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ICPP > 9 - ANS > Flashcards

9 - ANS Flashcards

1
Q

What is the anatomical structure of the parasympathetic nervous system?

A

S2 to S4

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2
Q

What is the anatomical structure of the sympathetic nervous system?

A
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3
Q

What neurotransmitters and receptors are involved in each synapse?

A
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4
Q

What is the main difference between nAchR and mAchR?

A

nAChR = LGIC

mChR = GPCR

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5
Q

What neurotransmitter is released from sympathetic post-ganglionic neurones?

A
  • Mainly noradrenaline

- In sweat glands and hair follicles it is ACh

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6
Q

Are there other neurotransmitters to NA and ACh?

A
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7
Q

What could be classified as the third divsion of the autonomic nervous system?

A

Enteric in GI tract

Thousands of neurones in microcircuit

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8
Q

What is the hormonal part of the sympathetic nervous system?

A
  • Post-ganglionic neurones are chromaffin cells in adrenal medulla that synthesise adrenaline
  • Whole cell depolarised by pre-ganglionic neurone, vesicles contain A fuse with membrane and release adrenaline into blood stream to act on adrenoreceptors
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9
Q

Summarise the neurotransmitters in the somatic and autonomic nervous system.

A
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10
Q

Why are beta 2 receptors classed as part of the sympathetic nervous system?

A

Dilate airways allowing more air and therefore more oxygen for respiration into the body

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11
Q

Where does NO generation occuring and what is it used to stimulate?

A

Locally

Causes penile erection, iris sphincter and cilliary muscles

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12
Q

What is dysauntomia?

A

Umbrella term for malfunctions of the ANS. Can be primary or occur secondarily to another condition (e.g to Parkinson’s)

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13
Q

What is NCS, POTS and MSA?

A

- Neurocardiogenic Synope - Fainting spells

- Postural Orthostatic Tachycardia Syndrome - Lightheaded, tachycardia, fainting, chest pains, temperature sensitivity. Mainly in young women who look healthy

- Multiple System Atrophy - Fatal dysautonomia in adults over 40. Neurodegenerative disease with similarities to Parkinson’s. Bed ridden after 2 years of diagnosis and dead in 5-10 years. Very rare

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14
Q

What are the clinical abnormalities in asthma?

A
  • Bronchospasms
  • Excess production of secretions
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15
Q

What are the basic steps of neurotransmission and highlight the steps that can be targeted by drugs?

A
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16
Q

How is acetylcholine synthesised and degraded?

A
17
Q

What drugs can target AChR?

A
  • Targets skeletal muscle and pre-ganglionic neurones

- Trimethapan (ganglion blocking drug) used in hypertensive emergencies and controlled hypotension in surgery. Nicotinic antagonist

18
Q

What is the issue with developing drugs to act on the parasympathetic nervous system?

A

5 Muscarinic ACh receptors and hard to make drugs that are selective so drug will bind to all receptors, causing unwanted side effects

19
Q

What is sludge syndrome?

A

Pathological effects of overstimulation of muscarinic AChR’s in the parasympathetic nervous system.

Usually caused by:

  • Drug overdose
  • Organophospphorous insecticides (parathion) and nerve gases (sarin)
  • Ingestion of magic mushrooms
20
Q

What is the treatment for SLUDGE syndrome?

A
  • Agents covalently bind to AChE to irreversibly deactive enzyme and raise ACh levels
  • Need drugs that either block muscarinic receptors or reverse covalent modification of AChE

- Atrophine and Pralidoxime

21
Q

What are some muscarinic agonists and antagonists?

A

Administered locally not systemically

Agonists:

  • Pilocarpine (glaucoma)
  • Bethanechol (stimulate bladder emptying)

Antagonists:

- Ipratropium (asthma but only certain causes)

  • Tiotropium (COPD)
  • Tolterodine, Darifenacin and Oxybutynin (overeactive bladder)
22
Q

What are sympathetic post-ganglionic neurones like?

A
  • Noradrenaline release
  • One neurone has lots of varicosities that are specialised for Ca2+ dependent noradrenaline release
  • Allows coordinate control over a large area
23
Q

How is noradrenaline and adrenaline synthesised?

A
24
Q

What happens to Noradrenaline/Adrenaline once it has been released?

A

1. Reuptake by noradrenaline transport proteins (NET)

- Uptake 1: Uptake back into pre-synaptic neurone via a Na dependent high affinity transporter

- Uptake 2: Low affinity transporter

2. Metabolism (10%)

  • Monoamine Oxidase (MAO)
  • Catechol-O-methlytransferase (COMT)

Can produce drugs that inhibit these enzymes so NA not broken down

25
Q

What receptors does NA interact with?

A

- Pre-synaptic adrenoreceptors: To feedback and regulate processes in nerve terminal like NA release

- Post-synaptic adrenoreceptors: Pass on message and then rapidly removed by NET

26
Q

Why is salbutamol such a good asthma treatment?

A

Relieves asthma no matter what has caused it

27
Q

Why would you use selective adrenoreceptor agonists?

A

To limit side effects, like cardiovascular side effects, as non-selective will act on both beta adrenoreceptors

28
Q

What are two drugs used to treat hypertension and other cardiovascular disorders?

A

Atenolol: B1 antagonist

Doxazosin: A1 antagonist

Bisprolol Fumarate: B1 antagonist

29
Q

What is thyrotoxicosis and how is it treated?

A
  • Excess of thyroid hormone in the body causing lots of symptoms
  • Beta agonists used to combat some of the symptoms, e.g high b.p.
  • Propanolol, Attenolol, Nadaolol
  • Methimazole and Propylthiouracil stop thyroid overproducing hormone

ICPP (12 decks)

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