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Step 1 > Pharm autonomic drugs > Flashcards

Pharm autonomic drugs Flashcards

1
Q

Number of neurons in sequence in the sympathetic versus parasymp versus somatic nervous systems

A

For sympathetic, it is two neurons in sequence (Ach, then norepi). For parasymp, it is two neurons in seq (Ach, then Ach), and somatic is a single neuron (Ach) to skeletal muscle

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2
Q

How is sympathetic to the sweat glands and sympathetic to the renal vasculature different from normal sympathetic innervation?

A

With normal, it is Ach then norepi; with sweat glands, it is Ach then Ach; for renal it is Ach then Dopamine receptor

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3
Q

Ach receptors

A

Nicotinic Ach receptors are the first ones; muscarinic Ach receptors are the second ones

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4
Q

Nicotinic Ach receptors

A

ligand-gated Na+/K+ channels

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5
Q

Muscarinic Ach receptors

A

G-protein coupled receptors that usually act through second messengers; 5 subtypes are M1, M2, M3, M4, and M5

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6
Q

alpha 1 receptors

A

G protein class q; increase vascular smooth muscle contraction, increase pupillary dilator muscle contraction, increase intestinal and bladder sphincter muscle contraction

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7
Q

alpha 2 receptors

A

G protein class I; decreased sympathetic outflow, decrease insulin release, decrease lipolysis, increase platelet aggregation, decrease acqueous humor production

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8
Q

beta 1 receptors

A

G protein class s; increase HR, increase contractiliy, increae renin release, increase lipolysis

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9
Q

beta 2 receptor

A

G protein class s; vasodilation, bronchodilation, increase lipolysis, increase insulin release, decreaes uterine tone (tocolysis), ciliary muscle relaxation, increase acqueous humor production

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10
Q

M1 parasymp receptor

A

G protein class q; CNS, enteric NS

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11
Q

M2 parasymp receptor

A

G protein class I; decrease HR and contractility of atria

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12
Q

M3 parasymp receptor

A

G protein class q; increase exocrine gland secretions, increase gut peristalsis, increase bladder contraction, bronchoconstriction, increase pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accomodation)

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13
Q

D1 dopamine receptor

A

G protein class s; relaxes renal vascular smooth muscle

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14
Q

D2 dopamine receptor

A

G protein class I; modulates transmitter release, esp in brain

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15
Q

H1 histamine receptor

A

G protein class q; increase nasal and bronchial mucus production, increase vascular permeability, contraction of bronchioles, pruritis, pain

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16
Q

H2 histamine receptors

A

G protein class s; increase gastric acid secretion

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17
Q

Vasopressin V1

A

G protein class q; increase vascular smooth muscle contraction

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18
Q

Vasopressin V2

A

G protein class s; increase water permeability and reabsorption in the collecting tubules of the kidney (V2 is found in the 2 kidneys)

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19
Q

Way to remember the G protein class

A

Qiss and qiq until you’re siq of sqs

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20
Q

How is Gq involved in the receptor pway?

A

Receptor activates Gq, which turns on phospholipase C, which leads to conversion of PIP2 into DAG and IP3; IP3 leads to increase in calcium into the cell and contraction of the smooth muscle; DAG activates protein kinase C

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21
Q

How are Gs and Gi involved in the receptor pway?

A

Gs turns on adenylate cyclase, whereas Gi inhib adenylyl cyclase; adenylyl cyclase converts ATP into cAMP, which activates protein kinase A, which increases calcium in the heart and inhibits myosin LCK in smooth muscle cells

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22
Q

How do cholinergic neurons work?

A

The choline needs to get into the cell, get aceylated by Acetyl-co-A, which turns it into Ach, which gets packaged into the vesicle; Then when calcium gets into the cell, the vesicle can be released; Achesterase chomps up the Ach back into choline and acetate and the cycle continues

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23
Q

Hemicholinum

A

inhibits the choline from getting into the neuron so that it cannot be made into Ach

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24
Q

Vesamicol

A

inhibits the Ach from being taken up into the vesicle in the cell

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25
Q

Botulinum

A

inhibits the release of the vesicle into the nerve terminal

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26
Q

How do noradrenergic neurons work?

A

Tyrosine gets taken up into the cell, then converted to DOPA, which is converted to dopamine; dopamine gets into the vesicle, where it is converted to norepi; the norepi is released when release-modulating receptors on the surface of the cell (ATII,pro, and alpha 2, inhib) signal it to be released by the intake of calcium into the cell

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27
Q

metyrosine

A

inhibits convesion of tyrosine into DOPA

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28
Q

Reserpine

A

inhibits the uptake of dopamine into the vesicle

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29
Q

Bretylium, guanethidine

A

inhibits release of vesicle into the post-synaptic area

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30
Q

Cocaine, TCAs, amphetamine

A

inhibit the reuptake of norepi in the presynaptic neuron

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31
Q

AT II receptor on the surface of the neuron

A

signals that the norepi vesicle should be released into the synapstic space

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32
Q

alpha 2 recepotr

A

norepi acting on the alpha 2 receptor inhibits the release of the norepi into the synapse (negative feedback)

33
Q

Bethanecol

A

cholinomimetic direct agonist; used for post-op ileus, neurogenic ileus, urinary retention; activates bowel and bladder smooth muscle; resistant to Achesterase

34
Q

Carbachol

A

cholimimetic direct agonist; constricts pupil and relieves intraocular pressure in glaucoma; this is just like acetycholine

35
Q

Methacholine

A

cholimimetic direct agonist; used for challenge test for diagnosis of asthma; stimulates muscarinnic receptors in the airway when inhaled

36
Q

Pilocarpine

A

cholimimetic direct agonist; potent stumulator fo sweat, tears, and saliva; open angle and closed angle glaucoma; contracts ciliary muscle of eye (open-angle glaucoma), pupillary sphincter (closed angle glaucoma), resistant to AChE

37
Q

donepezil, galantamine, rivastigmine

A

acetylcholinesterase inhib; used for alzheimer’s disease

38
Q

edrophonium

A

increase Ach; ued for dx of myasthenia gravis in the past; now MG is dx by anti-AChR Ab test

39
Q

neostigmine

A

increases Ach; postop and neurogenic ileus and urinary retention, MG, reversal f NMJ blockade post-op; no CNS penetration; Neo=no

40
Q

physostigmine

A

used to treat anticholinergic toxicity, crosses BBB; “phyxes” atropine overdose

41
Q

pyridostigmine

A

used to treate MG (long acting); does not penetrate CNS

42
Q

what to be careful with the cholinergic agents

A

Exacerbation of COPD, asthma, and peptic ulcers when giving to susceptible patients

43
Q

cholinesterase inhib poisoning

A

results in too much Ach; often due to organophosphates, such as parathion that irreversibly inhibit AChE; causes DUMBBELSS diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle and CNS, lacrimation, sweating, and salivation

44
Q

antidote for organophosphate poisoning

A

atropine (competitive inhib) with pralidoxime (regenerates AChEsterase if given early)

45
Q

atropine, homatropine, tropicamide

A

muscarinic antags that produce mydriasis and cycloplegia (i.e. affect the eye)

46
Q

benztropine

A

muscarinic antag that is used to treat parkinsons disease and acute dystonia

47
Q

glycopyrrolate

A

muscarinic antag that is used IV often pre-op to reduce airway secretions

48
Q

hyoscyamine, dicyclomine

A

muscarinic antag used as antispasmodic for IBS

49
Q

ipratropriu, tiotroprium

A

muscarinic antag used for COPD and asthma

50
Q

oxybutinin, solifenacin, tolterodine

A

muscarinic antag used to reduce bladder spasms and urge incontinence (overactive bladder)

51
Q

scopolamine

A

muscarinic antag used for motion sickness

52
Q

atropine

A

used to treat bradycardia and for opthalmic applications

53
Q

atropine’s effect on eye, airway, stomach, gut, bladder

A

increae pupil dilaton, cycloplegia, decrease airway secretions, decrease stomach acid, decrease motility in the gut, decrease urgency in cystitis

54
Q

Toxicity of atropine

A

increase body temp (due to decrease sweating), rapid pulse, dry mouth, dry, flushed skin, cycloplegia, constipation, disorientation; can cause acute angle-closure glaucoma in elderly (due to mydriasis), urinary retention in men with prostatic hyperplasia and hyperthermia in infants

55
Q

tetrodotoxin

A

Muscarinic antag; highly potent toxin that binds fast voltage gated Na channels in cardac and nerve tissue, preventing depol; causes nausea, diarrhea, paresthesias, weakness, dizziness, loss of reflexes, treatment is supportive; poisoning can result from poorly prepared puffer fish (Japan)

56
Q

Ciguatoxin

A

muscarinic antag; causes ciguatera fish poisoning; opens Na channels causing depol. Sx are like cholinergic poisoning: temp dyasthesia (cold feels hot and vice versa) is a spec finding; treatment is supportive

57
Q

scombroid poisoning

A

muscarinc antag; acute onset burning sensation in the mouth, flushing of face, erythema, urticaria, pruritis, HA. May cause anaphylaxis-like presentation; treat supportively with antihistamines or anti-anaphylactics; caused by eating dark meat fish improperly stored at room temp

58
Q

albuterol, salmeterol

A

B2 greater than B1 agonist; used for asthma or COPD control

59
Q

dobutamine

A

B1 greater than B2 and alpha; used in HF as an ionotrope more often then a chronotrope and in cardiac stress testing

60
Q

dopamine

A

D1 and D2, greater than beta, greater than alpha; used for unstable bradycardia, HF, shock; ionotropic and chronotropic alpha (?) effects predominate at high doses

61
Q

epinephrine

A

beta greater than alpha; used to treat anaphylaxis, asthma, open angle glaucoma; alpha effects predominate at high doses. Significantly stonger effect at beta 2 recepotr than norepi

62
Q

isopreterenol

A

b1 and b2; used for the electrophysiologic eval of tachyarrhythmias. Can worsen ischemia

63
Q

norepi

A

alpha 1 greater than alpha 2 greater than beta 1; used to treat hypotension (but decreases renal perfusion); signif weaker effect at beta 2 receptor than epi

64
Q

phenylephrine

A

alpha 1 greater than alpha 2; used to treat hypotension, used for ocular procedure (bc it is mydriatic), used to treat rhinitis

65
Q

amphetamine

A

indirect general sympathetic agonist bc it is a reuptake inhib, aso releases stored catecholamines; used to treat narcolepsy, obesity, ADHD

66
Q

cocaine

A

inidrect general sympathetic agonist; reuptake inhib; causes vasoconstriction and local anesthesia; never give beta blockers if cocaine intox is suspected because it can lead to unopposed alpha 1 activation and extreme HTN

67
Q

ephedrine

A

indirect general sympathetic agonist; releases stored catecholamines; used for nasal congestion, urinary incont, hypotension

68
Q

norepi versus isopreteronol

A

norepi increases systolic and diastolic pressures as a result of alpha 1 mediated vasoconstriction leading to incr mean arterial presure leading to relex bradycardia; isoproterenol has little allpha effect but causes b2 mediated vasodilation, resulting in decreased MAP and increased HR through B1 and reflex activity

69
Q

clonidine

A

alpha 2 agonist; used to hypertensive urgency, does nor decreae renal blood flow; also used for ADHD and Tourette’s; toxicity is CNS depression, bradycardia, hypotension, resp depression, miosis

70
Q

alpha methyldopa

A

alpha 2 agonist; used for HTN in pregnancy; toxicity has direct Coomb’s pos hemolysis, SLE-like syndrome

71
Q

phenoxybenzamine

A

irreversible nonselective alpha blockers; used to treat pheochromocytoma preop to prevent catecholamine crisis; can cause orthostatic hypotension, and reflex tachycardia

72
Q

Phentolamine

A

reversible non-selective alpha blocker used for patients on MAOis who eat tyramine containing foods; can, again, cause orthostatic hypotension, relfex tachycardia

73
Q

Prazosin, terazosin, doxazosin, tamsulosin

A

selective alpha 1 blocker; used for urinary sx of BPH, PTSD (prazosin), hypertension (except tamsulosin); side effects are orthostatic hypotension, dizziness, HA

74
Q

mirtazapine

A

selective alpha 2 blocker; used to treat depression; side effects are sedation, increased serum cholesterol, increase appetiite

75
Q

Effect of beta blockers (what are they used for clinically?)

A

used for angina to decrease HR and contractility, resulting in decreased oxygen consumption; used in SVT to decrease AV condution velocity (class II antiarrhythmics), HTN (decrease CO, decrease renin secretion), glaucoma (decr secretion of acqueous humor)

76
Q

toxicity of beta blockers

A

impotence, CV adverse effects (bradycardia, AV bock, HF), CNS adverse efffects (seizures, sedation, sleep alterations), dyslipidemia (metop), and asthma/COPD exacerbations

77
Q

Beta 1 selective antags

A

Acebutolol (partial agonist), atenolol, betaxolol, esmolol, metoprolol; mostly A-M (first half of alphabet)

78
Q

Nonselective beta antags

A

nadolol, pindolol, propranolol, timolol; mostly go from N to Z

79
Q

Nonselective alpha and beta antags

A

carvedilol, labetolol; “olol”

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