Glaucoma types, Pathogenesis, Diagnosis and Treatment

5,998 views 37 slides Mar 27, 2020
Slide 1
Slide 1 of 37
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37

About This Presentation

Glaucomas are ocular disorders characterized by changes in the optic nerve head (optic disk) and by loss of visual sensitivity and field.
There are two major types of glaucoma: open-angle glaucoma, which accounts for most cases and closed-angle glaucoma.


Slide Content

Glaucoma Dr. Chavan P.R. Pharm D

Definition Glaucomas are ocular disorders characterized by changes in the optic nerve head (optic disk) and by loss of visual sensitivity and field Glaucoma – Greek word- meaning clouded or swollen cornea

Damage to the optic nerve(optic neuropathy) is usually caused by raised ocular pressure IOP: Depends on the balance between production and removal of aqueous humour NORMAL IOP = between 10 and 21mmHg IOP > 21.7 is abnormal

Optic nerve The optic nerve is a bundle of nerve fibers. It carries visual information from the retina to the brain.

Aqueous flow The eye has an internal fluid circulation system. Fluid is produced at the base of the iris and flows through pupil in front of iris The fluid exits the eye at the angle between the iris and the cornea where it drains through a spongy meshwork.

IOP IOP is determined by The rate of aqueous production, The resistance encountered by the aqueous humour as it flows out of the passages, and The venous pressure of the episcleral veins that drain into the anterior ciliary vein.

Factor affecting IOP Age Sex Race Heredity Diurnal & Seasonal variation Blood pressure Obesity Drugs Posture Exercise Hormone Refractive error Eye movement Eyelid closure Inflammation Surgery

Causes of glaucoma Slow fluid drainage. Pressure builds up and damages the optic nerve. Optic nerve damage can occur at different pressure levels for different people.

Higher risk people Family history of glaucoma African American race Older age Diabetes Cardiovascular disease Migraine syndromes Nearsightedness (myopia) Eye trauma Prolonged use of topical or systemic corticosteroids

Types

Open n closed angle glaucoma Closed Angle Glaucoma Open Angle Glaucoma

CLINICAL PRESENTATION Open-angle glaucoma - slow progression - Peripheral visual changes - optic disc changes Closed-angle glaucoma - intermittent prodromal symptoms(blurred/hazy vision) -halos around lights and occasionally headache - cloudy, edematous cornea; - ocular pain; - nausea, vomiting, - abdominal pain, - Diaphoresis.

pathogenesis

pathogenesis

pathogenesis

pathogenesis

DIAGNOSIS Open-angle glaucoma-optic disk changes and visual field loss, with or without increased IOP Normal tension glaucoma refers to disk changes, visual field loss, and iop of less than 21 mm hg Ocular hypertension refers to iop of more than 21 mm hg without disk changes or visual field loss Closed-angle glaucoma - gonioscopy . IOP is generally markedly elevated ( e.G. , 40 to 90 mm hg), hyperemic conjunctiva, cloudy cornea, shallow anterior chamber, and occasionally edematous and hyperemic optic disk.

Optic disc assessment Visual field assessment Tonometry Contrast Sensitivity

DESIRED OUTCOME The goal of drug therapy in patients with glaucoma is to preserve visual function by reducing the IOP to a level at which no further optic nerve damage occurs.

EVALUATION OF THERAPEUTIC OUTCOMES I dentifying an effective, well-tolerated regimen; closely monitoring therapy; and patient adherence. IOP response is assessed every 4 to 6 weeks initially, every 3 to 4 months after IOPs become acceptable, and more frequently after therapy is changed The visual field and disk changes are monitored annually, unless glaucoma is unstable or worsening.

Patients should be monitored for tachyphylaxis , especially with β -blockers or apraclonidine . 25% to 30% reduction in IOP is desired, Targets as low as less than 10 mm Hg are desired for very advanced disease. Using more than one drop per dose increases the risk of adverse events and cost, but not efficacy. Patients should be educated about possible adverse effects and methods for preventing them.

Proper patient education

If more than one topical drug is required, instillation should be separated by 5 to 10 minutes to provide optimal ocular contact. Adherence to drug therapy should be monitored because it is commonly inadequate and a cause of therapy failure.

TREATMENT

TREATMENT Open angle glaucoma Treatment is indicated for ocular hypertension if the patient has a significant risk factor such as -IOP greater than 25 mm Hg, -vertical cup-disk ratio greater than 0.5, or -central corneal thickness less than 555 micrometers. Additional risk factors to be considered include family history of glaucoma, black race, severe myopia, and presence of only one eye.

Treatment is indicated for all patients with elevated IOP and characteristic optic disk changes or visual field defects. Historically, β -blockers (e.g., timolol ) were the treatment of choice and continue to be used if there are no contraindications to potential β blockade caused by systemic absorption. β -Blockers have the advantage of low cost owing to generic formulations. Prostaglandin analogs (e.g., latanoprost , bimatoprost and travoprost ) have the advantage of strong potency, unique mechanism suitable for combination therapy, good safety profile, and once-a-day dosing. Brimonidine has the theoretical advantage of neuroprotection, which has not yet been demonstrated in humans. Topical CAIs are also suitable for first-line therapy.

Carbachol , topical cholinesterase inhibitors, and oral CAIs (e.g., acetazolamide ) are used as last-resort options after failure of less toxic options.

Pilocarpine and dipivefrin , a prodrug of epinephrine, are used as third line therapies because of adverse events or reduced efficacy as compared with newer agents. The optimal timing of laser or surgical trabeculectomy is controversial, ranging from initial therapy to after failure of third- or fourth-line drug therapy. Antiproliferative agents such as fluorouracil and mitomycin C are used to modify the healing process and maintain patency.

TREATMENT Closed angle glaucoma Acute closed-angle glaucoma with high IOP requires rapid reduction of IOP. Iridectomy is the definitive treatment, which produces a hole in the iris that permits aqueous flow to move directly from the posterior to the anterior chamber. Drug therapy of an acute attack typically consists of an osmotic agent and secretory inhibitor (e.g., β -blocker, α 2 agonist, latanoprost , or CAI), with or without pilocarpine .

Osmotic agents are used because they rapidly decrease IOP. Examples include glycerin, 1 to 2 g/kg orally, and mannitol , 1 to 2 g/kg IV. Although traditionally the drug of choice, pilocarpine use is controversial as initial therapy. Once IOP is controlled, pilocarpine should be given every 6 hours until iridectomy is performed.

Topical corticosteroids can be used to reduce ocular inflammation and synechiae . Epinephrine should be used with caution because it can precipitate acute closed-angle glaucoma, especially when used with a β -blocker.

Thank you