glaucoma: Aqueous out flow:
d)conventionalroute(Trbecular meshwork): (80 percent of it )
Is a group of disorders which have in common: -The aqueous humor secretion is through the ciliary processes into the posterior
1)progressve characterstic optic neuropathy *(change s in the chamber then goes to the anterior chamber through the pupil it leaves the eye at
optic disc in post segment retina) the anterior chamber angle through trabeula meshwork, the Schemm's canal
intrascleral channels/collector channels and episcleral and conjunctivalveins.
2)visual fied defects *if no visual fild defect= no gluacoma
3)+/- raised IOP: b)Non-conventionalroute (uveo-scleral):(20 percent of it)
*one of the component but not the most important aqueous humor exits through the root of iris between the ciliary muscle bundles,then
through the suprachoroidal-scleral tissues.
*usually rised
*one of the main risk factor كلما كان مرتفع كلما زادة احتمالية المرض
Angle of anterior chamber and the importance of the angle:
the commonly accepted range for IOP is 10-22 1)open angle . 2)narrrow angel *أكثر عرضه للclose angle glaucoma
* maybe 24 espicially in old pt (rigid eyes)
▪️ structure of the angle:
Factors determining the IOP: 1)trabeccular meshwork
2)scleral spur
1-Rate of aquedus humor production. * Ant- chamber
2-The resistance to the outflow of aqueous from the eye. ▪️
3)part of the ciliary body (inside the angle)
seen by gonioscopy : visualized of ant-chamber by goniolens under high mignification
(slit lamb) for diagnosis
3-The level of episcleral venous pressure.
🔷
2 Angle closure glaucoma(narrow angle glaucoma):
-Develops in eyes with an already narrow angle of the anterior chamber.
-The eyes predisposed to develop narrow angle gaucoma are characteristically:
*small
Primary Glaucomas:
🔸🔶is a chronic,slowly progressive optic neuropathy characterized by:
1 open angle glaucoma (chronic simple glaucoma):*( outflow is normal)
*hypermetropic
*with shallow anterior chamber
*narrow angled
-atrophy and cupping of the optic nerve head -Less common type of glaucoma
-Characteristic pattern of visual field loss
🔸
-Increase IOP
🔸 It is familial and genetically determined.
It forms 90% of the cases of glaucoma
Risk factors of PACG:
age: near 60 yrs and more.
gender: females are more commonly affected than males.
Note: Race:higher in far eastern descents.
same characteristics with an IOP within normal limits called normal tension glucoma family history: 1st degree relatives are at increased risk.
🔸 3🔶Congenital Glaucoma:
Hypermetropia
risk factors of POAD :
glaucoma 1)IOP: the higher the IOP the greater the likelihood of glucoma
2)age: more common in order individuals
Clinical Features Of Angle Closure Glaucoma:
It has 4 stages:
is a form of developmental glaucoma that has it's onset at
birth or in the first 3 years of
3)black race: 4 times higher risk than others 1- Prodromal (subacute/intermittent) stage: life.
4)family history of POAG *The most important:
-Pathology is trabecular meshwork dysgenesis.
🔸
5)diabetes mellitus -transient high IOP (40-60mmHg) Clinical picture:
6)myopia -Colored haloes. A classical triad: epiphora,photophobia, and
by fatema okoff 🔸 Theories of optic nerve damage:
-Headache.
*Slit lamp: 🔸
blepharospasm.
Buphthalmos: if lOP increases before 3 years, this leads
🔸
1)mechanical theory: >Shallow AC. to enlargement of the globe and axial myopia.
🔸
-suggest thet the optic disc damage is due to the raised intraocular pressure that squeezes
🔹
>Corneal oedema (mild epithelial edema) Cornea enlarged >12mm.
🔸
the retinal ganglion cells axons and disturbs the axoplasmic flow.(does not explain normal It is precipitated by anxiety and over work and subsides without any Corneal odema.
🔸
tension glaucoma and ocular hypertension).
🔹
medication. Haab’s striae(breaks in Descemet membrane).
🔸
2)Vascular theory: R/ - Pilocarpine eye drops. Deep AC
🔸 Gonioscopy:changesinangle.
-due to reduced ocular blood perfusion and ischemia of the -bilateral Yag laser peripheral iridotomy.
optic nerve leading to the damage. OD .Cupping.
🔸 visual filld defects in chronic simple glaucoma:
🔹
2-Acute congestive stage:
Characterized by:
-Sudden onset of blurred vision sometimes to light perception. Treatment of congenital glaucoma:
1)paracentral supranasal small sctoma Surgical Intervention
-Severeocular pain &headache.
2)A nasal (Roenne step): a difference in sensitivity above & below the horizontal midline in is considered in these cases after decreasing the intraocular
-Nausea and vomiting
the nasal field
3)Bjerrum scotoma: upward extensions of scotomas from the blind spot( develop between
10-20 degree of fixation)
-Intense cilary congestion.
-Corneal edema. 🔹
pressure medically.
Gonictomy: a cicumferencial cut in the trabecular
4)Arcuate scotoma: elongation & coalescence of scotomas with fusion to the blind spot
-High IOP
-Shallow AC. 🔹
meshwork is made.
Trabeculotomy: Is an opening made through the
🔶 TREATMENT:
🔷
-Fixed mid dilated pupil
🔹
schlemm canal into the anterior chamber.
🔹 Treatment of acute congestivestage(emergency): Trabeculectomy.
Medical treatment:
🔹 Admission. DDx:
1)beta blockers (reduce IOP by decreasing aqueous secretion) > Megalocornea
2)carbonic anhydrase inhibitors(lower IOP by inhibiting aqueous secretion) Medical treatment: (pre-op.for24 hours):
classfication of glaucoma: 1. Pilocarpine E.D. > High myopia
3)prostaglandin analogues (enhance aqueous humour outflow through the uveoscleral
1)Primary: route ) 2. Systemic Acetazolamide.
3.Mannitol iv.
-Open angle glaucoma
-Angle closure glaucoma
🔸
4)miotics:
1 in POAG miotics reduce IOP by contraction of the ciliary muscle which increases the 4. Beta-blockers (timolol)
5.Topical steroids if the eye is acutely inflamed.
-congenital glucoma(open angle glaucoma in children) 🔸
facility of aqueous outflow through the trabecular meshwork.
2 in PACG contaction of the sphincter pupillae and the resultant miosis pulls the
peripheral iris away from the trabeculum thus opening the angle. 🔹
6. Analgesic.
Surgical treatment >>>>Trabeculectomy.
2) secondary glucoma 5)osmotic agent (they lower IOP by creating an osmotic gradient between blood and
vitreous so that water is drawn out from the vitreous ) 3-Chronic congestive stage:
It may develop after an acute attack or when the anglec loses progressively.(OP elevation
🔸
Surgical treatment:
trabeculectomy 🔸 drainage shunts may be only intermittent).
4 Stage of absolute glaucoma:
The eye is hard, sightless and painful
SECONDARY GLAUCOMAS:
🔹
-Lens related:
🔹 Lens dislocation.
🔹 Intumescent cataract (phacomorphic glaucoma).
Phacolytic glaucoma
-Inflammatory glaucoma:dueto iridocyclitis.
-Hyphema
-Neovascular glaucoma;due to rubiosis iridis.
-Postoperative;due to inflammation.
-Prolonged use of topical steroids.
d)conventionalroute(Trbecular meshwork): (80 percent of it )
Is a group of disorders which have in common: -The aqueous humor secretion is through the ciliary processes into the posterior
1)progressve characterstic optic neuropathy *(change s in the chamber then goes to the anterior chamber through the pupil it leaves the eye at
optic disc in post segment retina) the anterior chamber angle through trabeula meshwork, the Schemm's canal
intrascleral channels/collector channels and episcleral and conjunctivalveins.
2)visual fied defects *if no visual fild defect= no gluacoma
3)+/- raised IOP: b)Non-conventionalroute (uveo-scleral):(20 percent of it)
*one of the component but not the most important aqueous humor exits through the root of iris between the ciliary muscle bundles,then
through the suprachoroidal-scleral tissues.
*usually rised
*one of the main risk factor كلما كان مرتفع كلما زادة احتمالية المرض
Angle of anterior chamber and the importance of the angle:
the commonly accepted range for IOP is 10-22 1)open angle . 2)narrrow angel *أكثر عرضه للclose angle glaucoma
* maybe 24 espicially in old pt (rigid eyes)
▪️ structure of the angle:
Factors determining the IOP: 1)trabeccular meshwork
2)scleral spur
1-Rate of aquedus humor production. * Ant- chamber
2-The resistance to the outflow of aqueous from the eye. ▪️
3)part of the ciliary body (inside the angle)
seen by gonioscopy : visualized of ant-chamber by goniolens under high mignification
(slit lamb) for diagnosis
3-The level of episcleral venous pressure.
🔷
2 Angle closure glaucoma(narrow angle glaucoma):
-Develops in eyes with an already narrow angle of the anterior chamber.
-The eyes predisposed to develop narrow angle gaucoma are characteristically:
*small
Primary Glaucomas:
🔸🔶is a chronic,slowly progressive optic neuropathy characterized by:
1 open angle glaucoma (chronic simple glaucoma):*( outflow is normal)
*hypermetropic
*with shallow anterior chamber
*narrow angled
-atrophy and cupping of the optic nerve head -Less common type of glaucoma
-Characteristic pattern of visual field loss
🔸
-Increase IOP
🔸 It is familial and genetically determined.
It forms 90% of the cases of glaucoma
Risk factors of PACG:
age: near 60 yrs and more.
gender: females are more commonly affected than males.
Note: Race:higher in far eastern descents.
same characteristics with an IOP within normal limits called normal tension glucoma family history: 1st degree relatives are at increased risk.
🔸 3🔶Congenital Glaucoma:
Hypermetropia
risk factors of POAD :
glaucoma 1)IOP: the higher the IOP the greater the likelihood of glucoma
2)age: more common in order individuals
Clinical Features Of Angle Closure Glaucoma:
It has 4 stages:
is a form of developmental glaucoma that has it's onset at
birth or in the first 3 years of
3)black race: 4 times higher risk than others 1- Prodromal (subacute/intermittent) stage: life.
4)family history of POAG *The most important:
-Pathology is trabecular meshwork dysgenesis.
🔸
5)diabetes mellitus -transient high IOP (40-60mmHg) Clinical picture:
6)myopia -Colored haloes. A classical triad: epiphora,photophobia, and
by fatema okoff 🔸 Theories of optic nerve damage:
-Headache.
*Slit lamp: 🔸
blepharospasm.
Buphthalmos: if lOP increases before 3 years, this leads
🔸
1)mechanical theory: >Shallow AC. to enlargement of the globe and axial myopia.
🔸
-suggest thet the optic disc damage is due to the raised intraocular pressure that squeezes
🔹
>Corneal oedema (mild epithelial edema) Cornea enlarged >12mm.
🔸
the retinal ganglion cells axons and disturbs the axoplasmic flow.(does not explain normal It is precipitated by anxiety and over work and subsides without any Corneal odema.
🔸
tension glaucoma and ocular hypertension).
🔹
medication. Haab’s striae(breaks in Descemet membrane).
🔸
2)Vascular theory: R/ - Pilocarpine eye drops. Deep AC
🔸 Gonioscopy:changesinangle.
-due to reduced ocular blood perfusion and ischemia of the -bilateral Yag laser peripheral iridotomy.
optic nerve leading to the damage. OD .Cupping.
🔸 visual filld defects in chronic simple glaucoma:
🔹
2-Acute congestive stage:
Characterized by:
-Sudden onset of blurred vision sometimes to light perception. Treatment of congenital glaucoma:
1)paracentral supranasal small sctoma Surgical Intervention
-Severeocular pain &headache.
2)A nasal (Roenne step): a difference in sensitivity above & below the horizontal midline in is considered in these cases after decreasing the intraocular
-Nausea and vomiting
the nasal field
3)Bjerrum scotoma: upward extensions of scotomas from the blind spot( develop between
10-20 degree of fixation)
-Intense cilary congestion.
-Corneal edema. 🔹
pressure medically.
Gonictomy: a cicumferencial cut in the trabecular
4)Arcuate scotoma: elongation & coalescence of scotomas with fusion to the blind spot
-High IOP
-Shallow AC. 🔹
meshwork is made.
Trabeculotomy: Is an opening made through the
🔶 TREATMENT:
🔷
-Fixed mid dilated pupil
🔹
schlemm canal into the anterior chamber.
🔹 Treatment of acute congestivestage(emergency): Trabeculectomy.
Medical treatment:
🔹 Admission. DDx:
1)beta blockers (reduce IOP by decreasing aqueous secretion) > Megalocornea
2)carbonic anhydrase inhibitors(lower IOP by inhibiting aqueous secretion) Medical treatment: (pre-op.for24 hours):
classfication of glaucoma: 1. Pilocarpine E.D. > High myopia
3)prostaglandin analogues (enhance aqueous humour outflow through the uveoscleral
1)Primary: route ) 2. Systemic Acetazolamide.
3.Mannitol iv.
-Open angle glaucoma
-Angle closure glaucoma
🔸
4)miotics:
1 in POAG miotics reduce IOP by contraction of the ciliary muscle which increases the 4. Beta-blockers (timolol)
5.Topical steroids if the eye is acutely inflamed.
-congenital glucoma(open angle glaucoma in children) 🔸
facility of aqueous outflow through the trabecular meshwork.
2 in PACG contaction of the sphincter pupillae and the resultant miosis pulls the
peripheral iris away from the trabeculum thus opening the angle. 🔹
6. Analgesic.
Surgical treatment >>>>Trabeculectomy.
2) secondary glucoma 5)osmotic agent (they lower IOP by creating an osmotic gradient between blood and
vitreous so that water is drawn out from the vitreous ) 3-Chronic congestive stage:
It may develop after an acute attack or when the anglec loses progressively.(OP elevation
🔸
Surgical treatment:
trabeculectomy 🔸 drainage shunts may be only intermittent).
4 Stage of absolute glaucoma:
The eye is hard, sightless and painful
SECONDARY GLAUCOMAS:
🔹
-Lens related:
🔹 Lens dislocation.
🔹 Intumescent cataract (phacomorphic glaucoma).
Phacolytic glaucoma
-Inflammatory glaucoma:dueto iridocyclitis.
-Hyphema
-Neovascular glaucoma;due to rubiosis iridis.
-Postoperative;due to inflammation.
-Prolonged use of topical steroids.
