Glaucoma - Rai Flashcards
Glaucoma
chronic progressive ocular disease that toleads to progressive damage to the optic nerve and subsequent loss of visual field
major risk factor: increased IOP
Classification of Glaucoma
Based on Etiology
- Primary: open angle closure, congential
- Secondary: due to other ocular or systemic disease (inflammatory or lens induced glaucoma)
Based on Mechanism
- open angle glaucoma
- angle closure glaucoma
What is normal intraocular pressure?
10 to 21 mm Hg
Pathophysiology of IOP causing Optic Nerve damage
Mechanical Compression of Optic Nerve
Obstruction of blood supply and death of nerve fibers - causes hollowing of the optic nerve (cupping)
Eye Examination for Glaucoma
Check Vision
Refraction
Pupils (RAPD)
Measure IOP (Applanation, Tonopen, Schiotz, Pneumatonometer or palpation)
Gonioscopy
Examine Optic Nerve
Perimetry and Visual Fields - can do confrontation testing, or Humphrey Field Analyzer or Goldmen Perimetry
Imaging
ISNT Rule
“if it isn’t ISNT then it isn’t”
Rim width - distance between border of disc and position of blood vessel bending
Inferior > Superior > Nasal > Temporal
Characteristic Field Defects
Arcuate Defects
Nasal Step
Paracentral Defect
Annular Scotomas
Temporal Wedge
Tunnel Vision with temporal Island
Enlargment of Blind Spot
ACUTE VISION LOSS - - - REFER IMMEDIATELY
Acute Glaucoma
Keratitis
Endophthalmitis
Vitreous or Retinal Hemorrhage
Retinal Detachment
Acute Maculopathy
Retinal Vessel Occlusions
Optic Neuritis
Ischemic Optic Neuropathy
Cortical Infart
CHRONIC VISION LOSS - - - REFER NON-URGENTLY
Refractive Error
Media Disturbances in the tear film, cornea, lens or vitreous
Lesions of the nueral visual pathway from the retina to the visual cortex
Open Angle Glaucoma
usually no symptoms
identified on routine eye exams
some patients compalin of decreased peripheral vision
prognosis: depends on stage at time of diagnosis and ability to reduce and manage IOP
Managment of Chronic Glaucoma
establish a baseline
set a reasonable goal for IOP
lower the pressure
continue to observe patient, modifiy if necessary
Prostoglandin Analogs for Glaucoma
Xalatan, Travatan, Lumigan
- increase uveo-scleral outflow, reducing IOP
- administered once a day
ß Adgrenergic Antagonists
Timpotic, Betoptic S, Betagan
- reduces the production of aqueous humor by inhibiting cAMP, reduces IOP
- adminstered 1-2x a day
- side effects: corneal anesthesis, ptosis, hypotony, burining, superficial punctate keratitis, dry eye
- systemic: psychosis, fatigue, BRADYCARDIA, syncope, alopecia, nausea, impotence, ASTHMA, altered response to hypoglycemia, heart failure, tinnitus, depression, anxiety, hallucinations, dysarthria, CVA
Sympathomimetics
Epinephrine, Dipivefrin (Propine)
- reduces aqueous humor production, increases outflow through trabecular meshwork
- twice a day
- side effects: local irritation, pigmentation, corenal damage, macular edema, HTN, cardiac failure
Alpha Agonists: Iopidine, Alphagan
- reduce production of aqueous humor, possibly increases outflow
- 3x a day
- side effects: local allergy, dry nose and mouth, fatigue, trachyphylaxis
Parasympathomimetrics
Pilocarpine, Carbachol, Echothiophate
- increases outflow facility, reduces IOP
- 2x a day for echo, 4x a day for pilo
- side effects: browache, headache, occular allergy, pupillary constriction, RD, ocular inflammation
- parasympathetic effects
Describe the presentation of congenital glaucoma:
- Epiphora – watering eyes
- Photophobia
- Blepharospasm
- Buphthalmos – enlargement of the eye
- Haab’s Striae - Horizontal breaks in Descemet’s membrane
