Pharm Fall Ii Adrenergic Antagonists

Front 1

what are the 2 a receptor blockers

Back 1

phentolamine
phenocybenamine

Front 2

what are hte a1 blockers

Back 2

-azosin

prazosin
Terazosin
Doxazosin
tamsulosin

Front 3

what are the -azoin drugs

Back 3

the selsctive a1 blockers

dont forget tamsulosin

Front 4

what are the b blockers

Back 4

olol

Propanolol
Timolol

*the B1 selsctive are also olol

Front 5

what are hte b1 blockers

Back 5

olol (not propanolol, timolol)

b1
Metoprolol
Atenolol
Esmolol
Betaxalol
Nebivolol

Front 6

what are the olols

Back 6

b blockers

Front 7

what are the b blockers that havei ntrinsic sympathetic activity

Back 7

pindolol
acebutolol

Front 8

what are the b/a blockers

Back 8

labetalol
carvedilol

Front 9

what inhibits synthesis of NT

Back 9

metyrosine

Front 10

what drugs affect NT release

Back 10

guanethidine
reserpine

Metyrosine- inhibits synthesis

Front 11

whats the dif btwn phentolamine and phenoxybenzamine

Back 11

both are a blockers

Pentolamine is reversible
Phenoxybenzamine is irreversible

Front 12

what happens in general when a drug blocks both a1 and a2

Back 12

b receptor effects dominate

*a2 normally inhibits NE release, when a2 no longer works NE release in unmodulated and B effects are even more prevalent

Front 13

in general the effects of adrenergic blockers are most prevaent where

Back 13

heart

Front 14

a1 stim does... (4 major)

so blocking causes...

Back 14

1. Vasoconstriction
2. dilation
3. decreased GI motility, sphincters contract
4. ejaculation
5. nasal constriction, decongestant

when BLOCKED
1. dilation, decreased BP
2. orthostatic hypotension due to lack of BV tone
3. miosis
4. urinary ease
5. inhibit ejaculation
6. nasal congestion

Front 15

a2 stim does...

so blocking causes

Back 15

1 decrease NE, decrease SNS output

Blockade
1. increase NE release, increase SNS output
2. increase BP

Front 16

B1
B2
B3 causes....


so blockade causes

Back 16

B1- increase renin, increase HR, CO
B2- bronchoconstriction, increase CO, HR, glycogenolysis, increased intraocular pressure
B3. lipolysis

Blockade...

1. Decreased O2 demand, decreased HR/CO
2. Decrease renin (decrease BP over time)
3. bronchoconstriction
4. inhibit lipolysis, glycogenolysis
5. decrease intraocular pressure

Front 17

what R and mech decreases BP with b blockers

Back 17

well its kinda bc HR decreases but more importantly b1 no longer causes renin release so we have decreased BP from decreased renin

Front 18

what is the only non competative alpha blocker, what are all of the others

Back 18

phenyoxybenzamine

*all others are competitive reversible antagonists (phentolamine, prazosin,)

Competetive: Vmax, max effect, is the same. curve shifts right
Irreversible: Max effect is decreased

Front 19

what are the cardo effects of a blockade

Back 19

1. decreased BP, decreased constriction of a1
2. postural hypotension
3. reflex tachycardia
-decreased BP stim baroreflex to decrease vagal tone
-a2 block will increase NE release, NE can stim b1 to increase HR
4. Epi reversal: epi with a blocker means b effects dominate. BP is decreased. now epi looks like isoproterenol

Front 20

what are 2 reasons we may get reflex tachycardia with a block

Back 20

1. a2 block increases NE, NE can stim b1 to increase HR

2. a1 block causes decreased BP, we can then get reflex tachy with baroreceptor stim

Front 21

what is Epi reversel seen with, Epi effects no resemble what drug

Back 21

seen when Epi is given with A blocker

**b effects no dominate and BP is DECREASED
**effects resember isoproterenol (a b1/2 agonist)

Front 22

if you have increased HR and decreased BP what drug might it have been

Back 22

alpha blocker

BP is decreased bc we arent constricting a1 BV but then we have reflex tachy bc NE increased release and baroreceptor

Front 23

what are some side effects of a block

Back 23

1. meiosis
2. inhibit ejaculation
3. nasal stuffyness (normally we have nasal vasoconstriction that is a decongestant)
4. decreased resistance to urine flow. the sphincter isnt contracted so tight anymore. good for benign prostatic hypertrophy

Front 24

what might we give a guy to help him pee if he has BPH

Back 24

a agonist, it relaxes that sphincter a bit

Front 25

what is phentolamine

Back 25

Reversible a1/a2 antagonist

1. block a1 so decrease BP
2, HR increased via increased NE by a2 block, and baroreceptor
3. weird thing, GI stimulaiton bc of 5HT block, dont use in peptic ulcer

increased HR, decreased BP. dont use with coronary arterd disease or peptic ulcer

Front 26

ok so phentolamine is an a1/2 blocker so we expect decreased BP increased HR, what is the weird effect

Back 26

increase GI motility/secretion.
dont use in ppl with peptic ulcers

Front 27

what is phentolamine used for

Back 27

a1/2 block that increased HR, decreases BP and increases GI as a weird effect

1. HTN crisis
-(pheochromocytoma)
-ppl with increaed Tyramine and are taking MAOi
-abrupt clonidine withdrawl

Reverse NE effects of vasoconstriction to prevent necrosis

Front 28

what is phenoxybenzamine

Back 28

IRREVERSIBLE a blocker

*covalently binds to and inhibits a recetors

**bc its irreversible its a good tx for pheochromycytoma. this is a tumor that just spits out tons of SNS NT

hypotension can occur, esp when hypovolumic or postural hypotension
tachycardia can occur
nasal congestion bc of decreased constriction in the nose
inhibit ejaculation

Front 29

what is the irreversible a antagonist that is good to tx pheochromocytoma

Back 29

phenoxybenzamine

**can cause hypotension if hypovolumic
**can cause tachycardia (1. NE increase, 2 Reflex bc of decreased BP)

Front 30

what inhibits ejaculation

Back 30

the a bockers

a1 does ejaculation

Front 31

whats prazosin

Back 31

a1 selective antagonist (azosin is a1 antagonist)

used to tx HTN
decreased BP but less tachycardia bc there is no a2 blockade to increase NE to stim b1 to increase HR

block a1 R in urinary sphincter, increase ease of urination

**great for men with HTN and BPH, causes postural hypotension

DECREASE LDL, increase HDL bonus

Front 32

whats the dif in tachycardia seen in a1/2 antagonists and selective a1 antagonist

Back 32

less tachycardic with a1 selective

*when a2 is blocked we get increased NE which acts on b2 to increase hR

Front 33

talk to be about hte pharmacokinetics of prazosin

Back 33

a1 antagonist, -azosin

good oral abs, bound to plasma proteins
metabolized by liver. t1/2 increases with CHF

normal needs to be given 2/day

Front 34

what is a GREAT dug for men with BPH and HTN

Back 34

a1 antagonist, prazosin

tx HTN w/o reflex tachy cardia bc a2 not affected

will cause postural hypotention

another GREAT drug is terazosin or Doxazosin. these are the same as prazosins but are taken once a day and also do apoptosis of the prostate

ok so another really great one is Tamsulosin. its an a1 blocker that is specific for a1a, the a1R that are on prostate and bladder sphincter. relaxes hte prostate and sphincter. little effect on BP, will inhibit ejaculation

Front 35

the first dose phenomon is what, what class of drugs is it common in

Back 35

its common in a2 antagonists

*postural hypotension, take low doses when you are laying down

**also inhibits ejaculation
*dizziness
**nasal stuffiness

Front 36

postural hypotension
inhibit ejaculation
dizzy
nasal stuffiness

Back 36

a1 antagonist

**these are contraindicated in taking sildenafil, can cause SEVERE hypotension

Front 37

why is it kinda good ppl with ED and taking sildenafil shouldnt take a1 antagonists

Back 37

well really its bc it can cause seevere hypotension

BUT... its ironic bc a1 antagonitsts inhibit ejaculation. also cause postural hypotension and dizzy and nasal stuffiness

Front 38

whats terazosin/doxazosin

Back 38

azosin, its an a1 antagonist
automatically we know it does first dose- postural hypotension. inhibits ejaculation, and less tachycardia (simliar to prazosin)

Unique:
apoptosis of prostate, great for BPH
longer t/1/2, given once a day

Front 39

whats tamsulosin

Back 39

its the a1 selective that dosent ind in azosin

selective for a1 SPHINCTERS (a1a) not the BV

relaxes prostate and sphincters
little effect on BP
inhibits ejaculation

Front 40

whats the a2 antagonist

Back 40

yohimbine

Increased Ne release, increased HR and BP

**its an herbal to help with erection but its never been proven to work. it can cause incerased BP so caution in men with HTN. It antagonizes clonidine, the a2 stimulant

Front 41

whats the a2 stimulant,
whats the a2 antagonist

Back 41

stim: clonidine

inhibit: yohimbine

Front 42

the b antagonists that have intrinsic sympathetic activity are what? what about if used with a fll agonist

Back 42

partial agonist

competetive antagonist

Front 43

cardioselective b antagonists target which receptor

Back 43

b1,
propanolol

Front 44

what are hte cardio effects of b blockers

Back 44

1. decreased HR/contractiliry (b1), effect is strongest when SNS tone is activated in times of stress or exercise. bc heart has dom PNS effects a b block will prevent a huge increase in HR, more than it will decrease the HR

2. slowed conduction through atria and AV node

3,. decreased automaticity

4. decreased o2 consumptino of the ehart (good for angina esp exercise induced

5. decreased BP over long term bc b1 inhibit renin release, less whater retention, and also a bit bc CO is ddecreaed

6. inhibit vasodilation by b2 --> increased pressor effects. dont give to someone with pheochromocytoma w/o first giveing an a blocker

Front 45

what are the effects of b block in the lungs

Back 45

b2 want to dilate but its blocked so we constrict bronchioles

*not good for asthmatics
*use Ca channel blocker instead
*even the b1 selective (atenolol or metoprolol) can cause asthmatics problems

Front 46

what do beta blockers do in the eye

Back 46

decrease intraocular pressure

*b2 make aq humor

used topically but be sure it has no anesthetic effect, timolol is good but can also stim b2 so not good in asthmatics

Front 47

whats a metabolic effect of b blocker with hypoglycemia

Back 47

if you get hypoglycemic b2 are stim to go glycogenolysis to increase blood sugars, if the b R is blocked we will get hypoglycemic much more quickly

bad for DM
b blocker also blocks tremor and other things that clue you in that you are hypoglycemic

Front 48

whats the deal with pts with DM and b blockers

Back 48

dont want to use them but if we have to used a b1

B2 stim glycogemolysis if we get hypoglycemic, thi sis impaired in DM. and b blocker will also mask the signs of hypoglycemia

Front 49

what does chronic use of b blockers do to fat levels

Back 49

when b3 is blocked lipolysis is inhibited, increased VLDL, decreased HDL

not good with cardiovascular disease

Front 50

what does b blocker do to K

Back 50

can take K up into mm, increased serum K

Front 51

what are 5 alsolute must knows for b blockers

Back 51

1. Decreased BP with chronic use (b1 block will inhibit renin)

2. decreased intraocular pressure

3. local anesthetic

4. bronchoconstriction in asthma

5. impair recovery from hypoglycemia

Front 52

what can you tell me about the anesthetic properties of some adrenergic blockers

Back 52

b blockers may have some anesthetic effects, dont use them in the eye!

acebutolol,
labetalol
metoprolol
pindolol
propranolol

Front 53

what is the prototype b blocker

Back 53

propanolol

1. acts on b1/2
2. Slows HR/Conduciton through AV node
3. decrease force of contraction
**2/3 cause decreased O2 demand in the heart
4. inhibits lipolysis, glycogenolysis
5. local anestheric
6. bronchoconstriciton
7. decrease renin over time to decrease BP

Front 54

decreased BP with chronic use
decreased O2 demand
decreased lipolysis/glycogenolysis
anesthetic

these are all characteristic of what class of drug

Back 54

b blockers, non selective like propranolol

b1 inhibition decreases renin to decrease BP

Decreased O2 bc b1 is blocked to decrease HR, force of contraction, AV conduction

decreased lipolysis bc b3 block. decreased glycogenolysis bc of b2 block

b2 block also will bronchoconstrict

Front 55

whats the pharmacokinetics of propranolol

Back 55

b blocker (b1/2)

oral
slow abs, sustained release
enters CNS- sedation, depression
hepatic excretion

Front 56

if you have impaired recovery after hypoglycemia what might be thr problem

Back 56

b blocker, specifically b2

Front 57

what are some uses of b blockers, propranolol prototype

Back 57

1. decrease HTn with chronic use
2. decreased mortality after MI (decreased O2 demand)
3. tx arrhythemia
4. tx angina
5, prevent migrain
6. decrease pressure in portal vein, cirrhosis
7. blocks tremor- stage fright

* used in hyperthyroidism to decrease BP and HR

Front 58

is a b blocker reccomended after an MI

Back 58

yep, propanolol non selective b blocker

Front 59

what are some side effects of propranolol

Back 59

b blocker prototype

1. bronchoconstriction in asthmatics
2. exacerbate heart failure LATE in heart failure (its good to use it in early failure)
3. Bradycardia, decreased AV conduction, dont use with vermapamil, ca channel blocker
4. Overdose can cause hypotension and bradycardia
5. antagonist so R will upregulate, dont stop taking immediatly! can cause arrhythemia, HTN, angina
6. CNS penetration so depression, fatigue, sedation
7. mask effects of hypoglycemia, hard to recover
8. mask tremor
9. increase VLDL, decrease HDL long term

Front 60

what are the drug interactions of propranolol


what will increase/decrease metabolism

Back 60

metabolism is decreased with cimetedine

metaboism is increased with barbituates, phenytoin, rifampin, smoking.

calcuim channels have additive effects

Front 61

what increases the metabolism of propranolol

Back 61

its the prototype b blocker

increased metabolism means there is less available.
barbituates
phenytoin
rifampin
smoking

metabolism is reduced by cimetedine

Front 62

how are cimetedine and propranolol related

Back 62

cimetedine decreased the metabolism of propranolol

Front 63

whats the b blocker that is just like propranolol but...

Back 63

timolol, also a non selective b blocker

BUT it has no local anesthetic so it can be used in eye,

can be abs systemically so not to be taken with asthmatics

Front 64

whts teh drug that is like propranolol but wont make you so dang depressed

Back 64

nadolol

no selective b1/2 antagonist

Front 65

what are the b1 selective antagonists

Back 65

b1 are in the ehart and increase HR and force of contraction. Also increase release of renin

1. metoprolol: decreases HR, force of contraction. Tx HTN. good to use after MI. Also good for migraine prophylaxis
2. Atenolol: increase risk of DM II
3. Esmolol: really short duration (8min) must be IV
4. Bextaolol: glaucoma, less likely to cause bronchoconstriction than timolol
5. Nebivolol: most selective for b1, vasodilation with NO release, decrease cholesterol and glucose

Front 66

if you block b1 what happnes

Back 66

b1 cause increased HR and force of contraciton. also release renin so when they are blocked

1. HR and force of contraction decreases
2. tx HTN
3. Used after MI to increase life expectancy
4. Migraine prophylaxis

metprolol atenolol, esmolol, betaxolol, nebivolol

Front 67

what class of drugs are used for

1. tx HTN
2. used after MI
3. Migraine Prophylaxis

Back 67

b1 blockers

will decrease HR force, also decrease renin

metoprolol, atenolol, esmolol, betaxolol, nebivolol

Front 68

do selective or non selective b blockers have better exercise tolerance

Back 68

b2 cause dilation in sk mm

A b1 blocker will still allow dilation in sk mm so b1 provide better exerciese tolerance

Front 69

what are 2 reasons you might want to use a selective b1 over a non selective?

what are some examples of selective b1

Back 69

b1 are good to use after MI to decrease HR and force of contraction. decreaes renin so good for HTN

B1 better than b1/2 bc...
1. better exercise, b2 when blocked decrease BV dilation in the sk mm
2. b2 wont be blocked so we still can have glycogenolysis
*keep in mind even thorugh they are b1 selective they can still block b2 and so are risky in asthmatics

metprolol, atenolol, betaxolol, esmolol, nebivolol

Front 70

there is a reduced risk of hypoglycemia when this type of b blocker is used

Back 70

selective b1

metoprolol, atenolol, betaxolol, nebivolol, esmolol

Front 71

are b1 selective antagonists like metprolol, atenolol, bexatolol, nebivolol, and esmolol the answer for treating asthmatics with b blockers

Back 71

NOPE! even though they are b1 selective they may still block b2 and so are risky in asthmatics nad COPD

Front 72

tell me about betaxolol

Back 72

selective b1 antagonist
tx for glaucoma, less bronchostriction than tiimolol

Front 73

tell me about nebivolol

Back 73

b1 selective antagonist, most selective
b blocker that vasodilates via NO NOT an a1 block
also decreases cholesterol, TAG and glucose

Front 74

whats the selective b1 bocker that causes NO mediated vasodilation and can decrease cholesterol

Back 74

nebivolol

Front 75

whats the selective b1 antagonist that is used to tx glaucoma, less likely to stim bronshioles

Back 75

betaxolol

Front 76

tell me about esmolol

Back 76

selective b1 blocker

short duration
given IV

Front 77

what are the b antagonists with some intrinsic sympathetic activity? what are they used to treat?

Back 77

1. Pindolol
2. acebutolol, b1 selective

Tx HTN, angina,

*dont decrease HR as much

Front 78

whats pindolol

Back 78

b antagonist with ISA

tx HTN, angina

*dont decrease HR as much

Front 79

whats acebutolol

Back 79

b antagonist with ISA
b1 selective

Tx HTN, angina

*dont decrease HR as much

Front 80

what are hte combined a and b blockers

Back 80

1. Lebetalol- reversible
2. carvedilol

Front 81

whats labetalol

Back 81

blocks b1/b2 and a1

a1 block causes vasodilation- decrease BP

b block prevents compensatory increase in HR

given IV in emergencies. decrease BP with decreased HR too

done for: MI, CHF, HTN

Front 82

whats carvedilol

Back 82

blocks b1/2 and a1

vasodilation that decreases BP WIHTOUT reflex tachy!!

used for HTN, CHF, MI

Front 83

what are the drugs that can decrease BP w/o a compensatory increase in HR

Back 83

the b1/2 a1 antagonists

labetAlol
carvedIlol

we can get that rapid decrease in BP w/o the effects of reflex tachycardia. good for MI, HTN, CHF

Front 84

what are some clinical uses of b blockers (7)

Back 84

1. HTN
2. Ischemic heart disease
3. arrhythemia
4. Obstructive cardiac myopathy
5. dissecting aortic aneurysm
6. hyperthyroidism
7, migraine

Front 85

shoudl we use b blockers in ppl who have had an MI
what about HTN
what about aortic dissection
what about hyperthyroidism

Back 85

YES to all

and also ischemia, arrhythemia, obstructive myopathy, migraine

Front 86

talk to me about narrow angle glaucoma

Back 86

aka closed angle

*when the iris dilates it can block outflow of aq humor
*this is an emergency and is treated with cholinergics til you can have surgery

DONT USE A agonists, it will dilate teh eye

Front 87

what is open angle glausoma

Back 87

chronic, no surgery needed.

need to decrease produciton of aq humor and increase secretions, the dilation is less important


PG DOC!!!!!increase outflow of aq humor
B Blockers: Timolol, betaxolol
a antagonists: apraclonidine, brimonidine
diuretics
cholinergic agonists: pliocarpine

Front 88

what is the DOC for open angle gluacoma

Back 88

prostaglandin

help aq humor leak out

then B blockers: timolol, betalolol, b1 selective

a2 agonist: apraclonidine, brimonidine

carbonis anhydrase inhibitors

Cholinergic agonists: pliocarpine

Front 89

tell me about b blockers in teh tx of glaucoma

Back 89

used in open angle

*2 DOC, decrease production of aq humor, NO vision effects!! (no innervation on ciliary mm)

Timolol-
Betazolol- b1 selective, less bronchoconstriciton

Front 90

ok so we like tx open angle glaucoma with b antagonists like timolol and betaxolol (b1 selective) bc they will decrease produciton of aq humor and wont affect vision, do we use a agonists

Back 90

ya. A2 agonist, decrease aq humor production, increase outflow

apraclonidine
brimonidine

Front 91

whats hte deal with cholinergic agonists and glaucoma

Back 91

used as temp for narro angle til you can have surgery or...

bad choice for chronic tx of open angle bc it affects vision but things like pliocarpine, carbachol, phyostigmine, echothiophate

use only when nothing else will

Front 92

whats guanethidine

Back 92

inhibits release of NE

simliar mech to botchilism toxin

Front 93

whats reserpine

Back 93

depletes NE in vesicles

Front 94

whats metyrosine

Back 94

inhibits tyrosine hydroxylase so no Dopa can be made (RLE for NE synthesis)

used to tx pheochromocytoma b4 surgery