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LSM3211 > Autonomic Nervous Syetm: Cholinergic system > Flashcards

Autonomic Nervous Syetm: Cholinergic system Flashcards

1
Q

what is the parasympathetic system

A

regulates body functions during rest, digest and waste elimination
- increases the activity of gastrointestinal and genitourinary systems and decreases the activity of cardiovascular systems

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2
Q

what is the neurotransmitter for the cholinergic system

A

acetylcholine

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3
Q

which ones are cholinergic

A

preganglionic neurons and postganglionic para-sympathetic neurons

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4
Q

what ais the emaning of cholinergic and anticholinergic drugs

A

cholinergic drugs are used to increase parasympathetic activity, and used for such as urinary and intestinal stasis, glaucoma, alzheimer’s disease and myasthenia gravis

anticholinergics are drugs that decrease the parasympathetic activity and used for treatment of overactive urinary and interstinal conditions, asthma, and during various ophthalmic procedures

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5
Q

what is thr process for synthesis and storage of acetylcholine

A

ach is synthesised from choline and actyle-CoA via choline acetyltransferase
- choline accumulated in cholinergic presynaptic nerve ending via active transport mechanism linked to Na+ pump

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6
Q

what drug inhibits the cholineb iptake into nerve ending and what is the effect

A

hemicholinium
- decreased Ach sythesis

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7
Q

what happens after synthesis of ach

A

ach synthesized is actively transported into vesicles and stored by the vesicular acetylcholine transporter

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8
Q

what drug inhibits vesicular acetylcholine transporter

A

vacht can be inhibited by vesamicol and result in. reduced acetylcholine loaded into synaptic vesicles and released
result in less parasympathetic activity

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9
Q

process of release of acetylcholine

A

presynaaptic membrane depolarization opens voltage dependent ca2+ channels , and influx of the ion causes fusion of the synaptic vesicle membranes with the presynaptic membrane, leading to exocytosis of Ach

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9
Q

what drug prevents the release of Ach and how is it used

A

botulinum toxin prevents Ach release and used for dystonia and cosmetics

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10
Q

what is dystonia

A

movement disorder in thich a person’s muschels contract uncontrollably , contraction causes the affected body part to twist involuntarily, resulting in repetitive movements or abnormal postures

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11
Q

how is action of Ach terminated

A

acetylcholineeasterase(AchE)
there is also butyrylcholinesterase , that differ in their distribution, substrate specificity and function
they both convert Ach into choline and acetate

synapse and function to destroy Ach to prevent over stimulation

at skin, liver, brain muscle, and blood

when inhibited ,level of Ach increases

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12
Q

reversible AchE inhibitors

A

edrophonium
physostigmine
neostigmine

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13
Q

irrevisible AchE inhibitors

A

malathion and parathion( they are organophosphates)

since it is irrevisble, tjey increase the Ach levels exponentiallly

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14
Q

what is the function of pralidocime

A

reactives cholinestersae which are inactived by phosphorylation due to an organophosphate pesticide or related compound(malathion and parathion)
-thye have high level of affinity for phosphate groups

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15
Q

what is the warning for pralidoxime

A

it can only be used when we know that the AchE is inhibited by oligophosphates

if given without it, since they have weak inhibitory activity on AchE, further inhibit AchE and causes it to be worse

also they have to be administered very early when we know the action, bc when oligophosphates are administered, they undergo further medications that will result in a irreveisble process and then the phosphate group cannot be replaced

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16
Q

what are the post junctional receptors for Ach

A

muscarinic and nictonic
- target sites for activating drugs(direct acting cholinometics) and blocking drugs

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17
Q

the affinity of muscarinic receptors

A

muscarine
acetylcholine
nicotine

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18
Q

affinity of nicotinic receptors

A

nicorine
acetylcholine
muscarine

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19
Q

direct acting cholinomimetics

A

acts direcly on receptor

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20
Q

indirect acting cholinomimetics

A

inhibition of cholinesterase and prolong action of Ach

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21
Q

cholinoceptor antagonist

A

block muscranic receptor
block nicotinic receptor
cholinesterae regenerators which are not receptor blockers but are chemical antagonist of organophosphate acetylinesterase inhibitors

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22
Q

what are muscranic receptors

A

g protein couples receptors whcih respon to muscarine as well as Ach
- m1,m2,m3

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23
Q

signalling trasndcution involved for muschrnic receptor

A

m1 and m3 - phosphatidylinositol pathway
m2- cAMP pathway

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24
Q

effect of muscarinic agonist and receptor involved in brain

A

brain : m1: receptors involved in higher cognetive processes such as learning and memory

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25
Q

effect of muscarinic agonist and receptor involved in heart

A

cardiovascular effect :m2: decrease in cardia output preoducs a call in arterial pressure

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26
Q

effect of muscarinic agonist and receptor involved in smooth muscles

A

smooth muscle : m3: contraction of smooth mucels other than vascular smooth muscles
- increase in peristality activity of gastrointestinal tract
- contraction of bladder deterusor muscles and broonchila smooth muscles
—- contract more - pee more often

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27
Q

effect of muscarinic agonist and receptor involved in sweating lactimation, salivation and broncial secretion

A
  • critical for stimulation of exocrine glands
    combined effect of bronchial secretion and broncho constriction can interfere with breathing
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28
Q

effect of muscarinic agonist and receptor involved in eyes

A

parasympathetic nerve supply the constictor pypilla msucel
- runs circumferentially in the iris, and ciliary muscle
contraction of ciliary muscle in response to activation of M3 pulls the ciliary body inwards, thus relaxing the tensions on the suspensory ligament of lends, allowing fr the lens to bulge more
- reducing focal length
- accommodating the eyes for near vision
constictor pupillae important fro constricting the pupil in response to changes in light intensity and intraocualr pressure
- activation of the constrictor pupillary muscle by muscranic agonists in case of glaucoma lowers the intraocular pressure

  • aquarous humour can be cleared out rhu the canal of schemm
  • increase muscu secretion
  • improve nearby vision
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29
Q

effect of muscarinic agonist and receptor involved in stomach

A

m1 - acd productions

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30
Q

what type ot drug to use to make them pee less

A

used anticholigic drug to prevent bladder contractino due to Ach

31
Q

effect of muscarinic agonist and receptor involved in mouth

A

saliva sections

32
Q

effect of muscarinic agonist and receptor involved in gi tract

A

increse mortality

33
Q

muscaranic agonisy for glaucoma

A

aqu humour secreted slowly and n continously by cells of epithelium covering the ciliary body, and drains into the canal of schlemma

in acute glaucoma, drainage of aqu humaour become impeded when pupil is dilalated bc folding of the iris tissue occlues the drainage angle, causing the introocular pressure to rise

activation of the constrictor pupllae muschle by muscarinic agnoist in these circumstances lowers the intraocular pressure by improving drainage

34
Q

side effects of non selective muscranic agonist

A
  • blurrred vision
  • increased lactimation-tearing
    -increased salvation
    -bronchial constriction
    -hypertension-dizziness hwne getting up from lysing positon
    -abdominal cramping
    -increased gastric motility
    -diarrhea
    -urinary urgency
35
Q

name and funciton of non selective muscarinic antagonist effect

A

atropine
-blocks cholonegic activities

36
Q

non selective muscarinic antagonist effect on heart rate

A

heart rate: block sympathetic system: but only have inhibition is there is existing parasympathetic tone

37
Q

non selective muscarinic antagonist effect on smooth muscle

A

bronchial, biliary and urinary tract smooth muscle are all relaxed, incontinenct due to bladder overactivity is reduced by M3 antagonist

38
Q

non selective muscarinic antagonist
effect on gastrointestinal tract

A

only by atropine at large dose due to presence of alternative excitatory transmitters

39
Q

non selective muscarinic antagonist inhibition of secretion

A

salivary, lacrimal , bronchial, and sweat glands are inhibited, producing dry mouth and skin, gastic section only slightly reduced

40
Q

non selective muscarinic antagonist effect on eye

A

pupil is dilated(mydriasis) by atropine administration, ad becoming unresponsive to light, relaxation to fht eciliary muscle causes paralysis of accommodation, and near vision is impaired, intraocular pressure may rise

41
Q

non selective muscarinic antagonist effect on CNS

A

in theraputic dose, atropine has only small or no effect,

may cause mild restlessness,

higher dose can cause agitation and disorientation

in toxic dose, cause circulatory and respiratory collapse

chronic use of anticholinergic drugs may lead to decreased cholinergic activity in the brain and may decrease the cognitive decline

42
Q

do we give muscrainic antagonist to someone with glycoma? why?

A

for somone with glycoma, the intracellular pressure is alr higherbecuase of aqu humaour is notdraining out well
- to drain better they ned to make muscle contract
- but with antagonist the pressure will increase and as such we do not give the patient with glycoma antagonist

43
Q

muscaranic agnonist names and funciton and mechanism

A

activate receptor and increase ip3 and DAG

Bethanechol– relieved urinary retention

and pilocarpine– acute angle glucoma, can be given alongside physostigmine which is a revisible cholinerterase inhibitions

44
Q

where are the nicotic receptors agnost act on

A

ganglionic receptors or motor endplate

45
Q

nicotinic receptors function

A

function as ligand gated ion channel, they mediate fast exciattory synaptic transmission

  • binding site for nictoine and acetylcholine

can bd found in CNS and adrenal medulla

46
Q

nicotinic receptor subtypes and their responsibilities

A

muscle-skeletal neuromuscular junction

and ganglion - responsible for transmission at sympathetic and parasympathetic ganglia

they differ in their molecular structure and pharmacology

47
Q

drugs type that target nicotinic receptors

A

ganglion stimulating drugs

and neuromuscular blocking drugs

48
Q

ganglion stimulatinf drug name and what does it do

A

nicotine

  • opens Na and K channels in ganglia and neuromuscular end plates

both sympathetic and parasympathetic ganglia are stimulated, so effects are complex and dose-dependent
- no therapeutic uses
ganglion stimulating may be followed by depolarisation block

49
Q

actions that drugs can do to block neuromuscular transmission

A
  1. acting presynaptically to inhibit Ach synthesis or release
  2. acting on post synaptically on the endplate of NMJ
50
Q

how does neuromusclat blocking durg act postsynaptically on the end place of NMJ (non depolizing competitive blocker)

A

blocks Ach receptors without depolarizing the morot end plate

51
Q

how does neuromusclat blocking durg act postsynaptically on the end place of NMJ : depolarising blocker

A

activate Ach receptor thus causing president depolarising of morot end plate, which results in transmission block

52
Q

neuromuscular blockers clinical use

A

surgery to faciliate tracheal intubation and provide complete muscle relaxation to lower anesthetic doses, allowing for more rapid recovery from anesthesia and reducing postoperative respiratory depression

53
Q

name of non depolarising competitive drugs (neuromuscualr blocking drugs)

A

pancuronium
veruronium
atracurium

54
Q

what is the emchacnims of action for non depolairising competitive drugs of neuromuscular blocking drgs

A

non deploarins blokcing agent act as competitive antagonist at the Ach receptor of the endplate
- compete with Ach at the receptors without stimulating it , thus these drugs prevent depolarization of the muscle cell membrane and inhibit muscular contraction

55
Q

cholineraterse inhibitor vs nondepolarising competive blockers

A

at low dose, their competition overcome by the cholinesterase inhibitor as they increase Ach levels and Ach is the substrate for competition

choleinesterase inhibitor: neistigmine and adrophonium

56
Q

theraputic use of non depolarising competitive blockers of neuromuscular

A

muscle relaxation and paralysis

57
Q

pharmacology of the non depolarising competitive blockers of neuromuscular

A

administration and absorption: injected intravenous;y or occasionally intramuscularly since they are not effect orally

they penetrate membranes very poorly and do not enter cells or cross the blood brain barrier

many of the drugs are not metabolised and their actions are terminated by redistributioen

58
Q

name the muscular depolarising blocker

A

succinylcholine: muscle relaxant
- more presistent to degradation. by acetylcholinesterase and then can thus be more persistently depolasirsed the muscle fibers

59
Q

name the mechanism of the action of muscular depolarising blocker

A
  1. attract the nicotinic receptor and acts like Ach to depolarise the junction
  2. cause opening of sodium channel associated with nicotinic receptors ,
  3. result in depolarising of the receptors and transient twitching of the muscles
    4.unlike Ach,which is instantly destroyed by AchE, succinylcholine presist at high conc in synaptic cleft until plasma conc of the Sch Is reduced bc the breakdown by butyrycholinesterase or elimination by the kidney
  4. biphasic action of Sch from initial excitation tp eveunalt block of transmission result from continue depolarisation of the endplate and inactivation of NA + channel
    - causes resistance to depolasriasion and flaccid paralysis
60
Q

result of muscular depolarising blockers Succinylcholine

A

larger musccle gorup paralysed last
initlaly produce brief muscle fasciculatons that causes muscle soreness

61
Q

theraputic use of Succylcholine

A

rapid endotrachal intubation

62
Q

pharamokinetics of Succinylcholine

A

injected intravenously, bried duration of action result from redistribution and rapid hydrolysis by plasma butrylcholinesterase
- therefore sometimes give by conitnute infusion to maintain longer duration of effect

63
Q

adverse effect of Succylcholine

A

apnea: adminsteraction of succcinylcholine to a patient who Is deficient in plasma cholinesterase or who has an atypical form of the enzyme can lead to prolonged apnea due to paralysis of diaphragm

hyperkalemia: succylcholine increases K+ release from intracellular stores
- may be dangerous fro burn patients who have massive tissue damage in whic.h K + is rapidly lost within cells

64
Q

what is myasthenia gravis

A

weakness and rapid fatig of any muscle under voluntary control

65
Q

myasthenia gravis symptoms

A

affect any muscle that you can control voluntarily

  • eye muscle: drooping , double vision,
  • face and throat muschle : altered speaking, difficulty swallowing, problem chewing

neck and limb muscle

66
Q

primary cause of myasthnia gravis

A

auto immune disorder where immune system destroys recepts sites for acetylcholine , fewer muscle, fewer nerve signalling received, resulting in weakness

67
Q

treatment for myasthenia gravia

A

cholinesterase inhibitor: medication such as pyridostigmine enhances communication between nerves and muscle s

other used: corticosteroids, immunisuppressants

68
Q

Anti choline esterase inhibition means?

A

indirelct provide a cholinergic action by preventing degradation of Ach

  • result in accumulation of Ach in synaptic space
  • provoked response in all cholinocereptors in the body including muscarinic and nictonics receptors of the ANS
69
Q

AchE inhibitors : Short acting

A

adrophonium

70
Q

clinical purpose of adrophonium

A

reversal of neuromuscular block by non depolarising drugs
diagnosis off myasthenia gravis

71
Q

AchE inhibitors : Intermediate acting

A

neostigmine
pyridostigmine
physostigmine

72
Q

AchE inhibitors : long lasting acting

A

parathion
sarin

73
Q

clinical application of neostigmine

A

reversal of neuromuscualr block, treatment of myasthenia

74
Q

clinical applciation of pyridostihmine

A

treatment of myasthenia

75
Q

clinical application of physostigmine

A

reversal of severe atropine poisoning
occasionally used in acute glucoma

76
Q

clincail use of long acting

A

parathion: insecticides
sarin: nerve gas

LSM3211 (14 decks)

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