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AQUEOUS HUMOUR
PRODUCTION
ACTIVE SECRETION FROM NON-PIGMENTED EPITHELLIUM OF
THE CILIARY BODY AS RESULT OF A METABOLIC PROCESS
( Na+/K+ ATPase PUMP, CARBONIC ANHYDRASE)
OUTFLOW
TRABECULAR MESHWORK :
- UVEAL MESHWORK
- CORNEOSCLERAL MESHWORK
- ENDOTHELIAL (JUXTACANALICULAR) MESHWORK
SCHLEMM CANAL, CONNECT IN/DIRECTLY EPISCLERAL
VEINS
.
DEFINITION
GLAUCOMA IS AN OPTIC NEUROPATHY
WITH CHARACTERISTIC APPEARANCE OF
OPTIC DISC AND SPECIFIC PATTERN OF
VISUAL FIELD DEFECTS THAT IS
ASSOCIATED FREQUENTLY BUT NOT
INVARIABLY WITH RAISED IOP
VISUAL FIELD
MEASSUREMENT BY HUMPHREY PERIMETRY
CHARACTERISTIC PATTERN OF THE GLAUCOMATOUS FIELD
DEFECT:
- PARACENTRAL SCOTOMA
- A NASAL (ROENNE) STEP SCOTOMA
- ARCUATE-SHAPED DEFECTS
- PERIPHERAL SCOTOMA
- END STAGE CHANGES
GONIOSCOPY
.
CLASSIFICATION
.
1. PRIMARY GLAUCOMA
= PRIMARY OPEN ANGLE GLAUCOMA
= PRIMARY ANGLE-CLOSURE GLAUCOMA, 6 CLINICAL
STAGES:
A. LATENT ANGLE-CLOSURE GLAUCOMA
B. SUBACUTE (INTERMITTEN) ANGLE-CLOSURE
GLAUCOMA
C. ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA
D. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA
E. CHRONIC ANGLE-CLOSURE GLAUCOMA
F. ABSOLUTE ANGLE-CLOSURE GLAUCOMA
2. SECONDARY GLAUCOMA
= SECONDARY OPEN ANGLE GLAUCOMA
A. PRETRABECULAR GLAUCOMA, WHICH AQUEOUS
.
OUTFLOW
IS OBSTRUCTED BY A MEMBRANE COVERING THE TRABECULUM
+ FIBROVASCULAR TISSUE (NEOVASCULAR GLAUCOMA)
+ ENDOTHELIAL CELLS (IRIDOCORNEAL ENDOTHELIAL
= ICE SYNDROME)
+ EPITHELIAL CELLS (EPITHELIAL INGROWTH)
B. TRABECULAR GLAUCOMA, WHICH THE OBSTRUCTION
OCCURS
AS A RESULT OF CLOGGING UP OF THE MESHWORK BY:
+ PIGMENT PARTICLES (PIGMENTARY GLAUCOMA)
+ RED BLOOD CELLS ( RED CELL GLAUCOMA)
+ DEGENERATED RED CELLS (GHOST CELL GLAUCOMA)
+ MACROPHAGES AND LENS PROTEINS (PHACOLYTIC GLAU
+ PROTEINS ( HYPERTENSIVE UVEITIS)
3. CONGENITAL GLAUCOMA
A. TRUE PRIMARY CONGENITAL GLAUCOMA, WHICH IOP ELEVATED
DURING INTRAUTERINE LIFE
B. INFANTILE GLAUCOMA, WHICH MANIFESTS PRIOR TO THE 3TH
BIRTHDAY
C. JUVENILE GLAUCOMA, IOP RISED AFTER 3TH BIRTHDAY BUT
BEFORE
THE AGE OF 16 YEARS.
4. OCULAR HYPERTENSION
IOP MORE THAN 21 MMHG & ABSENCES OF DETACTABLE
GLAUCOMATOUS DAMAGE
5. NORMAL TENSION GLAUCOMA IS A VARIANT OF POAG,
CHARACTERIZED BY :
- IOP EQUAL TO OR LESS THAN 21 MMHG (DIURNAL TESTING)
- GLAUCOMATOUS OPTIC DISC DAMAGE & VISUAL FIELD LOSS
- OPEN ANGLE ON GONIOSKOPY
- ABSENCES OF SECONDARY CAUSES
Cont.. POAG
AETIOLOGIES
1. The ischaemic theory, postulates that compromise of the
.
microvas-culature with resultant ischaemia in the optic nerve
head
2. The direct mechanical theory, raised IOP directly damages the
retinal nerve fiber
RISK FACTORS
1. AGE . After the age of 65 years
2. RACE. More earlier & severe in black people than in white
3. FAMILY HISTORY with POAG
4. MYOPIA
5. RETINAL DISASES , central retinal vein occlusion,
rhegmatogenous
retinal detachment, retinitis pigmentosa
CONT..POAG
CLINICAL FEATURES
SYMPTOMS. Asymptomatic until significant loss of visual field has
.
occurred
SIGN : - Raised IOP (> 21 mmHg ) & diurnal fluctuation in IOP (> 5
mmHg)
- Optic disc changes
- Typical visual field changes
- Gonioscopy shows a normal open angle
MANAGEMENT
- Medical therapy ( timolol maleat, prostaglandine analough )
- Laser trabeculoplasty
- Trabeculectomy
Cont.PACG
PATHOGENESIS
is incompletely understood.
1. The dilatator muscle theory postulates that contraction of
the dilator pupillae exerts a posterior vector.
2. The sphincter muscle theory postulates that the sphincter
pupillae is the prime culprit in precipating angle closure.
Cont PACG
CLASSIFICATION
1. LATENT ANGLE-CLOSURE GLAUCOMA
Clinical features
-Symptoms are absent
-Slit lamp biomicroscopy
+ Axial anterior chamber depth is less than normal.
+ Convex-shaped iris-lens diaphragm
+ Close proximity of the iris to the cornea
-Gonioscopy : Shaffer grade 1 or 0
Treatment
- Prophylactic peripheral laser iridotomy
Cont.PACG
.
Cont.PACG
Cont ..PACG
Cont..PACG
Cont.PACG
RIMARY
CONGENITAL GLAUCOMA (PCG)
Affecting 1:10.000 births, 65 % boys
Sporadic, 10 % autosomal recessive
PATHOGENESIS
Isolated trabeculodysgenesis absence of the angle recess with the
Iris inserted directly into the surface of the trabeculum :
1. Flat iris insertion, iris inserteds flatly and abruptly into the
thickened
trabeculum at or anterior to the scleral spur
2. Concave iris insertion, superficial iris tissue sweeps over the iridotrabecular junction and the trabeculum
Cont .PCG
CLINICAL FEATURES
- Corneal haze ( epithelial & stromal oedema) lacrimation,
.
photopho
bia, blepharospasm
- Buphthalmos, large eye as result of stretching due to elevated IOP
Scleral thinner ( blue appearance), AC deep, lens subluxasion (zonular fibres stretch), axial myopia (increase axial length)
- Breaks in Descemet membrane (Haab striae)
- Optic disc cupping
SURGERY
- Goniotomy
- Trabeculotomy
- Trabeculectomy
TERMINOLOGY
When the IOP is found to be > 21 mmHg on two consecutive occasions, in the absence of detactable glaucomatous damage
MANAGEMENT
do not require treatment
only high risk should be treated because its effective in delaying
or
preventing the development of POAG
1. High risk factors
- retinal nerve fiber layer defects
- parapapillary changes
- IOP 30 mmHg or more
- IOP 26 mmHg or more & central corneal thickness < 555 um
- vertical CDR 0,4 or more & CCT < 588 um
ContOH
.
NORMAL
TENSION GLAUCOMA (NTG)
SIGN
- IOP usually in the high teens, but rarely the low teens
- ONH
+ both glaucomatous cupping or parapapillary changes are identical
POAG
+ splinter haemorrhages at the disc margin progressive damage of
NFL
+ acquired optic disc pits (localized excavations of the lamina cribrosa}
- VF defects, to be closer to fixation, deeper, steeper and more localized.
- peripheral vascular spasm
- migraine
- Nocturnal systemic hypotension, over treated systemic hypertension
- Reduced blood flow velocity in the a. ophthalmic
- Paraproteinaemia
Cont.. NTG
TREATMENT
- progressive VF loss
- IOP to reduce by at least 30 %
.
.
.