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BIOM 3090 > Agrenergic Drugs > Flashcards

Agrenergic Drugs Flashcards

1
Q

Many clinical applicaions/toxicities assocaited with adrenergic drugs involve the _____

why?

A

cardiovascular system

  • bc the SNS is the dominant system invovled in rapid regulation of blood pressure
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2
Q

equation for cardiac output

A

Heart Rate x Blood Volume = Cardiac output

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3
Q

what is peripheral vascular resistance?

A

PVR

  • vascular tone
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4
Q

How is blood pressure calculated?

A

CO x PVR = BP

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5
Q

what are the two main categories of adrenergic drugs?

A
  • sympathomimetics and adrenergic antagonists
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6
Q

what do sympathomimetic drugs do?

A

mimic the action of NE/epinephrine by either directly activating receptors (one or more subtypes depending on the drug) or indirectly increasing the level of NE at the synpase

  • this increases the activity at multiple receptor sub-types
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7
Q

what are adrenergic antagonists

A
  • agents that block receptor activation
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8
Q

what are the structure influences on sympathomimetic activity?

A
  1. Presence of -OH groups at m and p position of the aromatic ring is found in all catecholamines (including NE and epinephrine)
    • absense of one or both OH dec potency at receptors and secreases susceptibility to catechol-O-methyltransferase (COMT; degrades catecholamines)
  2. Addition of group at α-carbon makes the compound resistant to monoamine oxidase (MAO)
  3. Addition of a group on the amino end increases β-receptor activity and decreases α-receptor activity
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9
Q

what is amphetamine

A
  • indirect acting sympthomimetic drug
  • not broken down as quickly as NE or epinephrine
  • does not activate alpha or beta receptors directy
  • stimualtes release of NR from sympathetic neurons and also from neurons int he CNS

*at higher doses dopamine and serotonin are also affected

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10
Q

describe the receptor activity of Epinephrine

A

α1 = α2 and β1= β2

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11
Q

adrenergic drugs

A
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12
Q

describe the receptor activity of Norepinephrine

A

α1 = α2, β1>> β2

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13
Q

describe receptor activity of Phenylephrine

A

α1 > α2

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14
Q

describe the receptor activity of Clonidine

A

α2 > α1

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15
Q

Describe the receptor activity of Dobutamine

A

β1> β2

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16
Q

Describe the receptor activity of Isoproterenol

A

β1= β2

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17
Q

Describe the receptor activity of Albuterol

A

β2>> β1

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18
Q
A
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19
Q

what organs does the α1 receptor target

A

eye, blood vessels (organs and skin), adrenal medulla (kidney), bladder

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20
Q

what organs are affected when α2 receptor is targeted

A

eye, heart, adrenal medulla (kidney)

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21
Q

what organs are affected when β2 receptor is activated

A

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

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22
Q

how does eye respond to agrenergic activation

A

α1 contraction of dilator muscle = dilation of pupil (mydriasis)
α ↓ secretion of aqueous humor
β ↑ secretion of aqueous humor from ciliary epithelium into eye

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23
Q

how doe the bronchi respond to agrenergic activation

A

β2 receptor -smooth muscle relaxation (bronchodilation)

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24
Q

How does the heart respond to adrenergic receptor activation

A

β1 receptor -↑ heart rate/force of contraction

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25
Q

how does the GI tract respond to adrenergic receptor activation?

A

α1 contracts sphincter muscles
α2 ↓ ACh release (↓ motility)
β2 relaxes smooth muscle (↓ motility)

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26
Q

How does the urinary tract respond to adrenergic receptor activation?

A

α1 contracts sphincter muscles
β2 relaxes smooth muscle (↓ motility)

27
Q

how does the uterus respond to adrenergic receptor activation

A

β2 relaxes smooth muscle

28
Q

How does the skin respond to adrenergic receptor activation

A

α1 contraction of pilomotor smooth muscle

29
Q

How do blood vessels in the organ and skin respond to adrenergic receptor activation?

A

α1 vasoconstriction

30
Q

How do blood vessels in skeletal muscle respond to adrenergic receptor activation

A

β2 receptor - vasodilation

31
Q
A
32
Q

what are baroreceptors - what do they do

A
  • monitor blood pressure
  • when bp changes baroreceptors initiate reflex pathways for moment-to-moment regualtion of BP
  • if BP dec, sends message to CNS to inc SNS activity and decrease PSNS activity
33
Q

how do adrenergic drugs alter BP - give an exmaple

A
  • they alter CO or PVR but body tried to compensate
  • ex: dobutmaine activates β1 receptors to inc the rate and force of contraction
  • baroreceptors detect the inc BP and body responds by INC PSNS activity and DEC SNS activity
  • nce a drug is present and activating receptors in the heart, the increase in ACh and decrease in NE release will have little effect in the heart, however in the blood vessels a reduction in NE will cause vasodilation

**dobutmaine inc BP by inc heart rate and the body tries to compensate by dilating blood vessels - overall effect still inc in BP

34
Q
A
35
Q

describe effect phenylephrine on blood pressure

A
  • activates α1 receptors in blood vessels and causes vasocontriction
  • baroreceptors detect inc in BP so they INC PSNS activity and DEC SNS which dec HR
  • since BP=CO x PVR, if drug dec BP by affecting only CO OR PVR the body tried to compensate by altering the other

*overall drug effect is still greater than compensation of body

*phenylephrine causes an inc in BP

36
Q

Which sympathomimetic drug would be useful in the treatment of asthma? (asthma = bronchoconstriction)

A

Albuterol because it has a high affinity for β2 receptors which are found in the smooth muscle of bronchi.

37
Q

Why is phenylephrine used in nasal sprays to relieve congestion?

A
  • Nasal congestions is typically due to the swelling and inflammation of blood vessels supplying the mucous membranes of the airways.
  • Therefore, α1 agonists would temporarily relieve congestion by vasoconstriction (phenylephrine)
38
Q

what is clonidine

A
  • direct acting sympathomimetic with high affinity for alpha receptors
  • several therapetuic uses: opiate drug withdrawal, hypertension, pain, ADHD, glaucoma and diarrhea
39
Q

describe clonidine as treatment for glaucoma, diarrhea and hypertension

A

Glaucoma

  • *α-receptor agonist
  • dec aqueous humour production which which dec intracolular pressure

Diarrhea

  • α2 receptors on ACh-releasing nerve terminals in the GI tract that are activated by clonidine
  • dec ACh release and M3 receptor activation which decreases GI tract motility

Hypertension

  • acts on α2 receptors on adrenergic nerve terminals in the CNS
  • there receptors are found on NE releasing neurons that regulate the SNS system
  • result: decreased NE in the CNS which dec SNS activity and CO and PVR
40
Q

indirect acting sympathomimetics

A
  • tyramine, amphetamine and cocaine
41
Q

describe tyramine

A
  • indirect acting sympathomimetic
  • found in some cheeses and fermented foods
  • normally metabolized by MAO during the first pass through the liver, if taking a MAO inhibitor, tyramine from the diet would not be metabolized
  • Tyramine increases NE release which can be toxic and cause sympathetic excess.
42
Q

describe cocaine

A
  • prevents the re-uptake of NE back into the synaptic terminal of SNS neurons
  • this inc the levels of NE in the synaptic cleft
  • also stim the CNS by blocking NE, depamine and serotonin reuptake
43
Q

describe the toxicities associated with sympathomimetics

A
  • toxicities associated with the cardiovascular system (CVS) and CNS

CVS

  • β1 agonists cause tachycardia which can lead to arrhythmias and myocardial damage
  • agents that inc BP inc cardiac work which can lead to heart failure cardiac arrest and stroke
  • particular risk to elderly and those with high BP, previous HA or coronary artery disease

CNS

  • Toxicity rarely observed with direct agonists but indirect agonists might cause restlessness, tremors, insomnia, anxiety
  • adverse effects of cocaine include convulsions and cerebral hemorrhage in addition to arrhythmias and HA
44
Q

Describe adrenergic antagonists

A
  • block α or β receptors that are normally activated by NE or epinephrine
  • they decrease the level of NE in synpase by inhibiting the synthesis, storage or release of NE
  • in most organs SNS and PSNS activity are physiological antagonists - inhibition adrengeric systemhas the same effect as activation of PSNS
45
Q

adrenergic antagonists

A
46
Q

recetpor affinity of Prazoin

A

* adrenergic antagonist

α1 >>>> α2

47
Q

receptor affinity of phenoxybenzamine

A

*adrenergic antagonist

α1 > α2 (irreversible)

48
Q

receptor affinity of yohimbine

A

* adrenergic antagonist

α2 >> α1

49
Q

receptor affinity of metoprolol

A

*adrenergic antagonist

β1>>> β2

50
Q

receptor affintiy of propranolol

A

*adrenergic antagonist

β1= β2

51
Q

receptor affinity of butoxamine

A

*adrenergic antagonist

β2>>> β1

52
Q

effects of adrenergic inhibition of the eye

A

block α1 : constriction of pupil (miosis)
block β : ↓secretion of aqueous humor from ciliary epithelium into eye

53
Q

effect of adrenergic inhibition of the bronchi

A

block β2 : bronchoconstriction

54
Q

effects of adrenergic inhibition of the heart

A

block β1 : ↓ heart rate/force of contraction

55
Q

effects of adrenergic inhibition of the GI tract

A

block α1 : relaxes sphincter muscles
block α2 : ↑ACh release (↑ motility)
block : β2 ↑motility

56
Q

effects of adrenergic inhibition of urinary tract

A

block α1 : relax sphincter muscles
block β2 : contract smooth muscle

57
Q

effects of adrenergic inhibition of uterus

A

block β2 : contract smooth muscle

58
Q

effects of adrenergic inhibition on skin

A

block α1 : relaxation of pilomotor smooth muscle

59
Q

effects of adreneric inhibiton on blood vessels in rogan and skin

A

block α1 : vasodilation

60
Q

effects of adrenergic inhibiton on blood vessels in skeletal muscle

A

block β2 : vasoconstriction

61
Q

Baroreceptor Reflex Response to Antiadrenergic Drugs - Beta-blockers

A

Beta-blockers inhibit activation of β1 receptors - decreases heart rate and force of contraction

  • baroreceptors detect the decrease in BP and body inc SNS activity and dec PSNS activity
  • effects on heart would eb minimal due to presence of beta-blockers but inc SNS output would inc NE levels

inc in NE cause vasoconstriction via α1 receptors located on the smooth muscle cells of the blood vessels associated with the organs and skin.

62
Q

Baroreceptor Reflex Response to Antiadrenergic Drugs - alpha-blockers

A
  • inhibit activation of α1 receptors in the blood vessels -causes vasodilation - results in decreased peripheral vascular resistance and decreased BP.
  • baroreceptors detect the dec in BP and the body responds by inc SNS activity and decreasing PSNS activity
  • result in INC HR via NE mediated activation of β1 receptors
63
Q

A patient with asthma was prescribed propranolol for the treatment of glaucoma. Why might this drug choice be bad? What other drugs could be used instead?

A
  • Propranolol is a β2 receptor blocker (it DEC secretion of aqueous humour which is good) but could cause bronchoconstriction.
  • Any drug that reduces intraocular pressure but does not cause bronchoconstriction would be a better choice, such as clonidine.
64
Q

What adrenergic drugs could be prescribed for the treatment of hypertension in an individual with asthma?

A

prazosin: alpha blocker - vasoDILATION and no effect to bronchi

clonidine - dec relase of NE so dec SNS activity to DEC CO and PVR

metoprolol -

BIOM 3090 (22 decks)

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