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Autonomic Nervous System > Lecture summary > Flashcards

Lecture summary Flashcards

1
Q

What is the postganglionic sympathetic neurotransmitter?

A

NE (ACh in sweat glands and arterioles)

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2
Q

postganglionic parasymp. neurotransmitter?

A

ACh

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3
Q

What is the neurotransm. at the NMJunction?

A

ACh

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4
Q

What is the neurotransm at the presynaptic synapse in both the SNS and PNS?

A

ACh

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5
Q

Drugs that mimic NE

A

fight/flight responses

Heart rate UP

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6
Q

Drugs that mimic ACh

A

rest/digest responses

Heart rate DOWN

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7
Q

Precursors of ACh

A

Choline (diet) + Acetyl CoA

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8
Q

Where is ACh made?

A

Liver then goes to nerve terminal.

Done by high affinity Na- choline co-transporter

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9
Q

Inhibition of ACh synthesis

A

HEMICHOLINIUM (inhibits choline transporter)

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10
Q

Inhibition of ACh vesicular transporter?

A

VESAMICOL

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11
Q

By what mechanism is ACh released into the synaptic cleft?

A

Ca-dependent exocytosis

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12
Q

what breaks down ACh?

A

acetylcholinesterases-acetate and choline

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13
Q

Blockade of cholinesterase enzymes eg. Neostigmine (indirect)

A

increased autonomic activity but primary with increased cholinergic effects

At postganglionic nerve terminal with increased stimulation of muscarinic receptors, enhancing synaptic cholinergic activity, causing excessive salivation, bradycardia, bronchospasm and hypotension

increasing NMJ activity with muscle fasciculation and twitching and may result in a depolarisation block and paralysis

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14
Q

3 places where muscarinic receptors are located?

A

Cardiac
Smooth muscle
Exocrine glands

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15
Q

Nicotinic receptors: where?

A

Ganglia
Adrenal glands
NMJ

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16
Q

What is the precursor of NE

A

L-tyrosine

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17
Q

What is the rate limiting step of cat synthesis

A

Tyrosine hydroxylase

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18
Q

How is NE created from dopamine?

A

dopamine is formed in the cytoplasm of the nerve terminal is actively transported by vesicle transporter (VMAT: Vesicular MonoAmine Transporter) into the storage vesicle, where it is converted to norepinephrine by the enzyme dopamine beta-hydroxylase

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19
Q

Reserpine

A

Adrenergic blocking agent-blocks catecholamine STORAGE

ANTIHYPERTENSIVE

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20
Q

Adrenergic homeostasis

A
  1. Negative feedback: high NE in cytosol=inhibition of tyrosine hydroxylase
  2. NE binds to alpha2 receptors
  3. NET transporter for reuptake
  4. Diffusion and metabolism
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21
Q

Metyrosine

A

Blocks NE synthesis (Blocks tyrosine hydroxylase)

Anti-hypertensive

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22
Q

Muscarinic ACh receptors

A

GPCRs

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23
Q

Nicotinic ACh receptors

A

ligand-gated

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24
Q

ACh receptors 2

A

Muscarinic and Nicotinic

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25
Q

Adrenergic receptors 2

A

Alpha and Beta

7-transmembrane GPCRs

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26
Q

Alpha receptors

A

a1: postsynaptic
a2: presynaptic

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27
Q

Beta receptors

A

b1: heart, intestinal smooth muscle
b2: bronchial, vasc, uterine smooth muscle
b3: fat

28
Q

Muscle contraction

A

a1, a2

29
Q

Muscle relaxation

A

a1,a2,b2

30
Q

Increase heart rate and contraction force

A

b1

31
Q

PNS and bronchi

A

bronchoconstriction

32
Q

PNS and bladder

A

contracts

33
Q

Cholinergic drugs

A

Direct and indirect acting

34
Q

Direct cholinergic

A

Choline esters and natural alkaloids

35
Q

Indirect cholinergic

A

Anti-cholinesterase

36
Q

Choline ester

A

Bethanechol-longer half life ACh, not hydrolysed by cholinesterase
MUSCARINIC

37
Q

Natural alkaloid

A

Pilocarpine-closed angle glaucome

38
Q

Anticholinesterases

A

do not cross BBB-no central effects

39
Q

4 reversible anticholinesterases

A

EDROPHONIUM
Neostigmine
Physostigmine
Pyridostigmine

40
Q

Closed angle glaucoma

A

angle between cornea and iris is abnorm. small

raised IOP

41
Q

3 drugs that reduce IOP

A
  1. Pilocarpine-contracts ciliary muscle, aqueous outflow increased
  2. Timolol-beta blocker, it block B-2 receptors on the ciliary processes and reduce aqueous production. They may block vessels supplying the ciliary processes. The resulting vasoconstriction produces reduced ultrafiltration and aqueous formation.
  3. Brimonidine-reduce aqueous production.
    Alpha 2 adrenoceptor agonists, they decrease aqueous by stimulating alpha 2 adrenoceptors on the adrenergic nerve terminal innervating the ciliary body
42
Q

Myasthenia Gravis

A

autoimmune-induced decrease (70-90%) in the number of nAChRs at the NMJ

43
Q

Immediate and diagnostic treatment MG

A

Edrophonium

then Neostigmine and Pyridostigmine longterm (NM transmission rather than autonomic NS)

44
Q

Adverse effects AChE inhib.

A 
too much ACh symptoms
D-diarrhoea
U-urination
M-miosis
B-bronchoconstriction
E-excitation
L-lacrimation
S-salivation and sweating
45
Q

Anticholinergic drug
Antimuscarinic
Nonselective

A

Atropine

46
Q

Cholinergic ANTAGs

A

atropine: OP poisoning, muscarinic receptors, HR incr, mydriasis
(PRALIDOXIME ALSO IN OP POISONING-CHOLINESTERASE regen)
scopolamine: increase HR, mydriasis

Ipatropium bromide: anticholinergic, bronchodilator, nasal agent

47
Q

Nicotine recep antag

A

Pancuronium-inhibit skeletal muscle contraction

48
Q

Muscarinic recep antag

A

Glycopyrrolate – antimuscarinic/bronchodilator; used for reversal of neuromuscular blockade (preop)

Oxybutynin – antimuscarinic/urinary antispasmodic (urge incont)

Imipramine – TCA with strong antimuscarinic action, reduces incontinence

49
Q

Sympathomimetics

A

Sympathomimetics agonists may directly activate their adrenoceptors OR they may act indirectly to increase concentration of endogenous catecholamine transmitter in the synapse

50
Q

Indirectly acting sympathomimetics

A

Amphetamine derivatives and tyramine causes the release of the stored catecholimines

TCA and Coke: don’t like NET

51
Q

Directly acting sympathomimetics-non-cats

A

Clonidine (alpha 2 agonist-decr NE, decr BP)

52
Q

what does clonidine treat?

A

Resistant hypertension

53
Q

Sympathomimetics-
Direct acting
ALPHA 1

A

Phenylephrine – topical to eye for mydriasis and nasal decongestant

54
Q

Sympathomimetics-
Direct acting
ALPHA 2

A

Clonidine (anxiolytic, sedation, antihypertensive),
methyldopa (antihypertensive),
oxymetazoline (nasal decongestant)

55
Q

Sympathomimetics-
Direct acting
ALPHA 1 AND 2

A

Phenylpropanolamine (nasal decongestants)

56
Q

Sympathomimetics-
Direct acting
BETA 1

A

Dobutamine

mild α1 properties and greater inotropic than chronotropic effect

57
Q

Sympathomimetics-
Direct acting
BETA 2

A

Salbutamol
Formoterol, Salmeterol (LABA)
(asthma, pre-term labour)

58
Q

Epinephrine: topical

A

adjuvant of local anaes.
glaucoma
bleeding

59
Q

Epinephrine: systemic

A

Cardiac arrest
Anaphylactic shock
Acute bronchial asthma

60
Q

Amphetamine

A

CNS stimulant
Indirectly acting sympathomimetic

Amphetamine increases the release of norepinephrine, dopamine and serotonin from nerve terminal
Amphetamines bind to presynaptic membrane transporters responsible for the reuptake of norepinephrine ( NET), dopamine ( DAT) and serotonin ( SERT)
Uptake of amphetamine resulting in efflux of these monoamines from the cytoplasmic pool into extracellular space

Amphetamine causes the intracellular vesicular release of catecholamines within the nerve terminal causing redistribution of monoamines from the storage vesicles into the cytoplasmic pool
The will be release of NE in the synaptic junction

61
Q

Tyramine

A

Tyramine is an indirectly acting sympathomimetic ( a by-product of tyrosine metabolism)

Mechanism of action

Tyramine is taken up into nerve terminals by NET ( the norepinephrine reuptake transporter) and causes the release of cetacholamines. It is because of the feverse transport of NET
The effects of tyramine are increased in the presence of MAO inhibitors. MAO present in the nerve terminals metabolises both cytosolic amines such as NE as well as Tyramine converting them into inactive metabolites
Normally the bioavailability of dietary tyramine ( present in red wine and cheese) is relatively low due to the expression of MAO in the GUT tract and liver. When MAO is inhibited, high level of tyramine is absorbed , resulting in a “Hypertensive crisis” due to the release of NE from nerve terminals

62
Q

Alpha receptor antagonist

A

alpha 1: prazosin (BPH)
Doxazosin-HPT, BPH
Tamsulosin

63
Q

Beta recep antagonist

A

non-selective 1st gen: timolol-Glaucoma, HPT
non-selective 3rd gen: carvedilol
non-selective: propanolol (lipophilic)-HPT, MI, AP, hyperthyroid, migraine

Beta 1: atenolol, IHD

64
Q

alpha and beta antag

A

Carvedilol (hypertension, congestive heart failure) and Labetalol (hypertensive crisis)

65
Q

TCAs

A

These are important group of antidepressants in clinical practice, include amitriptyline and imipramine
TCA adverse effect profile is due to their ability to block muscarinic receptors, alpha 1 adrenoceptors and histamine receptors H1.
Anticholinergic effects atropine like effects, blurred vision, urinary retention, dry mouth
Sympathetic effects postural hypotension, reflex tachcardia
Histamine antagonism leading to sedation

Autonomic Nervous System (1 decks)

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