OPTHALMOLOGY

ANATOMY

PATHOLOGY
1. retinal diseases
a. diabetic retinopathy
b. retinal detachment
c. age related macular degeneration
d. CRA occlusion
e. CRV occlusion
2. Glaucoma
3. Cataracts
4. Conjunctival disease
a. Conjunctivitis
b. Sub-conjunctival hemorrhage
5. Keratitis
a. Herpes simplex keratitis
6. Peri-orbital cellulitis
7. Uveitis

1. RETINAL DISEASES
1a. DIABETIC RETINOPATHY
-

PATHOGENESIS: damage to the endothelial lining of the small blood vessels of

the eye progressive occlusion on a microscopic level obstruction and
increased pressure
NON-PROLIFERATIVE
Earliest form
Characterized by:
a. Dilation Of Veins
b. Microaneurysms
c. Retinal Edema
d. Retinal Hemorrhages (not as
dangerous as intra-vitreous because
they DONOT obstruct sight )

PROLIFERATIVE
Advanced form
Rapidly progresses into blindness
As the damage progressessecretes
angiogenesis factoroptic nerve getting
covered by abnormal
vesselshemorrhages in the vitreous
chambersight threatening.

PRESENTATION
a. Vision may decrease slowly or rapidly.
b. Vitreal hemorrhages may develop suddenly
c. Patient may complain of floaters in their vision.

DIAGNOSIS
a. screening on annual basis
b. Fluorescein angiography - identifies vessels which should undergo laser
photocoagulation which selectively destroys focal areas of the retina and
diminishes the production of angiogenesis Factor which causes the
proliferative retinopathy.

TREATMENT
a. Tight control of glucose, blood pressure(<140/90) and lipids (ldl<100, if CAD
ldl<70).
b. Proliferative retinopathy- immediate laser photocoagulation

1b. RETINAL RETACHMENT

-

PATHOGENESIS:
o spontaneous and may result from trauma
o Predisposing factors: myopia and surgical extraction of cataracts.
o Traction can also occur from:
Proliferative retinopathy from diabetes
Retinal vein occlusion
Age related macular degeneration

CLINICAL PRESENTATION:
o Blurry vision UNIlaterally w/o pain/redness
o Patient may complain of seeing floaters or flashes at the periphery of
vision.
o curtain coming down (retinal falls off the sclera behind it)

DIAGNOSIS
o Ophthalmologic examination

TREATMENT:
o Re-attach the retina by:
Leaning their head back to promote the chance that the retina will
fall back into place
Mechanical reattachment to the sclera surgically by
laser photocoadulation,
cryotherapy
injection of expansile gas into the vitreal cavity
buckle/belt can be placed around the sclera to push the sclera
forward so that it can come in contact with the retina
vitreous can be removed and the retina can be surgically attached
to sclera

1c. AGE- RELATED MACULAR DEGENERATION

-

PATHOGENESIS
o MCC of legal blindness in older persons
o Formation of deposits of drusen (extracellular material collecting into
yellowish deposits), small granular subretinal deposits that are age
related
- CLINICAL PRESENTATION
DRY
WET
- AKA atrophic
- AKA exudative form
- Slowly progressive visual loss
- Rapid distortions of vision over
in the elderly
weeks to months
- DIAGNOSIS: Drusen on dilated
- Abnormal growth of vessels from
eye exam
the chroroidal circulation into the
- TREATMENT: zinc, V c/e, beta
subretinal space
carotene
leakagesubretinal fluid and a
localized exudative renal
detachment
- DIAGNOSIS: Fluorescein
angiography
- TREATMENT: VEGF inhibitors
(Ranibizumab/Bevacizumab)

1d. and 1e. CENTRAL RETINAL ARTERY OCCLUSION VS CENTRAL RETINAL VEIN
OCCLUSION
Pathogenesis

Clinical
presentation
Ophthalmosc
opy

Diagnosis

Treatment

Central retinal artery occlusion

h/x of
a. carotid artery embolic
disease
b. temporal arteritis
c. cardiac thrombi/myxoma
d. thrombophilia (fac V
mutation)
- sudden painless
- UNILATERAL loss of vision
Pale retina
Diminished perfusion
Cherry red spot at fovea
Box-car segmentation of
the blood in the veins.
Undergo evaluation with
- Carotid artery imaging
- ECHO
- thrombophilia
a. Lay the patient flat
b. Supply O2
c. Ocular massage to
unobstruct the vessel
d. Acetazolamide and
thrombolytics
e. Anterior chamber
paracentesis
(decompress the
pressure and dislodge
the embolus)

Central retinal vein occlusion

o High risk for developing glaucoma
o Monitored for the possible use of
laser photocoagulation
o Young inherited causes of
thrombophilia
- Sudden loss of vision w/o
pain/redness.
Disk swelling
Venous dilation
Tortuosity
Retinal hemorrhages
Retinal hemorrhages (you cant have
hemorrhage in the retina if you dont
have blood getting into the eye)
NONE

2. GLAUCOMA
Pathogenesi
s

Open- angle
UNKNOWN

Diagnosis

Cup to disk ratio >0.3 on

tonometry

Treatment

Decreasing the production of

aqueous humorincreasing
drainage
1. Beta- blockers(timolol,
betaxolol, levobunolol)
2. Alpha agonists
(apraclonidine,
brimonidine)
3. Carbonic anhydrase
inhibitors (dorzolamide,
brinzolamide)
Increasing outflow of humor
1. prostaglandin analogs
(topical latanoprost,
travoprost, Bimatoprost)
2. mitotic agents
pilocarpine (allow greater
outflow of humor)
Surgery:
1. laser trabeculoplasty
2. surgical trabeculectomy

Closed- angle
Ophthalmologic emergency precipitated
by anticholinergic affects (TCA,
ipratropium)
Red, painful hard to palpate
Fixed midpoint pupil
Cornea hazy cloudiness, marked
diminishment of visual acuity.
1. IV Acetazolamide
2. IV urea
3. IV osmotic diuresis
(manitol/glycerol)
4. Pilocarpine (open canal of
schlemm)
5. Beta blockers (decrease the
production of humor)
6. Laser tubeculopathy

3. CATARACTS
-

PATHOGENESIS
o Opacification of lens
o Slowly progressive blurry vision over months to years
o Glare from the headlights of cars is problem at night
o Color perception if reduced in general
o Ass/w cigarette smoking

CLINICAL PRESENTATION
o Mature easily visible of P.E
o Earlier stages slit-lamp

TREATMENT
o Surgical removal with placement of intraocular lens

4. CONJUNCTIVAL DISEASES
-

PATHOGENESIS
o Any infectious agent (bacterial, viral, fungal)
CLINICAL PRESENTATION
BACTERIAL
VIRAL
- Unilateral
- Bilateral
- Marked purulent discharge from the
- Severe itching
eye
- Enlarged preauricular lymphadenopat
- In the morning with crusted eyelids
- Pupils are reactive and no photophobi
- Less itching
- Normally reactive pupil
TREATMENT: symptomatically with topical
- Normal ocular pressure
antihistamine/decongestants
- No impairement of visual acuity
TREATMENT: topical antibiotics

a. Erythromycin Ointment
b. Sulfacetamide Drops
c. Topical fluroquinolones
4A. SUBCONJUNCTIVAL HEMORRHAGE
- MCC- trauma, particularly in the presence of thrombocytopenia
- Collection of hematoma stops at limbus (b/w conjunctiva and cornea)
- Because this prevents the blood from covering the cornea
- There is no impairment of vision
- No intraocular/intra-vitreal damage
- NO specific therapy is necessary

5. KERATITIS
-

PATHOGENESIS
o Infection/inflammation of the cornea
o Usually, due to trauma to the cornea with the inoculation of bacterial/fungal
elements

5A. HERPES SIMPLEX KERATITIS

-

PRESENTATION
o Severe pain in the eye
o Sensation that something is caught under the eyelid

DIAGNOSIS

o Fluorescein staining with blue light - Characteristic dendritic pattern over the
cornea
-

TREATMENT
o Oral acyclovir, famcuclovir, valacyclovir
o Topical trifluridin 1% solution
o Idoxiuridine
o NEVER USE STEROIDS- worsen the growth of virus and acts as a fertilizer

6. PERIORBITAL CELLULITIS
-

PATHOGENESIS
o S. Aureus
o Streptococuus
o Invasion of dermis and subcutaneous tissue around the eye

TREATMENT
o Antistaphylococcal penicillins (oxacillin/nafcillin)
o If allergic to penicillin
Cephalosporins (1st gen (cephazolin))

7. UVEITIS
-

PATHOGENESIS
o Inflammation of the Uveal tract (iris, ciliary body, choroid)
o Etiology systemic (psoriasis, sarcoidosis, syphilis, reiters, IBD)
PRESENTATION
o Painful red eye with marked photophobia
o Pain occurs even when the light is shining in the unaffected eye (consensual
light reflex in which the affected pupil will constrict even when the light is
shined in the normal eye)
DIAGNOSIS

o Slit lamp exam

o Keratic precipitates (inflammatory cells may accumulate on the inside of the
cornea from aqueous humor, aka accumulating snowfall.