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Membranes & Receptors > ACh & NA > Flashcards

ACh & NA Flashcards

0
Q

What is another exception to neurotransmitters?

A

Pre-synaptic sympathetic activates chromaffin cells to release adrenaline (no post-synaptic neurone)

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1
Q

Which synapses have ACh as the major neurotransmitter?

A

Pre-synaptic sympathetic
Pre-synaptic parasympathetic
Post-synaptic parasympathetic NMJ

+ exception: post-synaptic sympathetic eccrine sweat gland innervation (ACh -> mAChR) & ejaculatory mechanisms

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2
Q

How is ACh synthesised?

A

choline acetyltransferase

Acetyl CoA + Choline —————————-> Acetylcholine

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3
Q

How is ACh packaged?

A

Vesicular ACh transporter (vAChT) transports ACh into vesicles coupled to the efflux of protons

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4
Q

How is ACh released?

A

Vesicle containing ACh brought closer to the membrane by the SNARE complex

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5
Q

What effect does botulin have on the release of ACh?

A

Botulin cleaves a specific part of the SNARE complex

Impaired targeting to synapse -> reduced ACh release -> PARALYSIS

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6
Q

How is ACh broken down?

A

acetylcholine esterase

Acetylcholine ————————-> Choline + Acetate

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7
Q

How is ACh recycled?

A

Choline and acetate diffuse back into the presynaptic membrane

Acetate converted to Acetyl CoA in the mitochondria (TCA cycle)

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8
Q

Give some examples of cholinergic and anticholinergic effects.

A

CHOLINERGIC ANTICHOLINERGIC
Diarrhoea Constipation
Urination Urinary retention
Miosis (contraction of pupils) Dilated pupils

     Bronchorrhoea (watery sputum)           Blurred near vision
            Bronchospasm                                   Dry mouth 
            Emesis (vomiting)                             Warm, dry, red skin 
            Lacrimation                                         Tachycardia 
              Sweating                                  Confusion & hallucination
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9
Q

Give the tissue, corresponding receptor type, and major physiological action of important ACh actions.

A

SAN M2 (&M3) Reduced c.AMP ——-> -ve chronotropy
AVN M2 (&M3) Reduced cardiac conduction velocity
Bronchi M3 (&M2) Increased [Ca2+]i ——> bronchoconstriction
Bladder M3 (&M1) Increased [Ca2+]i ——> contracts bladder
Glands M1/M3 Increased [Ca2+]i ——> stimulates secretion
Parasympathetic
neuro-effector M2 & M4 inhibits further ACh release
junction

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10
Q

Give some examples of cholinoceptor agonist drugs.

A

Carbachol: treats glaucoma

Bethanechol: urinary retention (use before surgery)

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11
Q

Give some examples of cholinoceptor antagonist drugs.

A

Atropine: reduced parasympathetic activity

Relaxes patient, reduces salivation

Side-effects: dry mouth, urinary retention, etc.

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12
Q

What is glaucoma? How can it be treated? Why can it lead to blindness?

A

Blockage of drainage of aqueous humor causing raised intraocular pressure

Reduced blood flow to optic nerve causes loss of peripheral vision and then blindness

Pilocarpine (M3 antagonist) ——-> increased drainage
Clonidine (alpha-2 agonist) ——-> reduced production & outflow of aqueous humor
Carbonic anhydrase inhibitors —-> reduced aqueous humor secretion

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13
Q

Outline the adrenaline synthesis pathway.

A

tyrosine hydroxylase DOPA decarboxylase
Tyrosine ——————-> DOPA ——-> dopamine —–>

dopamine-beta-hydroxylase
——————————-> noradrenaline —————–> adrenaline

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14
Q

Outline the release of noradrenaline.

A

Tyrosine transported into neurone by sodium symporter

Tyrosine converted into noradrenaline

Noradrenaline transported into vesicle via VMAT (vallinylmandelic acid transporter) coupled to proton efflux

Noradrenaline enters synaptic cleft

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15
Q

How is the action of noradrenaline regulated?

A

Autoinhibtion (negative feedback loop)

Noradrenaline in the synaptic cleft binds to autoreceptor (alpha-2) on membrane

Noradrenaline recycled back into presynaptic neurone via the NET/Uptake 1 (Na+ dependent; high affinity)

Left-over noradrenaline is taken up into the postsynaptic neurone via Uptake 2 (non-neuronal mechanism; low affinity)

16
Q

How can drugs take advantage of the noradrenaline negative feedback mechanism?

A

Alpha-2 agonists activate autoreceptor on presynaptic membrane and antagonise post-synaptic adrenoceptors

Prevent unwanted effects of noradrenaline release

17
Q

What is noradrenaline degraded and excreted as?

A

Noradrenaline in pre-synaptic neurone not recycled back into vesicles (~10%)

Monoamine oxidase (MAO) & catechol-O-methyltransferase (COMT)

Vallinylmendelic acid (VMA) and normetanephrine

These can be measured in the urine

18
Q

How can adrenaline be used to treat anaphylaxis?

A

Bronchodilation (prevents asphyxiation)

Vasoconstriction (increases blood pressure and redirects blood)

Glycogenolysis (increased ATP)

19
Q

What is the advantage of adrenaline and local anaesthetic? What is the danger of using these?

A

Adrenaline prolongs the effects of the local anaesthetic as vasoconstriction prevents dilution of drug

Danger: inject adrenaline and anaesthetic into vein —> anaesthetises heart —-> DEATH

20
Q

What is the important difference between adrenaline and noradrenaline?

A

Noradrenaline is neuronal, adrenaline is blood-borne

21
Q

What controls vasomotor tone?

A

Sympathetic nervous system (controls both vasodilatation and vasoconstriction)

22
Q

What does alpha-methyl tyrosine do? What condition can it be used to treat?

A

alpha-methyl tyrosine is a competitive inhibitor of tyrosine hydroxylase (rate-limiting step of adrenaline synthesis)

Pheochromocytoma: neuroendocrine tumour of adrenal medulla (chromaffin cells) causes excessive intermittent adrenaline and noradrenaline secretion (increased heart rate, blood pressure, & metabolism)

23
Q

What can alpha-methyl DOPA be used for?

A

alpha-methyl DOPA is a false substrate for DOPA decarboxylase - produces methyl-noradrenaline/adrenaline instead.

Inhibits sympathetic nervous system (reduced BP, depression, anxiety)

24
Q

What can guanethidine be used for?

A

Competitive inhibitor of NET

Packaged into vesicles instead of noradrenaline

Impairs sympathetic transmission

Side-effects: orthostatic hypertension, arrhythmias, heart failure, chest pain

25
Q

Give the receptor, tissue, and pharmacological action of sympathetic receptors.

A

SAN B1 (&B2) Positive chronotropy —> tachycardia
Ventricles B1 (&B2) Positive inotropy
Vasoconstriction/venodilation A1 (working skeletal muscle = B2)
Bronchiolar/intestinal/uterine B2 (&B3) Relaxation
Bladder ?B3 Constriction
Radial muscle contraction (A1) Iris contraction

26
Q

Give some an example of a sympathomimetic agent.

A

Amphetamines

Cause noradrenaline to leak from vesicles and into the synaptic cleft

27
Q

Give an example of an uptake 1 inhibitor.

A

Tri-cyclic inhibitors e.g. amitriptyline

act in CNS

28
Q

Give an example of an alpha-1 antagonist used to treat hypertension.

A

Doxazosin

Membranes & Receptors (11 decks)

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