Anatomy & physiology Flashcards
(156 cards)
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.
2
Q
Limbus
A
Corneoscleral junction
3
Q
Lacrimal gland
A
It continually releases fluid which cleanses and protects the eye’s surface as it lubricates and moistens it.
4
Q
Sclera
A
The white layer of theeyethat covers most of the outside of theeyeball.
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
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).
7
Q
Inferior lacrimal papilla & punctum
A
Drainage system for lacrimal fluid
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.
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)
10
Q
What are the 3 layers of the eyes?
A
Fibrous - outer layer
Uvea (vascular layer) - middle layer
Retina (photosensitive) -inner layer
11
Q
What are the 2 parts of the outer fibrous layer of the eyes?
A
- Sclera
2. Cornea
12
Q
Cilliary body
A
Controls iris, shape of lens and secretion of aqueous humour.
Contains smooth muscle and blood vessels
13
Q
Choroid
A
Nutrition and gas exchange
14
Q
What are the 3 parts of the Uvea (vascular, middle) layer of the eyes?
A
- iris
- ciliary body
- choroid
15
Q
What are the 2 eye segments?
A
Anterior and posterior
16
Q
Anterior segment of the eyes
A
In front of lens (lens behind cornea) - Divided into:
- anterior chamber
- posterior chamber
17
Q
Posterior segment of the eyes
A
Behind lens - makes up 2/3rds of eye
Contains vitreous body/humor
18
Q
Vitreous body/humour
A
The clear gel that fills the space between the lens and the retina of the eyeball of humans
19
Q
Anterior chamber of the eyes
A
Between cornea and iris
20
Q
Posterior chamber of the eyes
A
Between iris and suspensory ligaments
21
Q
Circulation of Aqueous
A
- Ciliary body produces Aqueous
- First goes to posterior chambers - nourishes lens
- Aqueous then passes through pupil
- Then into anterior chamber - nourishes cornea
- Aqueous reabsorbed into Canal of Schlemn
22
Q
Canal of Schelmn
A
Aqueous reabsorbed into scleral venous sinus (Canal of Schlemm) at iridocorneal angle
23
Q
Where is the Canal of Schelmn?
A
Iridocorneal angle
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.
25
The central vein of the retina
The only vein draining the retina
26
An end artery
An artery with insufficient anastomoses to maintain viability of the tissue supplied if arterial occlusion occurs
27
DANGER TRIANGLE of the face
Upper lip/external nose
28
Venous drainage of the eyes
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.
29
The retina
Contains millions of light-sensitive cells (rods and cones) and other nerve cells that receive and organize visual information. Your retina sends this information to your brain through your optic nerve, enabling you to see.
30
Fundoscopy
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.
31
Optic disc
1. The circular area in the back of the inside of the eye where the optic nerve connects to the retina.
2. Point of CN II formation
32
Blind spot
There are no photoreceptors in the optic disc - (hence the optic disc is the “blind spot”)
33
Macula
Part of the retina - greatest density of cones
34
Fovea
Centre of the macula - Depression of 1.5mm diameter
| Area of most acute vision
35
Complete interruption retinal artery branch/retinal vein
Loss of an area of visual field corresponding to the area of ischaemia
36
Complete interruption of flow of the central artery (end artery) or vein
Monocular blindness
37
Lateral rectus
```
Can only abduct eyeball
CN VI (Abducent)
```
38
Superior Rectus
```
When in abduction, SR can only elevate
CN III (Oculomotor)
```
39
Inferior rectus
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When in abduction, IR can only depress
CN III (Oculomotor)
```
40
Medial rectus
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Can only adduct eyeball
CN III (Oculomotor)
```
41
Inferior oblique
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When in adduction, IO can only elevate
CN III (Oculomotor)
```
42
Superior oblique
```
When in adduction, SO can only depress
CN IV (Trochlear)
```
43
How many extraocular muscles are there?
6
44
Levator palpebrae superioris
Small muscle of the superior orbit that elevates and retracts the upper eyelid.
45
A blowout fracture
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.
46
The orbicularis oculi muscle
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.
47
What cranial nerve innervates the orbicularis oculi muscle?
Temporal branch of the seventh cranial nerve (facial nerve)
48
Superior tarsus muscle
Known as Muller's muscle, is a structural muscle which functions to maintain the elevation of the upper eyelid.
49
Superior tarsus muscle innervation
It receives innervation from the sympathetic nervous system and is unique in that it consists of thin fibers of the smooth muscle.
50
Location of lacrimal gland
Under eyebrows (lateral end of face)
51
Lacrimal gland innervation
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).
52
What are the 3 branches of the trigeminal nerve?
```
CN V1 (ophthalmic nerve)
CN V2 (maxillary nerve)
CN V3 (mandibular nerve)
```
53
What does the CN V1 (ophthalmic nerve) innervate?
Sensory innervation to the upper eyelid, cornea, lacrimal gland and conjunctiva
54
What does the CN V2 (maxillary nerve) innervate?
Sensory innervation to skin of the lower eyelid
| and skin over the maxilla
55
What does the CN V3 (mandibular nerve) innervate?
Sensory innervation to skin over mandible and TMJ
| except angle of mandible
56
Vestibulo-ocular reflex
Turns the eyes in the opposite direction to a head movement
| Stabilises gaze on an object during head movement
57
Oculocardiac reflex
Reflex bradycardia in response to tension on extraocular muscles or pressure on eye
58
Sympathetic autonomic supply to the eyes
open eyes wider
get more light into eyes
emotional lacrimation
59
Parasympathetic autonomic supply to the eyes
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)
60
Autonomic reflexes of eye
parasympathetics constrict the pupil - in bright light and “rest & digest”
sympathetic innervation dilates the pupil
- the sick patient
61
Suspensory ligament of lens
Suspensory ligament of lens connects the circumferences of the lens & the ciliary body
62
Basal tears
For corneal health
clean/nourish & hydrate the avascular cornea
contain lysozyme - hydrolyses bacterial cell walls
63
Reflex tears
Extra tears in response to mechanical or chemical stimulation
64
What are the 3 types of tears?
basal tears
reflex tears
emotional tears
65
Presbyopia
Eye has reduced ability to focus on near objects because of age
66
Emmetropia
No refractive error
67
Hypermetropia
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
Myopia
Short-sightedness (eye is larger. Vision corrected by diverging lens)
69
Astigmatism
Not a perfectly curved lens, leading to blurriness
70
Cones
Color/day vision - are mostly packed in the fovea but still present in the periphery
71
Rods
Black&white/night vision - are not in the fovea but packed in the periphery
72
Intra-ocular pressure in the normal population
<21mmHg
73
Swinging light test
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
Miotics (drugs)
Constrict the pupil e.g. Pilocarpine
75
Mydriatics (drugs)
Dilate the pupil e.g. Tropicamide, atropine
76
Endopthalmitis
Infection of the entire eye
77
Keratitis
Infection of the cornea (layer over the pupil/iris)
78
Conjunctivitis
Infection of the conjunctiva (layer over the sclera)
79
Causes of sudden visual loss
```
Vascular occlusion/vitreous haemorrhage
Age related macular degeneration (wet)
Retinal detachment
Ischaemic optic neuropathy
Closed angle glaucoma
Optic neuritis
Stroke
Emergency referral
```
80
Choriodal neovascularisation
New blood vessels grow under the retina
81
Most common cause of blindness in the UK
Age-related macular degeneration
82
Age related macular degeneration
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
Risk factors for ARMD
```
Advancing age
Current smokers
Family history for ARMD
Hypertension
Dyslipidaemia
Diabetes
```
84
What are the 2 forms of ARMD?
Dry
| Wet
85
Dry Age Related Macular Degeneration
> 90% of cases
| > Characterised by drusen - yellow round spots in Bruch's membrane
86
Wet Age Related Macular Degeneration
> 10% of cases
> Characterised by choroidal neovascularisation
> Carries worst prognosis
> Leakage of fluid and blood can result in a rapid loss of vision
87
Symptoms of Wet ARMD
o Blurred central vision
o Diminished or changed colour perception
o Visual distortion (straight lines appear wavy or crooked)
o Visual hallucinations.
88
Treatment for Wet ARMD
1. Anti-VEGF (vascular endothelial growth factor) injection e.g. Ranibizumab
2. Laser coagulation surgery.
89
Metamophasia
Straight lines appear wavy or crooked
90
Ranibizumab
Anti-VEGF (vascular endothelial growth factor) injection used in wet ARMD
91
Investigations in ARMD
1. Slit-lamp microscopy
| 2. Fluorescein angiography if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy.
92
Why is there blurred central vision in wet ARMD?
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
Retinal detachment
Occurs when the neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium.
94
Symptoms of retinal detachment
> Persistent flashing lights
> Floaters
> Dark shadow in peripheral vision
> RAPD
95
Does retinal detachment cause permanent visual loss?
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
Causes of retinal detachment
```
o Myopia
o Previous detachment
o Family history
o Marfan’s syndrome
o Trauma
```
97
Investigations for Retinal detachment
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
Management for Retinal detachment
Surgery (to reattach the retina)
99
Relative afferent pupillary defect (RAPD)
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
How is Relative afferent pupillary defect (RAPD) investiigated?
Swinging light test
101
Central retinal artery occlusion (CRAO)
Causes sudden unilateral visual loss due to thromboembolism (from atherosclerosis) or arteritis of the central retinal artery
102
Central retinal artery occlusion (CRAO) features
▪ Pale retina with “thread-like” vessels
▪ Cherry red spot at the fovea
▪ RAPD
▪ Greatly reduced visual acuity
103
Risk factors for Central retinal artery occlusion (CRAO)
1. Risk factors for stroke
| 2. History of amaurosis fugax
104
Management of Central retinal artery occlusion (CRAO)
1. Ocular massage (to convert from CRAO to BRAO)
| 2. ECG/echo/carotid Doppler to assess for embolus
105
Central retinal vein occlusion
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
Features of Central retinal vein occlusion
1. Unilateral, painless blurred vision
2. Often occurs on waking
3. Metamorphosia
107
Risk factors for Central retinal vein occlusion
▪ Age
▪ Risk factors for stroke (as for CRAO)
▪ Raised intraocular pressure e.g glaucoma
▪ Polycythaemia
108
Treatment for Central retinal vein occlusion
1. Pan-retinal photocoagulation
| 2. Dexamethasone intravitreal implant
109
What are the 2 types of CRVO?
Ischemic and non-ischemic
110
Ischemic CRVO features
```
> Significantly decreased visual acuity
> Widespread dot, blot and flame haemorrhages
> Optic disc oedema
> Dilated, tortuous veins
> RAPD
```
111
Non-ischemic CRVO features
Retinal flame haemorrhages
| Cotton wool spots
112
What of the 2 types of CRVO is the most severe type?
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
Closed angle glaucoma
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
Risk factors for Closed angle glaucoma
> hypermetropia (long-sightedness)
> pupillary dilatation
> lens growth associated with age
115
What are the causes of Closed angle glaucoma?
1. Age
2. Female
3. Asian ethnicity
4. Hypermetropia
5. Drugs
116
Drug causes of Closed angle glaucoma
1. Nebulised ipratropium
| 2. Tricylclic antidepressents
117
Symptoms of closed angle glaucoma
```
> 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
Semi-dilated non-reacting pupil
Acute angle closure glaucoma
119
Management of Acute angle closure glaucoma
```
o IV acetazolamide
o IV mannitol
o Topical anti-hypertensives
o Topical steroids
o Topical pilocarpine
```
120
Acetazolamide
Stops aqueous production used in acute angle closure glaucoma
121
Definitive management of Acute angle closure glaucoma
Laser peripheral iridotomy creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle
122
Optic neuritis
Inflammation of the optic nerve
123
Optic neuritis causes
o Multiple sclerosis
o Giant cell arteritis
o Diabetes
o SLE
124
Features of Optic neuritis
```
> unilateral decrease in visual acuity
> poor discrimination of colours,
> 'red desaturation'
> pain worse on eye movement
> RAPD
> central scotoma
```
125
Management of Optic neuritis
1. high-dose steroids
| 2. recovery usually takes 4-6 weeks
126
Causes of gradual vision loss
```
● Cataract
● Age related macular degeneration (dry)
● Refractive error
● Diabetic neuropathy
● Inherited diseases
● Glaucoma (open angle)
● Access to eye-clinic (Non-urgent)
```
127
Cataracts
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
Cause of cataracts
```
Normal ageing process
Smoking
Increased alcohol consumption
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: hypocalcaemia
```
129
Most common cause of cataracts
Normal ageing process
130
Symptoms of cataracts
> Reduced vision
> Faded colour vision
> Glare: lights appear brighter than usual
> Halos around lights
131
Investigations in cataracts
1. Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
2. Slit-lamp examination. Findings: visible cataract
132
Management in cataracts
Surgical (phacoemulsification of the lens with insertion of the intra-ocular lens)
133
Causes of Dry ARMD
1. Damage to the cells of the macula as a result of build-up of waste products called drusen
2. Thickened retina
134
Symptoms of Dry ARMD
> Blurring of central vision
| > Can occur over 5-10 years
135
Investigations for Dry ARMD
Amsler grid testing
| Fundoscopy
136
What is drusen?
Damage to the cells of the macula as a result of build-up of waste products called drusen - found in dry ARMD
137
Management of Dry ARMD
Irreversible damage, so treatment is based on helping the person make the most of their remaining vision.
138
Pathophysiology of diabetic retinopathy
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
What are the 3 classifications of diabetic retinopathy?
1. Non-proliferative diabetic retinopathy (NPDR)
2. Proliferative retinopathy (PDR)
3. Maculopathy
140
Proliferative diabetic retinopathy
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
Maculopathy
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
What are the 3 classifications of Non-proliferative diabetic retinopathy (NPDR)?
1. Mild
2. Moderate
3. Severe
143
Mild NPDR features
1 or more microaneurysm
144
Moderate NPDR features
```
> microaneurysms
> blot haemorrhages
> hard exudates
> cotton wool spots ('soft exudates' )
> Venous beading/looping
```
145
Severe NPDR features
> blot haemorrhages and microaneurysms in 4 quadrants
> venous beading in at least 2 quadrants
> Intravenous micro-vascular abnormalities in at least 1 quadrant
146
Maculopathy management
If there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors
147
Non-proliferative retinopathy management
> Regular observation
| > If severe - panretinal laser photocoagulation
148
Proliferative retinopathy management
1. Laser photocoagulation
2. Intravitreal VEGF inhibitors
3. Severe/vitreous haemorrhage: vitreoretinal surgery
149
Glaucoma (chronic open angle)
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
What are glaucomas?
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
Risk factors for Open angle glaucoma
1. increasing age
2. genetics
3. Afro Caribbean ethnicity
4. myopia
5. hypertension
6. diabetes mellitus
7. corticosteroids
152
What drugs can cause open angle glaucoma?
Corticosteroids
153
Features of open angle glaucoma
1. peripheral visual field loss - nasal scotomas progressing to 'tunnel vision'
2. decreased visual acuity
3. optic disc cupping
154
Diagnosis of open angle glaucoma
o Tonometry
o Central corneal thickness
o Gonioscopy
155
Treatment for open angle glaucoma
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
Prostaglandin analogue
Increases the aqueous drainage
