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Abbey pharm shelf/step > pharmacology: adrenergic drugs > Flashcards

pharmacology: adrenergic drugs Flashcards

1
Q

where are alpha 1 receptors? effects?

A
  1. radial muscle eye (contraction = mydriasis without cyclopegia@)
  2. arterioles (contraction = increased TPR = increased diastolic pressure = increased afterload)
  3. veins (contraction = increased venous return = increased preload = increased systolic BP)
  4. bladder trigone and sphincter and prostatic urethra (contraction = urinary retention)
  5. male sex organs (vas deferens = ejaculation)
  6. liver (increased glycogenolysis)
  7. kidney (decreased renin release - safety valve - don’t want too much increase in BP)
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2
Q

where are alpha 2 receptors? effects?

A
  1. prejunctional nerve terminals (decreased transmitter release and NE synthesis
  2. platelets (aggregation)
  3. pancrease (decrease insulin secretion)
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3
Q

what type of receptor is alpha 1?

A

Gq = increased calcium

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4
Q

what type of receptor is alpha 2?

A

Gi couples = decreased cAMP

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5
Q

where are B1 receptors? effects?

A
  1. heart: oppose muscarinic 2
    SA node - (increased HR (positive chronotropy))
    AV node (increased conduction velocity (positive dromotrophy))
    atrial and ventricular muscle (increase force of contraction (positive inotropy), conduction velocity, CO and oxygen consumption)
    his-purkinje (increase automaticity and conduction velocity
  2. kidney: increase renin release (complementary effect with rest of Beta 1)
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6
Q

what type of receptor is beta 1?

A

Gs coupled: increase cAMP

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7
Q

what type of receptor is beta 2?

A

Gs coupled = increased cAMP

MOSTLY NOT INNERVATED - NE CAN’T REACH!! EPI!!!!!!!

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8
Q

where are beta 2 receptors? effects?

A
  1. blood vessels (all) - (vasodilation = decreased TPR = decreased diastolic pressure = decreased afterload)
  2. uterus (relaxation - prevent premature labor)
  3. bronchioles (dilation - relaxation)
  4. skeletal muscle (increased glycogenolysis - contractility (tremor))
  5. liver (increased glycogenolysis, gluconeogenesis, lipolysis)
  6. pancrease (increase insulin secretion - in order to allow glucose uptake)
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9
Q

which receptors are most sensitive?

A

beta receptors! when drugs have both effects, beta responses are dominant at low doses!! alpha at higher doses

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10
Q

where are D1 receptors located? effects?

A

renal, mesenteric, coronary vasculature (vasodilation - in kidney increased RBF, increased GR, increased Na+ secretion)

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11
Q

fenoldopam - mechanism and clinical

A

D1 agonist - used for severe hypertension (causes vasodilation)

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12
Q

what type of receptor is D1?

A

Gs coupled - increased adenylyl cyclase = increased cAMP

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13
Q

how is potential reflex bradycardia blocked with alpha 1 agonists?

A

M2 blockers

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14
Q

what is the direct acting alpha 1 agonist? clinical use?

A

phenylephrine - nasal decongestant and ophthalmologic use (mydriasis without cycloplegia)

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15
Q

phenylephrine effect on blood pressure

A

increase mean blood pressure via vasoconstriction of both arterioles and veins - no change in pulse pressure

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16
Q

what are the alpha 2 agonists? clinical use?

A

clonidine and methyldopa - mild to moderate hypertension (decrease sympathetic outflow)

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17
Q

what are the beta agonists? clinical use?

A

isoproterenol (B1=B2) - bronchospasm, heart block, bradyarrhythmias
dobutamine (B1>B2) - CHF (increased CO)

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18
Q

isoproterenol side effects

A

flushing, angina, arrhythmias

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19
Q

beta 1 agonist effects

A

increased HR, increased SV, increased CO, increased pulse pressure (d/t increase in contractility)

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20
Q

beta 2 agonist effects

A

decreased TPR, decreased BP

21
Q

what are the selective beta 2 agonists? clinical uses?

A

salmeterol (prophylaxis asthma), albuterol (asthma), terbutaline (premature labor)

22
Q

NE effect on BP

A

can NEVER lower BP because it has NO B2 activity

23
Q

low dose epinephrine effects

A

B1: increased HR, increased SV, increased CO, increased PP
B2: decreased TPR and decreased BP

24
Q

medium dose epinephrine effects

A

B1: increased HR, increased SV, increased CO, increased PP
B2: decreased TYPR, decreased BP
A1 effects!!!: increased TPR, increased BP (antagonism causes no change in BP)

25
Q

high dose epinephrine effects

A

similar to NE = A1 predominance (increased TPR and increased BP)

26
Q

how to distinguish between epinephrine and NE

A

CANNOT distinguish based on cardiovascular - bronchioles dilated with epi

27
Q

what are the beta 2 specific effects

A

smooth muscle relaxation; bronchioles, uterus, blood vessels

also: increased glycogenolysis, increased gluconeogenesis, increased mobilization and use of fat

28
Q

use of NE and epi

A

cardiac arrest, adjunct to local anesthetic, hypotension, anaphylaxis (epi only), asthma (epi only)

29
Q

what are the indirect-acting adrenergic receptor agonists? mechanism?

A

releasers (displace NE from mobile pool): tyramine, amphetamines, and ephedrine
reuptake inhibitors: cocaine and tricyclic antidepressant

30
Q

drug interaction with adrenergic receptor agonists releasers (tyramine, amphetamines, ephedrine)

A

MAOa inhibitors - causes HTN crisis when mixed with tyramine (red wine, cheese)

31
Q

alpha receptor antagonists effects? clinical uses?

A

decreased TPR, decreased mean BP (normal alpha 1 constriction) - may cause reflex tachycardia and salt/water retention
clinical: HTN, pheochromocytoma, BPH (a1 blocker)

32
Q

nonselective alpha receptor antagonist drugs? competitive/noncompetitive? clinical uses?

A

phentolamine - competitive - (acute management HTN)

phenoxybenzamine - noncompetitive (pheochromocytoma)

33
Q

MAO type A

A

mainly in liver, but Anywhere (metabolizes NE, 5HT, tyramine)

34
Q

MAO type B

A

mainly in brain (metabolizes DA)

35
Q

what are the selective alpha 1 blockers? clinical use?

A

-ZOSIN
prazosin, doxazosin, terazosin, tamsulosin
clinical? HTN and BPH (symptomatic treatment)

36
Q

what is the selective alpha 2 blocker? clinical use?

A

mirtazapine, antidepressant

37
Q

what are the beta receptor antagonists?

A

-olol

acebutolol, atenolol, metoprolol, pindolol, propranolol, timolol

38
Q

which beta receptor antagonists are beta 1 selective?

A

(A-M) acebutolol, atenolol, metoprolol

39
Q

which beta blocker causes the least amount of sedation? why?

A

atenolol - no CNS entry

40
Q

which beta blockers have no increase in blood lipids? why?

A

acebutolol, pindolol (because partial agonists)

41
Q

which beta blocker is best for asthmatics?

A

pindolol

42
Q

which beta blocker is used in social phobias?

A

propranolol

43
Q

uses for beta blockers

A

angina, HTN, post==MI

44
Q

labetalol and carvedilol

A

combined alpha-1 and beta blocking activity - NOT -olol becuase not full beta blockers

45
Q

carvedilol use

A

CHF

46
Q

labetalol use

A

hypertensive emergencies

47
Q

what does chronic use of beta blockers lead to?

A

receptor upregulation

48
Q

which adrenergic drugs are used to treat glaucome?

A

pilocarpine, echothiphate –> increased outflow d/t contraction of ciliary muscle which increases flow through canal of schlemm
timolol –> block actions of NE at ciliary epithelium (decrease aqueous humor formation)

Abbey pharm shelf/step (23 decks)

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