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Pharmacology And Toxicology > Pharmacology L9 > Flashcards

Pharmacology L9 Flashcards

1
Q

Drugs acting on the CNS include

A

Anti-Epileptics
Anti-Parkinsonians
Convultants: Tetanaus toxin

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2
Q

Drugs acting on the neuromuscular junction include

A

Anti-AChE drugs
Muscle Relaxants
Toxins: Botulinum toxin, Toxic anti-AChE

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3
Q

How does α-Bungarotoxin work

A

Blocks ACh binding to AChR by binding
irreversibly and competitively to the NMJ nAChR.

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4
Q

What does α-Bungarotoxin do

A

causes paralysis and respiratory failure

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5
Q

Schematic overview of NMJ:

A
  1. Action potentials in the motor neuron cause exocytosis of ACh containing synaptic vesicles
  2. ACh binds to receptors in the plasma membrane of the junctional folds of the skeletal muscle cell
  3. This triggers Na+ entry and action potential in the muscle cell
  4. Excess ACh is removed by the enzyme acetylcholinesterase
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6
Q

What is plasmalemma

A

Plasma membrane

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7
Q

How does plasmalemma excitation occur

A

It is caused by binding of ACh from motor neurons to nAChR on plasmalemma of muscle fibers.

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8
Q

What is the function of ion channel and pumps in plasmalemma excitation

A

maintenance of membrane potential
and triggering of action potential

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9
Q

DRUGS ACTING ON THE NEUROMUSCULAR JUNCTION include

A
  • Anticholinesterases
  • Neuromuscular blocking drugs
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10
Q

Examples of Anticholinesterases

A
  • Edrophonium; Reversal of NM block
  • Neostigmine; Diagnosis of MG
  • Pyridostigmine; Treatment of MG
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11
Q

Examples of Neuromuscular blocking drugs

A
  • Tubocurarine
  • Pancuronium
  • Suxamethonium
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12
Q

Neuromuscular blocking drugs may be subdivided into:

A

Presynaptic agents
Postsynaptic agents

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13
Q

What are Presynaptic agents

A

-inhibit ACh synthesis
- inhibit ACh release

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14
Q

What are Postsynaptic agents

A

They are used to cause clinical paralysis during anesthesia

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15
Q

Examples of Postsynaptic agents

A

-Non-depolarizing Competitive antagonists which block N-AChR
- Persistent depolarizing ACh receptor agonists

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16
Q

Presynaptic neuromuscular blocker that inhibits ACh synthesis:

A

Hemicholine - inhibits choline transport

17
Q

Presynaptic neuromuscular blocker that inhibits ACh release

A

Botulinum toxin - inhibits excocytosis of synaptic vesicle

18
Q

Example of Competitive antagonists which block nAChR

A

Non-depolarizing block is reversible by anti-AChE drug.
- Tubocurarine
- Pancuronium
- Atracurium

19
Q

Example of - ACh receptor agonist

A

Depolarizing block is NOT reversible by anti-AChE drugs
- Suxamethonium (succinylcholine)

20
Q

What is clinical spasticity

A

A medical condition that involves muscle time and hyperactive reflexes. It is not involved with the monosynaptic stretch reflex arch.

21
Q

What is the monosynaptic stretch reflex arch.

A

A pathway that causes muscle contraction in response to stretching

22
Q

What is the proposed cause of clinical spasticity

A

lesions in higher neuronal centres (brain, brain stem) damage the descending pathways that result in hyper- excitability of motoneurons in the spinal cord.

23
Q

Can drugs which act on the stretch reflex
arch may improve muscle spasms.

A

Yes

24
Q

What are PROPRIOCEPTORS

A

They measure the position of joints and lengths of muscles. They contain muscle spindles

25
Q

Where are the reflexes of PROPRIOCEPTORS mediated

A

at the spinal cord

26
Q

How are the la fibres stimulated

A

If a skeletal muscle is suddenly stretched by a blow on its tendon, the muscle spindles are also stretched

27
Q

what do la fibres do

A

directly stimulate the motoneurons of the same muscle, causing its contraction

28
Q

where are la fibres located

A

via the dorsal root to the anterior horn of the spinal cord

29
Q

what is the difference in reflex time between monosynaptic and postsynaptic STRETCH REFLEX

A

Since many more synapses are involved, the reflex time of postsynaptic reflex is longer than in the monosynaptic reflex

30
Q

How do you modify a simple stretch reflex

A

by modulating the activity of the respective excitatory and inhibitory synapses

31
Q

How to reduce the activity of a hyperactive stretch reflex

A
  • Ia fibres have to be reduced in their activity
  • Interneuron fibres have to be enhanced in their activity.
32
Q

Spasmolytic Drugs include

A

Diazepam:
Baclofen:

33
Q

How does Diazepam work

A

facilitates GABA-mediated presynaptic inhibition

34
Q

How does Baclofen work

A

interferes with release of excitatory transmitters

35
Q

Drugs with spasmolytic action outside the CNS

A

Dantrolene

36
Q

How does Dantrolene work

A

Directly modulates excitationcontraction coupling by
inhibiting calcium ion release
from the sarcoplasmic
reticulum of skeletal muscle
fibres and thereby reduces
muscle strength.

Pharmacology And Toxicology (6 decks)

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