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DIABETIC RETINOPATHY It Refers to Retinal Changes Seen in Patients with Diabetes Mellitus

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DIABETIC RETINOPATHY It Refers to Retinal Changes Seen in Patients with Diabetes Mellitus Ophthalmology APPLIED ANATOMY for Glaucoma Pathophysiology of glaucoma revolves around the aqueous humour dynamics. The principal ocular structures concerned with it are - ciliary body, angle of anterior chamber and the aqueous outflow system. 1. Ciliary body It is the seat of aqueous production. 2. Angle of anterior chamber Angle of anterior chamber plays an important role in the process of aqueous drainage. It is formed by root of iris, anterior-most part of ciliary body, scleral spur,trabecular meshwork and Schwalbe’s line (prominent end of Descemet’s membrane of cornea] Clinically the angle structures canbevisualisedby gonioscopic examination 3. Aqueous outflow system It includes the trabecular meshwork, Schlemm’s canal, collector channels, aqueous veins and the episcleral veins 1. Trabecular meshwork. It is a sieve-like structure through which aqueous humour leaves the eye. It consists of three portions. I. Uveal meshwork. It is the innermost part of trabecular meshwork and extends from the iris root and ciliary body to the Schwalbe's line. The arrangement of uveal trabecular bands create openings of about 25 μm to 75 μm. SMCI www.mayursayta.com M 9104448555 Page 1 Ophthalmology II. Corneoscleral meshwork. It forms the larger middle portion which extends from the sclera spur to the lateral wall of the scleral sulcus. It consists of sheets of trabeculae that are perforated by elliptical openings which are smaller than those in the uveal meshwork (5 μ-50 μ). III. Juxta canalicular (endothelial) meshwork. It forms the outermost portion of meshwork and consists of a layer of connective tissue lined on either side by endothelium. This narrow part of trabeculum connects the corneoscleral meshworkwith Schlemm’s canal. In fact the outer endothelial layer of juxtacanalicular meshwork comprises the inner wall of Schlemm’s canal. This part of trabecular meshwork mainly offers the normal resistance to aqueous outflow. 2. Schlemm’s canal. This is an endothelial lined oval channel present circumferentially in the scleral sulcus. The endothelial cells of its inner wall are irregular,spindle-shaped and contain giant vacuoles. The outerwall of the canal is lined by smooth flat cells and contains the openings of collector channels. 3. Collector channels. These, also called intrascleralaqueous vessels, are about 25-35 in numberand leave the Schlemm’s canal terminate into episcleral veins. SMCI www.mayursayta.com M 9104448555 Page 2 Ophthalmology Que. GLAUCOMA Definition Glaucoma is a group of disorders characterized by a progressive optic neuropathy resulting in a characterstic appearance of the optic disc and a specific pattern of irreversible visual field defects that are associated frequently with raised intraocular pressure (IOP). Classification Clinico-etiologically glaucoma may be classified as follows: (A) Congenital and developmental glaucomas 1. Primary congenital glaucoma (without associated anomalies). 2. Developmental glaucoma (with associated anomalies). (B) Primary adult glaucomas 1. Primary open angle glaucomas (POAG) 2. Primary angle closure glaucoma (PACG) 3. Primary mixed mechanism glaucoma (C) Secondary glaucomas Maintenance of intraocular pressure The intraocular pressure (IOP) refers to the pressure exerted by intraocular fluids on the coats of the eyeball. The normal IOP varies between 10 and 21 mm of Hg (mean 16 ± 2.5 mm of Hg). The normal level of IOP is essentially maintained by a dynamic equilibrium between the formation and outflow of the aqueous humour. Various factors influencing intraocular pressure can be grouped as under: (A) Local factors 1. Rate of aqueous formation influences IOP levels. It depends on permeability of ciliary capillaries and osmotic pressure of the blood. 2. Resistance to aqueous outflow(drainage). Most of the resistance to aqueous outflow is at the level of trabecular meshwork. 3. Increased episcleral venous pressure may result in rise of IOP. The Valsalva manoeuvre causes temporary increase in episcleral venous pressure and rise in IOP. SMCI www.mayursayta.com M 9104448555 Page 3 Ophthalmology 4. Dilatation of pupil In patients with narrow anterior chamber angle may cause rise of IOPowing to a relative obstruction of the aqueous drainage by the iris. (B) General factors 1. Heredity. It influences IOP, possibly by multifactorial modes. 2. Age. - IOP increases after the age of 40 years, due to reduced facility of outflow. 3. Sex.IOP is equal between the sexes in ages 20- 40 years. In older age groups increase in IOP with age is greater in females. 4. Diurnal variation of IOP. Usually, there is a higher IOP in the morning and lower in the evening. This has been related to diurnal variation in the levels of plasma cortisol. Normal eyes have a smaller fluctuation (< 5 mm of Hg) than glaucomatous eyes (> 8 mm of Hg). 5. Postural variations. IOP increases whenchanging from the sitting to the supine position. 6. Blood pressure. As such it does not have longtermeffect on IOP. However, prevalence ofglaucoma is marginally more in hypertensivesthan the normotensives. 7. Osmotic pressure of blood. An increase in plasma osmolarit y is associated with a fall in IOP, while a reduction in plasma osmolarityis associated with a rise in IOP. 8. General anaesthetics and many other drugs also influence IOP alcohol lowers IOP, tobacco smoking, caffeine and steroids may cause rise inIOP. In addition there are many antiglaucomadrugs which lower IOP. PATHOGENESIS OF GLAUCOMATOUS OCULAR DAMAGE Pathogenesis of retinal ganglion cell death Retinal ganglion cell (RGC) death is initiated when some pathologic event blocks the transport of growth factors (neurotrophins) from the brain to the RGCs. The blockage of these neurotrophins initiate a damaging cascade, and the cell is unable to maintain its normal function. The RGCs losing their ability to maintain normal function undergo apoptosis and also trigger apoptosis of adjacent cells. SMCI www.mayursayta.com M 9104448555 Page 4 Ophthalmology Retinal ganglion cell death is associated with loss of retinal nerve fibres. As the loss of nerve fibres extends beyond the normal physiological limit, The characteristic optic disc changes and specific visual field defects become apparent over the time. Etiological factors A. Primary insults 1. Raised intraocular pressure (Mechanical theory). Raised intraocular pressure causes mechanical stretch on the lamina cribrosa leading to axonal deformation and ischaemia by altering capillary blood flow. 2. Pressure independent factors (Vascular insufficiency theory). Factors affecting vascular perfusion of optic nerve head in the absence of raised IOP produce normal tension glaucoma (NTG). Failure of autoregulatory mechanism of blood flow. Vasospasm is another mechanism affecting vascular perfusion of optic nerve head. Ex. Raynaud's phenomenon Systemic hypotension in patients with night time administration of antihypertensive drugs has low vascular perfusion of optic nerve head resulting in NTG. Other factors such as acute blood loss and abnormal coagulability profile have also been associated with NTG. B. Secondary insults (Excitotoxicity theory) Neuronal degeneration is done by toxic factors such as glutamate (excitatory toxin), oxygen free radicals, or nitric oxide which are released when RGCs undergo death due to primary insults. secondary insult leads to continued damage mediated apoptosis, even after the primary insult has been controlled. SMCI www.mayursayta.com M 9104448555 Page 5 Ophthalmology PRIMARY OPEN ANGLE GLAUCOMA It is a type of primary glaucoma, where there is no obvious systemic or ocular cause of rise in the intraocular pressure. It occurs in eyes with open angle of the anterior chamber. Primary open angle glaucoma (POAG) also known as chronic simple glaucoma of adult onset and is typically characterized by slowly progressive raised intraocular pressure (>21 mmHg recorded on at least a few occasions) associated with characteristic optic disc cupping and specific visual field defects. ETIOPATHOGENESIS (A) Predisposing and risk factors. Heredity - POAG has a polygenic inheritance. The approximate risk of getting disease is 10% in the siblings, and 4% in the offspring of patients with POAG. Age. The risk increases with increasing age. Mostly at 5th and 7th decades. Myopes are more predisposed than the normals. Diabetics have a higher prevalence of POAG than non-diabetics. Cigarette smoking is also thought to increase its risk. High blood pressure - prevalence of POAG is more in hypertensives than the normotensives. Thyrotoxicosis prevalence of POAG is more in patients suffering from Graves’ ophthalmic disease than the normals. Pathogenesis of rise in IOP. It is certain that rise in IOP occurs due to decrease in the aqueous outflow facility due to increased resistance to aqueous outflow It is caused by age-related thickening and sclerosis of the trabeculae and an absence of giant vacuoles in the cells lining the canal of Schlemm. CLINICAL FEATURES Symptoms 1. The disease is insidious and usually asymptomatic, until it has caused a significant loss of visual field. 2. Patients may experience mild headache and eyeache. 3. Patient may notice a defect in the visual field. 4. Reading and close work often present increasing difficulties owing to accommodative failure due to constant pressure on the ciliary muscle and its SMCI www.mayursayta.com M 9104448555 Page 6 Ophthalmology nerve supply. Patients usually complain of frequent changes in presbyopic glasses. 5. Patients
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