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Neural Biology 1 > ocular pharmacology > Flashcards

ocular pharmacology Flashcards

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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

what are agonists ?

A

drugs that enhance the effectiveness of neuron

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3
Q

what are antagonists ?

A

suppress specific neuron

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4
Q

where do most ocular drugs work?

A

most ocular drugs use affect nerve/muscle synapses

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5
Q

what is skeletal muscle innervated by?

A
  • innervated by the somatic nervous system
  • ( single motor neuron )
  • releases ACH
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6
Q

what is smooth muscle innervated by ?

A
  • innervated by the autonomic nervous system
  • ( 2 neuron single chain ) separated by a ganglion
  • sympathetic ( close to spinal cord ) and parasympathetic ( close to the effector)
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7
Q

what does sympathetic system release?

A
  • post ganglionic neuron release nor-adrenaline at the effector ( alpha or beta receptors)
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8
Q

what does parasympathetic release?

A
  • post ganglionic fibre releases ACH at the effector ( muscarinic or nicotinic receptors )
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9
Q

explain chemical synapses ?

A
  • depolarisation of synaptic terminal
  • influx of calcium
  • migration of vesicles containing neurotransmitters to migrate to presynaptic membrane
  • fusion of vesicle with presynaptic membrane
  • release of transmitter by exocytosis
  • diffusion of transmitter across cleft down the concentration gradient
  • binding of transmitter to postsynaptic receptors
  • change in postsynaptic membrane permeability leading to IPSPs( open Cl or K you get hyper polarisation) or EPSPs( open Na) depending on ion channel opened
  • inactivation of transmitter ( enzymatic, reuptake into presynaptic neuron)
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10
Q

what are some types of neurotransmitters ?

A
  • Noradrenaline
  • Ach
  • Dopamine
  • Histamine
  • GABA
  • they all have their own set of neurotransmitter receptors
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11
Q

what is function of neurotransmitter receptors?

A

neurotransmitter receptors are important because its the receptors that determine which ions channels are open and shut in the posterior synaptic membrane

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12
Q

what are the 2 basic types of ACH receptors ?2

A
  • Ach can bind to
  • nicotinic - occurs at neuromuscular junction - open Na channels - therefore excitatory
  • muscarinic - open k and cl channels - therefore inhibitory
  • same neurotransmitter but 2 different effects depending on the receptor
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13
Q

what are the methods of transmitter inactivation ?

A
  • diffuse away
  • break it down with enzymes
    enzyme acts on Ach and splits into its components part which are re absorbed into presynaptic neuron
  • take it back up into presynaptic neuron
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14
Q

what enzyme destroys Nor-adrenaline?

A

monoamine oxidase- which is responsible for its reuptake in the presynaptic neuron

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15
Q

where can drug affect a neural and synaptic process?

A

drugs can affect any stage of the neural and synaptic process
1 - drug can affect synthesis of transmitters by stopping it or enhancing it
2- axonal transport -
3- storage of neurotransmitters in the vesicle
4- binding of neurotransmitter to postsynaptic membrane
5- conduction of action potential

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16
Q

what is the simplest drug to facilitate a synape?

A
  • the simplest drug to facilitate a synape would be to apply the neurotransmitter itself
  • this is rarely done as the body has mechanism for neutralising such transmitters
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17
Q

what is the first muscle that may be affected by drugs in the eye?

A
  • iris sphincter muscle
  • contraction causes pupil constriction ( miosis )
  • parasympathetic innervated -( from ciliary ganglion/ IIIrd nerve)
  • Muscarinic Ach receptor
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18
Q

what happens if you put pilocarpine in eye ?

A

binds to muscarinic receptors, acts as an Ach agonist activating Ach receptors and causing pupil constriction (miosis)

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19
Q

what happens if you put anti muscarinics in the eye ( e.g. atropine, tropicamide, cyclopentolate) ?

A

will block Ach receptors and result pupil dilation ( mydriasis )

20
Q

what happens to pupil diameter with age?

A
  • resting pupil diameter decreases with age due to a loss of sympathetic tone ( senile miosis )
  • this makes it harder for the old to read in lower light levels
21
Q

what is deadly nightshade ( atropa belladona ?

A

deadly night shade contains atropine which is an anti-muscarinic used by some women to dilate pupil, thus making them look younger

22
Q

what is atropine?

A
  • anti-muscarinic which binds to muscarinic receptors and stops ACH from acting on iris sphincter muscle and the pupils will dilate
23
Q

what happens when you put anticholinesterases ( eserine , physostigmine ) in the eye?

A

will enhance Ach levels and results in sphincter activation and pupil constriction by inactivating acetylcholinesterase

24
Q

what is iris dilator muscle ?

A
  • contraction causes pupil dilation ( mydriasis )
  • sympathetically innervated ( from superior cervical ganglion )
  • Alpha Nor-adrenalin receptors
25
Q

how to activate iris dilator muscle which would cause it to contract which causes dilation ?

A

use phenylepinephrine which acts as a direct agonists Nor- adrenalin causing pupil dialation

26
Q

how to cause the eye to dilate in the iris dilator muscle ?

A

use hydroxyamphetamine which acts by increasing the release of NA and hence also causes dilation

27
Q

how to cause the eye to constrict in the iris dilator muscle?

A

applying alpha-adrenergic blockers, (e.g. thymoxamine ) causing constriction

28
Q

what can you use cocaine for?

A

cocaine prevents the reuptake of NA and hence causes dilation

29
Q

what is ciliary muscle?

A
  • contraction results in accommodation
  • parasympathetic innervation ( from ciliary ganglion/IIIrd nerve)
  • muscarinic Ach receptors
30
Q

how can accommodation be blocked?

A
  • accommodation can be blocked ( cycloplegia ) by muscarinic receptor blockers such as atropine, cyclopentolate, scopolomine or tropicamide
31
Q

what are the ocular skeletal muscle?

A

6 EOM
orbicularis oculi
levator palpebrae superioris
- they can also be affected by drugs

32
Q

what is botulinum toxin?

A

inhibits the release of Ach at skeletal neuromuscular junction. it can therefore be used to turn a muscle off

33
Q

what is botulinum toxin used for ?

A
  • alleviate squint
  • induce eye closure ( botulinum tarsorrhaphy )
  • alleviate blepherospasm
34
Q

what can some drugs interfere with ?

A
  • some drugs can interfere with action potential transmission neuron and not affect muscle directly
35
Q

what is action potential ?

A 
thereshold depolarisation
open Na channels
large depolarisation 
Na channel shut
k channel open 
re-polarisation of neuron 
retransmitted in neuron through local circuits
36
Q

what do ocular anaesthetics work in the cornea?

A

most ocular topical anaesthetics (e.g. oxybuprocaine, amethocaine and lignocaine ) inhibit corneal sensory neurons by blocking sodium channels - neuron can’t depolarise

37
Q

what is Parkinson’s disease caused by?

A

low levels of dopamine in the substantia nigra

38
Q

why can’t dopamine be used to treat Parkinson’s ?

A
  • it does not cross the blood-brain barrier

- L-dopa, a precursor to dopamine does

39
Q

what can we use for Parkinson’s?

A
  • L-dopa, a precursor to dopamine which cross blood-brain barrier and reach substantia nigra
40
Q

how to slow heart down ?

A

by using beta blockers

the NA receptors on the heart, thereby slowing it down

41
Q

what are monoamines?

A 
Noradrenaline
dopamine
serotonin
- these are feel good transmitters 
- high levels are associated with feeling of well being
- low levels= depression
42
Q

how to alleviate depression ?

A

reuptake blockers for monoamines (e.g. prozack)

- raising level of monamine

43
Q

what are the long term effect of drugs?

A
  • if a system is deprived of neurotransmitter for an extended period, the number of receptors will increase ( up regulate)
44
Q

what will happen due to high levels of transmitter?

A
  • result in receptor down regulation

- as a result drugs will become less effective

45
Q

what happens when you stop using a drug?

A

the number of receptors will be low, even if the body is now producing the right amount of transmitter

Neural Biology 1 (58 decks)

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