Secondary Glaucoma
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-? Definition
? Types
? Causes
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? TreatmentSecondary Glaucoma
? Conditions with raised intraocular pressure
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due to pre existing ocular causes.? May manifest as-
a. Secondary open angle Glaucoma
b. Secondary angle closure Glaucoma
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c. Mixed pattern1] lens induced glaucoma/Phakogenic
i. Phacomorphic glaucoma
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i . Phacolytic glaucomai i. Phacoanaphylactic glaucoma
iv. Glaucoma associated with dislocated lens
[phakotopic]
v. Glaucoma capsulare/ Pseudoexfoliation
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syndrome
?Intra ocular inflammation (inflammatory glaucoma):
Associated with uveitis
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Inflammatory glaucoma
1] Iridocyclitis (both in acute phase & chronic phases)
2] Glaucomato-cyclitic crisis /Hypertensive
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uveitis (Posner and Schlossmann's syndrome)
3] Following perforated corneal ulcer
4] As a complication of Keratitis & scleritis
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3] Steroid-induced glaucomai. Iatrogenic cause
ii. It is associated with topical, periocular, systemic
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or intraocular steroid therapy.
iii. IOP rise after steroid therapy occurs more often
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with topical administration than with systemicadministration.
iv. Periocular injection of a long action steroid is
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the most dangerous route.
v. Intravitreal steroid use (Triamcinolone injection
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to treat intraocular neovascular orinflammatory disease) can also cause a rise in
IOP.
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vi. The response of IOP to steroids is genetically
determined
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vii. Rise in IOP occurs 6 weeks to 2 monthsviii. Response varies in people
ix. Reversible
X . But we need to treat till it comes down
Pathogenesis:
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i. deposition of mucopolysaccharides intrabecular meshwork
i . Reduced endothelial phagocytic activity
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i i. Inhibit synthesis of prostaglandins E and Fwhich otherwise increase aqueous out flow.
Treatment:
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i. Stop steroidi . Treat with Drug for POAG
i i. Surgery if medical treatment is unable to
prevent damage to optic nerve
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4] Pigmentary Glaucoma? Young myopic males
? Deposition of iris pigments in trabecular
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meshwork damage? Krukenberg's spindle (over corneal endothelium)
? Gonioscopy (Sampaolesi's line)
Glaucoma associated with intra ocular
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tumours
Causes:
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i.Episcleral venous hypertension
(obstruction beyond trabecular meshwork)
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ii. Obstruction of angle by seeding of tumour cel s
iii. Forward displacement of Lens-iris diaphragm
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eg- Thyroid exophthalmos,Carotico-cavernous fistula
Superior vena cava syndrome
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metastatic carcinoma of orbit
Retinoblastoma
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Iris melanomaPost-traumatic Glaucoma
[A] Blunt injury
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? Rise in IOP is biphasic- early which lasts for few hours
- After few months/years (angle recession)
? Gonioscopy is confimatory diagnosis- deeper
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angle recess with widening of ciliary band[B] Penetrating injury
[C] Chemical injury
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1.Neovascular glaucoma may be associated withall of the following except:
a.Diabetes
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b.Hypertensionc. Central retinal vein occlusion
d. Intraocular tumours
1.Treatment of malignant glaucoma includes all
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except:
a.Topical atropine
b.Topical pilocarpine
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c. IV mannitold. Vitreous aspiration
1.Secondary glaucoma following corneal
perforation is due to:
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a.Central anterior synechiae formation
b.Peripheral anterior synechiae
c. Intraocular haemorrhage
d. Angle recession
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1.Glaukomflecken is a feature of:
a.Acute narrow-angle glaucoma
b.Pseudoexfoliative glaucoma
c. Juvenile glaucoma
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d.Phacolytic glaucoma1.All of the following are true about pigmentary
glaucoma except:
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a.It occurs more often in young myopic menb.Iris transillumination defects are noted
c. It is associated with Krukenberg's spindle
d.The intensity of pigment deposit in the angle is
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related to iris colour? After blunt trauma to eye Raja develops
circumcorneal congestion. Now, which test
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should be done?? (a) Ultrasonography
? (b) Perimetry
? (c) Direct ophthalmoscopy
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? (d) intraocular pressure measurement.