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33 Cards in this Set

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Central Retinal Vein Occlusion
Defect: analogous to haemorrhagic stroke in brain
Onset: several days
Sxs: slowly progressing painless mild to profound visual dimming/blurring.
Signs: marked retinal vnous congestion/tortuosity, multiple blot, dot, linear retinal haemorrhages.
Assoc.: arterosclerotic retinopathy, ↑'d intracocular pressure, polycythaemia, hyperviscosity/coagubility.
Risks: neovascular glaucoma, retinal neovascularisation.
Acute Angle Glaucoma
True ophthalmic emergency
Defect: shallowing of ant. chamber, closure of ant. chamber angle, abrupt profund ↑ in intraocular pressure.
Sxs: profound progressive dimming/darkening of vision in eye. Severe pain/pressure sensation.
Signs: Red, congested eye, pupils dilated, poorly reactive to light.
Tx: anti-HTN, iridotomy.
Primary Open Angle Glaucoma
Defect: ↑intraocular pressure
Sxs: often asymptomatic. Slow bilat. loss of peripheral vision.
Signs: cup to disc ratio > 0.5.
Tx: Anti-glaucoma eyedrops, laser/metal surgery.
Microbial Corneal Infiltrates (Corneal ulcers)
Defect: infxn after corneal injuries or microbial conjunctivitis.
Sxs: painful
Signs: irregular white corneal lesions, intensely red eye, WBCs attracted to aqueous humour, layer out in anti. chamber to form hypopyon.
Tx: Ocular antibiotic drops.
Background Diabetic Retinopathy
Defect: Macular retinal oedema and progressive retinal capillary obliteration.
Sxs: progreesive loss of visual acuity.
Signs: tiny intraretinal red dots, "hard exudates", "cotton wool spots".
Tx: Focal laser therapy, intravitreal corticosteroid injection.
Proliferative Diabetic Retinopathy
Defect: Neovascularisation of the disc (NVD), which tend to be fragile and hemorrhage, obstructing vision. Proliferation of fibroblasts; vitreoretinal fibrovascular bands that contract to detach/distort retina.
Sxs: vision loss, blindness.
Tx: panrentinal photocoagulation, post. vitrectomy.
Hard exudate
Lipoproteinaceous intraretinal deposits, seen in Background Diabetic Retinopathy
Cotton Wool Spots
Ischaemic white spots of inner retina, seen in background diabetic retinopathy, vasospastic hypertensive retinopathy, arteriosclerotic hyptertensive retinopathy, and AIDS retinopathy.
Flame-Shaped Retinal Haemorrhage
Linear collexions of extravasated blood in the rential nerve fibre layer. Seen in Vasospastic and Arteriosclerotic HTN retinopathy.
Retinal Arterial Vasospasm
Marked ↓ of calibre and straightening of retinal arterioles. Primarily seen in vasospastic HTN retinopathy.
Elschnig Spots
Nummular patches of ischaemic outer retinal (pigment epithelial) clouding. Seen in vasospastic HTN retinopathy.
Vasopastic Hypertensive Retinopathy
Defect: acute systemic HTN.
Signs: cotton wool spots, flame-shaped retinal haemorrhages, retinal arterial vasospasm, Elschnig spots, exudative subretinal fluid in macula, intraretinal exudates, optic disc swelling (assoc. with HTN encephalopathy, poor prognosis)
Arteriiosclerotic Hypertensive Retinopathy
Defect: chronic HTN
Signs: ↑'d calibre/turtuosity of larger retinal arterioles, broadened light relfection along sclerotic arterioles, sclertotic clouding of arteriolar walls, venous nicking, flame-shaped retinal hemorrhage, cotton wool spots.
Venous Nicking
Compression of underyling rential veins, seen in Arteriosclerotic HTN retinopathy.
Combined Arteriosclerotic-Vasospastic Hypertensive Retinopathy
Development of vasospastic features superimposed on a prexisiting case of arteriosclerotic HTN retinopathy.
AIDS Retinopathy
Signs: cotton wool spots, which are not viral infiltrates, but Ag-Ab rxns. Occur in nearly 100% of pts. with HIV infxn.
Cytomegalovirus (CMV)
Class: Microbial Retinopathy in Immunosuppressed Pts.
Signs; 1+ broad, confluent white patches of necrotising retinitis with associated patches of extravasated intraretinal blood.
Retinal Detachment
Defect: separation of the outermost (retinal pigment epithelium) from the rest of the layers (sensory retina).
Process: mechanical tearing of the periphery when vitreous gelatin settles abruptly.
Age-related maculopathy
Defect: Age-related inability of the retinal pigment epithelium to fully digest photopigments. These accumulate as Drüsen, and build up as small droplets in Bruch's membrane.
die Drüsen
(German: glands)
Accumulations of un- or incompletely digested photochemical pigments from rods and cones. Appear as discrete or smudgy golden dots or globules deep to the retina. Tend to be concentrated in the macula. Seen in macular degeneration.
Dry Age-Related Maculopathy
Defect: Drüsen buildup, often assoc. with clumps of black macular pigment in early stages, central macular chorioretinal degeneration in late stages.
Onset: chronic, slow progression over course of years.
Tx: limited to oral antioxidants and zinc.
Wet Age-Related Maculopathy
Defect: choroidal neovascularisation; causes exudate of subretinal serosanguinous fluid, which becomes transformed into fibrotic disc/plate due to ingrowth of fibroblasts.
Sxs: abrupt onset, punctated progression of central vision loss.
Tx: focal laser photocoagulation, photodynamic therapy, intralesional injection of anti-VEGF, corticosteroids, submacular surgery, macular displacement.
Retinoblastoma
Defect: Malignant 1° intraocular neoplasm.
Sxs: leukocoria, strabismus, enlargement/clouding of cornea, eventual destruction of eye and metastasis.
Nonhereditary: usu. unilat. Tx: enucleation
Familial: bilat., autosomal dominant. Tx: chemo, then transcleral cryotherapy, laster, plaque radiation therapies.
Pseudotumour Cerebri
Defect: cause uncertain. ↑intracranial CSF pressure. Usu. affects obese, adolescent women.
Sxs: headaches, transient vision obscuration.
Signs: prominent swelling of optic disc, small brain ventricles.
Tx: CSF tap, drugs to reduce CSF production, CSF shunt.
Proptosis/Exophthalmos
Defect: ant. displacement of one or both eyes within the orbis.
Path: thyroid disease (thyroid eye disease), orbital tumours, inflammatory processes.
Sxs: if acute, eye appears congested and red.
CN III Palsy
Defect: CN III controls medial, sup., inf. rectus mm, sup. oblique, levator palpebrae sup., and sphincter mm.
Causes: Aneurysm of post. communicating art., enlarging neoplasm within cavernous sinus, or microvascular disease.
Sxs: ptosis, dilated pupils, nonreactive to consensual light, eye down and out, diplopia.
CN VI Palsy
Defect: CN VI controls the lat. rectus.
Causes: microvascular disease due to DM or HTN, neoplasm, demyelinating disease, aneurysm at base of brain.
Sxs: affect eye pulled in. Horisontal diplopia that's worse on attempted gaze into field of action of paretic mm.
Signs: frequ. face turn toward side with palsy to compensate.
Tx: usu. self-rresolves in 6-8 wks. if due to microvascular disease.
Horner's Syndrome
Defect: Interruption of sympathetic nn to the eye and face on one side.
Cause: Pancoast tumour (apex of lung) interrupt nn.
Sxs: ptosis, miosis, loss of facial sweating.
Ischaemic Optic Neuropathy in Giant Cell Arteritis
Defect: acute/subacute swelling of optic disc.
Cause: microcirculatory basis.
Sxs: profound dimming of vision, ↓visual acuity, Signs: Marcus Gunn pupil (relative afferent pupillary defect), oedematous/pale optic disc.
Tx: high dose corticosteroid.
Notes: usu. pts. 50+ age
Optic Neuritis in Multiple Sclerosis
Defect: MS; demyelination of CN II.
Sxs: ↓visual acuity, colour saturation. Dimming of vision, esp. peripheral.
Tx: Usu. self-limiting, resolves in 6-8 wks. High dose IV corticosteroid followed by po prednisone.
Notes: usu. pts. <30 age.
Myasthenia Gravis (ocular manifestations)
Defect: Type II autoimmune disease; Abs against ACh R. on mm fibres.
Path: extraocular mms particularly vulnerable.
Sxs: bilateral ptosis, diplopia, worse with exertion.
Notes: >50% pts. with ocular signs progress to systemic MG.
Cataract
Defect: clouding/opacification of the lens.
Sxs: progressive blurrin gof vision.
Signs: Red reflex contains dark spots or irregularities. Eventually, red reflex disappears when lens becomes completely opaque.
Tx: microsurgical replacement with inert polymeric lens. (IOL, intraocular lens)
Central Retinal Artery Occulsion (CRAO)
Defect: analogous to ischaemic stroke in brain.
Cause: atherosclerotic cartoid art. plaque, calcific cardiac valvular vegetations may provide source of embolus.
Sxs: sudden painless profound darkening of vision.
Sings: diffuse inner retinal cloudy swelling, marked attenuation of retinal arterioles and venules. Inner retinal neurones absent in the fovea. Embolus may be visible.
Tx: none available.