B1 specific blockers Flashcards
reduced side effects of B1 selective blocker
no B2 blockage:
- reduced risk of hypoglycemia as they don’t block glycogenolysis
- better exercise tolerance because they don’t block the dilation of blood vessels in skeletal muscle
B1 selective blocker that can cause T2DM
atenolol
B1 selective blockers (2) that aren’t atenolol but were grouped with it idk
metoprolol
bisoprolol
B1 selective blockers: COPD and asthma
COPD: proceed with caution
Asthma: still no, drug of last choice
drug that is less likely than timolol to cause bronchoconstriction in the tx of glaucoma
betaxolol
beta blocker which also produces dilation by increasing NO release
nebivolol
the most selective B1 drug
nebivolol
advantages to nebivolol
- lower BP without depressing left ventricular function
2. decreases central aortic pressure better
B1 specific antagonist with short duration of action, like less than 20 mins
esmolol, gotta give it IV
why esmolol so short acting
hydrolyzed by esterases in RBC
who esmolol is useful for
continuous IV drip in a pt who you might want to remove the beta blocker effect rapidly: CHF, bradycardia, hypotension
intrinsic sympathetic activity (ISA) means
partial agonists
selective B1 antagonists with intrinsic activity
acebutolol
drugs with ISA are thought to
produce less bradycardia, affect glucose/lipids less
B blockers with ISA treat
angina, htn
beta blocker with ISA and no other info
pindolol
less likelihood of systemic affects when treating glaucoma beta blocker with ISA
carteolol
labetolol blocks
B1, B2, some a1
labetolol/carvedilol effects
a1 decreases BP
B1 prevents increases in HR, less tachycardia than a1 blockage alone
hypertensive emergency drug
labetolol
carvedilol blocks
non-selective beta and a1
carvedilol treats
htn (w/o causing tachycardia)
improved mortality CHF
why does carvedilol help CHF
decreases free radicals and inhibits vascular smooth muscle mitogenesis
???
2 a2 agonists for glaucoma
apraclonidine
brimonidine
guanethidine MOA
inhibits release of NE from presynaptic nerve terminals, replaces NE, causing it to be depleted —> complete loss of sympathetic activity
drugs that prevent guanethidine from working
cocaine
tricyclic antidepressants
reserpine MOA
interferes with uptake and storage of biogenic amines in nerve terminals —> depletes NE, DA, serotonin. similar effects to methyldopa
metyrosine MOA
tryosine analogue blocks tyrosine hydroxylase (rate limiting step) —> no DA, Epi, NE
metyrosine is used to treat
pheochromocytoma in combo with phenoxybenzamine
