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lsm3211 > cholinergic and adrenergic > Flashcards

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
Q

what are the drugs affecting NA breakdown?

A

indirect sympathomimetic drugs
phenelzine (MAO inhibitor)
entacapone (COMT inhibitor)
inhibits MAO/COMT -> NA not broken down

25
Q

what is the difference between circulating catecholamines and NA from the sympathetic nerves?

A

duration of catecholamine circulating is significantly longer than neuronally released NA, effect is more prolonged

26
Q

what is an anaphylactic shock? (anaphylaxis)

A

severe allergic reaction: blood pressure plummets, airways narrow, breathing becomes difficult

27
Q

what is the MOA of adrenaline on anaphylaxis?

A

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
Q

how is ACh synthesised and stored?

A
  • 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
Q

what are the drugs involved in synthesis and storage of ACh?

A
  • hemicholinium: inhibits choline uptake into the nerve terminal
  • vesamicol: inhibits ACh from being stored in vesicles
30
Q

how is ACh released? what drug is involved?

A
  • presynaptic membrane depolarization -> Ca2+ channels open -> influx of ions -> vesicle fuses with presynaptic membrane -> exocytosis of ACh
  • botulinum toxin: inhibits release of ACh
31
Q

how is the action of ACh terminated?

A

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
Q

what happens when AChE is being inhibited? what are the two types of AChE inhibitors and examples

A

inhibit ache -> ach not broken down -> more ach -> more ach stimulation
- reversible ache inhibitors: edrophonium, physostigmine, neostigmine
- irreversible ache inhibitors: malathion, parathion

33
Q

what drug is used to reactive (inhibited) cholinesterase and how?

A

pralidoxime: binds to phosphate group (that was inhibiting ache) -> cholinesterase regenerated
needs to be administered early before aging occurs

34
Q

what are the two families of cholinoceptors?

A

muscarinic receptors
nicotinic receptors

35
Q

what type of receptor are muscarinic receptors and what are the receptors? what are the signal transduction pathways of the receptors?

A

GPCRs
M1 M2 M3 M4 M5
M1, M3: phosphatidylinositol (PI3K pathway)
M2: cAMP pathway

36
Q

what are the effects of muscarinic agonists on M1 receptor?

A
  • brain: stimulates (?) higher cognitive processes such as learning and memory
  • stomach: exocrine secretion
37
Q

what are the effects of muscarinic agonists on M2 receptor?

A

cardiovascular: decrease in cardiac output. arterial pressure drops

38
Q

what are the effects of muscarinic agonists on M3 receptor?

A

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
Q

what are the side effects of non-selective muscarinic agonist?

A

low bp -> hypotension
difficulty in breathing (bronchoconstriction)
stomach cramps, increased gastric motility
diarrhea
frequent urination/urgency
increased tears, saliva, mucus production
blurred vision

40
Q

what are the effects of nonselective muscarinic antagonists? what is an example of a muscarinic antagonist?

A

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
Q

what kind/type of receptor are nicotinic receptors? where are nicotinic receptors found?

A

ligand gated ion channels
muscle (skeletal neuromuscular junction)
the ganglion

42
Q

what are the targets of nicotinic drugs?

A
  • ganglion stimulating drugs
  • ganglion blocking drugs
  • neuromuscular blocking
43
Q

what is an example of ganglion stimulating drug and what happens?

A

nicotine
tachycardia, increased BP, GI motility ??, increased bronchial, salivary and sweat secretions

44
Q

what is an example of ganglion blocking drug and what happens

A

haxamethonium
hypotension, loss of cardiovascular reflexes, inhibition of secretions, GI paralysis, impaired urination
clinically obsolete

45
Q

what are the types of neuromuscular blocking drugs

A

non depolarizing competitive blockers
depolarizing blockers (acts like ACh)

46
Q

MOA of nondepolarizing blockers, dose effect, and examples

A
  • 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
Q

MOA of depolarizing blockers, effect, example

A

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
Q

what is myasthenia gravis and what is it caused by? how can it be treated?

A

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

lsm3211 (4 decks)

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