Ophtho2- Glaucoma

  1. Increased IOP is always the result of a(n) __________.
    decrease in outflow
  2. Decreased IOP is always the result of a(n) ___________.
    decrease in production (uveitis)
  3. All ___________ have glaucoma until proven otherwise.
    red eyes
  4. What is normal IOP?
    15-20mmHg
  5. Pressure on the inner cornea=
    pressure on the retina, which include the optic nerve, which is part of the brain (ie. you REALLY don't want to cut off perfusion to a part of your brain because you won't get it back)
  6. The _________ is the site of production of aqueous humor and is the __________.
    pars plicata ciliary body; blood-aqueous barrier
  7. Active secretion for aqueous production is driven by... (4)
    carbonic anhydrase, ATP, glucose, and the local environment
  8. How dos anterior uveitis lead to a decrease in aqueous production?
    it alters the local environment, ie. the pH and glucose conc
  9. Describe the flow of aqueous.
    ciliary epithelium--> b/w the iris and lens--> through the pupil--> into the anterior chamber--> to the iridocorneal angle--> through trabecular meshwork--> into the scleral venous plexus
  10. Describe the role of the trabecular meshwork and its purpose and when it is not physiologically normal.
    • Normally: the trabecular meshwork provides resistance to outflow, which leads to the development of the IOP
    • Glaucoma: trabecular meshwork is filled in with tissue--> no outflow--> increased IOP
  11. What is the prognosis for glaucoma?
    • It cannot be cured- you cannot decrease the amount of cells/ tissue that have filled in the trabecular meshwork; it is progressive.
    • It can only be managed- you can manage by decreasing the amount of aqueous production (carbonic anhydrase inhibitors), etc
  12. The ciliary musculature is under _____________ control; this is of clinical significance because...
    • parasympathetic; when these muscle contract, they open the trabecular meshwork--> less resistance to outflow--> decreased IOP
    • also, when you use atropine, the ciliary muscles are paralyzed and the trabecular meshwork closes--> increase IOP
  13. Why is atropine contraindicated in glaucoma?
    when you use atropine, the ciliary muscles are paralyzed (under parasympathetic control) and the trabecular meshwork closes--> increased IOP
  14. Why does glaucoma cause mydriasis?
    • paralysis of the iris sphincter (efferent damage)
    • retinal/ optic nerve degeneration (afferent damage- can't see--> pupil dilates to try and let more light in)
  15. Miosis in combination with increased IOP suggests...
    glaucoma and concurrent uveitis
  16. A sluggish to absent PLR is expected in the glaucomatous eye, BUT...
    look for consenual PLR...should be there
  17. ____(2)_____ are common with IOP> 40mmHg
    Diffuse corneal edema and/ or mydriasis
  18. Diffuse edema is the result of...
    endothelial cell damage and the increased hydrostatic pressure in the eye.
  19. Describe fundic exam findings with glaucoma. (4)
    • Evaluate retina for blood vessel size and distribution- vessels less vibrant and less numerous (called vascular attenuation)
    • Tapetal hyperreflectivity indicates loss of retina
    • Optic nerve is pale and dead- optic nerve atrophy
    • Optic nerve becomes cupped (neural tissue that filed the space is gone d/t infarction and pressure necrosis)
  20. What is the only diagnostic test to definitively diagnose glaucoma?
    IOP measurement- Tonopen/ Tonovet
  21. What are the 3 ways to measure IOP?
    • indentation tonometry
    • applanation tonometry
    • rebound tonometry
  22. __________ requires use of topical anesthetic, but the _________ does not.
    Tonopen (applanation tonometry); Tonovet (rebound tonometry)
  23. The _________ is a better instrument to measure IOP in horses.
    tonovet (rebound tonometry- no anesthesia necessary)
  24. Determination of IOP is indicated in all eyes with... (7)
    • diffuse corneal edema
    • anisocoria
    • fixed and dilated pupils
    • episcleral congestion
    • blindness
    • buphthalmos
    • anterior uveitis
  25. What is the etiology of primary glaucoma?
    • hereditary, not associated with any other ocular diseases
    • this is why you should regularly monitor pressures in predisposed breeds
  26. Glaucoma doesn't usually manifest clinical signs until IOP _________.
    • >40mmHg
    • [this is bad because by the time this happens, vision is already deteriorating]
  27. When primary glaucoma is diagnosed in one eye, there is a _______ chance it will develop in the other eye.
    • 50% (usually within 2 years)
    • IOP monitoring every 2-3 months in normal eye, prophylactic drugs (carbonic anhydrase inhibitor) in normal eye--> to prevent loss of vision in both eyes
  28. What is secondary glaucoma?
    result of some other event in the eye, which results in a decrease in aqueous humor access to the drainage angle or a decrease in outflow; must treat primary cause
  29. Is there a predisposition to bilateral involvement with secondary glaucoma?
    NO, except with breed-related anterior lens luxation
  30. What are etiologies of secondary glaucoma? (9)
    • anterior lens luxation
    • synechia (adhesions that impede flow of aqueous)
    • uveitis
    • Pre-iridal fibrovascular membrane (PIFM)
    • hypermature cataract
    • hyphema/ hypopyon
    • neoplasia
    • pigmentary
    • uveal cysts
  31. What are etiologies of anterior lens luxation? (4)
    • breed related (Terriers)
    • secondary to glaucoma
    • displacement by an intraocular neoplasia
    • trauma
  32. A lot of the causes of secondary glaucoma come to a common glaucoma etiology, called ____________.
    pre-iridal fibrovascular membrane (PIFM)
  33. What are the most common causes of PIFM, which can lead to secondary glaucoma? (3)
    • #1 uveitis
    • intraocular neoplasia
    • retinal detachment
  34. How does PIFM lead to secondary glaucoma?
    primary disturbance causes tissue hypoxia--> production of vascular growth factors d/t inflammation/neoplasia/etc--> vessels grow in front of the iris, down the face of the iris to the iridocorneal angle--> PIFM--> new vessels obstruct iridocorneal angle--> obstruct aqueous flow--> secondary glaucoma
  35. What are 2 ways tumors lead to secondary glaucoma?
    • physically obstructing aqueous flow
    • causing PIFM
  36. Equine glaucoma is almost always _________, typically as a result of __________.
    secondary; equine recurrent uveitis
  37. Patients with ___________ are true medical and/or surgical emergencies because...
    acute primary glaucoma; hours can make the difference b/w seeing and being blind (with chronic, the process has been there a while and it's probably already too far gone)
  38. What are clinical signs of acute primary glaucoma? (7)
    • diffuse corneal edema
    • decreased to absent menace
    • sluggish PLR
    • pupillary dilation
    • episcleral vessels engorged
    • pain- epiphora, blepharospasm
  39. You see a patient with red eye(s) with diffuse corneal edema. You can only do one diagnostic. What do you choose?
    intraocular pressures!
  40. How do you medically treat acute primary glaucoma? (3)
    • Emergency (gotta get your pressure down now):
    • prostaglandins (Latanoprost topical)- causes pupillary constriction, opens iridocorneal angle
    • osmotic agents (mannitol IV if prostaglandin didn't work)- sucks the fluid out of the eyeball within 20-30min, lasts 4-6hr
    • Long-term management:
    • carbonic anhydrase inhibitors (Methazolamide PO, Dorzolamide topical)- decrease aqueous production
    • always send home lantaprost drops
    • [glaucoma always ends up being a surgical case eventually]
  41. When are prostaglandins contraindicated for treatment of acute primary glaucoma? (2)
    • active uveitis
    • anterior lens luxation
  42. What are side effects of carbonic anhydrase inhibitors for long-term management of primary glaucoma? (5)
    • metabolic acidosis- panting, depression, vomiting, diarrhea
    • hypokalemia
    • [SEs are very rare]
  43. How do parasympathomimetics work in treatment of acute glaucoma? When are they contraindicated?
    • increases outflow by constricting ciliary muscles
    • contraindicated in eyes with anterior uveitis
  44. In what species are beta blockers used to treat acute glaucoma, and how do they work?
    • horses
    • reduce aqueous production
  45. What is the medical treatment for equine glaucoma? (3)
    • topical beta-blocker (Timolol)
    • topical prostaglandin (Dorzolamide- Trusopt)
    • topical carbonic anhydrase inhibitor (Cosopt)
  46. What are surgical treatments for acute primary glaucoma? (2)
    • [laser surgery]
    • cyclophotoabalation w/ diode laser- zap ciliary processes, permanently decrease aqueous production
    • filtering procedures- put implant under conj, tube in eyeball to transport fluid to conj, where vessels and lymphatics can carry it away
  47. Why isn't chronic glaucoma an emergency?
    these eyes are already blind and the damage to the retina and optic nerve is irreversible
  48. Treatment of chronic glaucoma is generally...
    surgical (treatment with drugs will never be cost effective)
  49. What are clinical signs of chronic glaucoma? (9)
    • diffuse corneal edema
    • buphthalmos (bulgy, enlarged eye)
    • episcleral vessels engorged
    • absent PLR
    • dilated pupil
    • corneal striae
    • absent menace response
    • retinal degeneration
    • cupped optic disc
    • +/- pain (pain is always present but there may not always be outward signs of it- convince your client that their dog is in pain!)
  50. What are surgical treatments for chronic glaucoma? (3)
    • evisceration with prosthesis- remove internal contents of the globe, insert silicone sphere, cornea vascularizes
    • enucleation
    • pharmacologic ablation (bad option)
Author
Mawad
ID
324461
Card Set
Ophtho2- Glaucoma
Description
vetmed Ophtho2
Updated