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cholinergic and adrenergic Flashcards

1
Q

what neurotransmitters are used postganglionic in the sympathetic division?

A

noradrenaline ((nor)adrenergic)

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2
Q

what neurotransmitters are used postganglionic in the parasympathetic division?
what receptors are used?

A

acetylcholine (ACh) (cholinergic)
muscarinic and nicotinic receptors

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3
Q

what neurotransmitters are used preganglionic in the autonomic nervous system?
what receptors are used?

A

acetylcholine (ACh) (all cholinergic) only nicotinic receptors

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4
Q

what neurotransmitters are used in the somatic nervous system?
what receptors are used?

A

acetylcholine
nicotinic receptors
no ganglions

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5
Q

what does the parasympathetic system regulate?
what are the physiological changes?

A
  • body functions during rest, digestion, waste elimination
  • increases GI activity
  • increases genitourinary activity
  • decreases cardiovascular system activity
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6
Q

what does the sympathetic system regulate?
what are the physiological changes?

A
  • controls activity during physical exertion and stress (fight or flight)
  • increased heart rate, increased sweating, pupil dilation
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7
Q

where is noradrenaline (norepinephrine) and adrenaline (norepinephrine) produced?

A

noradrenaline: adrenal medulla, adrenergic neurons
adrenaline: adrenal medulla

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8
Q

what are the adrenergic receptors?

A

a1: contraction of smooth muscles
a2: feedback inhibition
b receptors are post synaptic receptors
b1: increases heart rate and force of contraction (increases cardiac output)
b2: relaxation of smooth muscles in the lungs

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9
Q

function of a1 receptor

A

contraction of smooth muscles
- vasoconstriction -> increases peripheral vascular resistance and blood pressure
contracts bladder sphincters -> urinary retention
contracts iris dilator muscles -> dilation of pupils

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10
Q

function of a2 receptor

A

inhibits NA release
decreases insulin secretion from pancreatic islets

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11
Q

function of b1 receptor

A

increases heart rate and force of heart contraction (cadiac output)
increases release of renin from kidney cells -> raises blood pressure

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12
Q

function of b2 receptor

A

relaxes smooth muscles
- vasodilation
- bronchodilation (opens up airway during physical activity)
- relaxes uterine muscles

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13
Q

what is propranolol used for?

A

angina, hypertension
non selective b antagonist: reduces heart rate, blood pressure

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14
Q

what is epinephrine used for?

A

used in emergencies, increases heart rate, used for emergently treating asthma
mixed with local anesthetic to restrict to the area (due to vasoconstriction)
a/b agonist

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15
Q

what is salbutamol used for?

A

asthma
it is a b2 agonist: causes bronchodilation

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16
Q

what is phenylephrine used for?

A

nasal congestion
it is an a1 agonist: contracts smooth muscle -> vasoconstriction -> limits collection of fluids -> reduces congestion

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17
Q

what is clonidine used for?

A

hypertension and migraine
a2 partial agonist: aids inhibition of NA release

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18
Q

what are the drugs affecting NA receptors?

A

epinephrine, salbutamol, phenylephrine, clonidine, propranolol,

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19
Q

what drugs affect NA biosynthesis?

A

a-methyl-p-tyrosine
inhibits tyrosine hydroxylase (enzyme that converts tyrosine to L-DOPA)

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20
Q

what drug affects NA storage?

A

reserpine
inhibits VMAT
VMAT repackages NA into vesicles -> if not in vesicle, NA will be broken down by MAO
used for hypertension and mood disorders

21
Q

what are the TYPES of drugs affecting NA release/uptake?

A
  • indirect sympathomimetic drugs
  • a2 receptor agonist
22
Q

what are the indirect sympathomimetic drugs and how do they work?

A

amphetamine: affects release
- amphetamine and NA have similar structures. they compete for reuptake -> less NA gets reuptaken into vesicles via NET and VMAT. either gets transported out of into synaptic cleft or metabolised by MAO, but amphetamine has a bit of inhibitory effect on MAO
cocaine: affects reuptake
- blocks NET, NA cannot be reuptaken -> more in cleft -> increased synaptic activity

23
Q

what are the indirect sympathomimetic drugs and what are their effects?

A

amphetamine, cocaine
- increases heart rate and force of heart contractility
- constriction of blood vessels-> hypertension
- inhibition of gut motility (GI tract relaxes)
- CNS stimulant (improves mood), euphoria

24
Q

what are the a2 receptor agonists drugs and what is its effect?

A

clonidine -> inhibits release of NA -> anti-hypertensive

25
what are the drugs affecting NA breakdown?
indirect sympathomimetic drugs phenelzine (MAO inhibitor) entacapone (COMT inhibitor) inhibits MAO/COMT -> NA not broken down
25
what is the difference between circulating catecholamines and NA from the sympathetic nerves?
duration of catecholamine circulating is significantly longer than neuronally released NA, effect is more prolonged
26
what is an anaphylactic shock? (anaphylaxis)
severe allergic reaction: blood pressure plummets, airways narrow, breathing becomes difficult
27
what is the MOA of adrenaline on anaphylaxis?
overall: increase BP a1 agonist: increase vasoconstriction, increase peripheral vascular resistance, decrease mucosal edema b1 agonist: increase rate and force of heart contraction b2 agonist: increase bronchodilation, decrease mediators of inflammation
28
how is ACh synthesised and stored?
- acetyl CoA + choline -> (choline acetyltransferase) -> acetylcholine - choline accumulated in presynaptic nerve ending - ACh is actively transported into vesicles for storage by VAT (vesicle associated transporter)
29
what are the drugs involved in synthesis and storage of ACh?
- hemicholinium: inhibits choline uptake into the nerve terminal - vesamicol: inhibits ACh from being stored in vesicles
30
how is ACh released? what drug is involved?
- presynaptic membrane depolarization -> Ca2+ channels open -> influx of ions -> vesicle fuses with presynaptic membrane -> exocytosis of ACh - botulinum toxin: inhibits release of ACh
31
how is the action of ACh terminated?
acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) breaks down ACh -> choline + acetyl coa - ache has very high activity at the synapse to prevent overstimulation of the receptors - buche has very high activity in the liver, skin, brain, muscle, blood
32
what happens when AChE is being inhibited? what are the two types of AChE inhibitors and examples
inhibit ache -> ach not broken down -> more ach -> more ach stimulation - reversible ache inhibitors: edrophonium, physostigmine, neostigmine - irreversible ache inhibitors: malathion, parathion
33
what drug is used to reactive (inhibited) cholinesterase and how?
pralidoxime: binds to phosphate group (that was inhibiting ache) -> cholinesterase regenerated needs to be administered early before aging occurs
34
what are the two families of cholinoceptors?
muscarinic receptors nicotinic receptors
35
what type of receptor are muscarinic receptors and what are the receptors? what are the signal transduction pathways of the receptors?
GPCRs M1 M2 M3 M4 M5 M1, M3: phosphatidylinositol (PI3K pathway) M2: cAMP pathway
36
what are the effects of muscarinic agonists on M1 receptor?
- brain: stimulates (?) higher cognitive processes such as learning and memory - stomach: exocrine secretion
37
what are the effects of muscarinic agonists on M2 receptor?
cardiovascular: decrease in cardiac output. arterial pressure drops
38
what are the effects of muscarinic agonists on M3 receptor?
smooth muscle (other than vascular): contracts - increases peristaltic activity (GI tract) (can -> pain) - increases contraction of bladder -> increased urination - increase contraction of bronchial smooth muscles (bronchoconstriction) sweating, lacrimation (tears), salivation and bronchial secretion (can interfere w breathing) eye: contraction of ciliary muscle -> pulls ciliary body inward -> lens suspensory ligament relaxes -> lens bulge -> accommodates for near vision (impt in response to light intensity and (lowers) intraocular pressure)
39
what are the side effects of non-selective muscarinic agonist?
low bp -> hypotension difficulty in breathing (bronchoconstriction) stomach cramps, increased gastric motility diarrhea frequent urination/urgency increased tears, saliva, mucus production blurred vision
40
what are the effects of nonselective muscarinic antagonists? what is an example of a muscarinic antagonist?
M1: mild restlessness (therapeutic dose), agitation and disorientation (higher dose), gastric secretion only slightly reduced M2: tachycardia M3: (smooth muscle) relaxes bronchial, biliary and urinary tract smooth muscle (reduces incontinence), GI motility inhibited salivary, lacrimal, bronchial, sweat glands inhibited -> uncomfortably dry mouth and skin pupil dilated, unresponsive to light. ciliary muscle relaxes -> near vision impaired. intraocular pressure rises.
41
what kind/type of receptor are nicotinic receptors? where are nicotinic receptors found?
ligand gated ion channels muscle (skeletal neuromuscular junction) the ganglion
42
what are the targets of nicotinic drugs?
- ganglion stimulating drugs - ganglion blocking drugs - neuromuscular blocking
43
what is an example of ganglion stimulating drug and what happens?
nicotine tachycardia, increased BP, GI motility ??, increased bronchial, salivary and sweat secretions
44
what is an example of ganglion blocking drug and what happens
haxamethonium hypotension, loss of cardiovascular reflexes, inhibition of secretions, GI paralysis, impaired urination clinically obsolete
45
what are the types of neuromuscular blocking drugs
non depolarizing competitive blockers depolarizing blockers (acts like ACh)
46
MOA of nondepolarizing blockers, dose effect, and examples
- acts as competitive antagonists at the ACh receptors of the endplate - compete with ACh at the receptor without stimulating it low doses -> can be overcome by cholinesterase inhibitors high doses -> reduces cholinesterase inhibitors ability to reverse action of nondepolarizing blockers pancuronium, vecuronium, atracurium
47
MOA of depolarizing blockers, effect, example
succinylcholine (SCh) attaches to nicotinic receptor, acts like ACh to depolarize the junction Na+ channel opens -> depolarization -> blocks transmission bc continuous depolarization of endplate -> Na+ channels inactivated muscle relaxation and paralysis
48
what is myasthenia gravis and what is it caused by? how can it be treated?
weakness and rapid fatigue of muscles under voluntary control autoimmune, antibodies block or destroy muscle's receptor sites for acetylcholine -> fewer nerve signals -> weakness cholinesterase inhibitors -> enhancers communication between nerves and muscles

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