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Duke Elder (AD) > Slam Dunk Course > Flashcards

Slam Dunk Course Flashcards

1
Q

What are the 3 layers of the eye?

A

Global structure of the eyeball is made up:

  1. Fibrous tunic (sclera + cornea) = Outermost layer
  2. Vascular tunic (uvea) = Middle layer
  3. Neurosensory tunic = Inner layer
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2
Q

What are the components of the fibrous tunic layer of the eye?

A

Sclera - white part of the eye, provides attachment for rectus muscles, terminates at limbus.

Cornea - 5 layers in total, consisting of regular fibrous connective tissue.

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3
Q

What are the components of the vascular tunic layer of the eye?

A

Choroid - vessels for retina

Ciliary body - lens accommodation & produces aqueous humour

Iris - dictates aperture of the eye

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4
Q

Where in the eye does bilirubin accumuate?

A

Sclera is where bilirubin accumulatesespecially the dense connective tissue

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5
Q

What are the layers of the sclera?

A

Episclera (dense CT)

Sclera proper (collagen)

Lannina fusca (pigmented)

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6
Q

Which bones form the roof of the bony orbit?

A

Frontal
Lesser wing of sphenoid

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7
Q

Which bones form the floor of the bony orbit?

A

Maxilla
Palatine
Zygomatic

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8
Q

Which bones form the medial wall of the bony orbit?

A

Ethmoid
Maxilla
Sphenoid

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9
Q

Which bones form the lateral wall of the bony orbit?

A

Zygomatic
Greater wing of sphenoid

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10
Q

Which wall of the orbit is the thinnest?

A

The medial orbital wall is thinnest, followed by the bone of the floor of the orbit, but is strengthened by the ethmoid sinuses.

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11
Q

Which wall of the orbit is the most vulnerable to fracture?

A

The floor of the orbit is most vulnerable to fracture when there is direct force exerted on the ocular globe because it is thin and unsupported.

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12
Q

What is the shape of the walls of the orbit?

A

All the orbital walls are curvilinear in shape.

Their purpose is to maintain the projection of the ocular globe and to cushion it when subjected to blunt force.

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13
Q

What are orbital blowout fractures?

A

Orbital blowout fractures: incarceration of rectus muscles (IR), oedema ecchymosis, orbital compartment syndrome, upgaze restriction

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14
Q

What are the layers of the eyelid?

A
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15
Q

What are the anatomical layers of eyeball?

A

Skin
Orbicularis oculi
Submuscular adipose tissue
Orbital septum
Tarsal planes (connective tissue)
Levator apparatus
Conjunctiva

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16
Q

What is the role of the orbital septum?

A

DIvides the orbital content from lid content

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17
Q

What are the 3 components of the levator apparatus?

A

LPS (skeletal)
Superior tarsal muscle (Muller’s, SNS)
Inferior tarsal muscle (Muller’s, SNS)

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18
Q

What is the difference between a complete and partial ptosis?

A

Complete: Paralysis of LPS, due to CN Ill lesion (somatic nerves, skeletal muscle)

Partial: Paralysis of Muller’s muscle (found in the tarsal plate) due to Horner’s syndrome

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19
Q

What is the difference between a stye and chalazion?

A

Stye - a focal infection of a hair follicle, (folliculitis) or Meibomian gland. Painful.

Chalazion - a focal cyst of a Meibomian gland. Painless.

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20
Q

What are the three layers of the tear film?

A

Lipid layer - superficial, oily (MGs)

Aqueous layer - substrates, immune (lacrimal)

Mucinous layer - adhesion (epithelium)

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21
Q

What is the name for a focal infection of the lacrimal sac?

A

Dacrocystitis

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22
Q

What are the 5 layers of the cornea?

ABCDE

A

Tear film
Anterior corneal epithelium
Bowman’s capsule
Corneal stroma
Descement’s membrane
Endothelium

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23
Q

What are the 3 distinct regions of the conjunctiva?

A

Bulbar - covers sclera
Palpebral - lines inside of eyelid
Fornices - edges

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24
Q

What are the branches of the external carotid artery (ECA)?

‘Some Ancient Lovers Find Old Positions More Stimulating’

A

Superior thyroid
Ascending pharyngeal
Lingual Facial
Occipital
Posterior auricular
Maxillary
Superficial temporal

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25
Q

What is the anterior circulation of the brain?

A

Mainly ICA

ICA enters at carotid canal (petrous part of temporal bone)

Once in internal cavity, divides into: ACA, MCA

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26
Q

Through which bone does teh ICA enter the brain cavity?

A

Temporal bone

Specifically: carotid canal (petrous part)

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27
Q

Which arteries supply the posterior circulation of the brain?

A

Vertabral arteries

Vertebral arteries come off subclavian arteries

Travel posteriorly & ascend in transverse foramina of C1 - С6

Merge to form the basilar artery (located anterior of pons)

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28
Q

Where does the basilar artery form?

A

Anterior of the pons

Joining of the vertebral arteries

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29
Q

What are the 3 main mechanisms that can disrupt blood flow to the brain?

A
  1. Thromosis
  2. Embolism
  3. Haemorrhage

Infarction (secondary to occlusion)
Ischaemia (secondary to infarction)

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30
Q

What is amaurosis fugax?

A

Transient loss of vision (monocular blindness) due to an interruption in retinal blood flow.

Associated with vascular thromboembolic event, usually arising from ICA.

Other pathology: hypoperfusion, vasospasm, coagulopathies (leukaemia, myeloma), atherosclerosis.

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31
Q

What are the symptoms of amourosis fugax?

A
  1. Acute monocular, painless blindness
  2. Lasts seconds to minutes (rarely hours)
  3. Curtain coming down / generalised darkening
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32
Q

For a patient with amaurosis fugax, how should they be investigated?

A

Ophthalmic examination, vascular / stroke workup (carotid dopplers, echo, ECG), neuroimaging

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33
Q

For a patient with amaurosis fugax, how should they be managed?

A
  1. Control underlying RF (smoking, lipids, HTN)
  2. Aspirin, clopidogrel (anti-platelets)
  3. Steroids (if GCA)
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34
Q

What is the ‘stroke of the eye’?

A

Central retinal artery occlusion (CRAO)

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35
Q

What is central retinal vein occlusion?

A

Thrombosis of veins

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36
Q

Which parts of the eye are involved in refraction?

A

The cornea does 80% refraction, lens and vitreous does the other 20%, occurring due to convex lens.

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37
Q

Where does the retina terminate?

A

Ora serrata (sits behind the ciliary body)

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38
Q

What are the 2 major components of the retina?

A

Retinal pigmented epithelium (RPE) + Neurosensory retina

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39
Q

What is the blood supply to the retina?

A

Highly metabolic areas (RPE) from choroid

Low metabolic areas (inner retina) from retinal vessels & nutrition rom vitreous

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40
Q

What are the layers of the retina?

A

‘In New Generation It Is Ophthalmologists Examining Patient’s Retina’

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41
Q

What is phototransduction?

A

highly complicated process involving rhodopsin - a molecule that bleaches in light - and aims to convert light energy into neuronal impulse.

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42
Q

Is transduction a high or low metabolic process?

A

Odd arrangement, but transduction is a highly metabolic process, carried out by photoreceptors - turning light energy (photons- a type of quantum particle) into electrochemical energy.

Blood can be delivered more easily to the back of the eye than to the surface (choroidal > retinal vessels).

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43
Q

In the visual pathway, what is the ‘relay’ point?

A

LGN is a ‘relay’ point in the thalamus for filtering top-down & bottom-up information

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44
Q

What are the layers of the striate cortex?

A

Layer 1-5 - receives feedback from from LGN Layer 6 - provides feedback to LGN

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45
Q

Which part of the brain is involved in prosopagnosia?

A

Occipital facial area (OFA)
Face fusiform area (FFA)

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46
Q

Which part of the brain is involved in people recognition disorder?

A

Anterior temporal lobe (ATL)

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47
Q

What type of visual field defect is caused by a stroke?

A

Macular sparing homonymous hemianopia

Reason: The macula receives dual blood supply from the posterior cerebral arteries from both sides.

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48
Q

What are the extraocular muscles and their movements?

A

Each muscle has 3 movements

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49
Q

What is the major route of absorption of drugs given topically?

A

Cornea

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50
Q

What is the most common drug given intraocularly?

A

Intravitreal injections e.g. Anti-VEGF injections (ranibizumab) for proliferative diabetic neuropathy and wet AMD.

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51
Q

Which barriers do systemic drugs need to pass to reach the eye?

A

Blood-retinal barrier
Blood-aqueous barrier

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52
Q

What is the most common form of drug administration?

A

Topical administration into the inferior fornix represents the most common route of administration.

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53
Q

When giving drugs topically to the eye, what is important to remember?

A

The conjunctiva is an extremely vascular structure. Drugs can be lost through absorption into the systemic circulation.

Once the drug has been administered the amount available at the site of action (bioavailability) is affected by pre-corneal and corneal factors.

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54
Q

Pre-corneal factors affecting bioavailability of drugs: solution drainage?

A

Once in the fornix, the drugs enter the inferior meatus through the valve of Hasner, where high amounts of the drug are absorbed into the bloodstream.

Reduce by: pinching nose for 5 mins or giving gel/ointment (rather than drops)

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55
Q

What are some pre-corneal factors affecting the bioavailability of drugs?

A
  1. Solution drainage (valve of Hasner)
  2. Blink rate
  3. Tear volume & tear turnover time
  4. Disruption of the tear film
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56
Q

Pre-corneal factors affecting bioavailability of drugs: tear volume and turnover time?

A

Tear volume ranges from 7-8uL.

Transiently the fornix can hold 30uL.

Most applicators will deliver 50uL so a large volume is lost in over spill.

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57
Q

What is normal tear turnover time?

A

Normal tear turnover time is 0.5-2.2uL/minute

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58
Q

What are the three layers of the tear film?

A
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59
Q

How will disruption of the tear film affect bioavailability of drugs?

A

Anything that disrupts the integrity of the tear film e.g. meibomian gland dysfunction (MGD) will reduce drug residency time in the fornix.

The pH of the tear film 6.5-7.6. If the pH of the tear film is altered, drug ionisation and hence diffusion capacity is affected.

Some drugs will bind to tear film proteins such as albumin and lysozyme.

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60
Q

Which layer of the cornea is hydrophobic?

A

Epithelium is hydrophobic - will only allow lipid soluble drugs to pass through.

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61
Q

Outline corneal factors that affect bioavailability of drugs?

A
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62
Q

What does the blood-aqueous barrier consist of?

A
  1. Vascular endothelium of the iris/ciliary vessels
  2. The non-pigmented ciliary epithelium

Both cell layers express tight junctional complexes and prevent the entry of solutes into the anterior segment.

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63
Q

Which barrier prevents anything passing from the anterior segment of the eye?

A

Blood-aqueous barrier

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64
Q

Which barrier prevents anything passing to the anterior segment of the eye?

A

Blood-retinal barrier

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65
Q

What are the two cell types that make up the blood-retinal barrier?

A

The retinal capillary endothelial cells (inner BRB)

The retinal pigment epithelium cells (outer BRB)

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66
Q

What are the outer retinal layers of the blood-retinal barrier nourished by?

A

The choroid

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67
Q

What are the inner retinal layers of the blood-retinal barrier nourished by?

A

Retinal vessels

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68
Q

Which types of receptors does acetylcholine act on?

A
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69
Q

Where are acetylcholine receptors found in the eye? (6)

A
  1. EOM
  2. LPS
  3. Iris sphincter
  4. Ciliary body
  5. Lacrimal gland
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70
Q

Where in the eye is choline acetyltransferase present?

A
  1. Corneal epithelium
  2. Ciliary body
  3. Inner plexiform layer of the retina
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71
Q

What are two examples of Indirect parasympathomimetic drugs used in the eye?

A

Edrophonium, Physostigmine.

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72
Q

What are the actions of cholinergic agonists in the eye?

A
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73
Q

What is an example of a direct parasympathomimetic?

A

Pilocarpine

Used frequently in the treatment of glaucoma.

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74
Q

In which condition is edrophonium (indirect parasympathomimetic) used for diagnostic purposes?

A

Myasthenia Gravis

Ocular myasthenia can be made using the Tensilon Test. IV is edrophonium is administered. Any improvement in ptosis or diplopia confirms a positive diagnosis. Longer acting neostigmine can be used for treatment.

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75
Q

What are the side effects of cholinergic agonists/parasympathomimetics?

A

Systemic -salivation, bradycardia

Ocular - cataracts iris cysts, conjunctival toxicity

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76
Q

What are the actions of cholinergic antagonists?

A
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77
Q

In which condition is cholinergic antagonists often used in?

A

Used to prevent the formation of posterior synechiae in uveitis and iritis.
Posterior synechiae are adhesions between the posterior iris and anterior len surface.

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78
Q

In which examination are cholinergic antagonists used?

A

Routine funal exam

Also: provocation of glaucoma (test)

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79
Q

What are 3 examples of cholinergic antagonists?

A

Atropine
Cyclopentolate
Tropicamide

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80
Q

What are the actions to alpha agonists in the eye?

A

Smooth muscle contraction

Dilator pupillae muscle
Ciliary muscle
Constriction of conjunctival and episcleral vessels

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81
Q

What are 3 examples of topical alpha agonists?

A

Apraclonidine
Brimonidine
Clonidine

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82
Q

What are the side effects of alpha agonists?

A

Common: allergic conjunctivitis, conjunctival blanching

Systemic: hypotension, dry mouth

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83
Q

What drug can be used to differentiate between scleritis and episcleritis?

A

Instillation of phenylephrine drops can be used to differentiate between these 2 conditions.

The drug will cause constriction of the episcleral vessels in episcleritis but not in the deep plexus in scleritis.

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84
Q

What are some examples of topical beta blockers?

A

Timolol
Betaxolol
Levobunolol

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85
Q

What are some of the side effects of beta blockers?

A

Ocular: Conjunctivitis

Systemic: caution - heart block, heart failure, asthmatics

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86
Q

Where are beta-2 receptors found?

A

B2 receptors found on ciliary processes (this is different from the muscle) and trabecular meshwork

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87
Q

How do beta blockers affect aqueous?

A

Increase aqueous outflow
Decreased aqueous production

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88
Q

How do carbonic anhydrase inhibitors (CAIs) work?

A

Inhibit carbonic anhydrase which is found in ciliary body epithelium. It is a key enzyme in aqueous production.

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89
Q

What are some examples of topical carbonic anhydrase inhibitors?

A
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90
Q

What drugs are commonly given with carbonic anhydrase inhibitors for glaucoma treatment?

A

Generally combined with topical B antagonist (timolol) for glaucoma treatment

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91
Q

What are the side effects of carbonic anhydrase inhibitors (CAls)?

A

Systemic: renal stones, malaise, fatigue,

Ocular: stinging, allergic reactions

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92
Q

What are the 3 functions of the aqueous?

A
  1. To supply nutrition to the lens, corneal epithelium, corneal stroma but NOT the corneal epithelium. The corneal epithelium derives nutrition from tears.
  2. To maintain IOP. IOP is determined by the rate of aqueous secretion and rate of aqueous outflow. 10-21 mmHg.
  3. To remain transparent
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93
Q

How is the aqueous produced?

A

The passive diffusion of water and ions from the ciliary body and the active transport of Na and Cl. It is an active secretory process that involves Na/K ATPase pump and carbonic anhydrase type Il activity.

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94
Q

Outline the flow of aqueous.

A
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95
Q

Where is aqueous drained out?

A

Aqueous can be drained through the trabecular outflow (90%) or uveoscleral outflow (10%)

Trabecular: trabecular meshwork, Schlemm’s canal, episcleral veins

Uveoscleral: Drained by the venous circulation in the ciliary body, choroid and sclera

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96
Q

Outline the trabecular drainage of the aqueous.

A

Involves the trabecular meshwork, Schlemm’s canal, episcleral veins

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97
Q

Outline the uveoscleral drainage of the aqueous.

A

Drained by the venous circulation in the ciliary body, choroid and sclera

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98
Q

How do alpha agonists and beta antagonists affect aqueous flow?

A

Alpha agonists and B antagonists will suppress aqueous flow

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99
Q

What is the role of the orbicularis oculi pump?

A

70% tears drained by the lower canaliculus. Remainder drained by the upper.

With each blink fibres of orbicularis shorten the canaliculi and move the puncta medially. The lacrimal sac expands creating negative pressure and drawing in the tears.

When the eyes open and the muscles relax, the sac collapses and tears drain down the ducts.

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100
Q

What does the accomodation reflex involve? (3)

A
  1. Convergence of the eyes
  2. Pupillary constriction
  3. Increased biconvexity of the lens
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101
Q

How does accomodation change throughout life?

A

Accommodation begins to develop at 2 months and is well developed by 8 months. The ability to accommodate decreases with age and by 60 years accommodation is extremely poor (presbyopia) .

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102
Q

How does convergence of the visual axis occur in accomodation?

A

Contraction of the medial rectus via innervation of the oculomotor nerve

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103
Q

How does increased lens biconvexity occur in accomodation?

A

Circular ciliary muscle contracts, decreasing tension in zonular fibres, and allowing the lens capsule to contact and change the shape of he lens. The anterior pole moves forward, the axial width increases and the diameter of the lens decreases.

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104
Q
A

Stye/hordeolum

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105
Q

What is the difference between exteral and internal hordeolum?

A

External (stye): Infection of the glands of Zeis or Moll

Internal: Infection of meibomian gland within the tarsal plate

‘pus points TOWARDS you’

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106
Q

What are the symptoms of canaliculitis?

A

Unilateral red eye
Epiphora (watery eye)
Swollen lump on medical eyelid margin
Mucoid discharge when pressure applied over canaliculus
Granules at punctum

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107
Q

What pathogen is commonly implicated in canaliculitis?

A

Actinomyces israelii (anaerobic filamentous gram +ve)

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108
Q

What is dacrocystitis?

A

Infection of lacrimal sac secondary to obstruction in nasolacrimal duct causing stagnation of tears

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109
Q

What pathogens are commonly implicated in dacrocystitis?

A

Adults = Staph epidermidis Children = H influenzae

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110
Q

Which pathogens are commonly implicated in orbital cellulitis?

A

Strep pneumoniae
Staph aureus
H influenzae

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110
Q

What are some of the possible complicates of orbital cellulitis?

A

Orbital abscess, cavernous sinus thrombosis, brain abscess and meningitis, optic neuropathy, central retinal artery occlusion

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110
Q

What is cavernous sinus thrombosis?

A

A clot formed in the cavernous sinus usually as a result of a spreading infection from the paranasal sinuses, ear or orbital cellulitis

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111
Q

How does cavernous sinus thrombosis present?

A

Causes sudden onset headache, N&V, chemosis, proptosis

Can also cause diplopia due to CN 3, 4 or 6 compression

Lateral gaze palsy in CN 6 compression (first sign)

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112
Q

How is a cavernous sinus thrombosis diagnosed and managed?

A

Diagnosed with an MRA

Managed with IV abx/steroids + LMWH ( ± surgical invervention)

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113
Q

Which antibiotics are given in pre-septal cellulitis?

A

Co-amoxiclav

Important to treat as can progress into orbital cellulitis

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114
Q

What is orbital mucormycosis?

A
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115
Q
A

Bacterial keratitis

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116
Q

What investigations are done for bacterial keratitis?

A

Corneal scraping for microbiology (blood / chocolate agar)

Gram / Giemsa stain

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117
Q

Which pathogens are implicated in bacterial keratitis?

A

Contact lens wearers = Pseudomonas aeruginosa

Otherwise = Staph aureus

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118
Q

How does candidal fungal keratitis present?

A

Common in immunocompromised patients

Yellow-white infiltrate with ‘mushroom’/’collar stud’ morphology

Mx: Voriconazole drops

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119
Q

What investigations should be done for suspected fungal keratitis?

A

Gram & Giemsa staining, Sabouraud’s agar

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120
Q

How does filamentous funal keratitis (e.g. aspergillus) present?

A

Ocular trauma (e.g. tree branch)

Branch like stromal infiltrate pattern

Mx: Natamycin drops

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121
Q

What investigations should be done for acanthamoeba keratitis?

A

Corneal scraping - E.coli plated over non-nutrient agar

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122
Q

What condition presents with ring shaped stromal infiltrates?

A

Acanthamoeba keratitis

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123
Q

How is acanthamoeba keratitis managed?

A

Topical biguanides or chlorhexidine

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124
Q

How does epithelial HSV keratitis present?

A

Decreased corneal sensation

Decreased VA

Lacrimation

Foreign body sensation

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125
Q

What are the signs of herpes simplex keratitis?

A

Superficial punctate keratitis causing stellate / ‘star-shaped’/ ‘terminal buttons’

Classic dendritic ulcer visualised under fluorescein + Rose Bengal stain

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126
Q

What must you avoid in herpes simplex keratitis?

A

AVOID STEROIDS - can lead to ulcer and corneal perforation

Managed with topical acyclovir for epithelial

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127
Q

What causes endothelial/disciform HSV keratitis?

A

HSV antigen hypersensitivity

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128
Q

How does endothelial/disciform HSV keratitis present?

A

Insidious onset painless loss of vision

Circular central stromal oedema Intact epithelium on fluorescein staining

Wessely ring

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129
Q

How is disciform keratitis managed?

A

PO acyclovir for disciform

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130
Q

What causes herpes zoster ophthalmicus

A

Latent virus in the trigeminal ganglion may reactivate leading to shingles over the dermatome supplied by CNV(1)

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131
Q

What is interstitial keratitis?

A

Stromal inflammation +/neovascularization (infective or immune reaction)

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132
Q

What condition presents with non-ulcerated stromal keratitis with feathery mid-stromal scarring?

A

Interstitial keratitis

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133
Q

What are the three main causes of interstitial keratitis?

A

Syphilis: Congenital = BL, acquired =unilateral - treat IM benpen + topical steroids

Lyme disease: Borrelia bacteria via tick bite causing erythema migrans

Viral: HSV & VZV, EBV

134
Q

Which pathogens are implicated in bacterial conjunctivits?

A

Haemophilus influenzae most common in children

Staphylococcal species most common in adults

135
Q

How is bacterial conjunctivitis treated?

A

Can treat with topical chloramphenicol if severe

Topical fusidic acid in pregnant women (due to risk of aplastic anaemia with chloramphenicol)

136
Q

How is viral conjucntivitis distinguished from bacterial?

A

Viral will have preauricular lymph node swelling!

137
Q

What is the most common pathogen in viral conjunctivitis?

A

Adenovirus

VERY infectious! Should avoid sharing towels etc.

Treat with steroids!

138
Q

What are the 4 types of allergic conjunctivits?

A
  1. Seasonal and perennial allergic conjunctivitis
  2. Vernal keratoconjunctivitis (VKC)
  3. Atopic keratoconjunctivitis (AKC)
  4. Giant papillary conjunctivitis
139
Q

What are the symptoms of chlamydial conjunctivitis?

A

Unilateral red eye

White follicles

Preauricular lymphadenopathy

Mucopurulent/ ‘stringy’ discharge

140
Q

What is chlamydial conjunctivitis associated with?

A

Associated with Reiter’s / reactive arthritis (urethritis, arthritis and conjunctivitis)

Can’t see, pee or climb a tree

141
Q

How is chlamydial conjunctivitis managed?

A

STAT 1g azithromycin OR

100mg doxycycline for 14/7

142
Q
A

Trachoma

143
Q

What is the leading cause of infectious blindness worldwide?

A

Trachoma

144
Q

What is trachoma?

A

Type IV hypersensitivity reaction

145
Q

Which pathogen is implicated in trachoma?

A

Chlamydia trachomatis

Transmitted by musca sorbens fly (bazaar fly)

146
Q

What are the WHO stages of trachoma?

A

Inflammation follicular: 5+ follicles in upper tarsal conjunctiva

Inflammation intense: thickening of upper tarsal conj causing irritation

Scarring: repeated infections causing scaring and entropion

Trichiasis: ingrowing eyelashes towards cornea

Opacity: corneal inflammation leads to opacity

147
Q
A

Endophthalmitis

148
Q

What is endophthalmitis?

A

Infection of vitreous and aqueous humour

Post op complication (but can have endogenous causes too)

149
Q

How is endophthalmitis investigated?

A

Vitreous tap for culture

150
Q

Which pathogens are implicated in endophthalmitis?

A

Acute endophthalmitis within first week: Staph epidermidis

Delayed endophthalmitis (6 weeks +): Propionibacterium acnes

151
Q

How is endophthalmitis managed?

A

URGENT intravitreal abx

Pars plana vitrectomy if severe

Prevention = povidone-iodine preop, intracameral ABx peri-op, postop topical ABx

152
Q

What are the ocular features present in tuberculosis uveitis?

A

Conjunctivitis
Scleritis
Keratitis
Anterior uveitis: **Mutton fat KPs **
**Posterior uveitis **
Dacryoadenitis

153
Q

What is teh 2nd leading cause of infectious blindness worldwide?

First = trachoma

A

Onchocerciasis African River Blindness)

154
Q

What pathogen is implicated in african river blindness?

A

Onchocerca volvulus

Simulium black fly vector

Another name = Onchocerciasis

155
Q

What is a classical systemic feature in Onchocerciasis (African River Blindness)?

A

Maculopapular rash

156
Q

How is Onchocerciasis (African River Blindness) managed?

A

Ivermectin

157
Q
A

Cat Scratch Neuroretinitis

158
Q

What is cat scratch neuroretinitis?

A

Inflammation of optic nerve and neural retina causing oedema rom the nerve head to the macula

Caused by Bartonella henselae (gram -ve)

Commonly associated with cat-scratch disease (but noninfective causes too)

159
Q

What is CMV retinitis?

A

Opportunistic infection caused by cytomegalovirus

Occurs in AIDS patients when CD4+ count <50

160
Q

What are the possible complications of CMV retinitis?

A

Full thickness retinal infection that can lead to necrosis and retinal breaks and detachment

161
Q

How is CMV retinitis treated?

A

IV ganciclovir

162
Q

How is toxoplasmosis treated?

A

**Triple therapy **

  1. Pyrimethamine
  2. Sulfadiazine
  3. Corticosteroid
163
Q

How is toxoplasmosis diagnosed?

A

PCR (only needed if not clear from examination + fundoscopy)

164
Q

Which conditions are included in the term ‘uveitis’?

A

Iritis = iris, anterior chamber
Cyclitis = ciliary body
Choroiditis = posterior chamber
Iridocyclitis = anterior & posterior chamber

165
Q

What is uveitis initiated by in developed nations (usually)?

A

An autoimmune process or dysregulated immune response

HLA-B27

166
Q

In less developed countries, what is the leading cause of uveitis?

A

Infectious causes e.g. HHV 1-3, TB, syphilis, Lyme disease, delayed post-operative endophthalmitis

167
Q

Which cell type is present in chronic and granulomatous uveitis?

A

Macrophages

168
Q

Outline the adaptive immune response in uveitis

A
169
Q

What doe sit mean that the eye is immune privileged?

A

A limit is placed on local ocular immune and inflammatory responses (to preserve vision) - driven by the eye-driven systemic regulatory process (ACAID system)

ACAID = there is a delayed immune response / ¿ hypersensitivity reaction (12-24 hours at minimum for inflammation to occur) in response to antigens

170
Q

Which HLA is associatred with birdshot (chorioretinopathy)?

A

HLA-A29

171
Q

Which HLA is associated with Behcet’s?

A

HLA-B51

172
Q

Which HLA is associated with anterior uveitis?

A

HLA-B27

173
Q

Which HLA is associated with sympathetic ophthalmia?

A

HLA-DR4

174
Q

Which HLA is associated with panuveitis?

A

HLA-DR4

175
Q

Which HLA is associated with intermediate uveitis?

A

HLA-DR3

176
Q

Which HLA is associated with chronic iridocyclitis (IJA)?

A

HLA-DR5

177
Q

What are synechiae?

A

adhesions that are formed between adjacent structures within the eye usually as a result of inflammation

seen in uveitis

iris adheres to either the cornea (i.e. anterior synechia) or lens (i.e. posterior synechia)

178
Q

What are keratic precipitates?

A

acute, white, round, PMNs - as they age become pigmented & irregular

Upper image Bottom image = mutton fat precipitates
179
Q

What are mutton fat precipitates?

A

chronic, white-yellow, greasy, granulomatous, clumped-up cells macrophages +++

associated with sarcoidosis + syphilis

Bottom image Upper image = keratic precipitates
180
Q

What are (a) peripheral anterior synechiae and (b) posterior synechiae?

A

(a) adhesions between peripheral iris and angle of drainage

(b) adhesions between iris and anterior capsule of lens)

Photophobia (due to adhesions, the iris is unable to regulate eye aperture & ciliary spasm)

181
Q

What are koeppe nodules and bussaca nodules?

A

Koeppe nodules (inflammatory cell precipitates that lie at pupillary marginfound in both non & granulomatous)

Bussaca nodules (lie on the iris surface - pathognomonic for granulomatous uveitis)

182
Q

How is uveitis managed?

A
  1. Cycloplegics e.g. atropine 1% - prevent new synechiae and breaks existing adhesions
  2. Anti-inflammatory e.g. topical steroids
183
Q

What is intermediate uveitis and who does it affect?

A

Inflammation of vitreous body with minimal anterior / posterior signs.

Young, bilateral.

TO infiltrates in pars plana (pars planitis) and vitreous (vitritis).

184
Q

What signs are seen in intermediate uveitis?

A

Epiretinal membrane, snow banking, snow balls, vitritis (hazy)

185
Q

What is the pathophysiology of posterior uveitis?

A

Inflammation of choroid & retina (more often pan-uveitis). May target tissue (choroiditis) or vessels (choroidal vasculitis).

186
Q

Which type of uveitis presents with dyschromatopsia?

A

Posterior uveitis

187
Q

What does PORN stand for?

A

Progressive Outer Retinal Necrosis

187
Q

Which type of uveitis is associated with infectious causes?

A

Posterior uveitis

188
Q

Which parts of the eye are affected in uveitis?

A

Anterior (iris to ciliary body)

Intermediate (ciliary body to retina)

Posterior (choroid layer, retina, and retinal vessels) and panuveitis iris, ciliary body, and choroid layer)

189
Q

Which conditions are associated with HLA-B27? (4)

A
190
Q

HLA association in Behcet’s?

A

HLA-B51

191
Q

What are the A’s of ankylosing spondylitis?

A
192
Q

How does reactive arthritis present?

A

Reiter’s syndrome (Can’t see, can’t pee or climb a tree)

193
Q

How is thyroid eye disease managed?

A
194
Q

3 complications of thyroid eye disease?

A

Exposure keratopathy
Corneal erosions
Optic nerve compression

195
Q

What are the stages of diabetic retinopathy?

A
196
Q

Outline the pathophysiology of diabetic retinopathy.

A
197
Q

What are the 4 stages of hypertensive retinopathy?

A
197
Q

What are some of the complications of hypertensive retinopathy?

A

Central & Branch Retinal Vein Occlusions Malignant HTN (acutely high BP >180/120 & could cause acute-onset papilloedema / I ICP)

197
Q

Why does the consensual response occur?

A

Consensual response occurs as each pretectal nucleus is connected to BOTH EDW nuclei. Therefore, a unilocular light stimulus evokes a bilateral response.

198
Q

What is the role of the pretectal nucleus?

A

involved in the control of pupillary reflexes and contains several nuclei, including the pretectal olivary nucleus, which is believed to be the main pupillary center in primates.

198
Q

How does parasympathetic and sympathetic innervation affect the eye?

A
199
Q

What are the steps (and main nuclei) involved in pupil dilation?

A
199
Q

What causes RAPD?

A

Caused by incomplete optic nerve lesion or severe retinal disease

NOT by cataract

199
Q

What is an amourotic pupil?

A

Absolute Afferent Pupillary Defect

200
Q

What are some optic nerve diseases that result in RAPD?

A
  • Optic neuritis (Infectious, demyelinating)
  • Orbital disease (TED, sarcoid, tumours)
  • Drugs (ethambutol, methanol)
  • Ischaemic optic neuropathy
  • Glaucoma (unilateral; severe)
  • Trauma e.g. surgery, head injury, radiation
  • Congenital - Leber’s optic neuropathy
200
Q

What causes aniscoria?

A

Efferent lesions, iris(synechide) or pupillary muscles

201
Q

What are some retinal diseases that result in RAPD?

A
  • Ischaemic retinal disease - CRVO, CRAO
  • Retinal detachment - if the macula is detached or if at least two quadrants of retina are detached.
  • Severe macular degeneration - If unilateral and severe
  • Tumours- melanoma, retinoblastoma, and metastatic lesion if severe.
  • Retinal infection - CMV, HSV
202
Q

What are some bilateral causes of light-near dissociation?

The light reflex is absent or sluggish but the near response (accommodation) is normal

A
203
Q

What pharmacological test can be used to determine if a patient has Horner’s syndrome?

A

Cocaine 4% into both eyes

Affected eye: pupil does NOT dilate; eye is not producing noradrenaline
Unaffected eye: pupil dilates (normal response); prevents noradrenaline reuptake

204
Q

What are the 4 subdivisions of the optic nerve?

A

Intraocular: Optic disc, neve head: 1mm

Intra-orbital: 25-30 mm and extends from globe to optic foramen

Intra-canalicular: 6mm. Traverses the optic canal.

Intracranial: Joins the chiasm. 5mm-16mm. Longer nerve is more prone to damage.

205
Q

What are 6 signs of optic nerve dysfunction?

A
206
Q

How do you test contrast sensitivity?

A

Pelli-Robson Chart

207
Q

What is optic neuritis?

A

Optic neuritis is an inflammatory, infective or demyelinating process affecting the optic nerve

208
Q

What are the 4 major causes of optic neuritis?

A

Demyelinating - most common cause. Think MS!

Para-infectious - may follow viral infection or immunisation

Infectious- Lyme disease, meningitis, syphilis, cat-scratch fever

Autoimmune - associated with systemic autoimmune disorders (SLE, Sarcoid, thyroid eye disease)

209
Q

What is non-arteritic optic neuropathy?

A

Total or partial infarction of the optic nerve head caused by occlusion of the short posterior ciliary arteries

210
Q

What is arteritic optic neuropathy?

A

Usually referring to giant cell arteritis

211
Q

What is papilloedema?

A

Swelling of the optic nerve head **secondary to raised intracranial pressure (RIP). **

Swelling of the optic nerve head in the absence of RIP is known as disc swelling.

212
Q

What are the signs seen in papilloedmea?

A

Elevation of optic disc
Blurred disc margins
Swelling of optic nerve head Hyperaemia of optic disc
Flame haemorrhages
Exudated

213
Q

What is idiopathic intracranial hypertension?

A

Presence of RIP in the absence of intracranial mass or enlargement of the ventricles due to hydrocephalus

DIAGNOSIS OF EXCLUSION

90% of patients are obese women of child bearing age; amenorhoeic

214
Q

What drugs are associated with idiopathic intracranial hypertension?

A

tetracyclines, nalidixic acid

215
Q

How is idiopathic intracranial hypertension treated?

A

IV acetazolamide

Optic nerve sheath fenestrations (tiny slits in the optic nerve to allow CSF to flow out and reduce pressure)

216
Q

Why do you get a ptosis in CN III palsy?

A

Weakness of levator palpabrae muscle that causes a profound ptosis

Unopposed action of abducens nerve (‘out’ position in primary gaze) Normal abduction.

217
Q

Why do patients with CN III palsy have limited adduction?

A

Weakness of medial rectus limiting adduction

218
Q

Why do patients with CN III palsy have limited elevation?

A

Weakness of superior rectus and inferior oblique limiting elevation

219
Q

Why do patients with CN III palsy have limited depression?

A

Weakness of inferior rectus limiting depression

219
Q

Why do patients with CN III palsy have a dilated pupil?

A

Dilated pupil as PNS fibres travel along CN Ill in between brain stem and cavernous before reaching pupillary muscles

220
Q

What is the primary, secondary and tertiary actions of each of the eye muscles?

A
221
Q

What are some of the causes of a third nerve palsy?

A
222
Q

Outline the anatomy of the cavernous sinus

A
223
Q

What are the features of a CN 6 palsy?

A

Right esotropia
Failed abduction
Normal Adduction

224
Q

Which nerve might also be affected in CN 6 palsy?

A

CN 7

225
Q

What are some of the causes of CN 6 palsy?

A
226
Q

How does a CN 4 palsy present in the primary gaze and on adduction?

A

In the primary gaze (middle picture): Hypertropia and hyperdeviation of the affected eye due to unopposed action of inferior oblique.

On adduction (right picture): Hypertropia worsens on adduction due to overaction of inferior oblique

227
Q

In a CN 4 palsy, to which direction is the compensatory head tilt?

A

AWAY the lesion

228
Q

What are the 5 branches of the facial nerve (CN7)?

A
229
Q

What do signs involving both CN 6 and CN 7 suggest?

A

A lesion in the BRAIN

230
Q

What are the two types of squints?

A

Split into tropias / manifest or phorias / latent

Tropia / manifest = constantly present
Phoria/ latent = only detected on dissociation with an alternate cover-uncover test

231
Q

What is a concomitant vs incomitant squint?

A

Concomitant = deviation remains the same in all positions of gaze

Incomitant = angle / magnitude of deviated eye changes with position of the gaze

232
Q

What is amblyopia and how common is it?

A

Lazy eye

2% of the population (+ most common cause of unilateral decrease in VA in children)

233
Q

How is amblyopia treated?

A

If not fixed at a young age will become permanent

Occlusion therapy: good eye patched allowing visual connections to develop properly (can be pharmacological using atropine) - not tolerated very well

234
Q

What is the name for allied health professionals who assess diplopia, strabismus and eye movement defects?

A

Orthoptists

235
Q

What is binocular single vision (BSV)?

A

Use of both eyes together to achieve binocular depth perception - stereopsis

236
Q

What is the result of binocular single vision not developing correctly?

A

esotropia

237
Q

What is the AC/A ratio?

A

accommodative convergence to accommodation

238
Q

What is hypertropia and hypotropia?

A

Hypertropia = eye deviated superiorly and moves inferiorly with cover testing to fixate

Hypotropia = eye deviated inferiorly and moves superiorly with cover testing to fixate

239
Q

What is heterotropia and how common is it?

A

Manifest strabismus - One of the eyes is not directed towards a fixation point

5-8% of the population

240
Q

What is esotropia and exotropia?

A

Esotropia = eye deviated nasally and moves temporally with cover testing to fixate (convergent squint)

Exotropia = eye deviated temporally and moves nasally with cover testing to fixate

241
Q

What is accomodative esotropia?

A

Secondary to refractive errors or convergence excess

Associated with hypermetropia

242
Q

What is the most common childhood squint in the UK and what are the 2 subtypes?

A

Esotropia

Either accommodative or non-accommodative

243
Q

What is non-accomodative esotropia

A

Latent horizontal nystabmus
Normal refraction

SURGICAL management

244
Q

What is exotropia associated with?

A

Myopia

Esotropia is associated with hypertropia

245
Q

What is the most common type of exotropia?

A

Intermittent

246
Q

What are the two types of intermittent exotropia?

A

Distance or near

247
Q

How is constant exotropia managed?

A

SURGICAL

248
Q

What are the two possibilities for strabismus surgery?

A

Resection or recession

249
Q

In which patients are prisms used to treat strabismus?

A

Adults

250
Q

Which extraocular muscle has the closest and furthest insertions in relation to teh limbus?

A

Medial rectus has closest insertion to the limbus (5.5mm)

Superior rectus has furthest insertion from the limbus (7.7mm)

251
Q

What are antagonist-agonist and synergist muscles?

A

Antagonist-agonist muscles: Muscles in same eye that move the eye in different directions (e.g. right MR & right LR)

Synergist muscles: Muscles in the same eye that move the eye in the same direction (e.g. right IR & right SO)

252
Q

What are yolk muscles?

A

Muscles in different eyes that cause movement in the same direction (e.g. right LR and left MR) - both cause right gaze

253
Q

What is Hering’s law?

A

Yolk muscles involved in a particular direction of gaze receive equal and simultaneous flow of innervations

254
Q

What is Sherrington’s Law?

A

An increase in innervation of a muscle is accompanied by a decrease in innervation of its antagonist

255
Q

What is heterophoria?

A

Both eyes look straight but deviate on dissociation

Deviation of eye is normally hidden by the presence of fusion

It is revealed when fusion is broken e.g. during an alternating cover test

256
Q

What is duane retraction syndrome?

A

Rare congenital condition

Retraction of the globe on ADduction

Due to innervation of the LR muscle by CN3 rather than CN6

Associated with deafness and Goldenhar’s syndrome

257
Q

What is Brown syndrome?

A

Congenital / post trauma

Unilateral mechanical restriction of SO tendon

Leads to limited elevation on ADduction

Patients can’t look up and in
Some patients report a “click”

258
Q

How do you test visual acuity in infants up to 3 years (pre-verbal)?

A

Cardiff Acuity test / Cardiff cards

259
Q

How do you test visual acuity in children 18m to 4y (verbal)?

A

Kay Picture Tests

260
Q

How do you test visual acuity in children 4-5 years?

A

Keeler Crowded LogMAR test

261
Q

What is a retinoblastoma?

A

Malignant tumour of the retina - most common intraocular tumour of childhood + most sinister cause

262
Q

What is the genetic basis for retinoblastoma?

A

Loss of function of retinoblastoma tumour suppressor gene on chromosome 13

263
Q

How is retinoblastoma managed?

A

Mx: radioactive plaque or enucleation + adjuvant chemo

90-95% survival at 5 years with treatment

264
Q

What infection is congenital cataract associated with?

A

Rubella

265
Q

Which babies are most affected by retinopathy of prematurity?

A

Screen pre term babies (<30 weeks) + low birth weight (<1.5kg)

266
Q

What is the pathophysiology of retinopathy of prematurity?

A

Incomplete retinal vascularisation causes hypoxia

267
Q

What is seen in advanced case of retinopathy of prematurity?

A

Leukocoria seen in advanced cases due to a retinal detachment

268
Q

What is the management of retinopathy of prematurity?

A

ablation of avascular retina + laser

269
Q

How does a coloboma form?

A

Failure of choroidal fissure to close during embryological developmentmutation of PAX2 gene + also linked with foetal alcohol syndrome

Degree of visual impairment ranges from asymptomatic to significant loss of vision

White retinal reflex + severe amblyopia

270
Q

How is ptosis treated in children?

A

Require urgent frontalis suspension surgery (within 2-4 weeks) - Take part of fascia lata and insert it onto tarsal plate and frontalis muscle

271
Q

What is buphthalmos?

A

Buphthalmos is an enlargement of the eye and in children is a feature of congenital glaucoma

272
Q

What is the name of a congenital glaucoma?

A

Buphthalmos

273
Q

What is the definition of a congenital glaucoma / buphthalmos?

A

Corneal diameter > 12mm before 1 year

274
Q

What investigation is used for chlamydial conjunctivitis?

A

Giemsa stain

275
Q

What is the management of chlamydial conjunctivitis?

A

Erythromycin drops

276
Q

What is the management of gonococcal conjunctivitis?

A

IM / IV ceftriaxone

277
Q

What is the management of capillary haemangioma?

A

oral beta blockers

278
Q

What is congenital naso-lacrimal duct obstruction (Valve of Hanser)?

A

Tearing +/- conjunctivitis

Normally opens spontaneously by one year of age

If it does not open, can syringe and probe

279
Q

What is a limbal dermoid?

A

Benign congenital tumour often associated with eyelid coloboma or Goldenhar’s syndrome

280
Q

Why is a dermoid cyst?

A

Smooth round non-tender immobile lump on orbital rim

Gradually grows with risk of rupture

281
Q

What is a retinal haemorrhage associated with?

A

Cerebral haemorrhage

282
Q

What does higher pressures in the eye cause?

A

Higher pressures = mechanical damage (especially lamina cribosa). Local deformation results in axonal damage.

Remodelling & degeneration of neuronal glial cells (astrocytes, microglia) resulting in further atrophy of axons.

Disrupted axonal transport & atrophy of local cells results in rise in ROS and subsequent mitochondrial dysfunction.

283
Q

What is the definition of ocular hypertension?

A

Raised IOP (>21 mmHg) Open angles BUT, no optic neuropathy and visual field defect

284
Q

What is the cause of primary open angle glaucoma?

A

Progressive optic neuropathy with visual field loss.

Increased resistance to flow, resulting in an elevated lOP.

RF: M=F, age (>40), myopia, DM

3rd leading cause of blindness (worldwide).

285
Q

How does IOP cause neuronal death? (2 theories)

A
  1. Ischaemic (compromise in the microvasculature)
  2. Direct mechanical (force leads to neuronal apoptosis)
286
Q

What is Normal Tension Glaucoma (NTG)?

A

A variant of POAG - progressive optic neuropathy despite a normal or low lOP.

Systemic conditions (BP, migraines, vascular insult)

287
Q

What are the classic signs in normal tension glaucoma?

A
  • Optic disc cupping
  • Visual field defects
  • Peripapillary atrophy (usually focal - segments that are lighter)
  • Focal notching and thinning (segmental)
  • Drance haemorrhage
288
Q

What is acute angle closure glaucoma?

A

An ophthalmic emergency where the iris blocks the TM (primary, secondary if inflammatory)

289
Q

What is the pathophysiology of Acute Angle Closure Glaucoma (AACG)?

A

Primary due to physiological pupil block (e.g. stress, fatigue, change in room lighting)

This results in anterior lens surface obscuring aqueous flow posteriorly resulting in build up of pressure = iris bowing forward (bombé) = subsequent TM obstruction

Secondary = inflammatory

290
Q

What is the management of Acute Angle Closure Glaucoma (AACG)?

A

EMERGENCY - Peripheral iridotomy (PI)

In the meantime:
1. IV acetazolamide (then oral switch)
2. Topical anti-hypertensives (timolol 0.5%, iodipine 1%)
3. Cycloplegia (pilocarpine 2%)
4. Steroids (dexamethasone 1%) - If IOP remains high: IV mannitol 20%

291
Q

What is Inflammatory (uveitic) glaucoma?

A

Uveitis causes local inflammation (obstruction, cellular debris & trabeculitis) & leaky blood vessels (loss of blood-aqueous barrier).

292
Q

What causes inflammatory (uveitic) glaucoma?

A
  1. JIA
  2. Seronegative arthropathies (AS, Psoriatic, Reiter’s)
  3. Infectious (TB, syphilis, herpetic)
  4. Sarcoidosis
  5. Lens-induced (aphakic)
  6. Ocular disorders (Fuchs iridocyclitis)
293
Q

What are the classic signs of inflammatory (uveitic) glaucoma?

A
  • Synechiae (peripheral anterior)
  • Bulky ciliary bodies
  • Acute or chronic uveitis signs (nodules, perilimbal injections etc.)
  • Systemic signs
294
Q

How is Inflammatory (uveitic) glaucoma treated?

A

Treat the underlying cause of uveitis

Other treatments: oral anti-hypertensives, implantable steroids tenon corticosteroids

295
Q

What is rubeotic glaucoma?

A

Neovascularisation of the iris (rubeosis iridis). Known as 100 day glaucoma.

Due to proliferative DR or ischaemic insult (CRVO, CRAO, sickle cell crisis, carotid disease).

296
Q

What is the pathophysiology of rubeotic glaucoma?

A

Due to a process of neovascularisation, the iris starts to produce irregularlyshaped blood vessels. These are poorly formed and prone to leak. The AC may contain cells, flare or even hyphaema. The TM may contain irregular blood vessels as an extension from iris.

297
Q

What are the classic signs of rubeotic glaucoma?

A
  • Rubeosis iridis
  • Retinal pathology (diabetic retinopathy)
  • Neovascularisation of the trabecular meshwork
298
Q

How does traumatic glaucoma occur?

A

Blunt trauma is often well tolerated by the eye due to the 2 x humours, however, the more delicate structures (e.g. TM) are less resilient.

Blunt trauma results in a ‘coup-contrecoup injury’-like injury. There is expansion of fluid in the opposite end of injury. This sudden volume expansion (+ transmitted force) results in damage to TM, ciliary body & zonules.

Early onset: obstruction due to blood / pupil block
Late onset: tears, synechiae

299
Q

What are some possible signs seen in traumatic glaucoma?

A
300
Q

What is pseudoexfoliation syndrome?

A

Systemic condition due to abnormal protein synthesis that affects BM structure.

Filamentous, proteoglycans & aminoglycans are shed from lens ED, iris pigmented ED & non-pigmented ciliary body ED.

Pathological debris found in TM, as well as systemically (myocardium, lung, liver, etc).

301
Q

What are some of the classic signs seen in pseudoexfoliation syndrome?

A

Exfoliation flakes (AC)
Moth eaten (pupil, iris)
TM pigment
(Sampaolesi’s line)
Transilluminat ion defects (loss of iris shape)

302
Q

What is pigment dispersion syndrome?

A

Bilateral ocular condition when pigment rubs off the back of the iris (and ciliary body).

The classic triad consists of dense trabecular meshwork pigmentation, mid-peripheral iris transillumination defects, and pigment deposition on the posterior surface of the central cornea.

303
Q

What are 2 rare causes of glaucoma?

A

Pseudoexfoliation syndrome

Pigment dispersion syndrome

304
Q

Which type of glaucoma presents with NO iris bombe?

A

Malignant glaucoma

305
Q

What is malignant glaucoma?

A

Characterised by a shallow anterior chamber plus raised IOP, all despite treatment (iridotomy, glaucoma surgery).

306
Q

What is the normal range for cup:disc ratio (CDR)?

A

0-0.8

307
Q

How does one assess the optic nerve in clausoma?

A
308
Q

What are the two methods for measuring IOP?

A

Tonometry
Pachymetry

309
Q

What are the two methods of perimetry for testing visual fields?

A
310
Q

What is a gonioscope?

A

Gonioprisms are used to directly visualise the angle (Shaffer grading system).
Topical anaesthetic / topical lubricants required.

311
Q

What is OCT?

A

OCT uses light waves & can measure retinal nerve fibre layer (RNFL), optic nerve head (ONH) - including parameters such as disc, cup, and rim area measurements & other aspects of the retina.

312
Q

Which ocular anti-hypertensives decrease AQ vs. increase AQ outflow?

A
313
Q

What are the steps in medical management of glaucoma?

A
314
Q

What laser or surgical procedures can be used in management of glaucoma?

A

Selective laser trabeculoplasty (increased ciliary body drainage)

Trabeculectomy (small hole is created at sclera)

315
Q

How do cataracts present?

A

Change in vision: reduced VA, glare (halos around lights), difficulty seeing in dim light, monocular diplopia. Patient might have multiple changes in prescription.

Change in refraction: typically myopic shift

Change in fundal view: may have difficulty looking in’ before patient has difficulty ‘looking out’

316
Q

What is the structure of the lens?

A
317
Q

What are the 3 most common types of cataracts?

A
318
Q

How is a pre-operative cataract assessment done?

A
319
Q

How is the power of a lens calculated?

A
320
Q

Which drug can cause floppy eye syndrome, which can be a problem during cataract surgery?

A

Tamsulosin
Alpha-blocker

321
Q

What do the following terms mean:
1. Phakia
2. Pseudophakia
3. Aphakia

A
  1. Phakia: natural lens in situ
  2. Pseudophakia: cataract removed and IOL implanted
  3. Aphakia: cataract removed without IOL implanted
322
Q

What is a monofocal lens?

A

Monofocal e.g. toric lenses: Vision will be in focus at just one distance - either near, far, or intermediate distance. Toric lenses are particularly useful for correcting astigmatism. Patients may need to still wear glasses for reading (occasionally distance vision also)

323
Q

What is a significant intra-operative complication of cataract surgery?

A

Posterior capsule rupture
Mx: Vitrectomy

324
Q

What is the most common ACUTE post-op complication of cataract surgery?

A

Endophthalmitis (4-5 days after surgery) s.epdidermis,

325
Q

What is the most common SUB-ACUTE post-op complication of cataract surgery?

A

Cystoid macular oedema (6-8 weeks after)

Posterior capsule pacification (months to years) - image

Retinal Detachment (particularly if posterior capsule was breached)

Acute post-op complications:
Endophthalmitis (4-5 days after surgery) s.epdidermis,

326
Q

What is the refractive ability of the eye determined by?

A

Refractive properties of the cornea (43D) and natural lens (15D) (also includes aqueous and vitreous) .

Total refractive power of an emmetropic eye: 58D

327
Q

What may the refractive power in a myopic eye be?

A

Too great

More commonly due to a too long eyeball length

Duke Elder (AD) (6 decks)

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