Keratoconus is a non-inflammatory bilateral ectatic condition of the cornea that causes progressive thinning and conical protrusion. It typically starts during puberty and progresses slowly. Symptoms include irregular astigmatism and myopia. Signs include Fleischer's ring, Munson's sign, and irregular astigmatism on retinoscopy. Treatment options include glasses, rigid gas permeable contact lenses, INTACS, collagen cross-linking, and keratoplasty for later stages. Keratoglobus is a rare noninflammatory diffuse corneal ectasia present from birth. Lenticonus is a rare congenital anomaly of the crystalline lens characterized by a conical protrusion on the lens capsule.
Non-proliferative diabetic retinopathy (NPDR) is a complication of diabetes that causes progressive damage to the retinal blood vessels from high blood sugar levels. It has early stages where there are no symptoms, followed by blurred vision if untreated. Risk factors include the duration of diabetes and poor blood sugar control. As NPDR progresses, it can be classified from mild to severe based on findings like microaneurysms, hemorrhages, cotton-wool spots, and venous changes. Laser treatment may be used if the disease threatens vision. Maintaining good blood sugar control through diet, medication and regular eye exams can help prevent or delay vision loss from diabetic retinopathy.
This document provides an overview of central serous chorioretinopathy (CSC), including its pathogenesis, clinical presentation, diagnosis, course and treatment. CSC is characterized by a localized serous retinal detachment in the macula due to leakage of fluid from the choroid. It typically affects men ages 30-50 and can be associated with stress, corticosteroid use, hypertension and type A personality. Diagnosis is usually clinical but can be confirmed with fluorescein angiography showing characteristic leakage patterns or optical coherence tomography identifying subretinal fluid. While most cases resolve spontaneously, laser photocoagulation or photodynamic therapy may be used in persistent or recurrent cases to seal leaking sites and accelerate resolution.
This document discusses primary angle closure glaucoma (PACG), a type of glaucoma where the iris occludes the drainage angle of the eye, obstructing aqueous outflow. PACG is a leading cause of glaucoma worldwide and is particularly common in East Asian populations. It is classified based on the degree of iris occlusion and presence of optic nerve damage and vision loss. Risk factors include older age, female sex, Asian ethnicity, family history, hypermetropia, and shorter axial length. Symptoms include blurred vision, halos around lights, eye pain, and headache. Signs include elevated eye pressure, shallow anterior chamber, iris changes, and optic nerve damage. The document outlines methods for diagnosing
The document describes the embryology and anatomy of the eye lens. It discusses lens development from the optic vesicle and lens placode. Primary and secondary lens fibers develop from the lens vesicle. The lens nucleus changes from embryonic to fetal to infantile to adult. Dimensions and structures of the adult lens are provided, including the capsule, epithelium, fibers, and zonules. Biochemistry of the lens is covered, including proteins, water, electrolytes and metabolic pathways. Cataract formation and the role of glutathione are summarized. Accommodation mechanisms involving ciliary muscle constriction are briefly mentioned.
This document provides an overview of cataracts, including:
- Definitions and types of cataracts such as developmental, acquired, congenital, and secondary.
- Causes of cataracts including age, genetics, trauma, toxins, and medical conditions.
- Classification systems for cataracts based on location, shape, degree of opacity.
- Symptoms such as decreased vision and glare.
- Stages of cortical and nuclear cataracts.
- Secondary cataracts that develop due to underlying ocular diseases.
This document provides an overview of the anatomy and physiology of the human lens. It begins with a brief discussion of lens embryology, including the formation of the lens placode and vesicle. It then describes the microscopic structure of the adult lens, including the lens capsule, epithelium, and fibers. Key aspects of lens molecular biology are summarized, such as the predominant crystallin proteins and role of water. The document also reviews lens metabolism, with glucose being the primary energy source broken down via the glycolytic and sorbitol pathways.
Keratoconus is a non-inflammatory bilateral ectatic condition of the cornea that causes progressive thinning and conical protrusion. It typically starts during puberty and progresses slowly. Symptoms include irregular astigmatism and myopia. Signs include Fleischer's ring, Munson's sign, and irregular astigmatism on retinoscopy. Treatment options include glasses, rigid gas permeable contact lenses, INTACS, collagen cross-linking, and keratoplasty for later stages. Keratoglobus is a rare noninflammatory diffuse corneal ectasia present from birth. Lenticonus is a rare congenital anomaly of the crystalline lens characterized by a conical protrusion on the lens capsule.
Non-proliferative diabetic retinopathy (NPDR) is a complication of diabetes that causes progressive damage to the retinal blood vessels from high blood sugar levels. It has early stages where there are no symptoms, followed by blurred vision if untreated. Risk factors include the duration of diabetes and poor blood sugar control. As NPDR progresses, it can be classified from mild to severe based on findings like microaneurysms, hemorrhages, cotton-wool spots, and venous changes. Laser treatment may be used if the disease threatens vision. Maintaining good blood sugar control through diet, medication and regular eye exams can help prevent or delay vision loss from diabetic retinopathy.
This document provides an overview of central serous chorioretinopathy (CSC), including its pathogenesis, clinical presentation, diagnosis, course and treatment. CSC is characterized by a localized serous retinal detachment in the macula due to leakage of fluid from the choroid. It typically affects men ages 30-50 and can be associated with stress, corticosteroid use, hypertension and type A personality. Diagnosis is usually clinical but can be confirmed with fluorescein angiography showing characteristic leakage patterns or optical coherence tomography identifying subretinal fluid. While most cases resolve spontaneously, laser photocoagulation or photodynamic therapy may be used in persistent or recurrent cases to seal leaking sites and accelerate resolution.
This document discusses primary angle closure glaucoma (PACG), a type of glaucoma where the iris occludes the drainage angle of the eye, obstructing aqueous outflow. PACG is a leading cause of glaucoma worldwide and is particularly common in East Asian populations. It is classified based on the degree of iris occlusion and presence of optic nerve damage and vision loss. Risk factors include older age, female sex, Asian ethnicity, family history, hypermetropia, and shorter axial length. Symptoms include blurred vision, halos around lights, eye pain, and headache. Signs include elevated eye pressure, shallow anterior chamber, iris changes, and optic nerve damage. The document outlines methods for diagnosing
The document describes the embryology and anatomy of the eye lens. It discusses lens development from the optic vesicle and lens placode. Primary and secondary lens fibers develop from the lens vesicle. The lens nucleus changes from embryonic to fetal to infantile to adult. Dimensions and structures of the adult lens are provided, including the capsule, epithelium, fibers, and zonules. Biochemistry of the lens is covered, including proteins, water, electrolytes and metabolic pathways. Cataract formation and the role of glutathione are summarized. Accommodation mechanisms involving ciliary muscle constriction are briefly mentioned.
This document provides an overview of cataracts, including:
- Definitions and types of cataracts such as developmental, acquired, congenital, and secondary.
- Causes of cataracts including age, genetics, trauma, toxins, and medical conditions.
- Classification systems for cataracts based on location, shape, degree of opacity.
- Symptoms such as decreased vision and glare.
- Stages of cortical and nuclear cataracts.
- Secondary cataracts that develop due to underlying ocular diseases.
This document provides an overview of the anatomy and physiology of the human lens. It begins with a brief discussion of lens embryology, including the formation of the lens placode and vesicle. It then describes the microscopic structure of the adult lens, including the lens capsule, epithelium, and fibers. Key aspects of lens molecular biology are summarized, such as the predominant crystallin proteins and role of water. The document also reviews lens metabolism, with glucose being the primary energy source broken down via the glycolytic and sorbitol pathways.
This document provides an overview of different types of corneal dystrophies, including their classification, clinical features, histopathology, and management. It discusses epithelial and subepithelial dystrophies, corneal dystrophies of Bowman's layer, stromal corneal dystrophies, and Descemet membrane and endothelial dystrophies. The key points are that corneal dystrophies are inherited, bilateral, and slowly progressive disorders that begin early in life and are characterized by corneal opacification without relationship to environmental factors. Diagnosis involves classification based on the anatomical layer affected and treatment typically involves managing symptoms although surgery may be needed if vision is impaired.
The document summarizes the anatomy of the uveal tract, including the choroid, ciliary body, and iris. It describes the layers, blood supply, innervation, and functions of each structure in detail. The choroid lines the back of the eye and contains capillaries that nourish the outer retina. The ciliary body produces aqueous humor and helps with accommodation by suspending the lens. The iris divides the eye into anterior and posterior chambers and controls the pupil size to regulate light entry.
This document summarizes diabetic retinopathy and hypertensive retinopathy. It discusses the pathogenesis, risk factors, classification, clinical features and treatment of diabetic retinopathy. It describes how diabetes can damage retinal blood vessels and lead to proliferative changes. It also outlines the screening guidelines for diabetic retinopathy. The document also summarizes hypertensive retinopathy, describing how high blood pressure can cause vascular changes in the retina. It discusses the different grades of hypertensive retinopathy and the aim of treatment to control high blood pressure.
This presentation describes the nature of amniotic membrane grafts, Indications, and limitations with presentation of two cases of corneal perforations treated with it as a self experience
Fungal corneal ulcers are common, caused mainly by Aspergillus in India. Risk factors include ocular trauma, contact lens use, pre-existing eye conditions, and systemic immunosuppression. Diagnosis involves corneal scrapings, cultures, and stains showing fungal hyphae or spores. Treatment consists of topical natamycin or amphotericin B, sometimes with adjunctive debridement, intracameral/intracorneal injections, or therapeutic keratoplasty for severe cases. Systemic antifungals may also be used for extensive infections.
This document discusses cystoid macular edema (CME), including its pathogenesis, etiology, associated ocular conditions, manifestations, diagnosis and testing. Specifically, it focuses on pseudophakic or Irvine-Gass syndrome CME, which can occur after cataract surgery. The summary discusses how CME results from fluid accumulation in the retina, its appearance on fluorescein angiography, risk factors for pseudophakic CME like vitreous loss during surgery, and how it is diagnosed using techniques like optical coherence tomography.
Corneal degeneration refers to degenerative changes in the normal cells of the cornea under the influence of age or pathology. There are various types classified by location (axial or peripheral) or etiology (age-related or pathological). Common age-related degenerations include arcus senilis, Vogt's white limbal girdle, and Hassal-Henle bodies. Pathological degenerations comprise fatty degeneration, amyloidosis, calcific/band keratopathy, Salzmann's nodular degeneration, and pellucid marginal degeneration. Treatment options include phototherapeutic keratectomy, corneal transplantation, or superficial keratectomy depending on the type and severity of degeneration.
This document provides guidelines and information on glaucoma. It begins by outlining the preferred practice patterns for open angle glaucoma by the AAO and Canadian glaucoma guidelines. It then defines primary open-angle glaucoma and discusses clinical objectives such as monitoring optic nerve structure and function. Risk factors like elevated IOP, age, family history and type 2 diabetes are examined. The diagnostic process involving tests like visual fields, pachymetry and optic nerve imaging is summarized. Examination techniques like gonioscopy and optic nerve evaluation are also overviewed.
This document discusses diplopia (double vision), including its definition, causes, evaluation, and management. It begins by defining diplopia as seeing double due to misalignment of the eyes. The document then discusses the anatomy involved, types of diplopia (monocular vs binocular), approaches to evaluation, common causes like myasthenia gravis and various cranial nerve palsies, methods of examination, and treatment options which can include patching therapy, addressing underlying causes, eye exercises, and in some cases surgery.
This document discusses choroidal coloboma, beginning with definitions and epidemiology. It describes the embryonic development of the eye and how failure of fusion of the embryonic fissure can result in coloboma. Types of coloboma are classified based on location and presence of other anomalies. Complications like retinal detachment are discussed. Management of cataracts and other ocular issues in the context of coloboma are covered. The prognosis depends on factors like presence of microphthalmos, corneal diameter, and type and timing of surgery.
This document discusses different types of cataracts, including congenital and acquired cataracts. It describes various causes of congenital cataracts including genetic mutations, metabolic disorders, infections, and chromosomal abnormalities. Congenital cataracts affect approximately 0.03% of newborns and are a leading cause of childhood blindness. The document also discusses different types of cataracts including nuclear, lamellar, and cerulean cataracts. It provides information on diagnosing and treating pediatric cataracts through surgery and preventing amblyopia.
1) Intraocular lenses (IOLs) are artificial lenses implanted during cataract surgery to replace the clouded natural lens and correct vision. 2) IOLs have evolved over generations from rigid PMMA lenses to modern foldable designs made of silicone, acrylic, or hydrogel materials. 3) IOLs can be mono-focal, providing a single vision correction, or multi-focal, attempting to provide both near and distance vision without glasses. Accommodating IOL designs also aim to restore the eye's ability to focus at different distances.
This document discusses tear film dysfunction and dry eye. It begins with an introduction to the tear film, its components and functions. Various tests to evaluate tear film such as tear film breakup time, Schirmer's test, Rose Bengal staining, and Phenol Red thread test are described. Causes of tear film instability and diseases related to tear film dysfunction including evaporative dry eye and obstructive epiphoria are explained. Early signs of tear dysfunction and methods to check the tear outflow mechanism like Jones tests are also summarized.
Corneal edema after cataract surgery occurs when the corneal endothelium is damaged during surgery, reducing its ability to pump fluid out of the cornea and keep it clear. The endothelium does not regenerate, so surviving cells enlarge to cover the missing cells, impairing pumping. Causes include surgical instrumentation, intraocular lenses touching the endothelium, inflammation, and pre-existing conditions. Treatment focuses on eliminating causes, reducing inflammation and pressure, and restoring clarity through corneal transplantation if edema is severe or persistent.
- Tuberculosis (TB) can infect the eyes and is one of the leading causes of uveitis. It can spread to the eyes directly, via a hypersensitivity reaction, or hematogenously. Diagnosis is challenging as lab tests lack sensitivity and culture is not always possible. Treatment involves a combination of anti-TB drugs for 4-6 months along with corticosteroids for ocular inflammation. Drug-resistant strains pose a serious challenge to effective treatment.
The document discusses ocular trauma, providing classifications and guidelines for clinical evaluation and management. It describes the epidemiology of eye injuries and classifications for closed and open globe injuries. Evaluation involves history, exam, and potential investigations. Closed injuries include contusions while open injuries include ruptures and lacerations. Management depends on the injury type and aims to repair anatomy and maximize vision. Chemical burns require copious irrigation and treatments to normalize pH.
The retina is the light-sensitive tissue lining the back of the eye. It contains 10 layers including the retinal pigment epithelium, rods and cones, bipolar and ganglion cells. The retina is thinnest near the center and thickens toward the periphery. Key structures include the optic disc, macula with fovea for sharp central vision, and ora serrata marking the edge. The retina contains over 120 million light receptors and ganglion cells whose axons converge at the optic disc to form the optic nerve.
Optic atrophy refers to degeneration of the optic nerve resulting in vision loss and changes in the appearance of the optic disc. It can be primary, secondary, consecutive, or glaucomatous. Primary optic atrophy is caused by lesions along the visual pathway and results in a chalky white disc. Secondary optic atrophy follows optic nerve swelling and has a dirty grey-white appearance. Consecutive optic atrophy is caused by retinal or choroidal disease and leaves a waxy pallor. Glaucomatous optic atrophy is characterized by deep cupping of the disc. Diagnosis involves imaging and visual field testing while treatment focuses on the underlying cause.
This document summarizes the history and pathogenesis of pathological myopia. It discusses definitions of pathological myopia and classifications of myopia by degree, age of onset, and other factors. Risk factors for pathological myopia include race, age, gender, education level and familial inheritance. Complications include peripheral retinal degenerations which can lead to retinal detachment, myopic foveoschisis, macular holes, lacquer cracks, and choroidal neovascularization. Surgical treatments are discussed for various complications.
Glaucoma describes conditions characterized by raised intraocular pressure, optic nerve damage, and visual field loss. It is one of the leading causes of blindness worldwide. Primary open-angle glaucoma is the most common type, where the anterior chamber angle remains open and there is no identifiable cause for optic nerve damage other than statistically elevated pressure. It is typically asymptomatic until late in the disease when significant vision has already been lost. Treatment aims to lower pressure sufficiently to stop further visual field loss and involves topical eye drops or surgery.
Glaucoma is not a single disease process but a group of disorders characterized by a progressive optic neuropathy resulting in a irreversible visual field defects that are associated frequently raised intraocular pressure (IOP).
IOP is the most common risk factor but not the only risk factor for development of glaucoma.
This document provides an overview of different types of corneal dystrophies, including their classification, clinical features, histopathology, and management. It discusses epithelial and subepithelial dystrophies, corneal dystrophies of Bowman's layer, stromal corneal dystrophies, and Descemet membrane and endothelial dystrophies. The key points are that corneal dystrophies are inherited, bilateral, and slowly progressive disorders that begin early in life and are characterized by corneal opacification without relationship to environmental factors. Diagnosis involves classification based on the anatomical layer affected and treatment typically involves managing symptoms although surgery may be needed if vision is impaired.
The document summarizes the anatomy of the uveal tract, including the choroid, ciliary body, and iris. It describes the layers, blood supply, innervation, and functions of each structure in detail. The choroid lines the back of the eye and contains capillaries that nourish the outer retina. The ciliary body produces aqueous humor and helps with accommodation by suspending the lens. The iris divides the eye into anterior and posterior chambers and controls the pupil size to regulate light entry.
This document summarizes diabetic retinopathy and hypertensive retinopathy. It discusses the pathogenesis, risk factors, classification, clinical features and treatment of diabetic retinopathy. It describes how diabetes can damage retinal blood vessels and lead to proliferative changes. It also outlines the screening guidelines for diabetic retinopathy. The document also summarizes hypertensive retinopathy, describing how high blood pressure can cause vascular changes in the retina. It discusses the different grades of hypertensive retinopathy and the aim of treatment to control high blood pressure.
This presentation describes the nature of amniotic membrane grafts, Indications, and limitations with presentation of two cases of corneal perforations treated with it as a self experience
Fungal corneal ulcers are common, caused mainly by Aspergillus in India. Risk factors include ocular trauma, contact lens use, pre-existing eye conditions, and systemic immunosuppression. Diagnosis involves corneal scrapings, cultures, and stains showing fungal hyphae or spores. Treatment consists of topical natamycin or amphotericin B, sometimes with adjunctive debridement, intracameral/intracorneal injections, or therapeutic keratoplasty for severe cases. Systemic antifungals may also be used for extensive infections.
This document discusses cystoid macular edema (CME), including its pathogenesis, etiology, associated ocular conditions, manifestations, diagnosis and testing. Specifically, it focuses on pseudophakic or Irvine-Gass syndrome CME, which can occur after cataract surgery. The summary discusses how CME results from fluid accumulation in the retina, its appearance on fluorescein angiography, risk factors for pseudophakic CME like vitreous loss during surgery, and how it is diagnosed using techniques like optical coherence tomography.
Corneal degeneration refers to degenerative changes in the normal cells of the cornea under the influence of age or pathology. There are various types classified by location (axial or peripheral) or etiology (age-related or pathological). Common age-related degenerations include arcus senilis, Vogt's white limbal girdle, and Hassal-Henle bodies. Pathological degenerations comprise fatty degeneration, amyloidosis, calcific/band keratopathy, Salzmann's nodular degeneration, and pellucid marginal degeneration. Treatment options include phototherapeutic keratectomy, corneal transplantation, or superficial keratectomy depending on the type and severity of degeneration.
This document provides guidelines and information on glaucoma. It begins by outlining the preferred practice patterns for open angle glaucoma by the AAO and Canadian glaucoma guidelines. It then defines primary open-angle glaucoma and discusses clinical objectives such as monitoring optic nerve structure and function. Risk factors like elevated IOP, age, family history and type 2 diabetes are examined. The diagnostic process involving tests like visual fields, pachymetry and optic nerve imaging is summarized. Examination techniques like gonioscopy and optic nerve evaluation are also overviewed.
This document discusses diplopia (double vision), including its definition, causes, evaluation, and management. It begins by defining diplopia as seeing double due to misalignment of the eyes. The document then discusses the anatomy involved, types of diplopia (monocular vs binocular), approaches to evaluation, common causes like myasthenia gravis and various cranial nerve palsies, methods of examination, and treatment options which can include patching therapy, addressing underlying causes, eye exercises, and in some cases surgery.
This document discusses choroidal coloboma, beginning with definitions and epidemiology. It describes the embryonic development of the eye and how failure of fusion of the embryonic fissure can result in coloboma. Types of coloboma are classified based on location and presence of other anomalies. Complications like retinal detachment are discussed. Management of cataracts and other ocular issues in the context of coloboma are covered. The prognosis depends on factors like presence of microphthalmos, corneal diameter, and type and timing of surgery.
This document discusses different types of cataracts, including congenital and acquired cataracts. It describes various causes of congenital cataracts including genetic mutations, metabolic disorders, infections, and chromosomal abnormalities. Congenital cataracts affect approximately 0.03% of newborns and are a leading cause of childhood blindness. The document also discusses different types of cataracts including nuclear, lamellar, and cerulean cataracts. It provides information on diagnosing and treating pediatric cataracts through surgery and preventing amblyopia.
1) Intraocular lenses (IOLs) are artificial lenses implanted during cataract surgery to replace the clouded natural lens and correct vision. 2) IOLs have evolved over generations from rigid PMMA lenses to modern foldable designs made of silicone, acrylic, or hydrogel materials. 3) IOLs can be mono-focal, providing a single vision correction, or multi-focal, attempting to provide both near and distance vision without glasses. Accommodating IOL designs also aim to restore the eye's ability to focus at different distances.
This document discusses tear film dysfunction and dry eye. It begins with an introduction to the tear film, its components and functions. Various tests to evaluate tear film such as tear film breakup time, Schirmer's test, Rose Bengal staining, and Phenol Red thread test are described. Causes of tear film instability and diseases related to tear film dysfunction including evaporative dry eye and obstructive epiphoria are explained. Early signs of tear dysfunction and methods to check the tear outflow mechanism like Jones tests are also summarized.
Corneal edema after cataract surgery occurs when the corneal endothelium is damaged during surgery, reducing its ability to pump fluid out of the cornea and keep it clear. The endothelium does not regenerate, so surviving cells enlarge to cover the missing cells, impairing pumping. Causes include surgical instrumentation, intraocular lenses touching the endothelium, inflammation, and pre-existing conditions. Treatment focuses on eliminating causes, reducing inflammation and pressure, and restoring clarity through corneal transplantation if edema is severe or persistent.
- Tuberculosis (TB) can infect the eyes and is one of the leading causes of uveitis. It can spread to the eyes directly, via a hypersensitivity reaction, or hematogenously. Diagnosis is challenging as lab tests lack sensitivity and culture is not always possible. Treatment involves a combination of anti-TB drugs for 4-6 months along with corticosteroids for ocular inflammation. Drug-resistant strains pose a serious challenge to effective treatment.
The document discusses ocular trauma, providing classifications and guidelines for clinical evaluation and management. It describes the epidemiology of eye injuries and classifications for closed and open globe injuries. Evaluation involves history, exam, and potential investigations. Closed injuries include contusions while open injuries include ruptures and lacerations. Management depends on the injury type and aims to repair anatomy and maximize vision. Chemical burns require copious irrigation and treatments to normalize pH.
The retina is the light-sensitive tissue lining the back of the eye. It contains 10 layers including the retinal pigment epithelium, rods and cones, bipolar and ganglion cells. The retina is thinnest near the center and thickens toward the periphery. Key structures include the optic disc, macula with fovea for sharp central vision, and ora serrata marking the edge. The retina contains over 120 million light receptors and ganglion cells whose axons converge at the optic disc to form the optic nerve.
Optic atrophy refers to degeneration of the optic nerve resulting in vision loss and changes in the appearance of the optic disc. It can be primary, secondary, consecutive, or glaucomatous. Primary optic atrophy is caused by lesions along the visual pathway and results in a chalky white disc. Secondary optic atrophy follows optic nerve swelling and has a dirty grey-white appearance. Consecutive optic atrophy is caused by retinal or choroidal disease and leaves a waxy pallor. Glaucomatous optic atrophy is characterized by deep cupping of the disc. Diagnosis involves imaging and visual field testing while treatment focuses on the underlying cause.
This document summarizes the history and pathogenesis of pathological myopia. It discusses definitions of pathological myopia and classifications of myopia by degree, age of onset, and other factors. Risk factors for pathological myopia include race, age, gender, education level and familial inheritance. Complications include peripheral retinal degenerations which can lead to retinal detachment, myopic foveoschisis, macular holes, lacquer cracks, and choroidal neovascularization. Surgical treatments are discussed for various complications.
Glaucoma describes conditions characterized by raised intraocular pressure, optic nerve damage, and visual field loss. It is one of the leading causes of blindness worldwide. Primary open-angle glaucoma is the most common type, where the anterior chamber angle remains open and there is no identifiable cause for optic nerve damage other than statistically elevated pressure. It is typically asymptomatic until late in the disease when significant vision has already been lost. Treatment aims to lower pressure sufficiently to stop further visual field loss and involves topical eye drops or surgery.
Glaucoma is not a single disease process but a group of disorders characterized by a progressive optic neuropathy resulting in a irreversible visual field defects that are associated frequently raised intraocular pressure (IOP).
IOP is the most common risk factor but not the only risk factor for development of glaucoma.
Glaucoma is a group of eye disorders characterized by optic nerve damage and visual field loss. Primary open-angle glaucoma (POAG) is the most common type of glaucoma. It is caused by a gradual increase in eye pressure due to impaired outflow of fluid from the eye. Risk factors include older age, family history, race, and high eye pressure. Patients may be asymptomatic initially, but can experience vision loss over time without treatment to lower eye pressure and prevent further optic nerve damage. Diagnosis involves examining the optic disc for cupping, visual field testing, and measuring intraocular pressure. Early treatment can help prevent vision loss from POAG.
This document discusses glaucoma, defining it as an eye disease characterized by loss of retinal ganglion cells and their axons caused by increased intraocular pressure. It is the leading cause of irreversible blindness. There are two main types - open angle glaucoma, the most common type, and angle closure glaucoma. Diagnosis involves measuring intraocular pressure and examining the optic nerve and visual field. Treatment options include eye drop medications, laser treatments, and surgeries like trabeculectomy to improve fluid drainage from the eye. Nursing care focuses on managing pain, allaying fears, and educating patients.
The document provides information on the anatomy and physiology of the anterior segment of the eye. It discusses the ciliary body, anterior chamber, structures within the anterior chamber angle like the scleral spur, trabecular meshwork, Schlemm's canal, and how aqueous humor is produced and drained from the eye. It also provides definitions and classifications of glaucoma, risk factors for primary angle closure glaucoma, stages of primary angle closure glaucoma attacks, clinical features and diagnosis. Treatment of early stage primary angle closure involves miotic eye drops or laser iridotomy.
Glaucoma is a group of eye diseases characterized by optic nerve damage and visual field loss. It is often associated with elevated intraocular pressure but can sometimes occur with normal pressures. The two main types are open-angle glaucoma and angle-closure glaucoma. Congenital glaucoma is present at birth and results from impaired aqueous outflow, often due to developmental abnormalities in the trabecular meshwork. It is typically treated surgically through procedures like goniotomy or trabeculotomy to improve drainage and lower pressure. Long term monitoring is important as the disease can progress if not properly managed.
Congenital glaucomas are a group of disorders where abnormal high intraocular pressure results from developmental abnormalities of the anterior chamber angle that obstruct aqueous humor drainage. They can be primary, caused by trabecular meshwork maldevelopment, or secondary, associated with other ocular or systemic anomalies. Surgical treatment via goniotomy or trabeculotomy aims to create a drainage pathway and lower pressure. Medications may be used before or after surgery to control pressure. Early diagnosis and treatment leads to the best visual prognosis.
Glaucoma: the “silent thief of sight”
Glaucoma is a leading cause of preventable sight loss. Vision can often be preserved with early identification, good adherence to treatment and long-term monitoring.
1) Primary angle-closure glaucoma occurs when the iris blocks the drainage angle of the eye, preventing aqueous humor from draining properly and increasing intraocular pressure. It is usually caused by pupillary block from apposition of the iris and lens.
2) Acute primary angle closure presents with sudden severe eye pain, blurred vision, headache, and nausea. Chronic primary angle closure develops slowly over time with peripheral anterior synechiae formation.
3) Risk factors include hyperopia, smaller eye size, and increasing age when the lens thickens. Treatment involves medical management to lower pressure urgently followed by laser iridotomy or surgery to permanently open the drainage angle.
Glaucoma is a group of eye diseases that causes optic nerve damage and vision loss due to increased pressure in the eye (intraocular pressure). The two main types are open-angle glaucoma, which accounts for 90% of cases, and angle-closure glaucoma. Treatment options aim to lower intraocular pressure and prevent further vision loss through eye drop medications, laser treatments, or surgery. Glaucoma can also be caused secondary to other conditions like diabetes or inflammation and may be present from birth in rare cases of congenital glaucoma.
Glaucoma is a group of eye disorders characterized by optic nerve damage and vision loss caused by increased pressure in the eye. The document discusses the definition, epidemiology, causes, clinical features, diagnosis, and management of primary open angle glaucoma and primary angle-closure glaucoma. Key points include that glaucoma has various clinical manifestations, causes include blockage of aqueous outflow, signs involve optic nerve changes and visual field loss, and treatment aims to lower intraocular pressure through medication, laser treatment, or surgery.
This document provides an overview of glaucoma, including:
- Glaucoma is a group of optic neuropathies characterized by optic disc changes and visual field defects, often caused by elevated intraocular pressure. It is a leading cause of blindness worldwide.
- There are several types of glaucoma including open-angle glaucoma, closed-angle glaucoma, and normal tension glaucoma. Risk factors include age, family history, ethnicity, corneal thickness, and eye pressure.
- Examination techniques for diagnosing glaucoma include visual acuity testing, tonometry, gonioscopy, examination of the optic disc, and visual field testing. Perimetry helps assess severity and
This document provides information on various structures and diseases of the eye. It defines key eye structures like the cornea, iris, lens, retina and optic nerve. It also summarizes common eye conditions such as glaucoma, cataracts, diabetic retinopathy, age-related macular degeneration, and retinal detachments. For each condition, it lists important clinical findings, risk factors, symptoms, treatments and consequences of no treatment.
Glaucoma is a group of eye diseases characterized by increased intraocular pressure, optic nerve damage, and visual field loss. It is a leading cause of blindness worldwide. Cataracts are cloudy lenses that reduce vision and are most often age-related. They occur when the lens becomes less transparent over time. Risk factors for cataracts include diabetes, corticosteroid use, and glaucoma. Both conditions are generally treated surgically by removing the opaque lens or reducing eye pressure, but vision lost from glaucoma cannot be recovered. A combined study found diabetes significantly increases cataract risk while glaucoma is also an independent risk factor, potentially causing 5% of all cataracts.
you can get information about the glaucoma and its possible all types, its signs and symptoms, its pathogenesis, and its treatment (with medicines and with surgery).
you will know that how it affects the eye and causes the visual filed defects.
you will know that how it occurs in children and causes loss of vision.
you can get knowledge about the glaucoma, its different types, and its pathogenesis.......
how to treat it.......
its possible surgeries........
how it damages the eye and causes vision defects....
This document discusses glaucoma, including its definition, anatomy, types, risk factors, examination techniques, and classification. Specifically:
- Glaucoma is a disease of the optic nerve where damage to optic nerve fibers causes blind spots and vision loss.
- It involves abnormal drainage of the aqueous humor in the front of the eye, leading to increased intraocular pressure that damages the optic nerve over time.
- The main types are open-angle and closed-angle glaucoma. Risk factors include high eye pressure, family history, age, and certain medical conditions.
- Examination techniques to detect glaucoma include tonometry to measure intraocular pressure, fundoscopy to examine the optic disc
Approach to cases of congenital glaucoma, developmentalBipin Bista
This document discusses approaches to congenital glaucoma and developmental glaucoma associated with ocular and systemic disorders. It covers signs and symptoms, diagnostic examinations including vision testing, tonometry, and imaging. Primary congenital glaucoma is described along with theories of abnormal development. Specific conditions like Axenfeld-Rieger syndrome are also outlined. Management options are mentioned including medical therapy, various surgical procedures, and postoperative care.
Approach to cases of congenital glaucoma, developmentalShahrukh Kc
This document discusses approaches to congenital glaucoma and developmental glaucoma associated with ocular and systemic disorders. It covers signs and symptoms, diagnostic examinations including vision testing, external examination, and specific tests like tonometry and gonioscopy. Etiology and theories of abnormal development are explained. Primary congenital glaucomas, Axenfeld-Rieger Syndrome, Peters Anomaly, and Aniridia are discussed in detail including clinical features, management, genetics, and histopathology where relevant. Surgical and medical management strategies are also outlined.
NAVIGATING THE HORIZONS OF TIME LAPSE EMBRYO MONITORING.pdfRahul Sen
Time-lapse embryo monitoring is an advanced imaging technique used in IVF to continuously observe embryo development. It captures high-resolution images at regular intervals, allowing embryologists to select the most viable embryos for transfer based on detailed growth patterns. This technology enhances embryo selection, potentially increasing pregnancy success rates.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga
GASTROINTESTINAL INFECTIONS AND GASTRITIS
Osvaldo Bernardo Muchanga
Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
Gastritis and Gastric Health
Gastric Health is one of the most relevant concerns in human health, with gastrointestinal infections being among the main illnesses that affect humans.
Among gastric problems, we have GASTRITIS AND GASTRIC ULCERS as the main public health problems. Gastritis and gastric ulcers normally result from inflammation and corrosion of the walls of the stomach (gastric mucosa) and are generally associated (caused) by the bacterium Helicobacter pylor, which, according to the literature, this bacterium settles on these walls (of the stomach) and starts to release urease that ends up altering the normal pH of the stomach (acid), which leads to inflammation and corrosion of the mucous membranes and consequent gastritis or ulcers, respectively.
In addition to bacterial infections, gastritis and gastric ulcers are associated with several factors, with emphasis on prolonged fasting, chemical substances including drugs, alcohol, foods with strong seasonings including chilli, which ends up causing inflammation of the stomach walls and/or corrosion. of the same, resulting in the appearance of wounds and consequent gastritis or ulcers, respectively.
Among patients with gastritis and/or ulcers, one of the dilemmas is associated with the foods to consume in order to minimize the sensation of pain and discomfort.
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2. OUT LINE
• Relevant anatomy and Physiology
• Definition
• Pathogensis
• Classification
• Congenital glaucoma
• Primary glaucoma
• POAG
• PACG
• Secondary glaucoma
• Other types of Glaucoma
3. ANTOMY AND PHYSIOLOGY
• Pathophysiology of glaucoma revolves around the aqueous humor
dynamics.
The principal ocular structures concerned with it are
1. The pars plicata part of the ciliary body,
2. The angle of anterior chamber
3. The aqueous outflow system
4. 1. Ciliary Body
It is the main site of aqueous production
Ciliary body has two parts namely:
a) Pars plicata—The anterior one-third of ciliary body (about 2 mm) is
known as pars plicata. The ciliary processes are attached to this
part. Pars plicata part of the ciliary body secretes aqueous humor.
b) Pars plana—The posterior two-third of ciliary body (about 4 mm) is
known as pars plana. It is relatively avascular therefore posterior
segment of the eye is entered through the pars plana incision 3-5
mm behind the limbus.
5. 2. Angle of Anterior Chamber
• It plays an important role in the process of aqueous drainage. It is
formed by the root of iris, anterior
• most part of the ciliary body, scleral spur, trabecular meshwork and
Schwalbe’s line (prominent end
• of Descemet’s membrane of cornea)
6. 3. Aqueous Outflow System
It includes the trabecular meshwork, canal of Schlemm, aqueous veins and the episcleral veins.
• 1. Trabecular meshwork—It is a sieve-like structure through which aqueous humor gets filtered
• into the canal of Schlemm.
• 2. Canal of Schlemm—This is an endothelial lined oval channel present circumferentially in the
• scleral sulcus.
• 3. Aqueous veins—These are about 25-35 in number. They leave the canal of Schlemm at oblique
• angles to terminate into episcleral veins.
• 4. Episcleral veins—These are branches of anterior ciliary veins. There is pressure difference of
• about 5 mm Hg between the anterior chamber and the episcleral veins so that the aqueous drains
• continuously in them.
8. DEFINATION
Glaucoma is a chronic, progressive optic neuropathy caused by a group
of ocular conditions which lead to damage of optic nerve with loss of
visual function. The most common risk factor known is raised
intraocular pressure.
• Normal intraocular pressure = 10–20 mm Hg (Schiotz)
• Suspicious case = 20–25 mm Hg (Schiotz)
• Glaucoma = Above 25 mm Hg (Schiotz)
• Hypotony = Below 10 mm Hg (Schiotz
9. Etiology
Etiology
• The most important factor which causes rise of intraocular pressure is
obstruction to the drainage
• of the aqueous humor through the:
• i. Angle of the anterior chamber
• ii. At the pupil.
10. Pathogenesis
The glaucomatous damage is attributed to a combination of factors
which affect perfusion of optic nerve head.
1. Mechanical changes—The coats of the eye can withstand raised
intraocular pressure except at the lamina cribrosa which is pushed
backwards. This squeezes the nerve fibres within its meshes to disturb
the axoplasmic flow.
2. Vascular factors—The perfusion of optic nerve head may be affected
due to decreased blood flow in the capillaries and in annulus of Zinn
which supply nutrition to the laminar and postlaminar optic nerve
head.
12. CONGENITAL OR INFANTILE GLAUCOMA
(BUPHTHALMOS, HYDROPHTHALMOS)
It is defined as glaucoma appearing between birth and the age of 3-4
years.
There is raised intraoculartension present since birth. When the
glaucoma presents at puberty, it is known as Juvenile glaucoma.
13. Etiology
It is usually of a simple obstructive type due to congenital abnormality
at the angle of anterior chamber. It is transmitted as an autosomal
recessive trait.
1. The iris is not completely separated from the cornea.
2. Persistence of embryonic mesodermal tissue at the angle.
3. Absence of canal of Schlemm.
14. Types
• 1. Congenital glaucoma—It manifests at birth.
• 2. Infantile glaucoma—It presents between 1-3 years.
• 3. Juvenile glaucoma—It presents around puberty.
Syndromes Associated with Infantile Glaucoma.
1. von Recklinghausen’s disease, i.e. generalised neurofibromatosis.
2. Sturge-Weber syndrome—The capillary naevus of face is associated
with angiomatous ,conditions of the choroid and the brain.
15. Symptoms
• 1. Lacrimation - due to corneal oedema and erosion.
• 2. Photophobia - associated with corneal involvement.
• 3. There is defective vision- due to corneal oedema leading to hazy
cornea.
• 4. There is enlargement of cornea and the eye as a whole, due to
stretching of the sclera.
16. Signs
• 1. Enlargement of the eyeball as a whole is present with globular cornea.
• 2. There is corneal oedema and opacities due to endothelium damage and
rupture of Descemet’s membrane (Haabs’ striae). These occur because
Descemet’s membrane is less elastic than the corneal stroma. Tears are
situated in the periphery and are concentric with the limbus.
• 3. Deep anterior chamber with iridodonesis may be seen due to backward
displacement of the lens . Iris may have atrophic patches in the late stages.
• 4. Lens is flattened and displaced backwards due to stretching of the zonule
of Zinn.
• 5. Sclera becomes thin and bluish as the uveal tissue shines through it.
17.
18. Diagnosis
1 . Raised intraocular pressure—It is not raised markedly due to:
I . Extensibility or stretching of the sclera
ii . Uveoscleral outflow.
2 . Measurement of corneal diameter—Corneal enlargement occurs along
with the enlargement of the globe—buphthalmos (Bull-like eyes), specially
when the onset is before the age of 3 years.
A normal infant’s cornea measures about 10.5 mm in diameter.
3 . Fundus examination—The cupping of optic disc is seen due to stretching
of the lamina cribrosaand raised tension. Optic atrophy usually sets in after
the third year.
4. Gonioscopy—The angle of anterior chamber shows certain abnormalities.
19. Differential Diagnosis
i. Keratoglobus (megalocornea)—It is present since birth.
ii. Very high myopia—The eyeball is large as a whole.
iii. Raised intraocular pressure (IOP) in infants may be associated with:
• Retinoblastoma.
• Retinopathy of prematurity.
• Aniridia or absence of iris.
• Persistent primary hyperplastic vitreous.
20. Treatment
The treatment of congenital or infantile glaucoma is always surgical.
1. Medical Treatment
Systemic acetazolamide and mannitol IV along with local beta blockers,
e.g. timolol maleate control the intraocular pressure preoperatively.
Miotics are useless as they do not help in aqueous outflow.
2. Operative Treatment
i. Goniotomy
ii. Trabeculotomy
iii. Trabeculectomy
21.
22. PRIMARY OPEN ANGLE GLAUCOMA (POAG)
It is a chronic, slowly progressive condition with an insidious onset. This
presents an entirely different clinical picture from the acute closed
angle glaucoma.
Etiology:
It has a genetic basis. There is sclerosis of the trabecular meshwork in
any type of eye. The endothelial lining of the canal of Schlemm may
also be sclerosed.
23. Mechanism of Primary Open Angle Glaucoma
There is increased resistance to the outflow of the aqueous humor
offered by:
1. The sclerosed trabecular meshwork—Electron microscopic picture
shows following changes in the trabecular meshwork.
(i) Proliferation of endothelial lining with thickening of the basement
membrane.
(ii) Narrowing of intertrabecular spaces.
(iii) Deposition of amorphous material in the juxtacanalicular tissue.
2. The sclerosed endothelium lining of the canal of Schlemm—This
leads to narrowing or collapse of canal of Schlemm.
24. Associated Ocular Pathology
Following ocular diseases may be present in association with primary
open angle glaucoma:
• High myopia
• Fuchs endothelial dystrophy
• Retinitis pigmentosa
• Retinal vessel occlusion
• Retinal detachment.
25. Symptoms
1. There is painless, progressive loss of vision. Due to its insidious onset, it is
usually noticed when vision is completely lost in one eye and the other eye is
seriously impaired.
2. Mild headache and eyeache may be present.
3. A defect in the visual field (noticed by an intelligent patient) is often
present.
4. There is increasing difficulty in doing near work. Reading or close work is
often difficult due to accommodative failure as a result of pressure upon the
ciliary muscle and its nerve supply.
5. Light sense is defective. Light minimum is raised and dark adaptation is
slowed.
26. Signs
1. Visual acuity decreases gradually. However, it remains good till the
late stage as the central field of vision persists.
2. Cornea is usually clear.
3. Anterior chamber depth and angle are normal.
4. Pupillary reactions remain normal until the late stage when they
become sluggish.
27. Diagnosis
The diagnosis depends on the classical triad signs:
1. Raised intraocular pressure
↓
2. Cupping of the optic disc
↓
3. Visual field defects
37. 1. Baring of the blind spot 2. Small scotomatous areas 3. Seidel’s sign
4. Bjerrum’s arcuate scotoma 5. Double arcuate scotoma or 6. Temporal-central island
annular scotoma
38.
39. Treatment POAG
Methods
The treatment options available at present are medicines, laser or
surgery to lower the intraocular pressure.
1. Medical—It is always the treatment of choice in the early stages.
2. Surgical—It is considered to be the last resort.
3. Argon or diode laser trabeculoplasty (ALT or DLT)—It is the most
advanced technique.
4. Recent advanced procedures—These include laser filtration, seton
valves, deep sclerotomy and viscocanalostomy.
41. Treatment Con.
• In the event of failure of medical treatment of glaucoma
• Trabeculectomy (filtration surgery)
42.
43.
44.
45. PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG
This is a condition in which the intraocular tension is raised due to the
narrow or closed angle of the anterior chamber. There is obstruction to
the outflow of the aqueous humor.
RISK FACTORS
It has a genetic basis. It is typically seen in eyes which are:
I . Small and hypermetropic eye common in adults
II . Anatomical narrow angle of the anterior chamber
III. Shallow anterior chamber
IV . Iris—lens diaphragm is pushed forwards
46.
47. Convex Iris Lens Diaphragm | Shallow anterior chamber | Narrow entrance to chamber angle
Small and hypermetropic eye
49. Stages
The clinical course of the disease has been divided into five stages. The
condition however does not necessarily progress from one stage to the
other in an orderly sequence.
1. Primary angle-closure glaucoma suspect (latent)
2. Subacute or intermittent primary angle-closure glaucoma ( slight
emergency)
3. Acute primary angle-closure glaucoma
4. Chronic primary angle-closure glaucoma
5. Absolute primary angle-closure glaucoma
51. • Diagnosed by doing gonioscopy
• Goniolens
• Knowledge of normal angle is crucial
52.
53. Absolute Glaucoma
When chronic stage is not treated with or without sub-acut attackes
• Blind
• Painful
• Treatment :
• Pain relief with med and surgical procedures, if does not work
other options such as :
• Enucleation
• Laser/Cryotherapy
• Absolute alcohol
54. SECONDARY GLAUCOMA
• Secondary glaucoma occurs due to a specific anomaly or disease of the
eye.
Lens
• Intumescence
• Dislocation
• Phacolytic
Trauma
Uveitis
Neovascular
Pigmentary
56. NORMAL TENSION GLAUCOMA (NTG)
Definition:
The term normal tension glaucoma, also referred to as low tension
glaucoma is characterized by typical glaucomatous disc changes with
visual field defects, with an intraocular pressure remaining constantly
below 21 mm of Hg.
• It is a variant of primary open angle glaucoma
57. OTHER TYPES OF GLAUCOMA
APHAKIC GLAUCOMA
• It is a type of secondary glaucoma which occurs following extraction of the
lens.
Etiology
• It occurs after cataract surgery due to:
i. Delayed formation of anterior chamber—This results in the formation of
peripheral anterior synechiae. It may occur due to choroidal detachment or
leaking section
ii. The vitreous protruding through the pupil in the anterior chamber may
cause pupillary block
iii. Presence of vitreous in the anterior chamber blocks the angle.
58. OTHER TYPES OF GLAUCOMA
MALIGNANT GLAUCOMA
• Malignant glaucoma is a rare condition which may occur as a
complication of any intraocular surgery.
Etiology
Malignant glaucoma occurs typically in patients with
I . Primary narrow angle glaucoma operated for peripheral buttonhole
iridectomy or trabeculectomy (ciliolenticular block)
II . Aphakic eyes following vitreous phase disturbance (ciliovitreal block)