Blue 2-4 Flashcards

(35 cards)

1
Q

What is seen on temporal artery biopsy in GCA

A

Intimal thickening of the blood vessels
Necoriss of part of arterial wall
Granulomas containing muli-nucleated giant cells

Halo sign on US - thickening of arterial wall

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2
Q

Diagnostic criteria for IID

A

NOrmal nuerological evaluation
Normal neurimagine without hydrocephalus or mass
Normal CSF constituents
PResence of papilloedema
Elevated CSF opening pressure during LP
More than 25 cm H2O in adults, 28 in children

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3
Q

What drugs are associated with IIH

A

STAIN LONG

Steroid withdrawal
Tetracyclines
Vitamin A retinoids
Indomethacin
Nitrofurantoin
Lithium
OCP
Nalidixic acid
Growth hormone

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4
Q

What is the course and prognosis of NAAION. Risk of recurrence? Risk of fellow eye?

A

Vision deteriorate over 2 weeks, stabilises by 2 months

Prognosis of affected eye is good - 50% will have final vision of 6/9 or better
25% have final vision of 6/60 or worse

15-40% of eyes will recover 3 Snellen

10-20% change of deterioration of vision of affected eye at 2 years

3-8% change of recurrence

15-25% risk in fellow eye over 5 years

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5
Q

Features of Adie tonic pupil

A

Dilated pupil with sluggish response to light and poor response to near

Vermiform movements of iris

ciliary ganglion/short ciliary nerve damage

Accommodation more likely to be spared

Females 3:1

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6
Q

What test to assess Horner’s

A

Topical cocaine 4% or 10%
Topical apraclonidine 0.5% or 1%

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7
Q

How does cocaine test for Horner’s work?

A

Cocaine blocks reuptake of norepinerprine at NMJ which dilates normal pupil - Horner’s pupil dilates poorly as little/no norepinephrine

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8
Q

How does apraclonidine test for horners work

A

Alpha 2 agonist - in normal patients causes pupil constriction
Weak alpha 1 agonist promotes pupil dilation

In pupil that has lost sympathetic innervation, the pupil dilator muscle develops super senistivty to alpha 1 dilation of apraclonidine so Horner’s pupil will dilate

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9
Q

What tumours cause CAR

A

Small cell lung cancer
Gynae
Breast

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10
Q

What cells are affected in CAR and MAR

A

CAR - Cones>Rods
MAR Rods<cones

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11
Q

What antibody is associated with CAR

A

Antirecoveris

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12
Q

What are symptoms of CAR

A

Photosensitivty
Photopsia
Glare
Reduced central vision
Reduced colour vision

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13
Q

What does CAR appear in later stages

A

RPE thinning, mottling
Mimics retinitis pigmentosa

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14
Q

What is seen on ERG in CAR? OCT?

A

Global retinal dysfunction with severely reduced photopic a and b waves

OCT shows severe macular atrophy
Loss of photoreceptors
and IS/OS junction

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15
Q

Hamartoma vs choristoma

A

Hamatoma - abnormal tissue normal location
Choristoma - normal tissue abnormal locationh

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16
Q

What is seen in tamoxifen reitnoapthy

A

White intraretinal crystals int eh macular or paramacular area with or without oedema

17
Q

What is myopic CNV

A

Small flat greying membrane that may have a hyperpigemented border if chornic or recurrent

3 stages
1 direct damage to photoreceptors
2 regression of CNV - formation of fibrous pigemented scar (Forster-Fuch’s spot)
2-atrophy around regressed CNV

18
Q

What is Forster-Fuchs spot?

A

Fibrous pigmented scar from regression of myopic CNV

19
Q

What trials for IVI in myopic CNV?

A

REPAIR RADIANCE

PRN regimens of ranibizumab

2-4 injections median required

20
Q

What is photodynamic therapy?

A

Vertrporfin is used
Causes release of free radicals when activated by laser energy

Reacts with blood vessel endothelial cell membranes to cause histamine, thromboxane, TNFa release

Anti-inflammatory response leads to vasoconstriction, thrombosis, staiss and hypoxia

TReats CSCR, Choroidal haemangioma, polypoidal choroidal vasculopathy

21
Q

What is treatment for MAcTel type 2

A

No treatment unless CNV (then anti-VEGF)

22
Q

What vitamin can cause CMO

A

Vitamin B3 (niacin/nicotinic acid)

Toxic effect on Muller cell resulting in intracellular oedema - no leakage on FFA

23
Q

Which TB drug can treat non-resolving CSCR

A

Rifamipicin - causes catabolism of endogenous steroids - increase in cyp450 catabolism

24
Q

What are vasoproliferative tumours

A

REtinal lesion that may be primary or secondary
May be unilateral/bilateral
Inferotemporal quadrant
Subreitnal exudation
Can be associated with ERM/CMO

25
Type 1 mactel
Congenital and unilateral Possibly coats variant
26
Type 2 mactel
Acquired and bilateral USually in middle aged/older Bialteral capillary abnormalities in perifoveal region Confocal blur reflectance - increased relfectance of blur light (488nm) due to loss of macular pigements and structural alteraction
27
DMO in pseudophakic patient with CMT < 400um
Dexamethasone IV implant
28
What are high risk findings in PDR
NVD over 1/3 disc area Any NVD with VH NVE >= 1/2 disc area with VH Or 3 or more of: VH/preretinal haem Active neovascularisation Location of NV on or within one disc diameter of disc NVD>1/3 or NVE > 1/2 of disc area
29
What is CSMO
Retinal thickening at or within 500um of fovea Hard exudates at or within 500um of the fovea with adjacent retinal thickening An area or areas of retinal thickening on disc area in size part of which one disc diamter of the fovea
30
What did ETDRS report
Timing of PRP in PDR and outcome of focal laser treatment in DMO
31
What did the DCCT report
Intensive blood sugar control reduced risk of developing DR by 76% in T1 diabetics
32
What is Stikler syndrome
CT disorder of fibrillar collagen associated with RD, congenital megalophthalmos, deafness, cleft palate, arthritis, joint hypermobility Commonest cause of RRD in children Mostly type 1 Autosomal dominant COL2A1
33
What collagen is vitreous
2, 9 ,11
34
What condisions can cause optic disc drusen
Calcified intra and extracellular deposits RP Pseudoxanthoma elasticum Angioid streaks Alport's
35
Causes of electronegative ERG (full field , bright flash in scotopic conditions)?
X linked retinoschisis CSNB CRAOCRVO MAR Bridshot Batten disease