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PHAR2002 > Cholinergic Receptors > Flashcards

Cholinergic Receptors Flashcards

1
Q

Low doses of ACh cause ___ action produced by X and antagonised by Y

A

Muscarinic actions produced by muscarine and antagonised by atropine

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2
Q

High doses of ACh cause ___ action produced by X and antagonised by Y

A

Nicotinic actions produced by nicotine and antagonised by tubocurarine

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3
Q

While muscle receptors are ____ blocked by _____, ganglion receptors are blocked by ________

A

Potently, tubocurarine, hexamethonium

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4
Q

By definition all muscarinic receptors are blocked by _______

A

atropine

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5
Q

Some receptors have no innervation, such receptors do not normally see ___ but respond to ____

A

ACh, externally-applied agonists

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6
Q

Parasympathomimetic drugs

A

Mimic the effects of stimulating parasympathetic nerves

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7
Q

How do parasympathomimetic drugs act

A

1) By stimulating muscarinic receptors in the same way as ACh (muscarinic agonists)
2) By inhibiting cholinesterase to intensify + prolong action of ACh at synapse

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8
Q

Selectivity and speed of hydrolysis by ChE of ACh

A

N M, Rapid

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9
Q

Selectivity and speed of hydrolysis by ChE of Carbachol

A

N M, No

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10
Q

Selectivity and speed of hydrolysis by ChE of Methacholine

A

M, Slow

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11
Q

Selectivity and speed of hydrolysis by ChE of Bethanecol

A

M, No

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12
Q

Selectivity and speed of hydrolysis by ChE of Pilocarpine

A

M, No

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13
Q

Why are methacholine and carbachol more useful clinically than ACh?

A

Quaternary amines -> Longer duration of action as less quickly broken down by ChE

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14
Q

Why are methacholine and carbachol not given orally?

A

Quaternary amines are fully ionised so not absorbed when given orally nor readily absorbed from conjunctival sac

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15
Q

Why can pilocarpine be used topically?

A

Tertiary amine which is only partly ionised at physiological pH

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16
Q

Main effects of muscarinic agonists

A
  1. Bradycardia + reduced CO -> fall in bp
  2. Vasodilation
  3. Salivation, lacrimation + sweating
  4. Bronchoconstriction + increased bronchial secretion
  5. Contraction of bladder
  6. Increased G.I. motility
  7. Pupillary constriction -> low I.O. pressure
  8. Ciliary muscle contraction -> near vision accommodation
17
Q

Main clinical uses of muscarinic agonists:

A
  1. Reduction I.O. pressure in glaucoma (pilocarpine)
  2. Dry mouth relief (xerostomia; pilocarpine)
  3. Relief of urinary retention, when this results from failure of normal reflex pathway acting on bladder ( bethnechol; superseded by catherisation)
  4. Increasing G.I. motility during period of inactivity from abdominal surgery ( bethanechol; rarely)
18
Q

Competitive antagonists block _____ receptors without much _____

A

muscarinic, selectivity

19
Q

3 main antagonists at muscarinic receptors

A
  1. Atropine (nightshade berries)
  2. Hyoscine (scopolamine)
  3. Homatropine (synthetic analogue of atropine - briefer action)
20
Q

How are CNS effects avoided when using muscarinic antagonists?

A

Use quaternary derivatives since all 3 muscarinic antagonists are tertiary bases which are readily absorbed + enter brain easily

21
Q

Why are the elderly susceptible to cognitive impairment by antimuscarinic effects?

A

Many common classes of drugs have antimuscarinic side effects -> several types of drugs will have accumulated side effects

22
Q

Where is the site of a muscarinic receptor block?

A

At the organs innervated by It rather than PNS

23
Q

Peripheral inhibition of muscarinic receptor effects

A
  1. Block of secretions: saliva, tears, bronchial secretion, swelling
  2. Tachycardia -> block of vagal inhibition of heart
  3. Pupillary dilation (mydriasis) -> block of parasymp. influence on sphincter pupillae
  4. Inhibition of motility + secretions of GI tract
  5. Bronchi + bladder also relaxed
24
Q

Why is there no change in bp when vagal inhibition of heart is blocked?

A

Most blood vessels have no parasympathetic innervation

25
Q

Why mydriasis a bad thing?

A

Interfers with drainage via canal of Schlemm + thus raises IO pressure -: cycloplegia hence paralysis of accomodation

26
Q

Which inhibitiory effects require much larger doses and are not even complete?

A

G.I and smooth muscle since there are other transmitters that maintain G.I. + bladder function even when cholinergic transmission is fully blocked

27
Q

Atropine actions on CNS

A

No great effect in small doses but in high doses marked stimulation :

  • restlessness
  • disorientation
  • hallucination
  • > attention + memory deficit at low doses for elderly
28
Q

Hyoscine on CNS

A

Powerful CNS depressant -: sleep + amnesia

-> anti-emetic action

29
Q

Atropine-like drugs on CNS

A

supress the tremor of PD probs by blocking cholinergic transmission in basal ganglia

30
Q

2 therapeutic uses of inhibitors in anaesthetia

A
  1. Pre-anaesthetia med to inhibit salivary and bronchial secretion + cause drowsiness (hyoscine)
  2. During surgery to prevent vagal inhibition of heart ( occurs with some anaesthetics) + prevent parasympathomimetic actions of anti-cholinesterases -> effect on nmj?
31
Q

2 therapeutic uses of inhibitors in opthamology

A
  1. Dilate pupil fully and paralyse lens for opthalmological examination
  2. Prevent contraction of pupil following ophthalmic surgery
32
Q

What precaution needs to be taken when using inhibitors in opthamology

A

Pupilary dilation can increase IO pressure -> dangerous in glaucoma

33
Q

Why are atropine/ hyoscine not used for opthalomogical exams?

A

Blur vision for several ays so shorter acting synthetic analogue tropicamide or homatropine used

34
Q

What other therapeutic uses are there for inhibitors?

A
  1. Anticholinesterase poisoning
  2. Symptomatic relief of sm mu spasm in asthma -> poorly controlled by first-line agents/ bronchodilation COPD
  3. PD: initial or with levodopa
  4. Prevent motion sickness (hyoscine)
  5. Alleviate overactive bladder (tropium)

PHAR2002 (14 decks)

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