Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Autonomic Nervous System > Lecture summary > Flashcards

Lecture summary Flashcards

(65 cards)

Start Studying
1
Q

What is the postganglionic sympathetic neurotransmitter?

A

NE (ACh in sweat glands and arterioles)

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

postganglionic parasymp. neurotransmitter?

A

ACh

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

What is the neurotransm. at the NMJunction?

A

ACh

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

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

A

ACh

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

Drugs that mimic NE

A

fight/flight responses

Heart rate UP

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

Drugs that mimic ACh

A

rest/digest responses

Heart rate DOWN

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

Precursors of ACh

A

Choline (diet) + Acetyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is ACh made?

A

Liver then goes to nerve terminal.

Done by high affinity Na- choline co-transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Inhibition of ACh synthesis

A

HEMICHOLINIUM (inhibits choline transporter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Inhibition of ACh vesicular transporter?

A

VESAMICOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

By what mechanism is ACh released into the synaptic cleft?

A

Ca-dependent exocytosis

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

what breaks down ACh?

A

acetylcholinesterases-acetate and choline

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 places where muscarinic receptors are located?

A

Cardiac
Smooth muscle
Exocrine glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Nicotinic receptors: where?

A

Ganglia
Adrenal glands
NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the precursor of NE

A

L-tyrosine

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

What is the rate limiting step of cat synthesis

A

Tyrosine hydroxylase

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

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

Reserpine

A

Adrenergic blocking agent-blocks catecholamine STORAGE

ANTIHYPERTENSIVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Metyrosine

A

Blocks NE synthesis (Blocks tyrosine hydroxylase)

Anti-hypertensive

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

Muscarinic ACh receptors

A

GPCRs

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

Nicotinic ACh receptors

A

ligand-gated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ACh receptors 2

A

Muscarinic and Nicotinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Adrenergic receptors 2
Alpha and Beta | 7-transmembrane GPCRs
26
Alpha receptors
a1: postsynaptic a2: presynaptic
27
Beta receptors
b1: heart, intestinal smooth muscle b2: bronchial, vasc, uterine smooth muscle b3: fat
28
Muscle contraction
a1, a2
29
Muscle relaxation
a1,a2,b2
30
Increase heart rate and contraction force
b1
31
PNS and bronchi
bronchoconstriction
32
PNS and bladder
contracts
33
Cholinergic drugs
Direct and indirect acting
34
Direct cholinergic
Choline esters and natural alkaloids
35
Indirect cholinergic
Anti-cholinesterase
36
Choline ester
Bethanechol-longer half life ACh, not hydrolysed by cholinesterase MUSCARINIC
37
Natural alkaloid
Pilocarpine-closed angle glaucome
38
Anticholinesterases
do not cross BBB-no central effects
39
4 reversible anticholinesterases
EDROPHONIUM Neostigmine Physostigmine Pyridostigmine
40
Closed angle glaucoma
angle between cornea and iris is abnorm. small | raised IOP
41
3 drugs that reduce IOP
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
Myasthenia Gravis
autoimmune-induced decrease (70-90%) in the number of nAChRs at the NMJ
43
Immediate and diagnostic treatment MG
Edrophonium | then Neostigmine and Pyridostigmine longterm (NM transmission rather than autonomic NS)
44
Adverse effects AChE inhib.
``` too much ACh symptoms D-diarrhoea U-urination M-miosis B-bronchoconstriction E-excitation L-lacrimation S-salivation and sweating ```
45
Anticholinergic drug Antimuscarinic Nonselective
Atropine
46
Cholinergic ANTAGs
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
Nicotine recep antag
Pancuronium-inhibit skeletal muscle contraction
48
Muscarinic recep antag
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
Sympathomimetics
Sympathomimetics agonists may directly activate their adrenoceptors OR they may act indirectly to increase concentration of endogenous catecholamine transmitter in the synapse
50
Indirectly acting sympathomimetics
Amphetamine derivatives and tyramine causes the release of the stored catecholimines TCA and Coke: don't like NET
51
Directly acting sympathomimetics-non-cats
Clonidine (alpha 2 agonist-decr NE, decr BP)
52
what does clonidine treat?
Resistant hypertension
53
Sympathomimetics- Direct acting ALPHA 1
Phenylephrine – topical to eye for mydriasis and nasal decongestant
54
Sympathomimetics- Direct acting ALPHA 2
Clonidine (anxiolytic, sedation, antihypertensive), methyldopa (antihypertensive), oxymetazoline (nasal decongestant)
55
Sympathomimetics- Direct acting ALPHA 1 AND 2
Phenylpropanolamine (nasal decongestants)
56
Sympathomimetics- Direct acting BETA 1
Dobutamine | mild α1 properties and greater inotropic than chronotropic effect
57
Sympathomimetics- Direct acting BETA 2
Salbutamol Formoterol, Salmeterol (LABA) (asthma, pre-term labour)
58
Epinephrine: topical
adjuvant of local anaes. glaucoma bleeding
59
Epinephrine: systemic
Cardiac arrest Anaphylactic shock Acute bronchial asthma
60
Amphetamine
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
Tyramine
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
Alpha receptor antagonist
alpha 1: prazosin (BPH) Doxazosin-HPT, BPH Tamsulosin
63
Beta recep antagonist
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
alpha and beta antag
Carvedilol (hypertension, congestive heart failure) and Labetalol (hypertensive crisis)
65
TCAs
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)

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