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MSK > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is a terminal bouton?

A

Terminal bouton is the specialized presynaptic terminal at the end of an axon

forms a chemical synapse with the muscle membrane at the neuromuscular junction

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2
Q

Where are the cell bodies of the alpha motor neurones found?

A

Cell body in ventral horn of spinal cord (or brain stem)

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3
Q

What are the 4 main key structures of the skeletal neuromuscular junction?

A

(1) the terminal bouton (and surrounding Schwann cell)
(2) synaptic vesicles;
(3) the synaptic cleft
(4) the end plate region of the muscle cell membrane (sarcolemma) thrown into a series of junctional folds

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4
Q

Where do synaptic vessels release Ach from in the neurones?

A

Active zones

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5
Q

what are opposite Active zones in the neuromuscular junction?

A

Nicotinic ACh receptors are located at regions of the junctional folds

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6
Q

What are the key steps of neuromuscular transmission?

A
  1. Synthesis of ACh in cytoplasm of bouton
  2. Uptake of ACh into synaptic vesicles for concentration and storage
  3. Ca2+-dependent release of ACh into synaptic cleft by exocytosis
  4. Brief activation of nicotinic ACh receptors (nAChRs) by reversible binding of ACh
  5. Rapid termination of transmitter action by acetylcholinesterase (AChE) within the synaptic cleft
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7
Q

How is choline carried back into the pre synaptic cleft?

A

Choline transporter (symport with Na+)

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8
Q

How is acetylcholine synthesised?

A

ACh is synthesised in the cytosol from choline and acetyl coenzyme A (acetyl CoA) by the enzyme choline acetyltransferase (ChAT, or CAT)

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9
Q

How is ACh concentrated in vesicles?

A

vesicular ACh transporter

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10
Q

Arrival of the action potential at the terminal causes what?

A

depolarization
opening of voltage-activated Ca2+ channels
Ca2+ entry to the terminal

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11
Q

What causes vesicles at the active zone to release ACh via exocytosis?

A

Ca2+

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12
Q

what does the ACh bind to at the endplate region?

A

post synaptic nicotinic ACh receptors

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13
Q

how many ACh activate a nicotinic ACh receptor (nAChR)?

A

2

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14
Q

What type of molecule is the nicotinic ACh receptor (nAChR)?

ii. when does its gate open?

A

pentamers of glycoprotein subunits [(α1)2β1δε]* surrounding a central cation selective pore (formed by five M2 helices).

ii. in the presence of ACh

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15
Q

Which molecule is the nicotinic ACh receptor (nAChR) more permeable to Na+ or K+?

A

both equal

Na+ influx

K+ efflux

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16
Q

which has a more movement at the nAChR K+ efflux or Na+ influx?

A

Na+ influx- Na+ has greater driving force at resting potential

17
Q

what is the electrical response to one quantum of transmitter, due to the activation of nAChRs ?

A

miniature endplate potential (m.e.p.p)

18
Q

what do many m.e.p.ps summate to produce?

A

end-plate potential (e.p.p) -a graded (electrotonic) response

19
Q

E.P.P occur normally if they reach the threshold potential true or false?

A

true

20
Q

How does the Muscle Action Potential Cause Contractions?

A

Release of Ca2+ from Intracellular Stores

21
Q

How does Rapid termination of neuromuscular transmission occur?

A

hydrolysis of ACh by acetylcholinesterase (AChE), an enzyme associated with the end plate membrane

22
Q

what does AChE hydrolyses ACh to?

ii. how are these products reabsorbed into the presynaptic knob?

A

choline and acetate

ii. choline - choline transporter
acetate diffuses into cleft

23
Q

What are the symptoms of Neuromyotonia?

A

cramps
stiffness
slow relaxation (myotonia)
muscle twitches (fasiculations)

24
Q

What are the causes of neuromyotonia?

A

antibodies against voltage-activated K+ channels in the motor neurone disrupt function resulting in hyperexcitability and repetitive firing.

Latter results in prolonged e.p.p. and repetitive action potential discharge in skeletal muscle fibres

25
Q

How do you manage neuromyotonia?

A

anti-convulsants e.g. carbamazepine, phenytoin

block voltage-activated Na+ channels

26
Q

What are the signs and symptoms of Lambert-Eaton Myasthenic Syndrome (LEMS)?

A

Muscle weakness in limbs - improves upon exertion

associated with small cell carcinoma of the lung

27
Q

What are the causes of LEMS?

A

antibodies against voltage-activated Ca2+ channels in the motor neurone terminal result in reduced Ca2+ entry in response to depolarization and hence reduced vesicular release of ACh

28
Q

How do you manage LEMS?

A
  1. anticholinesterases (e.g. pyridostigmine)

increase the duration of action of ACh in the synaptic cleft

  1. potassium channel blockers (e.g. 3,4-diaminopyridine)

release of ACh by prolonging the action potential in the motoneurone terminal

29
Q

what are the signs and symptoms of Myasthenia Gravis (MG)?

A

progressively increasing muscle weakness during periods of activity

the eye and eyelid muscles is a presenting feature

30
Q

What are the causes of MG?

A

antibodies against nicotinic ACh receptors in the endplate result in reduction in the number of functional channels and hence the amplitude of the e.p.p.

31
Q

How do you manage MG?

A

anticholinesterases (e.g. edrophonium, pyridostigmine)

immunosuppressant agents (e.g. azathioprine)

32
Q

What is a Botulinum toxin?

A

Extremely potent exotoxin that acts at motor neurone terminals to irreversibly inhibit ACh release. Blocks exocytosis

33
Q

Give two examples where Botulinum toxin is useful.

A
  1. low dose can be used for over active muscles

2. age related wrinkles can be smoothened out using this

34
Q

How do Curare-like’ compounds affect postsynaptic action of acetylcholine ?

ii. what is the effect of this?

A

Act as competitive antagonists of nicotinic ACh receptors e.g. vecuronium, atracurium

ii. Reduce the amplitude of the endplate potential (e.p.p.) to below the threshold for muscle fibre action potential generation

35
Q

What is the clinical relevance of Curare-like compounds?

A

induces reversible muscle paralysis in certain types of surgery

MSK (7 decks)

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