ocular pharmacology Flashcards
what is the mode of action of most drugs ?
the mode of action of most drugs is to inhibit or facilitate neural processes such as action potential transmission or synaptic transmission
what are agonists ?
drugs that enhance the effectiveness of neuron
what are antagonists ?
suppress specific neuron
where do most ocular drugs work?
most ocular drugs use affect nerve/muscle synapses
what is skeletal muscle innervated by?
- innervated by the somatic nervous system
- ( single motor neuron )
- releases ACH
what is smooth muscle innervated by ?
- 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)
what does sympathetic system release?
- post ganglionic neuron release nor-adrenaline at the effector ( alpha or beta receptors)
what does parasympathetic release?
- post ganglionic fibre releases ACH at the effector ( muscarinic or nicotinic receptors )
explain chemical synapses ?
- 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)
what are some types of neurotransmitters ?
- Noradrenaline
- Ach
- Dopamine
- Histamine
- GABA
- they all have their own set of neurotransmitter receptors
what is function of neurotransmitter receptors?
neurotransmitter receptors are important because its the receptors that determine which ions channels are open and shut in the posterior synaptic membrane
what are the 2 basic types of ACH receptors ?2
- 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
what are the methods of transmitter inactivation ?
- 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
what enzyme destroys Nor-adrenaline?
monoamine oxidase- which is responsible for its reuptake in the presynaptic neuron
where can drug affect a neural and synaptic process?
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
what is the simplest drug to facilitate a synape?
- 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
what is the first muscle that may be affected by drugs in the eye?
- iris sphincter muscle
- contraction causes pupil constriction ( miosis )
- parasympathetic innervated -( from ciliary ganglion/ IIIrd nerve)
- Muscarinic Ach receptor
what happens if you put pilocarpine in eye ?
binds to muscarinic receptors, acts as an Ach agonist activating Ach receptors and causing pupil constriction (miosis)
what happens if you put anti muscarinics in the eye ( e.g. atropine, tropicamide, cyclopentolate) ?
will block Ach receptors and result pupil dilation ( mydriasis )
what happens to pupil diameter with age?
- 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
what is deadly nightshade ( atropa belladona ?
deadly night shade contains atropine which is an anti-muscarinic used by some women to dilate pupil, thus making them look younger
what is atropine?
- anti-muscarinic which binds to muscarinic receptors and stops ACH from acting on iris sphincter muscle and the pupils will dilate
what happens when you put anticholinesterases ( eserine , physostigmine ) in the eye?
will enhance Ach levels and results in sphincter activation and pupil constriction by inactivating acetylcholinesterase
what is iris dilator muscle ?
- contraction causes pupil dilation ( mydriasis )
- sympathetically innervated ( from superior cervical ganglion )
- Alpha Nor-adrenalin receptors
how to activate iris dilator muscle which would cause it to contract which causes dilation ?
use phenylepinephrine which acts as a direct agonists Nor- adrenalin causing pupil dialation
how to cause the eye to dilate in the iris dilator muscle ?
use hydroxyamphetamine which acts by increasing the release of NA and hence also causes dilation
how to cause the eye to constrict in the iris dilator muscle?
applying alpha-adrenergic blockers, (e.g. thymoxamine ) causing constriction
what can you use cocaine for?
cocaine prevents the reuptake of NA and hence causes dilation
what is ciliary muscle?
- contraction results in accommodation
- parasympathetic innervation ( from ciliary ganglion/IIIrd nerve)
- muscarinic Ach receptors
how can accommodation be blocked?
- accommodation can be blocked ( cycloplegia ) by muscarinic receptor blockers such as atropine, cyclopentolate, scopolomine or tropicamide
what are the ocular skeletal muscle?
6 EOM
orbicularis oculi
levator palpebrae superioris
- they can also be affected by drugs
what is botulinum toxin?
inhibits the release of Ach at skeletal neuromuscular junction. it can therefore be used to turn a muscle off
what is botulinum toxin used for ?
- alleviate squint
- induce eye closure ( botulinum tarsorrhaphy )
- alleviate blepherospasm
what can some drugs interfere with ?
- some drugs can interfere with action potential transmission neuron and not affect muscle directly
what is action potential ?
thereshold depolarisation open Na channels large depolarisation Na channel shut k channel open re-polarisation of neuron retransmitted in neuron through local circuits
what do ocular anaesthetics work in the cornea?
most ocular topical anaesthetics (e.g. oxybuprocaine, amethocaine and lignocaine ) inhibit corneal sensory neurons by blocking sodium channels - neuron can’t depolarise
what is Parkinson’s disease caused by?
low levels of dopamine in the substantia nigra
why can’t dopamine be used to treat Parkinson’s ?
- it does not cross the blood-brain barrier
- L-dopa, a precursor to dopamine does
what can we use for Parkinson’s?
- L-dopa, a precursor to dopamine which cross blood-brain barrier and reach substantia nigra
how to slow heart down ?
by using beta blockers
the NA receptors on the heart, thereby slowing it down
what are monoamines?
Noradrenaline dopamine serotonin - these are feel good transmitters - high levels are associated with feeling of well being - low levels= depression
how to alleviate depression ?
reuptake blockers for monoamines (e.g. prozack)
- raising level of monamine
what are the long term effect of drugs?
- if a system is deprived of neurotransmitter for an extended period, the number of receptors will increase ( up regulate)
what will happen due to high levels of transmitter?
- result in receptor down regulation
- as a result drugs will become less effective
what happens when you stop using a drug?
the number of receptors will be low, even if the body is now producing the right amount of transmitter
