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Systemic Pharmacology I > Parasympathetic Drugs > Flashcards

Parasympathetic Drugs Flashcards

1
Q

cholinomimetics are drugs that _____

A

mimic acetylcholine

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2
Q

direct acting cholinomimetics MOA

A

ACh receptor agonists

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3
Q

direct acting cholinomimetics MOA

A

cholinesterase inhibitors- inhibit the hydrolysis of endogenous ACh

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4
Q

all cholinergic agonists are metabolized by ____:

  • at ____
  • in the ____
  • in the ____
A

cholinesterase;
receptor;
blood;
liver

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5
Q

ACh, Carbachol, Bethanechol (synthetic choline esters)

A
  • not very lipid soluble (poorly absorbed)
  • highly charged molecules
  • differ in susceptibility to cholinesterase
  • mainly excreted by the kidneys
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6
Q

susceptibility to cholinesterase:

acetylcholine

A

rapidly hydrolyzed; brief duration of action

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7
Q

susceptibility to cholinesterase:

carbachol and bethanechol

A

more resistant to cholinesterase; longer duration of action

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8
Q

Pilocarpine, Nicotine, Muscarine (cholinomimetic alkaloids)

A
  • readily absorbed form most sites of administration
  • nicotine absorbed across skin
  • muscarine is toxic and crosses BBB
  • all mainly excreted by the kidneys
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9
Q

muscarinic receptors are ____ receptors;
activation produces ____;
organ function is _____

A

G-protein;
a cascade of 2nd messengers;
directly altered

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10
Q

there are also muscarinic receptors on the _____ (both parasympathetic and sympathetic);
activation causes _____;
organ function is _____

A

presynaptic nerve terminal;
an inhibition of ACh and/or NE release (feedback inhibition);
indirectly altered

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11
Q

nicotinic receptors are ____ receptors;
activation causes _____;
prolonged agonist binding causes _____

A

ion channel;
conformational change allowing sodium and potassium ions to diffuse down their concentration gradients (produces depolarization of nerve cell or neuromuscular end plate membrane);
the post-ganglionic neuron to stop firing- prevents recovery (depolarizing blockade) and the receptor becomes desensitized to agonist

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12
Q

muscarinic effects:

eye

A
  • contraction of iris sphincter (miosis)
  • contraction of ciliary muscle (accommodation)
  • above result in opening of TM and lowering IOP
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13
Q

muscarinic effects:

cardiovascular system

A

heart:

  • decrease in HR
  • hyperpolarization of SA and AV node
  • decreases duration of action potential and decreases contractility of atrial and ventricular cells

blood vessels:

  • vasodilation (decreases peripheral resistance)
  • in presence of endothelial damage (atherosclerosis), will cause vasoconstriction
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14
Q

muscarinic effects:

respiratory system

A
  • contraction of bronchial smooth muscle (bronchoconstriction)
  • stimulation of bronchial glands (increase mucous secretion)
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15
Q

muscarinic effects:

GI tract

A
  • increase smooth muscle motility
  • relax most sphincters
  • stimulate salivary and gastric glands to secrete
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16
Q

muscarinic effects:

genitourinary tract

A

-stimulate detrusor muscle and relax the trigone and sphincter muscles of bladder
(promote urination)

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17
Q

muscarinic effects:

miscellaneous glands

A

-stimulate secretion by sweat, lacrimal, and nasopharyngeal glands

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18
Q

nicotinic effects:

PNS

A
  • activation of nicotinic receptors in autonomic ganglia
  • sympatheticomimetic in cardiovascular system (increase HR and BP)
  • parasympatheticomimetic in GI and urinary tracts (all previously noted responses and nausea, vomiting, diarrhea, and urination)
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19
Q

activation of nicotinic receptors often resembles _____

A

simultaneous discharge of both para and sympathetic system

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20
Q

nicotinic effects:

NMJ

A

-causes depolarization followed by depolarization blockade

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21
Q

most indirect-acting cholinomimetics are ____; chemistry determines _____

A

simple alcohols or esters of alcohols;

duration of action

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22
Q

indirect-acting cholinomimetics that are derivatives of phosphoric acid (organophosphates) have _____;
many _____;
some used as _____

A

longest duration of action;
different compounds;
nerve gas or insecticides

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23
Q

absorption of indirect-acting cholinomimetics

A
  • variable absorption
  • physostigmine is well absorbed from all sites and can be used topically in the eye
  • organophosphates are absorbed from skin, lung, gut, and conjunctiva (dangerous to humans)
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24
Q

administration of indirect-acting cholinomimetics

A

any (including IV)

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25
Q

distribution and elimination of indirect-acting cholinomimetics

A
  • variable

- organophosphates are distributed to CNS (CNS toxicity is common, exception is echothiophate)

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26
Q

indirect-acting cholinomimetics MOA

A
  • increase concentration of endogenous ACh by inhibiting ACh-esterase
  • chemistry determines interaction with the enzyme
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27
Q

short-acting indirect-acting cholinomimetics MOA

A
  • edrophonium
  • forms reversible bond with the enzyme
  • not actually a substrate for ACh-esterase
28
Q

intermediate-acting indirect-acting cholinomimetics MOA

A
  • neostigmine, physostigmine, pyridostigmine

- resistant to part of enzyme action so takes longer

29
Q

long-acting indirect-acting cholinomimetics MOA

A
  • echothiophate, malathion, parathion, sarin

- forms phosphorylated enzyme complex that strengthens the bond with the drug

30
Q

indirect-acting cholinomimetics effects:

CNS

A
  • low concentrations: alerting response

- high concentrations: convulsions

31
Q

indirect-acting cholinomimetics effects:

eye, respiratory tract, GI tract, urinary tract

A

similar to the direct-acting cholinomimetics

32
Q

indirect-acting cholinomimetics effects:

cardiovascular system

A
  • increased activity in both sympathetic and parasympathetic ganglia as well as at muscarinic receptors
  • parasympathetic effects dominate due to direct muscarinic innervation (decreased HR and decreased cardiac output)
  • minimal effect on vascular smooth muscle (not innervated) (allows vasoconstriction and increased BP as a result of activity in the sympathetic ganglia)
33
Q

indirect-acting cholinomimetics effects:

neuromuscular junction

A
  • therapeutic concentrations prolong and intensify the actions of acetylcholine
  • increases strength of muscle contraction (esp. in patients with myasthenia gravis)
  • high or prolonged concentrations will cause depolarizing neuromuscular blockade
34
Q

clinical uses of cholinomimetics:

eye

A
  • cause contraction of the ciliary body (increases aqueous outflow)
  • older treatment of glaucoma
  • pilocarpine, carbachol, echothiophate
35
Q

clinical uses of cholinomimetics:

GI and urinary tract

A
  • used to treat disorders that involve a decrease in smooth muscle activity without obstruction
  • postoperative atony or urinary retention
  • neurogenic bladder (secondary to spinal cord injury)
  • bethanechol or neostigmine most common
  • can be used to increase salivary secretion (Sjogren’s syndrome)
  • pilocarpine, cevimeline
36
Q

clinical uses of cholinomimetics:

neuromuscular junction

A
  • treatment of myasthenia gravis
  • cholinesterase inhibitors used in treatment
  • edrophonium used more for diagnosis- pt displays an improvement in muscle strength after injection
  • pyridostigmine is most common for long-term treatment
  • neostigmine also used
  • reverse neuromuscular blockade produced during surgical anesthesia
  • neostigmine, edrophonium
37
Q

clinical uses of cholinomimetics:

treatment of Alzheimer’s

A
  • donepezil
  • galantamine
  • rivastigmine
38
Q

adverse effects of direct-acting cholinomimetics

A
  • nausea
  • vomiting
  • diarrhea
  • urinary urgency
  • salivation
  • sweating
  • flushing of the skin (vasodilation)
  • bronchial constriction
39
Q

adverse effects of cholinesterase inhibitors

A
  • same as direct-acting
  • also includes: muscle weakness, convulsions, respiratory failure

-the above often result from exposure to pesticides (organophosphates)

40
Q

cholinergic blockers:

  • interrupt _____
  • prevent ACh from _____
A

parasympathetic nerve impulses;

stimulating cholinergic receptors

41
Q

cholinoceptor antagonists:

  • ganglion blockers _____
  • muscarinic blockers can be further divided based on _____
A

have little clinical use;

affinity for certain receptor subtype (M1-M5)

42
Q

many muscarinic antagonists are _____, but ____ have also been formulated

A 
naturally occurring compounds (ex: atropine derived from nightshade plant);
synthetic compounds (ex: tropicamide)
43
Q

muscarinic antagonists:

absorption

A

most are well absorbed from the gut, conjunctiva, and across skin (some formulations)

44
Q

muscarinic antagonists:

distribution and elimination

A
  • most are widely distributed with CNS penetration

- eliminated via the kidney

45
Q

muscarinic antagonists MOA

A
  • block ACh action at muscarinic receptors
  • moderately selective for various muscarinic receptor subtypes
  • atropine is non-selective (useful in treating cholinomimetic toxicity)
46
Q

muscarinic antagonist effects:

CNS

A
  • atropine has minimal effects
  • scopolamine has marked effects- drowsiness and amnesia at normal doses, reversal of vestibular disturbances (Tx of motion sickness/sea sickness)
47
Q

muscarinic antagonist effects:

cardiovascular system

A

increased HR

48
Q

muscarinic antagonist effects:

eye

A
  • mydriasis (blockage of muscarinic activation of pupillary constrictor muscle allows unopposed sympathetic dilator activity)
  • cycloplegia (weakens contraction of ciliary muscle)
  • reduction in lacrimal secretion
49
Q

muscarinic antagonist effects:

respiratory system

A
  • bronchodilation

- decreased secretions in the lung

50
Q

muscarinic antagonist effects:

GI tract

A
  • decreased salivation
  • decreased production of stomach acid (very large doses)
  • decreased smooth muscle tone and propulsive movements
51
Q

muscarinic antagonist effects:

urinary tract

A

-relax bladder smooth muscle
-slows voiding
(reduced urinary activity)

52
Q

muscarinic antagonist effects:

sweat glands

A
  • reduces sweating

- can produce fever in young patients

53
Q

clinical uses of antimuscarinic drugs:

CNS disordesr

A
  • Parkinson’s disease (mainly adjunctive)

- treatment of motion sickness

54
Q

clinical uses of antimuscarinic drugs:

ocular disorders

A
  • accurate refraction (usually homatropine or cyclopentolate)
  • dilated fundus exam (usually tropicamide or cylcopentolate)
  • treatment of uveitis (prevents synechia, usually homatropine or cyclopentolate)
55
Q

atropine duration of effect

A

7-10 days

56
Q

homatropine duration of effect

A

1-3 days

57
Q

cyclopentolate duration of effect

A

1 day

58
Q

tropicamide duration of effect

A

6 hours

59
Q

clinical uses of antimuscarinic drugs:

respiratory disorders

A
  • pre-anesthesia (prevent airway secretions and laryngospasm; usually atropine or scopolamine)
  • COPD and asthma (causes bronchodilation; usually ipratropium or tiotropium via inhaler)
60
Q

clinical uses of antimuscarinic drugs:

urinary disorders

A

-treatment of urinary urgency or bladder spasm (usually oxybutynin)

61
Q

clinical uses of antimuscarinic drugs:

cardiovascular system

A

-treatment of bradycardia and some types of arrhythmias

62
Q

clinical uses of antimuscarinic drugs:

cholinergic poisoning

A
  • considered a medical emergency
  • common in rural communities (insecticides)
  • no effective method for directly blocking nicotinic effects
  • antimuscarinic therapy- atropine preferred, usually multiple doses required
  • cholinesterase regenerator compounds- pralidoxime; can “regenerate” phosphorylated enzyme, must be used rapidly
63
Q

adverse effects of antimuscarinic drugs

A
  • mydriasis (contraindicated in patients w/ glaucoma)
  • cycloplegia
  • dry mouth
  • tachycardia
  • flushed skin
  • agitation
  • delirium
  • elevated body temperature
64
Q

many antihistamines, antipsychotics, and antidepressants have _____ activity

A

muscarinic cholinoreceptor antagonist activity

65
Q

cholinoreceptor agonists cause _____

A

SLUD

  • salivation
  • lacrimation
  • urination
  • diarrhea
66
Q

cholinoreceptor antagonists have ____

A

the opposite effect of SLUD

  • dry mouth
  • dry eyes
  • urinary retention
  • constipation

Systemic Pharmacology I (7 decks)

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