Pharmacology Exam 3- Adrenergic Inhibition

Front 1

sympatholytic definition (what is it, used for what)

Back 1

drugs inhibiting adrenergic transmission.

used for hypertension

Front 2

adrenergic inhibition elicits what responses? (4)

Back 2

decrease heart rate
decrease BP
decrease blood flow to skeletal muscles
increase blood flow to skin and splanchic region (organs)

Front 3

pre-junctional sympatholytics types (4)

Back 3

autoreceptor agonists (a2, DA2)
NE depleting agents
nerve terminal membrane stabilization agents
"false" transmitters

Front 4

post-junctional adrenergic inhibitor types of agents (2)

Back 4

1) a1 antagonists (competitive/non-competitive)
2) beta adrenergic blockers (b1/b2 or b1)

Front 5

3 a2 receptor agonists

Back 5

clonidine
guanabenz
a-methyldopa

Front 6

a2 receptor agonist mechanism (4)

Back 6

1) decrease total peripheral resistance
2) inhibits NE release (negative feedback) from nerve terminal-->hypotension
3) decrease hart rate
4) decrease cardiac output

Front 7

2 benefits of using a2 receptor agonists

Back 7

1) does not elicit baroreflex
2) no orthostatic hypotension

Front 8

side fx of a2 receptor agonist (4)

Back 8

1) xenostomia
2) sedation
3) fluid retention
4) CNS stimulation (opposite?)

Front 9

bromocriptine
indication

Back 9

DA2 receptor agonist
used for anti-parkinson CNS effects (DA2 is not autoreceptor in CNS)

Front 10

peripheral side effects of bromocriptine (2)

Back 10

1) postural hypotension during initial therapy
2) development of cardiac arrhythmia

Front 11

explain how inhibition of NE release by synaptic depletion works

Back 11

reduce conc. of NE inside vesicles

Front 12

Metyrosine MoA
use

Back 12

inhibit tyrosine hydroxylase
inoperable pheochromocytoma

Front 13

reserpine MoA

Back 13

blocks storage of biogenic amines into vesicles by inhibiting VMAT

Front 14

reserpine route, duration, potency

Back 14

very potent
oral/parenteral
long duration but maximal response takes a while to achieve

Front 15

downside with parenteral admin of reserpine

Back 15

you can get initial release of NE, but conc. goes down over time

Front 16

effect of reserpine (2)

Back 16

bradycardia
decreased MAP

Front 17

adverse effects of reserpine (3)

Back 17

primarily CNS:
sedation/depression
parkinsonian symptoms

GI motility reduce = increased ulcers

Front 18

MoA of guanethidine (2)

Back 18

1) competes with NE for NET, and for VMAT into vesicles thus depleting NE (over time)
2) stabilizes neuronal membrane to interfere with exocytosis once inside the terminal

Front 19

route of admin for guanethidine
indication
CNS effects?
affect other biogenic amines?

Back 19

orally effective
for the most severe hypertensions
does not cross BBB
minimal effects observed with DA and Epi (derivatives/precursors)

Front 20

what types of agents interfere with guanethidine?

Back 20

agents that inhibit transport- NET (cocaine/reuptake inhibitors like tricyclic antidepressants) antagonizes guanethidine action

Front 21

describe the action of false transmitters (like methyldopa) class of drug

Back 21

replace DOPA in NE synthesis resulting in false transmitter a-methyl NE synthesis and replacement of NE in vesicle

Front 22

a-methyl NE vs. NE effects on PNS/CNS (2)

Back 22

MNE has much reduced efficacy at receptors in PNS but is potent stimulator of a2 receptors in brainstem which inhibits vasomotor center (hypotension)

Front 23

adverse effects of a-methyldopa (7)

Back 23

1) sedation
2) postural hypotension
3) dizziness
4) sleep disturbance
5) impotence
6) dry mouth
7) nasal congestion

Front 24

adverse effects of chronic a-methyldopa therapy (4)

Back 24

1) hemolytic anemia
2) leukopenia
3) hepatitis
4) lupus like problems

Front 25

a1 adrenergic blocker function

Back 25

inhibit contraction/constriction of vasculature

Front 26

2 subtypes of a1 antagonists

Back 26

irreversible (noncompetitive)
reversible (competitive)

Front 27

b1/b2 blockers function (2)

Back 27

inhibit cardiac output (b1)
inhibit dilation/relaxation (b2)

Front 28

b1 selective blocker function

Back 28

inhibit cardiac output

Front 29

prazosin, terazosin, doxazosin (ZOSIN) receptor selectivity

Back 29

a1

Front 30

phenoxybenzamine receptor selectivity

Back 30

a1 and a2, but a1 > a2

Front 31

phentolamine receptor selectivity

Back 31

a1 = a2

Front 32

yohimbine, tolazoline receptor selectivity

Back 32

a2 >> a1

Front 33

labetalol receptor selectivity

Back 33

b1 = b2 > or equal to a1 > a2

Front 34

atenolol
metoprolol
betaxolol

receptors

Back 34

b1

Front 35

propranolol
pindolol
timolol

receptors

Back 35

b1 = b2

Front 36

butoxamine (experimental) receptors

Back 36

b2

Front 37

phenoxybenzamine type of inhibitor

MoA? (2)

Back 37

irreversible, noncompetitive antagonist

MoA- alkylates a1 and a2 receptors (covalent bond)
inhibits NET by covalently binding to it to form a cyclic intermediate (inactive)

Front 38

phenoxybenzamine duration of action
route (2)
indications (2)

Back 38

24 hr
oral or IV
pheo- to manage hypertension preoperation, or if tumor is inoperable
and adjunct therapy to severe hypertension

Front 39

side fx to phenoxybenzamine (2)

Back 39

reflex tachycardia (due to decrease MAP)
postural hypotension

Front 40

prazosin:
type of inhibitor/MoA
important "pro" of prazosin

Back 40

competitive antagonist of a1 receptors

does not elicit reflex tachycardia (though mechanism is unknown- has nothing to do with b1 inhibition).

Front 41

why do some mixed a2/a1 antagonists cause tachycardia? (2)

Back 41

normal a2/a1 mixed antagonists can sometimes elicit tachycardia due to inhibition of negative feedback-->more release of NE-->stimulation of b1 receptor though

or reflex tachycardia

Front 42

route of admin for prazosin
duration of action

Back 42

effective orally
12 hr

Front 43

terazosin: indication and MoA

Back 43

competitive selective inhibitor of a1
used to relieve urinary incontinence associated with BPH

Front 44

phentolamine: MoA
side fx?

Back 44

competitively inhibits a1/a2 receptors (equally)

can elicit tachycardia/increased cardiac output due to a2 stimulation (inhibit negative fb-->more NE release)

Front 45

why is phentolamine considered a "dirty drug"?

Back 45

also interacts with M and H receptors (in addition to a1/a2)

Front 46

usage of phentolamine

Back 46

regitine test: diagnosis of pheo
check if you can significantly reduce BP after administration. if so, probably pt has high amounts of epi in circulation.

Front 47

selective b1 blockers are better for treating htn because...
but still contraindicated why?

Back 47

less prone to induce constriction of bronchiol smooth muscle (important in pt with ASA (asthma) although in patients with actual asa you might want to avoid beta 2 blockers all together because they are selective for b1, but not entirely specific)

Front 48

b1/b2 mixed antagonists (4)

Back 48

propranolol
timolol
pindolol
nadolol (Long half life)

Front 49

propranolol clinical usage (4)

Back 49

antihtn
anti arrhythmia
AP (angina pectoris)
migraines

Front 50

2 b1/b2 blockers that are used as prophylactics for MI recurrence

Back 50

timolol/propranolol

Front 51

pindolol indication

Back 51

htn

Front 52

timolol indication (3)

Back 52

htn
glaucoma
ap

Front 53

nadolol indication

Back 53

htn

Front 54

elimination halflife of esmolol
indication (2)

Back 54

super short- 9 min
ACUTE treatment of sinus tachycardia
atrial flutter

Front 55

betaxolol halflife
indication

Back 55

super long: 14-22 hr
glaucoma

Front 56

atenolol halflife
indication

Back 56

medium: 6.5 hr
htn

Front 57

metoprolol halflife
indications (3)

Back 57

medium: 5 hr
prophylactic for MI
htn
ap

Front 58

side fx of propranolol (2)

Back 58

ataxia
dizziness
(esp with initial therapy)

Front 59

side fx of metoprolol (2)

Back 59

ataxia
dizziness
(esp with initial therapy)

Front 60

side fx of atenolol/nadolol compared with propranolol/metoprolol

Back 60

fewer CNS effects (ataxia/dizziness) due to diminished ability in crossing BBB

Front 61

beta receptor blockers must be used with great caution or avoided in what 2 types of pt? why?

Back 61

COPD/asa- some b2 actions even in b1 blockers
OR
cardiac insufficiency pts as you may induce cardiac failure by blocking b1 (decrease cardiac output due to decrease contractility/heart rate)

Front 62

look over principle sites of action slide for drugs

Back 62

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