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Pharmocolgy > P7: Drugs and Neuromuscular Transmission > Flashcards

P7: Drugs and Neuromuscular Transmission Flashcards

1
Q

Which motor division does the NMJ belong to?

A

Somatic Motor Division

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2
Q

Describe a somatic motor neurone (4)

A
  • Single myelinated neurone
  • Originates from CNS
  • Terminates at NMJ
  • Branched
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3
Q

Where do action potentials transmitted across the neuromuscular junction pass along?

A

The Sacrolemma

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4
Q

What are T-tubules?

A
  • Invaginations in the sarcolemma

- Perpendicular to the length of the myofibrils

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5
Q

What does transmission of an action potential along the t-tubule membrane cause?

A
  • Activation of voltage-gated Ca2+ channels in the sarcoplasmic reticulum
  • Ca2+ entry causes actin/myosin contraction and shortening of the myofibril
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6
Q

How does actin/myosin contraction affect the myofibril?

A

Causes it to shorten

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7
Q

What is the job of the T-tubules?

A

Permit rapid transmission of the action potential across the whole myofibre

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8
Q

What do spontaneous exocytosis of vesicles cause?

A

miniature end plate potentials (mEPP)

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9
Q

During Neuromuscular transmission what does a calcium influx cause?

A
  • Release of roughly 50 synaptic vesicles
  • Producing an EPP
  • Which initiates an AP in the muscle fibre
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10
Q

What breaks down ACh?

A

Acetylcholinesterase

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11
Q

Describe the action of Hemicholinium

A
  • Hemicholinium competes with the choline reuptake transporter
  • Inhibiting ACh synthesis
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12
Q

Describe the action of Botulinum toxin

A
  • Botulinum toxin prevents fusion of vesicles to the presynaptic membrane
  • Inhibiting ACh release
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13
Q

Name 2 drugs that may be used as calcium channel blockers

A
  • Streptomycin

- Tetracycline

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14
Q

Describe the action of Black Widow spider venom

α-latrotoxin

A
  • Promotes exocytosis

- Resulting in large release and block due to depletion.

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15
Q

Which type of botulinum toxin are toxic to humans?

What are botulinum toxin type A and B used for medically?

A
  • A,B,E and F

- Muscle spasms, excessive sweating, neuropathic pain, cosmetics

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16
Q

How do non-depolarising Neuromuscular blockers work?

competitive antagonists

A
  • Prevent access of ACh to the nicotinic neuromuscular receptor
  • Preventing depolarization of the motor end plate (D-tubocurarine)
17
Q

How do depolarising Neuromuscular blockers work?

agonists

A
  • Produce excessive depolarization of the motor end plate by over-stimulating the nicotinic neuromuscular receptor (succinylcholine)
18
Q

Name some non-depolarising neuromuscular blockers

A
  • Tubocurarine
  • Atacurium
  • Pancuronium
  • Vercuronium
19
Q

How can you reverse the effects of a non-depolarising neuromuscular blocker?

A

With anticholinesterase treatment (neostigmine)

20
Q

What are some side effects of non-depolarising blockers

Especially tubocurarine

A
  • Histamine releaser
  • Ganglionic blocker
  • Sympathetic transmission blocker
21
Q

Name 2 depolarising neuromuscular blockers

A
  • Suxamethonium

- Succinylcholine

22
Q

What are depolarising neuromuscular blockers used to treat?

A

Spastic paralysis

23
Q

How do you you enhance the effects of depolarising neuromuscular blockers?

A

By using anticholinesterases

24
Q

How do you terminate depolarising neuromuscular blockers?

A

Requires plasma cholinesterase to terminate its action

25
Q

Describe the action of suxamethonium (3)

Phase I Block

A
  1. Suxamethonium binds to N2 nicotinic receptors
  2. Na+ enters the channel, causing motor end plate depolarisation
    and muscle contraction
  3. Suxamethonium is not metabolised at the synapse, so depolarisation persists and the depolarised membrane remains unresponsive to subsequent impulses
26
Q

What is a Phase II block?

A
  • Desensitisation
27
Q

Name some side effects of depolarising blockers

A
  • Stimulation of muscarinic receptors (bradycardia, increased salivation, gastric secretions)
  • Excessive K+ release from muscles - Hyperkalemia
  • Increase intraocular pressure
  • Prolonged paralysis - until hydrolysed by cholinesterase
  • Genetic variation
28
Q

What are the clinical uses for NMJ blockers

A
  • Skeletal muscle relaxant during general anaesthesia - reduces necessary GA cones
  • Convulsions
  • Orthopaedics - relaxation when manipulating fractured or dislocated bones
29
Q

What is Myasthenia Gravis?

A
  • Acquired autoimmune disease characterized by muscle weakness due to decreased neuromuscular signal transmission
  • ACh function is inhibited as antibodies bind to postsynaptic nicotinic receptor at NMJ.
30
Q

How can you treat Myasthenia Gravis?

A
  • Acetylcholinesterase inhibitors relieve symptoms through potentiation of ACh signalling
31
Q

Name 2 drugs that can treat Myasthenia Gravis

A
  • Physostigmine

- Pyridostigmine

32
Q

Name the common visual problems with myasthenia gravis

A

Double vision

Diplopia

Pharmocolgy (22 decks)

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