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Adrenergic Drugs Flashcards

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1
Q

why do many clinical applications and toxicities associated with adrenergic drugs involve the cardiovascular system

A
  • it is an SNS dominant system involved in rapid regulation of blood pressure
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2
Q

what makes up blood pressure

A

cardiac output x vascular time (PVR)

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3
Q

what categories can adrenergic drugs be divided into

A

sympathomimetics (direct or indirect)
adrenergic antagonists

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4
Q

what are the different types of sympathomimetics (adrenergic drugs)

A

direct acting: activate receptors directly
indirect acting: increase level of NE at synapse, therefore increase activity at multiple receptor sub-types

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5
Q

what do structural differences in sympathomimetic drugs determine

A
  • presence of -OH groups increase potency and susceptibility to COMT
  • additional methyl group on the a-carbon makes it resistant to MAO
  • addition of a methyl group at the N-terminal end alters receptor affinity
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6
Q

what is the difference in structure between NE and EP

A

EP has an extra methyl group therefore changes which receptors it binds

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7
Q

how is receptor affinity altered by the size of groups added at the N-terminal end of a sympathomimetic

A
  • large groups = increased B-receptor activity
  • small groups = increased a-receptor activity
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8
Q

which direct acting agonists have mixed affinity

A

epinephrine: a1 = a2, B1 = B2
norepinephrine: a1 = a2, B1&raquo_space; B2

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9
Q

which direct acting agonists have affinity for a-receptors

A

phenylephrine: a1&raquo_space; a2
clonidine: a2&raquo_space; a1

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10
Q

which direct acting agonists have affinity for B-receptors

A

dobutamine: B1 > B2
Isoproterenol: B1 = B2
albuterol: B2&raquo_space; B1

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11
Q

what are the direct acting adrenergic agonists

A

norepinephrine
epinephrine
phenylephrine
clonidine
dobutamine
isoproterenol
albuterol

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12
Q

what are the indirect acting adrenergic agonists

A

tyramine
amphetamine
cocaine

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13
Q

what drugs are adrenergic antagonists

A

prazosin
yohimbine
metoprolol
propranolol
butoxamine

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14
Q

where are a1 receptors found

A

bladder
stomach
blood vessels (organs and skin)
eye
sphincters

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15
Q

where are B1 receptors found

A

heart
adrenal medulla
eye?

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16
Q

where are B2 receptors found

A

eye
blood vessels (skeletal muscle)
bronchi
stomach
small intestine
bladder
uterus (genitals)

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17
Q

what is the difference between NE and EP secretion

A
  • NE is released from nerve terminals at target tissue
  • EP is secreted from the adrenal medulla and circulates via blood to tissues
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18
Q

what mechanism do adrenoreceptors (a and B) uswe to send signals

A

GPCR messenger systems

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19
Q

what effect do a1 receptors have in GPCR systems

A

increase IP3 and DAG production - stimulatory effect

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20
Q

what effect do a2 receptors have in GPCR systems

A

decrease cAMP production - inhibitory effects

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21
Q

what effect do all beta receptors (B1, B2, B3) have in GPCR systems

A

increase cAMP production - stimulatory effect

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22
Q

what effects do different adrenergic receptors have in the eye

A

contraction of dilator/radial muscle (dilate pupil - mydriasis) = a1
decrease aqueous humor = a1, a2
increase aqueous humor = B1, B2

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23
Q

what effects do adrenergic receptors have in the heart

A

B1 in the heart = increase rate and force of contraction

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24
Q

what effects do adrenergic receptos have in blood vessels

A

a1 in BV of organs and skin = vasoconstriction
B2 in BV of skeletal muscles = vasodilation

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25
how do baroreceptors monitor BP
- when BP changes, baroreceptors initiate reflex pathways for moment-to-moment regulation - when BP drops, baroreceptors message CNS to decrease PSNS and increase SNS activity
26
how do adrenergic drugs alter BP
- alter CO and/or PVR - body tries to compensate
27
how do baroreceptors respond to the drug dobutamine to monitor BP
- activate B1 receptors in heart - increase rate and force of contraction - baroreceptrs detect increased BP and tell CNS to increase PSNS and decrease SNS - cause vasodilation
28
how do baroreceptors respond to the drug phenylephrine to monitor BP
- activates a1 in blood vessels of organs and skin - causes vasoconstriction - baroreceptors detect increased BP and tell CNS to increase PSNS and decrease SNS - cause decreased heart rate
29
all organs with smooth muscles have ___ receptors and all organs with sphincters have ___ receptors
1. B2 2. a1
30
adrenoceptors in bronchi (and effects of direct agonists)
- B2 = relaxation (bronchodilation) - responds to isoproterenol, albuterol and EP
31
adrenoreceptors in the GI tract (and effects of direct agonists)
- B2 = relax SM - caused by isoproterenol, albuterol and EP - a2 = decrease ACh release - caused by NE, EP and clonidine - a1 = contracts SM at sphincters - caused by NE, EP and phenylephrine
32
adrenoreceptors in the bladder (and effects of direct agonists)
- B2 = relaxes SM - caused by isoproterenol, albuterol and EP
33
adrenoreceptors in the skin (and effects of direct agonists)
- a1 = contraction of pilomotor SM - caused by NE, EP and phenylephrine
34
what sympathomimetic drug would be useful for treating asthma (bronchoconstriction)
albuterol - activates B2 receptors to cause bronchodilation (could also say isoproterenol)
35
why is phenylephrine used in nasal spray
it is an a1 agonist - when a1 receptors on blood vessels are activated is causes blood vessels in the nose to constrict and reduces fluid accumulation
36
what are some theraputic uses for clonidine (a2 agonist
- a2 always inhibits activity - opioid withdrawal. pain, hypertension, glaucoma, diarrhea
37
clonidine as treatment for glaucoma
- binds to a2 which decreases aqueous humor and therefore intraoccular pressure
38
clonidine as treatment for diarrhea
- binds to a2 receptors on ACh releasing neurons in the GI tract - activates a2 to decrease ACh release - decreases M3 receptor activation and therefore GI tract motility
39
clonidine as treatment for hypertension
- binds a2 receptors on adrenergic nerve terminals in the CNS - causes decrease in NE in the CNS and therefore SNS output - action in the CNS responsible for decreased BP
40
Tyramine - an indirect acting sympathomimetic
- increased NE release by pushing it ou of the pre-synaptic terminal - can be toxic - sympathetic excess - normally metabolized by MAO during first pass through the liver - if taking MAO inhibitor, tyramine from diet wont be metabolized
41
amphetamine - indirect acting sympathomimetic
- stimulates release of NE by the reverse transporter - crosses the BBB - stimulates CNS
42
cocaine - indirect acting sympathomimetic
- prevents re-uptake of NE by inhibiting transporter - crosses the BBB - stimulates CNS
43
why is cocaine sometimes administered for nasopharyngeal surgery
- inhibits NE re-uptake - NE activates a1 to cause vasoconstriction - constricts BV to prevent excessive bleeding - also has anesthetic properties
44
which sympathomimetic drugs can prolong the duration of action of a local anesthetic
- any direct a1 agonist - NE, EP, amphetamine - tyramine - cocaine
45
how can B1 agonists (e.g cocaine) cause toxicities in the CV system
- cause tachycardia which leads to arrhythmias/myocardial damage - increase blood pressure which can lead to heart failure, cardiac arrest and stroke
46
why must you be careful when administering B1 agonist drugs to elderly people
-can be at risk for cardiac arrest or stroke if they have high BP since B1 agonists increase BP
47
does the CNS experience toxicity from direct adronergic agonists
rarely
48
how does the CNS experience toxicity sue to indirect adronergic agonsist
- multiple transmitters increased (NE, dopamine, serotonin) - multiple receptors activated
49
symptoms of sympathomimetic toxicities in the CNS (due to indirect agonists)
restlessness hyperactivity insomnia aggression tremor anxiety seizures hyperthermia hemorrhage
50
adrenergic antagonists that block a receptors
prazosin: a1 >>> a2 yohimbine: a2 >> a1
51
adrenergic antagonists that block B receptors
metoprolol: B1 >>> B2 propranolol: B1 = B2 butoxamine: B2 >>> B1
52
why do adrenergic antagonists have the same effect as PSNS activation
the locations that adrenergic agonists work on have no PSNS input (only SNS)
53
effects of adrenergic antagonists in the eye
block a1: pupil constriction (mitosis) block B1 and B2: decrease production of aqueous humor
54
effects of adrenergic antagonists in the heart
block B1: decrease rate and force of contraction
55
effects of adrenergic antagonists in blood vessels
block a1: vasodialation (organs and skin) block B2: vasoconstriction (skeletal muscles)
56
baroreceptor reflex response to beta-blockers
- block B1: decrease rate and force of contraction - when they detect decreased BP they cause decreased PSNS and increased SNS - causes vasoconstriction via a1 (organs and skin)
57
beroreceptor reflex to alpha blockers
- block a1: vasodilation of BV - when they detect decreased BP they cause decreased PSNS and increased SNS - causes increased heart rate via B1
58
effects of adrenergic antagonists in the Bronchi
block B2: bronchoconstriction
59
effects of adrenergic antagonists in the GI react
block B2: increased motility block a2: increased ACh release (increased motility) block a1: relaxes sphincters
60
effects of adrenergic antagonists in the urinary bladder
block B2: contracts urinary bladder block a1: relaxes sphincters
61
why is propranolol good to treat hypertension but bad for asthma
hypertension: B1 receptor inhibition causes decreased rate and force of contraction asthma: B2 receptor inhibition in brochi causes bronchoconstriction
62
what adrenergic drugs could be a good choice to treat someone who has hypertension but also asthma
- drugs that target B1 but not B2 - prazosin, clonidine, metoperol
63
which adrenergic drugs could be used to treat cardiac arrest
- a B1 agonist to stimulate the heart - epinephrine, dobutamine
64
which adrenergic drugs could be used to treat anaphylactic shock (bronchoconstriction and CV collapse)
- a B1 agonist to stimulate heart and B2 agonist to relax bronchi - epinephrine, isoproterenol

Pharmacology (21 decks)

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