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Pharmacology > Pharmacology of the Peripheral Nervous System > Flashcards

Pharmacology of the Peripheral Nervous System Flashcards

1
Q

drugs that affect the ANS are used in what

A
  • anesthesia and emergency medicine
  • treatment of allergic reactions, cardiovascular disease, gastrointestinal/urologic disorders, asthma, psychiatric disorders, and glaucoma
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2
Q

adverse rxns to PNS drugs are due to

A

expression through interactions with receptors in the ANS

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3
Q

drugs that directly affect somatic responses at skeletal muscles are used when?

A
  • during surgical procedures and in the ICU to limit movement
  • in treatment of myasthenia gravis
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4
Q

see slides 2&3

A

see slides 2&3

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5
Q

where do neurohumoral transmissions occur

A

btwn nerve cells (across synapses) and btwn nerve cells and effectors cells (across neuroeffector junctions)

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6
Q

what are the 2 major neurotransmitters in the PNS

A
  1. Acetylcholine (ACh)

2. Norepinephrine (NE)

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7
Q

what are the steps in neurotransmission

A
  1. synthesis of neurotransmitter
  2. sotrage of neurotransmitter
  3. release of neurotransmitter
  4. receptor binding (recognition) of neurotransmitter
  5. inactivation of neurotransmitter
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8
Q

see slide 6

A

see slide 6

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9
Q

what type of neurotransmitter is acetylcholine

A

a cholinergic

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10
Q

where is acetylcholine stored

A

in synaptic vesicles via a proton antiporter

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11
Q

see slides 8-12

A

see slides 8-12

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12
Q

what are the adrenergic receptors

A

alpha1, alpha2 (3 subtupes each)

beta1, beta2, beta3

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13
Q

what are the cholinergic receptors

A

nicotinic receptors: Nn, Nm (sodium channels compromised of 5 subints)

muscarinic receptors: M1,M2,M3,M4,M5

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14
Q

where are alpha 1 receptors located

A
  • vascular smooth m.
  • pupillary radial m.
  • genitourinary smooth m.
  • sphincters
  • pilomotor smooth m.
  • sweat glands
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15
Q

what are the physiological responses of Alpha 1 receptors

A 
Contraction (vasoconstriction;  TPR)
Contraction (dilates pupil)
Contraction
Contraction
Contraction (erects hair)
Secretion
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16
Q

where are alpha 2 receptors located

A 
Some vascular smooth muscle
Presynaptic (NE, some ACh nerves)
Platelets
Pancreas
CNS
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17
Q

what are the physiological responses of Alpha 2 receptor

A 
Contraction (vasoconstriction)
Inhibits NT release
Aggregation
Inhibits insulin release
Multiple sites ( sympathetic outflow)
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18
Q

see slides 14-21

A

see slides 14-21

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19
Q

what are the catecholamines

A
  1. epinephrine
  2. norepinephrine
  3. dopamine
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20
Q

what are the uses of Epinephrine

A

Anaphylaxis, Vasoconstrictor added to local anesthetics, topical hemostatic, cardiac rescue

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21
Q

what are the uses of norepinephrine

A

blood pressure support

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22
Q

what are the uses of dopamine

A

severe CHF; cardiogenic/septic shock

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23
Q

see slide 23

A

see slide 23

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24
Q

what are the types of Adrenergic Agonists

A
  1. direct
  2. indirect (amphetamine, tyramine)
  3. mixed (ephedrine)
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25
Q

the clinical effects of alpha receptor agonists are due to what

A

activation of alpha-adrenergic receptors in vascular smooth m.

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26
Q

what are the clinical effects of alpha receptor agonists

A
  • peripheral vascular resistance is increased
  • blood pressure is maintained or elevated
    - useful in some patients with hypotension or shock
  • also are used topically as nasal decongestants
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27
Q

what are the direct acting Alpha-1 Selective agonists

A
  • Phenylephrine
  • methoxamine
  • several “azoline” derivaties
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28
Q

what are mixed acting Alpha-1 Selective agonists

A

Metaraminol

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29
Q

what is the therapeutic use of alpha-2 selective agonists

A
  • used for the treatment of hypertension (topically in opthalmology)
  • capacity to lower BP results from activation of alpha2- receptors in the CV control centers of the CNS which suppress the outflow of sympathetic nervous system activity form the brain
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30
Q

what are the adverse effects of alpha-2 selective agonists

A

dry mouth and sedation

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31
Q

name 3 alpha-2 selective agonists

A
  1. Clonidine
  2. Guanfacine, Guanabenz
  3. Methyldopa (prodrug)
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32
Q

what is the therapeutic use of Beta Receptor Agonists

A
  • treatment of bronchoconstriction in pts with asthma or chronic obstructive pulmonary disease
  • occasionally used for cardiac stimulation
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33
Q

name 2 nonselective Beta Agonists

A
  1. isoproterenol

2. Epinephrine (also activates alpha receptors)

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34
Q

what causes the adverse effects of Beta adrenergic agonists

A
  • stimulation of cardiac Beta-1 receptors

- drugs with preferential affinity for Beta-2 receptors compared with Beta-1 receptors have been developed

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35
Q

what are the selective Beta-2 agonists

A 
Metaproterenol
Terbutaline
Albuterol, Pributerol, Fenoterol
Bitolterol (prodrug)
Salmeterol (long acting)
Formoterol (long acting)
36
Q

what are the adverse effects of Beta Agonists

A

Tachycardia, skeletal muscle tremor, restlessness, apprehension and anxiety, increased plasma glucose, decreased plasma K+

37
Q

see slide 32

A

see slide 32

38
Q

name a noncompetitive, nonselective alpha blocker

A

Phenoxybenzamine

39
Q

name 2 competitive, nonselective alpha blocker

A

Phentolamine; Tolazoline

40
Q

name 5 competitive selective alpha1 blockers

A

Prazosin, Terazosin, Doxazosin, Alfusozin, Tamsulosin (α1A)

41
Q

what are the adverse effects of alpha blockers

A
  • Decrease in peripheral resistance;  mean blood pressure
  • Increase in heart rate and cardiac output (mediated by baroreceptor reflex; less with alpha1 selective blocking agents)
  • Improve urine flow in prostatic hypertrophy
42
Q

what are the adverse effects if alpha blocker (continued)

A 
Postural hypotension
Tachycardia
Nasal stuffiness
Weight gain
Psychomotor slowing in some individuals
Inhibition of, or retrograde, ejaculation
Epinephrine “reversal”.
43
Q

what are the clinical uses of alpha blockers

A

Hypertension
Benign prostatic hypertrophy; urinary flow obstruction
Local vasoconstrictor excess (eg, vasoconstrictor + local anesthetic)
Pheochromacytoma (temporary symptomatic control)

44
Q

how do Beta blockers differ

A
  • in their relative affinity for beta receptors subtypes and pharmacokinetics
  • some beta blockers are weak partial agonists of the beta receptors (intrinsic sympathomimetic activity)
  • some retain a degree of local anesthetic-like (so-call membrane stabilizing) effect
45
Q

see slide 39

A

see slide 39

46
Q

what are the side effects of beta blockers

A
  • decreased HR
  • lower BP
  • enhance cardiac efficiency (improve the balance btwn cardiac oxygen supply and demand)
  • antiarrhythmic effects
  • lower intraocular pressure
  • bronchoconstriction
  • metabolic effects
  • exacerbate symptoms of PVD
  • CNS effects (fatigue, sleep, disturbances, depression)
47
Q

what are the antiarrhythmic effects of beta blockers

A
  • depress SA node
  • decrease ectopic pacemaker activity
  • slow atrial and AV node refractory pd
48
Q

what are the metabolic effects of beta blockers

A
  • inhibit lipolysis

- delay recovery from, and mask symptoms of hypoglycaemia

49
Q

what are the clinical uses of beta blockers

A

Hypertension
Supraventricular and ventricular arrhythmias
Angina pectoris
Hypertropic obstructive cardiomyopathy
Post-myocardial infarction (early phase treatment and prophylaxis)
Certain patients with congestive heart failure
Signs and symptoms of hyperthyroidism
Prophylaxis of migraine
Treatment of glaucoma
Social phobia; performance anxiety
Alcohol withdrawal; patients with akathisia

50
Q

see lecture h/o

A

see lecture h/o

51
Q

see slide 44

A

see slide 44

52
Q

how is ACh synthesized

A

choline + acetyl CoA –> Acetylcholine + CoA-SH

53
Q

where is ACh stored

A

in storage vesicles

54
Q

release of ACh is blocked by what

A

botulinum toxin; stimulated by spider venom

55
Q

what are the natural alkaloids

A
  1. Muscarine
  2. Pilocarpine
  3. Nicotinic
56
Q

what is Muscarine isolated from

A

from the mushroom Amanita muscaria

57
Q

where does muscarine act

A

almost exclusively at muscarinic receptors

58
Q

where is Pilocarpine isolated from

A

chief alkaloid obtaiined from the leaflets of S/A shrubs

59
Q

what is the MOA of Pilocarpine

A

acts on muscarinic agonist

60
Q

what is the therapeutic use of Pilocarpine

A
  • is a MIOTIC agent in the treatment of glaucoma and in the treatment of xerostomia
  • sweat and salivary glands are extremely sensitive to the drug
61
Q

what type of receptors are nicotinic receptors

A

ligand-gated ion channels

62
Q

activation of nicotinic receptors cause what

A
  • a rapid increase in cellular permeability to Na+ and Ca++

- depolarization and excitation

63
Q

what are the 2 agents of Nictonic

A
  • nicotine

- lobeline

64
Q

what are synthetic congeners

A

chemically related to ACh

  • undergo slower rate of hydrolysis
  • clinical uses limited to muscarinic effects of bladder and GI-tract
65
Q

what effects do acetylcholinesterase inhibitors cause

A

-accumulation of Ach at all cholinergic synapses

66
Q

what is the therapeutic use of acetylcholinesterase inhibitors

A
  • myasthenia gravis
  • glucoma
  • paralytic ileus
  • atony of the urinary bladder
  • Alzheimer’s disease
  • as pesticides and chemical warfare agents
67
Q

acetylcholinesterase can reverse the paralysis of

A

competitive NM blockers and reduce symptoms of atropine-like toxicity

68
Q

what are the side effects of acetylcholinesterase inhibitors

A
  • intoxication manifest as an intense cholinergic response (“cholinergic crisis”)
  • effects also exerted on skeletal m. and CNS
69
Q

what are the different classification of AChE inhibitors

A

competitive reversible
alternate substrates; slowly reversible
irreversible (organophophates)

70
Q

what are the effects of AChE inhibitors on eye

A

miosis; blurred vision; spasm of accommodation

71
Q

what are the effects of AChE inhibitors on the GI

A

salivation; increased secretions; increased tone and motility; urination; vomiting; diarrhea

72
Q

effects of the AChE inhibitors on respiratory tract

A
  • increased bronchial secretions; watery

nasal discharge; bronchoconstriction; weakness or paralysis of respiratory muscles

73
Q

what are the effects of AChE inhibitors on the cardiovascular system

A
  • bradycardia; decreased cardiac output; hypotension; atrial flutter
74
Q

what are the effects of AChE inhibitors on the CNS

A

tremor; anxiety; restlessness; convulsions; coma

75
Q

what are the effects of AChE inhibitors on skeletal muscle

A

fasciculation; increased force of

muscle contraction followed by weakness; muscle paralysis due to depolarizing-type neuromuscular blockade

76
Q

which AChE inhibitors are used to treat Alzheimer’s Disease

A

Tacrine (reversible)
Donepezil (reversible)
Rivastigmine (carbamate)
Galantamine (reversible)

77
Q

what is the function of antimuscarinic such as atropine

A

-reduces the effect of ACh at muscarinic sites

78
Q

see slide 55

A

see slide 55

79
Q

what are muscarinic receptor antagonists

A

-are drugs (organic esters) that inhibit the actions of Ach on autonomic cholinergic nerves and on smooth m. cells that lack parasympathetic innervation

80
Q

what drugs are classificed as belladonna alkaloids

A

atropine and scopolamine

81
Q

what is the MOA of muscarinic receptor antagonists

A

-are competitive antagonists of muscarinic agonists competing for a common binding site on the receptor

82
Q

what are the effects of atropine at low doses

A

Slight cardiac slowing followed by slight increases in heart rate, decreased salivation, inhibition of sweating. At moderate does dryness of mouth is pronounced with tachycardia, mydriasis, and cycloplegia

83
Q

what are the effects of atropine at high doses

A

Reduced tone and motility in GI tract; decrease in vagus stimulated gastric, pancreatic, intestinal and biliary secretions; urinary retention

84
Q

what are the side effects of atropine

A

Pulse rapid and weak; iris obliterated; vision very blurred; skin is flushed, hot, and dry; ataxia, restlessness, excitement, hallucinations, delirium, coma

85
Q

what are the clinical uses of muscarinic blockers

A 
Reduce GI tone/motility and bladder voiding
Ocular exams
Anesthesia ( ↓ vagal influences)
Reverse sinus bradycardia
Motion sickness
Treat acute mushroom; AChE(-) poisoning
Adjunct in Parkinson’s disease 
Adjunct in bronchial asthma (“tropiums”)
86
Q

what are the limited clinical use of ganglionic blocking agents

A

controlled hypotension; “bloodless” surgical field

Pharmacology (23 decks)

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