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Block 3 Up To Quiz 1 > Cholinergic Pharmacology Pt 2 > Flashcards

Cholinergic Pharmacology Pt 2 Flashcards

1
Q

Cholinergic agonists

A

can interact directly with nicotinic or muscarinic receptors or both (agonists)

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2
Q

parasympathomimetics

A

drugs producing only muscarinic effects

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3
Q

Direct acting agonists

A
  1. Choline esters
  2. Naturally occurring alkaloids
  3. Ganglionic stimulating agents
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4
Q

Carbachol

A
  • nicotinic and muscarinic agonist
  • choline ester
  • longer lasting than but has both nicotinic and musarinc effects
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5
Q

methacholine

A
  • muscarinic agonist
  • choline ester
  • mostly muscarinic
  • decrease nicotinic effect
  • mostly cardiac
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6
Q

Choline esters

A
  • Carbachol, Methacholine, Bethanechol

- somewhat selective, resistant to action of cholinesterase (hydrolysis) competed to Ach so longer duration fo action

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7
Q

Bethanechol

A
  • choline ester
  • muscarinic specific
  • mostly GI and bladder
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8
Q

Naturally occurring alkaloids

A
  • muscarinic agonists

- muscarine and pilocarpine

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9
Q

Ganglionic stimulating agents

A
  • nicotinic agonists
  • Nicotine
  • Lobeline
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10
Q

Ganglionic stimulating agents effects

A
  • no therapeutic usage
  • produce generalized stimulation of autonomic ganglia and mixed symp and parasympathetic responses
  • blood pressure increase bc vasoconstriction bc symp ganglia stimuli and release epinephrine from adrenal medulla
  • gut motility increase or decrease
  • secretion salvia, bronchial mucus, and sweat increased
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11
Q

Ganglionic stimulating agents effects at v high doses

A
  • at v high doses cause blockade bc depolarization block, reflecting inactivation sodium channels and desensitization nicotinic receptors
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12
Q

Anticholinergic/ cholinergic antagonists

A

muscarinic antagonists

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13
Q

muscrinic antagonists

A

Atropine, scopolamine, homatropine

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14
Q

Muscarinic antagonists fx

A
  • competitive inhibitors at parasympathetic neuroeffect junctions
  • can block nicotinic sites at V high concentrations
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15
Q

muscarinic antagonisti are derived from

A
  • alkaloids derived from deadly nightshade, jimosn weed, henbane or synthetic analogs of these products
  • these are toxicologically important
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16
Q

Pharmacological actions of muscarinic antagonists heart

A
  • tachycardia deepening on vagal tone (horse + dog)
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17
Q

Pharmacological actions of muscarinic antagonists blood vessels

A
  • not innervated (most muscarinc receptor in blood vessels not innervated), little effect
  • block vasodilation induced by choline esters
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18
Q

Pharmacological actions of muscarinic antagonists GI and urinary tracts

A

decrease tone, motility, and secretions

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19
Q

Pharmacological actions of muscarinic antagonists respiratory

A

increase luminal diameter, decrease bronchial secretions

- low doses stimulate respiration high doses inhibit

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20
Q

Pharmacological actions of muscarinic antagonists eye

A

relax sphincter muscle of iris and colliery muscles of sense -> mydriasis and cycloplegia (loss ability to accommodate near vision)
-increased intraocular pressure bc canals of Schelmm blocked

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21
Q

muscarinic antagonists and glaucoma

A

contraindicated

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22
Q

Pharmacological actions of muscarinic antagonists sweating

A

impaired (sympathetic; horse is excetption bc horse is noradernergic sweater)

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23
Q

Pharmacological actions of muscarinic antagonists salivation

A

reduced -> dry mouth

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24
Q

Pharmacological actions of muscarinic antagonists CNS

A
  • moderate doses stimulate medullary and higher centers
  • higher doses -> restlessness, disorientation, delirium, hyperthermia (bc of effect on medulla and higher centers)
  • even higher doses depression, coma, death bc medullary paralysis
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25
Q

Ganglionic blocking agents

A
  • nicotinic antagonists (competirei antagonists)
  • non-depolarizing
  • block symp and parasympathetic ganglia -> loss tone to organ
  • not used in vet med
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26
Q

non-depolarizing ganglionic blockers

A
  • hexamethonium (H6) and trimethaphan
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27
Q

nonâ-depolarizaing ganglionic blockers fx

A

competitively compete with ACh for nicotinic receptor sites at ganglia and adrenal medulla
net response organ system depends on predominant tone

28
Q

parasympathetic predominant tone

A

USE GBH (Use great big hug)

  • Urinary bladder
  • Salivary gland
  • Eye (Iris and ciliary muscle)
  • GI
  • Bronchioles
  • Heart
29
Q

sympathetic predominant tone

A

AVS

  • Arterioles
  • Veins
  • Sweat glands
30
Q

types ganglionic blocking agensts

A
  • non-depolarizing ganglionic blockers

- depolarizing ganglionic blockers

31
Q

depolarizing ganglionic blockers

A
  • Nicotine and Lobeline
32
Q

depolarizing ganglion blockers mechanism action

A
  • cause initial sustained depolarization followed by receptor blockade bc inactivation Na+ channels and desensitized receptor
33
Q

nicotine

A
  • depolarizing ganglionic blocker
  • also functions as depolarizing blocker at NMJ
  • Has been used as incedicide and wildlife capture drug
34
Q

depolarization ganglion blockers poisining

A

characterized by initial stimulation of ganglia followed by blockade, death caused by antagonist effects (at respiratory muscle NMJs)

35
Q

prejunctional anticholinergics

A
  • antagonists
  • don’t discriminate between muscarinic and nicotinic synapses/ junctions
  • Hemicholinium
  • Botulinus Toxin
  • Opioids
  • Local Anestethics
36
Q

hemicholinium

A
  • HC-3
  • blocks choline transport system, little to no effect on choline acetyltransferase
  • inhibition choline uptake -> limit synthesis ACh and decrease amount transmitter available for release
37
Q

Botulinus toxin

A
  • prevents release vesicular ACh at all cholinergic fibers

- peripheral respiratory paralysis -> death

38
Q

Opioids

A
  • stimulate enkephalin receptors in gut -> inhibition of release of acetylcholine
39
Q

Local Anestetics

A
  • block sodium channels and inhibit generation and propagation of action potentials
40
Q

Indirectly acting agonists

A
  • cholinesterase inhibitors
  • act on acetylcholinesterase and butyrycholinesterase
    3 types:
    1. Short acting/ reversible inhibitors
    2. Carbamylating Esters
    3. Phosphorylating Agents
41
Q

Acetylcholinesterase (AChE(

A
  • true or specific ChE
  • normal metabolism for termination of cholinergic transmission
  • AChE= generally membrane associated and found in nerve terminals in PNS, NMJ, on erythrocytes, and in gray matter of CNS
42
Q

Butyrylcholinesterase (BuChE)

A
  • aka serum or pseudo cholinesterase

- generally soluble and found in blood serum and in white matter of CNS

43
Q

Short acting reversible cholinesterase inhibitors

A
  • indirectly acting agonists

- Enrophonium (Tension)

44
Q

Enrophonium

A

-aka Tension
the following also true for general short acting reversible cholinesterase inhibitors?:
- shortest acting AntiChE
- Combines with AChE primarily at cation binding site forming rapidly reversible enzyme-inhibitor complex

45
Q

Enrophonium as diagnostic tool

A
  • inhibit Ache get more Ach; if -> more weakness issue is too much Ach as opposed to not enough receptors
46
Q

Carbamylating esters

A
  • type indirectly acting agonist
  • Physostigmine (Eserine)
  • Neostigmine (prostigmine)
  • Pyridostigmine
  • all reversibly inhibit ChE for few hours
47
Q

Phosphorylating agents

A
  • aka organophosphates
  • essentially irreversibly inhibit ChE and new enzyme must be synthesized for recovery to occur
  • importantly clinically for toxicity and poisoning
48
Q

Organophosphates characteristics

A
  • v lipid soluble (except echothiophate)
  • high vapor pressures (volatile)
  • extremely toxic bc of above characteristics
49
Q

types organophosphates

A
  • phosphates and phosphothionates
50
Q

phosphates examples

A
  • DFP
  • Paraoxon
  • Dichlorvos
  • Echothiophate
51
Q

Phosphothionates

A
  • Parathion
  • Malathion
  • these must be converted to phosphonates via P450 oxidation enzyme in liver to be active
52
Q

Organophosphates used for

A

insecticides, pesticides, nerve gas

53
Q

signs cholinesterase inhibitor poisoinig

A

DUMBBELSS

D- D+
U- urination
M- miosis
B- bronchospasm
B- bradycardia
E- Neuromuscular excitation 
L- lacrimation 
S- sweating
S- salivation
54
Q

Pharmacological effects organophosphate poisoning muscarinic

A
  • salivation
  • miosis
  • V+
  • defication
  • hyper motility GI tract
  • urination
  • bradycardia
  • hypotension
  • severe bronchoconstriction
  • excess bronchial secretions
55
Q

Pharmacological effects organophosphate poisoning nicotinic effects

A
  • NMJ: skeletal muscle fasciculations, twitching… patalysis
  • ganglia- not observed often, sympathetic usually predominates
56
Q

Pharmacological effects organophosphate poisoning CNS

A
  • ataxia, confusion
57
Q

Pharmacological effects organophosphate poisoning cause of death

A

usually respiratory failure but bronchoconstriction and convulsions (CNS) can be life threatening too

58
Q

Treatment of organophosphate poisoning

A

Atropine

Pralidoxime

59
Q

Atropine

A
  • blocks muscarinic effects overwhelming the system

- Give IV slowly

60
Q

Pralidoxime

A
  • aka 2-Pam aka protopam, obidoxime, or diacetyl monoxime
  • Give IV prior to “aging” (phosphorylation)
  • charged so will not cross blood brain barrier and will not reverse CNS effects
  • useful for nerve agent poising like nerve gas
61
Q

Mechanism of action organophosphates steps

A
  1. Inhibition (phosphorylation)
  2. Reactivation (dephospho rylation)
  3. Aging
  4. Regeneration/ Recovery
62
Q

Inhibition (phosphorylation)

A

OP reacts covalently w/ active site AChE

63
Q

Reactivation (dephospho rylation)

A

spontaneous reactivation can occur but is V slow; 2Pam can reactive enzyme prior to aging

64
Q

Aging

A

loss of alkyl group, enzyme irreversibly inihibited and v resistant to regneration with 2-PAM

65
Q

Regeneration/ Recovery

A

if enzyme not reactivated with 2-PAM new AChE must be synthesized only small fraction AChE need to be resynthesizes for full functional recovery

66
Q

Acetylcholine esterase sites and 2-PAM

A
  • anionic site and serine molecule= catalytic site where hydrolysis cleavage event occurs; carbonyl transferred to serine -> stable intermediate that stays bound for longer, site regenerated can accept acetyl choline molecule organophosphates have phosphate bind ot serine -> permanent inactivation of enzyme, pralidoxime (2-PAM) gets phosphate off serine and reactivates enzyme

Block 3 Up To Quiz 1 (24 decks)

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