactive form of receptor and behave like competitive antagonists (“off”)
B antagonists that block Ca entry:
What does this do?
carvedilol
betaxolol
prevents contraction
B antagonist that produces NO:
nebivolol
B antagonists that are also a-1 R antagonists?
carvedilol
labetolol
B antagonist that has antioxidant activity?
carvedilol
What results from long term administration of beta blockers?
drop in peripheral vasc resistance
Beta blocker with no effect on renin? Most effective if elevated renin?
pindolol
propranolol
What effect does lipid solubility have on antihypertensives?
drugs that do NOT penetrate BBB (low sol) are effective anti-HTN
Who should NOT take beta blockers?
patients with:
- compensated HF, acute MI, cardiomeg
- AV conduction defects, as these drugs cause bradycardia
- bronchospastic disease (due to bronchoconstriction via beta-2)
Beta blockers should not be stopped abruptly because:
they can exacerbate angina and increase risk of sudden death (receptors are upregulated)
Lipophilic beta blockers may cause:
CNS depression, causing mental disorders, fatigue, vivid dreams
How do beta blockers affect plasma lipids?
increase triglycerides
decrease HDL
What type of beta blockers reduce cholesterol and LDL?
those with intrinsic sympathomimetic activity and cardioselectivity
Activation of what receptors mediates lipolysis?
alpha1
beta 1, 2, 3
What is the effect of using beta blockers post MI?
improved mortality
Non-CV uses for beta blockers?
tremor thyrotoxicosis anxiety migraines prevent bleeding from esoph varices glaucoma
Effects of ganglionic blockade on arterioles?
vasodilation
hypotension
Effects of ganglionic blockade on veins?
dilation/pooling
decreased venous return/CO
Effects of ganglionic blockade on heart?
tachycardia
Nicotinic receptors are ______ channels which mediate
post-synaptic ligand gated ion initial EPSP (caused by Na/K)
MOA of trimethaphan:
competes with ACh for ganglionic receptor binding
Causes dry mouth, vision problems, urinary retention, constipation?
ganglionic blockers
MOA of reserpine:
binds to NT storage vesicles and inhibits vesicle transporter VMAT2
=no storage/concentration of dopamine and NE