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Pharmacology > Lecture 8: Cholinergic antagonists > Flashcards

Lecture 8: Cholinergic antagonists Flashcards

1
Q

Cholinergic receptor blockers mostly act on muscarinic/nictotinic receptors?
why?

A

Mostly act on muscarinic.

If they acted on Nicotinic they’d simply block all ganglia…

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2
Q

what major type of innervation is mainly reduced by cholinergic antagonists?

A

Parasympathetic innervation (because antagonists act mainly on muscarinic receptors)

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3
Q

How would you call blockers that act on nicotinic receptors? what would there effect be?

A

They’re called ganglionic blockers. They’d inhibit both sympathetic and parasympathetic innveration

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4
Q

What type of receptors do neuromuscular blocking agents bind? what’s their major use?

A

They bind nicotinic receptors at the neuromuscular juntion.

They’re mostly used as adjuvants in anesthesia (allowing to have sedation with lower doses of anesthetics)

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5
Q

Antimuscarinic agents can inhibit some sympathetic stimulation. where and how?

A

They can do it at the salivary and sweat glands which have muscarinic receptors triggering sympathetic response (salivation).

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6
Q

What is Atropine classified as? (what does it bind?)

A

It’s an anti-muscarinic drug. It has very high affinity for muscarinic receptors, even higher than Ach itself.

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7
Q

How is Atropine binding classified? competitive/non-competitive? what does it clinically mean?

A

Atropine is a competitive inhibitor, meaning higher doses of Ach can bypass its effect (for example usage of anticholinesterase inhibitors)

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8
Q

Where is Atropine active? NS? PNS? Both?

A

Both CNS and PNS

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9
Q

how long is the duration of action of Atropine?

A

4 hours

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10
Q

What are the major effects of atropine on the ocular system?

A
  • Mydriasis (dilation of pupil)
  • unresponsiveness to light
  • cycloplegia (inability to focus near vision (requires constriction of pupils))
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11
Q

How does Atropine affect the GI?

Give another drug having the same effect

A
  • Antispasdomic activity in the GI

Other drug is Scopolamine

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12
Q

What’s the effect of Atropine on the cardiovascular system? How can it be explained?

A

At low doses, atropine causes BRADYCARDIA.
This is because atropine blocks the M1 receptors which are on the inhibitory presynaptic neurons. These neurons would lower the release of Ach.
By binding to them, we have more Ach release and thus bradychardia.
At higher doses (>1mg), the M2 receptors on SA node are blocked and we have increase in cardiac rate (these are muscarinic and would have lowered HR).

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12
Q

How does Atropine affect blood pressure / blood vessels diameter? explain why

A

Blood pressure is NOT changed.
Vessels relax in response to NO (produced in response to Ach). When Ach is inhibitted, no NO is produced and the vessels do not relax: this does not mean they constrict. They just keep their normal dimensions.

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13
Q

What is Enuresis?

How would you treat it

A

Enuresis is involuntary voiding of urine.
Can be treated with Atropine but has too many side effects.
We’d rather use α adrenergic agonists (α1)

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14
Q

How is atropine calssified in regard to secretions?

A

It’s an antisecretory agent (secretions of upper respiratory tract, lacrimation, salivation, sweating, etc…)

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15
Q

The major side effects of Atropine?

A
  • dry mouth
  • blurred vision
  • sandy eyes (dry eyes)
  • tachycardia
  • constipation
  • hallcinations & delirium
  • Collapse of the circulatory and respiratory systems
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16
Q

The major side effects of Atropine?

A
  • dry mouth
  • blurred vision
  • sandy eyes (dry eyes)
  • tachycardia
  • constipation
  • hallucinations & delirium
  • Collapse of the circulatory and respiratory systems
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17
Q

What drug is scopolamine similar to? what’s the main difference?

A

Scopolamine is similar to Atropine except that it has an even greater action on the CNS (action on nausea/vomiting centers)

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18
Q

Scopolamine can be subject of abuse at high doses, give 2 reasons:

A
  1. Can cause Euphoria

2. Can block short-term memory (used in anesthesia)

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19
Q

What is Ipratropium mostly used for?

A

It’s useful to treat asthma. It is a muscarinic bloccker thus inhibiting any vagal stimulation that usually keeps airways constricted.

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20
Q

How does Sympathetic stimulation affect the respiratory passages?

A

Sympathetic stimulation causes bronchodilation

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21
Q

How is Asthma primarily treated? When is Ipratropium medicated? why?

A

Asthma is primarily treated with Adrenergic agonists. Ipratropium is medicated in patients that shouldn’t take adrenergic agonists such as those with high blood pressure where an adrenergic agonist would cause further vasocontriction and higher BP.

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22
Q

Give 2 ganglionic blockers

A

Nicotine & Mecamylamine

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23
Q

Many neuromuscular blockers are derived from this naturally occuring chemical.

A

Curare

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24
Q

What’s the effect of nicotine on ganglia?

A

Nicotine is the natural substrate to nicotinic receptors. Its presence causes depolarization (stimulation) followed by paralysis of ganglia.
At lower doses we can expect increased blood pressure, cardiac rate and peristalsis and secretions which all fall at higher doses.

25
Q

How do non-depolarizing neuromuscular blocking drugs cause sedation?

A

They block the nicotinic receptors at NM plate, inhibitting Ach from binding. These are competitive inhibitors that can be overcame by a higher dose of Ach.
At high doses, they can block the ion channels of the end plate making their effect very hard to bypass.

26
Q

What muscles are usually affected first by neuromuscular blocking drugs? what are last?

A

ordered from first to last:

Facial and eye muscles / fingers / limbs / Neck / Trunk / intercostal / Diaphragm

27
Q

How do neuromuscular blocking drugs affect BP and bronchiolar diameter?

A

BP drops and bronchoconstriction

28
Q

Apart from sedative effect during surgeries, what field HEAVILY relies on neuromuscular blocking agents? why?

A

Orthopedic surgeries because they often need 0 tension on bone while operating on them (complete flacid muscles)

29
Q

What 2 neuromuscular junction blocking drugs ARE metabolized? why is this clinically relevant?

A

Vecuronium and Rocuronium are deacetylated by the liver.
This is important because we’d have to expect lower clearance rate (higher bioavailability) in patients with diseased kidney.

30
Q

Give 2 drugs that can enhance neuromuscular blockade

A
  • Halogenated hydrocarbon anesthetics by sensitizing the neuromuscular junction to the effect of neuromuscular blockers.
  • Aminoglycoside antibiotics: inhibit Ach release from cholinergic nerves.
31
Q

What 2 neuromuscular junction blocking drugs ARE metabolized? why is this clinically relevant?

A

Vecuronium and Rocuronium are deacetylated by the liver.
This is important because we’d have to expect lower clearance rate (higher bioavailability) in patients with diseased liver.

32
Q

Give a DEPOLARIZING neuromuscular blocking drug.

A

Succinylcholine.

33
Q

What drug can block short-term memory?

A

Scopolamine

34
Q

What are the effects of Succinylcholine on the neuromuscular junction?

A

It is a DEPOLARIZING neuromuscular blocker and has 2 phases:
Phase I: membrane depolarizes, causing fasciculations (brief quick contractions) of the muscles.
Phase II: Receptors are desensitized, membrane repolarizes and we have flacid paralysis (even if Ach is added).

36
Q

Discuss α2 adrenergic receptors:

  • excitatory/inhibitory
  • location
  • response to molecule
A
  • inhibitory
  • presynaptic nerve terminal, platelets, Fat, GI
  • NE & E
37
Q

Discuss α1 adrenergic receptors:

  • excitatory/inhibitory
  • location
  • response to molecule
A
  • excitatory
  • in skin, splanchnic, GI & sphincters, Iris
  • NE (and Epi when at low doses)
    understand that they’re on the smooth muscles of skins, viscera (liver/kidney/iris/ejaculatory ducts) and GI and cause vasoconstriction when excited.
38
Q

Discuss α2 adrenergic receptors:

  • excitatory/inhibitory
  • location
  • response to molecule
A
  • inhibitory
  • presynaptic nerve terminal, platelets, Fat, GI
  • NE & E
39
Q

Discuss β1 adrenergic receptors:

  • excitatory/inhibitory
  • location
  • response to molecule
A
  • excitatory
  • Heart
  • NE & E
40
Q

Discuss β2 adrenergic receptors:

  • excitatory/inhibitory
  • location
  • response to molecule
A
  • inhibitory
  • smooth muscles of skeletal muscles, bronchial smooth muscles, GI tract & bladder
  • NE & E
41
Q

The pupil of the eye is controlled by 2 muscles.

what are they and how do they affect the pupil upon contraction?

A
  1. Radial muscle: When they contract they stretch the pupil (they’re attached to pupil and (sclera?)).
  2. Sphincter muscles: When they contract they close the pupil
42
Q

What type of receptor do ciliary muscles have? What happens upon their contraction?

A

They have α1 receptors

Upon contraction they stretch the pupil.

43
Q

What type of receptors do sphincter muscles have? What happens upon their contraction?

A

They have muscarinic receptors

Upon contraction they close the pupil.

44
Q

What happens to the lens upon accomodation? What muscle/receptor is responsible for it? When do we accomodate?

A

Accomodation occurs when we need close vision (like reading): The lens needs to be LESS spherical, more elongated.
This is done by contraction of ciliary muscles under α1 activity.

45
Q

How will a muscarinic agonist affect the vision?

A

Muscarinic agonist will act on the sphincter muscles (of pupil), making the less MORE spherical and less elongated: we can’t have a net near vision: Cycloplegia (can only see distant objects).

46
Q

Both muscarinic antagonists & α1 agonist cause Mydriasis. How to tell which is the real reason?

A

I need to check if I have cycloplegia. If I have it then I had no accommodation, then ciliary muscles didn’t contract: So it wasn’t α1 agonist but rather a muscarinic antagonist.

47
Q

If I have Mydriasis with no cycloplegia, what could be the cause?

A

An α1 agonist: Ciliary muscles contracted, causing mydriasis and extending the lens, allowing for near vision.

48
Q

If I have Mydriasis with cyclopegia, what could be the cause/

A

A muscarinic antagonist. Sphincter muscle of pupil relaxed, giving me mydriasis but ciliary muscles didn’t contract and elongate the lens: I can’t focus near sight vision.

49
Q

Which yould cause cycloplegia? α1 agonist of muscarinic antagonist?

A

Muscarinic antagonist.

50
Q

Where is the ciliary fluid made, under action of what receptor?

A

It is made in the ciliary body (posterior to the iris) under action of β1.

51
Q

Where is the ciliary fluid recycled?

A

In the canal of schlemm, which is anterior to the iris.

52
Q

when talking about glaucoma, what angle are we refering to?

A

The angle between the iris & cornea

53
Q

which type of glaucoma is painful and acute? Which is painless and chronic?

A

The open angle glaucoma is painless and chronic .

The closed angle glaucoma is acute and painful (have few hours to treat before retinal damage).

54
Q

roughly, what causes increased intra-ocular pressure in open/closed angle glaucomas?

A

In open angle glaucoma, the Canal of Schlem is reachable but itself non-functional.
In closed angle glaucoma, the canal of schlem is not reachable, although functional by itself.

55
Q

What drug family is used in open angle glaucoma? explain the logic behind it

A

We use β1 antagonists (timolol)
The canal of Schlem is reachable but not functional so the only fix to that is to stop producing the intraoccular fluid. Remember β1 receptors are responsible for fluid secretion from the ciliary body

56
Q

What drug family is used in close angle glaucoma? explain the logic behind it

A

We use Muscarinic agonists.
This acts on the ciliary body and the iris anterior to it. The muscarinic agonist will make these structures RELAX and thus decrease in size, allowing an opening to the Schlemm canal and thus better drainage.

57
Q

What type of glaucoma patient would see his case worsened by usage of atropine?

A

Patients with close-angle glaucoma.

58
Q

What’s the main the main usage of tropicamid?

A

used as ophtalmic solutions: it causes mydriasis & cyclopegia

59
Q

What’s the main the main usage of Cyclopentolate?

A

used as ophtalmic solutions: it causes mydriasis & cyclopegia

60
Q

Is myosis associated with near/distant vision?

A

Myosis is associated with near vision so Cyclopegia is caused my mydriasis.

61
Q

What neuromuscular blocking agent causes histamine release? What other drug took its place?

A

The drug is Atracurium which causes histamine release (lowers BP, XX(?)). It is replaced by cisatracurium.

62
Q

What neuromuscular blocking drug has a rapid onset of action making it useful for tracheal intubation? (2)

A

Rocuronium: It needs 1 minute to cause the blockade.

Succinyl-choline might be used as well.

Pharmacology (5 decks)

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