This document summarizes various degenerative conditions of the conjunctiva, cornea, and retina. It describes conditions such as pterygium, pinguecula, and concretions of the conjunctiva. For the cornea, it discusses recurrent erosion, arcus senilis, and lipid keratopathy. Regarding the retina, it outlines microcystoid degeneration, retinoschisis, and paving stone degeneration. The document provides details on the signs, symptoms, etiology, and treatment of these various ocular degenerative diseases.

1. OPTOM FASLU MUHAMMED

2.  Degenerations may be unilateral or bilateral
and are secondary phenomena after previous
disease

3. Degenerative Conditions of
Conjunctiva
 Concretions
 Pinguecula
 Pterygium
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4. Concretions (Lithiasis)
 They are minute hard, yellow, projectile lesions seen in
palpabral conjunctiva.
 Concretions are due to collection of epithelial cells and
inspissated mucous in depressions called Henle’s
gland.
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6.  They produce foreign body sensation. Commonly
found in elderly patients who have suffered from
Trachoma.
 Treatment: Removal under topical Anaesthesia with a
sharp hypodermic needle.

7. Pinguecula
 It’s a triangular patch on the bulbar conjunctiva in
palpabral aperture in elderly patients especially those
exposed to strong sunlight, dust ,wind , drying etc
 The pinguecula is due to hyaline infiltration and
elastotic degeneration in sub-mucous tissue.

9.  Yellow triangular raised lesion with apex away from
cornea are seen in palpabral aperture.
 Nasal side is affected first then the temporal.
 The patch looks like fat (pinguis = fat). The lesion is
stationary at a moderate size. The pinguecula becomes
more prominent in congested / inflammed eye.

10.  No treatment is usually required. If removal is desired
for cosmetic purposes

11. Pterygium
 Pterygium (A wing) is a triangular encroachment of
bulbar conjunctiva on to the cornea.
 The conjunctiva invade the cornea destroying the
superficial layers of the stroma and bowman
membrane , the corneal tissue is covered by
conjunctival epithelium.

13. Etiology
 Commonly seen in dry ,sunny, hot climate with sandy
soil, ultra-violet light also act as etiological factor

14. Signs
 A triangular encroachment of conjunctiva upon the
cornea with numerous small deep opacities in front of
the apex.
 It usually follows pinguecula first develop on nasal
side, in case of double pterygium temporal side is
affected later.

15.  Progressive pterygium is thick vascular growth with
punctate opacities in front of the apex.
 Atrophic pterygium is thin and pale growth with few
obliterated vessels. It is characterized by formation of
dense fibrous tissue and is associated with
considerable corneal astigmatism.

16. Prophylaxis
 UV rays filters, protective glasses
 Artificial tears

17.  If small and does not cause cosmetic problem, it be
left.
 Subconjunctival resection of pterygium leaving a bare
sclera adjacent to limbus
 Sub-conjunctival transplantation of pterygium.

18. Degenerative Conditions of Cornea
 Epithelial
 I. Keratitis sicca
 II. Recurrent erosion
 III. Keratomalacia
 IV. Neuroparalytic keratopathy

19. Stromal
 Arcus senilis
 Terrien’s ulcer
 Calcific band keratopathy
 Salzmann’s nodular degeneration
 Lipid keratopathy
 Limbus girdle of Vogt
 Delle
 Anterior crocodile shagreen

20. Keratitis sicca
 Because the watery part of the tear secretion is lacking,
corneal epithelial punctate erosions develop in
exposed areas

21. Recurrent erosion
 The epithelium forms small blebs and then desquamates
In recurring cycles.
 The condition usually follows incomplete healing of a
traumatic corneal abrasion, most commonly a fingernail,
paper, or plant injury.
 The cause is uncertain but seems to be a defect
in the epithelium that produces an abnormal
basement membrane.

22. Keratomalacia
 Keratomalacia, caused by a deficiency of vitamin A, is
characterized by diffuse, excessive keratinization of all
mucous membrane epithelia, including the cornea and
conjunctiva
 The condition occurs most often in children , who
characteristically complain of night blindness

23. Neuroparalytic keratopathy
 Early neuroparalytic keratopathy, which may resemble
recurrent erosion, often progresses to almost total
corneal epithelial desquamation.
 Frequently, it is complicated by secondary infection
that leads to perforation.

24.  The condition is caused by a lesion any where along
the course of the ophthalmic division of the fifth
cranial nerve and results in partial or complete loss of
corneal sensitivity

25. Stromal
Arcus senilis
 Lipid deposit is limited to the peripheral cornea and
central sclera.
 It starts earliest at the inferior pole of the cornea, then
involves the superior, becoming annular in the late
stage.
 lipid first concentrates in the area of Descemet’s
membrane, then in the area of Bowman’s membrane

27. Terrien’s ulcer
 The lesion, a limbal depression or gutter, starts as fine,
yellow-white, punctate opacities supranasally,usually
bilaterally, and spreads circumferentially,rarely
reaching inferiorly.

29. Calcific band keratopathy
Calcific band keratopathy starts in the nasal and temporal
periphery with a translucent area at the level of Bowman’s
membrane; the semiopaque
The extreme peripheral cornea remains clear, but the central
cornea ultimately may become involved.

31. A deposition of calcium salts on and in Bowman’s
membrane apparently is related to abnormal epithelial
activity.
Calcific band keratopathy may be secondary to primary
hyperparathyroidism; increased vitamin D absorption;
chronic renal failure; ocular disease,especially uveitis ;
long-standingglaucoma; local pilocarpine therapy

32. Salzmann’s nodular degeneration
 The condition, an elevated white or yellow corneal area,
usually is unilateral (but may be bilateral)
 occurs mainly in women
 It is superimposed on an area of old corneal injury

33.  the epithelium shows areas of both hypertrophy and
atrophy, with a marked increase of subepithelial
basement membrane material and scar tissue.

35. Lipid keratopathy (secondary lipidic degeneration)
 Lipid keratopathy may be unilateral or bilateral and
follows old injury, especially surgical.
 Clinically, it appears as a nodular, yellow, often
elevated corneal infiltrate.
 Histologically, the lipid deposition is located mainly
in between Bowman’s membrane and epithelium.

37. Limbus girdle of Vogt
The limbus girdle of Vogt appears as a symmetric,
yellowish-white corneal opacity forming a half-moon–
like arc running concentrically within the limbus
superficially in the interpalpebral fissure zone, most
commonly nasally

38. Delle (singular form of dellen)
A delle is a reversible, localized area of corneal
stromal dehydration and corneal thinning owing to a
break in the continuity of the tear film layer secondary
to elevation of surrounding structures

39. Anterior crocodile shagreen
The condition consists of a central corneal opacification at the level
of Bowman’s membrane that presents as a mosaic of polygonal
gray opacities
1. The condition may occur as a dystrophy
with bilaterality and a dominant inheritance pattern.
2. It also may occur as a degeneration after trauma or associated
with such conditions as megalocornea, iris malformations, and
band keratopathy.
3. A peripheral variety may be seen as an aging

40. Degenerative Conditions of retina
Microcystoid Degeneration
 Outer plexiform layer is the commen site of the
lesion
 All persons 8 years of age or older show the lesion.
 The tendency is toward relatively equal bilateral
involvement. The temporal neural retina is involved
more than the nasal, and the superior sectors are
affected more than the inferior

41.  The degeneration always seems to begin at the ora
serrata.
 Early, the cysts are limited to the middle layers of the
neural retina. Later, they may extend to the external
and internal limiting membranes of the neural retina.

42.  The septa separating the cysts are composed of glial–
axonal tissue rich in the cytochrome oxidase enzyme
system.
 microcysts coalesce, an intraneural retinal macrocyst
or retinoschisis cavity is formed when the macrocyst is
at least 1.5 mm in
 length

43.  Reticular peripheral cystoid degeneration
 Reticular peripheral cystoid degeneration appears
clinically posterior to typical peripheral microcystoid
degeneration.
 The subsurface retinal vasculature arborizes into fine
branches throughout the reticular lesion.

44.  The inferior and superior temporal regions, each
involved to approximately the same extent
 Reticular peripheral cystoid degeneration are located
in the nerve fiber layer of the neural retina.

45.  Early, the cysts are located completely within the nerve
fiber layer;
 later, they may extend from the internal limiting
membrane to the inner plexiform layer.
 The cysts contain hyaluronic acid

46. Degenerative Retinoschisis
 reticular degenerative (adult) type ,typical
degenerative senile (adult)type
 defined as an intraneural retinal tissue loss or splitting
at least 1.5 mm in length
 It is most common after the age of 40, and rare before
the age of 20 years.

47.  it is found in the peripheral inferior temporal quadrant
 Neural retinal holes are seen in this condition
 area of the retinoschisis enlarges, the involved neural
retina is destroyed

48.  Paving Stone (Cobblestone)Degeneration
 The lesions are located primarily between the ora
serrata and equator and are separated from the ora
serrata by normal neural retina.
 The lesions are nonelevated, sharply demarcated,
yellow–white, single or multiple, and separate or
confluent.
 most common in the inferior temporal quadrant

49.  the lesions are characterized by:
Neural retinal thinning in an area devoid of pigment
epithelium
 An absent choriocapillaris or a partially obliterated
choriocapillaris or sometimes only minimal
abnormalities such as thickening of the walls of the
choriocapillaris are seen
 The disorder involve outer retina
& result in RPE atrophy

50. Peripheral Retinal Albinotic Spots
I. Areas of hypopigmentation in the neural retinal
periphery are caused by depigmentation of the RPE.
II. Although the lesions probably are degenerative, a
congenital cause cannot be ruled out.

51.  Myopic Retinopathy
 “high” myopia (greater than 6 diopters of myopia)
affects the neural retina most severely in the posterior
pole and in the periphery
 The globe is enlarged mainly in its posterior third,
with thinning of the sclera.

52.  optic disc and usually extending temporally
 Thinned sclera bulges posteriorly to form a staphyloma
that is lined by a thin and atrophic choroid.
 Bruch’s membrane may develop small breaks
 peripheral neural retina also becomes thin and
atrophic

53. Macular Degeneration
 It is characterized by a sharply demarcated, dome-
shaped elevation of the RPE.
 Most RPE detachments are between one-fifth to one-
half disc diameter, rarely reaching two disc diameters.

54.  The symptoms are those of metamorphopsia, positive
scotoma, and micropsia. Decreased contrast
Decreased color
 The condition recurs in approximately one-fourth to one-
third of patients and occasionally may become bilateral.
 the involved area, most often in the macula, shows fluid
under the neural retina
 Most cases heal spontaneously with restoration of normal
vision.

55. Age-Related Dry Macular Degeneration
 Dry ARMD is characterized by a gradual reduction of
central vision.
 The cause is unknown.

56.  High intake of saturated fat and cholesterol is
associated with an increased risk for early ARMD.
Exposure to sunlight and soft and hard drusen also
have been implicated as a risk factors.
 the retinal damage is limited to the foveomacular area
and causes a gradual and subtle visual loss

57.  increased and decreased pigmentation are seen in the
macula.
 The atrophy of the RPE tends to spread and form well
demarcated borders, called geographic atrophy of
macular degeneration.
 Hyperopia also may be a risk factor.

58.  The changes usually are bilateral and found in people
older than 50 years of age
 The choriocapillaris may be partially or completely
obliterated.

59. Age-Related Exudative Macular Degeneration
 exudative ARMD rarely occurs in people younger than
60 years of age.
 The cause is unknown.

60.  risk increases with age, especially 75 years and older,
and in women.
 main risk factor is age-related macular choroidal
degeneration
 High intake of saturated fat and cholesterol also is
associated with an increased risk for early ARMD.
 .

61.  Exudative ARMD may be associated with moderate to
severe hypertension, particularly among patients
receiving antihypertensive therapy.
 Hyperopia also may be a risk factor
 Large, soft drusen seem to predispose the eye to
exudative ARMD.

62.  The age-related macular choroidal degeneration
becomes complicated by neovascular invasion.
 The new vessels grow from the choroid (from the
choriocapillaris) through Bruch’s membrane, usually
under the RPE
 Finally, a hemorrhage between Bruch’s membrane and
RPE occurs

63.  the haemorrhage may remain localized, it usually
breaks through the RPE under the neural retina; rarely
it may extend into the choroid, the neural retina, or
even the vitreous.