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Pharmacology Exam 3 (Toy's) > Pharmacolgy of NMJ > Flashcards

Pharmacolgy of NMJ Flashcards

0
Q

Muscarinic is associated with what nervous system response

A

Rest & digest (parasympathetic)

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1
Q

What are the two cholinoceptors

A
  • muscarinic

- Nicotinic

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2
Q

Nicotinic receptors are associated with nervous system response

A

Excitatory

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3
Q

What is the neurotransmitter at both muscarinic and nicotinic receptors

A

Ach

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4
Q

Characteristic of muscarinic receptors

A
  • G protein linked

- Regulate 2nd messenger production

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5
Q

Where are muscarinic subsets located

A
  • heart
  • airway smooth muscle
  • salivary gland
  • tissues innervated by cholinergic postganglionic nerves
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6
Q

Muscuranic stimulation will cause what type of response (heart, lungs, salivary glands, nervous tissue)

A
  • decrease HR
  • bronchoconstriction
  • increase saliva
  • increased muscle relaxation
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7
Q

Nicotinic characteristics

A
  • selective ligan gated ion channel receptors
  • Cholinoceptor selectivity
  • excitatory mainly, does have inhibitory receptors
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8
Q

Where are nicotinic receptors located

A
  • In PNS cells, postganglionic SNS cells and skeletal muscle endplates
  • N1 @ autonomic ganglia, N2 @ NMJ
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9
Q

Cholinoceptor direct activation Vs. Indirect activation

A
  • Direct activation acts on muscarinic and nicotinic receptors directly.
  • Indirect activation inhibits the hydrolysis of Ach (acts on acetylcholinesterase enzyme)
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10
Q

Where is Ach broken down?

A

NMJ

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11
Q

What drug and/ or neurotransmitter are choline esters?

A

Ach, Succinylcholine

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12
Q

What drug/ neurotransmitters are alkaloids/ amines

A

muscarine, nicotine

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13
Q

What is the effect of a Beta-methyl group at a nicotinic receptor?

A

reduces the potency

methacoline, challenge test; bethanecol, urinary retention

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14
Q

How are esters absorbs (r/t rate of absorption) and distributed? What is the reason for this absorption/ distribution rate rate?

A

-Esters are poorly absorbed and distributed due to hydrophillic properties

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15
Q

What hydrolizes Ach and at what rate?

A

Ach rapidly hydrolyzed by acetylcholinesterase

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16
Q

What hydrolyzes succinylcholine?

A

Pseudocholinesterase

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17
Q

What contributes to ester compounds with longer DOA

A

Greater resistance to acetylcholinesterase (ex. Metacholine 3x more resistant)

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18
Q

What type (structure) of alkaloid is Nicotine. How does it (type) effect its absorption?

A

Tertiary alkaloid, lipid soluble, well absorbed

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19
Q

What type (structure) of amine is Muscarine and how does it effect rate of absorption?

A

Quarternary amine. Less completely absorbed. Decrease lipid solubility. (can still be toxic, eg. certain mushrooms)

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20
Q

(2) Ways(MOA) in which a direct acting, muscarinic cholinoceptor stimulants can work

A
  1. Ach activates muscarinic receptors directly on effector organ
  2. Ach interacts w/ muscarinic receptor on nerve terminal to inhibit release of neurotransmitter (- feedback loop); likely involves 2nd messenger
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21
Q

Nicotinic MOA

A

Depolarization of nerve cells or neuromuscular endplate

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22
Q

Define: Neuromuscular blockade

A

If depolarization of nerve cell becomes prolonged, the response is abolished (neuron stops firing), skeletal muscle relaxes.

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23
Q

Cardiovascular effects of cholinoceptor stimulation

A
  • Decrease HR, contraction, and conduction velocity

- Muscarinic agonist release EDRF (endothelium-derived relaxing factor)

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24
Q

Result of the release of EDRF(endothelium-derived relaxing factor) from muscarinic agonist in small doses vs. large doses

A
  • small doses:Venous & arterial dilation

- large dose: Direct vasoconstriction effect

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25
Q

Effect of Cholinoceptor stimulation on CNS

A

(Think nicotine stimulation w/ CNS)

  • Nicotine tremor
  • Stimulation or respiratory center
  • High levels cause Sz.
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26
Q

**What happens with Stimulation of cholinoceptors at NMJ

A

-Depolarization of endplate (r/t increased permeability to Na+ & K+ ions (caused by nicotine stimulation)

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27
Q

How do indirect acting cholinoceptors (stimulants) work?

A

Inhibit acetylcholinesterase thereby allowing increased concentration of Ach

28
Q

Where is the primary effect of indirect acting cholinomimetics

A
  • AT the active site of the enzyme

- Some have direct action on nicotinic receptors

29
Q

In terms of the amount manufactured, what is the most common use for INDIRECT-acting cholinomimetics

A

Insecticides

30
Q

How do the therapeutic and industrial structures of INDIRECT-acting cholinomimetics compare

A
  • Differences are in chemical structure and pharmacokinetics.
  • The pharmacodynamics are almost always the same.
31
Q

3 commonly used groups of INDIRECT-acting Cholinoceptor stimulants (with examples)

A
  1. Organic derivatives of phosphoric acid (organophosphates)
  2. Simple alcohols w/ quaternary ammonium group (edrophonium)
  3. Carbamic acid esters of alcohol with quaternary ammonium (neostigmine) or tertiary amine group (physostigmine)
32
Q

Characteristic of Organophosphate INDIRECT-acting Cholinoceptor stimulants (with examples)

A

-Highly lipid soluble, well absorbed by skin

  • Soman, potent nerve gas
  • Paratione & malathione insecticides are converted to phosphate derivatives in plants & animals and are better for insecticide use
33
Q

***** Quartenary carbamates vs. tertiary amines (INDIRECT-acting Cholinoceptor stimulants) absorption rates

-drug example of each

A
  • Quaternary carbamates (Neostigmine) is poorly absorbed via skin, lungs, PO
  • Tertiary amines (Physostigmine) are well absorbed (Eserine eye drops) and more readily distributed to CNS
34
Q

How does affinity of INDIRECT-acting Cholinoceptor stimulants effect potency

A
  • differences in potency reflects differences in affinity

- Increase infinity = increased potency (and the opposite)

35
Q

3 MOA of INDIRECT-acting Cholinoceptor stimulants drugs. (Mechanisms in which they inhibit ach-esterase)

A
  1. Reversible inhibition
  2. Formation of carbamyl esters (reversible)
  3. Irreversible inactivation
36
Q

Uses for Edrophonium

A
  • Skeletal muscle relaxant reversal

- Tensilon Challenge (Myasthania gravis/ cholinergic crisis dx.)

37
Q

Why are drugs that form carbamyl esters effective at inhibiting ach-esterase. (what makes them good INDIRECT-acting Cholinoceptor stimulants)

A

Carbamylated Ach-esterase can’t hydrolyze Ach

38
Q

Drugs that are Carbamyl esters

A
  1. Neostigmine
  2. Pyridostigmine
  3. Physostigmine
39
Q

Use for INDIRECT-acting Cholinoceptor stimulants

A

Muscle relaxant reversal

40
Q

Where do cholinesterase inhibitors bind to block enzyme’s action?

A

anionic and esteric sites

41
Q

In reference to ech-esterase enzyme site, where & how does Neostigmine, pyridostigmine, and edrophonium bind.

A
  • Neostigmine & pyridostigmine covalently bind at esteratic site
  • Edrophonium hydrogen binds to anionic site
42
Q

Which type INDIRECT-acting Cholinoceptor stimulant has irreversible inactivation? Why?

A
  • Organophosphates form irreversible bond with enzyme to for an ineffective complex
  • can’t be hydrolyzed
  • Reversal effects require new enzyme production
43
Q

Myasthenia Gravis

A
  • Affects skeletal muscle NMJ
  • Autoimmune process produces antibodies, which decrease functional nicotinic receptors on end plates.
  • Symptoms: weakness, and fatigue which improves with rest and worsens with exercise. Often difficulty w/ speaking, swallowing, breathing
44
Q

Drug class that Myasthenia gravis (MG) patients are VERY sensitive to and why?

A

NDMRs (functional receptors are blocked)

45
Q

Drugs used to treat MG, and why

A
  • Cholinesterase inhibitors

- Increase Ach present, therefor increase stimulation to nicotinic receptors

46
Q

MG crisis vs. Cholinergic crisis

A
  • MG crisis: pt. weak because not enough drug/ ach present

- Cholinergic crisis: pt. weak because too much much drug / ach

47
Q

How is MG vs. Cholinergic crisis differentiated to diagnose?

A

Tensilon Challenge

48
Q

What is involved in a Tensilon Challenge

A
  • Edrophonium is given. If pt. gets better, than MG crisis was the problem. (Ach levels were low…increased with drug..pt. feels better)
  • If pt. gets worst, than Cholinergic crisis is the problem (pt. has too much Ach r/ too much ach-esterase,causing increased levels makes pt. worst)
49
Q

Neuromuscular blockade mechanisms

A
  • Channel blockade (closed ion channel blockade: pre-syneptic block) (open ion channel blockade- Succinylcholine)
  • Receptor desensitization (mechanism unknown): agonist receptor binding, but no ion channel
50
Q

Drug class and drug of Open ion channel Neuromuscular blockade mechanism

A
  • NDMR

- Succinylcholine

51
Q

How are esters absorbed…metabolized…and cleared in the body?

A
  • Poorly absorbed r/t hydrophillic properties
  • Hepatic metabolism
  • Urinary Clearance
52
Q

What inhibits the action of Ach

A

acetylcholinesterase

53
Q

Effect of direct acting cholinoceptor stimulation vs. indirect acting.

A

Results/ effects are the same

54
Q

Where do cholinesterase inhibitors bind to block enzyme’s action

A

At the anionic and esteric sites

55
Q

What is the difference between a Myasthenia Gravis Crisis and a Cholinergic crisis?

A
  • Myasthenia G. crisis requires more drug (weakness from not enough cholinesterase inhibitor present)
  • Cholinergic crisis has too much drug present (weakness from depolarizing blockade from too much Ach present)
56
Q

Define malignant Hyperthermia

A

an AUTOSOMAL DOMINANT inherited skeletal muscle disorder. Dx. by muscle biopsy. During a crisis Ca+ is greatly increased & there’s a problem w/re-uptake d/t defective channel receptors leading to sustained muscle contractions> severe cellular O2 debt>demand for ATP>glycolysis>lactic acidosis>membrane instability>cellular rupture>rhabdomyolysis

57
Q

What are the 2 NMBDs that undergo Hoffman’s hydrolysis?

A
  • Atracurium

- Cisatracurium

58
Q

Ultra short acting NMBD

A

Succinylcholine

59
Q

Short acting NMBD

A

Mivacurium (Mivacron)

60
Q

Intermediate acting NMBD

A
  • Veruronium (Norcuron)
  • Rocuronium (Zemuron)
  • Atricurium
  • Cisatricurium
  • DTC (Curare)
61
Q

Long acting NMBD

A

-Pancuronium
-Pipecuronium
(-Gellamine)

62
Q

Biisoquaternarty aminosteroid NMBD

A
  • Pancuronium

- Pipecuronium

63
Q

Isoquinolinium NMBD

A

DTC (Curare)

64
Q

Benzisoquinolinium NMBD

A
  • Mivacurium (Mivacron)
  • Atricurium (Tracurium)
  • Cisatracurium (Nimbex)
  • (Doxacurium)
65
Q

Monoquaternary Aminosteroid NMBDs

A
  • Vecuronium (Norcuron)

- Rocuronium (Zemron)

66
Q
  • NMBDs that you can give a priming dose.

- How much is the priming dose

A

Can give 10% priming dose with:

  • Cisatracurium (Nimbex)
  • Vecuronium (Norcuron)
  • Rocuronium (Zemron)
67
Q

The 2 NMBDs whose hydrolysis can be affected by atypical pseudocholinesterase

A
  • Succinylcholine

- Mivacurium (Mivacron)

68
Q

NMBD used for rapid sequence intubation (RSI)

A
  • Succinylcholine
  • Rocuronium

(Vecuronium not really good for RSI r/t prolong onset)

Pharmacology Exam 3 (Toy's) (5 decks)

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