Title 19. GLAUCOMA.pdf ✅

PHARMD GURU Page 1 DEFINITION: Glaucomas are ocular disorders that lead to an optic neuropathy characterized by changes in the optic nerve head (optic disc) that is associated with loss of visual sensitivity and field. CLASSIFICATION:  Most common forms of Glaucoma’s are: 1) Open-angle glaucoma & 2) Closed-angle glaucoma.  Five major types of glaucoma exist. These are: OPEN-ANGLE (CHRONIC) GLAUCOMA: Open-angle, or chronic, glaucoma has no signs or symptoms except gradual vision loss. This loss may be so slow that your vision can suffer irreparable damage before any other signs become apparent. According the National Eye Institute (NEI) Trusted Source, this is the most common type of glaucoma. ANGLE-CLOSURE (ACUTE) GLAUCOMA: If the flow of your aqueous humor fluid is suddenly blocked, the rapid buildup of fluid may cause a severe, quick, and painful increase in pressure. Angle-closure glaucoma is an emergency situation. You should call your doctor immediately if you begin experiencing symptoms, such as severe pain, nausea, and blurred vision. CONGENITAL GLAUCOMA: Children born with congenital glaucoma have a defect in the angle of their eye, which slows or prevents normal fluid drainage. Congenital glaucoma usually presents with symptoms, such as cloudy eyes, excessive tearing, or sensitivity to light. Congenital glaucoma can run in families. GLAUCOMA
PHARMD GURU Page 2 SECONDARY GLAUCOMA: Secondary glaucoma is often a side effect of injury or another eye condition, such as cataracts or eye tumors. Medicines, such as corticosteroids, may also cause this type of glaucoma. Rarely, eye surgery can cause secondary glaucoma. NORMAL TENSION GLAUCOMA: In some cases, people without increased eye pressure develop damage to their optic nerve. The cause of this isn’t known. However, extreme sensitivity or a lack of blood flow to your optic nerve may be a factor in this type of glaucoma. ETIOLOGY: The back of your eye continuously makes a clear fluid called aqueous humor. As this fluid is made, it fills the front part of your eye. Then, it leaves your eye through channels in your cornea and iris. If these channels are blocked or partially obstructed, the natural pressure in your eye, which is called the intraocular pressure (IOP), may increase. As your IOP increases, your optic nerve may become damaged. As damage to your nerve progresses, you may begin losing sight in your eye. What causes the pressure in your eye to increase isn’t always known. However, doctors believe one or more of these factors may play a role:  Dilating eye drops  Blocked or restricted drainage in your eye  Medications, such as corticosteroids  Poor or reduced blood flow to your optic nerve  High or elevated blood pressure PATHOPHYSIOLOGY:  There are two major types of glaucoma: primary open-angle glaucoma (POAG) or ocular hypertension, which accounts for most cases and is therefore the focus of this
PHARMD GURU Page 3 chapter, and closed-angle glaucoma (CAG). Either type can be a primary inherited disorder, congenital, or secondary to disease, trauma, or drugs.  In POAG, the specific cause of optic neuropathy is unknown. Increased intraocular pressure (IOP) was historically considered to be the sole cause. Additional contributing factors include increased susceptibility of the optic nerve to ischemia, excitotoxicity, autoimmune reactions, and other abnormal physiologic processes.  Although IOP is a poor predictor of which patients will have visual field loss, the risk of visual field loss increases with increasing IOP. IOP is not constant; it changes with pulse, blood pressure, forced expiration or coughing, neck compression, and posture. IOP demonstrates diurnal variation with a minimum pressure around 6 pm and a maximum pressure upon awakening.  The balance between the inflow and outflow of aqueous humor determines IOP. Inflow is increased by β-adrenergic agents and decreased by α2- and β-adrenergic blockers, dopamine blockers, carbonic anhydrase inhibitors (CAIs), and adenylate cyclase stimulators. Outflow is increased by cholinergic agents, which contract the ciliary muscle and open the trabecular meshwork, and by prostaglandin analogues and β- and α2-adrenergic agonists, which affect uveoscleral outflow.  Secondary OAG has many causes, including exfoliation syndrome, pigmentary glaucoma, systemic diseases, trauma, surgery, ocular inflammatory diseases, and drugs. Secondary glaucoma can be classified as pretrabecular (normal meshwork is covered and prevents outflow of aqueous humor), trabecular (meshwork is altered or material accumulates in the intertrabecular spaces), or posttrabecular (episcleral venous blood pressure is increased).  Many drugs can increase IOP (Table 65–1). The potential to induce or worsen glaucoma depends on the type of glaucoma and on whether it is adequately controlled.  CAG occurs when there is a physical blockage of the trabecular meshwork, resulting in increased IOP.
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