Adrenergic Pharmacology Flashcards

1
Q

Precursor to catecholamines

A

Tyrosine

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2
Q

Pathway for norepinephrine

A

Tyrosine–>L DOPA–>Dopamine–>Norepinephrine

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3
Q

a2 stimulation

A

Results in negative feedback in presynaptic terminal

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4
Q

b2 receptors

A

Only stimulated by epinephrine, not NE

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5
Q

COMT

A

Metabolizes NE in synapse

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6
Q

MAO

A

Make sure that the NE mobile pool that is not recycled into vesicles is destroyed so not too much NE is released

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7
Q

Methyl Tyrosine

A

Blocks conversion of tyrosine–>L dopa and therefore decreases NE release

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8
Q

MAO inhibitors

A

Block degradation of excess NE mobile pool in presynaptic cell–can cause excess NE release

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9
Q

a1 effect on blood vessels

A

Constriction and increased BP
Arterioles: Increased TPR, increased afterload, increased diastolic BP
Veins: Increased preload and increased systolic pressure

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10
Q

a1 effect on eye

A

Dilation

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11
Q

a1 effect on kidney

A

Decreased renin release

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12
Q

a1 effect on liver

A

increased glycogenolysis

Decreased insulin

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13
Q

a1 effect on bladder

A

Increased sphincter tone and urinary retention

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14
Q

a2 effect

A

Decreased synthesis and release of NE

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15
Q

B1 effect on heart

A

Increased HR, Increased conduction velocity, increased contractility, increased SV and increased systolic pressure

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16
Q

B1 effect on kidney

A

increased renin release

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17
Q

B1 effect on ciliary body in eye

A

Increased aqueous humor

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18
Q

B2 effect on vessels

A

Vasodilation, decreased TPR and decreased diastolic pressure

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19
Q

B2 effect on bronchioles

A

Bronchodilation

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20
Q

B2 effect on uterus

A

Relaxation–can delay preterm labor

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21
Q

B2 effect on liver

A

Glycogenolysis and gluconeogenesis

Increased insulin

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22
Q

a1 agonists

A

Increase in BP with no change in pulse pressure

Does not effect HR but reflex bradycardia may occur due to increase in BP

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23
Q

Phenylephrine

A

a1 agonist
Can be used for septic shock
Use as a nasal decongestant due to vasoconstriction preventing mucus

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24
Q

a2 agonists

A

Increase negative feedback so decrease release of NE
Can help with muscle spasticity by causing muscle relaxation
Will decrease insulin so caution in diabetics

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25
Q

Isoproterenol

A

Beta Agonist
B1=B2
use for bradycardia and heart block (B1) and asthma (B2)
Side effects: tachycardia, hypotension, flushing, headache

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26
Q

Dobutamine

A

B1 agonist
Use for congestive heart failure management
Side effects: tachycardia due to reflex from vasodilation

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27
Q

Albuterol

A

B2 agonist
Used for acute asthma
Side effects: palpitations, tremor, anxiety, restlessness

28
Q

Terbutaline

A

B2 agonist

Used for premature labor

29
Q

Salmetrerol

A

long acting B2 agonist, delayed onset, good for prophylaxis of asthma

30
Q

Formoterol

A

Long acting b2 agonist, prompt onset, good for acute and prophylaxis

31
Q

Norepinephrine always

A

Activates a1, a2, B1
Increases BP (a1 and B1 causes increased systolic BP and a1 causes slight increase in diastolic BP): increase in pulse pressure
B1 causes increase in HR, however reflex bradycardia will occur due to increased BP

32
Q

Epinephrine

A

Effects are dose dependent

Activates a1, a2, B1, B2

33
Q

Low dose epi

A

B1 and B2 agonist

Use for anaphylactic shock

34
Q

High dose epi

A

a1 and B1 primarily (looks more like NE)…B2 is masked by a1 effects
Use for heart stopping

35
Q

how to differentiate between high dose epi and NE

A

Need to block a1 to see if B2 becomes unmasked

Will cause hypotension if it is high dose epi

36
Q

Effect of low dose epi on HR and BP

A

B1: increased HR, increased SV, increased CO
B2: decreased TPR, decreased BP
Increased pulse pressure and mean pressure decreases

37
Q

Effect of medium dose epi on HR and BP

A

B1: increased HR, increased SV, increased CO
B2: decreased TPR, decreased BP
a1: increased TPR, increased BP
Increased pulse pressure, mean pressure stays constant

38
Q

Effect of high dose epi on HR and BP

A

B2 effect masked by a1=increased TPR and increased BP

Potential reflex bradycardia–can make ischemia worse

39
Q

Uses of NE and epi

A
Cardiac arrest
Adjunct to local anesthetic 
Hypotension
Anaphylaxis: Epi only
Asthma: Epi only
40
Q

Dopamine

A

Can be used in shock management due to similarity to NE

41
Q

Low dose dopamine

A

D1

Vasodilation on renal, coronary, mesenteric vessels

42
Q

Medium dose dopamine

A

D1 and B1

Adds inotropic effect to D1 to preserve blood flow to heart and kidneys

43
Q

High dose dopamine

A

D1, B1, a1

a1 can help maintain BP

44
Q

Indirect acting adrenergic receptor agonists: releasers

A

Displaces NE from mobile pool causing an increase in NE availability

45
Q

Releasers can interact negatively with

A

MAO inhibitors and Tyramine rich food

Can cause hypertensive crisis due to too much NE

46
Q

Examples of reuptake inhibitors of NE

A

Cocaine and TCAs

47
Q

a receptor antagonists

A

Decrease TPR and decreases mean BP
Used to fight hypertension
May cause reflex tachycardia and salt/water retention

48
Q

B1 receptor antagonists

A

Decreases HR, SV, and CO: good for anti-arrhythmic and decrease O2 demand and angina
Decreases renin release: good for anti CHF
Decreases aqueous humor production: good for anti glaucoma

49
Q

B2 receptor antagonists

A

Aggregates bronchospasm in asthmatics, makes metabolic effects worse in diabetics

50
Q

General use of beta blockers

A

Angina, hypertension, post MI
Anti arrhythmic
Glaucoma

51
Q

Chronic use of beta blockers leads to

A

Upregulation and tolerance

Important to taper dose to avoid excessive CV effects

52
Q

Additive bradycardia occurs when

A

Take beta blocker with calcium channel blocker

Can cause AV block

53
Q

What can be used in Beta blocker OD

A

glucagon

Binds to Gs coupled receptors and reverses B blockade toxicity without interfering Beta receptor

54
Q

1st generation beta blockers

A

nonselective
N-Z
“-olol”

55
Q

2nd generation beta blockers

A

B1 selective
A-M
“-olol”

56
Q

3rd generation beta blockers

A

Also act as vasodilators
Nonselective + a1 antagonist: used in CHF
Selective B1 and NO release: used in HTN

57
Q

Clonidine

A

a2 agonist

58
Q

Methyldopa

A

a2 agonist

59
Q

Phentolamine

A

a1 blockers nonselective

60
Q

Labetalol

A

A1 + b blocker

61
Q

Amphetamines

A

Increase release of NE

62
Q

Methylphenidate

A

Increase release of NE

Treatment of ADHD

63
Q

Atomexetine

A

Increase release of NE

Treatment of ADHD

64
Q

Modafinil

A

Increase release of NE

treatment of narcolepsy

65
Q

B2 blocking effects

A

Bronchoconstriction, decreased aqueous humor, impotence

66
Q

Beta blockers can decrease

A

Renin

Can be used for hypertension but not first line