W10 Maculopathies and Hypertension Flashcards
ERM description and presentation:
Fibrocellular, avascular proliferation of glial cells forming translucent sheet.
Presents decreased VA ~6/12
ERM signs and symptoms:
irregular light reflex on red-free photography
retinal striae > wrinkles > distorted BV
Macular pseudo holes, cystoid macula oedema, haemorrhages
Metamorphopsia
ERM progression
ERM contraction > retinal structure disruption > macula/vasculature distortion >
photoreceptor dislocation, local elevation, haemorrhages, retinal oedema
ERM patho:
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
ERM types:
Idiopathic: most common, u/>50y, 10% bilateral, 90% w/PVD
Secondary: u/retinal detachment Sx, then disease, trauma, vit. Inflammation, BRB loss
Macula hole stage 2:
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
Macula hole secondary causes:
HT/Proliferative D. Retinopathy, ERM, cystoid macula oedema, rhegamatogenous RD, Best’s disease, ^myopia, Blunt trauma, ocular disease, BEST’s disease, vitreomacular traction syndrome
ERM management:
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
Macula hole description:
Full thickness loss of retina at central macula
Idiopathic occur in females 2:1, 65y, 10% bilateral
Macula hole patho:
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
Muller cell cone:
Central glial component at fovea, maintains orient and placement of retinal foveal components.
Macula hole Stage 1:
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
Macula hole stage 3:
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)
Macula hole stage 4:
Full sized hole with complete PVD
Usually with noted Weiss ring, circle of condensed vitreous that was attached around ON
Symptoms of macula hole:
1: asymptomatic, slight metamorphopsia
2: decreased VA (6/15-6/120)
3: decreased VA (6/60-6/240)
Eccentric fixation can resolve better VA
Signs of macula hole:
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
Vitrectomy procedure:
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
Lamellar macula hole patho:
An aborted macula hole
Inner retinal layers lost from foveal PVD but outer photoreceptor layers retained
Continued progression unlikely as vitreofoveolar separation has completed
Lamellar macula hole signs/symptoms:
Asymptomatic (6/9)
Circular defect at inner retinal layer without thickening/cystic formation
Often with pseudo-operculum
Fluroescein angiography shows no abnormality
Macula pseudo hole patho:
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
Managing macula hole:
VA
Macula assessment on fundoscopy
Amsler grid > enlarged central spot / central metamorphopsia/scotoma
OCT
Regular monitoring 3-12mo > vitrectomy
Vitrectomy indications:
Other macula patho: epiret. Pucker, VMT
RD
Complications from ant. Seg. Sx (lens dislocation)
Trauma (haemorrhage)
D. Retinopathy (vit. Haem.)
Endophthalmitis / severe uveitis
CSR description:
Central Serous CHORIORETINOPATHY
Accumulation of fluid under retina and/or RPE, causing localised detachment of neurosensory retina and/or RPE
CSR patho:
*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
CSR risks:
Stress
Corticosteroids
Males 20-50yo
Type A personality (competitive)
CSR symptoms:
Decreased VA 6/15, may improve with hyperopic refraction
Metamorphopsia / central scotoma
CSR signs:
Amsler distortion
OCT dome
FFA shows sites to fluid pooling
CSR management:
Self resolves 95% in few months *rarely retains slight metamorphopsia
Change lifestyle
Chronic(5%)/recurrent(40%) require photodynamic therapy or anti-VEGF
HT discription:
Hypertension is elevated BP
Stage 1: >140/90 mmHg
2: > 160/100
3: > 180/110
Malignant HT (1%): >200/140
HT stats:
%50 < 55, %60 < 65, 70% < 75
BP = cardaic output*peripheral resistance
HT risks:
^heart rate
^blood volume (renal retention)
^BV resistance (arteriosclerosis)
Age, stress, smoking, obesity, physical inactivity
Essential HT causes:
Primary: most common, related to genes for renin-angiotensin system. Compounded by environment conditions (smoking, obesity, salt)
Pathophysiological changes in HT:
^BP > Arteriosclerosis/Arteriolosclerosis > lumen size loss / ^BV resistance
^BP > Atherosclerosis > atheromatous plaque in intima layer > thrombosis
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
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
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
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
Hypertensive retinopathy stages:
Vasoconstrictive
Sclerotic
Exudative
Related conditions > HT choroidopathy, HT optic neuropathy
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
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
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)
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
CWS:
Microvascular damage > NFL ischemia > NF swelling > adjacent NF compression > ^ischemia/swelling of axons
Swollen axons disrupt spacing > altered refractive composition > visible spot
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
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
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
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
Angiotensin receptor blockers in HT:
“candesartan”
Inhibits AT2 from binding to AT2 type1 receptors > decreased adrenal gland activation > decreased vasoconstriction/water retention
Management of HT:
ACE inhibitors
Angiotensin receptor blockers
A1-adrenoreceptor antagonists
B-blockers
Calcium channel blockers
Diuretics
Hypertensive choroidopathy signs:
Elshnig spots: well-demarcated yellow/white areas of RPE atrophy, later develops central pigmentation
Sigrist streaks: hyperpigmented streaks overlying choroidal arteries
A1 adrenoreceptors antagonists in HT:
“prazosin”
Binds a1 adrenoreceptors on vascular smooth muscle > prevents catecholamine-induced vasoconstriction > arterial dilation
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
B-blockers in HT control:
“propanolol”
Binds b1 receptors on heart > decreased cardiac output > decrease BP
C/B retinal artery occlusion from HT patho:
Atherosclerosis > BV plaque > seperation > emboli (contains cholesterol/CA) travel upstream > occlusion in central/branch artery
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
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)
Ca channel blockers in HT control:
“verapamil”
Binds Ca channels in heart and vasculature > intracellular Ca loss > decreased heart contractility/conduction > ^ vasodilation
Ocular conditions secondary to hypertension:
CRAO / BRAO
CRVO / BRVO
Non-arteritic anterior ischemic optic neuropathy (NAION)
Stroke
Diabetic retinopathy
Virchow’s triad:
Endothelial injury
Stasis
Hypercoagulable stress
AV nipping > turbulent flow of venous blood > endo. Wall damage / stasis > hypercoagulability / thrombosis formation
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
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
