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M202 > W31 Glaucoma and ARMD Pathophysiology and Management > Flashcards

W31 Glaucoma and ARMD Pathophysiology and Management Flashcards

1
Q

Vision (overview-for info)

A
  • Eye converts light that falls on the retina into an electrical signal in photoreceptor cells
  • Carried to the brain (occipital cortex) through the optic nerve
  • Eye focusses light/objects on
    retina
    =Refraction- most occurs at cornea
  • Accommodation
    -Lens
    -Fine tuning
    -Ciliary muscles
    Pupil size
    -Amount of light entering eye
    -Iris
    Autonomic nervous system innervates both the ciliary muscles and the iris
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2
Q

Pupil size
What is it controlled by? (2)
What is Miosis?
Mydriasis?

A
  • Controlled by relative tone of two muscle groups of iris
    1. Parasympathetic
    2. Sympathetic
  • Miosis - Pupillary constriction
    -contraction of the circular muscle
    -Drugs:
    =muscarinic receptor agonists
  • Mydriasis – pupil dilation
    -contraction of the radial muscle
    -Drugs:
    =Muscarinic receptor antagonists
    -paralyze the circular muscle (most powerful muscle)
    -α1-adrenoceptor agonists
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3
Q

What is Accommodation? (for info)

A

Accommodation of the eye refers to its ability to adjust its focus to see objects clearly at different distances. This adjustment is primarily carried out by changes in the shape of the lens inside the eye. When you look at something close, the muscles around the lens tighten, making the lens thicker and more curved. This allows the eye to focus the light rays from the close object onto the retina at the back of the eye, resulting in a clear image. Conversely, when you look at something far away, the muscles relax, making the lens thinner and flatter to focus the light rays onto the retina for distant vision. This ability to adapt the focus of the eye is crucial for clear vision at varying distances

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4
Q

Accommodation:

A
  • Near (to see close things) : lens must become more curved to refract light from near objects so that it is focused on the retina
  • Circular constrictor ciliary muscles
    -Affects tension on lens
  • Only parasympathetic innervation
    -(ACh – Muscarinic Receptors)
  • When no innervation (Far vision)
    -Relaxed (Larger)
    -Increases tension on ligaments
    -Pulls lens flat (less refraction/bending of light)
  • Parasympathetic innervation (Near
    vision)
    -Contracts
    -Less tension
    -Lens bulges
    allows focus on close objects
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5
Q

PUPIL SIZE:
Parasympathetic & Sympathetic
Which is responsible for pupil constriction and dilation?
What light can be seen?
Receptors?

A
  1. Parasympathetic
    - Circular conctrictor
    - Muscarinic receptors
    - Bright light and close vision
  2. Sympathetic= Controlled interest, heightened awareness, if you see people you like, your pupils dilate
    - Radial dilator
    - Alpha 1 adrenoreceptors
    - Dim light and dim vision
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6
Q

Which receptors are on smooth muscle?
Which receptors are at the NMJ?

A

Muscarinic receptors
Nicarinic receptors

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7
Q

Aqueous Humor (Jelly like)

A
  • Posterior and anterior chamber filled with aqueous humor
  • Maintenance of intraocular pressure
    -15 mm Hg
    -Balance between production and drainage
  • continuously secreted into the posterior chamber by epithelium of the ciliary body
  • flows through the pupil to the anterior
    chamber
  • Most leaves the eye through the
    trabecular meshwork (1) that drains via
    Schlemm’s canal into the veins (2)
  • About 10% drains through the sclera (3)
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8
Q

Production and drainage

A
  • Production (of aqueuous humour)
  • Sympathetic Nervous System
  • Ciliary body
    -β2-adrenoceptor - increased AH
    -α2-adrenoceptor - reduced AH
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9
Q

Production and drainage
What angle is drainage affected by
Does constriction or dilation enhance drainage of aqueous humour? (refer to diagram)

A
  • Affected by iridocorneal angle
    =angle between iris and cornea
  • If shallow anterior chamber,- smaller angle (narrow)- route of drainage becomes smaller
  • Dilation of pupil
    -When iris circular muscle relaxes/ radial
    contracts– muscle in region of angle thickened –can reduce drainage through meshwork
    -Can lead to increase in pressure in eye
  • Constriction of pupil
    -Constriction of circular muscle of iris
    -Moves iris away from meshwork
  • Widens angle
    -Enhances drainage through meshwork
  • Uveoscleral outflow – increased by
    prostaglandins
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10
Q

Topical application of drugs to eye

A
  • Can act locally at cornea
  • Drugs Penetrate to anterior chamber and ciliary body
    -Generally paracellularly through cornea
    -Little diffusion to posterior sections of eye (back of eye)

Cornea: High water content
* Lipid solubility less important
* Requires low molecular weight
* Formulations that avoid irritation of conjunctiva
* Poor absorption
-Also spillage
-Drainage into nasolacrimal duct
=Reduced by shutting eye and compressing duct with finger

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11
Q

Drugs for the eye:
What are mydriatic drugs?
What are cycloplegic drugs?

A
  • Mydriatic drugs: dilate the pupil
    -either by producing paralysis of the circular muscle of the iris, or by
    contracting the radial muscle
  • Cycloplegic
    -Cycloplegic drugs paralyse the ciliary muscle and prevent accommodation for near vision. (ie affect lens)
  • Anti muscarinic drugs (antagonistic) (atropine, tropicamide)
    -Mydriatic and cycloplegic
    -Eg Tropicamide – dilating pupil for examination
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12
Q

What is Glaucoma? (NICE-for info)

A

Glaucoma is a group of eye diseases that cause progressive optic neuropathy and in which intraocular pressure (IOP) is a key modifiable factor.

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13
Q

Glaucoma

A

Progressive optic neuropathies
Progressive visual defects
* initially as scotomas (blind spots) in
the peripheral visual field
* Enlarge
* Tunnel vision
* Blindness
In many cases intraocular pressure
increased
* Causes where pressure normal less
clear
Two forms
* Open-angle glaucoma
* Angle-closure glaucoma (less
common)

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14
Q

What is intraocular pressure?

A
  • IOP keeps the eye in the shape of a globe and is maintained by the balance between production and outflow of aqueous humour.
  • Raised IOP is the main risk factor for developing glaucoma as the raised pressure may damage nerve fibres of the optic nerve, or blood vessels supplying these nerve fibres.
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15
Q

Measuring IOP: What device is used?

A

Applanation tonometry (tonometer) - checks eye pressure

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16
Q

Glaucoma
What can a raised IOP cause?
Where is the site of damage?

A
  • Intraocular pressure can cause mechanical stress and strain on the posterior structures of the eye

Site of damage
* Where axons leave eye
* Cell death of retinal ganglion (RG) cells
* Degeneration of retinal ganglion cells
* Loss of RG axons

(Rod/Cone cell- Bipolar cell-Ganglion cell)

17
Q

Glaucoma- back of the eye

A
  • Causes a big effect at the back of the eye where the optic nerve leaves
  • Changes in the optic nerve head
  • Deepening and widening of the
    depression (cup) of the optic disc
18
Q

What are the Symptoms of glaucoma?
What are the emergency symptoms?

A
  • Usually symptomless to begin with
  • Develops slowly over period of years and begins to affect peripheral vision
  • May have blurred vision or see rainbow-coloured circles around lights

Emergency symptoms (usually due to acute angle-closure glaucoma):
* Intense eye pain
* N+V
* Red eye
* Headache
* Tenderness around eyes
* Rings around lights
* Blurred vision

19
Q

2 types of Glaucoma?

A

Open-angle glaucoma:
* Increased resistance to aqueous outflow through the trabecular
meshwork
-Eg Schlemm’s canal obstructed
-Increase in intraocular pressure

Angle-closure glaucoma:
* Less common
* Site of aqueous outflow is obstructed
by apposition of the iris,
-Resulting in an anatomically closed angle
-Physical treatment – first line

20
Q

Types of glaucoma – open angle? (3)

A

Primary open angle glaucoma (POAG) is, by far, the most common type of glaucoma.
* Mainly affects people over the age of 40 years.
* Is usually insidious in onset, and follows a chronic course.
* Usually affects both eyes, but one eye may be more affected than the other.
* Is typically associated with raised intraocular pressure (IOP).

Normal tension (pressure) glaucoma occurs in a significant minority of people with POAG where glaucoma develops with normal IOP.

Secondary POAG is much less common and due to a variety of causes

21
Q

Primary open-angle glaucoma (POAG) risk factors?

A
  • Raised IOP
  • Age – increases with increased age
  • FHx – sibling increased risk 8x, parent 2x
  • Ethnicity – 2-3x more common in black than white people
  • Corticosteroid use – oral or inhaled
  • Myopia – due to mechanical factors
  • T2DM – 2x risk compared to pts without diabetes
  • Hypertension and CVD – may cause small increase
22
Q

Types of glaucoma – closed angle? (2)

A
  • Primary angle closure glaucoma (PACG) is the most common type of angle
    closure glaucoma.
  • Secondary PCAG is much less common and due to a variety of causes
23
Q

Primary closed-angle glaucoma (PCAG) risk factors?

A
  • Age – increases with increased age
  • Sex – 2-3x more common in women than men
  • Ethnicity – more common Asian people
  • Eye size – small hyperopic eyes more common
  • FHx – a hereditary element may play a role in some people
24
Q

Screening for glaucoma:

A
  • Older age
  • Family hx of glaucoma
  • Ethnicity- 40+ and Black African family origin- annually
25
Q

Prognosis of glaucoma

A
  • Depends on severity of ocular hypertension, corneal thickness and age
  • Early treatment that reduces ocular hypertension leads to better outcomes
  • About 10% of blindness registrations in UK due to glaucoma
  • POAG – around 5-10% of people will go blind, others will have varying degrees of sight loss
  • Any sight lost at any stage cannot be restored
  • Around 50% of people treated will have no further sight loss after 20 years
  • PCAG – much less common that POAG, but accounts for 50% of cases of glaucoma-related blindness worldwide
  • Outlook good with prompt treatment – recognition is key
  • The other eye has a 40-80% chance of an episode of PCAG over the next 5-10 years
26
Q

Treatment options for glaucoma:

A

Mild ocular hypertension – poss. watchful waiting
Eye drops
* First-line – prostaglandin analogues (PGAs)
* Second-line if unsuccessful or not tolerated – switch to an alternative PGA, or
* A topical beta-blocker.
* Switching to, or adding in, a second-line drug treatment, which are: a non-generic PGA, a topical sympathomimetic, a topical carbonic anhydrase inhibitor, a topical miotic or a combination of treatments.

  • If treatment is recommended by an ophthalmologist based on an IOP of
    24mmHg or more and an identified risk of visual impairment, first-line treatment is 360° selective laser trabeculoplasty (SLT).
27
Q

Treatments- 1st line for OAG?

A

Open-angle glaucoma
* reducing intraocular pressure
* the only modifiable risk factor
* To slow the rate of disease progression sufficiently to prevent visual impairment

Prostaglandin Analogues (first line)
-latanoprost, travoprost, bimatoprost

Increased uveoscleral outflow of aqueous humor
* may be in part due to a reduction in collagen in the trabecular meshwork
* also increase blood flow to the optic nerve
=may contribute to neuroprotection in the retina

28
Q

PGAs- Patient and carer advice?

A
  • Changes in eye colour- Increase in the brown pigment in the iris can occur which may be permanent
  • Changes in eyelashes and vellus hair can also occur
29
Q

Treatments: Sympathetic nervous system? (2)
examples?

A

β-Adrenoceptor Antagonists
* Betaxolol, Timolol
* Reduce the formation of aqueous humour by the ciliary body

Sympathomimetics
* α2 adrenoceptor agonists
* Apraclonidine, brimonidine
* reduce aqueous humour production and increase uveoscleral outflow

*Caution in asthma, HypoTN and Bradycardic patients

30
Q

Treatments: other (not as common)

A
  • Carbonic Anhydrase Inhibitors
    -acetazolamide, brinzolamide, dorzolamide
  • Carbonic anhydrase in the eye is responsible for about 70% of the Na+ that enters the anterior chamber, which is accompanied by water to maintain
    isotonicity
  • Inhibition reduces aqueous humor production

Miotic Drugs (Muscarinic Agonists)
* Pilocarpine
* Contracts the circular sphincter muscle of the iris
* Produce miosis, pupil constriction - opens the drainage channels in the
anterior chamber of the eye

31
Q

360° selective laser trabeculoplasty (SLT)

A
  • involves a low-energy laser being fired at the trabecular meshwork
  • thought to work by selectively targeting melanin pigment that occurs in a
    proportion of cells in the trabecular meshwork, leaving non-pigmented cells
    unscathed
  • increases the drainage capacity of the trabecular meshwork but causes little
    damage to the structures there
  • if needed, it can be safely repeated.
32
Q

PCAG treatment?

A
  • Always an emergency and treated in secondary care
  • Initially intravenous acetazolamide and topical pilocarpine, beta-blockers,
    and steroids.
  • Surgical procedures can then be considered, including:
  • iridotomy (hole lasered in iris to promote fluid drainage)
  • phacoemulsification (use of ultrasound to break up lens to remove)
  • iridoplasty (similar to iridotomy)
33
Q

Counselling in glaucoma?

A
  • Adherent to treatment absolutely vital to preserving vision
  • Counsel on use of specific drops and get patient to show how they use them
  • Provide an eye-drop dispenser device if appropriate
  • Store drops correctly (some need to be in fridge)
  • Report adverse effects as can switch if necessary
  • Certain benefits available if pts lose sight
  • Can usually drive, but need to inform DVLA if glaucoma in both eyes
34
Q

AGE-RELATED MACULAR DEGENERATION

A

Main cause of irreversible visual loss in the developed countries
Macula
* High-resolution, colour vision (lots of rods and cones)
* Within this is the fovea= Highest density of cones
Advanced forms are characterized by a central vision loss
* Dry (non-exudative) ARMD
* Wet (exudative) ARMD
Risk factors
* Age, smoking obesity, genetics (inc complement factor H gene)

35
Q

Pathology of ARMD

A

Early:
* Deposition of Drusen – lipid droplets
Dry (non-exudative) ARMD
* Proliferative changes in the retinal pigment epithelium
* Macula: cell migration into the photoreceptor layer and drusen
* Most cases of ARMD are dry – more minor visual disturbance
* Not routinely treatable

36
Q

Pathology of Wet ARMD

A

Pathology
* Wet (exudative) ARMD
* similar to dry AMD
* additional development of new blood vessels (choroidal neovascularisation)
under the macula
* Vessels leak blood and protein
* Severe macular visual loss in 70% of affected eyes within 2 years
* Evidence of increased vascular
endothelial growth factor (VEGF-A)
-by retinal pigment epithelial cells

VEGF-A is an angiogenic protein
* induces growth of new blood
vessels and increases vascular
permeability
* Contributes to vision loss

37
Q

Treatments of ARMD

A
  • Monoclonals – anti –VEGF ranibizumab or bevacizumab
  • Soluble decoy receptor: aflibercept
    -Binds to VEGF – inhibits activation of VEGF receptors
  • Inhibit VEGF
  • Inhibits growth of new blood vessels
  • Intravitreal injection
38
Q

Summary

A

Accommodation
* Ciliary muscles controlled by parasympathetic innervation
* Pupil size
-Parasympathetic – contraction
-Sympathetic – dilation
Pressure – related to aqueous humor
* β2-adrenoceptor – increased production
* α2-adrenoceptor – reduced production
* Constriction of pupil can increase drainage
Glaucoma - 2 types
* Prostaglandin analogues
* Adrenoreceptor antagonists (beta)
* Adrenoreceptor agonists (alpha)
* Muscarinic agonists
ARMD
* VEGF inhibitors

M202 (72 decks)

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