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Pathophysiology - Eye Disorders
Terms in this set (90)
Eyelid Inflammation (Blepharitis)
inflammation of anterior or posterior structures of eyelids.
Involves eyelid skin, eyelashes & associated anterior glands.
Causes of Anterior Blepharitis
1. Seborrhea (dandruff) or 2. Bacteria.
-Staph is most common bacterial cause.
-Bacterial causes usually result in more erythema (redness) and ulcers
Manifestations of Anterior Blepharitis
irritation, burning, redness, photophobia & itching of the eyelid margins.
Involves rim and posterior region of eyelid.
Causes of Posterior Blepharitis
usually meibomian gland dysfunction; bacterial can occur but less likely.
Manifestations of Posterior Blepharitis
-Irritation, photophobia, abnormal secretions due to inflamed, plugged, & dilated meibomian glands & orifices
-Lid margins are often rolled inward & tears may be frothy and greasy due to meibomian secretions.
Infection of sebaceous glands of eyelid; can be internal or external.
Manifestations of Hordeolum
pain, swelling, redness.
Granulomatous inflammation of a meibomian gland
Manifestations of a Chalazion
-Small non-tender nodule on upper or lower eyelid
-Conjunctiva around chalazion is often red
-If large enough, vision may become distorted
Hordeolum vs. Chalazion
inflammation of the conjunctiva
Can vary in severity from mild redness with tearing to severe redness and purulent discharge
Manifestations of Conjunctivitis
Foreign body sensation, scratching or burning sensation, itching and photophobia.
Severe eye pain + photophobia suggests corneal irritation rather than conjunctiva.
Usually seasonal and found in persons with other allergic diseases.
Immunoglobulin E (IgE) mediated hypersensitivity reaction precipitated by small airborne allergens.
Manifestations of Allergic Conjunctivitis
most common symptom is eye pruritis, bilateral watery eye discharge or tearing, conjunctival erythema.
Hyperacute Bacterial Conjunctivitis
-abrupt onset with copious amounts of yellow-green discharge
Causes of Hyperacute Bacterial Conjunctivitis
N. gonorrhea & N. meningitides
Manifestations of Hyperacute Bacterial Conjunctivitis
-Redness, chemosis & lid swelling
- Also can see tender, swollen preauricular lymph nodes.
-Can lead to corneal ulceration with perforation
-Gonococcal ocular infection left untreated results in corneal ulceration with ultimate perforation and sometimes permanent loss of vision.
Acute Bacterial Conjunctivitis
- burning, tearing, & purulent discharge
-usually self-limited disorder lasting about 10-14 days if untreated.
Causes of Acute Bacterial Conjunctivitis
S. pneumoniae, S. aureus, H. influenzae
Manifestations of Acute Bacterial Conjunctivitis
Sticky eyelids with possible eyelid involvement.
Chronic Bacterial Conjunctivitis
-often associated with blepharitis
-Burning, foreign body sensation, eyelash crusting
CAUSES - adenovirus, HSV & enterovirus
Adenovirus - commonly associated with pharyngitis, fever, & malaise
MANIFESTATIONS - redness, tearing & minimal exudates
Herpes Simplex Conjuntivitis
Unilateral infection, irritation, mucoid discharge, pain & mild photophobia.
Vesicles can develop on eyelids & lid margins.
Often associated with HSV keratitis.
Caused by Chlamydia trachomatis.
Severe strains can be complicated by process of trachoma (corneal ulceration, scarring & blindness).
More serious forms of infection are caused by a different strain (serotypes A through C) and leads to ulceration and scarring of the cornea.
How is Chlamydial Conjunctivitis Spread?
Spread by contaminated genital secretions and occurs in newborns with infected mothers.
Also can be contacted through swimming in unchlorinated pools.
What is the leading cause of preventable blindness in the world?
Chlamydial Conjuctivitis cause by a more serious, different strain.
Pathological Process of Chlamydia trachomatis
Corneal abrasions can be extremely painful, but with minor it usually will heal in a few days.
INTEGRITY OF THE CORNEAL EPITHELIUM AND ENDOTHELIUM IS NECESSARY TO MAINTAIN HYDRATION OF THE CORNEA WITHIN A LIMITED RANGE; DAMAGE TO EITHER STRUCTURE LEADS TO EDEMA AND LOSS OF TRNASPARENCY
Healing process of corneal trauma
-Epithelial corneal layer can regenerate & heal after trauma without scarring, deeper abrasions heal slower & have a higher risk for infection
-Abrasions to deepest layer heal with scarring & permanent opacification which impairs light transmission
IF STROMA OF CORNEA IS DAMAGED, HEALING OCCURS MORE SLOWLY, AND THE DANGER OF INFECTION IS INCREASED
INJURIES TO BOWMAN'S MEMBRANE AND THE STROMAL LAYER HEAL WITH SCAR FORMATION AND PERMANENT OPACIFICATION
OPACITIES IMPAIR LIGHT AND DISTORT VISION
Manifestations of Corneal Trauma
pain, photophobia, corneal edema and possibly long-term visual distortions.
With corneal edema, the cornea appears dull, uneven and hazy, visual acuity decreases, and iridescent vision (rainbow around lights) occurs.
-Iridedescent vision results from epithelial and subepithelial edema, which splits white light into its compenent parts, with blue in the center and red on the outside.
Causes of Corneal Trauma
Prolonged and uninterrupted wearing of hard contact lenses, which can deprive the epithelium of oxygen, disrupting the integrity corneal edema also occurs after a sudden rise in intraoccular pressure.
inflammation of cornea
Causes of Keratitis
infections, hypersensitivity reactions, ischemia, defects in tearing, & trauma
CAN ALSO BE CAUSED BY INTERRUPTION OF SENSORY INNERVATION THAT OCCURS WITH EXCESSIVE LOCAL ANESTHETICS
EXPOSURE TRAUMA CAN RESULT FROM DEFORMITIES OF THE LID, PARALYSIS OF LID MUSCLES OR SEVERE EXOPTHALMUS
Manisfestations of Keratitis
extreme pain, photophobia, blurred vision, lacrimation, FB sensation.
Ulcerative vs. Non-Ulcerative Keratitits
Non-ulcerative - all epithelial layers are affected but epithelium remains intact
-Causes: syphilis, tuberculosis, lupus
Ulcerative - part of epithelium is destroyed with ulcer formation
-Causes: bacteria (Staph, Strep, Chlamydia), exposure trauma, extended-wear contact lenses
ACANTHAMOEBA IS A FREEE-LIVING PROTOZOAN THAT THRIVES IN CONTAMINATED WATER; ACANTHAMOEBA KERATITIS IS AN INCREASINGLY SERIOUS AND SIGHT-THREATENING COMPLICATION OF WEARING A SOFT CONTACT LENS, PARTICULARLY WHEN HOMEMADE SALINE SOLUTIONS ARE USED FOR CLEANING; CAN ALSO OCCUR IN NON-CONTACT LENS WEARERS AFTER EXPOSURE TO CONTAMINATED WATER OR SOIL
Most common cause of corneal ulceration
Herpes Simplex Keratitis
Herpes Simplex Keratitis
Primary infection causes follicular conjunctivitis, corneal irritation & blepharitis with rounded cobblestone lesions.
After primary infection, virus may persist in a latent state in trigeminal nerve.
What precipitates recurrence of herpes simplex keratitis?
Stress-related factors precipitate recurrence.
RECURRENT INVOLVEMENT IS USUALLY UNILATERAL
Manifestations of herpes simplex keratitis
usually unilateral; irritation, photophobia, tearing, & possible blurred vision.
-Corneal lesion has a typical branching pattern
SOME REDUCTION IN VISION CAN OCCUR WHEN LESION AFFECTS THE CENTRAL PART OF THE CORNEA
HERPETIC LESIONS THAT INVOLVE THE STROMAL LAYER PRODUCE INCREASINGLY SEVERE CORNEAL OPACITIES; THOUGHT TO HAVE AN IMMUNE RATHER THAN AN INFECTIOUS CAUSE.
Causes of herpes simplex keratitis
MOST CASES ARE CAUSED BY HSV TYPE 1 , EXCEPT IN NEONATAL INFECTIONS ACQUIRED THROUGH THE BIRTH CANAL (80% ARE TYPE 2).
Varicella Zoster Opthalmicus
Reactivation of varicella virus ("shingles")
Who is at higher risk of Varicella Zoster Opthalmicus?
Immunocompromised pts at higher risk.
Manifestations of Varicella Zoster Opthalmicus?
Malaise, fever, headache; burning & itching of periorbital area (1-2 days before rash)
Rash starts as vesicles, then becomes pustular & finally begins crusting
Involvement of the tip of the nose indicates a high likelihood
Ocular signs include conjunctivitis, keratitis, and possible uveitis.
What % of shingles cases involve varicella zoster ophthamicus?
represents about 10-25% of all cases of herpes zoster.
Uveal tract involves 3 regions: choroids, ciliary body, and iris
Definition - inflammation of all 3 regions of uveal tract
Causes of Uveitis
usually from autoimmune diseases (lupus, rheumatoid arthritis, sarcoidosis).
Manifestations of Uveitis
severe photophobia, ciliary flush, irregular shaped pupil, hypopyon (collection of inflammatory cells in anterior chamber of eye).
Optic neuropathy characterized by optic disk cupping & visual field loss usually resulting from an increase in intraocular pressure resulting from abnormalities in the balance between aqueous production & outflow
Causes of Glaucoma
Most commonly due to interference with outflow from the anterior chamber.
CAN OCCUR AS A CONGENITAL OR ACQUIRED DISORDER AND MAY MANIFEST AS A PRIMARY OR SECONDARY DISORDER.
Primary vs. Secondary Causes of Glaucoma
PRIMARY- no evidence of preexisting ocular or systemic disease
SECONDARY- usually from inflammatory diseases
-Tumors or from blood cells of trauma produced hemorrhage that obstruct the outflow of aqueous humor.
2 Types of Glaucoma
1. angle closure (narrow-angle)
2. open (wide) angle
Manifestations of Glaucoma
Temporary or permanent impairment of vision results from pressure-induced degenerative changes in the retina and optic nerve & from corneal edema & opacification.
How to detect optic nerve damage from glaucoma?
Optic nerve damage can be detected by an opthalmoscopic examination.
Cause of Angle-closure (Narrow-angle) Glaucoma
occlusion of anterior chamber angle by iris; usually bilateral.
Acute attacks precipitated by prolonged pupillary dilation which increases IOP
Occurs from inherited anatomic defect causing a shallow anterior chamber
MOST LIKELY TO DEVELOP IN EYES WITH PREEXISTING NARROW ANTERIOR CHAMBERS
USUALLY OCCURS AS THE RESULT OF AN INHERITED ANATOMIC DEFECT THAT CAUSES A SHALLOW ANTERIOR CHAMBER
SEEN MORE COMMON IN PEOPLE OF FAR-EASTERN, ASIAN, ESKIMO DESCENT AND IN PEOPLE WITH HYPERMETROPIC EYES
ACUTE ATTACKS OFTEN PRECIPITATED BY PROLONGED PUPILLARY DILATION (CAUSES IRIS TO THICKEN (BLOCKS CIRCULATION BETWEEN ANTERIOR & POSTERIOR CHAMBER
OTHER CONDITIONS CAUSING EXTENSIVE AND PROLONGED DILATION OF THE PUPIL - EMOTIONAL UPSET, PHARMACOLOGIC AGENTS (ATROPINE)
Manifestations of Narrow-angle Glaucoma
acute pain, blurred vision, enlarged fixed pupil; with prolonged attacks the eye becomes red; headache, N & V are also possible
Open (Wide) angle Glaucoma
Most common form of glaucoma and usually manifests after age 35
Characterized by abnormal increase in intraocular pressure occurring without obstruction at the iridocorneal angle
Cause of open (wide) angle glaucoma
Exact cause remains unclear
Occurs because of an abnormality of the trabecular meshwork that controls the flow of aqueous into the Canal of Schlemm
Manifestations of open (wide) angle glaucoma
Causes progressive damage to optic nerve resulting in gradual visual field loss
lens opacity interfering with the transmission of light to the retina
Most common cause of age-related visual field loss in the world
Pathogenesis - not completely understood
Risk Factors for Cataracts
aging, genetics, drugs, injury, environmental & metabolic influences, long-term sunlight, heavy smoking, congenital, drugs
FOUND IN 50% OF PEOPLE BETWEEN 65 - 74 YO & 70% OF THOSE OLDER THAN 75.
Types of Cataracts
Caused by foreign body injury to lens or blunt eye trauma
Foreign body can interrupt lens capsule & allow aqueous & vitreous humor to enter lens & initiate cataract formation
Present at birth due to genetic defects, toxic & environmental agents and viruses
Most are not progressive & are not dense enough to cause significant visual impairment
MATERNAL RUBELLA INFECTION DURING THE FIRST TRIMESTER OF PREGNANCY CAN CAUSE CONGENITAL CATARACT
CATARACTS AND OTHER DEVELOPMENTAL DEFECTS OF THE OCULAR APPARATUS DEPEND ON THE TOTAL DOSE AND THE MBRYONIC STAGE AT THE TIME OF EXPOSUREDURING THE LAST TRIMESTER OF PREGNANCY, GENETICALLY OR ENVIRONMENTALLY INFLUENCED MALFORMATION OF THE SUPERFICIAL LENS FIBERS CAN OCCUR
MOST CONGENITAL CATARACTS ARE NOT PROGRESSIVE AND ARE NOT DENSE ENOUGH TO CAUSE SIGNIFICANT VISUAL IMPAIRMENT
What is the most common cause of age-related vision loss?
Most common cause of age-related vision loss
With normal aging, nucleus & cortex of lens enlarge & new fibers form in outer zones & compress the old inner fibers
Metabolic changes occur, lens proteins become more insoluble & concentrations of calcium, sodium, potassium, phosphate increase, which gradually results in loss of lens transparency
Manifestations of Senile Cataracts
most bilateral; result in gradual blurring & vision distortion ultimately leading to severe vision loss.
Central Retinal Artery Occlusion
Complete occlusion of central retinal artery results in sudden unilateral blindness
Uncommon; most often caused by embolism
Because retina has a dual blood supply, the survival of retinal structures is possible if blood flow is restored
Infarct swells & opacifies; because fovea centralis receptors are supplied by vessels from choroid they survive resulting in a bright red spot surrounded by a pale retina
Central Retinal Artery Occlusion Pathophysiology
PThe blood supply to the choroid comes ultimately from the ophthalmic artery (#1 in figure). There are variations but quite posterior branches will become the central retinal artery, and ciliary arteries on each side of the optic nerve. These vessels divide into 2 long posterior ciliary arteries and ~20 short posterior ciliary arteries that enter the eye immediately adjacent and around the optic nerve. The short posterior ciliary arteries directly supply the choroid and the long posterior ciliary arteries travel in the suprachoroidal space anteriorly then supply the choroid anteriorly via recurrent branches. The ophthalmic artery continues to provide branches for the posterior (#7 in Figure) and anterior (#8 in Figure) ethmoidal vessels. The superior oblique muscle is shown for orientation.
Disorders of retinal vessels resulting in retinal exudates, microaneurysms, hemorrhages, & neovascularization
outpouchings of vessels
formation of new vessels resulting from endothelium releasing VEGF
preretinal, intraretinal, subretinal
opacities result from inflammatory processes, often resulting in the destruction of the underlying retinal pigment & choroid layer.
Non-proliferative Diabetic Retinopathy
Proliferative Diabetic Retinopathy
Hypertensive (HTN) Retinopathy
Non-proliferative Diabetic Retinopathy
Cause - uncertain (hyperglycemia, HTN, Chol)
Third leading cause of blindness in US
Confined to retinal capillary wall resulting in vessel thickening & microaneurysm formation
Ruptured capillaries cause small intraretinal hemorrhages & microinfarcts
Most common cause of decreased VA is macular edema due to fluid accumulation in the retina from a breakdown in the blood-retina barrier
Proliferative Diabetic Retinopathy
Characterized by retinal neovascularization
Vessels grow in front of retina along posterior surface of vitreous or into the vitreous
-Weak vessels bleed easily & can cause vitreous hemorrhage
-Vessels attach firmly to retinal surface & posterior surface of vitreous & can result in retinal detachment
Hypertensive (HTN) Retinopathy
Long-term uncontrolled HTN results in thickening of arteriolar walls, which decrease perfusion pressure in capillaries.
Edema, microaneuryms, intraretinal hemorrhages, exudates, & cotton wool spots
Normally, retinal vessels are transparent & seen as a red line; arteries in persons with hypertensive retinopathy appear paler "copper & silver wiring)
Compressed veins under thickened arteries exhibit AV (arteriovenous) nicking
Separation of sensory retina from pigment layer
Cause of Retinal Detachment
traction on inner sensory layer or tear in with vitreous accumulating between the 2 layers
Vitreous normally adheres to retina; if vitreous shrinks it results in retinal traction
Retinopathies, eye surgery, inflammation or exudates
Prolonged detachment leads to permanent destruction of neural retina & blindness of involved area
Manifestations of Retinal Detachment
painless, sudden visual loss; may be preceded by floaters or spots
Loss of central vision due to destruction changes of the area surrounding the central fovea
Cause is poorly understood
Risk Factors for Macular Degeneration
Leading cause of blindness in individuals > 75
age, female, caucasian, cigarette smoking, & decreased dietary intake of carotene
2 Types of Macular Degeneration
Non-exudative (dry) Macular Degeneration
Atrophy and degeneration of central retina
Does not involve leakage from blood vessels
Changes occur on the retina consisting of pale, yellow spots called drusen (remnants of materials in pigment epithelium)
Most people with drusen do not experience significant loss of central vision & the atrophic changes may stabilize or progress very slowly
Exudative (wet) Macular Degeneration
Characterized by the formation of choroidal neovascularization in between the neural retina & pigment retinal layer
New vessels are weak & prone to leakage resulingt in separation of 2 layers or retinal detachment
Natural course is toward irreversible loss of central vision
Ultimaely leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated.
% of people with wet type macular degeneration
Only about 10% of patients suffering from macular degeneration have the wet type.Macular degeneration is not painful, which may allow it to go unnoticed for some time.
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