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Pharmacology > Autonomics > Flashcards

Autonomics Flashcards

1
Q

Differentiate between the Sympathetic and Parasympathetic Nervous Systems.

A

SNS: Fight/Flight
PNS: Rest/Digest

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2
Q

In the sympathetic nervous system, preganglionic neurons are very _____ and end in ganglionic neurons very _____ to the spinal cord.

A

Short and close

Postganglionic neurons are long and travel further to site

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3
Q

In the parasympathetic nervous system, preganglionic neurons are very ______ and travel _____ distances.

A

Long and long

Post ganglionic neurons are shorter with short distances to travel

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4
Q

In the sympathetic nervous system; what neurotransmitter is present in the pre and post ganglions neurons and what receptors do they act on.

A

Pre ganglionic: Acetylcholine acts on the Nicotinic receptor
Post ganglionic: Norepinephrine acts on Adrenergeric (alpha and beta)receptors and Acetylcholine acts on Muscarinic (sweat glands)

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5
Q

In the parasympathetic nervous system; what neurotransmitter is present in the pre and post ganglions neurons and what receptors do they act on.

A

Pre ganglionic: Acetylcholine acts on Nicotinic receptors

Post ganglionic: Acetylcholine acts on Muscarinic receptors

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6
Q

In the somatic nervous system; what neurotransmitter is present in the neurons and what receptors does it act on.

A

Acetylcholine at the Nicotinic receptor

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7
Q

For sympathetic innervation neurons arise from:

A

Lumbar, thoracic regions.

Short pre, long post

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8
Q

For parasympathetic innervation neurons arise from:

A

Cranial, sacral

Long pre, short post

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9
Q

The primary neurotransmitter of the sympathetic nervous system is:

A

Norepinephrine

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10
Q

Catecholamines produced in neurons include:

A

Dopamine
Norepinephrine
Epinephrine

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11
Q

How can tyramine and MAOI’s lead to a hypertensive crisis?

A

Tyramine is metabolized by MAO, in the setting of taking an MAOI this does not happen. Excess tyramine displaces NE from vesicles, increased available NE, this can causes a hypertensive crisis.

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12
Q

Nonselective adrenoreceptors agonists include:

A

Norepinephrine
Epinephrine
Dobutamine

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13
Q

Non-selective alpha agonists include:

A

Oxymetazoline (afrin) and Tetrahydrozoline

Clinically these agents are used topically so alpha-1 effects usually predominate

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14
Q

Alpha-1 selective agonists include:

A

Phenylephrine and Pseudoephedrine

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15
Q

Alpha-2 selective agonists include:

A

Clonidine, guanabenz, guanfacine, alpha-methyldopa

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16
Q

Selectivity of alpha agonists phenylephrine and clonidine:

A

Phenylephrine a1>a2»»>B

Clonidine a2>a1»»>B

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17
Q

Selectivity of mixed alpha and beta agonists NE and epi:

A

NE: a1=a2 B1»B2
Epi: a1=a2; B1=B2

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18
Q

What are the main tissues alpha-1 agonist effect and what are their actions?

A 
Smooth muscle (innervated)=contraction 
Pupillary dilator muscle= contraction/dilate pupils
Pilomotor smooth muscle= erects hair
Prostate=contraction 
Heart=Increases forces of contraction
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19
Q

What are the main tissues alpha-2 agonist affect and what are their actions?

A

Negative feedback; sends message to decrease catecholamine release

Platelets=Aggregation
Adrenergic muscle terminals=Inhibits transmitter release
Some vascular smooth muscle= contraction
Fat cells= Inhibits lypolysis

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20
Q

B-selective adrenoreceptor agonists include:

A

Nonselective: Isoproterenol (Isuprel)- not used
B1 selective: Dobutamine, Xamoterol- not used
B2 selective: Metaproterenol, terbutaline, albuterol, salmeterol, formoterol, perbuterol, bitolterol

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21
Q

Selectivity of B agonists; dobutamine, isoproterenol, terbutaline/albuterol:

A

Dobutamine B1>B2»»»a
Isoproterenol B1=B2»»>a
Terbutaline/albuterol B2»B1»»a

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22
Q

Functional effects of B1 (tissue and action)

A

Heart= increases force and rate of contraction

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23
Q

Functional effects of B2 (tissues and actions)

A

Respiratory, uterine, vascular smooth muscle= Relaxation
Skeletal muscle= Promotes K uptake
Liver= Activates glycogenolysis

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24
Q

Functional effects of B3 (tissue and action)

A

Fat cells= lipolysis

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25
Q

Selectivity of Dopamine agonists:

A

Dopamine: D1=D2»B»a
Fenoldopam: D1»D2

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26
Q

Functional effects of D1 and D2 (tissues and actions)

A

D1
Smooth muscle= dilates renal blood flow

D2
Nerve endings= Modulates transmitter release

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27
Q

CV effects of sympathomimetics:

A

a1: vasoconstriction=incr. BP
a2: neg. feedback=dec. BP
b1: increased CO=incr. BP
b2: peripheral vasodilation-dec. BP

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28
Q

What type of agonist would be used to accommodate for vision?

A

a1= causes mydriasis (pupil dilation)

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29
Q

How are a1, a2, and b1 used in regulation of intraocular pressure?

A

a1, a2=increased humoral outflow (=dec. pressure)

B1= increased production of aqueous humor (=dec. this to decrease pressure)

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30
Q

Respiratory effects of sympathomimetics:

A

a1=reduces mucosal secretion (decongestant)

b2= bronchial dilation

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31
Q

GI effects of sympathomimetics:

A

a2, b2= decreased peristalsis (direct smooth muscle relaxation)
a2= decreased digestive secretions

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32
Q

GU effects of sympathomimetics:

A

Bladder- a1= contraction of urethral sphincter; b2 relaxation (decreases UOP)
Erectile tissue- a1= facilitates ejaculation
Uterus- B2= relaxation (inhibits labor)

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33
Q

Direct Acting Sympathomimetics: Catecholamines

Epinephrine:

A

a1: vasoconstriction
B1: cardiac stimulation
B2: vasodilation

ex-anaphylaxis

34
Q

Direct Acting Sympathomimetics: Catecholamines

Norepinephrine:

A

a1: vasoconstriction
B1: cardiac stimulation

ex-sepsis

35
Q

Direct Acting Sympathomimetics: Catecholamines

Isoproterenol:

A

B1-cardiac stimulation

36
Q

Direct Acting Sympathomimetics: Catecholamines

Dopamine:

A

Dose dependent
D1/D2-renal vasodilation(lower dose)
a1- vasoconstriction (higher dose)
B1-cardiac stimulation (higher dose)

37
Q

Direct Acting Sympathomimetics: Non-Catecholamines are not inactivated by ________.

A

COMT (enzyme that breaks down catecholamines)

=longer duration of action, better access into brain

38
Q

Direct Acting Sympathomimetics: Non-Catecholamines:

a1 agonists:

A

Phenylephrine- mydriatic, decongoestant, pressor
Methoxamine- increases BP
Midodrine (ProAmatine)- postural hypotension
Oxymetazoline tetrahydrozoline, xylometazoline- nasal and ocular decongestants

39
Q

Direct Acting Sympathomimetics: Non-Catecholamines:

a2 agonists:

A

Clonidine- CNS receptors, decreases BP

Apraclonidine- ciliary receptors, reduces intraocular pressure

40
Q

Direct Acting Sympathomimetics: Non-Catecholamines: B2 agonists:

A

Albuterol, terbutaline, pirbuterol, botolterol, metaproterenol- asthma, COPD
Salmeterol, formorterol- long duration of action
Ritodrine- relaxes uterus to delay premature labor

41
Q

Indirect Acting Sympathomimetics:

A

Enhance the release of catecholamines

Amphetamine-increases release of NE and dopa
Methamphetamine- similar to amphetamine but higher CNS effects
Methylphenidate (Ritalin), permoline (Cylert)- amphetamine variants used for ADHD

42
Q

MOA of alpha antagonists:

A

a-receptor responds faster than B-receptor
Blocks stimulatory effects of NE at a-receptor

Reversible: Phentolamine
Irreversible: Phenooxybenzamine

43
Q

CV effects of a-antagonism:

A

a1:
decreases PVR and lowers BP
postural hypotension d/t failure of vasoconstriction upon standing up
a2:
(blocks negative feedback) Increase NE release from nerve terminals

44
Q

GU effects of a-antagonism:

A

Blockade in prostate and bladder cause muscle relaxation and ease micturition

45
Q

Phentolamine, phenoxybenzamine

A

a- antagonist
vasodilation, lowers BP

diabetic neuropathy, enhance male sexual function, reverse side effects of clonidine withdrawal

46
Q

Prazosin (minipress), terazosin (Hytrin), doxazosin (Cardura), tamsulosin (Flomax)

A

a-antagonists

-Hypertension, BPH

47
Q

Yohimbine

A

a-antagonist

Diabetic neuropathy, enhance male sexual function, reverse side effects of clonidine withdrawal

48
Q

B antagonist CV effects:

A

Decreases CO, BP
Increases Na+ retention

Propranolol (antag) wins over epi= vasodilation>constriciton

49
Q

B antagonist Resp effects:

A

Increases airway resistance

50
Q

B antagonist ocular effects:

A

Decreases aqueous humor production

51
Q

B antagonist metabolic effects:

A

Decreases carb metabolism which decreases insulin release
Decreases renin secretion with decrease angiotensin II (lowers BP)
Decreases Na+ excretion
Decreases lipolysis

52
Q

Timol:

A

B antagonist
Used for glaucoma by decreasing aqueous humor production
Topical ocular hypotensive agent

53
Q

Betaxolol:

A

B antagonist

Used for glaucoma by decreasing aqueous humor production

54
Q

______ is the only neurotransmitter working in the PSNS.

A

Acetylcholine

55
Q

What is botulinum toxin’s effect on Acetylcholine?

A

Prevents exocytosis of presynaptic vesicles which prevents release of Ach at nicotinic receptors/neuromuscular junction

56
Q

Neostigmine and pyridostigmine:

A

AChE inhibitors
Use in treating disease of the neuromuscular junction (myasthenia gravis)

Neostigmine also increases smooth muscle motility to ease abdominal distension

57
Q

Physostigmine (Isopto):

A

AChE inhibitor

Increases outflow of aqueous humor to treat glaucoma

58
Q

Tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne):

A

AChE inhibitors

Used to treat AD and other cognitive dysfunction

59
Q

AE and CI of AChE inhibitors:

A

AE: Peripheral ACh effects of GI tract: N/V/D, anorexia, flatulence, abdominal cramping (dose dependent)
CI: Unstable or severe cardiac disease (AV block), uncontrolled epilepsy, active PUD

60
Q

Why is ACh not administered?

A

Broad activity and rapid hydrolysis of AChE

61
Q

Methacholine:

A

Muscarinic Agonist
Used to diagnose asthma
Causes bronchoconstriction

62
Q

Carbachol:

A

Muscarinic Agonist

Miosis and decreased intraocular pressure

63
Q

Bethanechol:

A

Muscarinic Agonist

GI and urinary tract motility- post op and post-partum urinary retention, neurogenic bladder

64
Q

Succinylcholine:

A

Nicotinic Agonist
Resistant to AChE
Induction of paralysis by means of depolarizing blockade
Continuous activation of nicotinic receptor channels results in neuronal depolarization of blockade

65
Q

What are muscarinic antagonists MOA?

A

By antagonizing muscarinic receptors they causes sympathetic responses to predominate

66
Q

Atropine:

A

Muscarinic Antagonist
Mydriasis for eye exams
Reverse symptomatic brady
Inhibits excessive salivation and mucus secretion during surgery
Prevents vagal reflexes induced by surgical trauma of visceral organs

67
Q

Scopolamine:

A

Muscarinic Antagonist
Treats motion sickness
Transdermal patch

68
Q

Ipraroprium (Atrovent), tiotropium (Spiriva),

A

Muscarinic Antagonists
Bronchodilators
Used to treat COPD

69
Q

Oxybutynin (Ditropan), tolterodine (Detrol)

A

Muscarinic Antagonists
Used to treat overactive bladder
Work at non-specific M-rc

70
Q

Darifenacin (Enablex), Solifenacin (Vesicare)

A

Muscarinic Antagonists
Used to treat overactive bladder
M3 specific

71
Q

AE and CI for Muscarinic Receptors:

A

AE: Anticholinergic effects
Blurred vision, dry mouth, ileus, urinary retention, flushing, agitation, tachycardia
CI: angle-closure glaucoma
Use caution with elderly

72
Q

MOA of Nicotinic Antagonists:

A

Prevent ACh binding to nicotinic receptors and subsequent muscle depolarization

73
Q

Pancuronium, Vecuronium, Rocuronium:

A

Nicotinic receptors

Induce paralysis

74
Q

What is the MOA of AChE inhibitors?

A

Elevates concentration of endogenously release ACh in the synapse
=increases transmission at NM junction, increased parasympathetic tone, increases central cholinergic activity

75
Q

Muscarinic Effects:

A 
SLUG BAM 
Salivation, secretions, sweating
Lacrimation 
Urination 
GI upset (vomiting, diarrhea)
Brady, bronchoconstriction, bowel movement 
Abdominal cramps, Anorexia 
Miosis
76
Q

Anticholinergic Effects:

A 
ABCDS
Anorexia
Blurry vision
Constipation, confusion 
Dry mouth
Sedation, stasis of urine

Can’ts
Cant: Pee, See, Spit, Shit

77
Q

a-agonism Fight/flight properties:

A 
Vasoconstriction 
Urethral constriction 
Dec. humoral outflow 
Prostate contraction 
Decreased peristalsis 
Platelet inhibtion
78
Q

a- antagonism Rest/Digest properties:

A 
Vasodilation 
Urethral relaxation 
Miosis 
Prostate relaxation 
Nasal congestion
79
Q

b1 agonism Fight/Flight properties:

A

Increase CO/BP

Increased aqueous humor

80
Q

b2 agonism Fight/Flight properties:

A 
Bronchodilation
Increase Na retention 
Peripheral vasodilation 
Decreased peristalsis 
Uterine relaxation
81
Q

B1 antagonism : Rest/Digest properties:

A

Decrease CO/HR/BP

Decrease aqueous humor

82
Q

B2/B3 antagonism: Rest/Digest properties:

A

Bronchoconstriction

Metabolic effects

Pharmacology (48 decks)

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