1. Glaucoma is:
    a group of diseases characterized by visual field loss secondary to optic nerve damage.
  2. Pemanent Blindness can occur with ______
    • Glaucoma.
    • It is the leading cause of preventable blindness
  3. There are two types of Glaucoma:
    • 1. Open Angle Glaucoma
    • 2. Acute Angle-Closure Glaucoma (aka Narrow Angle aka Closed Angle)
  4. Statistics of Open Angle Glaucoma:
    • 90 % of cases
    • Leading cause of blindness among African Americans & 3rd among whites
  5. Risks of Open Angle Glaucoma:
    • Elevation of IOP (intraocular pressure)
    • African Americans
    • family history
    • advancing age
  6. Signs/Symptoms of Open Angle Glaucoma:
    • insidious(slow onset/don't notice) until extensive damage
  7. Screening for Open Angle Glaucoma:
    every 2 years for high risk individuals until age 45 then aannual persons without risk factors screening every 4 years until age 45 then every 2 years
  8. Prognosis for Open Angle Glaucoma:
    • No CURE
    • the goal is to reduce IOP to slow/stop progression
  9. Treatment of Open Angle Glaucoma:
    • Chronic drug therapy to decrease IOP
    • Surgery if drug therapy fails
  10. 1st Line drugs for Open Angle Glaucoma:
    • Beta-adrenergic blocking agents (Beta Blockers)
    • Alpha 2 adrenergic agonists
    • Prostaglandin analogs
  11. 2nd Line drugs for Open Angle Glaucoma:
    • Cholinergic Agonists
    • Carbonic Anhydrase Inhibitors
    • Nonselective Adrenergic Agonists
  12. Route for Open Angle Glaucoma:
  13. Drug evaluation for Open Angle Glaucoma:
    • Decreased IOP
    • Pharmacotherapy is usually prescribed when IOP is > 21 mmHg.
    • Some prescribers wait until IOP is 28 mmHg to 30 mmHg.
  14. Onset/Peak/Duration of Open Angle Glaucoma:
    • Onset: 6-8 weeks to reach
    • Peak: 2-4 months before checking for therapeutic effectiveness
    • Effects continue for 2-4 weeks after drug is discontinued
  15. Note to Remember for Open Angle Glaucoma:
    • Because drugs in different classes have different mechanisms of action, combined therapy can be more effective than monotherapy.
    • Overall important concept in drug therapy for many diseases.
  16. Statistics of Angle-Closure Glaucoma:
    5% of glaucoma cases
  17. Risks of Angle-Closure Glaucoma:
    • displacement of the iris from TRAUMA
    • Asian descent
    • older adults
  18. Signs/Symptoms of Angle-Closure Glaucoma:
    • Unilateral
    • extremely painful
    • headaches
    • bloodshot eyes
    • foggy vision
    • halos around bright lights
    • bulging iris
    • irreversible loss of vision can occur within 1-2 days
  19. Treatment for Angle-Closure Glaucoma:
    • Surgery
    • Drug Therapy to control the acute attack
  20. Drugs for Angle-Closure Glaucoma:
    • Osmotic agents
    • short-acting mitotics
    • carbonic anhydrase inhibitors
    • topical beta-adrenergic blocking agents to suppress symptoms
  21. Process of Giving Eye Drops:
    • Wash Hands
    • Cleanse exudates from eyes
    • Tilt client head
    • Gently pull lower lid down and client look up
    • Instill drops in the "sac" not the eye
    • Apply gentle pressure for 30 sec. to 1 min over inner canthus to prevent absoprtion thru tear duct
    • To avoid cross contamination, dropper should not touch the client's eyes, lashes, etc.
  22. Classes of Glaucoma Drugs
    • Prostaglandins-1st line
    • Autonomic Agents: beta-adrenergic blockers, nonselective sympathomimetics, alpha-adrenergic agonists, and cholinergic agonists
    • Carbonic anhydrase inhibitors
    • Osmotic diuretics
  23. Prostaglandins approved for glaucoma:
    • Lantanoprost (Xalatan)-prototype
    • Bimatoprost (Lumigan)
    • Travaprost (Travatan)
    • Unoprostone (Rescula)
  24. How do Prostaglandins work?
    • Lowers IOP by relaxing the ciliary muscle.
    • Causes fewer side effects than beta blockers
    • Use daily in the EVENING (bc it can be irritating to eye)
    • Drops
  25. Travoprost is more effective in
    African Americans than the other prostaglandins
  26. Common side effects of Prostaglandins:
    • A browning pogmentation of the iris that may be irreversible
    • A browning of the eyelid
    • Growth of eyelashes (Latesse!)
  27. Lesser side effects of Prostaglandins:
    • Blurred vision
    • Burning
    • Stinging
    • Conjunctival hyperemia and punctuate keratopathy
    • Rare side effect=migraine
  28. Adverse effects/toxicity of Prostaglandins:
    • respiratory infection
    • angina
    • muscle or joint pain
  29. Patient Education for Prostaglandins:
    • Remove contact lenses before use and 15 minutes after instillation
    • Proper installation technique
  30. Autonomic Agents for Glaucoma:
    • beta-adrenergic blockers
    • nonselective sympathomimetics
    • alpha-adrenergic agonists
    • cholinergic agonists
  31. Beta-Adrenergic Blockers for Glaucoma include:
    • betaxolol
    • levobetaxolol
    • carteolol
    • levobunolol
    • metipranolol
    • timolol
    • Are 1st line drugs; although Prostaglandins are becoming 1st line
  32. How do beta-adrenergic blockers work and why is your patient getting it?
    • Open-angle glaucoma
    • Decreases IOP 20-30% by decreasing production of aqueous humor by the ciliary body.
    • Exact mechanism of action is UNKNOWN.
    • Route: drops
    • Frequency: daily or bid
  33. Local/Systmeic Effects for Beta-Adrenergic Blockers:
    • LOCAL: stinging, conjunctivitis, blurred vision, photophobia, dry eyes
    • SYSTEMIC: cardiac arrhythmias, N/V, constipation, impotence, decreased libido, dizziness, vertigo, pulmonary edema, stroke, bradycardia, CHF
  34. Patient Education for Beta-Adrenergic Blockers:
    • proper instillation to reduce systemic absorption
    • may mask s/s of hypoglycemia
    • discontinue gradually about 48 hours prior to surgery
    • wear sunglasses if photophobic
    • don't drive if dizziness
    • report any systemic side effects
  35. Contraindications of Beta-Adrenergic Blockers:
    • drug-drug interactions if absorbed systemic
    • increases effects of insulin, verapamil, NSAIDS
  36. Alpha 2 Adrenergic Agonists include:
    • apraclonidine (Lopidine)-used for short term therapy only or as a pre-op med. Does NOT cross the BBB.
    • brimonidine (Alphagan)-only alpha 2 adrenergic agonist approved for long term use. Crosses BBB.
  37. Why is my patient getting Alpha 2 Adrenegic drops?
    • open angle glaucoma
    • ocular hypertension
    • mydriasis (dilate pupils for an exam)
    • pre-op to control bleeding
  38. How do Alpha 2 Adrenergic Agonists work?
    reduces aqueous humor production
  39. Contraindications for Alpha 2 Adrenergic Agonists:
    • hypersensitivity to epi
    • narrow angle glaucoma
    • abraded cornea
  40. Side Effects and Patient Education for Alpha 2 Adrenergic Agonists:
    • signiificant if absorbed systemically
    • cardiac
    • neurologic
    • BP
    • sweating
    • tremors
    • Patient Education: crosses placenta, installation techniques, what side effects to report to MD
  41. Cholinergic Agonists aka
  42. Mitotics include:
    pilocarpine (IsoptoCarpine)-widely used in the past; 2nd line drug
  43. Why is my patient getting Mitotics and how do they work?
    • Open angle glaucoma and angle closure glaucoma
    • Activates cholinergic receptors in the eye and produces miosis (constriction of pupil)
  44. Frequency of Cholinergic agonists:
    • open angle (chronic): every 4-12 hours
    • closed angle (acute): every 5-10 minutes for 3-6 doses
  45. Contraindications and Nursing Implications of Mitotics:
    • Teach proper instillation
    • Hold if pupillary constriction occurs
  46. Serious Adverse Effects/ Toxicity of Cholinergic Agonists:
    with systemic absorption: salivation, tachycardia, hypertension, bronchospasm, sweating, N/V
  47. Non-selective sympathomimetics include:
    • Dipivefrin HCL (Propine)
    • Epinephrine
  48. How do non-selective sympathomimetics work and why are they taking it?
    • Stimulate the sympathetic nervous system to produce mydriasis(pupil dilation) increasing outflow of aqueous humor thereby reducing IOP
    • These drugs are not as effective as the beta adrenergic blockers or prostaglandins.
    • Open angle Glaucoma
  49. Side Effects of Non-selective sympathomimetics:
    • orthostatic hypotension
    • facial flushing
    • headache
    • palpitations
    • anxiety
    • nausea
  50. Adverse Effects of Non-selective sympathomimetics:
    • severe headache
    • electrolyte imblanaces
    • edema
    • tachycardia
    • hypertension
    • CNS reactions (especially patients with cardiac history)
  51. Contraindications of Non-selective sympathomimetics:
    • assess for sensitivity to sulfites
    • avoid with MAOIs
    • narrow angle glaucoma
    • opthalmic beta-blockers
    • digitalis
  52. Carbonic Anhydrase Inhibitors (CAIs) include:
    • acetazolamide (Diamox)
    • brinzolamide (Azopt)
    • dorzolamide (Trusopt)
    • methazolamide
  53. How do CAIs work? Frequency? Route?
    • Job=decrease IOP
    • Frequency=bid or qid or po preperations once to qid depending on drug
    • Route=drops or systemically
  54. Topical Side Effects of CAIs:
    • photosensitivity blurred vision
    • dry eye
    • bitter taste
    • local itching
    • sensation of foreign body in the eye
    • headache
  55. Systemic Side Effects of CAIs:
    • diuresis
    • electrolyte imbalances
    • blood dyscrasias
    • flaccid paralysis
    • hepatic impairment
    • diarrhea
    • paresthesia
  56. Administration considerations of CAIs:
    • administer early to avoid nocturia
    • administer oral form with food or meal to decrease GI effects
    • may crush tablet
    • caution in people with adrenocortical insufficiency
  57. Contraindications of CAIs:
    • sensitivity to sulfonamides
    • hyponatremia
    • hypokalemia
    • hepatic or renal dysfunction
    • can affect bone marrow function
  58. Drug Interactions of CAIs; and Labs??
    • interferes with renal excretion of quinidine, salicylates, and lithium
    • Labs=false positive results in tests for urinary protein, Na, K, bicarb, uric acid, thyroid uptake, and WBC
  59. Osmotic Diuretics include:
    • mannitol
    • urea
    • glycerin
    • isosorbide
  60. Why is my patient taking osmotic diuretics?
    occasionally used pre-op and post-op with ocular surgery or as emergency treatment for acute closed angle glaucoma attacks
  61. How do osmotic diuretics work?
    quickly reduce plasma volume and reducing formation of aqueous humor
  62. Osmotic diuretics are taken:
  63. Adverse Effects of Osmotic Diuretics:
    • headache
    • tremors
    • dizziness
    • dry mouth
    • fluid and electrolyte imbalance
    • thrombophlebitis or clot near IV site
  64. Side Effects of Osmotic Diuretics:
    • hypotension
    • facial flushing
    • headache
    • palpitations
    • anxiety
    • nausea
  65. Drugs for eye exams and surgery:
    • Cycloplegics
    • Mydriatics
  66. Cycloplegics are:
    drugs that paralyze the ciliary muscle
  67. Mydriatics are:
    drugs that dilate pupils
  68. Cycloplegics and Mydriatics are used for:
    • diagnosis and surgical treatment of opthalmic disorders
    • There are two classes: Anticholinergic and Adrenergics
  69. Anticholinergics include:
    • Atropine
    • Scopolamine
  70. Anticholinergics are used for; and they work by:
    • eye exams, surgery, uveitis
    • produces mydriasis and cycloplegia
  71. Admin considerations for Anticholinergics:
    • use with caution in clients with glaucoma
    • compress the lacrimal duct 2-3 minutes after admin
  72. Route for Anticholinergics:
    opthalmic ointment
  73. Local Side Effects of Anticholinergics:
    • blurred vision
    • photophobia
    • allergic lid reactions
  74. Systemic Side Effects of Anticholinergica:
    • confusion
    • delirium
    • drowsiness
    • dry mouth
    • flushing
    • tachycardia
  75. Adverse Reactions of Anticholinergics:
    • slurred speech
    • hallucinations
    • tachycardia
    • psychiatric and behavioral problems
    • fever
    • respiratoey depression
    • coma
Card Set
Drug Therapy for the Eyes