Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

LSM3211 > Autonomic Nervous Syetm: Cholinergic system > Flashcards

Autonomic Nervous Syetm: Cholinergic system Flashcards

(77 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the neurotransmitter for the cholinergic system

A

acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

which ones are cholinergic

A

preganglionic neurons and postganglionic para-sympathetic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

hemicholinium
- decreased Ach sythesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what happens after synthesis of ach

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

reversible AchE inhibitors

A

edrophonium
physostigmine
neostigmine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

irrevisible AchE inhibitors

A

malathion and parathion( they are organophosphates)

since it is irrevisble, tjey increase the Ach levels exponentiallly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

the affinity of muscarinic receptors

A

muscarine
acetylcholine
nicotine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

affinity of nicotinic receptors

A

nicorine
acetylcholine
muscarine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

direct acting cholinomimetics

A

acts direcly on receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

indirect acting cholinomimetics

A

inhibition of cholinesterase and prolong action of Ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are muscranic receptors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

signalling trasndcution involved for muschrnic receptor

A

m1 and m3 - phosphatidylinositol pathway
m2- cAMP pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
effect of muscarinic agonist and receptor involved in brain
brain : m1: receptors involved in higher cognetive processes such as learning and memory
25
effect of muscarinic agonist and receptor involved in heart
cardiovascular effect :m2: decrease in cardia output preoducs a call in arterial pressure
26
effect of muscarinic agonist and receptor involved in smooth muscles
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
27
effect of muscarinic agonist and receptor involved in sweating lactimation, salivation and broncial secretion
- critical for stimulation of exocrine glands combined effect of bronchial secretion and broncho constriction can interfere with breathing
28
effect of muscarinic agonist and receptor involved in eyes
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
29
effect of muscarinic agonist and receptor involved in stomach
m1 - acd productions
30
what type ot drug to use to make them pee less
used anticholigic drug to prevent bladder contractino due to Ach
31
effect of muscarinic agonist and receptor involved in mouth
saliva sections
32
effect of muscarinic agonist and receptor involved in gi tract
increse mortality
33
muscaranic agonisy for glaucoma
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
side effects of non selective muscranic agonist
- 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
name and funciton of non selective muscarinic antagonist effect
atropine -blocks cholonegic activities
36
non selective muscarinic antagonist effect on heart rate
heart rate: block sympathetic system: but only have inhibition is there is existing parasympathetic tone
37
non selective muscarinic antagonist effect on smooth muscle
bronchial, biliary and urinary tract smooth muscle are all relaxed, incontinenct due to bladder overactivity is reduced by M3 antagonist
38
non selective muscarinic antagonist effect on gastrointestinal tract
only by atropine at large dose due to presence of alternative excitatory transmitters
39
non selective muscarinic antagonist inhibition of secretion
salivary, lacrimal , bronchial, and sweat glands are inhibited, producing dry mouth and skin, gastic section only slightly reduced
40
non selective muscarinic antagonist effect on eye
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
non selective muscarinic antagonist effect on CNS
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
do we give muscrainic antagonist to someone with glycoma? why?
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
muscaranic agnonist names and funciton and mechanism
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
where are the nicotic receptors agnost act on
ganglionic receptors or motor endplate
45
nicotinic receptors function
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
nicotinic receptor subtypes and their responsibilities
muscle-skeletal neuromuscular junction and ganglion - responsible for transmission at sympathetic and parasympathetic ganglia they differ in their molecular structure and pharmacology
47
drugs type that target nicotinic receptors
ganglion stimulating drugs and neuromuscular blocking drugs
48
ganglion stimulatinf drug name and what does it do
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
actions that drugs can do to block neuromuscular transmission
1. acting presynaptically to inhibit Ach synthesis or release 2. acting on post synaptically on the endplate of NMJ
50
how does neuromusclat blocking durg act postsynaptically on the end place of NMJ (non depolizing competitive blocker)
blocks Ach receptors without depolarizing the morot end plate
51
how does neuromusclat blocking durg act postsynaptically on the end place of NMJ : depolarising blocker
activate Ach receptor thus causing president depolarising of morot end plate, which results in transmission block
52
neuromuscular blockers clinical use
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
name of non depolarising competitive drugs (neuromuscualr blocking drugs)
pancuronium veruronium atracurium
54
what is the emchacnims of action for non depolairising competitive drugs of neuromuscular blocking drgs
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
cholineraterse inhibitor vs nondepolarising competive blockers
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
theraputic use of non depolarising competitive blockers of neuromuscular
muscle relaxation and paralysis
57
pharmacology of the non depolarising competitive blockers of neuromuscular
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
name the muscular depolarising blocker
succinylcholine: muscle relaxant - more presistent to degradation. by acetylcholinesterase and then can thus be more persistently depolasirsed the muscle fibers
59
name the mechanism of the action of muscular depolarising blocker
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 5. 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
result of muscular depolarising blockers Succinylcholine
larger musccle gorup paralysed last initlaly produce brief muscle fasciculatons that causes muscle soreness
61
theraputic use of Succylcholine
rapid endotrachal intubation
62
pharamokinetics of Succinylcholine
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
adverse effect of Succylcholine
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
what is myasthenia gravis
weakness and rapid fatig of any muscle under voluntary control
65
myasthenia gravis symptoms
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
primary cause of myasthnia gravis
auto immune disorder where immune system destroys recepts sites for acetylcholine , fewer muscle, fewer nerve signalling received, resulting in weakness
67
treatment for myasthenia gravia
cholinesterase inhibitor: medication such as pyridostigmine enhances communication between nerves and muscle s other used: corticosteroids, immunisuppressants
68
Anti choline esterase inhibition means?
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
AchE inhibitors : Short acting
adrophonium
70
clinical purpose of adrophonium
reversal of neuromuscular block by non depolarising drugs diagnosis off myasthenia gravis
71
AchE inhibitors : Intermediate acting
neostigmine pyridostigmine physostigmine
72
AchE inhibitors : long lasting acting
parathion sarin
73
clinical application of neostigmine
reversal of neuromuscualr block, treatment of myasthenia
74
clinical applciation of pyridostihmine
treatment of myasthenia
75
clinical application of physostigmine
reversal of severe atropine poisoning occasionally used in acute glucoma
76
clincail use of long acting
parathion: insecticides sarin: nerve gas

LSM3211 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions