DONE ANS Part 2

Question 1

What enzyme degrades ACh and what are the products?

When does degradation of neurotransmitters occur?

Answer 1

(Acetyl)cholinesterase = AChE

Acetate + choline

When there is more activity @ synapses, most is not degraded, is transported into synaptic vesicles

Question 2

What is the name of a ganglion-blocking drug to block nACh receptors in the ANS?

Answer 2

Trimetaphan = decrease BP

Question 3

What AChE inhibitor can be used to treat myasthenia gravis?

Answer 3

Pyridostigmine

Question 4

Why are there often side effects to cholinergic drugs?

Answer 4

Lack of selectivity

E.g. non-selective mACh receptor agonist = will decrease HR, cause bronchoconstriction + increased sweating/salivation

Question 5

What are the effects of a massive discharge of the parasympathetic nervous system?
Why does this occur?

Answer 5

SLUDGE

Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis (vomiting)

Covalent-modification of AChE = raise ACh (reverse with pralidoxime)
Over-stimulation of mACh receptors (block with atropine)

Question 6

What are noradrenergic varicosities?

Answer 6

Branching axonal network in sympathetic post-ganglionic neurones
Each is a site for calcium-dependent noradrenaline release

Question 7

What is the synthesis of noradrenaline?

Answer 7

Tyrosine > into noradrenergic varicosity > convert to DOPA > dopamine > NA

Question 8

What are the two ways in which NA action can be terminated?

Answer 8

Re-uptake into pre-synaptic terminal (by high affinity Na+ dependent transporter = NET)

When NA has not been into a vesicles = metabolised by monoamine oxidase or COMT (inhibit enzymes = NA storage high)

Question 9

What beta-2 adrenoceptor agonist is used in asthma?

Why is its selectivity important?

Answer 9

Salbutamol to oppose bronchoconstriction

Limits cardiovascular side effects (+ve inotropy + chonotropy as are beta 1)