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Systemic Pharmacology I > Parasympathetic Drugs > Flashcards

Parasympathetic Drugs Flashcards

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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
distribution and elimination of indirect-acting cholinomimetics
- variable | - organophosphates are distributed to CNS (CNS toxicity is common, exception is echothiophate)
26
indirect-acting cholinomimetics MOA
- increase concentration of endogenous ACh by inhibiting ACh-esterase - chemistry determines interaction with the enzyme
27
short-acting indirect-acting cholinomimetics MOA
- edrophonium - forms reversible bond with the enzyme - not actually a substrate for ACh-esterase
28
intermediate-acting indirect-acting cholinomimetics MOA
- neostigmine, physostigmine, pyridostigmine | - resistant to part of enzyme action so takes longer
29
long-acting indirect-acting cholinomimetics MOA
- echothiophate, malathion, parathion, sarin | - forms phosphorylated enzyme complex that strengthens the bond with the drug
30
indirect-acting cholinomimetics effects: | CNS
- low concentrations: alerting response | - high concentrations: convulsions
31
indirect-acting cholinomimetics effects: | eye, respiratory tract, GI tract, urinary tract
similar to the direct-acting cholinomimetics
32
indirect-acting cholinomimetics effects: | cardiovascular system
- 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
indirect-acting cholinomimetics effects: | neuromuscular junction
- 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
clinical uses of cholinomimetics: | eye
- cause contraction of the ciliary body (increases aqueous outflow) - older treatment of glaucoma - pilocarpine, carbachol, echothiophate
35
clinical uses of cholinomimetics: | GI and urinary tract
- 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
clinical uses of cholinomimetics: | neuromuscular junction
- 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
clinical uses of cholinomimetics: | treatment of Alzheimer's
- donepezil - galantamine - rivastigmine
38
adverse effects of direct-acting cholinomimetics
- nausea - vomiting - diarrhea - urinary urgency - salivation - sweating - flushing of the skin (vasodilation) - bronchial constriction
39
adverse effects of cholinesterase inhibitors
- same as direct-acting - also includes: muscle weakness, convulsions, respiratory failure -the above often result from exposure to pesticides (organophosphates)
40
cholinergic blockers: - interrupt _____ - prevent ACh from _____
parasympathetic nerve impulses; | stimulating cholinergic receptors
41
cholinoceptor antagonists: - ganglion blockers _____ - muscarinic blockers can be further divided based on _____
have little clinical use; | affinity for certain receptor subtype (M1-M5)
42
many muscarinic antagonists are _____, but ____ have also been formulated
``` naturally occurring compounds (ex: atropine derived from nightshade plant); synthetic compounds (ex: tropicamide) ```
43
muscarinic antagonists: | absorption
most are well absorbed from the gut, conjunctiva, and across skin (some formulations)
44
muscarinic antagonists: | distribution and elimination
- most are widely distributed with CNS penetration | - eliminated via the kidney
45
muscarinic antagonists MOA
- block ACh action at muscarinic receptors - moderately selective for various muscarinic receptor subtypes - atropine is non-selective (useful in treating cholinomimetic toxicity)
46
muscarinic antagonist effects: | CNS
- 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
muscarinic antagonist effects: | cardiovascular system
increased HR
48
muscarinic antagonist effects: | eye
- 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
muscarinic antagonist effects: | respiratory system
- bronchodilation | - decreased secretions in the lung
50
muscarinic antagonist effects: | GI tract
- decreased salivation - decreased production of stomach acid (very large doses) - decreased smooth muscle tone and propulsive movements
51
muscarinic antagonist effects: | urinary tract
-relax bladder smooth muscle -slows voiding (reduced urinary activity)
52
muscarinic antagonist effects: | sweat glands
- reduces sweating | - can produce fever in young patients
53
clinical uses of antimuscarinic drugs: | CNS disordesr
- Parkinson's disease (mainly adjunctive) | - treatment of motion sickness
54
clinical uses of antimuscarinic drugs: | ocular disorders
- accurate refraction (usually homatropine or cyclopentolate) - dilated fundus exam (usually tropicamide or cylcopentolate) - treatment of uveitis (prevents synechia, usually homatropine or cyclopentolate)
55
atropine duration of effect
7-10 days
56
homatropine duration of effect
1-3 days
57
cyclopentolate duration of effect
1 day
58
tropicamide duration of effect
6 hours
59
clinical uses of antimuscarinic drugs: | respiratory disorders
- pre-anesthesia (prevent airway secretions and laryngospasm; usually atropine or scopolamine) - COPD and asthma (causes bronchodilation; usually ipratropium or tiotropium via inhaler)
60
clinical uses of antimuscarinic drugs: | urinary disorders
-treatment of urinary urgency or bladder spasm (usually oxybutynin)
61
clinical uses of antimuscarinic drugs: | cardiovascular system
-treatment of bradycardia and some types of arrhythmias
62
clinical uses of antimuscarinic drugs: | cholinergic poisoning
- 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
adverse effects of antimuscarinic drugs
- mydriasis (contraindicated in patients w/ glaucoma) - cycloplegia - dry mouth - tachycardia - flushed skin - agitation - delirium - elevated body temperature
64
many antihistamines, antipsychotics, and antidepressants have _____ activity
muscarinic cholinoreceptor antagonist activity
65
cholinoreceptor agonists cause _____
SLUD - salivation - lacrimation - urination - diarrhea
66
cholinoreceptor antagonists have ____
the opposite effect of SLUD - dry mouth - dry eyes - urinary retention - constipation

Systemic Pharmacology I (7 decks)

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