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Week 130 - Visual Disturbance > General Ophthalmology > Flashcards

General Ophthalmology Flashcards

0
Q

What is hypermetropia?

A

Long-sighted ness

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1
Q

What is myopia?

A

Short-sightedness

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2
Q

What is astigmatism?

A

Unevenly curved cornea causing a refractive error

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3
Q

What is presbyopia?

A

Age-related long-sightedness

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4
Q

What two structures of the eye are responsible for refracting light onto the retina?

A

Cornea and lens

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5
Q

What structure controls the concavity of the lens?

A

The ciliary body and zonules (ligaments)

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6
Q

Is the refractive error positive or negative for short-sightedness?

A

Positive

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8
Q

Why do Pancoast tumours cause the symptoms of ptosis, anhydrosis and miosis?

A

Due to disruption of the sympathetic fibres to the head and neck, including occulosympathetic fibres.

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9
Q

A patient presents with partial right-sided ptosis, a dilated right pupil with deviation of that eye inferiorly and laterally oriented. What is likely to be wrong?

A

Occulomotor nerve palsy (eye moves in direction of the one remaining intact muscle: the lateral rectus, not innervated by the occulomotor nerve)

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16
Q

Why might you want to x-ray a patient presenting with partial unilateral ptosis, miosis and anhydrosis?

A

Because you may need to rule out a more sinister cause for those symptoms such as a Pancoast tumour

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17
Q

What is the Edinger-Westphal nucleus and what does it supply?

A

It is the accessory parasympathetic nucleus of the oculomotor nerve (CN III). It supplies the constricting muscles of the iris and the ciliary muscles.

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18
Q

What is emmetropia?

A

Normal sight

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19
Q

What causes myopia (short-sightedness)?

A

The eye grows to become too long (front to back) which means the light doesn’t reach the retina so distant objects appear blurred.

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20
Q

What sort of sight are most babies born with?

A

Hyperopia. The eyes continue to grow and elongate until around the age of 8 years. Children before this point are able to accommodate to overcome this though (not possible with short-sightedness)

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21
Q

From what germ layer does the retina originate?

A

The ectoderm

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22
Q

The retina is considered an out-pouching of what organ?

A

The brain

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23
Q

How does aqueous humour drain from the anterior chamber to the circulating blood?

A

Via the trabecular meshwork and Canal of Schlemm

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24
Q

What are the 3 layers of the meninges (outside-in)?

A

Dura mater
Arachnoid
Pia mater

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25
Q

Which anatomical feature of the eye has the greatest number of pain receptors?

A

The choroid

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26
Q

Damage to the Canal of Schlemm can result in what?

A

Glaucoma

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27
Q

What is the emergency eye service in Wales called?

A

Rapid Access Clinic for Eyes (RACE)

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28
Q

How do you test visual acuity?

A

Using a Snellen chart or Logmar

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29
Q

How do you test eye movements?

A

Get patient to look at you finger / held object and keeping head still follow the object in an ‘H’ formation

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30
Q

How do you test visual fields?

A

First both eyes: wiggle finger individually at 10, 2, 4 & 8 o’clock then both together (10 & 2) and (4&8). Then cover one eye at a time: bring in a red tipped pin / pen from bottom and top diagonals starting out of peripheral vision. Test against your own peripheral vision.

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31
Q

What is acuity?

A

The ability to see fine detail

32
Q

When recording a Snellen result what do both the numerator (top number) and denominator (bottom number) represent?

A 
Numerator = distance from the chart in metres
Denominator = lowest line read
33
Q

What would testing VA with a pinhole do?

A

Correct refractive error

34
Q

What is the driving standard for Snellen results?

A

6/12

35
Q

What is considered normal visual acuity?

A

6/6 (Snellen) or 0.0 (LogMAR)

36
Q

How do you test for a relative afferent pupillary defect?

A

With the swinging light test

37
Q

How can a relative afferent pupillary defect (RAPD) be detected with the swinging light test?

A

In a normal swinging light test both pupils with constrict initially with light and then relax a little. With RAPD when shining the light in the affected eye both pupils dilate rather than constrict.

38
Q

What pathologies can be seen when assessing the red reflex?

A

Ocular media abnormalities: foreign bodies, cataract, haemorrhage, floaters
Retinoblastomas

39
Q

Why might a VDRL be performed in the case of sudden visual loss?

A

To test of syphilis (which can cause blindness)

40
Q

Why might you test for antinuclear antibodies in the instance if sudden visual loss?

A

To test for SLE (systemic lupus erythematosis) which can attack any bodily organ

41
Q

In the presence of light are rod cells switched on or off?

A

Off

42
Q

What does the phototransduction cascade achieve?

A

It is a series of molecular steps that result in turning off rod cells. In-so-doing informing other cells that light is present. These messages get converted into neural impulses to inform he brain

43
Q

Which type of cell is more sensitive to light - rods or cones?

A

Rods

44
Q

Where a rods most concentrated?

A

In the periphery of the retina

45
Q

Where are cones most concentrated?

A

Fovea / macula

46
Q

Which have slower absolute refactory periods rods or cones?

A

Rods (so it takes a long time for eyes to adjust to sudden dim light)

47
Q

What molecule in rhodopsin is altered by light contacting it?

A

Retinal

48
Q

When light changes retinal’s shape what occurs next?

A

The shape of rhodopsin changes too and binds to a molecule called transducin

49
Q

What does transducin do in the phototransduction cascade?

A

Its alpha unit binds to phosphodiesterase which inturn converts cGMP to GMP

50
Q

What impact does the reduction of cGMP have in the phototransduction cascade?

A

It closes Na+ channels on the rod cell causing hyperpolarisation therefore switching off the rod cell.

51
Q

Explain the final stage in the phototransduction cascade with regard to bipolar cells.

A

When a rod cell is switched off ‘ON-centre’ bipolar cells switch ON. They activate retinal ganglion cells which sends impulses down the optic nerve to allow brain to recognise that light is entering the eye.

52
Q

What does guanylate cyclase do?

A

Catalyses the conversion of GTP to cGMP

53
Q

What change does light manifest in retinal?

A

Changes it from 11-cis retinal to all-trans retinal

54
Q

What separates the alpha unit from transducin for it to bind to phosphdiesterase?

A

Activated opsin

55
Q

Which neurotransmitter it’s released in photoreceptor action potentials?

A

Glutamate (excitatory)

56
Q

What three types of cone cell are there? List in order of wavelength at which they are stimulated

A

Blue, green, red. Red = being the longest wavelength

57
Q

Deficiencies in production of what accounts for colour vision defects?

A

Opsins

58
Q

99% of red-green deficiencies are coded on which chromosome?

A

X (hence more common in men but still present in some women if both X chromosomes carry the fault)

59
Q

What is protanopia?

A

Red weakness

60
Q

What is deuteranopia?

A

Green weakness

61
Q

Which chromosome is associated with blue weakness and what is this weakness called?

A

Chromosome 7; tritanopia

Autosomal dominant, males = females, rare!

62
Q

What might you use to detect a colour deficiency in a patient?

A

Ishihara plates

63
Q

What is the 3rd and least abundant type of photoreceptor?

A

Retinal ganglion cell (2%)

64
Q

What do retinal ganglion cells contain?

A

Melanopsin (photopigment blue)

65
Q

How do RGCs project and what do they regulate?

A

Via retinohypothalamic tract - regulate melatonin production

66
Q

What is melatonin and where is it produced?

A

Hormone which regulates circadian rhythms and acts as an antioxidant (intracelluarly, protects DNA).
Produced in pineal gland, skin, retina, GIT

67
Q

Where in the brain is the primary visual cortex?

A

The occipital pole

68
Q

If a patient has a RAPD in their left eye where has the lesion occurred? Is this anterior or posterior to the chiasm?

A

The left optic nerve. Anterior to the chiasm

Week 130 - Visual Disturbance (3 decks)

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