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CPR Week 3 > 3.3.5. Cholinergics, Anticholinergics > Flashcards

3.3.5. Cholinergics, Anticholinergics Flashcards

1
Q

Discuss neurotransmitter release in the somatic nervous system

A

i. ACh is released from the neuron into the neuromuscular junction ii. ACh binds to nicotinic receptors on skeletal muscle nAChRM.

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2
Q

Discuss neurotransmitter release in the parasympathetic nervous system

A

i. ACh is released by long preganglionic neurons and interact with nictonic receptors (nAChRN) on the short post-ganglionic neurons. ii. The post-ganglionic neurons release ACh and interact with muscarinic receptors on the end organ.

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3
Q

Discuss neurotransmitter release in the sympathetic nervous system

A

i. ACh is released by short preganglionic neurons and interact with nictonic receptors (nAChRN) on the long post ganglionic neurons. ii. The post ganglionic neurons release norepinephrine which interact with adrenergic receptors on the end organ

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4
Q

Discuss how the adrenal gland relates to the sympathetic nervous system and what neurotransmitters are related to it

A

The adrenal gland is also a part of the sympathetic pathway Neurons release ACh which interacts with the adrenal gland The adrenal gland then releases epinephrine into the bloodstream.

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5
Q

Where are muscarinic receptors in the parasympathetic pathway?

A

In the parasympathetic pathway: Muscarinic receptors are located in cardiac and smooth muscle, gland cells, and nerve terminals

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6
Q

Where are muscarinic receptors in the sympathetic pathway? What is different about these?

A

Muscarinic receptors are located in sweat glands. Post-ganglionic sympathetic neurons to sweat glands release ACh, not NE. Released ACh acts on muscarinic receptors in the vicinity of these nerve terminals.

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7
Q

There are muscarinic receptors in the sympathetic pathway that are not able to connect with the normal route, and thus seem physiologically unclear. Discuss this

A

There are muscarinic receptors on peripheral blood vessels; these are not innervated. These receptors respond to exogenously administered muscarinic agonists. Physiological significance is unclear.

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8
Q

What do we mean by muscarinic receptor subtypes? How do they relate to pharmacology?

A

There are 5 known subtypes of muscarinic receptor, each with a unique pattern of distribution in brain and periphery. The subtypes can be discriminated pharmacologically. At this time, few drugs in the clinic act preferentially at one site

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9
Q

Where do we see M1 receptors expressed?

A

Sympathetic postganglionic neurons, CNS neurons, some presynaptic neurons

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10
Q

Where so we see M2 receptors expressed?

A

Myocardium, smooth muscle, and presynaptic neurons

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11
Q

Where so we see M3 receptors expressed?

A

Exocrine glands, blood vessels (smooth muscle, ganglia, and endothelium)

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12
Q

Where so we see M4 receptors expressed?

A

Mainly in the brain (post ganglionic nerve terminals)

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13
Q

Where so we see M5 receptors expressed?

A

Mainly in the brain (in dopamine neurons)

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14
Q

What is pirenzepine?

A

Selective agonist for M1 receptors

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15
Q

What is AF-DX 116?

A

Selective agonist for M2 receptors

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16
Q

What is tiotropium?

A

Selective agonist for M1 and M3

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17
Q

There are two primary transduction pathways for the 5 muscarinic receptor subtypes. What are they?

A

G q/11 G i/o

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18
Q

Discuss G q/11

A

Primary transduction pathway for M1, 3, and 5 Works by activating PLC, IP3, and DAG

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19
Q

Discuss G i/o

A

Primary transduction pathway for M2 and 4. Works by inhibiting adenylyl cyclase and opening K+ channels.

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20
Q

Most cholinergic subtypes _____ (do/do not) distinguish between subtypes.

A

Do not

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21
Q

Discuss the excitatory muscarinic receptors (M1,3,5) in more detail

A

Activation of M1,3, or 5 in endothelial cell → activation of Gq → stimulates phospholipase C Phospholipase C cleaves PIP2 to produce IP3 and diacylglycerol Diacylglycerol → activation of protein kinase C → Response IP3 → increase in Ca2+–> response

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22
Q

Discuss the inhibitory muscarinic receptors in more detail (M2 and 4)

A

M2 and M4 are inhibitory receptors Activation of M2 or M4 in endothelial cell causes activation of Gi/o The alpha part of the G protein is going to inhibit adenylate cyclase This leads to less cAMP and Protein kinase A → inhibition of calcium channels and a pacemaker channel The beta/gamma part of the G protein activates potassium channels.

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23
Q

What esters are direct acting cholinergic receptor agonists?

A

Acetylcholine Bethanecol Carbachol Methacholine

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24
Q

Discuss the use of Acetylcholine clinically.

A

Acetylcholine - not used clinically - too indiscriminate (too rapidly hydrolyzed by cholinesterase; low concs M-selective; higher concentrations induce nicotinic effects)

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25
Q

Discuss the use of Carbachol clinically

A

Carbachol - not used clinically - very slowly hydrolyzed; both muscarinic and nicotinic effects

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26
Q

Discuss Bethanecol’s use clinically

A

Bethanecol - very slowly hydrolyzed; specific muscarinic agonist; may be used post-operatively to treat urinary retention, abdominal distension, adynamic ileum, gastric atony

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27
Q

Discuss Bethanecol’s use clinically

A

Bethanecol - very slowly hydrolyzed; specific muscarinic agonist; may be used post-operatively to treat urinary retention, abdominal distension, and various other GI issues

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28
Q

What is Pilocarpine and what do we use it for

A

Pilocarpine - topical miotic; glaucoma (decreases intraocular pressure).

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29
Q

What are the effects of muscarinic receptor agonists on the heart?

A

Decrease the HR However, a decrease in BP could override this by causing a reflexive increase in HR

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30
Q

Muscarinic agonists on Blood vessels?

A

Decrease tone in the arterioles and small blood vessels and decrease blood pressure

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31
Q

Muscarinic agonists on other smooth muscles?

A

Increase tone and increase contraction

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32
Q

Muscarinic agonists on Exocrine systems?

A

Increase salivation, mucous secretions

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33
Q

Muscarinic agonists on the Iris sphincter?

A

Miosis (pupillary constriction)

34
Q

Muscarinic agonists on the GI tract?

A

Increase tone, contractions, peristalsis

35
Q

Muscarinic agonists on respiration

A

Bronchoconstriction

36
Q

Muscarinic agonists on urinary bladder

A

Decrease bladder capacity

37
Q

Mechanism of action of ACh in small blood vessels

A

In arterioles and small blood vessels, ACh acts on M3 receptors located on endothelial cells lining the blood vessel lumen 1. Increases intracellular Calcium 2. Activates NO synthase to make NO 3. NO diffuses from the endothelial cell to the adjacent smooth muscle cell 4. NO activates guanyl cyclase, generating cyclic GMP 5. Cyclic GMP causes a muscle relaxation. The end result is a reduction of peripheral resistance and a fall in blood pressure

38
Q

How do anticholinergics work?

A

Mechanism of Action: Competitive antagonism of muscarinic cholinergic receptors. Anticholinergics inhibit the action of the parasympathetic nervous system and effects of cholinergics on end-organs of the parasympathetic nervous system

39
Q

Difference between tertiary amine and quaternary amines

A

They are both anticholinergics, but tertiary can enter the CNS while Quaternary have restricted distribution and cannot.

40
Q

Pirenzepine was discussed earlier as a chlinergic antagonist, i.e., an anticholinergic. What is its effect and use?

A

pirenzepine (tricyclic antidepressant: decreases stomach acid)

41
Q

What tertiary amines do we have?

A

Atropine Scopolamine Homatropine Benztropine Oxybutynin Tolterodine Pirenzepine BASHPOT

42
Q

What quaternary Amines do we have

A

Propantheline Ipratropium Tiotropium

43
Q

What anticholinergic do we use for opthamology?

A

Homatropine

44
Q

What anticholinergic do we use for Parkinsons?

A

Benzotropine

45
Q

What anticholinergics do we use for urinary incontinence?

A

Oxybutynin and Tolterodine

46
Q

What do we use propantheline for?

A

Preanesthetic used to inhibit secretions and GI motility

47
Q

What anticholinergics do we use for COPD and asthma?

A

Ipratropium and Tiotropium

48
Q

Atropine toxicity effects on secretions?

A

Decreases them (sweating, respiratory and salivation)

49
Q

Atropine toxicity effects on the eye

A

Mydriasis (dilate pupils) Cycloplegia (paralysis of accomadation)

50
Q

Effect of Atropine toxicity on the heart

A

Tachycardia

51
Q

Effect of Atropine toxicity on the GI/GU system

A

Decrease contractions of all of it. Decrease in GI secretions as well

52
Q

Effect of Atropine toxicity on the CNS

A

Delirium, excitation “Mad as a Hatter”

53
Q

What are Belladonne alkaloids, their effects and how do we treat?

A

Atropine and scopolamine Symptoms are those of atropine toxicity Treat with anticholinesterase sedative

54
Q

What can we use scopalamine for therapeutically?

A

Antimotion sickness and also as a CNS sedative

55
Q

Autonomic ganglia and adrenal medulla innervated by _____ fibers.

A

Autonomic ganglia and adrenal medulla innervated by cholinergic fibers.

56
Q

Postsynaptic receptors are ____ ____ receptors.

A

Postsynaptic receptors are nicotinic cholinergic receptors.

57
Q

Response to nicotine in the body

A

Low concentrations of nicotine are ganglionic stimulants (in tobacco smokers) Moderate concentrations of nicotine produce a depolarizing block of ganglionic transmission Both sympathetic and parasympathetic ganglia are affected

58
Q

Pre-ganglionic sympathetic and parasympathetic neurons release ____ as the primary transmitter.

A

Pre-ganglionic sympathetic and parasympathetic neurons release ACh as the primary transmitter.

59
Q

The initial pulse of ACh release induces a rapid ____ by activating ____ receptors to induce what?

A

The initial pulse of ACh release induces a rapid EPSP by activating nAChN receptors to induce a rapid influx of sodium in the post-synaptic neuron and membrane depolarization.

60
Q

These ___ ___ and ___ ___ events appear to play a modulatory role, in controlling ganglionic excitability and may vary in importance in the transmission process in different autonomic ganglia.

A

These later IPSP and slow EPSP events appear to play a modulatory role, in controlling ganglionic excitability and may vary in importance in the transmission process in different autonomic ganglia.

61
Q

Discuss slow IPSP, slow EPSP and a late slow EPSP

A

A much slower IPSP, induced by ACh activating M2 receptors, follows the initial EPSP. The IPSP is followed by an even slower “slow EPSP” associated with M1 or M3 receptor activation. Finally a late slow EPSP is developed as a result of peptide release within the ganglion and activation of peptidergic receptors.

62
Q

chemoreceptors in aortic arch and carotid body stimulate what

A

Respiratory stimulation

63
Q

Chemoreceptors in the emetic trigger zone cause what?

A

Nausea and vomiting

64
Q

Chemoreceptors in the hypothalamus cause what?

A

Vasopressin (ADH) secretion

65
Q

chemoreceptors are what kind of receptors?

A

nACh receptors

66
Q

Relate smoking to nAChN receptors and motor reflexes

A

Motor Reflexes - stimulation or depression (via nAChN receptor in spinal cord); in smokers, most obvious effect is depression of knee jerk. (Note: nicotine has very little activity at nAChM receptors on muscle).

67
Q

Stimulating nACh receptors at low doses causes what?

A

increased cortical neuron firing frequency, associated with increased acetylcholine turnover, resulting in increased alertness after low doses. motor stimulation at low doses,

68
Q

Stimulating nACh receptors at high doses causes what?

A

depression at high doses, with very rapid tolerance to stimulant effects

69
Q

If you smoke you don’t have to worry about:

A
  1. Ulcerative Colitis 2. Alzheimer’s Disease 3. Pain (its a good pain reliever)
70
Q

Acute toxicity with nicotine and what does it cause?

A

acute intoxication (“green tobacco sickness”) - nausea, vomiting, weakness, headache, sweating, salivation.

71
Q

Discuss chronic nicotine toxicity

A

chronic toxicity: cardiovascular toxicity, hypertension, chronic obstructive pulmonary disease, low birth rate babies; craving, dependence and addiction associated with tobacco use

72
Q

Death caused by nicotine? Treatment options?

A

Deaths due to oral nicotine are rare, due to early vomiting and first-pass metabolism. Treatment: induce vomiting or gastric lavage; artificial respiration.

73
Q

Phases of tobacco smoking

A
  1. Gas phase (Monoxide, hydrogen cyanide, ammonia, etc) 2. Particulate phase - Nicotine is the major pharmacologically active component
74
Q

Discuss the mechanism of the nicotine reward system

A

The rewarding effect of nicotine involves the ventral tegmental area (VTA) dopamine neurons. Nicotine excites dopamine neurons via acting on nAChRNs (a4b2) expressed on dopamine neurons

75
Q

Therapies for nicotine dependnece

A
  1. nicotine replacement therapy (patches, etc.) 10% effective 2. Antidepressants (buproprion) 23% at one year but discontinued often due to side effects like tremors, headache and skin rash 3. nAChN partial agonist (varenicline)
76
Q

Examples of ganglionic blocking agents

A

Tetraethylammonium ions, hexamethonium, trimethaphan

77
Q

Describe where in the pathway that Hemicholinium, Vesamicol, and Botulinum act to stop transmission

A
78
Q

What are our indirect agonists and how do they work in general?

A

Neostigmine

Pyridiostigmine

Physostigmine

Donezepil

Edrophonium

These all are indirect agonists because they stop anticholinergics (thus increasing ACh endogenously)

79
Q

What do we use for Alzheimer’s Disease?

A

Donepezil

Rivastigmine

Galantamine

80
Q

How do we treat atropine poisoning and why?

A

Physostigmine, it’s an anticholinesteras that increases endogenous ACh and can cross the blood brain barrier

CPR Week 3 (16 decks)

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