Eye > Cornea > Flashcards

Cornea Flashcards

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1
Q

How is corneal vascularization classified by depth?

A

• Superficial: From superficial limbal plexus.
• Interstitial: From anterior ciliary arteries.
• Deep/retrocorneal pannus: Seen in syphilitic interstitial keratitis.

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2
Q

What is pannus?

A

Fibrovascular tissue growth between epithelium and Bowman’s layer; degenerative or inflammatory.

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3
Q

What are the types of pannus?

A

Pannus trachomatosus
Pannus leprosus
Pannus phlyctenulosus
Pannus degenerativus

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4
Q

Define micropannus.

A

Vascularization extending beyond 1–2 mm from normal vasculature.

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5
Q

Causes of micropannus

A

Inclusion conjunctivitis
Vernal conjunctivitis
Superficial limbic keratoconjunctivitis
Staphylococcal blepharitis,
Childhood trachoma
Contact lens wear.

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6
Q

Define gross pannus

A

Vascularization extending >2 mm from normal vasculature.

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7
Q

Gross Pannus causes.

A

Trachoma
Staphylococcal blepharitis
Atopic keratoconjunctivitis
Rosacea
HSV

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8
Q

progressive pannus vs regressive pannus

A

Progressive → Infiltration ahead of vascularization.
Regressive → Vascularization ahead of infiltration.

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9
Q

Characteristic of superficial vessels in cornea

A

Arborizing Dichomotous branching
Sub epithelial
Red color
Can be traced beyond limbus

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10
Q

Characteristic of Deep vessels in cornea

A

Straight Stromal Pink
non branching
Can’t be traced beyond limbus

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11
Q

Arrangement patterns of deep corneal vessels?

A

Terminal loops, Brush, Parasol, Umbel, Network, Interstitial arcade.

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12
Q

Which corneal layers are involved in pannus formation?

A

Between epithelium and Bowman’s layer.

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13
Q

What does the term “pannus” literally mean.

A

Cloth

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14
Q

Deep or retrocorneal pannus is commonly seen in which condition?

A

Syphilitic interstitial keratitis.

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15
Q

What surgical methods are used to treat corneal vascularization?

A

• Peritomy: Remove annulus of conjunctival & subconjunctival tissue (3–4 mm from limbus)
• Superficial keratectomy: For superficial or circumferential vascularization
• Argon laser photocoagulation

radiation therapy
Destroys superficial vessels by causing endarteritis from endothelial trauma.

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16
Q

What is the first stage of a corneal ulcer and its key features?

A

Progressive Infiltration

Microbial invasion
Stromal infiltration
Gray white opacity
Pain Red Edema

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17
Q

What is the second stage of a corneal ulcer and its key features?

A

Active Ulceration

NECROSIS
Sloughing
Hypopyon
Edema

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18
Q

What is the third stage of a corneal ulcer and its key features?

A

Regression

Inflammation subsides
MARGINS demarcated
Less edema
VASCULARIZATION

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19
Q

What is the fourth stage of a corneal ulcer and its key features?

A

Cicatrization

Scar
OPACIFICATION
Epithelization
Vascularization subsides

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20
Q

Definition of ulcer

A

Break in the continuity of the Co epi with inflammation and necrosis of the surrounding tissue

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21
Q

Risk factors for the development of fungal keratitis

A

OCULAR FACTORS
Trauma
Chronic corneal inflammation
Contact lens wear
Drugs Corticosteroids, Anesthetics
Corneal surgery Penetrating Keratoplasty Refractive surgery

SYSTEMIC FACTORS
Diabetes mellitus HIV positive patients Leprosy

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22
Q

Corneal Biopsy instrument

A

dermatologic trephine or Elliot’s trephine

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23
Q

Amphoterecin concentration
Eyedrop
Intrastromal

A

0.15%
5ug in 0.1ml

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24
Q

Sensitivity of
Gram’s stain
KOH wet mount
Calciflour

A

31.6% - 98%
72.2% - 91%
80%

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25
Voriconazole concentration Eyedrop Intrastromal
5% 50ug
26
Thick corneal nerves found in
1. **Keratoconus**– Commonest association; due to stromal thinning and nerve prominence. 2. **Neurofibromatosis**– Especially type 2; thickened nerves may be visible at the slit lamp. 3. **Multiple endocrine neoplasia type 2B (MEN 2B)**– Characteristic finding with mucosal neuromas. 4. **Leprosy**– Due to Mycobacterium leprae involvement of corneal nerves. 5. **Refsum’s disease** – Peroxisomal disorder with phytanic acid accumulation. 6. Other rare causes – **Meesmann corneal dystrophy, Fuchs’ endothelial dystrophy (occasionally), acanthamoeba keratitis** (due to inflammation).
27
Corneal graft grading
0 0paque 1 pupil border visible 2 iris is visible but details hazy 3 slightly hazy Co. iris details visible 4 Clear “”OBHVC””
28
What does LASIK stand for?
Laser-Assisted In Situ Keratomileusis
29
What does SMILE stand for?
Small Incision Lenticule Extraction
30
What does SILK stand for?
Smooth Incision Lenticule Keratomileusis (ELITA = Enhanced Lenticule Intrastromal Technique using Advanced energy)
31
What type of laser is used in LASIK?
Excimer for ablation + Femtosecond for flap
32
What type of laser is used in SMILE?
Femtosecond laser (VisuMax, 500 kHz) “Visu had a Max SMILE”
33
What type of laser is used in SILK/ELITA?
Femtosecond laser (Lenticule 2.0, ~2 MHz) “He ate a Silky Lenticule”
34
What is the typical energy per pulse in SMILE?
~130–180 nJ
35
What is the typical energy per pulse in SILK/ELITA?
~10–50 nJ (lower energy)
36
What is the repetition rate in SMILE?
500 kHz
37
What is the repetition rate in SILK/ELITA?
Up to 2 MHz
38
What is the incision size in LASIK?
~20 mm (flap)
39
What is the incision size in SMILE?
2–4 mm
40
What is the incision size in SILK/ELITA?
~2.5–3 mm
41
Which refractive surgery has the strongest biomechanics?
SMILE and SILK (flapless, better corneal strength)
42
Which refractive surgery has the fastest visual recovery?
LASIK and SILK (faster than SMILE)
43
What are the main advantages of LASIK?
Fast recovery, accurate, widely established
44
What are the main advantages of SMILE?
Flapless, less dry eye, biomechanical stability
45
What are the main advantages of SILK/ELITA?
All SMILE benefits + **smoother interface**, faster recovery, less energy damage
46
What is the main limitation of LASIK?
Flap-related complications, ectasia risk
47
What is the main limitation of SMILE?
Steep learning curve, difficult dissection in some cases
48
What is the main limitation of SILK/ELITA?
Very new, limited long-term data, Zeiss-only technology
49
What is the definition of Peripheral Ulcerative Keratitis (PUK)?
Destructive inflammatory disease of peripheral cornea characterized by: ① Epithelial defect, ② Stromal inflammation, ③ Progressive stromal melting,
50
Why is the corneal periphery more prone to ulceration in PUK?
Thicker and loosely structured collagen nutrition by perilimbal capillaries, more access to blood supply and lymphatic increased lymphocyte/macrophage presence limbal vessels with immune complexes increased epithelial proliferation.
51
What is the basic pathogenesis of PUK?
Exposure to foreign antigen → Antibody production → Immune complex formation → Complement activation → Neutrophil/macrophage recruitment → Release of collagenase/proteinase (IL-1, TNFα) → Stromal disruption and melting.
52
List the important ocular infectious etiologies of PUK.
Bacterial (including TB), Viral, Fungal,.
53
List the important non-infectious ocular etiologies for PUK.
Autoimmune: Mooren's ulcer Neurogenic causes Trauma: lid/lash disease Iatrogenic “TINA”
54
List the systemic non-infectious associations of PUK.
Rheumatoid arthritis, Wegener's granulomatosis (Granulomatosis with polyangiitis), Polyarteritis nodosa, Sjogren's syndrome, Inflammatory bowel disease, Pemphigoid.
55
Key clinical features of PUK?
Peripheral crescentic ulceration, epithelial defect, subepithelial infiltration, circumferential spread, overhanging edge, limbitis, scleritis, cell and flare.
56
What is Mooren's Ulcer?
An idiopathic peripheral ulcerative keratitis without scleral or limbal involvement; associated with HLA-DR17/DQ2.
57
Name the chief sequelae of PUK.
Peripheral thinning and scarring, perforation, contact lens appearance of cornea.
58
Outline the management principles of PUK.
Identify and treat underlying etiology, control infection (if present), corneal scraping and culture, use topical and systemic immunosuppression, support healing (lubricant, cycloplegic), treat complications (glue, patch graft, keratoplasty).
59
What is the primary treatment for non-infectious PUK?
Topical steroids, systemic immunosuppression, N-acetylcysteine (collagenase inhibitor), conjunctival resection, surgical intervention if needed.
60
When are oral steroids indicated in Mooren's ulcer?
Bilateral Unilaterally Severe Young patients recurrence.
61
How is an infectious etiology of PUK managed?
Corneal scraping for culture, empirical/rational antibiotic therapy, adjust based on organism, address non-healing or perforation with glue/BCL, patch graft, or keratoplasty.
62
What is the 'overhanging edge' in PUK?
It refers to the edge of the ulcer, where infiltrated tissue overlaps the stromal defect due to tissue melting.
63
List non-infectious differential diagnoses for peripheral corneal ulceration.
Degenerative conditions (Terrien's marginal degeneration, pellucid marginal degeneration) neoplastic (ocular surface squamous neoplasia) Dalen trauma/chemical injury contact lens-related changes eyelid disease.
64
What is the main physiologic function of the cornea?
To act as a major refracting medium for a clear retinal image.
65
Enlist the anatomical factors responsible for corneal transparency.
Uniform arrangement of epithelium, peculiar stromal lamellae arrangement, corneal avascularity.
66
What is the physiological factor responsible for corneal transparency?
Relative dehydration of cornea.
67
Enlist the factors affecting corneal transparency.
Epithelium and tear film, stromal lamellae arrangement, avascularity, hydration, cellular factors.
68
Explain Maurice theory of corneal transparency.
Regular lattice arrangement of stromal fibrils (< wavelength of light) causes transparency by destructive interference of scattered light.
69
Explain Goldman theory of corneal transparency.
Transparency is due to small fibril size relative to wavelength of light, lattice arrangement not essential.
70
Enlist the hydration factors responsible for corneal transparency.
Stromal swelling pressure, imbibition pressure, epithelial/endothelial barrier function, endothelial pump mechanisms, evaporation of water from tear film, intraocular pressure.
71
What is stromal swelling pressure?
Pressure (~60 mmHg) exerted by stromal GAGs drawing water into cornea.
72
What is imbibition pressure and how is it calculated?
Negative pressure opposing stromal swelling; in vivo IP = IOP - SP.
73
Enlist the endothelial pump mechanisms controlling corneal hydration.
Na+/K+ ATPase pump, bicarbonate-dependent ATPase, carbonic anhydrase, Na+/H+ pump.
74
What happens if IOP exceeds stromal swelling pressure?
Corneal edema develops, reducing transparency.
75
Enlist the theories of corneal vascularization.
Chemical theory (VSF, VIP), mechanical theory (loosening of stroma), combined theory, role of leukocytes.
76
Enlist the types of corneal vascularization.
Superficial vascularization, deep vascularization, retrocorneal pannus.
77
Enlist the cellular factors affecting corneal transparency.
Keratocytes (collagen, proteoglycans), corneal crystallins (transketolase, aldehyde dehydrogenase).
78
Enlist the factors affecting drug permeability across cornea.
Lipid solubility, molecular size and weight, concentration, ionic form.
79
Which form of drugs penetrates epithelium vs stroma better?
Non-ionized (lipid-soluble) drugs penetrate epithelium, ionized drugs penetrate stroma.
80
What is the main physiologic function of the cornea?
To act as a major refracting medium for a clear retinal image.
81
Enlist the anatomical factors responsible for corneal transparency.
Uniform arrangement of epithelium, peculiar stromal lamellae arrangement, corneal avascularity.
82
What is the physiological factor responsible for corneal transparency?
Relative dehydration of cornea.
83
Enlist the factors affecting corneal transparency.
Epithelium and tear film, stromal lamellae arrangement, avascularity, hydration, cellular factors.
84
Explain Maurice theory of corneal transparency.
Regular lattice arrangement of stromal fibrils (< wavelength of light) causes transparency by destructive interference of scattered light.
85
Explain Goldman theory of corneal transparency.
Transparency is due to small fibril size relative to wavelength of light, lattice arrangement not essential.
86
Enlist the hydration factors responsible for corneal transparency.
Stromal swelling pressure, imbibition pressure, epithelial/endothelial barrier function, endothelial pump mechanisms, evaporation of water from tear film, intraocular pressure.
87
What is stromal swelling pressure?
Pressure (~60 mmHg) exerted by stromal GAGs drawing water into cornea.
88
What is imbibition pressure and how is it calculated?
Negative pressure opposing stromal swelling; in vivo IP = IOP - SP.
89
Enlist the endothelial pump mechanisms controlling corneal hydration.
Na+/K+ ATPase pump, bicarbonate-dependent ATPase, carbonic anhydrase, Na+/H+ pump.
90
What happens if IOP exceeds stromal swelling pressure?
Corneal edema develops, reducing transparency.
91
Enlist the theories of corneal vascularization.
Chemical theory (VSF, VIP), mechanical theory (loosening of stroma), combined theory, role of leukocytes.
92
Enlist the types of corneal vascularization.
Superficial vascularization, deep vascularization, retrocorneal pannus.
93
Enlist the cellular factors affecting corneal transparency.
Keratocytes (collagen, proteoglycans), corneal crystallins (transketolase, aldehyde dehydrogenase).
94
Enlist the factors affecting drug permeability across cornea.
Lipid solubility, molecular size and weight, concentration, ionic form.
95
Which form of drugs penetrates epithelium vs stroma better?
Non-ionized (lipid-soluble) drugs penetrate epithelium, ionized drugs penetrate stroma.
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