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OPTO3003 > W10 Maculopathies and Hypertension > Flashcards

W10 Maculopathies and Hypertension Flashcards

1
Q

ERM description and presentation:

A

Fibrocellular, avascular proliferation of glial cells forming translucent sheet.
Presents decreased VA ~6/12

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2
Q

ERM signs and symptoms:

A

irregular light reflex on red-free photography
retinal striae > wrinkles > distorted BV
Macular pseudo holes, cystoid macula oedema, haemorrhages
Metamorphopsia

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2
Q

ERM progression

A

ERM contraction > retinal structure disruption > macula/vasculature distortion >
photoreceptor dislocation, local elevation, haemorrhages, retinal oedema

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3
Q

ERM patho:

A

Idiopathic: *PVD > ILM defects > triggering migration/proliferation of glial cells, and proliferation of hyalocytes remaining on ILM
Secondary: *Vit irritation(Sx) > proliferative vitreoretinopathy following liberation / proliferation of RPE and glial cells within vit cavity

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3
Q

ERM types:

A

Idiopathic: most common, u/>50y, 10% bilateral, 90% w/PVD
Secondary: u/retinal detachment Sx, then disease, trauma, vit. Inflammation, BRB loss

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4
Q

Macula hole stage 2:

A

Small full thickness hole
Desinence forms in ceiling of cystic cavity, pulled by vitreofoveolar attachment.
seperates partially or fully.
Almost always continues to stage 3

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4
Q

Macula hole secondary causes:

A

HT/Proliferative D. Retinopathy, ERM, cystoid macula oedema, rhegamatogenous RD, Best’s disease, ^myopia, Blunt trauma, ocular disease, BEST’s disease, vitreomacular traction syndrome

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4
Q

ERM management:

A

Mild (<6/12): monitor for spontaneous ERM seperation
Symptomatic / (>6/12): epiretinal peel w/vitrectomy
Trypan blue stain 0.15%, silicon oil/gas replacement
75% ^VA, 25% unchanged, 2% VA loss, 75% cataract in 2y
ERM can regrow

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4
Q

Macula hole description:

A

Full thickness loss of retina at central macula
Idiopathic occur in females 2:1, 65y, 10% bilateral

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5
Q

Macula hole patho:

A

Traction from persistent vitreoretinal attachment remining after PVD, or vit. Fluid motion forcing tangential traction on vitreoretinal interface.
Traction pulls Muller cell cone from foveal photoreceptors > cystic lesion > dehiscence of cystic cavity > centrifugal displacement of photoreceptors

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5
Q

Muller cell cone:

A

Central glial component at fovea, maintains orient and placement of retinal foveal components.

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6
Q

Macula hole Stage 1:

A

1a (impending): muller cone detaches from photoreceptor layer forming cystic cavity
Inner/outer retinal layers still intact
1b (occult): loss of foveal depression, displacement of outer retinal layers.
50% stage 1 holes resolve spontaneously

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7
Q

Macula hole stage 3:

A

Full sized macula hole
Vitreofoveolar traction Continues desinence into photoreceptor layer
Roof detachment forms pseudo-operculum
Pos. Hyaloid face may separate from retina (partial PVD)

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7
Q

Macula hole stage 4:

A

Full sized hole with complete PVD
Usually with noted Weiss ring, circle of condensed vitreous that was attached around ON

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8
Q

Symptoms of macula hole:

A

1: asymptomatic, slight metamorphopsia
2: decreased VA (6/15-6/120)
3: decreased VA (6/60-6/240)
Eccentric fixation can resolve better VA

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9
Q

Signs of macula hole:

A

1a: flat foveal depression
1b: yellow macula ring
2: retinal defect <400um, circle/oval/crescent shape
3: retinal defect >400um, red base with yellow/white dots surround by grey subretinal fluid and pseudo-operculum. May have noted pigmented demarcation line at edge of subretinal fluid cuff

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10
Q

Vitrectomy procedure:

A

Topical anaesthetic > subconj. Anaesthetic injection
Three incisions in sclera for fluid flow/instruments
PVD via pos. Hyaloid removal
Vit. Dissection > removal via aspiration
Tractional membrane removal w/ Trypan blur
Vit replaced via Perfluorocarbon liquid
Causes cataracts via vit. Ascorbate loss

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10
Q

Lamellar macula hole patho:

A

An aborted macula hole
Inner retinal layers lost from foveal PVD but outer photoreceptor layers retained
Continued progression unlikely as vitreofoveolar separation has completed

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10
Q

Lamellar macula hole signs/symptoms:

A

Asymptomatic (6/9)
Circular defect at inner retinal layer without thickening/cystic formation
Often with pseudo-operculum
Fluroescein angiography shows no abnormality

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11
Q

Macula pseudo hole patho:

A

Similar to full-thickness holes
No loss of retinal tissue, with normal foveal thickness
Formed by perifoveal retinal distortion secondary to epiretinal membrane or vitreomacular traction

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12
Q

Managing macula hole:

A

VA
Macula assessment on fundoscopy
Amsler grid > enlarged central spot / central metamorphopsia/scotoma
OCT
Regular monitoring 3-12mo > vitrectomy

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12
Q

Vitrectomy indications:

A

Other macula patho: epiret. Pucker, VMT
RD
Complications from ant. Seg. Sx (lens dislocation)
Trauma (haemorrhage)
D. Retinopathy (vit. Haem.)
Endophthalmitis / severe uveitis

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13
Q

CSR description:

A

Central Serous CHORIORETINOPATHY
Accumulation of fluid under retina and/or RPE, causing localised detachment of neurosensory retina and/or RPE

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14
Q

CSR patho:

A

*idiopathic
Abnormality in choroid/RPE > choroid BV dysfunction > fluid leakage/build-up under RPE > RPE function disruption > local BRB loss > pooling under retina > neurosensory detachment from RPE

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15
CSR risks:
Stress Corticosteroids Males 20-50yo Type A personality (competitive)
16
CSR symptoms:
Decreased VA 6/15, may improve with hyperopic refraction Metamorphopsia / central scotoma
17
CSR signs:
Amsler distortion OCT dome FFA shows sites to fluid pooling
17
CSR management:
Self resolves 95% in few months *rarely retains slight metamorphopsia Change lifestyle Chronic(5%)/recurrent(40%) require photodynamic therapy or anti-VEGF
18
HT discription:
Hypertension is elevated BP Stage 1: >140/90 mmHg 2: > 160/100 3: > 180/110 Malignant HT (1%): >200/140
19
HT stats:
%50 < 55, %60 < 65, 70% < 75 BP = cardaic output*peripheral resistance
20
HT risks:
^heart rate ^blood volume (renal retention) ^BV resistance (arteriosclerosis) Age, stress, smoking, obesity, physical inactivity
21
Essential HT causes:
Primary: most common, related to genes for renin-angiotensin system. Compounded by environment conditions (smoking, obesity, salt)
21
Pathophysiological changes in HT:
^BP > Arteriosclerosis/Arteriolosclerosis > lumen size loss / ^BV resistance ^BP > Atherosclerosis > atheromatous plaque in intima layer > thrombosis
21
Secondary HT causes:
5% from: Renal artery stenosis, kidney disease (^water retention > ^BP) Pheochromocytoma (adrenal gland tumour > ^nor/adrenaline > ^sympathetic activity > BV constriction / ^heart rate
21
Late stage atherosclerosis:
Plaque enlarges > narrow lumen / ^BV resistance > ^BP Plaque may rupture > leakage into blood > thrombosis > ^lumen occlusion Plaque/thrombus may separate > emboli in smaller BV downstream
22
Plaque formation in Atherosclerosis:
HT/DM/smoking/obesity > endo. Damage > ^vascular permeability > Leukocyte/lipid adhesion to endo > intima invasion > macro. Phagocytose lipoproteins > lipid-laden foam cells / inflammation > intima smooth muscle proliferation / ^ECM production > atheromatous plaque of leukocyte/lipid/ECM/smooth muscle
22
Hard exudates in HT:
Damaged endo./tight J. > plasma leak in retina > oedema Fluid "dries" > retained lipid/debris yellow hard exudate > phagocytosed by macro. Leakage usually self limiting > only hard exudate present on examination
22
Hypertensive retinopathy stages:
Vasoconstrictive Sclerotic Exudative Related conditions > HT choroidopathy, HT optic neuropathy
22
HT vasoconstrictive stage:
HT > Vasocon. Factors (angiotensin II, adrenaline, vasopressin) released > retinal BV ^vascular tone > ^arteriolar narrowing (norm 1:3 > HT 2:3 AV ratio) Vessels with arteriosclerosis show focal narrowing from loss of elasticity/immobility of hardened wall
23
HT exudative stage:
Late stage chronic HT > endo damage > BRB loss > Microaneurysms (outpouching wall > tight junction strain > leak/haemorrhage) Retinal/macula oedema/hard exudate Retinal haemorrhages Cotton wool spots
23
HT sclerotic stage:
Chronic ^BP > media BV layer hyperplasia > intima thickening / hyaline degeneration > ^BV attenuation ^BV tortuosity (focal change in wall hardening) ^arteriolar light reflex (copper>silver wiring) AV nipping (venous compression where AV share adventitial sheath)
23
Retinal haemorrhages in HT:
Flame: NFL, bright red, arcuate, pools between axons More common in HT than DM (BP in NFL arterioles) Dot/blot: OPL/NFL, small, dark red, round Damage to pre-venular capillaries, small from intraretinal compression Pre-retinal / sub-hyaloid: ILM-NFL / ILM-Vit. Hyaloid. Appear as D- / Boat- respectivley Associated with damaged superficial retinal arterioles
23
CWS:
Microvascular damage > NFL ischemia > NF swelling > adjacent NF compression > ^ischemia/swelling of axons Swollen axons disrupt spacing > altered refractive composition > visible spot
24
CRAO/BRAO presentation:
Sudden painless loss of vision, narrow/attenuated arteries Whitening of retina within hours (ion transport loss in ganglion axons > axonal oedema) Cherry red spot (lack of NFL w/pigmented compounds at fovea) Vision loss at fovea related to axonal ischemia preventing signals leaving eye Severe > RAPD
24
Hypertensive optic neuropathy:
^BV constriction > decreased blood flow in short posterior ciliary arteries > ON ischemia > nerve fibre swelling / axoplasmic stasis ^intracranial pressure (from HT) > ON compression > axoplasmic stasis / swelling Presents bilateral ON oedema Late stage > ON atrophy: ganglion cell death > glial proliferation > pale OD
24
Optometrist management HT retinopathy:
GP ref. Change diet/lifestyle (exercise/salt) Note acute/chronic signs: Acute (mac. Oedema/hard exudates/haem) indicate poor BP control > regime change Chronic (AV nip./metal wiring) will remain regardless of HT control
24
Hypertensive choroidopathy patho:
Rare, following severe acute ^BP, usually young adult Choroid BV without autoregulation HT > ^vasoconstrictive factors > ^^choroid BV constriction > BV/capillary narrowing/occlusion > RPE necrosis (pale patches under retina) > sub-retinal exudates > localised serous RD
24
Angiotensin receptor blockers in HT:
"candesartan" Inhibits AT2 from binding to AT2 type1 receptors > decreased adrenal gland activation > decreased vasoconstriction/water retention
24
Management of HT:
ACE inhibitors Angiotensin receptor blockers A1-adrenoreceptor antagonists B-blockers Calcium channel blockers Diuretics
24
Hypertensive choroidopathy signs:
Elshnig spots: well-demarcated yellow/white areas of RPE atrophy, later develops central pigmentation Sigrist streaks: hyperpigmented streaks overlying choroidal arteries
24
A1 adrenoreceptors antagonists in HT:
"prazosin" Binds a1 adrenoreceptors on vascular smooth muscle > prevents catecholamine-induced vasoconstriction > arterial dilation
24
ACE inhibitors in HT:
"Captopril" Inhibits angiotensin converting enzyme from converting angiotensin 1 to angiotensin 2 > decreased adrenal gland activation > decreased vasopressin/aldosterone release > reduced vasoconstriction/water retention
24
B-blockers in HT control:
"propanolol" Binds b1 receptors on heart > decreased cardiac output > decrease BP
24
C/B retinal artery occlusion from HT patho:
Atherosclerosis > BV plaque > seperation > emboli (contains cholesterol/CA) travel upstream > occlusion in central/branch artery
24
C/B retinal vein occlusion in HT:
Virchow's triad > clot(thrombus) in vein > blood flow blockage > ^vein pressure > ^tortuosity/thickening > vein ischemia (deoxygenated blood stasis) > leakage > "blood and thunder" blot/flame haemorrhages, exudates, oedema Causes sudden painless loss of vision
24
NAION from HT:
Non-arteritic anterior optic neuropathy HT > blood flow loss in short posterior ciliary arteries > ON ischemia > ganglion cell axon swelling > oedema > loss of visual signal transmission > sudden painless VA loss / colour loss (red desaturation) / RAPD Similar presentation to AAION (caused by autoimmune arteritis)
24
Ca channel blockers in HT control:
"verapamil" Binds Ca channels in heart and vasculature > intracellular Ca loss > decreased heart contractility/conduction > ^ vasodilation
24
Ocular conditions secondary to hypertension:
CRAO / BRAO CRVO / BRVO Non-arteritic anterior ischemic optic neuropathy (NAION) Stroke Diabetic retinopathy
24
Virchow's triad:
Endothelial injury Stasis Hypercoagulable stress AV nipping > turbulent flow of venous blood > endo. Wall damage / stasis > hypercoagulability / thrombosis formation
24
Stroke relation to HT:
Ischemic strokes most common cause from emboli/thrombosis in brain Loss of brain function > sudden painless VF loss (homonymous hemianopia) / CN palsy / EOM loss / visual processing loss
24
Diabetic retinopathy in relation to HT:
HT > increased risk of ocular complication from DM > increased development of D. Retinopathy/maculopathy HT control is now part of DM management

OPTO3003 (18 decks)

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