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OPH > Module 6 > Flashcards

Module 6 Flashcards

1
Q

Cornea

A

Development:

  • Epithelium = surface ectoderm –> secretes primary stroma
  • Mesenchymal neural crest = endoderm, stroma, anterior iris stroma, ciliary muscle
  • Endothelium –> Descemet’s membrane at 30-35 days
  • Mesoderm between epithelium and endoderm, continuous with the sclera –> stroma
  • lids open days 14, thinning of cornea in initial 4 weeks, then increase in thickness over next 6 months
  • Neural crest mesenchyme - pupillary membrane –> anterior chamber
  • Cornea - 48D of plus power towards the convergence of an image on retina
  • Oxygen from tear film, nutrients from aqueous.
  • tight junctions create protective barrier. The subepithelial nerve plexus is extensive and also serves to protect the eye.
  • Immunoglobulins are provided via the tear film. Tear film is approx 7um thick.
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2
Q

Epithelium

A

Stratified, squamous, non-keratinised, non-secretory. 50-60um. 5-7 layers.
Most superficial layer - microvilli and microplicae
Superficial layer - flattened squamous cells, squames, tight juntions
2-3 layers interdigitating wing cells in intermediate layer
Basal layer tightly adhered to basement membrane 50nm thick.

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3
Q

Epithelial cell adhesion

A

Superficial cells - numerous desmosomes, but also tight junctions which surround the cell.
Wing cells attached to superficial cells by desmosomes. Gap junctions between wing cells allow intercellular communication
Basal cells - desmosomes and gap junctions, less than wing cells. Hemidesmosomes attach epithelium to basement membrane

Basement membrane roles: maintaining structure, anchorage, barrier, filtration or storage, involved in biological processes - embryonic development and cellular differentiation.

Basement membrane - formed by epithelial and stromal cells. Lamina lucida and lamina densa. Cillagen IV, laminin, proteoglycans.

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4
Q

Stroma

A

500um thick = 90% corneal thickness. Highly organised. Meshes with sclera.
Stromal fibroblasts, keratocytes, secrete lamellar fibroblasts.
Proteoglycans (keratin and chondroitin) cross-link the lamellae.
Predominantly type I, some type III, V and VI
Keratocytes - constantly remodelling the stroma, produce proteases which allow this, over production –> melting keratomalacia

Inner most layer of stroma is Descemet’s membrane, it is 12um thick and is secreted by endothelium

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5
Q

Endothelium

A

low cuboidal, single-layered endothelium.
No specialised adhesive junction between endothelium and Descemet’s membrane.
Lateral membrane - desmosomes, tight and gap junctions.
Leaky barrier between aqueous and stroma but impedes free flow.
Gap junctions - intercellular communication.
Mitochondria +++, smooth and rough endoplasmic reticulum, golgi apparatus
NaK ATPase pump maintains corneal hydration
Not self renewing. Enlarges and slides to fill defects

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6
Q

Corneal innervation

A

Myelinated nerves pass from the trigeminal nerve through the anterior stroma in leashes. On penetration through the basement membrane the sheath is lost and naked nerve ending sends terminus up between the cells layers.
300-400 more nerve endings than the epidermis, reduced in brachys which predisposed them to injury

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7
Q

Corneal nutrition

A

Tear film - oxygen

Limbal bloods vessels and aqueous - glucose and amino acids

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8
Q

Limbus

A

Junction between corneal and conjunctival epithelia. Anatomically location includes Schlemm’s canal and the trabecular meshwork, usually only superficial portion that is termed the limbus.
Epithelium in this transition zone is 10-12 layer thick, no goblet cells. Cell-cell and cell-substrate junctions are similar to those of the cornea.
Basal cells have undulating extensions into the underlying matrix –> increase SA for absorption of nutrients.
Basal cells have less hemidesmosomes cf. cornea and are hypothesised to be stem cells for the corneal epithelium.
Connective tissue more loosely arranged than cornea. Large radial folds in the stroma - palisades of vogt. Limbal epithelium reaches down into the valley between the palisades, protects the stem cell population.
Limbal vasculature supplies: peripheral cornea, conjunctiva, episclera, limbal sclera, peripheral uvea. Arterial - anterior ciliary arteries from rectus muscles. Drained by venules reversing over same direction

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9
Q

Resting state

A

Corneal epithelium - self renewing, constant state of healing as squames shed into tear pool and replaced by cells from limbus and basal layers.
When damage occurs, healing kicks in, essentially an exaggeration of the normal physiological process.
Normal circumstances corneal mass doesn’t change. X+Y=Z
X=proliferation of basal cell, Y=contribution to cell mass by centripetal movement
z=epithelial cell loss
Replication form peripheral stem cells of the cornea is exaggerated during traumatic epithelial loss

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10
Q

Epithelial wound healing

A

Requires: cell migration, cell proliferation and cell adhesion
Latent phase: 4-6 hours post trauma, no decrease in wound size, sloughing necrotic cells, intracellular components upregulated. Basal and squamous cells in the area thicken and separate. Hemidesmosomes between basal cells and basement membrane disappear. Tight junctions disappear but desmosomal attachments are not completely severed. PMN cells arrive via the tear fluid 3 hours post trauma. Lost of columnar appearance of basal cells, epithelium is thinner during this phase. Ruffling and folding of plasma membrane –> finger like projects (filopodia and lamellipodia).

Linear phase: cells flatten and spread across defect until covered. Glycogen provides energy for this. Actin filaments at leading edge of migrating cells. Desmosomes allow the cells to move as a sheet. Temporary adhesions, focal contacts, are formed during migration - actin filament bundles inserting into cells. Intracellular contractile mechanisms draw the trailing cells forward. Fibrin and fibronectin –>PAF–>plasminogen to plasmin which lyses cell adhesions allowing them to advance forward and form new adhesions. This continues until wound closure and wound is usually closed initially with a single layer of cells. Migration and cells proliferation are independent but compliment each other. Healing considered complete once epithelium anchored down by hemidesmosomes, can be complete in 1 week if basement membrane intact, if not can be up to 6 weeks for new basement epithelium to be constructed by stroma and epithelium.

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11
Q

Stromal wound healing

A

Stromal healing cannot begin until re-epithelialisation is complete. Fibroblasts migrate into wounded and lay down new collagen - not regular and hence opaque scar results. Remodels with time and opacity may become smaller.

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12
Q

Corneal disease

A

Colour change: blue/grey, red, white, black/brown
Causes: oedema, vascularisation, pigmentation, fibrosis, cellular infiltration, lipid deposition (common in dogs, not in cats), calcium deposition

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13
Q

Oedema

A

Fluid –> stroma; epithelial or endothelial dysfunction.
Mild = hazy or steamy. Dense = blue eye.
May form cysts/bullae which then burst and are difficult to heal

Epithelial dysfunction = ulcer
Endothelial dysfunction = primary (endothelial dystrophy, breed related or degeneration, age) or secondary (glaucoma - increased IOP, uveitis - IO inflammation, lens luxation, IO mass, iatrogenic post sx)

Full ophthalmic examination, fluorescein staining. Measure IOP. Ocular US if not possible to see in the eye.

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14
Q

Vascularisation - red

A

Superficial and deep vascularisation
Angiogenic factors released by anoxic/injured cornea.
superficial - tree like, from conjunctiva
deep - brushes or hedges, from limbus
Granulation tissue sometimes seen, usually non-healing ulcers such as those seen in Boxers

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15
Q

Pigmentation - black/brown

A

Chronic corneal disease

  • melanin: superficial or endothelial
  • sequestrum in cats
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16
Q

White

A

Fibrosis - from stromal healing.
Cellular infiltrate- white/pink - superficial and proliferative. Scraping can assist dx, or keratectomy
Lipid - white/sparkly - various causes, superficial or deep, cholesterol or trglycerides
Calcium - white/gritty - degenerative, usually in elderly dogs, check for other old age diseases - renal or cardiac disease

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17
Q

Non-ulcerative corneal diseases

A

Infiltrative: cellular, neoplastic, non-cellular
Non-infiltrative: congenital or aquired
Infectious

18
Q

Infiltrative - cellular

Chronic superficial keratitis (pannus)

A

Chronic superficial keratitis (pannus) - dogs, GSDs, collies, greyhounds. 3-5 years, red eyes. ventro-lateral limbus and spread across cornea. Conj, including TEL without corneal dz = plasmoma.
Worse seasonally due to UV light
Bx –> plasma cell
Dx –> bx but also CS usually enough
Tx –> CCS or ciclosporin. Repeated courses throughout life. lipid and pigment deposition persist despite tx, keratectomy if vision is severely impaired.

19
Q

Infiltrative - cellular

Eosinophilic keratoconjunctivitis

A

IM dz in cat.
White/pink deposits (cottage cheese) in the superficial corneal stroma and epithelium.
Young to middle aged cats.
Dx –> cytology on scrapings. MCTs and eosinophils.
Poss part of EGC. Poss linked to FHV.
Tx: CCS, ciclosporin. Seasonal recurrence.

Megoestrol acetate has been advocated but undesirable AE.

20
Q

Infiltrative - cellular

punctate keratitis

A

Shetland sheepdogs, min LH dachshunds
flu +ve punctate corneal opacities
tx with CCS

21
Q

Infiltrative - neoplastic

A

Rare

SCC: limbus, reported in cats and dogs. In dogs can be associated with chornic keratitis.

Limbal/epibulbar melanoma: dogs, slow growing benign tumour. Mostly Labs and GSDs. Sx resection and treatment with strontium 90 is the treatment of choice. May require reconstruction.

Others - haemangiomas and haemangiosarcoma

22
Q

Infiltrative - non-cellular

Lipid (crystalline stromal) dystrophy

A

Lipid deposited in stroma, subepithelially. No inflammation flu -ve.
Inherited and seen in many breeds but mode uncertain in dogs
CKCS and rough collies - autosomal dominant
Huskies - recessive, variable expression

young adults, bilateral and symmetrical, one may be impacted before the other
Central/paracentral, crystalline appearance, once formed often static
In bitches may be associated with hormonal cycle, worth checking serum lipid and lipoproteins if marked or progressive.

Pathology: cholesterol, defect in corneal fibroblast/keratocyte; accumulates lipid and then dies. Tx: none unless progressive

23
Q

Infiltrative - non-cellular

Lipid keratopathy

A

Lipid deposition, vascularisation. +/- hyperlipoproteinaemia (HDL cholesterol - smaller lipoproteins raised if any)
Associated with anterior segment inflammation, localised corneal disease, previous corneal or ocular insult

Pathology: fibroblast cell death as for lipid dystrophy, lipid-filled foam cells in progressive lesions - macrophage derived. Corneal neovascularisation is esablished lipid keratopathy.

24
Q

Infiltrative - non-cellular

Arcus lipoides corneae (ALC)

A

Bilateral. peripheral accumulation of lipid.
A result of excessive insudation of plasma proteins therefore hyperlipoproteinaemia!
Larger lipoproteins (triglycerides) –> arcus
Smaller lipoproteins (cholesterols) –> lipid keratopathy

Opacity is located peripherally in the corneal stroma, superficial stroma.
Opacities become vascularised, but delicate cf. lipid keratopathy.

Hyperlipoproteinaemia is usually secondary e.g. to hypoT4

Pathology: peripheral non-crystalline triglyceride rich lipid deposition. Cellular involvement and cell death later. May have subtle neovascularisation if cell death sufficient.

Tx: lipid and lipoprotein profile, primary rare, secondary is common. Dietary manipulation. Tx underlying cause.

25
Q

Corneal calcification

A 
>14 years old
May follow corneal damage and degeneration
Seen in older dogs
HyperCa sometimes
Renal and cardiac dz sometimes
Poor prognosis for dog's general health
Tx: EDTA ointment or drops
26
Q

Non-infiltrative disease - congenital

A

Dermoids: if they involve cornea usually noted at limbus. Asymptomatic if hairless. Keratectomy = tx. GSD and St Bernard

Micro and megalocornea: rare, no other congenital conditions are seen otherwise would be MODs. Bilateral, non progressive. Poss in association with microphthalmia or buphthalmos. FHV may result in MODs including corneal defects.

Persistent pupillary membranes: may attach to posterior cornea, opacity at point of contact

Transient opacities: following eye opening. Clear rapidly and no clinical significance

keratoconus: bilateral thinning of the central cornea sporadically or in association with lenticonus. keratoglobus: limbal to limbal thinning

Lysosomal storage diseases: accumulation of abnormal products within the cell lysosomes. Neuro abnormalities dominate. Retinal changes, blindness, corneal clouding. Diffuse corneal clouding = neurometabolic storage dz = mucopolysaccharides I, VI, ?VII, GM1 and GM2 gangliosidosis and mannosidosis.

27
Q

Non-infiltrative disease - acquired

A

Dystrophies: breed predisposition, may effect epithelium stroma or endothelium

Endothelial dystrophy: most commonly ESS, chihuahua, boxer and boston terrier. May be impaired function rather than reduced number. Late to middle aged. May be seen in old dogs due to loss (degeneration).
CS: stromal oedema, bilateral but one eye may be impacted before the other, may be develop keratoconus or keratoglobus. Bullous keratopathy –> non-healing ulcers.
Mx: reduce corneal oedema with NaCl ointment, and tx secondary problems. Contacts for ulcers. Thermal keratoplasty advocate, scarring squeezes fluids out and prevents fluid entry. Opacity may be worse so doesn’t restore vision. Gunderson flaps are a good way of reducing oedema and improving vision.

28
Q

Non-infiltrative disease - acquired

A

Endothelial dystrophy in the cat: occasionally seen, progress, bilateral and severe. Cat is otherwise normal.

Stromal dystrophy: Manx cats, autosomal recessive

Macular corneal dystrophy: stromal opacity, inherited in labradors, developes around 5 years. DNA test (carbohydrate sulfotransferase-6 mutation).

Exposure and neurotrophic keratitis: CN V (neurotrophic) or CN VII (neuroparalytic)palsy will result in keratitis due to absence of blink reflex. Also factor in brachys. Incomplete blink and tear film spreading, exposure of central cornea.

29
Q

Non-infiltrative disease - acquired

A

Corneal sequestrum: only in cats. Any breed but more brachys. Likely the cornea’s response to chronic damage. Seen in association with FHV, entropion, KCS, chronic exposure keratitis. CE - required to uncover any concurrent problems. Lesions starts as brown pigment in the stroma, increases in size and gets darker, extending into anterior stroma and breaking into epithelium. Plaque seen to appear above epithelium as then starts to cause discomfort at this stage. May slough spontaneously, but takes a long time. Tx: If underlying cause and tx that, superficial keratectomy with grafts or lenses as necessary. IFN has been tried as tx recently

30
Q

Non-infiltrative disease - acquired

A

Keratoconjunctivitis sicca:

  • STT1 reduced, middle aged dogs, WHWT + others, progressive corneal opacity, vascularisation and pigmentation
  • CS: discharge, conjunctivitis, non-healing ulcers, melting ulcers
  • Dx: STT1
  • Tx: ciclosporin, false tears, ABs if secondary infection, tacrolimus, sx

Epithelial inclusion cyst: smooth round corneal lesions, when corneal epithelium seeds into the stroma. Aetiology not always clear, congenital, post trauma or sx, Non-painful and flu -ve. Tx is by excision.

31
Q

Infectious dz

A

FHV:

  • acute = cat flu signs; conjunctivitis, keratitis, URT signs
  • ulceration and symblepharon as a result of corneal stem cell damage, can be extensive and effectively blind a kitten due to conjunctival growth over defect
  • Carrier/chronic status: dendritic ulceration from active viral replication and stromal keratitis, symblepharon, conjunctivitis, non-healing ulcers, dry eye.
  • CS: intermittently sore watery eyes. Rose bengal best for picking up dendritic ulcers
  • Stromal keratitis is a perpetuation of cat’s own immune-response to viral antigen
  • possible may contribute to corneal sequestrum and eosinophilic keratoconjunctivitis
  • Dx: hx and CS. PCR best to confirm but false pos and neg. Serum not useful due to vaccs
32
Q

Infectious dz

A

Mycobacterium: mycobacterium keratitis rare. Dx acid-fast bacilli in corneal scrapings

Mycotic keratitis: once rare in the UK. Consider in refractory keratitis cases. Ulcerative disease most common and H/o topical or steroid tx. Very painful, paucity of blood vessels, white/icing sugar appearance to the stroma and ulcer surface. Tx: voriconazole or clotrimazole or keratectomy and graft.

33
Q

Ulcerative corneal disease

A

Full hx including vacc status. Breed tendencies should be kept in mind.
Uncomplicated ulcers should heal within 7 days, if it doesn’t then why?
Tx: uncomplicated ulcer - topical ABs and analgesia

Assessment: why is it there? how deep? is it infected? Other factors?
Depth: superficial, deep, descemetocoele, rupture. Slit beam!!!!

34
Q

Ulcerative corneal disease

A

Indolent ulcers:

  • superficial ulcer that fails to heal, not infected, oedema, +/- vasc, pain, epiphora, flu staining, dogs, middle-aged, Boxers, staffies, corgis
  • Full ophthalmic exam, eyes and adnexa and STT, flu staining +/- rose bengal.
  • Superficial ulcers more painful than deep ulcers
  • complicating factors: repeated trauma (hairs or FB), dry eye, oedema, infiltrate, IM (CSK, punctate keratitis)
  • SCCEDS super chronic corneal epithelial defects: defect in basement membrane formation and epithlial cell adhesion.
  • Boxers but can be seen in older dogs and cats
  • May see over exuberant healing response which results in granulation tissue protruding from the corneal surface
  • Tx: aim is to remove or disturb the abnormal basement membrane with keratotomy or keratectomy. Remove abnormal matrix as well as damage stroma and stimulate wound healing response. Analgesia and ABs, sometimes systemic preferred to avoid preservatives.
35
Q

Ulcerative corneal disease

A

Surgical options for non-healing ulcers:
- debridement: LA, dry sterile cotton bud, circular rubbing, remove all loose epithelium
Post- op: pain-relief, contact lens, lubrication, ABs.
- keratotomy: LA, +/- sedation, debride and then grid or punctate keratotomy
Post- op: pain-relief, contact lens, lubrication, ABs.
- phenol cautery: old fashioned, LA, debride, one drop on coton bud, rub ulcer bed, flush with 20ml sterile water.
Post- op: pain-relief
- diamond burr: new, LA, debride with cotton bud and then use to mechanically debride the area
Post- op: pain-relief, contact lens, lubrication, ABs.
- superficial keratectomy: GA, magnification, keratectomy knife/beaver blade, experience needed
Post- op: pain-relief, contact lens, lubrication, ABs, temp tarsorrhaphy

36
Q

Ulcerative corneal disease

A

Cats with non-healing ulcers: debride, contact lens, TEL, tarrsorrhaphy, antivirals, superficial keratectomy, medial canthoplasty.

Do not burr, phenol or grid non-healing ulcers in cats!!! Increase risk of forming a sequestrum!

37
Q

Melting ulcers - keratomalacia

A

Rapidly progressing ulcers which occur when the stroma is digested by proteases and collagenases. Produced by pathogenic organisms but also inflammatory cells and resident corneal cells. Cornea becomes liquefied.

Pseudomonas and B-haemolytic streps are a common cause. Brachys and dry eye can see sterile melts.

Mx: hospitalise if poss, cytology (+/- C&S), topical broad spectrum ABs q1-2hours for first 48 hours, anti-colleagenase tx (EDTA, serum and tetracyclines) frequently for first 48 hours, systemic NSAIDs +/- atropine for ciliary spasm (except in KCS due to dropping tears), potent analgesia, avoid CCS topically and systemically, corneal cross linking

38
Q

Thermal and chemical injuries

A

Emergency. Copious irrigation. Lubrication and topical antibiotics. NSAID and analgesia +/- atropine. Chemical injuries - test pH as acids are less destructive than alkalis. anticollagenases may be required. Scarring is a very probable complication and symblepharon may be seen if stem cells at limbus destroyed.

39
Q

Corneal cross linking (CXL)

A

Formation of chemical bridges by exposure to photoactivated riboflavin (Vit B2).
Riboflavin exposed to UV-A light at a peak of 370nm, generates free radicals up to a depth of 300um.

Stabilises cornea
microbicidal
bacteriostatic

photoactivated chromophore for infectious keratitis-corneal cross-linking (PACK-CXL) successful as a standalone in human melting ulcers.

Implemented into melting ulcer protocols would likely improve patient outcome

Infectious ulcers 80-90% gram +ve, 10-20% gram -ve.

40
Q

Episclera

A

Episclera - collagen, blood vessels, elastic fibres, fibroblasts, melanocytes, phagocytic cells, and nerves. Most developed limbus to extraocular muscle insertions, then blends with tenon’s capsule

Episcleritis: dogs>cats. diffuse or nodular. uni or bi.

  • Diffuse - corneal oedema and lipid deposition.
  • Nodular - subtle oedema, and lipid deposition.
  • Not painful cf. secondary to other inflammatory dz.
  • R/o other systemic dz.
  • Dx: bx
  • Tx: CCS or ciclosporin, topical or systemic if unresponsive. Recurrence possible.
41
Q

sclera

A

Sclera - relatively avascular, compact arrangement of collagen, Similar cell types but sparser.

Scleritis: not obvious as tissue is at greater depth, usually salmon pink rather than bright red. Nodular or diffuse, uni or bi.

  • Fundic exam advised in case posterior scleral involvement.
  • uncomfy
  • possible component of multisystemic inflammatory dz
  • topical and systemic CCS and recurrence possible

OPH (13 decks)

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