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Ophthalmology Year 2 > Anatomy & physiology > Flashcards

Anatomy & physiology Flashcards

1
Q

Iris

A

The colored tissue at the front of the eye that contains the pupil in the center.

Theirishelps control the size of the pupil to let more or less light into the eye.

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2
Q

Limbus

A

Corneoscleral junction

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3
Q

Lacrimal gland

A

It continually releases fluid which cleanses and protects the eye’s surface as it lubricates and moistens it.

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4
Q

Sclera

A

The white layer of theeyethat covers most of the outside of theeyeball.

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5
Q

Conjunctival fornix

A

Is loose soft tissue lying at the junction between the palpebralconjunctiva(covering the inner surface of the eyelid) and the bulbarconjunctiva

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6
Q

Thelacrimal lake

A

Is the pool of tears in the lower conjunctival, which drains into the opening of the tear drainage system (the lacrimal punctum).

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7
Q

Inferior lacrimal papilla & punctum

A

Drainage system for lacrimal fluid

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8
Q

Cornea

A

Acts as the eye’s outermost lens. It functions like a window that controls and focuses the entry of light into the eye. Thecorneacontributes between 65- 75 percent of the eye’s total focusing power.

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9
Q

Conjunctiva

A

A loose connective tissue that covers the surface of the eyeball (bulbar conjunctiva) and reflects back upon itself to form the inner layer of the eyelid (palpebral conjunctiva)

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10
Q

What are the 3 layers of the eyes?

A

Fibrous - outer layer
Uvea (vascular layer) - middle layer
Retina (photosensitive) -inner layer

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11
Q

What are the 2 parts of the outer fibrous layer of the eyes?

A
  1. Sclera

2. Cornea

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12
Q

Cilliary body

A

Controls iris, shape of lens and secretion of aqueous humour.
Contains smooth muscle and blood vessels

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13
Q

Choroid

A

Nutrition and gas exchange

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14
Q

What are the 3 parts of the Uvea (vascular, middle) layer of the eyes?

A
  1. iris
  2. ciliary body
  3. choroid
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15
Q

What are the 2 eye segments?

A

Anterior and posterior

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16
Q

Anterior segment of the eyes

A

In front of lens (lens behind cornea) - Divided into:

  1. anterior chamber
  2. posterior chamber
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17
Q

Posterior segment of the eyes

A

Behind lens - makes up 2/3rds of eye

Contains vitreous body/humor

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18
Q

Vitreous body/humour

A

The clear gel that fills the space between the lens and the retina of the eyeball of humans

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19
Q

Anterior chamber of the eyes

A

Between cornea and iris

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20
Q

Posterior chamber of the eyes

A

Between iris and suspensory ligaments

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21
Q

Circulation of Aqueous

A
  1. Ciliary body produces Aqueous
  2. First goes to posterior chambers - nourishes lens
  3. Aqueous then passes through pupil
  4. Then into anterior chamber - nourishes cornea
  5. Aqueous reabsorbed into Canal of Schlemn
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22
Q

Canal of Schelmn

A

Aqueous reabsorbed into scleral venous sinus (Canal of Schlemm) at iridocorneal angle

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23
Q

Where is the Canal of Schelmn?

A

Iridocorneal angle

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24
Q

The arterial supply of the eyes

A

Provided by several branches from the ophthalmic artery, which is derived from the internal carotid artery in most mammals.

These branches include the central retinal artery, the short and long posterior ciliary arteries, and the anterior ciliary arteries.

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25
Q

The central vein of the retina

A

The only vein draining the retina

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26
Q

An end artery

A

An artery with insufficient anastomoses to maintain viability of the tissue supplied if arterial occlusion occurs

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27
Q

DANGER TRIANGLE of the face

A

Upper lip/external nose

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28
Q

Venous drainage of the eyes

A

Carried out by the superior and inferior ophthalmic veins. These drain into the cavernous sinus, a dural venous sinus in close proximity to the eye.

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29
Q

Theretina

A

Contains millions of light-sensitive cells (rods and cones) and other nerve cells that receive and organize visual information. Yourretinasends this information to your brain through your optic nerve, enabling you to see.

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30
Q

Fundoscopy

A

A procedure in which the back portion of the eye called the fundus is examined. Fundus includes the blood vessels that feed the eye, the retina, the optic disk, and the choroid.

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31
Q

Optic disc

A
  1. The circular area in the back of the inside of theeyewhere theopticnerve connects to the retina.
  2. Point of CN II formation
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32
Q

Blind spot

A

There are no photoreceptors in the optic disc - (hence the optic disc is the “blind spot”)

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33
Q

Macula

A

Part of the retina - greatest density of cones

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34
Q

Fovea

A

Centre of the macula - Depression of 1.5mm diameter

Area of most acute vision

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35
Q

Complete interruption retinal artery branch/retinal vein

A

Loss of an area of visual field corresponding to the area of ischaemia

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36
Q

Complete interruption of flow of the central artery (end artery) or vein

A

Monocular blindness

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37
Q

Lateral rectus

A 
Can only abduct eyeball
CN VI (Abducent)
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38
Q

Superior Rectus

A 
When in abduction, SR can only elevate
CN III (Oculomotor)
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39
Q

Inferior rectus

A 
When in abduction, IR can only depress
CN III (Oculomotor)
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40
Q

Medial rectus

A 
Can only adduct eyeball
CN III (Oculomotor)
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41
Q

Inferior oblique

A 
When in adduction, IO can only elevate
CN III (Oculomotor)
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42
Q

Superior oblique

A 
When in adduction, SO can only depress
CN IV (Trochlear)
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43
Q

How many extraocular muscles are there?

A

6

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44
Q

Levator palpebrae superioris

A

Small muscle of the superior orbit that elevates and retracts the upper eyelid.

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45
Q

A blowout fracture

A

A break in the floor or inner wall of the orbit or eye socket. A crack in the very thin bone that makes up these walls can pinch muscles and other structures around the eye, keeping the eyeball from moving properly.

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46
Q

The orbicularis oculi muscle

A

Is a muscle located in the eyelids. It is a sphincter muscle arranged in concentric bands around the upper and lower eyelids. The main function is to close the eyelids.

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47
Q

What cranial nerve innervates the orbicularis oculi muscle?

A

Temporal branch of the seventh cranial nerve (facial nerve)

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48
Q

Superior tarsus muscle

A

Known as Muller’s muscle, is a structural muscle which functions to maintain the elevation of the upper eyelid.

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49
Q

Superior tarsus muscle innervation

A

It receives innervation from the sympathetic nervous system and is unique in that it consists of thin fibers of the smooth muscle.

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50
Q

Location of lacrimal gland

A

Under eyebrows (lateral end of face)

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51
Q

Lacrimal gland innervation

A

The sensory innervation to the lacrimal gland is via the lacrimal nerve. This is a branch of the ophthalmic nerve (in turn derived from the trigeminal nerve).

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52
Q

What are the 3 branches of the trigeminal nerve?

A 
CN V1 (ophthalmic nerve) 
CN V2 (maxillary nerve) 
CN V3 (mandibular nerve)
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53
Q

What does the CN V1 (ophthalmic nerve) innervate?

A

Sensory innervation to the upper eyelid, cornea, lacrimal gland and conjunctiva

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54
Q

What does the CN V2 (maxillary nerve) innervate?

A

Sensory innervation to skin of the lower eyelid

and skin over the maxilla

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55
Q

What does the CN V3 (mandibular nerve) innervate?

A

Sensory innervation to skin over mandible and TMJ

except angle of mandible

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56
Q

Vestibulo-ocular reflex

A

Turns the eyes in the opposite direction to a head movement

Stabilises gaze on an object during head movement

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57
Q

Oculocardiac reflex

A

Reflex bradycardia in response to tension on extraocular muscles or pressure on eye

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58
Q

Sympathetic autonomic supply to the eyes

A

open eyes wider
get more light into eyes
emotional lacrimation

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59
Q

Parasympathetic autonomic supply to the eyes

A
  1. Get less light into eyes (to protect the retina from bright light or when asleep)
  2. focus on near objects
  3. Reflex lacrimation (to wash away the stimulant foreign body & clean the cornea)
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60
Q

Autonomic reflexes of eye

A

parasympathetics constrict the pupil - in bright light and “rest & digest”

sympathetic innervation dilates the pupil
- the sick patient

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61
Q

Suspensory ligament of lens

A

Suspensory ligament of lens connects the circumferences of the lens & the ciliary body

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62
Q

Basal tears

A

For corneal health
clean/nourish & hydrate the avascular cornea
contain lysozyme - hydrolyses bacterial cell walls

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63
Q

Reflex tears

A

Extra tears in response to mechanical or chemical stimulation

64
Q

What are the 3 types of tears?

A

basal tears
reflex tears
emotional tears

65
Q

Presbyopia

A

Eye has reduced ability to focus on near objects because of age

66
Q

Emmetropia

A

No refractive error

67
Q

Hypermetropia

A

Long sightedness (eye is smaller. Vision is corrected by converging lens) - Because the lens needs to cause the light to converge (come closer) before it hits the retina

68
Q

Myopia

A

Short-sightedness (eye is larger. Vision corrected by diverging lens)

69
Q

Astigmatism

A

Not a perfectly curved lens, leading to blurriness

70
Q

Cones

A

Color/day vision - are mostly packed in the fovea but still present in the periphery

71
Q

Rods

A

Black&white/night vision - are not in the fovea but packed in the periphery

72
Q

Intra-ocular pressure in the normal population

73
Q

Swinging light test

A

Rapid changes of light stimulation from one eye to the other. Both pupils should stay equally constricted

Light shining in one eye causes constriction of the pupil (direct response) and in the other eye (consensual response) so both eyes contract

74
Q

Miotics (drugs)

A

Constrict the pupil e.g. Pilocarpine

75
Q

Mydriatics (drugs)

A

Dilate the pupil e.g. Tropicamide, atropine

76
Q

Endopthalmitis

A

Infection of the entire eye

77
Q

Keratitis

A

Infection of the cornea (layer over the pupil/iris)

78
Q

Conjunctivitis

A

Infection of the conjunctiva (layer over the sclera)

79
Q

Causes of sudden visual loss

A 
Vascular occlusion/vitreous haemorrhage 
Age related macular degeneration (wet)
Retinal detachment
Ischaemic optic neuropathy
Closed angle glaucoma 
Optic neuritis
Stroke
Emergency referral
80
Q

Choriodal neovascularisation

A

New blood vessels grow under the retina

81
Q

Most common cause of blindness in the UK

A

Age-related macular degeneration

82
Q

Age related macular degeneration

A

Degeneration of the central retina (macula) is the key feature with changes usually bilateral.

ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen.

83
Q

Risk factors for ARMD

A 
Advancing age
Current smokers 
Family history for ARMD
Hypertension
Dyslipidaemia 
Diabetes
84
Q

What are the 2 forms of ARMD?

85
Q

Dry Age Related Macular Degeneration

A

> 90% of cases

> Characterised by drusen - yellow round spots in Bruch’s membrane

86
Q

Wet Age Related Macular Degeneration

A

> 10% of cases
Characterised by choroidal neovascularisation
Carries worst prognosis
Leakage of fluid and blood can result in a rapid loss of vision

87
Q

Symptoms of Wet ARMD

A

o Blurred central vision
o Diminished or changed colour perception
o Visual distortion (straight lines appear wavy or crooked)
o Visual hallucinations.

88
Q

Treatment for Wet ARMD

A
  1. Anti-VEGF (vascular endothelial growth factor) injection e.g. Ranibizumab
  2. Laser coagulation surgery.
89
Q

Metamophasia

A

Straight lines appear wavy or crooked

90
Q

Ranibizumab

A

Anti-VEGF (vascular endothelial growth factor) injection used in wet ARMD

91
Q

Investigations in ARMD

A
  1. Slit-lamp microscopy

2. Fluorescein angiography if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy.

92
Q

Why is there blurred central vision in wet ARMD?

A

Blind spot appears in the middle of your visual field. This tends to become larger over time as more and more rods and cones degenerate in the macula.

93
Q

Retinal detachment

A

Occurs when the neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium.

94
Q

Symptoms of retinal detachment

A

> 

Persistent flashing lights 
Floaters
Dark shadow in peripheral vision
RAPD
95
Q

Does retinal detachment cause permanent visual loss?

A

It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected. If left untreated and symptomatic, retinal detachment will inevitably lead to permanent visual loss.

96
Q

Causes of retinal detachment

A 
o	Myopia 
o	Previous detachment 
o	Family history 
o	Marfan’s syndrome 
o	Trauma
97
Q

Investigations for Retinal detachment

A

Any patients with new onset flashes and floaters should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage.

98
Q

Management for Retinal detachment

A

Surgery (to reattach the retina)

99
Q

Relative afferent pupillary defect (RAPD)

A

Sign observed during the swinging light test. The patient’s pupils constrict less when the light is shone into the affected eye, giving the appearance of dilatation as the light moves from eye to eye.

A normal response would be equal constriction of both pupils, regardless of which eye the light is directed against. In RAPD, light directed in the affected eye will cause only mild constriction of both pupils. While light in the unaffected eye will cause a normal constriction of both pupils.

100
Q

How is Relative afferent pupillary defect (RAPD) investiigated?

A

Swinging light test

101
Q

Central retinal artery occlusion (CRAO)

A

Causes sudden unilateral visual loss due to thromboembolism (from atherosclerosis) or arteritis of the central retinal artery

102
Q

Central retinal artery occlusion (CRAO) features

A

▪ Pale retina with “thread-like” vessels
▪ Cherry red spot at the fovea
▪ RAPD
▪ Greatly reduced visual acuity

103
Q

Risk factors for Central retinal artery occlusion (CRAO)

A
  1. Risk factors for stroke

2. History of amaurosis fugax

104
Q

Management of Central retinal artery occlusion (CRAO)

A
  1. Ocular massage (to convert from CRAO to BRAO)

2. ECG/echo/carotid Doppler to assess for embolus

105
Q

Central retinal vein occlusion

A

A blockage of this vein that causes the vein to leak blood and excess fluid into the retina. This fluid often collects in the macula causing blurred central vision.

106
Q

Features of Central retinal vein occlusion

A
  1. Unilateral, painless blurred vision
  2. Often occurs on waking
  3. Metamorphosia
107
Q

Risk factors for Central retinal vein occlusion

A

▪ Age
▪ Risk factors for stroke (as for CRAO)
▪ Raised intraocular pressure e.g glaucoma
▪ Polycythaemia

108
Q

Treatment for Central retinal vein occlusion

A
  1. Pan-retinal photocoagulation

2. Dexamethasone intravitreal implant

109
Q

What are the 2 types of CRVO?

A

Ischemic and non-ischemic

110
Q

Ischemic CRVO features

A 
>	Significantly decreased visual acuity
>	Widespread dot, blot and flame haemorrhages 
>	Optic disc oedema
>	Dilated, tortuous veins
>	RAPD
111
Q

Non-ischemic CRVO features

A

Retinal flame haemorrhages

Cotton wool spots

112
Q

What of the 2 types of CRVO is the most severe type?

A

Ischaemic CRVO is the more severe form of the disease. It may present initially as the ischemic type, or it may progress from the non-ischaemic. Patients may also end up with neovascular glaucoma and a painful blind eye.

113
Q

Closed angle glaucoma

A

Occurs when the iris bulges forward to narrow or block the drainage angle formed by the cornea and iris. As a result, fluid can’t circulate through the eye and pressure increases.

114
Q

Risk factors for Closed angle glaucoma

A

> hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age

115
Q

What are the causes of Closed angle glaucoma?

A
  1. Age
  2. Female
  3. Asian ethnicity
  4. Hypermetropia
  5. Drugs
116
Q

Drug causes of Closed angle glaucoma

A
  1. Nebulised ipratropium

2. Tricylclic antidepressents

117
Q

Symptoms of closed angle glaucoma

A 
>   severe pain: may be ocular or headache
>   decreased visual acuity
>   symptoms worse with mydriasis 
>   hard, red-eye
>   haloes around lights
>   semi-dilated non-reacting pupil
>   corneal oedema results in dull or hazy cornea
>   systemic upset may be seen
118
Q

Semi-dilated non-reacting pupil

A

Acute angle closure glaucoma

119
Q

Management of Acute angle closure glaucoma

A 
o	IV acetazolamide
o	IV mannitol
o	Topical anti-hypertensives
o	Topical steroids
o	Topical pilocarpine
120
Q

Acetazolamide

A

Stops aqueous production used in acute angle closure glaucoma

121
Q

Definitive management of Acute angle closure glaucoma

A

Laser peripheral iridotomy creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle

122
Q

Optic neuritis

A

Inflammation of the optic nerve

123
Q

Optic neuritis causes

A

o Multiple sclerosis
o Giant cell arteritis
o Diabetes
o SLE

124
Q

Features of Optic neuritis

A 
>   unilateral decrease in visual acuity 
>   poor discrimination of colours, 
>   'red desaturation'
>   pain worse on eye movement
>   RAPD
>   central scotoma
125
Q

Management of Optic neuritis

A
  1. high-dose steroids

2. recovery usually takes 4-6 weeks

126
Q

Causes of gradual vision loss

A 
●	Cataract
●	Age related macular degeneration (dry)
●	Refractive error
●	Diabetic neuropathy
●	Inherited diseases
●	Glaucoma (open angle)
●	Access to eye-clinic (Non-urgent)
127
Q

Cataracts

A

A common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision.

128
Q

Cause of cataracts

A 
Normal ageing process
Smoking
Increased alcohol consumption
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: hypocalcaemia
129
Q

Most common cause of cataracts

A

Normal ageing process

130
Q

Symptoms of cataracts

A

> Reduced vision
Faded colour vision
Glare: lights appear brighter than usual
Halos around lights

131
Q

Investigations in cataracts

A
  1. Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
  2. Slit-lamp examination. Findings: visible cataract
132
Q

Management in cataracts

A

Surgical (phacoemulsification of the lens with insertion of the intra-ocular lens)

133
Q

Causes of Dry ARMD

A
  1. Damage to the cells of the macula as a result of build-up of waste products called drusen
  2. Thickened retina
134
Q

Symptoms of Dry ARMD

A

> 

Blurring of central vision

> Can occur over 5-10 years

135
Q

Investigations for Dry ARMD

A

Amsler grid testing

Fundoscopy

136
Q

What is drusen?

A

Damage to the cells of the macula as a result of build-up of waste products called drusen - found in dry ARMD

137
Q

Management of Dry ARMD

A

Irreversible damage, so treatment is based on helping the person make the most of their remaining vision.

138
Q

Pathophysiology of diabetic retinopathy

A

Hyperglycaemia causes increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes

Endothelial dysfunction leads to increased vascular permeability. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia.

139
Q

What are the 3 classifications of diabetic retinopathy?

A
  1. Non-proliferative diabetic retinopathy (NPDR)
  2. Proliferative retinopathy (PDR)
  3. Maculopathy
140
Q

Proliferative diabetic retinopathy

A
  1. retinal neovascularisation - may lead to vitrous haemorrhage
  2. fibrous tissue forming anterior to retinal disc
  3. more common in Type I DM, 50% blind in 5 years
141
Q

Maculopathy

A
  1. based on location rather than severity,
  2. hard exudates and other changes on macula
  3. check visual acuity
  4. more common in Type II DM
142
Q

What are the 3 classifications of Non-proliferative diabetic retinopathy (NPDR)?

A
  1. Mild
  2. Moderate
  3. Severe
143
Q

Mild NPDR features

A

1 or more microaneurysm

144
Q

Moderate NPDR features

A 
>   microaneurysms
>   blot haemorrhages
>   hard exudates
>   cotton wool spots ('soft exudates' )
>   Venous beading/looping
145
Q

Severe NPDR features

A

> blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
Intravenous micro-vascular abnormalities in at least 1 quadrant

146
Q

Maculopathy management

A

If there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors

147
Q

Non-proliferative retinopathy management

A

> Regular observation

> If severe - panretinal laser photocoagulation

148
Q

Proliferative retinopathy management

A
  1. Laser photocoagulation
  2. Intravitreal VEGF inhibitors
  3. Severe/vitreous haemorrhage: vitreoretinal surgery
149
Q

Glaucoma (chronic open angle)

A

The angle in your eye where the iris meets the cornea is as wide and open as it should be, but the eye’s drainage canals become clogged over time, causing an increase in internal eye pressure and subsequent damage to the optic nerve.

150
Q

What are glaucomas?

A

Glaucomas are optic neuropathies associated with raised intraocular pressure (IOP). They can be classified based on whether the peripheral iris is covering the trabecular meshwork, which is important in the drainage of aqueous humour from the anterior chamber of the eye.

151
Q

Risk factors for Open angle glaucoma

A
  1. increasing age
  2. genetics
  3. Afro Caribbean ethnicity
  4. myopia
  5. hypertension
  6. diabetes mellitus
  7. corticosteroids
152
Q

What drugs can cause open angle glaucoma?

A

Corticosteroids

153
Q

Features of open angle glaucoma

A
  1. peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
  2. decreased visual acuity
  3. optic disc cupping
154
Q

Diagnosis of open angle glaucoma

A

o Tonometry
o Central corneal thickness
o Gonioscopy

155
Q

Treatment for open angle glaucoma

A
  1. first line: prostaglandin analogue eyedrops
  2. second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
  3. if more advanced: surgery or laser treatment can be tried
156
Q

Prostaglandin analogue

A

Increases the aqueous drainage

Ophthalmology Year 2 (2 decks)

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