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0V015 Biology & Pathology > L51 Ocular Pharmacology > Flashcards

L51 Ocular Pharmacology Flashcards

1
Q

What is the mode of action of most drugs?

A

The mode of action of most drugs is to inhibit or facilitate neural processes such as action potential transmission or synaptic transmission

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2
Q

Drugs that enhance the effectiveness of a neurone are known as what?

A

Agonists

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3
Q

Drugs that suppress specific neurones are known as what?

A

Antagonists

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4
Q

What is skeletal muscle innervated by?

A

Skeletal muscle is innervated by the somatic nervous system (single motor neuron)

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5
Q

What is smooth muscle innervated by?

A

Smooth muscle is innervated by the autonomic nervous system (2 neuron chain)

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6
Q

In the sympathetic nervous system what neurotransmitter is used upon the effector and what receptors is this picked up by?

A

Nor-adrenaline Alpha or beta receptors

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7
Q

In the parasympathetic system what neurotransmitter is used upon the effector?

A

Acetyl choline Muscarinic or nicotinic receptors

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8
Q

Compare the Sympathetic and Autonomic Nervous system.

A
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9
Q

Describe what happens at a chemical synapse

A
  • Depolarisation of synaptic terminal
  • Influx of calcium
  • Migration of vesicles containing neurotransmitter
  • Fusion of vesicle with presynaptic membrane
  • Release of transmitter by exocytosis
  • Diffusion of transmitter across cleft down concentration gradient
  • Binding of transmitter to postsynaptic receptors
  • Change in postsynaptic membrane permeability leading to Inhibitry Post Synaptic Potentials or Excitatory Post Synaptic Potentials depending on ion channels opened
  • Inactivation of transmitter (enzymatic, reuptake etc)
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10
Q

Nicotinic Receptors:

Where are they found?

What do they do?

What kind of receptor are they- excitatory or inhibitory?

A

Nictonic receptors are found at neuromuscular junctions.

Open Na+ channels

Excitatory

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11
Q

Muscarinic Receptors:

Where are they found?

What do they do?

What kind of receptor are they- excitatory or inhibitory?

A

Occur in heart for example.

Opens K+ and Cl- channels

Inhibitory

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12
Q

The simplest drug to facilitate a synapse would be to apply the neurotransmitter itself - however this is rarely done, why?

A

The body has mechanisms for neutralising such transmitters e.g. if you tried to inject acetylcholine into the body,the body would just produce more acetylcholinesterase to break that down.

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13
Q

Contraction of the iris sphincter muscle causes what?

A

•pupil constriction (miosis)

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14
Q

What type of receptors does the iris sphincter muscle have?

A

•Muscarinic Ach receptors

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15
Q

How is the iris sphincter muscle innervated?

A

•Parasympathetically innervated (from ciliary ganglion/IIIrd nerve)

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16
Q

If you wanted to stimulate the iris sphincter muscle what would you use and why?

A

You have two options:

An acetylcholine agonist such as Pilocarpine - this would bind to the muscarinic acetylcholine receptors of the sphincter muscle causing them to contract (miosis)

or

Anti-cholinesterases (e.g. eserine, physostigmine) will enhance Ach levels, and hence result in sphincter activation and pupil constriction, by inactivating acetylcholinesterase. (basically you destroying the thing that destroys the thing).

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17
Q

If you wanted to stop the pupil constricting what drug would you use and why?

A

Anti muscarinics (e.g. atropine, tropicamide, cyclopentolate) as they will block Ach receptors and result in dilation (mydriasis).

(it is a receptor blocker)

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18
Q

What is senile miosis?

A

Resting pupil diameter decreasing with age due to a loss of sympathetic tone.

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19
Q

What does contraction of the iris dilator muscle cause?

A

Contraction causes pupil dilation (mydriasis)

20
Q

How is the iris dilator muscle innervated?

A

Sympathetically innervated from the superior cervical ganglion

21
Q

What kind of receptors are present on the iris dilator muscle?

A

Alpha Nor-adrenaline receptors.

22
Q

If you wanted to dilate the pupil what drugs (name them) could you use and why?

A

An agonist for Nor-adrenaline (e.g. Phenylepinephrine). This would act as an artificial nor-adrenaline causing dilation.

A drug such as hydroxyamphetamine. This acts by increasing the release of Nor-adrenaline hence causing dilation. (fun fact - amphetamine is a class of recreational drug and therefore and due to this those that are on amphetamine have dilated pupils).

Cocaine (very very small amounts) as it prevents the uptake of Nor-adrenaline hence causing dilated pupils.

23
Q

If you wanted to constrict the pupil what sort of drugs (name them) would you use and why?

A

The iris dilator muscle can be relaxed by applying alpha-adrenergic blockers (e.g. thymoxamine) causing constriction.

24
Q

What does the contraction of the ciliary muscle result in?

A

Accommodation

25
Q

What is the ciliary muscle innervated by?

A

Parasympathetically innervated (from ciliary ganglion/IIIrd nerve)

26
Q

What kind of receptors does the ciliary muscle have?

A

Muscarinic Acetylcholine receptors

27
Q

What type of drug can be used to block accommodation and give examples of them?

A

Muscarinic receptor blockers such as atropine, cyclopentolate ,scopolamine or tropicamide as they stop contraction of the ciliary muscle.

28
Q

What are the ocular skeletal muscles?

A

6 EOMs, orbicularis oculi and levator palpebrae superioris

29
Q

What is the more common name for botulinum toxin?

A

Botox

30
Q

What does botulinum toxin do and therefore what may it be used to treat?

A

Botulinum toxin inhibits the release of Acetylcholine at skeletal neuromuscular junctions. It can, therefore, be used to ‘turn a muscle off’.

This can be used to

  • alleviate squint
  • alleviate blepharospasm (Blepharospasm is an abnormal contraction of the eyelid muscles)
  • induce eye closure (botulinum tarsorrhaphy)
31
Q

What is the disadvantage of using botox to treat eye conditions?

A

It only lasts 6 weeks so you have to keep going back to top it up.

32
Q

True or false- Not all drugs work at the nerve-muscle junction. Some interfere with action potential transmission.

A

True

33
Q

How do most ocular topical anesthetics work?

A

Most ocular topical anaesthetics (e.g. oxybuprocaine, amethocaine and lignocaine) inhibit corneal sensory neurons by blocking sodium channels.

34
Q

What are some examples of ocular topical anaesthetics?

A

oxybuprocaine, amethocaine and lignocaine

35
Q

What is parkinsons caused by?

A

Due to a lack of dopamine in a motor part of the brain called the Substania Nigra

36
Q

Why can dopamine not be administered straight to resolve the lack of dopamine which causes Parkinsons?

A

Dopamine cannot be administered as it is too big to pass through the blood-brain barrier.

37
Q

What do we administer to those with Parkinson’s and why?

A

L dopa (as it is small enough to cross the blood-brain barrier) - it acts as a precursor to dopamine

38
Q

What is heart rate increased by?

A

Sympathetic innervation

39
Q

What drugs may be used to slow down heart rate?

A

Beta receptors are present in the heart therefore beta-blockers block the acetylcholine receptors thereby slowing down the heart rate.

40
Q

What are some examples of monoamines and what are they?

A

Noradrenaline, Dopamine, and serotonin.

They are our ‘feel good’ receptors.

41
Q

What are high levels of monoamines associated with?

A

Feelings of well being. Happiness

42
Q

What is one of the causes of depression?

A

Low monoamine levels

43
Q

What may be used to treat depression?

A

Reuptake blockers for monoamines e.g. prozack.

Selective serotonin reuptake inhibitors.

44
Q

How do amphetamines, cocaine and other ‘recreational drugs’ make you feel good?

A

Amphetamines, cocaine, and other ‘recreational drugs’ work by raising monoamine levels.

45
Q

What are some long term effects of drug use?

A
  • If a system is deprived of neurotransmitter for an extended period, the number of receptors will increase (upregulation)
  • Conversely, high levels of the transmitter will result in receptor downregulation
  • As a result, drugs will become less effective over time
  • Furthermore, when you stop using the drug the number of receptors will be inappropriate, even if your body is now producing the right amount of transmitter.

0V015 Biology & Pathology (57 decks)

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