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222 Cards in this Set
- Front
- Back
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Major areas for drug treatment of glaucome
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NPE of ciliary body, alpha 2 and beta 2 receptors --> sympathetics produce aqueous.
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Pilocarpine
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Direct acint Parasympathomimetic
MAO: Congration of ciliary muscle enhances pathway of the CONVENTIOANL flow via pulling on scleral spur. OUtfkiw us enhanced through juxtacanicular tissue. it BLOCKS uveoscleral pathway; |
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Piolcarpine side effects
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Miosis, brow ache, REtINAL detachment, secondary cataracts and iris cysts.
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Carbachol
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Used when piollcarpine is ineffecitve. Parasympathomimetic direct acting
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Anticholinesterases
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Indirect acting Parasympathomimetics
MAO: strong contraction of ciliarty muscle pulling on scleral spur to open CONVENTIONAL pathway |
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Other indirect acting parasympathomimetic drufs
PIED |
Echothiphate iodide
demercarium bromide isofluorphate physostigamine sulphate |
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Indirect acing parasympathmemic side effects
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POSTERIOR synchiae, cataracts, stroma miosis and accomodation, retinal detachment, iris cysts
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Sympathomimetic drugs
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PURPLE CAP
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Parasympathomimetic drugs
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GREEN CAP
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Sympathomimetic Alpha Stimulators
Aclonodine |
Aprclonidine
Stimulates alpha 2 receptors Decreases aqueous production by stimulating an INHIBITORY G protein, G decreases cAMP in the NPE cell= inhibits aqueous production. DRUG OF CHOICE FOR ANGLE CLOSURE ATTACKS --> GOOD FOR SHORT TERM Causes: Tachphylaxis, dry mouth, lid retraction |
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Sympathomimetic Alpha Stimulators
Brimonidine Alphagan |
Selective alph 2 agonist.
Decreases aqueous production by stimulating an inhibitory G protein. Decreases cAMP. Enhance uveoscleral outflow - Can be used long term DRUG OF CHOICE FOR LOW OR NOMRAL TENSION GLAUCOMA. NEUROPROTECTIVE EFFECT ON ONH. NO tachyplyaxis |
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Alphagan P
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Purite is the P, its a preservative. Shows less allergic reactions
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Direct Acting Alpha and Beta Stimulators
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Epinephrine
Propine --> prodrug of epinephrine INCREASES activity of enodthelial cells --> ENHANCES CONVENTIONAL system ENHANCES phagocytosis of debris thru meshwork ENHANCES UVEOscleral flow by releasing prostaglandins which relax ciliary body. Also causes some increase of inflow ONLY DECREASES IOP BY 2 OR 3 MM HG |
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Propine side effects
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LOADS of them:
Adenchrome: dark deposits on the cong, tox reactions with long term use Cystoid macula edema due to prostaglandin release lid retraction NEVER use on those with tachcardias or hyperentions |
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Sympatholytic drugs --> BETA BLOCKERS
1. What is the GOLD STANDARD? |
Timoptic XE/Timolol
Gel form before bed. Decreases active section by BLOCKING beta 2 recpetors of NPE --? Blocks formation of cAMP Very effective in lowering IOP. Short and long term drift may occur. BECOMES less effective with continued use. Beginning has a 30% drop of pressure. - HAVE PATIENTS punctal occlude - Causes bronchiole constriction - Pulmony effects - GI disturbances - Cardiac effects |
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Sympatholytic drugs --> BETA BLOCKERS
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Levobunolol
Metipranolol Carteolol Betoxolol- less pulmonary issues, but less effective Betoptic Cosopt |
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Carbonic Anhydrase Inhibitors
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Orange Cap
VERYY effective decreases IOP via INHIBITON of active secretion processes, thereby decreasing aqueous production. INHIBITS bicarbonate formation ACUTE TREATMENT only due to side effects. |
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Carbonic Anhydrase Inhibitors side effects
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Diarrhea, blood dyscrasia, depletion of sodium and potassium, anorexia, depression, decreased libido
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Carbonic Anhydrase Inhibitors
Dorzolamide |
Topical carbonic anhydrase inhibitor and beta blocker
not good at lowering pressure alone --> USE IN COMBOO Has a bitter taste |
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Carbonic Anhydrase Inhibitors
Azopt |
not as effective as an oral CA
Fewer side effects |
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DRUG OF CHOICE
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Prostaglaninds!!!
Increase uveoscleral outflow |
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Prostaglandin of choice- gold standard
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Xalatan
Receptors in cilary muscle leads to biosynthesis of the matrix of metalloproteinases. Alters colalgen in ciliary muscle and increases sspace among fiverse REDUCES hydraulic resistance's in uveoscleral outflow pathway NO effect on blood aqueou layer Side effects: Darkens iris coloration, lengthens eyelastions, darkens skin, can cause cystoid macualr edema triggers herpes simplex MUST BE REFRIGERATED |
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Other prostaglandins
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Lumigan: effects episcleral veins and mimics prostamides
Travatan: very effective, more on african americans. Used in VA hospitals |
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Hyperosmotics
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Used for patients with angle closure:
Glyercol and manntol. reduces active secrtion, increaes osmotic pressure in ciliary body and veitreous. pulls aq out of eye to lower IOP |
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1.Extravan
2. Nabuctate |
1. combo of a prostaglandin and beta bloder
2. Mariguana derivate. Best when smoked |
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Mesodermal mesenchyme
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blood vessel and blood elements
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Crest mesenchyme
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melanocytes and connective tissue
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Neural ectoderm
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dilator and sphincter muscle
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2nd wave of neural crest cells
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6-7th week corneal stroma
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3rd wave of neural crest mesenchyme
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ATVL anterior leaf of iris
ABL |
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Mesodermal mesenchyme
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blood vessel and blood elements
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Crest mesenchyme
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melanocytes and connective tissue
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Neural ectoderm
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dilator and sphincter muscle
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2nd wave of neural crest cells
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6-7th week corneal stroma
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3rd wave of neural crest mesenchyme
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ATVL anterior leaf of iris
ABL |
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Fourth wave of mesenchyme
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posterior leaf
fibroblasts and melanocytes |
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Atrophy of the ATVL occurs
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6th month --> we get the posterior ciliary arteries extending from posterior leaf to form major circle of iris.
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Anterior iris epithelium is continuous with
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pigented epithelium of ciliary body
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Iris muscles develop from anterior epithelium via
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neuroectoderm
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Sphincter development
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after 13-14 weeks iris loses melanin and forms actin which lets spincter to move away from anterior epithelium and into stroma
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Dilator development
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occurs during 6th month and ends 5 motnhs postnasally
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Last feature of the iris to appear
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pupil --> atrophy of ATVL during 6th month
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Iris coloartion occurs during
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5-6th month postnasally
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Crypts of fucs develope _____-- due to atrophy of __________-
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postnatally
anterior border layer |
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Congenital absense of iris
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Aniridia
BILATERAL rim of optic cup fails to proliferate can get gluacoma and catract |
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Typical Iris coloboma
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6 oclock
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Atpyical iris coloboma
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anywhere not at 6 oclock
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Albinoism
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NORMAL amount of melanocytes, but failure to produce enough melanin
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Microcoria
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pupil smaller than .5 mm
due to failure of the last phase of iris differentiation. MALFORMATION of the dilator muaxkw |
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Ciliary neural crest mesenchyme develops into
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connective tissue stroma, melanocytes, ciliary muscle
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Ciliary body neural ectoderm develops into
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inner nonpigmented and outer pigmented CB epithelium
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Aqueous product occurs during
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4th mon prenatally
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Ciliary muscle is fully developed ___________
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at 1 year of age --> no accomodation prior
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Crypts of fuchs develop-------
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POSTnatally as a result of ABL atropy
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Depth of anterior chamber
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3.5-3.7 mm
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Volume of anterior chamber
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250 microliters
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Angle of anterior chamber:
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20-45 derees
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Structures that contribute to the anterior chamber angle
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SS FATS
Scleral spur Schwalbe's line Face of ciliary body anterior surface of iris trabecular meswork schlemm's canal |
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Hyperopes have a __________ angle than myopes
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Smaller
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Function of the anterior chamber angle
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pathwy for aqueous to exit eye. Is the plumbing.
Produces MPS and enzymes |
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Traecualr meshwork is composed of
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cords and sheets of connective tissue surrounded by MPS and an endothelial covering
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MPS
Mucopolysaccaride |
SLOWS down flow of aqueous... is a viscous gel
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Uveal meshwork
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2-3 cord layers thick
adjacent to anterio chamber aqueous --> sieve GROSS filtration. RADIAL around the eye |
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Corneoscleral meshwork
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20 layers of pores
CLOSER to schlemm's canal FINE filtration run CIRCUMFERENTIALLY inserts into scleral spur mostly |
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Anterior trabecualr meshwork
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nonfiltering portion
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Posterior embrotoxin
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thickened schwalbe's line
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Scleral spur
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aids in aqueous flow when ciliary contracts --> ELASTIN
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Do corneal or trabecular meshwork endothelial cells undergo mitosis?
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NO
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Capthepsin B,G,D
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breaks down MPS produced by the endothelial cells. Released in cyclical fashion to control variation of aquous flow. Some steroids can bind to these and cause an increase in MPS and a decrease in aqueous flow --> INCREASES IOP
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Trabecular endothelial cells are innervated by
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Sympathetic alpha and beta recepotrs --? Increases outflow of aqueous
Epinephrine speeds up filtration by enhancing trabecular meshwork activity. --> Pilocarpine |
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Juxtacanalicular tissue
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last sheet of corneoscleral meshowrk and inner wall of Schlemm
offfers GREATEST reistance to flow of aqueous CONTRACTION of ciliary body pulls on scleral spur which pulls on trabecular meshwork and juxtacaniluar tissie. ENHANCES outflow thru CONVENTIONAL pathway |
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Schlemm's canal
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circumference 36 mm --> Internal Scleral Sulcus.
Endothelial lining of inner wall contains zonula occludens so that fluid only gets thru one way. Transported intraceullarly via Pincytosis and giant vacuoles--> PRESSURE dependent. MORE IOP means MORE vacuoles needed Vacuoles are responsible for the pressure gradient created by slow moving aqeuous in juxtacanilar --> no backflow. |
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Outer wall of schlemm
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effect collegect channels, pathway for aq to exit
BLOOD drains to anterior ciliary vein |
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Blood in the anterior chamber is known as:
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Hyphema --> caused by trauma to iris.
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Uveal Scleral outflow pathway --> Unconventional
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NOT pressure dependent. Percolate thru ciliary muscle and travel to emissary channels of sclera.
ENHANCED by Prostaglandins --> GOLD STANDARD!!!! Xalatan, Lumihan, Travitan XTL PILOCARPINE SLOWS DOWN uveal scleral outflow when it enhances conventional pathway. |
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Future anterior chamber structures are formed by
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neural crest cells
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Enlargement of the anterior chamber:
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growth of eyeball
forward growth of optic cup enlargement of ciliar Scleral and corneal differentiation |
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At 4 month, anterior chamber:
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NO aqueous production
narrow not recessed no schlemm canal |
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6 months, anterior chamber:
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Production of aqueous!
2 layers of meshwork: corneoscleral and uveal meshwork |
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7 months, anterior chamber:
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scleral spur fully formed
anle reession BARKAN's membrane formed |
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BARKAN's membrane
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undifferentiated tissue that is translucent. It is a membrane that is made up of corneal endothelium. Can lead to congeintal glaucoma due to it growing over developing tm, and left over remnants.
POORY DEVELOPED NEURAL CREST MESENCHYME |
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Canal of schlemm
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venous system of mesodermal origin
-smal plexus of venous canaliculi -appears at 3 months |
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Scleral spur appears at ___ months
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4 months
Not well established till 8 months. FINAL differentiation occurs postnatally |
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Trabecular meshwork development
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Does not differentiate and appear till 4-6 months.
6th month we have separation from corneoscleral and uveal portions 8th month- mature |
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Congenital glaucoma
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at birth-3 months
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Infantile glaucoma
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3 months-3 years
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Juvenile glaucoma
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3 years-34 years
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Primary Infantile Glaucoma
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Defect in in TM and anterior chamber angle
GONIDYGENESIS -can see some blue sclear to due stretching from igh IOP--> Buphthalmos See: extreme photophobia, blepharospasm, epiphoria, enlarged corneal diameter corneal edema due to elevated IOP HAAB STRIAE IS HALLMARK SIGN!!!!!!! |
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Neural crest derivations
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melanocytes, parts of orbit
95% of sclera, corneal stroma and endothelium stroma of iveal tract, ciliary muscle, meninges |
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Diseases and malformation from neural crest are known as:
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Angular neurocristopathies
-abnormalities in migration of neural crest cells |
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Axenfeld-Rieger Syndrome
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Developmental arrest of tissue of neural crest origin in third trimester of gestration.
White line in posterior aspect of cornea. BILATERAL AD Abnormal iris, anterior chamber angle, peripheral cornea. Many other developmental problems present |
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Peter's anomaly
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Incomplete migration and differentiation of neural crest cells of the central corneal endothelium and descement's membrane
OR Defective involvement of the central cornea, lens iris HALLMARK: CENTRAL corneal defect in descements membrane with endothelium thinning and opacification of corneal stroma Bilateral AD/AR 3 Types: 1. No keratolenticular contact or cataract 2. Kertolenitcular contact or cataract present 3. Associated with Axenfeld-Rieger --> RARE |
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Sturge-Weber Syndrome
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NEURO-ocular syndrome.
-Port wine stains Anormality in neural crest cells. Can lead to glaucoma --> trabeculodygensisi. See ELEVATED episcleral venous pressure |
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Uveitis
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inflammation of the uveal tract and anterior segment. cells in flare
can be caused by breakdown in blood aqueuous barrier can lead to 2ndy gluacoma due to cloggin |
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Iridocyclitis
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inflammation of iris and ciliary body
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Functions of aqueous
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1. Internal blood supply to the lens, cornea, vitreous, and anterior chamber
2. elimniates waste by acting as a venous drainage 4. lyphatic drainage is the trabecular meshwork that serves as a path for large molecular weight molecules |
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Anterior chamber volume
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.25 ml
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posterior chamber Volume
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.06 ml
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Viscousity is proportioal to
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protein content
aq viscousity is a little greater than water. increase protein content, increase viscousity and decrease aq outlow |
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normal index of refaction for aqueous
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1.336
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crstalloid
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a solution containing very small particles < 1 micron in size.
They are homogenous and transparent |
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colloid
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not homogenous
larger particles make it opalescent this is aqueous |
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Tyndall effect
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results in an opalescent appearance. Light shines ont a colloid and will refect off goving particles a smoky appearance. Cells and flare!
aq is the size of a colloid but with clarity similar to a crystalloid |
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Diffusion
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spontaneous movemment of moelcuels requring no additional energy, but maily occuring by thermal convention
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Brownian movement
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random movement of particles in a fluid tofill all available spaces --> can changea crsyalloid into a colloid.
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dislysis
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ion distribution across a semipermeable membrane without pressure added to the system. NO ADDED PRESSURE
allows passage of Na and Cl ions |
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Gibbs-Donan equilibrium
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Predicts the movement of carged particles and moelcules across a semipermeable membrane under osmotic and chemical pressure.
Proteins do not move but do effect Na and Cl movment so that a true equilirium CANNOT be reached due to these proteins |
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Ultrafiltration
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dialysis under hydrostatic pressure
ADDITION of pressure that pushes particles across the semipermeable membrane. Occurs in capillaries, esieclaly nonfenestrated ones. 20-30% of aq is produced this way Nonfenestrated capillariese are present in ciliary body stroma and allow most elements to leak thru wlls. Tight junctions of the nonpigmented epithelium of ciliary body act as the sempermeable membrane for aqueous production!!!!!!!!!!!!!!! Pressure is due to blood pressure |
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Responsible for production of aq
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Tight junctions of the nonpigmented epithelium of ciliary body act as the sempermeable membrane for aqueous production!!!!!!!!!!!!!!!
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Responisble for aq ultrafiltration pressure factors:
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-pressure in ciliary capillaries, local autonomic innervation of smooth muscles
- intraolcar pressure (WORKS AGAINST ultrafiltration, makes less IOP be produced --> negative feedbackloop) Osmotic pressure resulting from high protein concentrations in ciliary body and stroma. Pulls water from aq into stroma and thus IS AGAINST aq production, as well. ONLY blood pressure favors Aqueous production! |
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For filtration and production of aq to occur
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Capilly pressure must be GREATER than IOP +Osmotic pressure!!!
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Avg capillary pressure is about
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27-28 mm Hg
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Average IOP
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16
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Average osmotic pressure
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14 mmHg
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Percentage of aq produced y ultrafiltration based on te math:
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30-40%
An average capillary pressure of greater than 40 mmHg is needed to drive ultrafiltration, and the average is 27-28. |
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2nd process of aqueous production
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ACTIVE SECTRION
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What % of aq is responsible for active secretion?
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60-80%
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Active secretion is caused by
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basal infoldigns of NPE laer of the ciliary body that is under control of Beta 2 receptors. The active secretion ustilizes the Na/K/ATPase pump which makes this system
PRESSURE INDEPENDENT on the production of aq. It is, however, ENERGY dependent |
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Is active secretion of aq pressure dependent?
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NO... but it is energy! dependent and erquires O2 and gucose.
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energy dependent active secretion of aq pump
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Na K 2 Cl- moves from stroma into pigmented epithelium
Na moves into NPE from pigmented epithelium CO2 +h20 forms HCO3- Carbonic ANHYDRASE Gets pumped OUT of cell thru Aquaporin 1 channels |
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PRIMARY DRIVING FORCE of aq production is
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Chemo-osmotic imbalance from actions o the NA/K ATPase pump
Can treat gluacome by reducing carbonic anhydrase production |
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Drugs that block the Na/K atpase pump
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Oubain and Vanadate
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CA Inhibitors
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Diamox- sudden instant angle closure
Neptazan Truspot/Asopt |
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Alpha 2 receptor
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Stimulated by Neuroepinephrine
stimulate inhibitory G proteins to DECREASE aq production --> Alphagan |
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Beta 2 receptors
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Stimulated by epinephrine, receptors block excitatory G protein and decrease aq production
--> timolol |
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Lasix Furosemide
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Blocks Na uptake at pe and blocks Na/KCL smport to decrease aq production
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Cornea and aq
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Aq gives cornea glucose, and some oxygen, amino acids
Corneal wastes are removed --> lactic aid |
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Posterior chamber aq
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hih glucose, vitamin C, aminod acids, little lactice acid
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Aqueous versus plasma
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has higher vitamin C, amino acids, Cl and Na.
Has less glucose, HCO3, proteins and IgG then plasma |
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blood aq barrier pore size
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104 A
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The eye and immunosupression
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keeps WBC to a minimum, cytokines and neuropetides inhibits T cell activateion, less scaring
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Detox pump
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removes toxic substances from aq and drains into vortex in NPE
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Prostaglanins
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brakdown blood aq barrier
stimulated by alpha receptors via sympthetic derived from aracadonic acid. |
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Substance P
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contraction of sphincter of iris which results in miosis
Inovled in pain response |
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after injury, miosis of pupils occurs and is due to
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substance P release via prostaglandins
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Flare is
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proteins
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cells in aqueous are
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wbc
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prostaglandins work in two ways
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initially it increases IOP
but then beings to INCREASE uveoscleral outflow so that it DECREASES IOP can call hyperemia though |
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Xalatan Latanaprost
PG wonder drug |
topical
stimulates melanogensis to INCREASE pigmentation of iris INCREASES uveal-scleral outflow INCREASES length of eyelashes other drugs: Travatan and Lumigan |
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Complications of chronic inflammation related to PG release:
1. Cystoid Macular Edema |
intraretinal cysts
decreased VA |
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Aq flow out from anterior chamber:
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150 microliters per hour
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Flow of aq:
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Ciliary body -> posterior chamber -->pupil --> anterior chamber --> two pathways to trabecular meshwork and Schlemm or uveal pathway to vortex veins
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Aqueous is produced at a rate of:
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2.5 microliters per minute
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production of aq_______ as we age
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decreases
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Krukenberg spindle
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due to changes in thermal convection current.Normally cornea is cooler than iris so that aq near iris is heated and then cooled at cornea and falls back to iris.
If pigment is present in anterior chamber the PIGMENT can be depositsed on cornea in a VERTICAL pattern --> pigment disperion syndrome. Can clog meshwork and outflow --> PIGMENTARY glaucoma. |
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Which gender has higher IOPs on average?
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Females
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At what age does IOP start to change?
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40
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What season is IOP lowest?
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lower in summer, higher in winter, can be due to blood pressure changes in the season.
If pressure difference is greater than 5 for seasonal variation in glaucom patients, it is a RED FLAG |
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Effect of incresed blood pressure on IOP
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In response to increase in BP, the eye, under AUTONOMIC CONTROL, keeps blood vessels CONSTRICTED or DILATED as needed to protect eye --> keeps pressure NORMAL
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Pressure highest during what time of day?
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EARLY morning 3-5 AM --> cortisol is being released which prevents lysosomes that break down MPS in the juxtacanilar tissue from working --> makes q more viscous.
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waters effect on iop
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increase
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Alcohol effec on iop
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DECREASE, strong diuretic, decreases blood volume
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upside down effect on iop
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INCREASE IOP
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Myopes tends to have ___________ IOP
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higher
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Flow of aq into EYE
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Flow= Cin(Pa-IOP)
Ease of aq enter eye(pressure in ciliary body pushing aq out-pressure pushing back in) ONLY considers the pressure dependent portion of aq production: 20% |
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Psuedofacility
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IOP high enough to actually stop the production of aq via ultrafilatration. This occurs when IOP approaches DIASTOLIC BP 50-60 mm Hg!!!!
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Flow OUT of eye
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Cout(IOP-Pepiscleral venous) + Uveal scleral pathway.
80% of outflow IS pressure dependent If IOP reaches 50-60 mm Hg outflow SHUTS DOWN and Schlemm's canal COLLAPSES |
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For every 1 mm Hg increase in Pressure of episceral venous pathway Pe there is
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a .8 mm Hg INCREASE IN IOP
ANYTHING effecting EPISCLERAL VEINS HAS A HUGE IMPACT ON IOP |
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Things that effect Pressure of episcleral pathway
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GONIO
Hanging upside down Tight necktie Valsalva maneuver |
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For every 1 mm Hg increase in Ciliary Body arterial pressure Pa
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there is a .2 mm Hg change in IOP!!!
Blood vessels have local autonomic controls to protect itself from changes in Blood pressure |
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Acid in blood's effect on iop
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decrease aq pressure
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Carotid occlusion's effct on iop
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SLIGHT DECREASE IN IOP on one eye vs the other. ABNORMAL EYE IS THE ONE WITH LOW IOP
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Tarsal plate composed of
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dense connective tissue --> provides protection from projectiles
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Cilia of eyelid
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eyelashes --> innvervated by CN V for blink reflex
eyebrows --> innvervated by CN V |
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Protective Reflex
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CN 7 --> EFFERENT LIMB
palpebral portion of orbicularis oculi |
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Spontaneous Blink Reflex
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Blink 12-15 blinks per minute
allows for lubrication of eye by spreading tears and drainage. involves basal ganglia and midbrain rretincular. See deficiet in Parkinson's efferent limb is CN 7 |
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Flow of tears
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lacrimal lake --> puncta --> lacrimal caniculi --> lacrimal sac --> nasolacrimal duct --> nasal cavity at inferior metus lateral to inferior nasal concha
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Dazzle reflex
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eyelid closes in response to BRIGHT light
Afferent lumb is CN II Effect lumb is CN VII Bilateral reflex |
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Menace reflex
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closure of eyelid in response to impending danger/threat
Info travels ot visual cortex because we have to see danger CN II afferent |
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Corneal reflex
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Protective reflex is described by closure of eyelids. Like blinking resuls from touching the cornea or a puff of air.
CN V innervation Pathway: CN V --> reticular formation --> both nuclei of CN VII --> CN VII --> CN V is the afferent limb; CN VII --> efferent limb |
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Auditory Reflex
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Eyelid closes in response to a loud sound
CN VIII afferent lumb CN VII is efferent lumb |
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Bell's Phenomenon
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OCCURS DURNING SLEEP, and during forceful blinking.
Eyes move UP AND OUT to put cornea out of danger. Inolves superior rectus and levator In this phenomenon--> LEVATOR IS INHIBITED --? physiologic synkinesis |
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CN 7 muscle innervation
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1. Oribtal portion of orbicularis oculi
2. Cirrygatir supercili (inserts middle of brow) --> produces vetical lines on forehead 3. Procerus- horizontal wrinkle of nose |
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Skin around eye is
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thinner and elastic tissue is finer
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Blrpharochalasis
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allergies
Loosening of the eyelid (chalasis means lossening) Swelling presents |
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Dermatochalasis
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COMMON in elderly
Lossening of skin. Secondary folds present. Thin tissue and loss of elasticity, weakened orbital septum causes protrusion of extraconal fat --> puffy appearance |
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Palpebral fissure dumensions
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29-30 mm horizontally
11-15 vertically |
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Larger palpebral fissure in
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infants, females, myopes, young, caucasions.
With age it NARROWS |
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Senile ptosis
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sagging of skin --> no damage to CN III, cam block pupil and get decreased VA
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Narrow Palpebral Fissure
True Lid Ptosis |
1.unilateral CN III or bilateral (nuclear lesions)
Congenital --> FAT test 2. Aquired. Orbiulcaris oculi- CN VII Levator palpebrae superiorious- CN 3 Sympathetics--> superior tarsal muscle of mueller. ALL INOVLED. If you see ptosis you MUST CHECK PUPILS First nuetralize CN 7 by pushing up on forehead in order to relax frontalis. Look at pupils. Ptosis + LARGE pupils in bright light --> PARASYMPATHETIC damage/CN 3!!! Levator is screwed up Ptosis + SMALL pupils in Dark --> DILATOR/sympathetics damaged --> Mueller problem |
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Ptosis + SMALL pupils in Dark
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DILATOR/sympathetics damaged --> Mueller problem
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Ptosis + LARGE pupils in bright light
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--> PARASYMPATHETIC damage/CN 3!!! Levator is screwed up
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If nothing wrong with pupil and you have a lid ptosis
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Could be neuromusclar --> Nicotinic acetocholingeric receotprs.
Myargwnia Gravic --> only effects striate skeletal muscles and pupil is spared because its smooth. Pupil sparing CN 3 disease: diabetes |
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Prelid period --> 1 month
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tube closes here.
Neural crest is guided by fibernecton and glycosaminoglycans Neural crest contribues to bone, carticlage, connective tissue, meninges, melanoctes |
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First branchia arch
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mandibular branch --> lower and upper jaw
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2nd branchial arch
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muscles of facial expression
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Lid folds --> 6th-7th week
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Superior fold --> frontonasal process --> mesoderm + surface ectoderm
Ingerior laid fold --> maxillary process Surface ectoderm gives rise to the skin, ciliary, and glands |
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Fusion of lid folds
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9th week. Meet in midline. Due to cell division that plugs tissue and keeps eyelid close.
NECESSARY in order to prevent keratinization of kornea. If lid doesn't close fully --> COLOBOMA. TISSUES form after fusion |
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Eyelid differentiaion/specialization
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Surface extoderm: hair, skin, glands, INSIDE palepbral conj
Neural crest: Orbital spetum melanocytes, connective tissue Mesoderm: blood, muscles |
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Separation of eyelids
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6-7th month.
Due to dead cells slouthing off and breakign the seal. |
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Cryptophthalmos
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skin of eyelid is continuous with skn on cheeck, no real eyelid development.
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Microblepharon
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shortening of vertical dimension of eyelid so that ti doesnt close totally
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Eyelid coloboma
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congenital absense of eyelid tissue. MOstly unilateral.
Can be related to exposure keratitis |
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Ankylopblepharon
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Failure of lid margin to SEPARATE, lids can still be fused. Surgery to separate
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Entropion
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Inward turning of eyelid margin, OVERDEVELOPMENT of marginal fibers of orbicularis oculi.
Circular fibers at lid margin keep contraction and cause eyelids to turn inward. Related to tarsal plate hypoplasia |
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Ectropion
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Malposition of eyelid so that lid marin turns away from globe--> can lead to expoure keratitis. Seen with Bell's Palsy
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Epicanthus
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Abnormal folds of skin at medial canthus. Can be normal and common. Semilunar folds of skin that can give the impression of a STRABISMUS
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Epicanthus inversus
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folds of skin from LOWER lid --> associated with Wardenburg snydrome and down syndrome
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Epiblepharon
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Horizontal folds of kin at lid marin, rolls lashes toward eye
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Euryblepharon
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ENLARGED horizontal palpebral fissure. Eyelid pulled down and see lateral displacement --> exposure problems
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Blepharopimosis
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Dimunation in both directions of palpebral fissue. Associated with congential ptosis and epicanthus
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Occulodermal melanocytosis
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Blue gray pigment of skin. Pigment follows distribution of V opthalmic and maxillary divisions!! Can see unilateral glaucoma -->pigmentary GLAUCOMA??
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Hemanogioma
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Portwine stain, straberry nevus
Congenital hamartoma appears after birth. Tumor like nodule of overgrow of mature cells. Projecting bud of endothelial cells |
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Harmaroma
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A benign tumor filled with blood or lipid.
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Dermoid
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Rubbery,firm, subcutaneous masses found along oribtal rim, composed of tissues not nomrall present in region of that body.
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Choristoma
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mass composed of tissue that are not normaly present in particular region. Large fleshy tumor found in lateral aspects. See residual bone, cartilae, teeth.
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Congenital ptosis
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Abonmrality of eyelid motility. Ptosis is a malpractice of upper eyelid.
Usually uniteral Can e associated: Blepharophimosis Marcus Gunn jaw winking syndrome Extraocular muscle palsies Will likely have EXTROPIA because of the functio nof the levator function. Can also be seen with congenital horner's --> sympathetic mueller |
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Waardenberg 3 manifestsations
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AD!! --> no other systemic problems
Eyelid anomalies Pigmentary abnormalities auditory problems Ptosis, TELECANTHUS!!!!!!!!!!!!!! (lateral displacemnt of medial canthus) HALLMARK eterochromia iridis white forelock of hair partial albinins auditory problems |
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TELECANTHUS
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lateral displacemtn of medial canthus --> HALLMARK OF WAARDENBERG
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Marcus Gunn Snydrome
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Conjential trigemino-ocular motor synkinesis. Muscle of Jaw and lid levator move together unintenitally.
See unilateral ptosis Inolves V3 |
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Aquired ptosis
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Associate with good levator muscle function
Can be involutional/senile Neurogenic Traumatic Mechanical due to lid tumors |
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Testing lid lag
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levator tone increases on upward and decreases downward. Have target look from above to downward. If unliateral it could be throid disease
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Diagnose Myathenia grivas using
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Tensilon test
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Normal position of eye within orbit
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16
Worry if its > 21 |
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Blepharitis
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iflammation of lid margins
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Blepharoconjuncvitis
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most common is stapyloccus
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Trichasis
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inward turning if eyelashes
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Distachilasis
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extra row of lasses
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Alopecia
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loss of lashes
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Chalzaion
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chroniic lipogrANULMATOUS INFLAMATION OF MEIBOMIAN GLAND. occurs spontaneously. CUT VERTICALLY
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Internal hordeolum
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localized staph infection of meibomean gland
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External hordeom
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A stye! involves sebaceous and gland of Zeiss.
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