This document discusses different types and treatments of glaucoma. It describes open angle glaucoma as a genetically predisposed degenerative disease affecting the trabecular meshwork that causes the intraocular pressure to rise insidiously. The main drug classes used to treat glaucoma are discussed, including beta blockers like timolol and betaxolol, alpha agonists like dipivefrine and brimonidine, prostaglandin analogues like latanoprost and travoprost, and carbonic anhydrase inhibitors. Miotic drugs are also mentioned. Angle closure glaucoma is characterized by a narrow iridocorneal angle that can cause rapid rises in pressure, and its treatment
Glaucoma is a progressive optic nerve damage generally associated with raised intraocular pressure. The main treatment is to lower intraocular pressure by reducing aqueous humor production or promoting drainage. Common drug classes for glaucoma treatment include beta-adrenergic blockers, alpha-adrenergic agonists, prostaglandin analogs, and carbonic anhydrase inhibitors. These drugs work to lower intraocular pressure by various mechanisms like reducing aqueous humor formation or increasing outflow facility. Side effects of drugs can include ocular issues like stinging or systemic effects like bronchospasm.
This document discusses the pharmacotherapy of glaucoma. It begins by introducing glaucoma as a group of ocular disorders united by intraocular pressure-associated optic neuropathy. It then covers the classification and mechanisms of action of various topical and systemic glaucoma drugs. The topical drugs discussed include cholinergic agents, adrenergic agonists, beta blockers, prostaglandin analogs, and carbonic anhydrase inhibitors. The mechanisms of these drugs include decreasing aqueous production and increasing outflow through different pathways. Side effects of the various drug classes are also summarized.
This document discusses various medical treatments for glaucoma, including topical eye drop medications from different drug classes. It describes the mechanisms of action, administration, efficacy and side effects of prostaglandin analogues, beta blockers, carbonic anhydrase inhibitors, alpha-2 agonists, miotics, osmotic agents, and some combination drug preparations. The document provides detailed information on commonly used glaucoma drugs to help clinicians select appropriate treatment options based on a patient's needs and risk factors.
Glaucoma treatment aims to lower elevated eye pressure and prevent further optic nerve damage. Treatment may involve prescription eye drops or surgery. The main treatments are prostaglandin analogues, beta blockers, alpha agonists, and carbonic anhydrase inhibitors, which work by reducing fluid buildup in the eye. Eye drops are usually the first approach but sometimes multiple drugs are combined or surgery is needed. Lowering eye pressure through medication or surgery can help reduce glaucoma risk and vision loss if treatment begins early. Lifestyle changes like exercise may also help control eye pressure.
This document summarizes various classes of anti-glaucoma medications, including their mechanisms of action and examples of drugs. It focuses on prostaglandins, describing how latanoprost, bimatoprost, and travoprost work. It also discusses adrenergic medications, carbonic anhydrase inhibitors, cholinergic drugs, and hyperosmotic agents for treating glaucoma. Side effects are provided for each class.
This document discusses different types and treatments of glaucoma. It describes open angle glaucoma as a genetically predisposed degenerative disease affecting the trabecular meshwork that causes the intraocular pressure to rise insidiously. The main drug classes used to treat glaucoma are discussed, including beta blockers like timolol and betaxolol, alpha agonists like dipivefrine and brimonidine, prostaglandin analogues like latanoprost and travoprost, and carbonic anhydrase inhibitors. Miotic drugs are also mentioned. Angle closure glaucoma is characterized by a narrow iridocorneal angle that can cause rapid rises in pressure, and its treatment
Glaucoma is a progressive optic nerve damage generally associated with raised intraocular pressure. The main treatment is to lower intraocular pressure by reducing aqueous humor production or promoting drainage. Common drug classes for glaucoma treatment include beta-adrenergic blockers, alpha-adrenergic agonists, prostaglandin analogs, and carbonic anhydrase inhibitors. These drugs work to lower intraocular pressure by various mechanisms like reducing aqueous humor formation or increasing outflow facility. Side effects of drugs can include ocular issues like stinging or systemic effects like bronchospasm.
This document discusses the pharmacotherapy of glaucoma. It begins by introducing glaucoma as a group of ocular disorders united by intraocular pressure-associated optic neuropathy. It then covers the classification and mechanisms of action of various topical and systemic glaucoma drugs. The topical drugs discussed include cholinergic agents, adrenergic agonists, beta blockers, prostaglandin analogs, and carbonic anhydrase inhibitors. The mechanisms of these drugs include decreasing aqueous production and increasing outflow through different pathways. Side effects of the various drug classes are also summarized.
This document discusses various medical treatments for glaucoma, including topical eye drop medications from different drug classes. It describes the mechanisms of action, administration, efficacy and side effects of prostaglandin analogues, beta blockers, carbonic anhydrase inhibitors, alpha-2 agonists, miotics, osmotic agents, and some combination drug preparations. The document provides detailed information on commonly used glaucoma drugs to help clinicians select appropriate treatment options based on a patient's needs and risk factors.
Glaucoma treatment aims to lower elevated eye pressure and prevent further optic nerve damage. Treatment may involve prescription eye drops or surgery. The main treatments are prostaglandin analogues, beta blockers, alpha agonists, and carbonic anhydrase inhibitors, which work by reducing fluid buildup in the eye. Eye drops are usually the first approach but sometimes multiple drugs are combined or surgery is needed. Lowering eye pressure through medication or surgery can help reduce glaucoma risk and vision loss if treatment begins early. Lifestyle changes like exercise may also help control eye pressure.
This document summarizes various classes of anti-glaucoma medications, including their mechanisms of action and examples of drugs. It focuses on prostaglandins, describing how latanoprost, bimatoprost, and travoprost work. It also discusses adrenergic medications, carbonic anhydrase inhibitors, cholinergic drugs, and hyperosmotic agents for treating glaucoma. Side effects are provided for each class.
Management of glaucoma aims to lower intraocular pressure (IOP) through various treatment modalities including medications, laser procedures, and surgery. Medications work by decreasing aqueous production or increasing outflow, with prostaglandin analogues and beta-blockers being first-line options. Laser trabeculoplasty and iridotomy can improve outflow and treat angle closure glaucoma. When medical management fails, trabeculectomy creates a fistula to lower IOP through filtration surgery. The document provides details on mechanisms, examples, dosages, and side effects of different glaucoma treatment classes and options.
Glaucoma 4 therapy of glaucomas, dr.k.n.jha,09.11.16ophthalmgmcri
This document discusses the management of glaucomas. The key points covered are: the goals of glaucoma therapy which are to preserve vision by reducing intraocular pressure (IOP) with minimal side effects; medical therapies include eye drops that work by various mechanisms to lower IOP such as beta-blockers, parasympathomimetics, carbonic anhydrase inhibitors, and prostaglandin analogues; surgical options include trabeculectomy which creates a fistula to drain aqueous humor from the anterior chamber externally to lower IOP; complications of glaucoma treatments can include side effects of medications or issues following surgery like infection and hypotony.
The document discusses various medical treatments for glaucoma, including different drug classes and their mechanisms of action, indications, contraindications and side effects. It provides detailed information on adrenergic agonists, beta-adrenergic antagonists, carbonic anhydrase inhibitors, and combined medications used to treat glaucoma. Key points covered include how the drugs work to lower intraocular pressure, when they should and should not be used, and common adverse effects.
Medical treatment of primary open angle glaucomaAdithya Phadnis
The document discusses goals and approaches for treating glaucoma. The primary goal is lowering intraocular pressure to reduce risk of vision loss. Medical approaches include various drug classes that decrease aqueous production or increase outflow, while surgical options are considered when pressure cannot be controlled through medical therapy alone. Follow-up care involves regular exams and testing to monitor pressure and disease stability.
This document provides an overview of glaucoma, including its anatomy, pathophysiology, classification, and pharmacological treatment. Glaucoma involves progressive optic neuropathy and vision loss due to increased intraocular pressure. It is classified into primary and secondary types. The main drugs used for treatment are prostaglandin analogues, beta blockers, alpha agonists, cholinergic agonists, and carbonic anhydrase inhibitors, which work to reduce aqueous humor production or increase outflow. Emerging therapies aim to provide neuroprotection to retinal ganglion cells. Surgery may also be used in some cases.
This document discusses beta-blockers and their uses in glaucoma. It first classifies beta-blockers as non-selective or cardioselective. It then discusses their mechanisms of action and indications, including hypertension, angina, heart arrhythmias, heart failure, and glaucoma. For glaucoma specifically, it explains that beta-blockers work by reducing aqueous humor production and intraocular pressure. Timolol is noted as the prototype beta-blocker preferred for ophthalmic use. The document also summarizes other drug classes used for glaucoma like prostaglandin analogues, alpha-agonists, carbonic anhydrase inhibitors, and parasympathomimetics.
This document discusses new drugs and therapies for glaucoma that are currently in development. It outlines several novel drug targets and mechanisms of action that are being investigated, including ROCK inhibitors, adenosine receptor agonists, BkCa channel modulators, siRNAs, cannabinoids, and local calcium channel blockers. It also discusses neuroprotective strategies such as antioxidants, memantine, neurotrophic growth factors, gene therapy, and stem cell therapy that aim to prevent further neural damage in glaucoma. Overall, the document provides an overview of the many innovative approaches that are being researched to better treat glaucoma beyond current first-line therapies.
3 4 cholinergic pharmacology younus h johan 2016younus johan
This document discusses drugs used to treat glaucoma, including cholinergic agents, beta-blockers, alpha agonists, prostaglandins, diuretics, and anticholinergic drugs. Cholinergic agents like pilocarpine work by improving aqueous humor drainage to lower intraocular pressure. Beta-blockers like timolol and alpha agonists like brimonidine decrease aqueous humor production. Prostaglandins increase outflow through the uveoscleral pathway. Diuretics and carbonic anhydrase inhibitors lower production of aqueous humor. Anticholinergic drugs are used for mydriasis, cycloplegia, peptic ulcers, and urinary disorders.
The document discusses various classes of medications used to treat glaucoma by reducing intraocular pressure, including beta-blockers, parasympathomimetics, adrenergic agonists, carbonic anhydrase inhibitors, and prostaglandin analogues. It provides details on the mechanisms of action, common medications, dosages, efficacy and side effects for each class. Beta-blockers such as timolol work by reducing the production of aqueous humor in the eye. Parasympathomimetics like pilocarpine increase outflow of aqueous humor through contraction of the ciliary muscle. Adrenergic agonists decrease aqueous humor production through vasoconstriction and inhibition of enzyme activity. Carbon
Drugs used in glaucoma are aimed at lowering intraocular pressure (IOP) by reducing aqueous humor production or increasing outflow. The main drug classes include beta-blockers, alpha-agonists, prostaglandin analogues, carbonic anhydrase inhibitors, and miotics. Beta-blockers and prostaglandin analogues are usually first-line treatments for open-angle glaucoma as they can lower IOP by 20-35% with once-daily dosing and minimal side effects. For acute angle-closure glaucoma, emergency treatment includes hypertonic agents, acetazolamide, and miotics to rapidly lower severely elevated IOP and prevent vision loss before definitive treatment with
This document discusses various glaucoma drugs, including prostaglandins, beta-blockers, alpha agonists, carbonic anhydrase inhibitors, osmotics, and miotics. Prostaglandins such as latanoprost and travoprost are often used as first-line treatment due to their greater IOP lowering effect compared to alternatives. Common side effects include conjunctival hyperemia and iris pigmentation changes. Beta-blockers lower IOP by decreasing aqueous production and common systemic side effects include bronchospasm. New drugs discussed include latanoprostene bunod and ROCK inhibitors.
This document summarizes different types of anti-glaucoma drugs. It discusses the classification of these drugs based on their mechanism of action, which includes reducing aqueous production, increasing aqueous outflow, or both. The main classes covered are beta blockers, prostaglandin analogues, parasympathomimetics, sympathomimetics, carbonic anhydrase inhibitors, and hyperosmotics. Specific drugs are provided within each class along with their indications, mechanisms, dosages, and potential side effects. Combination drug therapies are also mentioned. Treatment protocols are outlined for primary open angle glaucoma and acute primary angle-closure glaucoma.
Drugs used in glaucoma and myasthenia gravisSatyajit Ghosh
1) Drugs used to treat glaucoma work by lowering intraocular pressure through reducing aqueous humor production or increasing outflow. Topical medications include beta blockers, alpha agonists, prostaglandin analogs, carbonic anhydrase inhibitors, and miotics.
2) Angle closure glaucoma requires emergent treatment to rapidly lower pressure including intravenous mannitol or glycerol, oral acetazolamide, and topical pilocarpine and timolol.
3) Myasthenia gravis results from antibodies destroying acetylcholine receptors. Diagnosis involves physical exams, blood tests for antibodies, and electrodiagnostic tests. Treatment includes acetylcholinesterase inhibitors for symptoms and immunos
This document summarizes newer treatment modalities for glaucoma. It discusses how lowering intraocular pressure remains the primary treatment but may not stop disease progression. It then outlines several novel treatment approaches being investigated, including cannabinoids, cellular cytoskeletal modulators, memantine, and Rho kinase inhibitors. Clinical trials have been conducted or are ongoing for some of these alternative therapies to potentially treat glaucoma through neuroprotective mechanisms rather than solely lowering pressure. However, many of these novel agents have shown toxicity or failed to meet efficacy endpoints to date.
Ocular hypotensive drugs are used to reduce intraocular pressure and treat glaucoma. There are several classes of ocular hypotensive drugs: 1) Prostaglandin analogues like latanoprost which increase outflow of aqueous humor, 2) Beta-blockers like timolol which reduce aqueous production, 3) Alpha-2 adrenergic agonists like brimonidine and apraclonidine which decrease aqueous production, 4) Carbonic anhydrase inhibitors like acetazolamide which suppress aqueous humor production, and 5) Cholinergic agonists or miotics like pilocarpine which contract the iris sphincter muscle and ciliary body to facilitate aqueous outflow. Hyper
Glaucoma refers to a group of diseases characterized by optic neuropathy, visual field defects, and raised intraocular pressure. The document discusses the medical management of glaucoma including targeting intraocular pressure, evaluating patients, and selecting initial treatments such as beta blockers, prostaglandin analogues, adrenergic agonists, cholinergic drugs, carbonic anhydrase inhibitors, and hyperosmotic agents. Neuroprotective drugs that may help preserve vision by various mechanisms including blocking glutamate receptors and calcium channels are also reviewed. The ultimate goal of glaucoma treatment is to preserve vision and quality of life through long term management and control of intraocular pressure.
This document discusses the pharmacology of glaucoma. It describes that surgery is indicated for angle closure glaucoma, while medications are used to treat primary open-angle glaucoma by lowering intraocular pressure. The main classes of medications mentioned are beta blockers, carbonic anhydrase inhibitors, alpha agonists, sympathomimetics, prostaglandin analogues, and parasympathomimetics; each works by a different mechanism to reduce aqueous humor production or increase outflow to lower pressure in the eye.
Glaucoma is a chronic progressive optic neuropathy caused by an imbalance between the rate of aqueous humor formation and drainage, leading to damage of the optic nerve and loss of vision. It is defined as an intraocular pressure of over 21 mmHg. The aqueous humor is produced by the ciliary epithelium and normally drained through two routes - the conventional trabecular route which drains around 90% and the uveoscleral pathway which drains around 10%. Glaucoma is diagnosed by tonometry and treated through lifelong drug therapy, laser treatment, or surgery to lower intraocular pressure and prevent further vision loss.
This document discusses different classes of medications used to treat glaucoma, including alpha adrenergic agonists, miotics, and carbonic anhydrase inhibitors. It provides details on specific drugs within each class, such as brimonidine and apraclonidine, which are alpha adrenergic agonists that lower intraocular pressure by reducing aqueous humor production. Miotics were previously widely used but now only as a last option due to side effects. Carbonic anhydrase inhibitors like acetazolamide and dorzolamide lower intraocular pressure by reducing aqueous humor formation in the ciliary epithelium. The document also briefly describes the mechanisms of angle closure and open angle glaucoma.
Management of glaucoma aims to lower intraocular pressure (IOP) through various treatment modalities including medications, laser procedures, and surgery. Medications work by decreasing aqueous production or increasing outflow, with prostaglandin analogues and beta-blockers being first-line options. Laser trabeculoplasty and iridotomy can improve outflow and treat angle closure glaucoma. When medical management fails, trabeculectomy creates a fistula to lower IOP through filtration surgery. The document provides details on mechanisms, examples, dosages, and side effects of different glaucoma treatment classes and options.
Glaucoma 4 therapy of glaucomas, dr.k.n.jha,09.11.16ophthalmgmcri
This document discusses the management of glaucomas. The key points covered are: the goals of glaucoma therapy which are to preserve vision by reducing intraocular pressure (IOP) with minimal side effects; medical therapies include eye drops that work by various mechanisms to lower IOP such as beta-blockers, parasympathomimetics, carbonic anhydrase inhibitors, and prostaglandin analogues; surgical options include trabeculectomy which creates a fistula to drain aqueous humor from the anterior chamber externally to lower IOP; complications of glaucoma treatments can include side effects of medications or issues following surgery like infection and hypotony.
The document discusses various medical treatments for glaucoma, including different drug classes and their mechanisms of action, indications, contraindications and side effects. It provides detailed information on adrenergic agonists, beta-adrenergic antagonists, carbonic anhydrase inhibitors, and combined medications used to treat glaucoma. Key points covered include how the drugs work to lower intraocular pressure, when they should and should not be used, and common adverse effects.
Medical treatment of primary open angle glaucomaAdithya Phadnis
The document discusses goals and approaches for treating glaucoma. The primary goal is lowering intraocular pressure to reduce risk of vision loss. Medical approaches include various drug classes that decrease aqueous production or increase outflow, while surgical options are considered when pressure cannot be controlled through medical therapy alone. Follow-up care involves regular exams and testing to monitor pressure and disease stability.
This document provides an overview of glaucoma, including its anatomy, pathophysiology, classification, and pharmacological treatment. Glaucoma involves progressive optic neuropathy and vision loss due to increased intraocular pressure. It is classified into primary and secondary types. The main drugs used for treatment are prostaglandin analogues, beta blockers, alpha agonists, cholinergic agonists, and carbonic anhydrase inhibitors, which work to reduce aqueous humor production or increase outflow. Emerging therapies aim to provide neuroprotection to retinal ganglion cells. Surgery may also be used in some cases.
This document discusses beta-blockers and their uses in glaucoma. It first classifies beta-blockers as non-selective or cardioselective. It then discusses their mechanisms of action and indications, including hypertension, angina, heart arrhythmias, heart failure, and glaucoma. For glaucoma specifically, it explains that beta-blockers work by reducing aqueous humor production and intraocular pressure. Timolol is noted as the prototype beta-blocker preferred for ophthalmic use. The document also summarizes other drug classes used for glaucoma like prostaglandin analogues, alpha-agonists, carbonic anhydrase inhibitors, and parasympathomimetics.
This document discusses new drugs and therapies for glaucoma that are currently in development. It outlines several novel drug targets and mechanisms of action that are being investigated, including ROCK inhibitors, adenosine receptor agonists, BkCa channel modulators, siRNAs, cannabinoids, and local calcium channel blockers. It also discusses neuroprotective strategies such as antioxidants, memantine, neurotrophic growth factors, gene therapy, and stem cell therapy that aim to prevent further neural damage in glaucoma. Overall, the document provides an overview of the many innovative approaches that are being researched to better treat glaucoma beyond current first-line therapies.
3 4 cholinergic pharmacology younus h johan 2016younus johan
This document discusses drugs used to treat glaucoma, including cholinergic agents, beta-blockers, alpha agonists, prostaglandins, diuretics, and anticholinergic drugs. Cholinergic agents like pilocarpine work by improving aqueous humor drainage to lower intraocular pressure. Beta-blockers like timolol and alpha agonists like brimonidine decrease aqueous humor production. Prostaglandins increase outflow through the uveoscleral pathway. Diuretics and carbonic anhydrase inhibitors lower production of aqueous humor. Anticholinergic drugs are used for mydriasis, cycloplegia, peptic ulcers, and urinary disorders.
The document discusses various classes of medications used to treat glaucoma by reducing intraocular pressure, including beta-blockers, parasympathomimetics, adrenergic agonists, carbonic anhydrase inhibitors, and prostaglandin analogues. It provides details on the mechanisms of action, common medications, dosages, efficacy and side effects for each class. Beta-blockers such as timolol work by reducing the production of aqueous humor in the eye. Parasympathomimetics like pilocarpine increase outflow of aqueous humor through contraction of the ciliary muscle. Adrenergic agonists decrease aqueous humor production through vasoconstriction and inhibition of enzyme activity. Carbon
Drugs used in glaucoma are aimed at lowering intraocular pressure (IOP) by reducing aqueous humor production or increasing outflow. The main drug classes include beta-blockers, alpha-agonists, prostaglandin analogues, carbonic anhydrase inhibitors, and miotics. Beta-blockers and prostaglandin analogues are usually first-line treatments for open-angle glaucoma as they can lower IOP by 20-35% with once-daily dosing and minimal side effects. For acute angle-closure glaucoma, emergency treatment includes hypertonic agents, acetazolamide, and miotics to rapidly lower severely elevated IOP and prevent vision loss before definitive treatment with
This document discusses various glaucoma drugs, including prostaglandins, beta-blockers, alpha agonists, carbonic anhydrase inhibitors, osmotics, and miotics. Prostaglandins such as latanoprost and travoprost are often used as first-line treatment due to their greater IOP lowering effect compared to alternatives. Common side effects include conjunctival hyperemia and iris pigmentation changes. Beta-blockers lower IOP by decreasing aqueous production and common systemic side effects include bronchospasm. New drugs discussed include latanoprostene bunod and ROCK inhibitors.
This document summarizes different types of anti-glaucoma drugs. It discusses the classification of these drugs based on their mechanism of action, which includes reducing aqueous production, increasing aqueous outflow, or both. The main classes covered are beta blockers, prostaglandin analogues, parasympathomimetics, sympathomimetics, carbonic anhydrase inhibitors, and hyperosmotics. Specific drugs are provided within each class along with their indications, mechanisms, dosages, and potential side effects. Combination drug therapies are also mentioned. Treatment protocols are outlined for primary open angle glaucoma and acute primary angle-closure glaucoma.
Drugs used in glaucoma and myasthenia gravisSatyajit Ghosh
1) Drugs used to treat glaucoma work by lowering intraocular pressure through reducing aqueous humor production or increasing outflow. Topical medications include beta blockers, alpha agonists, prostaglandin analogs, carbonic anhydrase inhibitors, and miotics.
2) Angle closure glaucoma requires emergent treatment to rapidly lower pressure including intravenous mannitol or glycerol, oral acetazolamide, and topical pilocarpine and timolol.
3) Myasthenia gravis results from antibodies destroying acetylcholine receptors. Diagnosis involves physical exams, blood tests for antibodies, and electrodiagnostic tests. Treatment includes acetylcholinesterase inhibitors for symptoms and immunos
This document summarizes newer treatment modalities for glaucoma. It discusses how lowering intraocular pressure remains the primary treatment but may not stop disease progression. It then outlines several novel treatment approaches being investigated, including cannabinoids, cellular cytoskeletal modulators, memantine, and Rho kinase inhibitors. Clinical trials have been conducted or are ongoing for some of these alternative therapies to potentially treat glaucoma through neuroprotective mechanisms rather than solely lowering pressure. However, many of these novel agents have shown toxicity or failed to meet efficacy endpoints to date.
Ocular hypotensive drugs are used to reduce intraocular pressure and treat glaucoma. There are several classes of ocular hypotensive drugs: 1) Prostaglandin analogues like latanoprost which increase outflow of aqueous humor, 2) Beta-blockers like timolol which reduce aqueous production, 3) Alpha-2 adrenergic agonists like brimonidine and apraclonidine which decrease aqueous production, 4) Carbonic anhydrase inhibitors like acetazolamide which suppress aqueous humor production, and 5) Cholinergic agonists or miotics like pilocarpine which contract the iris sphincter muscle and ciliary body to facilitate aqueous outflow. Hyper
Glaucoma refers to a group of diseases characterized by optic neuropathy, visual field defects, and raised intraocular pressure. The document discusses the medical management of glaucoma including targeting intraocular pressure, evaluating patients, and selecting initial treatments such as beta blockers, prostaglandin analogues, adrenergic agonists, cholinergic drugs, carbonic anhydrase inhibitors, and hyperosmotic agents. Neuroprotective drugs that may help preserve vision by various mechanisms including blocking glutamate receptors and calcium channels are also reviewed. The ultimate goal of glaucoma treatment is to preserve vision and quality of life through long term management and control of intraocular pressure.
This document discusses the pharmacology of glaucoma. It describes that surgery is indicated for angle closure glaucoma, while medications are used to treat primary open-angle glaucoma by lowering intraocular pressure. The main classes of medications mentioned are beta blockers, carbonic anhydrase inhibitors, alpha agonists, sympathomimetics, prostaglandin analogues, and parasympathomimetics; each works by a different mechanism to reduce aqueous humor production or increase outflow to lower pressure in the eye.
Glaucoma is a chronic progressive optic neuropathy caused by an imbalance between the rate of aqueous humor formation and drainage, leading to damage of the optic nerve and loss of vision. It is defined as an intraocular pressure of over 21 mmHg. The aqueous humor is produced by the ciliary epithelium and normally drained through two routes - the conventional trabecular route which drains around 90% and the uveoscleral pathway which drains around 10%. Glaucoma is diagnosed by tonometry and treated through lifelong drug therapy, laser treatment, or surgery to lower intraocular pressure and prevent further vision loss.
This document discusses different classes of medications used to treat glaucoma, including alpha adrenergic agonists, miotics, and carbonic anhydrase inhibitors. It provides details on specific drugs within each class, such as brimonidine and apraclonidine, which are alpha adrenergic agonists that lower intraocular pressure by reducing aqueous humor production. Miotics were previously widely used but now only as a last option due to side effects. Carbonic anhydrase inhibitors like acetazolamide and dorzolamide lower intraocular pressure by reducing aqueous humor formation in the ciliary epithelium. The document also briefly describes the mechanisms of angle closure and open angle glaucoma.
Alpha adrenergic agonists like brimonidine and apraclonidine are medications used to treat glaucoma by reducing aqueous humor production or increasing its outflow to lower intraocular pressure. Apraclonidine lowers IOP by 25% and has common side effects like itching and dryness. Brimonidine is more alpha2 selective and lowers IOP by 20-27%. Miotics were once commonly used to treat glaucoma but now are rarely used due to side effects like pupil changes and headaches. Carbonic anhydrase inhibitors like acetazolamide and dorzolamide reduce aqueous formation to lower IOP, with side effects like paresthesia and acidosis.
GLAUCOMA
,dignosis , types of glaucoma , risk factors oo glaucoma and treatment , the clasis of drugs that use in treatment of glaucoma.
prepared by : Hardi Sdiq
university of sullaimani
collage of pharmacy
Glaucoma is caused by damage to the optic nerve from raised intraocular pressure. The main treatments are medications that lower IOP by reducing aqueous humor production or increasing outflow. The major drug classes include prostaglandin analogues, beta blockers, alpha agonists, carbonic anhydrase inhibitors, and parasympathomimetics. Newer drugs target the Rho kinase pathway or are nitric oxide donors. The goal of treatment is to lower IOP to a target level while minimizing side effects like hyperemia, allergy, and systemic effects.
This document discusses the treatment of various types of glaucoma. There are several types of open angle glaucoma that are treated with various eye drop medications including beta blockers, prostaglandin analogues, alpha-2 agonists, parasympathomimetics, and carbonic anhydrase inhibitors. These work by reducing aqueous humor production or increasing outflow. Common side effects include dryness, redness, blurred vision, and systemic effects like bronchospasm, bradycardia, and heart failure. Close angle glaucoma is treated with medications to lower pressure like acetazolamide and pilocarpine as well as laser iridotomy. Pigmentary glaucoma can be treated with mi
Glaucoma is a group of eye disorders characterized by abnormally high intraocular pressure that can damage the optic nerve and result in vision loss. The document defines glaucoma and identifies primary open-angle glaucoma and primary angle-closure glaucoma as the two most common types. Risk factors include aging, genetics, eye injuries or surgeries, and certain medical conditions. Treatment involves medications or surgery to reduce pressure in the eye in order to prevent further vision loss from optic nerve damage.
MYDRIATIC AND MIOTIC AGENTS AND DRUGS USED IN GLAUCOMA Rishabh Sharma
A brief Pathophysiology Presentation on the topic " MYDRIATIC AND MIOTIC AGENTS AND DRUGS USED IN GLAUCOMA "
Includes Both Open Angle and Closed Angle Glaucoma , their Mechanism Of Onset , Pathophysiology and Treatment ( Drugs Used In Glaucoma )
This document discusses the medical management of glaucoma. It covers principles of diagnosis and assessment, results of clinical trials on glaucoma treatment, pharmacokinetics of topical drugs, educating patients, follow up, and various classes of anti-glaucoma medications including cholinergic stimulants, beta-blockers, alpha-adrenergic receptor antagonists, prostaglandin analogs, and carbonic anhydrase inhibitors. Side effects and administration of these drug classes are also outlined.
This document summarizes medical treatments for glaucoma, including various drug classes and specific agents. It discusses the mechanisms of action, efficacy, side effects, and considerations for prostaglandin analogues, beta blockers, alpha-2 agonists, carbonic anhydrase inhibitors, miotics, osmotic agents, and fixed combination therapies. Key points include: prostaglandins are often first-line due to efficacy and safety profile; beta blockers may be preferred in some cases but should not be used at bedtime; alpha-2 agonists have neuroprotective effects but require caution in young children; and fixed combinations can improve compliance while maintaining efficacy of individual components.
Dr. Sneha Dange will present on the pharmacotherapy of glaucoma. The presentation will cover the anatomy of the eye relevant to glaucoma, the goals of glaucoma treatment, and an overview of current pharmacotherapy options including beta blockers, alpha agonists, prostaglandin analogues, cholinergic agonists, carbonic anhydrase inhibitors, and hyperosmotic agents. Recent advances discussed will include antioxidants, forskolin, and Ginkgo biloba as complementary treatments.
Medical Management of Glaucoma (2) (1).pptxAleenaS18
This document discusses the medical management of glaucoma through pharmacological agents. It begins by classifying topical and systemic antiglaucoma medications. It then covers the mechanisms of action, pharmacokinetics, indications, and side effects of various drug classes - including prostaglandin analogues, beta blockers, alpha agonists, and carbonic anhydrase inhibitors. The document emphasizes the importance of balancing efficacy of IOP reduction with minimization of side effects and adherence to treatment.
drug relative to eyes with their meiotic and mydriatic effect.
In the presentation discus about spasm of accommodation and cycloplegic action on eye . pharmacological action , dosage also discussed of condition developed on eye i.e. Glaucoma
Glaucoma is a group of eye diseases that damage the optic nerve and can cause vision loss. It is usually caused by an increase in pressure within the eye due to blocked drainage canals. There are two main types - open angle glaucoma caused by partial blockage and closed angle glaucoma caused by sudden, complete blockage. Treatment aims to lower intraocular pressure through eye drops, oral medication, laser therapy or surgery depending on the severity. Surgical treatment is usually a last resort but is the primary approach for closed angle glaucoma emergencies. Post-operative care involves anti-inflammatory and antibiotic eyedrops.
This document summarizes various drugs used to treat common eye disorders, organized by drug class. It lists the pharmacology, action, and example products for each class. The main classes covered are: sympathomimetics, miotics, beta-adrenergic blockers, carbonic anhydrase inhibitors, osmotic diuretics, mydriatics, prostaglandin analogues, local anesthetics, cycloplegic mydriatics, ophthalmic anti-infectives, NSAIDs, ophthalmic steroid anti-inflammatories, vasoconstrictors, and antiallergy medications. For each class it provides a brief 1-2 sentence description of the pharmacological action and lists 1
The document discusses thermoregulation and normal body temperature. It notes that the hypothalamus contains heat- and cold-sensitive neurons that detect core and skin temperatures and trigger various neuronal mechanisms to increase or decrease body heat through processes like vasodilation, sweating, shivering and chemical thermogenesis. These keep the body's core temperature within a normal range of 36.1-37.8°C (97.0-100°F) orally. Fever results when pyrogens raise the hypothalamic set point.
The spinothalamic system transmits somatosensory information about pain, temperature, and crude touch from the skin to the thalamus. It consists of first-order neurons in the dorsal horn that synapse on second-order neurons in the spinal cord. These second-order neurons decussate and ascend contralaterally to the thalamus. They then synapse on third-order neurons that project to the somatosensory cortex. The system includes the lateral and anterior spinothalamic tracts, which are important for localization of painful or thermal stimuli. It also includes smaller tracts that project to the reticular formation and tectum.
An illustration about what happens from the beginning to the end of a septic shock & what are the factors that cause it.
*There are notes provided in some slides.
The document summarizes the descending motor tracts that transmit signals from the brain to lower motor neurons and muscles. It focuses on the pyramidal tracts, including the corticospinal tract which controls voluntary limb movement, and corticobulbar tract which controls head and neck muscles. The corticospinal tract originates in motor areas of the cortex and projects through the brainstem and spinal cord. The corticobulbar tract projects to motor nuclei controlling cranial nerves.
Genetic factors can cause inherited bleeding disorders through mutations in single genes, variants in genes, or chromosomal imbalances. The document discusses two main inherited bleeding disorders: von Willebrand disease and hemophilia. Von Willebrand disease is caused by mutations in the von Willebrand factor gene and is characterized by a decreased von Willebrand factor level. Hemophilia A is caused by factor VIII deficiency due to mutations on the X chromosome, while hemophilia B is caused by factor IX deficiency. The severity of hemophilia depends on the factor level.
G6PD deficiency is an X-linked genetic condition characterized by low levels of the enzyme glucose-6-phosphate dehydrogenase, which helps maintain red blood cell health. People with G6PD deficiency are prone to hemolytic anemia during times of oxidative stress, such as certain infections, foods like fava beans, drugs, and chemicals. The condition is most common in people from the Mediterranean and Africa and provides some protection against malaria.
Epilepsy is characterized by recurrent seizures caused by abnormal neuronal activity in the brain. Seizures can have various presentations depending on the affected brain region. Epilepsy has genetic and acquired causes such as brain injuries, tumors, or infections. Diagnosis involves tests like EEG, MRI, and bloodwork to identify structural or metabolic abnormalities. Treatment focuses on medications, dietary changes, surgery, or devices like vagus nerve stimulators to reduce or eliminate seizures. Identifying a patient's epilepsy syndrome provides guidance on determining causes and appropriate treatments.
This document discusses different types of ear discharge including wax, pus, mucus, blood, and cerebrospinal fluid. It notes that ear discharge can be caused by conditions like otitis externa, otitis media, otomycosis, and trauma. Signs and symptoms of ear discharge include ear pain, swollen ear, itchy ear, vertigo, and tinnitus. The color and consistency of the discharge provides clues to the underlying cause, with purulent discharge indicating infection, mucoid discharge a perforated eardrum, and bloody or clear fluid potential trauma or skull base surgery.
Hematopoiesis occurs in bone marrow where large numbers of white blood cells and red blood cells are generated each hour. Specifically, 2-5 x 108 white blood cells and 1 x 1010 red blood cells are produced per hour through hematopoiesis in bone marrow. This process is essential for generating new blood cells to replenish and maintain the levels in circulation.
Abstract of depression assessment:
- How to assess
- Differential diagnosis for physiologic causes vs. psychological
- Rating scales
*There are notes provided in some slides
Cranial hematomas can be either extra-axial (outside the brain), occurring between membranes covering the brain, or intra-axial (inside the brain). The most common extra-axial hematomas are epidural, subdural, and subarachnoid hematomas. Epidural hematomas typically result from injuries that rupture the middle meningeal artery. Subdural hematomas are caused by tears in bridging veins, while subarachnoid hematomas usually stem from ruptured cerebral aneurysms. In newborns, common cranial hematomas include caput succedaneum, cephalohematoma, and subgaleal hematoma, which are usually due to difficult childbirth and
Autoimmune thyroiditis is an autoimmune disease where antibodies are produced against thyroid antigens, potentially causing inflammation and destruction of thyroid tissue leading to hypothyroidism. It has genetic and environmental risk factors and a higher prevalence in women. Primary hypothyroidism can be caused by autoimmune thyroiditis (Hashimoto's thyroiditis), which is characterized by lymphocytic infiltration of the thyroid gland and sometimes enlargement. Symptoms include weight gain, fatigue, dry skin and hair, and depression.
Anatomical description & illustration of:
- Ankle joint, it's relation with both leg and foot, movements.
- Foot bones, joints, ligaments, movements, arches and clinical significance in both ankle & foot.
*There are notes provided in some slides
Acute myelogenous leukemia (AML) is a cancer of the blood and bone marrow characterized by the rapid growth of abnormal white blood cells that build up in the bone marrow and interfere with normal blood cell production. AML is most common in adults around age 50 and has an overall low survival rate of 15-30%. Risk factors include other blood disorders, genetic conditions like Down syndrome, and exposure to chemicals or radiation. Signs and symptoms include fatigue, fever, bleeding, bone pain, and an enlarged spleen or lymph nodes. Laboratory tests show abnormal blood cell counts and the presence of immature white blood cells in the bone marrow. Immunophenotyping helps distinguish AML from other leukemias. Classification systems organize A
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Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
Know the difference between Endodontics and Orthodontics.Gokuldas Hospital
Your smile is beautiful.
Let’s be honest. Maintaining that beautiful smile is not an easy task. It is more than brushing and flossing. Sometimes, you might encounter dental issues that need special dental care. These issues can range anywhere from misalignment of the jaw to pain in the root of teeth.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
Lecture 6 -- Memory 2015.pptlearning occurs when a stimulus (unconditioned st...AyushGadhvi1
learning occurs when a stimulus (unconditioned stimulus) eliciting a response (unconditioned response) • is paired with another stimulus (conditioned stimulus)
How to Control Your Asthma Tips by gokuldas hospital.Gokuldas Hospital
Respiratory issues like asthma are the most sensitive issue that is affecting millions worldwide. It hampers the daily activities leaving the body tired and breathless.
The key to a good grip on asthma is proper knowledge and management strategies. Understanding the patient-specific symptoms and carving out an effective treatment likewise is the best way to keep asthma under control.
Are you looking for a long-lasting solution to your missing tooth?
Dental implants are the most common type of method for replacing the missing tooth. Unlike dentures or bridges, implants are surgically placed in the jawbone. In layman’s terms, a dental implant is similar to the natural root of the tooth. It offers a stable foundation for the artificial tooth giving it the look, feel, and function similar to the natural tooth.
low birth weight presentation. Low birth weight (LBW) infant is defined as the one whose birth weight is less than 2500g irrespective of their gestational age. Premature birth and low birth weight(LBW) is still a serious problem in newborn. Causing high morbidity and mortality rate worldwide. The nursing care provide to low birth weight babies is crucial in promoting their overall health and development. Through careful assessment, diagnosis,, planning, and evaluation plays a vital role in ensuring these vulnerable infants receive the specialize care they need. In India every third of the infant weight less than 2500g.
Birth period, socioeconomical status, nutritional and intrauterine environment are the factors influencing low birth weight
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
2. MYDRIATICS
Agents that induce dilation of the pupil.
To permit examination of the retina and other deep structures of the eye, and also to
reduce painful ciliary muscle spasm.
Anticholinergic drugs:
• Block action of acetylcholine that constricts pupillae muscle.
• Relaxation of ciliary muscle.
• Increase intraocular pressure.
Adrenergic drugs:
• Contract radial muscles of the iris.
• Increase drainage of aqueous humor.
3. TIMOLOL
Non-selective beta blocker
• Eye drops: used to treat open-angle glaucoma by reducing aqueous humor
production through blockage of the β receptors on the ciliary epithelium.
• Adverse effects: burning sensation, eye redness.
4. DORZOLAMIDE
Carbonic anhydrase inhibitor (diuretic)
• Used topically to lower increased intraocular pressure (20%) in open-
angle glaucoma and ocular hypertension.
• Inhibition of carbonic anhydrase II in the ciliary processes of the eye decreases
aqueous humor secretion, who are insufficiently responsive to beta-blockers.
• Dorzolamide/timolol
• Adverse effects: Ocular stinging, burning, itching and bitter taste.
Editor's Notes
Inhibition of carbonic anhydrase II in the ciliary processes of the eye decreases aqueous humor secretion, presumably by slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport.