Common Ophthalmology pathologies Flashcards
What are the features of glaucoma?
increased intraocular pressure in the eye causing optic nerve damage (Glaucomatous cupping of the optic disc) due to the impaired drainage of aqueous humour from the anterior chamber of the eye. This results in visual field loss that starts peripherally and progresses centrally. 30-40
Early Glaucoma is completely asymptomatic, however there are often changes in the peripheral (superior due to inferior nasal field nerve fiber loss) visual fields that are undetected by the patient. 30-40% nerve fibres can be lost before demonstrable visual defect, 90% before becoming symptomatic because of compensation by other eye/brain. Early changes in the optic disc= OVAL CUP (due to infarction of the nerve fibres causing expansion of the cup)
Intermediate Glaucoma enlarged cup but a return to a normal shape. Arcuate scotoma is the pattern of vision loss associated.
Advanced stage glaucoma cup=disc and ring scotoma pattern of vision loss (aka tunnel vision).
What are the causes of optic disc swelling. Describe their pathophysiology.
Papilloedema (bilateral) due to raised ICP e.g. due to tumour, haemorrhage,
optic neuritis (MS)
arteritic anterior ischaemic optic neuropathy
non-arteritic anterior ischemic optic neuropathy
malignant HT
What are the stages of Diabetic Retinopathy? Describe the features seen on Opthalmoscopy.
- Background/ Non-Proliferative: Early changes are observed but pt asymptomatic. Microaneuyrsms (focal dilatation of capillaries), haemorrhages (red): dot, blot, flame shaped, hard exudates (yellow-white) (distinct edges- leaked lipoproteins), cotton wool spots (greyish) due to focal areas of infarction of axons in the retina (indistinct edges), intraretinal microvascular abnormalities (IRMA).
Common after 8-10y of DM but may be mild-severe.
NO NEW VESSELS
In severe Non-proliferative, dark haemorrhages, beading/ loops of veins, and other IRMA. Will progress to Proliferative within 12/12. - Proliferative: Neovascularization (abnormal new blood vessels due to release of angiogenic growth factors) is the hallmark of this stage. Either NVD (of the disc) or NVE ( elsewhere except for disc). Pattern of these vessels- like seaweed/ ink in water (irreg branching). High risk of bleeds with due to the fragility of these endothelial buds that rupture easily causing pre-retinal/ vitreous haemorrhage. More common T1DM.
Late features: retinal fibrosis, traction retinal detachment, iris neovascularization – neovascular glaucoma due to growth of vessels in the angle.
What is the pathophysiology of Diabetic retinopathy?
- Hyperglycaemia which leads to altered Hb and resulting hypoxia of the retina (highly metabolically active neurones)
- Hypoxia results in changes in the blood vessels (capillaries, arterioles, venules) and cytoskeleton, “ultrastructural changes” such as:
- thickened Basement Memb of arterioles
- decreased mitochondria
- increased stickiness of platelets
- more rigid RBC - These changes in particular to the BM and the RBC lead to the formation of micro emboli occluding the microvasculature leading to further hypoxia and ischaemia.
- In the venous system, intramuscular pericytes die by apoptosis in clusters leading to sectional dilatation- saccular/ out-touching stagnating venous flow leading to leakage of the contents, retinal oedema and contributing to hypoxia. Macrophages engulf leaked plasma proteins forming hard exudates in the retina.
- Retina tries to respond to the hypoxia by opening parallel pre-existing channels of blood flow to divert past occlusions but these shunt vessels (IRMA) are not sufficient to provide relief therefore ultrastructural changes persist.
- Prolonged ischaemia results in the release of angiogenesis factors e.g. VEGF causing the retinal vascular bed to sprout abnormal vessels particularly veins.
- Diabetic Maculopathy can accompany background or proliferative retinopathy.
What are the RF for cataracts? How is cataracts treated?
- Ageing
- Trauma: blunt, sharp, XR, radiotherapy, chemical injuries, UV light
- DM
- Malnutrition
- F more than M
- Systemic steroids
- smoking
Extracapsular surgery using phacoemulsification + aspiration of the lens with maintenance of the posterior capsule to support implanted lens. Dexamethasone + gentamicin/ cefuroxime is used post-surgery to reduce risk of Refractory uveitis.
What is the ddx for acute red eye?
- Haemorrhage
2. Congestion on surface of eye which is generalised: ciliary/ conjunctival, or localised.
What are the two types of haemorrhage that may cause red eye?
- Subconjunctival: where posterior border of blood patch is visible. More common older patients, those on aspirin/ warfarin, foreign body, sometimes trauma. May shift in location due to gravity.
- Retrobulbar: this is blood accumulating behind the eye ball. The posterior border of the blood patch is not visible.
Signs: raised pressure (behind eye can compress Optic n), proptosis (like exophthalmos), reduced eye movement, dilated pupil (indicates optic n compromise). These last two signs indicate an emergency.
Common cause: iatrogenic, trauma, head injury/ fracture floor of orbit, bleeding disorders.
CAN CAUSE SUDDEN IRREVERSIBLE BLINDNESS
V homogenous red sclera but NOT congestion- no blood vessels visible, as though sclera has been dyed red. Even when patient moves the affected eye, no posterior border will be visible.
What are the generalised congestive causes of red eye?
Conjunctivitis: viral, bacterial, allergic Keratitis (cornea) Acute Glaucoma Iridocyclitis Uveitis (iris, ciliary body, choroid)
What are the localised congestive causes of red eye?
episcleritis (autoimmune). tender. common SLE, RA. No effect on site. Anti-inflamms either steroidal/ non-steroidal.
Scleritis- severe pain, localised pain.
phylctenular conjunctivitis
How do you differentiate circumcorneal and conjunctival congestion?
circumcorneal/ ciliary: dusky red, blood flow from limbus to fornix, vessels do not blanch with topical vasoconstrictors/ move with conjunctiva.
conjunctival: bright red (bc involves superficial vessels), blood flows from fornix to limbus (periphery to cornea), vessels blanch (go white!) with topical vasoconstrictors (phenylephrine) and move with the conjunctiva, more marked in the fornices (i.e. where conjunctiva reflect onto lids) and the periphery of the bulbar conjunctiva (i.e. where conjunctiva is covering sclera).
What are the features of Horner’s Syndrome? What is it caused by?
- Partial ptosis (disruption to muller’s/tarsal muscle which only lifts eyelid slightly whereas main lifter is levator palpebrae superioris which is supplied by CNIII)
- Anhydrosis
- Meiosis due to unopposed action sphincter papillae (ANAISOCORIA)
- Apparent enopthalmos
- If longstanding/ congenital heterochromia of irises
It is due to disruption of the sympathetic output to the eye and face. This disruption can be anywhere along the path of the output from the hypothalamus, along the spinal cord, through the cervical sympathetic chain, the sup cervical ganglion the path along the common carotid (ECA for sweat glands) and ICA and then via the different individual nerves to the eyelid and pupil.
Describe the types of Glaucoma?
Open angle 1° and 2°
Narrow angle 1° and 2°
Normal tension Glaucoma
OPEN 1°: idiopathic and most common type due to reduced drainage through trabecular meshwork. usually bilateral and slowly progressing (years).
Rarely seen before age 40.
OPEN 2°: caused by clogging of the trabecular meshwork. Pigment Dispersion syndrome- pigment cells of iris are shed when iris touches lens clogging meshwork. Pseudoexfoliation fibrous deposition from lens etc that occludes trabecular meshwork. Other causes: inflammatory (uveitis), neovascular (DM/ central retinal vein occlusion) retinal ischaemic causes release of vasoproliferative factors resulting in new vessels occluding the angle and therefore blocking outflow.
NARROW 1°: “wrong size” eye (small) long-sighted hypermetropic.
NARROW 2°: lens growth causes the lens to abut the iris.
What is raised intraocular pressure called? and how is it identified?
Ocular HT (provided no damage to the 0ptic nerve evident) Above 21 mmHg (provided cornea is of average thickness).
What normal process causes narrowing of the Angle of the anterior chamber?
Continued lens growth through life can sometimes causes the narrowing of the angle due to the pushing of the lens onto the iris.
What are the RF for Open Angle Glaucoma?
Increased Intra Ocular P Fhx African American Myopic DM
