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Billy Week 136 > Clinical > Flashcards

Clinical Flashcards

(48 cards)

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1
Q

AION symptoms

A 
Sudden- may wake up with it
Painless
RAPD
Severe visual loss - often altitudinal
Can be arteritic
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2
Q

Causes of RAPD

A

.

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3
Q

AION signs

A

Cotton wool spots (ischaemia)
Pale swollen optic disc
RAPD
Peri-papillary haemorages

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4
Q

AION investigations

A

Same day ophthalmology referral

Fundoscopy

Urgent bloods (CRP/ESR; if arthritic ESR may be >100)

Temporal biopsy if ?arteritic ( over 55 and severe, or raised CRP/ESR)

MRI brain if under 55 to rule out MS

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5
Q

AION management

A

If arteritic AION can’t be ruled out; high dose IV steroids then taper, followed by PO steroids for aorudn 2 years

Bisphosphonates, calcium, vitamin D if starting steroids

Consider anti-platelets

Manage other risk factors e.g. AF, DM, HTN

Also lipids, glucose, think risk factors

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6
Q

CRAO symptoms

A

Painless.
Acute; often wake up with it.
Can be severe visual loss.
Unilateral.

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7
Q

CRAO signs

A

Cupping of optic disc
Cherry red spot
Pale surrounding retina

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8
Q

CRAO investigations

A

Fundoscopy

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9
Q

CRAO management

A

Same day ophthalmology referral

Ocular massage to dislodge clot
Thrombolytics?

Reduce future risk factors:

  • DM/HTN/AF control
  • Exercise
  • Weight loss
  • Stop smoking
  • Reduce alcohol
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10
Q

RD symptoms

A

Can be acute or progressive.
Painless.
Unilateral.
Decreased VA.
Black curtain moving down or shadow moving in to centre.
Prior photopsia, cobwebs, floaters, shadows.

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11
Q

RD signs

A

Bulging retina with vessels (hill with paths).
RAPD.
Maybe associated tear.
Maybe associated PVD or VH.

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12
Q

RD investigations

A

Fundoscopy

Slit lamp exam (ophthalmologist)

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13
Q

RD management

A

Same day ophthalmology referral.

Laser/surgical retinopexy.

Laser/cryo repair of retinal tears.

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14
Q

RD description(s)

A

Detachment of retinal pigment epithelium from underlying neural retina

Can be rhegmatogenous (filled with fluid), non-rhegmatogenous (tractional) or non-rhegmatogenous (exudative).

Rhegma usually due to a pull on the retina.

Tractional usually due to neovascularisation (DR).

Exudative usually malignancy or inflammation.

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15
Q

AACG description

A

Acutely raised IOP due to blockage of outflow of aqueous humour through the iridocorneal junction (canal of schlemm). Often due to the iris bowing and pressing against and blocking the trabecular network.

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16
Q

AACG symptoms

A 
Acute.
Very painful.
N&V.
Red eye (ciliary flush).
Headache.
Hazy cornea.
Decreased VA.
Haloes around light.
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17
Q

AACG signs

A

Mid-dilated fixed pupil, often oval.

Hazy cornea.

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18
Q

AACG investigations

A

Gonioscopy - visualise occluded anterior chamber angle.

Tonometry - raised IOP (up to 20 = N)

Slit-lamp exam: shows shallow angle.

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19
Q

AACG management

A

Same day ophthalmology referral

PO/IV acetazolamide
TOP pilocarpine

Once under control:
- Laser or surgical iridotomy

Pain relief
Anti-emetics

Add in other IOP lowering drugs:

  • Beta blocker (timolol)
  • TOP CA inhibitor (dorzolamide)
  • PG analogue (bimatoprost, latanoprost)
  • Sympathomimetics (apraclonidine, brimonidine, phenylephrine)
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20
Q

ON symptoms

Study These Flashcards
A 
Hours to a week.
1. Painful; peri-orbital or ocular and worse on movement.
2. Dyschromatopsia.
3. Decreased VA.
Phosphenes.
Pulfrick's phenomenon.
Uthhoff's phenomenon.
RAPD.
Swollen optic disc.
Pale optic disc.
21
Q

ON investigations

Study These Flashcards
A

Fundoscopy:

  • swollen optic disc
  • RAPD
  • pale optic disc (been going on for a while)

MRI brain: to rule out white matter lesions (MS)

22
Q

ON management

Study These Flashcards
A

Same day ophthalmology referral.

May need neurology referral.

IV methylprednisolone: not routinely given; only if other eye is poor vision, need sight for job etc.

Pain relief.

23
Q

ON description

Study These Flashcards
A

Inflammatory, usually demyleinating process affecting optic nerve.

24
Q

VH description

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A

Haemorrhage into the potential spaces within or around vitreous body.

Can be haemorrhage of:

  • Normal vessels (e.g. tear in retina due to PVD, RD)
  • Abnormal vessels e.g. neovasc or CRVO
  • Adjacent structures (e.g. malignancy, choroid)
25
VH symptoms
Varies in severity: smaller bleeds may just cause some floaters and haziness and maybe red tint to vision, but can be complete loss of vision. ``` Often sudden. Painless. Decreased VA. Often preceding floaters, cobwebs, shadows. Hazy/smoky vision. Photopsia. Photophobia. Worse when lying down as blood settles at back. ```
26
VH signs
Diminished red reflex. | Red mist on fundoscopy.
27
VH investigations
Complete eye exam Fundoscopy / slit lamp: blood seen Ultrasound if slit lamp can't detect cause. Look for clues in contralateral eye: - Dot + blot -> DR - Drusen -> MD - Vein dilatation -> CRVO, HTN
28
VH management
Same day ophthalmology referral Treat AACG if it develps Patch to limit eye movement Elevate head of bed Follow up as O/P R/V any antiplatelets / anticoagulants
29
Phenylephrine MOA
Alpha adrenergic agonist Increase uveoscleral outflow of aqueous Decrease production of AH
30
Timolol MOA
Beta blocker Decrease production of AH
31
Acetazolamide MOA
CA inhibitor Decrease production of AH
32
Latanoprost MOA
PG analogue Increase uveoscleral outflow of AH by inducing metalloproteinase enzymes in ciliary body to break down ECM
33
Pilocarpine MOA
Parasympathomimetic Increase uveoscleral outflow of AH by contracitng ciliary muscle which tightens trabec network Also causes miosis by activating M3 receptors of pupillary sphincter muscles
34
AEs of timolol
Bradycardia | Bronchoconstriction
35
Contraindications of timolol
``` (Asthma) (COPD) Heart failure Bradycardia Heartblock ```
36
CA inhibitors AE
Acidosis Nausea Depression Superficial punctate keratitis
37
Pilocarpine AEs
Brow ache Myopia Decreased vision in low light
38
CRVO symptoms
``` Sudden - often wake up with it Painless Unilateral Loss of visual acuity May be severe ```
39
CRVO description
Veins are continuous with arteries, if they get blocked an ischaemic process begins which triggers vascular leakage which makes the whole thing worse. Causes include - thrombus (most common) - raised IOP causing compression - vessel disease (adj artery gets wider and compresses vein Around 25% become ischemic which is the worse sort
40
CRVO signs
Non-ischaemic: Mild RAPD Dot + blot haemorrhages Flame haemorrhages Ischaemic: Marked RAPD Worse haemorrhages widespread Cotton wool spots
41
CRVO investigations
Slit-lamp exam Tonometry (? neovascular glaucoma) FLUORESCEIN ANGIOGRAPHY: can visualise capillary filling!
42
CRVO management
Same day ophthalmology referral Manage raised IOP if that's the cause e.g. acetazolamide/dorzolamide + pilocarpine Intravitreal anti-vegf if neovasculariation is detected; needed around 6 weekly, regular checks Pan-retinal photocoagulation: also for neovasc; needed every few months
43
Possible complication of CRVO
Ischaemia causes VEGF release -> neovascularisation -> haemorrhage of new vessels, or glaucoma due to vessels growing into trabelcular network
44
PVD description
Vitreous membrane separates from the retina. Common in older adults; around 75% of over 65s. The vitreous membrane separates the VH from the retina. It can occur due to syneresis with ageing, and can pull on the retina and cause a retina tear or RD Increased risk of RD is greatest in first 6 weeks
45
PVD symptoms
``` No visual impairment. Painless. Floaters, cobwebs, shadows. Photopsia. Weiss ring. ```
46
PVD signs
Floaters. Weiss ring. Haemorrhage may be seen. Associated RD/VH may be seen.
47
PVD investigation
Indirect ophthalmoscopy and slit-lamp exam: - floaters - Weiss ring - Haemorrhage - RD - VH
48
PVD management
If new onset flashes or floates with visual field loss or signs of RD/VH, needs same day referral If new onset flashes or floaters but no visual field loss, 24 hour referral. No treatment, just treat tears with laser or cryotherapy. Educate on how to look out for RD/RT as high risk.

Billy Week 136 (1 decks)

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