45 drug related retinopathies
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This document discusses three categories of drug-related retinopathies: 1) antimalarials such as hydroxychloroquine and chloroquine, 2) phenothiazines like chlorpromazine and thioridazine, and 3) crystalline maculopathies from tamoxifen and canthaxanthin. Antimalarials can cause bull's-eye maculopathy, with hydroxychloroquine posing a very small risk and chloroquine risking toxicity over 300g cumulative dose. Phenothiazines may cause plaque-like pigmentation or focal/diffuse loss of retinal pigment epithelium and choroid. Tamoxifen can deposit crystalline rings in the macula while canth
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Vortex keratopathy, characterized by whorl-like corneal epithelial deposits, can be caused by long-term use of antimalarial drugs like chloroquine and hydroxychloroquine. Amiodarone, used to treat arrhythmias, can also cause slowly reversible corneal deposits. Prolonged use of chlorpromazine above 500 mg daily is linked to irreversible corneal and lens deposits. Prolonged administration of medications containing silver or gold can lead to gray-brown or purple corneal deposits respectively, through argyrosis or chrysiasis.
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Toxic responses of the ocular and visual system
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Ocular side effects of systemic drugs
Many systemic drugs have reported
ocular and visual side effects that impact patient management.
It is important to be familiar with the associated side effects which can be mild and transient or may seriously threaten vision.
Glaucoma types, Pathogenesis, Diagnosis and Treatment
Glaucomas are ocular disorders characterized by changes in the optic nerve head (optic disk) and by loss of visual sensitivity and field.
There are two major types of glaucoma: open-angle glaucoma, which accounts for most cases and closed-angle glaucoma.
Ocular pharmacology ii, dr.kurinchi, 22.06.17
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Systemic drugs affecting cornea
Vortex keratopathy, characterized by whorl-like corneal epithelial deposits, can be caused by long-term use of antimalarial drugs like chloroquine and hydroxychloroquine. Amiodarone, used to treat arrhythmias, can also cause slowly reversible corneal deposits. Prolonged use of chlorpromazine above 500 mg daily is linked to irreversible corneal and lens deposits. Prolonged administration of medications containing silver or gold can lead to gray-brown or purple corneal deposits respectively, through argyrosis or chrysiasis.
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This document discusses various drug toxicities that can affect the posterior segment of the eye. It classifies toxicities into pigmentary retinopathies, crystalline retinopathies, retinal vasculopathies, retinal folds, and cystoid macular edema. Many drugs are described such as chloroquine, tamoxifen, gentamicin, and latanoprost that can cause retinal damage through mechanisms such as binding to melanin, forming intraretinal crystals, vascular effects, or disrupting the blood-retinal barrier. Symptoms vary but can include vision loss, with many toxicities being reversible upon drug cessation. Careful monitoring is important to detect and manage drug-induced retinal damage
Ocular side effects of systemic drugs
This document discusses the ocular side effects of various systemic drugs. It begins by explaining how drug molecules can reach ocular tissues through blood circulation. It then discusses three major drug accumulation sites - the cornea, lens, and vitreous. Specific drugs like chloroquine, amiodarone, and chlorpromazine are mentioned as examples of drugs that can cause corneal side effects like keratopathy. Steroids, chlorpromazine, and allopurinol are provided as examples of drugs that may cause lens side effects like cataracts. Finally, various drugs like antimalarials, phenothiazines, tamoxifen, and interferon-alpha are discussed in relation to potential retinal side effects they
Toxic responses of the ocular and visual system
This document provides an overview of toxic responses in the ocular and visual system. It discusses various sites in the eye that can be affected by toxicants including the cornea, lens, retina, optic nerve, and central visual system. Evaluation methods for ocular toxicity and visual function are also outlined, such as the Draize test and various ophthalmologic and electrophysiological techniques. The mechanisms of several toxicants that can damage different ocular tissues are then reviewed.
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Ocular side effects of systemic drugs
Many systemic drugs have reported
ocular and visual side effects that impact patient management.
It is important to be familiar with the associated side effects which can be mild and transient or may seriously threaten vision.
Glaucoma types, Pathogenesis, Diagnosis and Treatment
Glaucomas are ocular disorders characterized by changes in the optic nerve head (optic disk) and by loss of visual sensitivity and field.
There are two major types of glaucoma: open-angle glaucoma, which accounts for most cases and closed-angle glaucoma.
Ocular pharmacology ii, dr.kurinchi, 22.06.17
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This presentation emphasizes the importance of screening for chloroquine retinopathy according to new AAO guidelines. While bull's eye maculopathy is a classic late-stage sign, initial photoreceptor damage typically occurs parafoveally in Europeans and peripherally near the arcades in Asians. Screening tests like automated visual fields and SD-OCT can detect toxicity before visible RPE damage, as irreversible progression often occurs by the time bull's eye maculopathy appears. Risk of toxicity depends on daily dose, with very thin patients at increased risk when dose is based on ideal rather than actual weight.
Glaucoma 2011
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Glaucoma is a group of eye diseases that damage the optic nerve and can cause vision loss. It is usually caused by an increase in pressure within the eye due to blocked drainage canals. There are two main types - open angle glaucoma caused by partial blockage and closed angle glaucoma caused by sudden, complete blockage. Treatment aims to lower intraocular pressure through eye drops, oral medication, laser therapy or surgery depending on the severity. Surgical treatment is usually a last resort but is the primary approach for closed angle glaucoma emergencies. Post-operative care involves anti-inflammatory and antibiotic eyedrops.
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glaucoma slides
This document provides an overview of glaucoma, including risk factors, types, and treatment options. It discusses several key points:
- Glaucoma is the leading cause of blindness worldwide and causes permanent vision loss due to damage to retinal ganglion cells.
- Elevated intraocular pressure is a major risk factor, and treatment aims to lower pressure to preserve vision.
- Studies have shown patients whose pressure was consistently below 18 mmHg had little progression, while those over 18 mmHg at more visits faced greater risk of vision loss.
- Diurnal fluctuations in pressure are also correlated with visual field loss, so controlling pressure throughout the day is important.
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This document discusses various medical treatments for glaucoma, including topical eye drop medications from different drug classes. It describes the mechanisms of action, administration, efficacy and side effects of prostaglandin analogues, beta blockers, carbonic anhydrase inhibitors, alpha-2 agonists, miotics, osmotic agents, and some combination drug preparations. The document provides detailed information on commonly used glaucoma drugs to help clinicians select appropriate treatment options based on a patient's needs and risk factors.
Glaucoma ppt.
Glaucoma is an eye disease that is often associated with elevated intraocular pressure, in which damage to the eye (optic) nerve can lead to loss of vision and even blindness.
Glaucoma
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This document provides an overview of glaucoma, including its pathophysiology, types, diagnosis, and treatment. Glaucoma is an optic neuropathy characterized by optic nerve damage and visual field loss. It is traditionally associated with elevated intraocular pressure but can occur with normal pressure as well. The two main types are open-angle glaucoma, the most common, and closed-angle glaucoma, which has a sudden onset. Treatment involves medications, laser therapy, or surgery to lower intraocular pressure and prevent further nerve damage.
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Medical management of glaucoma
This document discusses the medical management of glaucoma. It covers principles of diagnosis and assessment, results of clinical trials on glaucoma treatment, pharmacokinetics of topical drugs, educating patients, follow up, and various classes of anti-glaucoma medications including cholinergic stimulants, beta-blockers, alpha-adrenergic receptor antagonists, prostaglandin analogs, and carbonic anhydrase inhibitors. Side effects and administration of these drug classes are also outlined.
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GLAUCOMA PPT
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Glaucoma is a progressive optic neuropathy caused by loss of retinal neurons and nerve fibers, resulting in blindness if left untreated. There is a dose-response relationship between intraocular pressure and risk of damage to the visual field. Types of glaucoma include primary (congenital, hereditary, adult), and secondary (inflammatory, traumatic, phacolytic). Treatment involves drugs that lower intraocular pressure such as cholinergic agonists, beta blockers, alpha agonists, prostaglandin analogues, and carbonic anhydrase inhibitors. Prostaglandins are often first choice drugs due to their efficacy and rare systemic side effects.
Glaucoma
This document provides information about glaucoma, including definitions, classifications, risk factors, clinical features, examination findings, and management strategies. It discusses primary open angle glaucoma as the most common type, which can cause progressive, painless vision loss if intraocular pressure is not controlled. It also covers primary angle closure glaucoma and congenital glaucoma. Surgical treatments like trabeculectomy may be used if medical therapy with eye drops is insufficient to stop disease progression. Early detection and treatment are important to prevent irreversible vision loss from this sight-threatening condition.
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one of my education lecture in ophthalmic hospital about glaucoma patho-physiology and management as illustrated in applied therapeutic 10th edition - clinical pharmacy department
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Glaucoma is a group of eye disorders that cause damage to the optic nerve, resulting in vision loss. It is typically associated with elevated pressure inside the eye (intraocular pressure). The two major types are open-angle glaucoma and narrow-angle glaucoma, referring to the drainage angle inside the eye. Most types cause no symptoms until noticeable vision loss occurs. Treatment involves lowering intraocular pressure through eye drops, laser treatment, or surgery depending on severity. Maintaining healthy lifestyle habits such as exercise, diet rich in vitamins and omega-3 fatty acids, and avoiding smoking may help reduce glaucoma risk.
Glaucoma 4 therapy of glaucomas, dr.k.n.jha,09.11.16
This document discusses the management of glaucomas. The key points covered are: the goals of glaucoma therapy which are to preserve vision by reducing intraocular pressure (IOP) with minimal side effects; medical therapies include eye drops that work by various mechanisms to lower IOP such as beta-blockers, parasympathomimetics, carbonic anhydrase inhibitors, and prostaglandin analogues; surgical options include trabeculectomy which creates a fistula to drain aqueous humor from the anterior chamber externally to lower IOP; complications of glaucoma treatments can include side effects of medications or issues following surgery like infection and hypotony.
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This presentation emphasizes the importance of screening for chloroquine retinopathy according to new AAO guidelines. While bull's eye maculopathy is a classic late-stage sign, initial photoreceptor damage typically occurs parafoveally in Europeans and peripherally near the arcades in Asians. Screening tests like automated visual fields and SD-OCT can detect toxicity before visible RPE damage, as irreversible progression often occurs by the time bull's eye maculopathy appears. Risk of toxicity depends on daily dose, with very thin patients at increased risk when dose is based on ideal rather than actual weight.
Glaucoma 2011
glaucoma diagnosis and treatment
prepared by Hardi Sdiq
university of sulaimani
college of pharmacy
Glaucoma - symptomes and treatment
Glaucoma is a group of eye diseases that damage the optic nerve and can cause vision loss. It is usually caused by an increase in pressure within the eye due to blocked drainage canals. There are two main types - open angle glaucoma caused by partial blockage and closed angle glaucoma caused by sudden, complete blockage. Treatment aims to lower intraocular pressure through eye drops, oral medication, laser therapy or surgery depending on the severity. Surgical treatment is usually a last resort but is the primary approach for closed angle glaucoma emergencies. Post-operative care involves anti-inflammatory and antibiotic eyedrops.
Medical treatment of primary open angle glaucoma
The document discusses goals and approaches for treating glaucoma. The primary goal is lowering intraocular pressure to reduce risk of vision loss. Medical approaches include various drug classes that decrease aqueous production or increase outflow, while surgical options are considered when pressure cannot be controlled through medical therapy alone. Follow-up care involves regular exams and testing to monitor pressure and disease stability.
Primary open angle glaucoma (poag)
Primary open angle glaucoma (POAG) is the most common type of glaucoma. It is characterized by an open anterior chamber angle, increased intraocular pressure (IOP), and glaucomatous optic nerve damage and visual field loss. Elevated IOP is the primary risk factor. Treatment involves medical therapy to lower IOP through various drug classes, laser trabeculoplasty to increase outflow, and surgeries like trabeculectomy or newer minimally invasive procedures if medication is insufficient. The goal is to lower IOP enough to prevent further optic nerve damage and vision loss.
glaucoma slides
This document provides an overview of glaucoma, including risk factors, types, and treatment options. It discusses several key points:
- Glaucoma is the leading cause of blindness worldwide and causes permanent vision loss due to damage to retinal ganglion cells.
- Elevated intraocular pressure is a major risk factor, and treatment aims to lower pressure to preserve vision.
- Studies have shown patients whose pressure was consistently below 18 mmHg had little progression, while those over 18 mmHg at more visits faced greater risk of vision loss.
- Diurnal fluctuations in pressure are also correlated with visual field loss, so controlling pressure throughout the day is important.
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This document discusses various medical treatments for glaucoma, including topical eye drop medications from different drug classes. It describes the mechanisms of action, administration, efficacy and side effects of prostaglandin analogues, beta blockers, carbonic anhydrase inhibitors, alpha-2 agonists, miotics, osmotic agents, and some combination drug preparations. The document provides detailed information on commonly used glaucoma drugs to help clinicians select appropriate treatment options based on a patient's needs and risk factors.
Glaucoma ppt.
Glaucoma is an eye disease that is often associated with elevated intraocular pressure, in which damage to the eye (optic) nerve can lead to loss of vision and even blindness.
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This document provides an overview of HEENT disorders therapeutics, focusing on glaucoma. It defines glaucoma and discusses the two main types: open-angle glaucoma and closed-angle glaucoma. For each type, it covers risk factors, pathophysiology, clinical presentation, diagnosis, and treatment goals and approaches. Treatment typically begins with medications to lower intraocular pressure and may progress to laser therapy or surgery if medication is not effective. The document provides detailed information on evaluating and managing both chronic open-angle glaucoma and acute angle-closure glaucoma.
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The document discusses various medical treatments for glaucoma, including different drug classes and their mechanisms of action, indications, contraindications and side effects. It provides detailed information on adrenergic agonists, beta-adrenergic antagonists, carbonic anhydrase inhibitors, and combined medications used to treat glaucoma. Key points covered include how the drugs work to lower intraocular pressure, when they should and should not be used, and common adverse effects.
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This document discusses the medical management of glaucoma. It covers principles of diagnosis and assessment, results of clinical trials on glaucoma treatment, pharmacokinetics of topical drugs, educating patients, follow up, and various classes of anti-glaucoma medications including cholinergic stimulants, beta-blockers, alpha-adrenergic receptor antagonists, prostaglandin analogs, and carbonic anhydrase inhibitors. Side effects and administration of these drug classes are also outlined.
Hyphema
This document discusses hyphema, which is blood in the anterior chamber of the eye. It defines hyphema and lists its potential causes such as trauma, medical conditions, and surgeries/medications. The document outlines methods for grading hyphema based on the amount of blood in the anterior chamber. It also discusses the clinical features, workup, potential complications like increased eye pressure, and treatment approaches like medical management with anti-inflammatory drugs and surgery if needed to prevent complications. The prognosis depends on factors like the severity of hyphema and any associated eye damage.
GLAUCOMA PPT
This presentation summarizes glaucoma, including its etiology, pathophysiology, classification, clinical manifestations, diagnosis, and treatment. Glaucoma refers to a group of eye disorders characterized by optic nerve damage and vision loss due to increased intraocular pressure. It is classified as primary open-angle glaucoma or primary angle-closure glaucoma. Clinical features may include loss of peripheral vision, optic nerve cupping, and visual field defects. Diagnosis involves measuring intraocular pressure, examining the anterior chamber angle and optic disc. Treatment options include non-pharmacological methods as well as topical eye drops to lower pressure such as beta-blockers, alpha-2 agonists, prostaglandins, and
Glaucoma
Glaucoma is a progressive optic neuropathy caused by loss of retinal neurons and nerve fibers, resulting in blindness if left untreated. There is a dose-response relationship between intraocular pressure and risk of damage to the visual field. Types of glaucoma include primary (congenital, hereditary, adult), and secondary (inflammatory, traumatic, phacolytic). Treatment involves drugs that lower intraocular pressure such as cholinergic agonists, beta blockers, alpha agonists, prostaglandin analogues, and carbonic anhydrase inhibitors. Prostaglandins are often first choice drugs due to their efficacy and rare systemic side effects.
Glaucoma
This document provides information about glaucoma, including definitions, classifications, risk factors, clinical features, examination findings, and management strategies. It discusses primary open angle glaucoma as the most common type, which can cause progressive, painless vision loss if intraocular pressure is not controlled. It also covers primary angle closure glaucoma and congenital glaucoma. Surgical treatments like trabeculectomy may be used if medical therapy with eye drops is insufficient to stop disease progression. Early detection and treatment are important to prevent irreversible vision loss from this sight-threatening condition.
Glaucoma
one of my education lecture in ophthalmic hospital about glaucoma patho-physiology and management as illustrated in applied therapeutic 10th edition - clinical pharmacy department
Glaucoma
Glaucoma is a group of eye disorders that cause damage to the optic nerve, resulting in vision loss. It is typically associated with elevated pressure inside the eye (intraocular pressure). The two major types are open-angle glaucoma and narrow-angle glaucoma, referring to the drainage angle inside the eye. Most types cause no symptoms until noticeable vision loss occurs. Treatment involves lowering intraocular pressure through eye drops, laser treatment, or surgery depending on severity. Maintaining healthy lifestyle habits such as exercise, diet rich in vitamins and omega-3 fatty acids, and avoiding smoking may help reduce glaucoma risk.
Glaucoma 4 therapy of glaucomas, dr.k.n.jha,09.11.16
This document discusses the management of glaucomas. The key points covered are: the goals of glaucoma therapy which are to preserve vision by reducing intraocular pressure (IOP) with minimal side effects; medical therapies include eye drops that work by various mechanisms to lower IOP such as beta-blockers, parasympathomimetics, carbonic anhydrase inhibitors, and prostaglandin analogues; surgical options include trabeculectomy which creates a fistula to drain aqueous humor from the anterior chamber externally to lower IOP; complications of glaucoma treatments can include side effects of medications or issues following surgery like infection and hypotony.
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This document discusses various electrophysiological tests used to objectively assess visual pathway function, including the electroretinogram (ERG), electrooculogram (EOG), and visually evoked potentials (VEP). It focuses on the ERG test, describing the basic principles, waveforms, responses, electrodes, and specialized forms (e.g. bright flash ERG, focal ERG, multifocal ERG, pattern ERG). Clinical uses include evaluating retinal diseases like diabetic retinopathy, retinal detachment, retinitis pigmentosa, and more. Abnormal ERG findings typically include reduced amplitude and delayed peak times, varying with the specific disease.
Electroretinography
This document discusses electroretinography (ERG), which measures the low voltage electrical activity of the retina. It provides a brief history of ERG and describes the different cellular components that contribute to the ERG waves. The document outlines ERG protocols, materials, and analysis methods. It discusses factors that can influence the ERG and clinical applications for evaluating retinal function and diseases.
ERG
This document discusses electroretinography (ERG), a technique for evaluating retinal function by recording electrical responses from the retina to light stimulation. It provides details on:
- The history and components of the ERG
- Procedure for performing ERG including electrode placement and light stimulation methods
- The different ERG waveforms and what parts of the retina they represent
- Clinical applications of ERG for evaluating various retinal diseases and conditions like retinitis pigmentosa, retinal toxicity, and more
- Limitations and sources of artifacts in ERG testing
Chloroquine
This document summarizes information about the anti-malarial drug chloroquine. It discusses chloroquine's classification as a 4-aminoquinoline, pharmacokinetics including rapid absorption and high tissue distribution, and mechanism of action in concentrating in the parasite's food vacuole and preventing heme polymerization. The document also briefly mentions chloroquine's pharmacological effects including its activity against various malaria parasites and infections. Common adverse effects include cardiovascular, CNS, and ocular toxicity with long term use. Chloroquine is used to treat malaria, giardiasis, and certain other infections and inflammatory conditions.
Electrofisiologia
El documento describe diferentes pruebas de electrofisiología ocular como el electrorretinograma (ERG) y el electrooculograma (EOG). El ERG mide los potenciales de acción de la retina en respuesta a la estimulación luminosa y separa la respuesta en ondas que reflejan la actividad de fotorreceptores, células bipolares y epitelio pigmentario. El EOG mide el potencial eléctrico entre la parte anterior y posterior del ojo para evaluar la función del epitelio pigmentario retinal.
Case presentation-Retinitis Pigmentosa Albecanse
A 21-year-old female presented with dimness of vision, more at night, for the past 12 months. On examination, her best corrected vision was 6/6 in the right eye and 6/9 in the left eye. Fundus examination revealed pale discs, attenuated vessels with periarteriolar sheathing, and numerous yellow-white scattered lesions and bony spicule pigmentary lesions in the peripheral retina of both eyes. The provisional diagnosis was retinitis punctata albescens with myopia.
case presentation on retinitis pigmentosa (low vision aid)
This document summarizes a case presentation for a 75-year-old female patient seeking low vision aids. She has a history of retinitis pigmentosa and diabetes. Her best corrected vision is 6/60 and 6/30. Low vision aids trialed included an Optima device for distance and a +8D spectacle magnifier for near. These devices, along with indicators and a flood light, were prescribed to help with mobility and reading tasks. Retinitis pigmentosa was discussed, which causes progressive vision loss starting with night blindness and constricting peripheral vision. Low vision aids like reverse telescopes and infrared scopes can help address tunnel vision and night blindness issues common in retinitis pigmentosa patients.
Optic neuritis
The document discusses optic neuritis, including its causes, symptoms, diagnosis, and treatment. Specifically, it notes that optic neuritis is characterized by loss of central vision, visual acuity, and color perception, along with an afferent pupil defect. It can be caused by conditions like multiple sclerosis, infections, granulomatous diseases, and others. Diagnosis involves visual field testing, color vision testing, and MRI imaging of the optic nerve. Treatment focuses on corticosteroids to reduce inflammation acutely and prevent future attacks.
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Management of psoriasis.pptx (Recent advances)
Psoriasis is an inflammatory skin disease that is associated with multiple comorbidities and substantially diminishes patients' quality of life. Topical therapies remain the cornerstone for treating mild psoriasis. Therapeutic advancements for moderate to severe plaque psoriasis include biologics that inhibit TNF-α, p40IL-12/23, IL-17, and p19IL-23, as well as an oral phosphodiesterase 4 inhibitor.
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Dermatology
This document provides information on various dermatological conditions including:
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41 principles retinal detachment surgery
This document outlines principles of retinal detachment surgery, including scleral buckling procedures, pneumatic retinopexy, and vitrectomy. Scleral buckling involves configuring scleral buckles, localizing retinal breaks, applying cryotherapy, and inserting an explant. Pneumatic retinopexy uses gas injection and postoperative positioning. Vitrectomy is used for giant retinal tears, proliferative vitreoretinopathy, and diabetic tractional retinal detachments to release traction and unfold retinal flaps. The causes and techniques addressed aim to reattach the retina and prevent early failure.
29 primary angle closure glaucoma
Intermittent angle-closure glaucoma occurs when the iris temporarily blocks the drainage angle, causing a spike in eye pressure. Acute congestive angle-closure glaucoma is a medical emergency characterized by a sudden, complete blockage of the drainage angle and severe symptoms. Treatment involves lowering eye pressure with medications, hyperosmotic agents, or YAG laser iridotomy. Post-congestive angle-closure glaucoma develops after an acute attack and is marked by iris and corneal changes. Chronic angle-closure glaucoma has similar visual field loss and optic nerve damage as open-angle glaucoma but the drainage angle is partially blocked.
26 ectopia lentis
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25 abnormal lens shape
This document discusses three abnormalities of lens shape: 1) Lenticonus, which is an axial bulge of the posterior or anterior lens that can be unilateral and sporadic or bilateral and familial/associated with Lowe syndrome. 2) Coloboma, which is a defect in the iris, choroid, or retina that can be associated with giant retinal tears. 3) A small lens, which can be microphakia with a small diameter or microspherophakia with a small spherical diameter, and may be familial or associated with Lowe or Weill-Marchesani syndrome.
23 congenital cataract
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20 corneal surgery
This document summarizes various corneal surgery procedures:
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2. Keratoprosthesis involves insertion of an artificial lenticule into the corneal stroma for patients with bilateral blindness from conditions like ocular pemphigoid.
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19 congen corneal anoms
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18 corneal ectasias
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17 corneal dystrophies
This document summarizes various types of corneal dystrophies:
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03 diffuse eyelid diseases
This document discusses various diffuse eyelid diseases categorized into allergic, infectious, and miscellaneous causes. Allergic causes include acute edema from insect bites or urticaria/angioedema, contact dermatitis from topical medications, and atopic dermatitis which is associated with asthma/hay fever and causes chronic itching/scratching. Infectious causes involve preseptal cellulitis from skin trauma/insects, herpes simplex causing vesicles/crusting, herpes zoster ophthalmicus causing painful vesicles/pustules, impetigo causing golden-yellow crusting, erysipelas causing acute spreading cellulitis, and necrotizing fasciitis causing
14 peri corn thin & ulcer
This document discusses various causes of peripheral corneal thinning and ulceration. It is divided into conditions that present without systemic disease such as dellen, Terrien marginal degeneration, and Mooren ulcer, and those associated with systemic diseases like rheumatoid arthritis, Wegener granulomatosis, and polyarteritis nodosa. For each condition, the document describes signs, causes, progression, and recommended treatments.
13 peripheral corneal inflam
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10 allergic conjunctivitis
This document discusses three types of allergic conjunctivitis: allergic rhinoconjunctivitis, vernal keratoconjunctivitis, and atopic keratoconjunctivitis. Allergic rhinoconjunctivitis involves a hypersensitivity reaction to airborne antigens and is associated with nasal and eyelid swelling. Vernal keratoconjunctivitis commonly affects children and males in warm climates and involves itching, discharge, and tearing, with papillae forming on the eyelids that can rupture and form giant papillae. Atopic keratoconjunctivitis typically affects young patients with atopic dermatitis and causes red, thickened, fissured eyelids, with
11 immunobullous diseases
This document discusses several immunobullous diseases:
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2) Stevens-Johnson syndrome is an acute, self-limiting disease typically affecting young men with oral and eye lesions that are often hemorrhagic and necrotic. Eye complications can include symblepharon.
3) Other diseases discussed include toxic epidermal necrolysis, epidermolysis bullosa, pemphigus vulgaris, and linear IgA bullous dermatosis
09 conjunctival infections
This document describes various infectious conjunctival diseases including bacterial, viral, and chlamydial causes. Bacterial conjunctivitis can be caused by simple bacteria or gonorrhea. Viral conjunctivitis can be caused by adenovirus, molluscum contagiosum, herpes simplex virus, or chlamydia. Adenoviral conjunctivitis may cause pharyngoconjunctival fever in children or epidemic keratoconjunctivitis in adults. Chlamydial conjunctivitis includes adult and neonatal forms as well as trachoma, a chronic infection caused by Chlamydia trachomatis. Each disease is characterized by signs and symptoms and discussed
08 infection lacrimal
1. The document discusses various infections of the lacrimal passages including congenital nasolacrimal duct obstruction, congenital dacryocele, chronic canaliculitis, and acute and chronic dacryocystitis.
2. Treatment for congenital nasolacrimal duct obstruction includes massage, antibiotic drops, and probing if no improvement by 12-18 months, with a 90% cure rate from first probing.
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45 drug related retinopathies
- 1. DRUG - RELATED RETINOPATHIES 1. Antimalarials • Chloroquine • Hydroxychloroquine 2. Phenothiazines 3. Crystalline maculopathies • Tamoxifen • Canthaxanthin • Chlopromazine • Thioridazine
- 2. Antimalarials Hydroxychloroquine - very small risk of toxicity Chloroquine - risk of toxicity with cumulative dose of 300 g VA - 6/18 to 6/24 Early bull’s eye maculopathy VA - CF End-stage VA - 6/36 to 6/60 Advanced bull’s eye maculopathy
- 3. FA of bull’s eye maculopathy Increased background choroidal fluorescence due to RPE window defect
- 4. Phenothiazines Chlorpromazine - very small risk of toxicity • Coarse, plaque-like pigmentation Thioridazine - risk of toxicity if daily dose exceeds 800 mg • Focal loss of RPE and choriocapillaris • Diffuse loss of RPE and choriocapillaris
- 5. Crystalline maculopathies Tamoxifen • Crystalline, ring-like macular deposits Canthaxanthin • Only with very high doses • May cause visual impairment • Glistening dots arranged in doughnut shape at posterior poles • Visually innocuous • If used over prolonged periods of time
- 6. Crystalline maculopathies Tamoxifen • Crystalline, ring-like macular deposits Canthaxanthin • Only with very high doses • May cause visual impairment • Glistening dots arranged in doughnut shape at posterior poles • Visually innocuous • If used over prolonged periods of time