Peripheral Nervous System Flashcards

(19 cards)

1
Q

How can altering a drug target’s function help treat disease?

A

Drugs can enhance or inhibit target functions to restore balance in disease states

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2
Q

What are the two branches of the Peripheral Nervous System?

A

Somatic - Controls voluntary movement (skeletal muscle)
Autonomic - Controls involuntary functions (cardiac, digestion)

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3
Q

What is the neuromuscular junction (NMJ?)

A

A synapse where motor neuron transmits signals to skeletal muscle via acetylcholine (ACh)

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4
Q

What are the key steps in synaptic transmission at the NMJ?

A

1 - Choline uptake into the nerve terminal
2 - ACh synthesis and packaging into vesicles
3 - Action potential arrival, leads to depolarisation
4 - Calcium channel activation, triggers vesicle function
5 - ACh release and receptor binding at muscle membrane
6 - Muscle depolarisation -> Contraction
7 - AChE breakdown of ACh, stopping the signal

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5
Q

What are drug targets at the NMJ?

A
  • Nicotinic ACh receptors -> Influence depolarisation (agonists/antagonists)
  • Acetylcholinesterase (AChE) -> Inhibitors prevent breakdown, prolonging signal transmission
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6
Q

What causes Myasthenia Gravis?

A

Autoimmune depletion of nicotinic ACh receptors leads to weak muscle contraction

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7
Q

What are symtpoms of Myasthenia Gravis?

A

Muscle weakness and fatigue
Drooping eyelids (in humans)
Weak mouth (in dog)

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8
Q

How is Myasthenia Gravis treated?

A

AChE inhibitors (neostigmine, physotigmine) –> Increase ACh avaliability at synapse

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9
Q

How do muscle relaxants work?

A

Block ACh transmission at NMJ –> Prevent muscle contractions (e.g., tubocurarine)

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10
Q

What is tubocurarine and how was it historically used?

A
  • Found in Amazon blowgun poison (“tube curare”)
  • Paralyses prey when entering the bloodstream but harmless if ingested
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11
Q

How does botulinum toxin affect NMJ transmission?

A
  • Blocks vesicle fusion and ACh release, preventing muscle contractions
  • Clinical uses: Muscle spasm relief, urinary incontinence, cosmetic injections
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12
Q

What are the differences between the somatic and autonomic nervous system?

A
  • Somatic: Voluntary control, single neuron, ACh -> nicotinic receptors
  • Autonomic: Involuntary control, ganglia, ACh or noradrenaline (NA)
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13
Q

What are the two branches of the autonomic nervous system?

A

Sympathetic (Fight or flight) - Increase heart rate, dilates pupils
Parasympathetic (rest and digest) - Lowers heart rate, stimulates digestion

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14
Q

What are the primary neurotransmitters in the ANS?

A

Acetylcholine (ACh)
Noradrenaline (NA)

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15
Q

What recepors do these neurotransmitters target?

A

Nicotinic ACh receptors -> Autonomic ganglia (neuronal communication)
Muscarinic ACh receptors -> Parasympathetic effectors (GPCRs)
Adrenoreceptors -> Sympathetic effectors (GPCRs)

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16
Q

How does receptor specificity impact drug targeting?

A

Muscarinic receptors (M1-M3) -> Pharmacologically indistinct, requiring selective drug delivery
Adrenoreceptors -> Distinct tissue distribution, allowing targeted drugs

17
Q

What drugs act on parasympathetic system?

A

Pilocarpine (mACh agonist) -> Treats glaucoma (reduces eye pressure)
Atropine (mACh antagonist) -> Used in anaesthesia (prevents heart rate slowing)

18
Q

What drugs act on the sympathetic system?

A

Phenylephrine (α1 agonsit) -> Decongestant, dilates pupils
Atenolol (β1 antagonist) -> Lowers blood pressure, reduces heart rate
Salbutamol (β2 agonist) -> Treats asthma (bronchodilation)

19
Q

What are the key drug targets in the PNS?

A

NMJ -> Treat uscle disorders
Autonomic receptors -> Regulate heart rate, digestion, blood flow
Selective targeting -> More effective with sympathetic adrenoreceptor drugs due to distinct receptor distribution