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PA20016 > Ocular pharmacology > Flashcards

Ocular pharmacology Flashcards

1
Q

What is the function of eyes?

A

Translating images from the external world onto the retina where they are translated into electrical signals.

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2
Q

What happens if there is damage or change in the condition of the tissue layers in the eye?

A

Eyesight will be reduced.

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3
Q

What is the pupil size regulated by?

A

The size of the iris as it relaxes and contracts.

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4
Q

What are the two major chambers in the eye?

A

The anterior and vitreous chamber.

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5
Q

What is the ciliary body made up of?

A

Muscle and epithelium.

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6
Q

What are the two types of smooth muscle in the eye?

A

Radial (dilator) and sphinteric (constrictor). The radial muscle contracts to pull the iris outwards and make the pupil bigger, whereas the sphincteric muscle is down the centre of the iris that constricts to pull the iris inwards.

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7
Q

What is the purpose of the ciliary muscle?

A

It changes the refractory index of the lens and is involved in accommodation - the ability to accommodate the vision.

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8
Q

What nerve innervates the eye?

A

The medullary nerve three through the parasympathetic system.

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9
Q

What do cranial parasympathetic axons innervate?

A

The ciliary ganglion at the back of the eye.

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10
Q

What do postganglionic fibres innervate?

A

The sphincteric constrictor smooth muscle.

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11
Q

What is miosis?

A

Constriction of the pupil by the sphincteric constrictor.

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12
Q

What is mydriasis?

A

Dilation of the pupil.

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13
Q

What is the difference in pupil dilation in fight and flight vs. rest and digest?

A

Fight/flight - mydriasis, rest/digest - miosis.

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14
Q

Where are sympathetic fibres involved in the iris from?

A

The superior cervical ganglion.

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15
Q

What is the idea of the consensual pupil response?

A

Response in one eye will stimulate the same response in the other eye.

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16
Q

What receptors and neurotransmitters does the parasympathetic nervous system work on in pupil size?

A

ACh on M3 muscarinic receptors.

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17
Q

What do effect do M3 antagonists have?

A

Mydriasis.

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18
Q

What neurotransmitters and receptors does the sympathetic nervous system work on in pupil size?

A

NA on alpha1 adrenoceptors.

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19
Q

What effect did the plant, angels trumpet, have on the pupil?

A

No pupillary light reflex and no accommodation. Muscarinic receptors were blocked due to atropine/hyoscyamine and scopolamine.

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20
Q

What are the parasympathetic nervous system effects on the eye?

A

Miosis - Contraction of the constrictor pupillae, contraction of the ciliary muscle (near sight), mydriasis - relaxation of the constrictor pupillae and relaxation of cilliary muscle (far sight).

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21
Q

What is an example of a muscarinic antagonist?

A

Atropine.

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22
Q

What is an example of a muscarinic agonist?

A

Pilocarpine.

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23
Q

What effect does phospholipase C have?

A

Intracellular calcium release which causes muscle contraction.

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24
Q

What type of innervation does the ciliary muscle have?

A

Only parasympathetic. Sympathetic activation will cause changes in blood vessel tone.

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25
Q

What the sympathetic mechanism of action on the eye?

A

NA binds to alpha1 receptors to cause IP3 release, increasing calcium. This causes contraction of vascular smooth muscle blood, and contraction of radial smooth muscle and the pupil dilates.

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26
Q

What is the parasympathetic mechanism of action on the eye?

A

ACh binds to M3 receptors which causes IP3 release and contraction of sphincter smooth muscle (constrict pupil) and contraction of ciliary smooth muscle.

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27
Q

What do mydriatics do?

A

They block the constrictor muscle to cause pupillary dilation.

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28
Q

What do cycloplegics do?

A

They paralyse cilliary muscle and block accommodation.

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29
Q

What is anterior uveitis?

A

Inflammation of the posterior synechia. If this is constricted there is less adhesion and rubbing

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30
Q

What can be used to treat anterior uveitis?

A

Mydriatics and cycloplegics.

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31
Q

What else can cycloplegics and mydriatics be used to treat?

A

Ocular examinations and amblyopia (lazy eye).

32
Q

Why can cycloplegics be used to treat lazy eye?

A

Use this in the good eye to paralyse this muscle so the patient is forced to use the weaker eye.

33
Q

Are there any adrenergic receptors on ciliary muscle?

A

No.

34
Q

What is atropine?

A

An adrenergic agonist that causes radial contraction.

35
Q

What is glaucoma?

A

A major disease of the eye that if untreated can lead to blindness. There is loss of peripheral vision initially.

36
Q

What causes glaucoma?

A

Consequence of raised intra-ocular pressure of over 21mmHg.

37
Q

What is intraocular pressure determiend by?

A

Rate of formation and rate of drainage of aqueous humour.

38
Q

What is aqueous humour?

A

It is produced continously by the ciliary body epithelium and maintains itnraocular pressure, provides nutrients to the cornea, lens etc. and is released into the posterior chamber.

39
Q

What is the main cause of increased intra-ocular pressure?

A

There is obstruction of drainage through the trabecular meshwork and canal of Schlemm, causing effect in the rest of the eye.

40
Q

What is aqueous humour formation stimulated by?

A

Beta agonists and inhibited by alpha agonists.

41
Q

How do alpha1 agonists inhibit aqueous humour formation?

A

They are vasconstrictors that reduce the blood supply to the ciliary body.

42
Q

How do alpha2 agonists inhibit aqueous humour formation?

A

They cause decrease cAMP levels. They directly inhibit AH formation due to decreased NA release from sympathetic fibres.

43
Q

What do adrenoceptor agonists do?

A

They reduce aqueous humour production.

44
Q

What is dipivefrin?

A

A pro-adrenaline molecule that is broken down by esterases in the eye to form adrenaline.

45
Q

Why are alpha2 agonists more popular?

A

To avoid off target effects on the beta receptors due to decreased beta stimulation.

46
Q

What is aqueous humour formation dependent on?

A

cAMP dependent.

47
Q

What is timolol?

A

A beta blocker.

48
Q

What else does aqueous humour formation require?

A

Active transport of HCO3- out of the cilliary body, along with Na+.

49
Q

What does carbonic anhydrase catalyse?

A

CO2+ + H2O —> H2CO3, which then dissociates into HCO3-.

50
Q

What can carbonic anhydrase inhibitors be used to treat?

A

To reduce aqueous humor formation, as there needs to be active transport for bicarbonate for the formation.

51
Q

Where does aqueous humour travel?

A

It is produced by the ciliary body and flows from the posterior chamber through the iris into the anterior chamber.

52
Q

Where does most of the drainage of aqueous humour occur?

A

The trabecular meshwork (90%) and 10% from uveoscleral outflow.

53
Q

How can glaucoma be treated?

A

Improved drainage of AH through the trabecular network which is useful in raised and normal pressure glaucoma.

54
Q

What drugs can be used to treat glaucoma?

A

Carbachol, pilocarpine, anticholinesterases, latanoprost PGF2alpha analogue.

55
Q

What is closed-angle glaucoma?

A

The angle between the iris and the cornea is narrowed which blocks the flow of AH from the posterior to the anterior chamber. The onset can be sudden and result in rapid irreversible change.

56
Q

What is the emergency treatment for closed-angle glaucoma?

A

Osmotic agents to drag the fluid out - increase the blood osmolarity so water leaves the vitreous humour, reducing the volume of VH and decreasing intra-ocular pressure.

57
Q

What is the difference between vitreous humour and aqueous humour?

A

Aqueous humour - fills both the anterior and posterior chambers of the eye, vitreous humour is located in the vitreous chamber (space between lens and retina).

58
Q

What are some other treatments for glaucoma?

A

Laser trabeculoplasty, laser iridectomy, surgical scleral flap.

59
Q

What is laser trabeculoplasty?

A

Burning small holesin the trabecular meshwork to aid drainage.

60
Q

What is laser iridectomy?

A

Removing small portions of the iris.

61
Q

What is another eye disease, related to age?

A

Age-related macular degeneration.

62
Q

What is the macula?

A

A region of the retina essential for sharp vision.

63
Q

What is dry AMD?

A

Slow onset of degeneration of the macula.

64
Q

What is wet AMD?

A

Rapid onset of degeneration of the macula.

65
Q

What is neovascularization?

A

Excessive growth of leaky blood vessels under the retina.

66
Q

How can neovascularization be prevented?

A

Photodynamic therapy - verteporfin followed by laser photoactivation.

67
Q

What is blood vessel growth and leak stimulated by?

A

Vascular endothelial cell growth factor (VEGF).

68
Q

What can be used to stop blood vessel growth?

A

Anti-VEGF antibodies or VEGF receptor constructs that arrest progression.

69
Q

What is dry eye condition?

A

A clinical condition associated with decreased secretion.

70
Q

How can dry eye syndrome occur?

A

Radiotherapy, Sjogren’s syndrome or keratoconjunctivitis.

71
Q

How can pilocarpine be used to treat dry eyes?

A

It increases tears via muscarinic activation.

72
Q

How else can dry eyes be treated?

A

Glucocorticoids/immunosuppressives, lifitegrast.

73
Q

What are allergic eye diseases?

A

Excessive immune response to something in the enviroment.

74
Q

What causes allergic eye disease?

A

IgE mediated mast cell degranulation - itch and reddening.

75
Q

Treatments for allergic eye disease?

A

H1 receptor antagonists, mast cell stabilisers (cromones - sodium cromoglycate), glucocorticoids (long term risk of glaucoma or cataracts).

PA20016 (10 decks)

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