Pain, Redness, & Swelling Layers of Cornea

HORDEOLUM A Anterior Epithelium

INTERNAL EXTERNAL B Bowman’s Membrane
Meibomian glands Sty/gland of Zeis C Corneal Stroma
Skin or conjunctival Skin D Descemet’s Membrane
surface E Endothelium
Vertical incison Horizontal incision
Layers of Retina
PTERYGIUM PINGUECULA Bruch’s membrane
Crosses the limbus Yellow nodules at nasal Pigment epithelium
side of cornea Rods and cones
UV, drying & windy Does not cross the cornea External limiting membrane
environment Outer nuclear layer
Hyaline + elastic tx Hyaline + elastic tx Outer plexiform layer
Inner nuclear layer
Tx: excision with No treatment or weak
Inner plexiform layer
conjunctival autografts topical steroids
Ganglion cell layer
(prednisolone 0.12%) or
Nerve fiber layer
topical NSAIDs
Internal limiting membrane
MYOPIC HYPEROPIC
HTN Retinopathy
Concave lens Convex lens Grade
0 No visible changes
1 Vascular attenuation
2 Grade 1 + AV nicking
3 Grade 2 + retinal edema, cotton wool spots,
flame hemorrhages
4 Grade 3 + optic disc edema, macular star
Types of Cataract Surgery
Diabetic Retinopathy Classification
 ECCE (Extracapsular Cataract Extraction)
1. Non-proliferative Retinopathy
o Phacoemulsification
- microaneurysms
o MSICS (manual sutureless small
- flame-shaped hemorrhages
incision cataract surgery)
- cotton wool spots
 ICCE (Intracapsular Cataract Extraction)
- IRMA
 Phacofragmentation
2. Maculopathy
Signs of Glaucoma
- Focal or diffuse retinal thickening or edema
 enlargement of optic disc cup with disc
- Hard exudates
pallor in area of cupping; “bean pot cup”
 nasal displacement of vessels 3. Proliferative Retinopathy
 cup:disc > 0.5 - New vessels on optic disk (NUD)
 increased intraocular pressure
 atrophy of retinal nerve fiber layer
 fixed dilated pupils
1st line sa Bailey-Love
Symptoms of Glaucoma - HZVDS
 visual field loss 1st line sa Snellen
 eye pain - E
 haloes Goldmann Applanation Tonometry
 nausea and vomiting - gold standard to measure pressure
Management of chemical injury
Types of Glaucoma
- irrigation
OPEN ANGLE ANGLE CLOSURE
Ptosis
Asymptomatic, Sudden onset
progressive, bilateral visual - drooping of the superior eyelid
loss Lamina papyracea
IOP < 21 mmHg IOP >60-80 mmHg - weakest bone of orbit
Degenerative process in Occluded trabecular
trabecular meshwork & meshwork
decrease in aqueous
drainage
1. Draw and label the anterior and posterior chambers of the eye disk or field changes vomiting. Other findings
associated with include increased IOP, a
elevated IOP, a shallow anterior
normal-appearing chamber, a steamy
open anterior chamber cornea, a fixed, and
angle, and no other moderately dilated pupil,
reason for IOP and ciliary injection.
elevation.
Treatment Trabeculectomy – OPHTHALMIC
good option in patients EMERGENCY!
who progress despite Treatment is initially
medical treatment directed at reducing the
IOP. IV and oral
acetazolamide (along with
topical agents such as beta-
blockers & apraclonidine, and, if
necessary, hyperosmotic agents)
will usually reduce the IOP.
Pilocarpine 2% should be
instilled ½ hour after
commencement of treatment, by
2. Draw the excretory portion of the lacrimal system which time reduction of iris
ischemia and lowering of IOP
allow the sphincter papillae to
respond to the drug.
Topical steroids may also
be used to reduce secondary
inflammation.
Once the IOP is controlled,
laser peripheral
iridotomy should be
undertaken to form a permanent
connection between the anterior
and posterior chambers, thus
preventing recurrence of the iris
bombe. This is most often done
neodymium:YAG
with the
laser. Surgical
peripheral iridectomy is
the conventional treatment if laser
treatment is unsuccessful, but
Tears drain from the lacrimal lake via the upper and lower puncta and ALPI may be performed. The
canaliculi to the lacrimal sac, which lies in the lacrimal fossa. The fellow eye should always undergo
nasolacrimal duct continues downward from the sac and opens into the prophylactic laser
inferior meatus of the nasal cavity, lateral to the inferior turbinate. iridotomy.
Tears are directed into the puncta by capillary attraction & gravity and by the blinking action of Prognosis Without treatment, If treatment is delayed,
the eyelids. The combined forces of capillary attraction in the canaliculi, gravity, and the
pumping action of Horner’s muscle, which is an extension of the orbicularis oculi muscle to a
may progress to the peripheral iris may
point behind the lacrimal sac, all tend to continue the flow of tears down the nasolacrimal duct complete blindness. If adhere to the trabecular
into the nose (page 18). anti-glaucoma drops meshwork (anterior
control the IOP in an synechiae), producing
3. Differentiate open and closed angle glaucoma in terms of eye that suffered irreversible occlusion of
pathophysiology, clinical manifestation, treatment (medical, laser, extensive the anterior chamber
surgical), & prognosis (page 222) glaucomatous angle requiring surgery.
Primary open-angle ACUTE angle-closure damage, the Optic nerve damage is
(page 232) prognosis is good. common.
Pathophysiolo Degenerative process Elevation of intraocular When the process is
gy in the trabecular pressure is a detected early, most
meshwork, including consequence of glaucoma patients can
deposition of obstruction of aqueous be successfully
extracellular material outflow by occlusion of managed medically.
within the canal. The the trabecular meshwork
consequence is a by the peripheral iris. 4. Mom has Open angle glaucoma. What is your advice to her
reduction in aqueous Acute angle closure children? What age should you start screening?
drainage leading to a (“acute glaucoma”) The major problem in detection of primary open-angle glaucoma is the
rise in intraocular occurs when sufficient absence of symptoms until relatively late in the disease. When patient
pressure. iris bombe develops to first notice field loss, substantial optic nerve damage has already
cause occlusion of the occurred. If treatment is to be successful, it must be started early in
anterior chamber angle the disease, and this depends on an active screening program. At
by the peripheral iris. present, it is necessary to rely for early diagnosis predominantly on
Clinical Absence of symptoms Sudden onset of visual regular ophthalmic assessment of first-degree relatives of affected
manifestation until relatively late in loss accompanied by individuals. Age?
the disease. excruciating pain, halos,
Glaucomatous optic and nausea and
5. What is the accommodative power of the eye? Discuss the
physiology of this phenomenon (page 405?)
The eye changes refractive power to focus on near objects by a
process called accommodation. Contraction of the ciliary muscle
results in thickening and increased curvature of the lens, probably due
to relaxation of the lens capsule.

6. Differentiate types of conjunctivitis (cause, treatment, clinical manifestations). Page 83

VIRAL BACTERIAL CHLAMYDIAL ALLERGIC
CAUSE Hyperacute/purulent – N
gonnorhea, Neisseria kochiim N
meningitides
Acute mucopurulent/ catarrhal –
“pinkeye”; S pneumonia, H.
aegyptocus
CLINICAL Bilateral irritation and injection,
MANIFESTATI purulent exudate with sticky lids on
ONS waking, and occasionally lid edema.
Infection usually starts in one eye
and may be spread to the eye by
direct contact form the hands. It
may be spread from one to another
by fomites.
TREATMENT

7. Clinical manifestation of epithelial and stromal herpetic keratitis

(page 121?)

Epithelial Keratitis – the epithelial changes vary widely from simple

edema and vacuolation to minute erosions, filament formation, partial
keratinization, etc. The lesions vary also in their location on the cornea.
Types: see page 121
Stromal Keratitis – accumulation of inflammatory cells; edema
manifested as corneal thickening, opacification, or scarring; “melting”
or necrosis, which may lead to thinning or perforation; and
vascularization.