this ppt explains PG level vascular occlusion retinopathies in OPTHALMOLOGY
SOURCE- PARSON DISEASES OF EYE
CONTAINS FUNDOSCOPY AND FFA IMAGES WITH LATEST TREATMENTS
Central retinal artery occlusion (CRAO) results from obstruction of blood flow through the central retinal artery, causing ischemia of the inner retina. It presents suddenly with severe, painless vision loss. Examination typically reveals a cherry red spot at the macula and whitening of the inner retina. The cause is usually thrombotic or embolic, with cholesterol emboli being common. Prognosis depends on the extent of retinal ischemia, with only minimal chances of vision improvement over time. Management involves ruling out underlying cardiovascular conditions and considering prophylactic treatment to prevent further embolic events.
Central retinal artery occlusion (CRAO) results from obstruction of blood flow through the central retinal artery, causing ischemia of the inner retina. It presents suddenly with severe, painless vision loss. Examination typically reveals a cherry red spot at the macula and whitening of the inner retina. The cause is usually thrombotic or embolic, with cholesterol emboli being common. Prognosis depends on the extent of retinal ischemia, with only minimal chances of vision improvement over time. Management involves ruling out underlying cardiovascular conditions and considering prophylactic treatment to prevent further embolic events.
Central retinal artery occlusion (CRAO) results from obstruction of blood flow through the central retinal artery, causing ischemia of the inner retina. It presents with sudden, painless vision loss. Examination typically reveals a cherry red spot at the macula and whitening of the inner retina. Ancillary testing such as OCT, FFA, and ERG can help evaluate the extent of retinal damage. Prompt diagnosis and treatment of underlying causes is important to prevent further vascular events.
Central retinal artery occlusion (CRAO) results from obstruction of blood flow through the central retinal artery, causing ischemia of the inner retina. It presents with sudden, painless vision loss. Examination typically reveals a cherry red spot at the macula and whitening of the inner retina. Ancillary testing such as OCT, FFA, and ERG can help evaluate the extent of retinal damage. Prompt diagnosis and treatment of underlying causes is important to prevent further vascular events.
The document discusses retinal arterial occlusion, including the central retinal artery and its branches. It describes the anatomy and blood supply of the retina. There are several potential mechanisms of retinal arterial occlusion, most commonly atherosclerosis-related thrombosis. Clinical presentations vary depending on the site of occlusion, such as central retinal artery occlusion presenting with a cherry red spot and cilioretinal artery occlusion causing pericentral scotomas. Management includes treating the acute event to restore vision as well as workup and management of any underlying systemic conditions. However, visual recovery is often poor due to retinal infarction.
This document discusses various retinal vascular diseases and associated findings. It covers central retinal vein occlusion and the associated findings except for neovascular glaucoma. It notes that the most common cause of neovascular glaucoma is ischemic central retinal vein occlusion. The document also discusses ophthalmic artery occlusion findings compared to central retinal artery occlusion. Additional topics covered include hypertensive retinopathy, sickle cell retinopathy, Coats disease, retinal artery macroaneurysms, and other retinal conditions like radiation retinopathy. Treatment options are provided for several of the conditions.
The document summarizes various causes of sudden vision loss including retinal artery obstruction, retinal vein obstruction, ischemic optic neuropathy, optic neuritis, vitreous hemorrhage, and acute glaucoma. It then describes the blood supply of the eye from the central retinal artery, anterior ciliary arteries, and posterior ciliary arteries. It provides details on retinal vein occlusion including presentation, risk factors, and treatments such as anti-VEGF injections. It also discusses retinal artery occlusion presenting with sudden severe vision loss and visible emboli, as well as treatments focused on underlying causes.
Central retinal vein thrombosis can cause sudden vision loss in elderly patients. On examination, there are typically extensive hemorrhages extending from the optic disc to the retinal periphery, along with edema of the disc and retina. Risk factors include older age, hypertension, cardiovascular disease, and diabetes. Treatment options include anti-VEGF drugs which have been shown to reduce macular edema, as well as corticosteroid implants. Laser treatment is only beneficial for neovascularization complications.
Central retinal artery occlusion (CRAO) results from obstruction of blood flow through the central retinal artery, causing ischemia of the inner retina. It presents suddenly with severe, painless vision loss. Examination typically reveals a cherry red spot at the macula and whitening of the inner retina. The cause is usually thrombotic or embolic, with cholesterol emboli being common. Prognosis depends on the extent of retinal ischemia, with only minimal chances of vision improvement over time. Management involves ruling out underlying cardiovascular conditions and considering prophylactic treatment to prevent further embolic events.
Central retinal artery occlusion (CRAO) results from obstruction of blood flow through the central retinal artery, causing ischemia of the inner retina. It presents suddenly with severe, painless vision loss. Examination typically reveals a cherry red spot at the macula and whitening of the inner retina. The cause is usually thrombotic or embolic, with cholesterol emboli being common. Prognosis depends on the extent of retinal ischemia, with only minimal chances of vision improvement over time. Management involves ruling out underlying cardiovascular conditions and considering prophylactic treatment to prevent further embolic events.
Central retinal artery occlusion (CRAO) results from obstruction of blood flow through the central retinal artery, causing ischemia of the inner retina. It presents with sudden, painless vision loss. Examination typically reveals a cherry red spot at the macula and whitening of the inner retina. Ancillary testing such as OCT, FFA, and ERG can help evaluate the extent of retinal damage. Prompt diagnosis and treatment of underlying causes is important to prevent further vascular events.
Central retinal artery occlusion (CRAO) results from obstruction of blood flow through the central retinal artery, causing ischemia of the inner retina. It presents with sudden, painless vision loss. Examination typically reveals a cherry red spot at the macula and whitening of the inner retina. Ancillary testing such as OCT, FFA, and ERG can help evaluate the extent of retinal damage. Prompt diagnosis and treatment of underlying causes is important to prevent further vascular events.
The document discusses retinal arterial occlusion, including the central retinal artery and its branches. It describes the anatomy and blood supply of the retina. There are several potential mechanisms of retinal arterial occlusion, most commonly atherosclerosis-related thrombosis. Clinical presentations vary depending on the site of occlusion, such as central retinal artery occlusion presenting with a cherry red spot and cilioretinal artery occlusion causing pericentral scotomas. Management includes treating the acute event to restore vision as well as workup and management of any underlying systemic conditions. However, visual recovery is often poor due to retinal infarction.
This document discusses various retinal vascular diseases and associated findings. It covers central retinal vein occlusion and the associated findings except for neovascular glaucoma. It notes that the most common cause of neovascular glaucoma is ischemic central retinal vein occlusion. The document also discusses ophthalmic artery occlusion findings compared to central retinal artery occlusion. Additional topics covered include hypertensive retinopathy, sickle cell retinopathy, Coats disease, retinal artery macroaneurysms, and other retinal conditions like radiation retinopathy. Treatment options are provided for several of the conditions.
The document summarizes various causes of sudden vision loss including retinal artery obstruction, retinal vein obstruction, ischemic optic neuropathy, optic neuritis, vitreous hemorrhage, and acute glaucoma. It then describes the blood supply of the eye from the central retinal artery, anterior ciliary arteries, and posterior ciliary arteries. It provides details on retinal vein occlusion including presentation, risk factors, and treatments such as anti-VEGF injections. It also discusses retinal artery occlusion presenting with sudden severe vision loss and visible emboli, as well as treatments focused on underlying causes.
Central retinal vein thrombosis can cause sudden vision loss in elderly patients. On examination, there are typically extensive hemorrhages extending from the optic disc to the retinal periphery, along with edema of the disc and retina. Risk factors include older age, hypertension, cardiovascular disease, and diabetes. Treatment options include anti-VEGF drugs which have been shown to reduce macular edema, as well as corticosteroid implants. Laser treatment is only beneficial for neovascularization complications.
The document discusses the retina and macula. It begins by describing the layers of the retina and macula, including the fovea. It then discusses the cell types found in each layer, such as photoreceptors, bipolar cells, and ganglion cells. The document goes on to explain retinal vasculature and how the retina is supplied by the central retinal artery. It concludes by briefly mentioning common imaging techniques used to examine the retina and macula.
This document discusses central retinal vein occlusion (CRVO), a retinal vascular disorder where the central retinal vein becomes blocked. It has a prevalence of 0.4% and can be caused by compression of the vein, intraluminal thrombosis, or inflammation. CRVO is classified as perfused or non-perfused based on fluorescein angiography and the degree of retinal capillary non-perfusion. Treatment focuses on managing macular edema and neovascularization, common complications. While no treatment reverses CRVO itself, risk factor modification and therapies targeting edema and neovascularization can help preserve vision.
This document summarizes retinal artery occlusion, including classifications, epidemiology, clinical features, risk factors, evaluation, treatment, and prognosis for different types. Central retinal artery occlusion typically causes sudden, painless vision loss and has a poor visual prognosis. Branch retinal artery occlusion often causes partial vision loss and has a better prognosis, with vision recovering to 20/40 or better in most cases. Cilioretinal artery occlusion can occur in isolation or with central retinal vein occlusion, and isolated cases typically have a good visual outcome.
Central Retinal Artery Occlusion (CRAO) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of CRAO.
Also encompasses salient points for PGMEE
Eale’s disease is an idiopathic inflammation of the peripheral retinal veins that causes recurrent vitreous hemorrhage. It typically affects young adult males and is characterized by sudden floaters or vision loss due to bleeding in the vitreous. Treatment includes corticosteroids, laser photocoagulation, and vitreoretinal surgery for complications like retinal detachment. Optic neuritis refers to inflammatory disorders of the optic nerve with possible causes including multiple sclerosis, infections, and autoimmune diseases. Symptoms include sudden monocular vision loss and pain with eye movements. Signs include reduced visual acuity and a relative afferent pupillary defect.
This document provides information on vascular disorders of the retina. It begins with the anatomy and blood supply of the retina. It then discusses diabetic retinopathy in detail, including pathogenesis, signs, diagnosis and treatment. It also briefly covers hypertensive retinopathy and retinal vein occlusion, describing their pathophysiology, classification systems, clinical presentation and management. The document focuses primarily on providing an overview of diabetic retinopathy and its various stages and complications.
Traumatic chorioretinal pathologies can result from both penetrating and non-penetrating ocular injuries. Males under 40 are most commonly affected. Closed globe injuries may cause commotio retinae, while open globe injuries risk choroidal rupture. Indirect injuries like Valsalva retinopathy or Terson syndrome can also cause intraocular bleeding. Traumatic macular holes and retinal detachments require surgical repair like vitrectomy. Overall ocular trauma remains a major cause of blindness worldwide.
This document provides an overview of several retinal vascular diseases including sickle cell disease, vasculitis, cystoid macular edema, Coats disease, macular telangiectasia, phakomatoses, radiation retinopathy, Valsalva retinopathy, and Purtscher retinopathy. Key details are provided on the pathogenesis, clinical presentation, diagnosis, and management of each condition. The document is intended as an educational guide for retinal specialists and contains technical terminology related to retinal anatomy and diseases.
3. The document discusses various types of retinal examinations and retinal breaks that can lead to retinal detachment. It describes the 3 mirrors used in retinal examination - the central, equatorial, and gonioscopy mirrors. It then covers the anatomy of the retina and vitreous before discussing different types of peripheral retinal lesions, posterior vitreous detachment, and the definitions and characteristics of retinal breaks such as holes, tears, giant retinal tears, and dialysis. Finally, it lists risk factors for retinal detachment based on the type of break and other ocular and systemic factors.
This document provides an overview of vitreoretinal diseases and the anatomy of the vitreous and retina. It discusses examination of the normal eye, symptoms of vitreoretinal disorders, and abnormal fundus features seen on examination. Specific conditions covered include retinal detachment, age-related macular degeneration, diabetic retinopathy, and effects of systemic diseases like hypertension and AIDS. Management approaches for various vitreoretinal diseases are also summarized.
This document discusses central retinal artery occlusion (CRAO) and branch retinal artery occlusion (BRAO). CRAO is caused by an embolism blocking blood flow through the central retinal artery, typically in patients around 60 years old. It results in sudden painless vision loss. BRAO is less common and blocks a branch retinal artery, usually causing sectoral vision loss. Both can be caused by emboli from atherosclerosis and are medical emergencies treated by attempts to restore blood flow through the blocked vessel. Outcomes are generally poor with permanent vision loss for CRAO and variable recovery for BRAO.
This document discusses the evaluation and management of sudden visual loss. It begins by distinguishing between acute transient visual loss lasting less than 24 hours and acute persistent visual loss lasting at least 24 hours. Important aspects of the history and examination are outlined. Causes of visual loss are then categorized as media problems, retinal problems, neural pathway problems, and psychogenic problems. Specific conditions are described within each category along with distinguishing examination findings and appropriate management. Immediate treatment is recommended for conditions such as central retinal artery occlusion and acute angle closure glaucoma, while other conditions require emergent or urgent referral.
Central retinal vein occlusion occurs when the central retinal vein becomes blocked, disrupting blood flow out of the retina. It can be caused by physical blockage at the lamina cribrosa or hemodynamic factors that obstruct blood flow. Histopathology shows occlusion at or behind the lamina cribrosa. Risk factors include hypertension, diabetes, glaucoma, and low physical activity. Investigations may include blood tests, imaging like fluorescein angiography, and screening for thrombophilias in younger patients. Features include retinal hemorrhages, edema, and delayed venous filling on angiography. Prognosis is generally poor for ischemic cases due to vision loss from macular edema, nonperfusion, and neovascular
DISEASES OF THE RETINA - COGENITAL,VASCULAR,ALLPREETHABALAJI21
1. The document discusses various congenital and developmental disorders of the retina including anomalies of the optic disc, nerve fibers, and vascular elements.
2. Specific conditions covered include drusen, situs inversus, hypoplasia, aplasia, and coloboma. Inflammatory disorders of the retina such as retinitis, chorioretinitis, and retinal vasculitis from various etiologies are also discussed.
3. Common vascular disorders of the retina like retinal artery occlusions, retinal vein occlusions, diabetic retinopathy, and sickle cell retinopathy are reviewed in detail.
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.
This document discusses neovascular glaucoma, also known as rubeotic glaucoma. It begins by defining the terminology and describing the clinical features. The main causes of neovascular glaucoma are diabetic retinopathy, central retinal vein occlusion, and carotid artery occlusive disease, all of which result in ocular tissue hypoxia. This hypoxia leads to the release of angiogenic factors like vascular endothelial growth factor that induce new blood vessel growth on the iris and in the anterior chamber angle, causing glaucoma. Later sections discuss theories of neovasculogenesis, angiogenic and vasoinhibitory factors, clinical course, differential diagnosis, medical management, and surgical options.
This document discusses retinal vascular occlusions, including arterial and venous occlusions. It provides details on the arterial supply and venous drainage of the retina. For retinal artery occlusions, it describes the etiology as embolism, atherosclerosis or inflammatory changes. Clinical features include sudden painless vision loss and a cherry red spot in the macula. Treatment may include ocular massage or thrombolytics within 4-6 hours. Retinal venous occlusions are associated with thrombus formation and compression of veins. Clinical features include blurred vision and retinal hemorrhages. Treatment focuses on managing risk factors and treating macular edema or neovascularization.
Nutritional deficiency Disorder are problems in india.
It is very important to learn about Indian child's nutritional parameters as well the Disease related to alteration in their Nutrition.
The document discusses the retina and macula. It begins by describing the layers of the retina and macula, including the fovea. It then discusses the cell types found in each layer, such as photoreceptors, bipolar cells, and ganglion cells. The document goes on to explain retinal vasculature and how the retina is supplied by the central retinal artery. It concludes by briefly mentioning common imaging techniques used to examine the retina and macula.
This document discusses central retinal vein occlusion (CRVO), a retinal vascular disorder where the central retinal vein becomes blocked. It has a prevalence of 0.4% and can be caused by compression of the vein, intraluminal thrombosis, or inflammation. CRVO is classified as perfused or non-perfused based on fluorescein angiography and the degree of retinal capillary non-perfusion. Treatment focuses on managing macular edema and neovascularization, common complications. While no treatment reverses CRVO itself, risk factor modification and therapies targeting edema and neovascularization can help preserve vision.
This document summarizes retinal artery occlusion, including classifications, epidemiology, clinical features, risk factors, evaluation, treatment, and prognosis for different types. Central retinal artery occlusion typically causes sudden, painless vision loss and has a poor visual prognosis. Branch retinal artery occlusion often causes partial vision loss and has a better prognosis, with vision recovering to 20/40 or better in most cases. Cilioretinal artery occlusion can occur in isolation or with central retinal vein occlusion, and isolated cases typically have a good visual outcome.
Central Retinal Artery Occlusion (CRAO) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, types, associated conditions and management of CRAO.
Also encompasses salient points for PGMEE
Eale’s disease is an idiopathic inflammation of the peripheral retinal veins that causes recurrent vitreous hemorrhage. It typically affects young adult males and is characterized by sudden floaters or vision loss due to bleeding in the vitreous. Treatment includes corticosteroids, laser photocoagulation, and vitreoretinal surgery for complications like retinal detachment. Optic neuritis refers to inflammatory disorders of the optic nerve with possible causes including multiple sclerosis, infections, and autoimmune diseases. Symptoms include sudden monocular vision loss and pain with eye movements. Signs include reduced visual acuity and a relative afferent pupillary defect.
This document provides information on vascular disorders of the retina. It begins with the anatomy and blood supply of the retina. It then discusses diabetic retinopathy in detail, including pathogenesis, signs, diagnosis and treatment. It also briefly covers hypertensive retinopathy and retinal vein occlusion, describing their pathophysiology, classification systems, clinical presentation and management. The document focuses primarily on providing an overview of diabetic retinopathy and its various stages and complications.
Traumatic chorioretinal pathologies can result from both penetrating and non-penetrating ocular injuries. Males under 40 are most commonly affected. Closed globe injuries may cause commotio retinae, while open globe injuries risk choroidal rupture. Indirect injuries like Valsalva retinopathy or Terson syndrome can also cause intraocular bleeding. Traumatic macular holes and retinal detachments require surgical repair like vitrectomy. Overall ocular trauma remains a major cause of blindness worldwide.
This document provides an overview of several retinal vascular diseases including sickle cell disease, vasculitis, cystoid macular edema, Coats disease, macular telangiectasia, phakomatoses, radiation retinopathy, Valsalva retinopathy, and Purtscher retinopathy. Key details are provided on the pathogenesis, clinical presentation, diagnosis, and management of each condition. The document is intended as an educational guide for retinal specialists and contains technical terminology related to retinal anatomy and diseases.
3. The document discusses various types of retinal examinations and retinal breaks that can lead to retinal detachment. It describes the 3 mirrors used in retinal examination - the central, equatorial, and gonioscopy mirrors. It then covers the anatomy of the retina and vitreous before discussing different types of peripheral retinal lesions, posterior vitreous detachment, and the definitions and characteristics of retinal breaks such as holes, tears, giant retinal tears, and dialysis. Finally, it lists risk factors for retinal detachment based on the type of break and other ocular and systemic factors.
This document provides an overview of vitreoretinal diseases and the anatomy of the vitreous and retina. It discusses examination of the normal eye, symptoms of vitreoretinal disorders, and abnormal fundus features seen on examination. Specific conditions covered include retinal detachment, age-related macular degeneration, diabetic retinopathy, and effects of systemic diseases like hypertension and AIDS. Management approaches for various vitreoretinal diseases are also summarized.
This document discusses central retinal artery occlusion (CRAO) and branch retinal artery occlusion (BRAO). CRAO is caused by an embolism blocking blood flow through the central retinal artery, typically in patients around 60 years old. It results in sudden painless vision loss. BRAO is less common and blocks a branch retinal artery, usually causing sectoral vision loss. Both can be caused by emboli from atherosclerosis and are medical emergencies treated by attempts to restore blood flow through the blocked vessel. Outcomes are generally poor with permanent vision loss for CRAO and variable recovery for BRAO.
This document discusses the evaluation and management of sudden visual loss. It begins by distinguishing between acute transient visual loss lasting less than 24 hours and acute persistent visual loss lasting at least 24 hours. Important aspects of the history and examination are outlined. Causes of visual loss are then categorized as media problems, retinal problems, neural pathway problems, and psychogenic problems. Specific conditions are described within each category along with distinguishing examination findings and appropriate management. Immediate treatment is recommended for conditions such as central retinal artery occlusion and acute angle closure glaucoma, while other conditions require emergent or urgent referral.
Central retinal vein occlusion occurs when the central retinal vein becomes blocked, disrupting blood flow out of the retina. It can be caused by physical blockage at the lamina cribrosa or hemodynamic factors that obstruct blood flow. Histopathology shows occlusion at or behind the lamina cribrosa. Risk factors include hypertension, diabetes, glaucoma, and low physical activity. Investigations may include blood tests, imaging like fluorescein angiography, and screening for thrombophilias in younger patients. Features include retinal hemorrhages, edema, and delayed venous filling on angiography. Prognosis is generally poor for ischemic cases due to vision loss from macular edema, nonperfusion, and neovascular
DISEASES OF THE RETINA - COGENITAL,VASCULAR,ALLPREETHABALAJI21
1. The document discusses various congenital and developmental disorders of the retina including anomalies of the optic disc, nerve fibers, and vascular elements.
2. Specific conditions covered include drusen, situs inversus, hypoplasia, aplasia, and coloboma. Inflammatory disorders of the retina such as retinitis, chorioretinitis, and retinal vasculitis from various etiologies are also discussed.
3. Common vascular disorders of the retina like retinal artery occlusions, retinal vein occlusions, diabetic retinopathy, and sickle cell retinopathy are reviewed in detail.
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.
This document discusses neovascular glaucoma, also known as rubeotic glaucoma. It begins by defining the terminology and describing the clinical features. The main causes of neovascular glaucoma are diabetic retinopathy, central retinal vein occlusion, and carotid artery occlusive disease, all of which result in ocular tissue hypoxia. This hypoxia leads to the release of angiogenic factors like vascular endothelial growth factor that induce new blood vessel growth on the iris and in the anterior chamber angle, causing glaucoma. Later sections discuss theories of neovasculogenesis, angiogenic and vasoinhibitory factors, clinical course, differential diagnosis, medical management, and surgical options.
This document discusses retinal vascular occlusions, including arterial and venous occlusions. It provides details on the arterial supply and venous drainage of the retina. For retinal artery occlusions, it describes the etiology as embolism, atherosclerosis or inflammatory changes. Clinical features include sudden painless vision loss and a cherry red spot in the macula. Treatment may include ocular massage or thrombolytics within 4-6 hours. Retinal venous occlusions are associated with thrombus formation and compression of veins. Clinical features include blurred vision and retinal hemorrhages. Treatment focuses on managing risk factors and treating macular edema or neovascularization.
Nutritional deficiency Disorder are problems in india.
It is very important to learn about Indian child's nutritional parameters as well the Disease related to alteration in their Nutrition.
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...Donc Test
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)MuskanShingari
Statistics- Statistics is the science of collecting, organizing, presenting, analyzing and interpreting numerical data to assist in making more effective decisions.
A statistics is a measure which is used to estimate the population parameter
Parameters-It is used to describe the properties of an entire population.
Examples-Measures of central tendency Dispersion, Variance, Standard Deviation (SD), Absolute Error, Mean Absolute Error (MAE), Eigen Value
PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
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.
The Children are very vulnerable to get affected with respiratory disease.
In our country, the respiratory Disease conditions are consider as major cause for mortality and Morbidity in Child.
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) CosmeticsMuskanShingari
Acne is a common skin condition that occurs when hair follicles become clogged with oil and dead skin cells. It typically manifests as pimples, blackheads, or whiteheads, often on the face, chest, shoulders, or back. Acne can range from mild to severe and may cause emotional distress and scarring in some cases.
**Causes:**
1. **Excess Oil Production:** Hormonal changes during adolescence or certain times in adulthood can increase sebum (oil) production, leading to clogged pores.
2. **Clogged Pores:** When dead skin cells and oil block hair follicles, bacteria (usually Propionibacterium acnes) can thrive, causing inflammation and acne lesions.
3. **Hormonal Factors:** Fluctuations in hormone levels, such as during puberty, menstrual cycles, pregnancy, or certain medical conditions, can contribute to acne.
4. **Genetics:** A family history of acne can increase the likelihood of developing the condition.
**Types of Acne:**
- **Whiteheads:** Closed plugged pores.
- **Blackheads:** Open plugged pores with a dark surface.
- **Papules:** Small red, tender bumps.
- **Pustules:** Pimples with pus at their tips.
- **Nodules:** Large, solid, painful lumps beneath the surface.
- **Cysts:** Painful, pus-filled lumps beneath the surface that can cause scarring.
**Treatment:**
Treatment depends on the severity and type of acne but may include:
- **Topical Treatments:** Such as benzoyl peroxide, salicylic acid, or retinoids to reduce bacteria and unclog pores.
- **Oral Medications:** Antibiotics or oral contraceptives for hormonal acne.
- **Procedures:** Such as chemical peels, extraction of comedones, or light therapy for more severe cases.
**Prevention and Management:**
- **Cleanse:** Regularly wash skin with a gentle cleanser.
- **Moisturize:** Use non-comedogenic moisturizers to keep skin hydrated without clogging pores.
- **Avoid Irritants:** Such as harsh cosmetics or excessive scrubbing.
- **Sun Protection:** Use sunscreen to prevent exacerbation of acne scars and inflammation.
Acne treatment can take time, and consistency in skincare routines and treatments is crucial. Consulting a dermatologist can help tailor a treatment plan that suits individual needs and reduces the risk of scarring or long-term skin damage.
Selective alpha1 blockers are Prazosin, Terazosin, Doxazosin, Tamsulosin and Silodosin majorly used to treat BPH, also hypertension, PTSD, Raynaud's phenomenon, CHF
As the world population is aging, Health tourism has become vitally important and will be increased day by day. Because
of the availability of quality health services and more favorable prices as well as to shorten the waiting list for medical
services regionally and internationally. There are some aspects of managing and doing marketing activities in order for
medical tourism to be feasible, in a region called as clustering in a region with main stakeholders groups includes Health
providers, Tourism cluster, etc. There are some related and affecting factors to be considered for the feasibility of medical
tourism within this study such as competitiveness, clustering, Entrepreneurship, SMEs. One of the growth phenomenon
is Health tourism in the city of Izmir and Turkey. The model of five competitive forces of Porter and The Diamond model
that is an economical model that shows the four main factors that affect the competitiveness of a nation and its industries
in this study. The short literature of medical tourism and regional clustering have been mentioned.
Can Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptxFFragrant
There are many traditional Chinese medicine therapies to treat blocked fallopian tubes. And herbal medicine Fuyan Pill is one of the more effective choices.
Congestive Heart failure is caused by low cardiac output and high sympathetic discharge. Diuretics reduce preload, ACE inhibitors lower afterload, beta blockers reduce sympathetic activity, and digitalis has inotropic effects. Newer medications target vasodilation and myosin activation to improve heart efficiency while lowering energy requirements. Combination therapy, following an assessment of cardiac function and volume status, is the most effective strategy to heart failure care.
Spontaneous Bacterial Peritonitis - Pathogenesis , Clinical Features & Manage...Jim Jacob Roy
In this presentation , SBP ( spontaneous bacterial peritonitis ) , which is a common complication in patients with cirrhosis and ascites is described in detail.
The reference for this presentation is Sleisenger and Fordtran's Gastrointestinal and Liver Disease Textbook ( 11th edition ).
2. NORMAL FFA
• TO UNDERSTAND THE IMAGING OF THE VARIOUS DISEASES WE
FIRST MUST KNOW THE NORMAL FFA OF EYE
• NORMAL VASCULATURE FILLING AND PATTERN IS OBSERVED
• MACULA APPEARS AS DARK BECAUSE IS RELATIVELY AVASCULAR
• An obstruction, complete or partial, permanent or temporary,
may affect either the retinal arteries or veins.An obstruction,
complete or partial, permanent or temporary, may affect either
the retinal arteries or veins.
4. CRAO
• Obstruction of a retinal artery is usually due to an embolus;
superadded spasm often completes the occlusion
• There may be associated arteriosclerosis, hypertension or
Buerger disease .or giant cell arteritis
• Obstruction by an embolus is often secondary to a plaque of
atheroma situated at the bifurcation of the common carotid
artery in the neck, or occasionally to a diseased mitral or aortic
valve
• Hollenhorst plaque= Cholesterol emboli
5. • Might involve the whole artery (panretinal) or a peripheral
branch when the effects are localized
• CRAO is nearly always at the lamina cribrosa, where the vessels
normally become slightly narrowed. Such an accident causes
sudden and complete retinal ischaemia and this tissue rapidly
loses function. The eye becomes suddenly blind, although
when the causative factor is minute emboli, premonitory
obscurations of vision may occur
• Examination of the fundus reveals a very typical picture- Cherry
red spot at macula. (Oedema at ganglion cell layer which is
absent at foveola)
6.
7. • The larger arteries are reduced to threads; the smaller are invisible
but the veins are little altered except on the disc where they are
contracted. Within a few hours, the retina loses its transparency,
becoming opaque and milky-white, especially in the neighbourhood
of the disc and macula. At the fovea centralis, where the retina is
extremely thin, the red reflex from the choroid is visible and appears
as a round cherry-red spot, presenting a strong contrast to the
cloudy white background.
• Clinical features include- Sudden painless LOV, consective optic
atrophy,
• When obstruction to the blood flow is not complete, the flow may be
partially restored in the course of a few days, in which case gentle
pressure upon the globe may break up the column of venous blood
into red beads separated by clear interspaces. The beads move in a
jerky fashion through the vessels, sometimes in the normal direction
of blood flow, sometimes in the opposite direction (the ‘cattle-truck’
appearance). If the veins are easily emptied of blood or arterial
8. • The white appearance of the retina takes several weeks to clear
up but eventually the membrane regains its transparency and
appears normal; it is, however, completely atrophic apart from
the outer layers which receive their nourishment from the
choroid
• The vessels are contracted or reduced to white threads,
although some of them refill at a later stage due to the
establishment of a feeble collateral circulation through an
anastomosis with the ciliary system around the disc. The disc is
atrophic. There is no direct pupillary reaction and light
perception is lost. (RAPD/ Marcus gunn pupil)
• In some cases, a certain degree of central vision persists in
spite of apparent complete occlusion of the central artery
9. • This is due to the presence of cilioretinal arteries which, when
present, always supply the macular region and naturally escape
occlusion, or due to a macular branch of the central artery
given off proximal to the block.
• This is due to the presence of cilioretinal arteries which, when
present, always supply the macular region and naturally escape
occlusion, or due to a macular branch of the central artery
given off proximal to the block.
10.
11. • Treatment seldom helps, but attempts should be made to
relieve spasm or drive an embolus into a less important branch
if the patient is seen early. Massaging the globe is probably the
most effective method but paracentesis has been employed for
this purpose; to be effective, such measures must be adopted
without delay. Inhalation of amyl nitrite produces
vasodilatation. Branch occlusion may be relieved in this way.
The normal result of an occlusion of the central artery,
however, is blindness.
• Alternative vasodilators used: sublingual isosorbide dinitrate +
corbogen inhalation.
• IV mannitol
• Paracentesis
12. FEATURES OF VENOUS STASIS
RETINOPATHY
• Unilateral disc oedema with variable retinal vascular changes in
young healthy adults.
• The individual is usually 20–40 years of age and the initial
symptom is a vague, unilateral fogginess of vision
• Visual acuity remains good and vitreous haemorrhage is never
present. Neuro-ophthalmological examination is negative and
fluorescein angiography shows venous stasis with delayed
venous drainage
• There is generally no permanent visual defect
13. • The fundus picture simulates that of central venous thrombosis
and probably results from phlebitis affecting the central vein
within the optic nerve head. The cause is unknown, although
increased levels of circulating IgM have been reported in a large
number of patients
• Venous thrombosis usually occurs in elderly people with
cardiovascular disease or glaucoma. In these cases, the
obstruction is usually in the central vein just behind the lamina
cribrosa where the vein shares a common sheath with the
artery so that the two are affected by the same sclerotic
process
• At other times in arteriosclerotic patients, the block may be
peripheral, usually at a bifurcation or where a sclerosed artery
crosses a vein, an event which is particularly prone to occur in
14. • In young people, it may be due to an infective periphlebitis in
which case a branch of the central vein is affected
• Thrombosis may also be due to local causes, such as a chronic
glaucoma, orbital cellulitis or facial erysipelas. In all cases, the
condition is to be regarded as a danger signal and
constitutional investigation and treatment should be
assiduously undertaken.
15.
16. CRVO
• In CRVO, all the veins of the retina become enormously
engorged with blood and extremely tortuous, and the retina is
covered with haemorrhages.
• Sight is much impaired, though not as rapidly as in obstruction
of the central retinal artery
• In many cases, tortuous new vessels are formed upon the optic
disc ; in others, a collateral circulation is effected by similarly
tortuous new vessels in the retina
• Eventually the affected retina becomes atrophic with fine
pigmentary changes.
17.
18. • The prognosis is rendered worse by the fact that secondary
glaucoma ensues in 2–3 months in a considerable number of
cases, due to neovascularization at the angle of the anterior
chamber.
19. BRVO
• In BRVO when a single branch of the central vein is blocked, the
oedema and haemorrhages are limited to the area supplied by
the vein
• In these cases, the visual defect is partial but not exactly
sectorial as in the case of occlusion of a branch of the artery
• The prognosis for central vision is better, but unfortunately
blockage of the superior temporal vein frequently involves the
macula
• Eyes with intact or complete perifoveal capillary arcades have a
better visual prognosis than eyes with incomplete arcades as
demonstrated by angiography.Secondary glaucoma rarely
20.
21. • No treatment is effective in cases of venous occlusion once the
blockage has become complete.
• If there is widespread capillary occlusion, panphotocoagulation of the
retina (or cryoapplications if the media are hazy) may forestall
neovascular glaucoma and rubeosis iridis
• Widespread capillary occlusion is associated with cotton-wool spots,
delayed arteriovenous transit time, large vessel leakage and retinal
oedema
• In branch occlusion, destruction of areas of poor perfusion (as seen by
closure of retinal capillaries in an angiogram) may relieve persistent
oedema and inhibit neovascularization
• Photocoagulation should not be done until most of the intraretinal
blood is absorbed. Anti-VEGF therapy, as intravitreal injections, is now
an established treatment to improve visual recovery and prevent late