Pharmacology Flashcards

1
Q

All skeletal muscle motorneurones are myelinated, T/F?

A

False - they are myelinated until they reach the muscle where they divide into unmyelinated branches

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2
Q

What are the “important” areas of the NMJ? (4)

A

1) Active Zone (presynaptic; ACh vesicles)
2) Synaptic Cleft
3) Sarcolemma of muscle containing nicotinic ACh receptors
4) End plate

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3
Q

ACh is made from which precursors

A

Choline + Acetyl CoA

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4
Q

Which enzyme synthesises ACh?

A

ChAT (choline acetyltransferase)

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5
Q

Which enzyme packages the ACh into vesicles?

A

Vesicular ACh transporter

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6
Q

An action potential causes which events in the pre-synaptic terminal/buton? (2)

A

Opening of calcium channels (voltage gated) allowing calcium into the cell + triggering exocytosis

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7
Q

What is the ACh receptor composed of?

A

5 M2 receptors arranged into a pore

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8
Q

What is the net effect on the post-synaptic muscle cell once ACh has bound?

A

ACh receptors open, allowing sodium in and potassium out. Net gain is depolarisation as more sodium flows in than potassium out.

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9
Q

What is an end-plate potential?

A

The potential of the muscle fibre once the ACh receptors have opened allowing depolarisation

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10
Q

What is the mepp?

A

Miniature end plate potential - the amount of electrical activity elicited by one quantum of neurotransmitter binding

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11
Q

In normal skeletal muscle, one AP triggers how many twitches?

A

1 (there is 1: 1 coupling)

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12
Q

Why are sodium channels required on the muscle fibre & why must these be open in contraction?

A

They continually refresh the AP, without them it would tail off

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13
Q

Skeletal muscle fibre is/ is not “all or none”?

A

It is (i.e. a threshold has to be reached to trigger contraction)

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14
Q

In muscle fibres, where does calcium come from? What is its purpose?

A

Exclusively from the SR (c.f. cardiac which gets it from ECM and SR) and enables coupling by interacting with troponin

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15
Q

Which enzyme terminates ACh signalling?

A

Acetylcholinesterase

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16
Q

Botulinum toxin is directed against what structure/function of skeletal contraction?

A

It blocks fusion of the ACh-filled vesicles with the membrane; preventing the presynaptic terminal from releasing them.

17
Q

Myasthenia gravis is a muscle weakness driven by what pathophysiology?

A

Antibodies against the nicotinic ACh receptor

18
Q

Neuromyotonia underlying pathophysiology

A

Antibodies against potassium channels (causes hyperexcitability / spasticity)

19
Q

LEMS underlying pathophysiology

A

Antibodies against calcium channels on the neurone

20
Q

Curare is a reversible/ irreversible receptor binder?

A

Reversible (used in surgery)

21
Q

How does curare work?

A

Competitive antagonist of ACh receptor, reduces amplitude of epp and thus it will not reach threshold for contraction

22
Q

Does botulinum cause reversible/ irreversible muscle paralysis?

A

Irreversible

23
Q

On which membrane is acetylcholinesterase associated?

A

End-plate membrane

24
Q

Acetylcholinesterase works slowly/quickly

A

Very quickly

25
Q

Full list of corticosteroid side-effects?

A

Weight gain, muscle wastage, skin atrophy, osteoporosis, diabetes, hypertension, glaucoma, cataracts, fluid retention, adrenal suppression, immunosuppression and AVN of femoral head

26
Q

Side effect of gold/ penicillinamine therapy?

A

Proteinuria, GN, BM suppression