Pharmacology

Question 1

skeletal muscle innervated by

Answer 1

motor neurones

Question 2

whats transmitted at neuromusuclar junction

Answer 2

acetylcholine

Question 3

Pathway to skeletla muscle

Answer 3

Cell body (ventral horn of spinal cord) > myelinated axon > unmyelinated axon terminals > neuromuscular junction

Question 4

Features of skeletal neuromuscular junction:

Answer 4

-terminal bouton (+ surrounding schwann cell), -synaptic vesicles, -synaptic cleft, -end plate region.

Question 5

ACh =

Answer 5

Choline + acetylCoA

Question 6

Explain activation of post-junctional nicotinic ACh receptor

Answer 6

Calcium goes in binds to vesicle membranes which allows it to fuse to membrane and release ACh. These activate nAChRs.

Question 7

In the junction what hydrolyses ACh into choline + acetate

Answer 7

Acetylcholinesterase

Question 8

Explain EPP (end plate potential)

Answer 8

nAChRs gates close in absence of ACh. Gate opens when two molecules of ACh bind to exterior. The driving force for Na+ is greater than for K+ at resting membrane potential, influx of Na+ is greater than efflux of K+: a depolarisation known as the EPP is generated.

Question 9

nAChRs are …

Answer 9

Pentameric

Question 10

EPP msut reach threshold to …

Answer 10

initiate contraction

Question 11

Drugs and toxins can …

Answer 11

reduce amplitude of EPP casuing skeletal muscle paralysis

Question 12

Action potential journey

Answer 12

Goes deep into muscle fibres through T-tubules causing release of Ca2+ in SR, which combines with troponin at bridges to cause contraction.

Question 13

Anti-cholisterases

Answer 13

reverisbly blocks AChE (anticholisterases)

Question 14

Nerve gases

Answer 14

irreversibly block AChE

Question 15

Neuromyotonia

Answer 15

(NMT or Isaac’s sydrome) autoimmune, reduced K+ conductance in motor neurones causes hyperexcitability (repetitive firing)

Question 16

Lambert Eaton Myasthenic Syndrome (LEMS)

Answer 16

Autoimmune (asscoiated with small cell carcinoma of the lung), reduced Ca2+ conductance presynapticlly, decreased ACh, muscle weakness

Question 17

Botulism

Answer 17

Caused by botulinum toxic (can be used to treat overactive muscles), decreased release of ACh, paralysis

Question 18

Myasthenia Gravis (MG)

Answer 18

Autoimmune, reduced number of nAChRs (Nicotinic ACh receptors), muscle weakness (reduced amplitude of EPP)

Question 19

‘Curare-like’ compounds

Answer 19

Competitive anatgonists of nAChRs, reduce EPP to below threshold for muscle AP generation, used in surgery to produce reversible paralysis (e.g. vecuronium, atracurium)