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201 Cards in this Set
- Front
- Back
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name the 3 types of blinking
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spontaneous
reflex forced |
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describe spontaneous blinking
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most common blink
maintains optics and comfort |
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what causes spontaneous blinking
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palpebral portion of orbicularis
|
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average blink rate
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15 per min
|
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reflex blinking caused by what*
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sensory stimuli:
auditory touch/irritation dazzle menance |
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touch or irritation can cause reflex blinking how
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CN 5 senses it and CN 7 causes the blink
|
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dazzle reflex blink
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caused by bright lights
CN 2 senses i CN 7 causes the blink |
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menace reflex blink
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CN 2 senses it and begins at FRONTAL lobe
CN 7 causes the blink |
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forced blinking
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vol forced closure do BOTH palbebral AND orbital portions of orbicularis
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blinking causes what portion of tear film to be secreted
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lipid secretion via holocrine method
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describe what a blink does
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upper lid blinks LATERAL to MEDIAl thereby SPREADING tear film over cornea and bulbar conj
MUCUS layer spread over corneal epithelium with each blink |
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how are tears drained
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when eyes are closed tears will do the following:
puncta --> canaliculi --> lacrimal sac --> NLD --> Hasner --> IM |
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what does Horner's muscle do
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Horner's muscle is part of orbicularis that surrounds lacrimal sac
when eye closes it contracts pumping tears into the lacrimal sac |
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what does the preseptal orbicularis do
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contracts and stretches lacrimal sac laterally widening
tears are sucked in via the negative partial pressure that is generated |
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tears and optics
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provide smooth surface for vision
air and tear film have great difference in n |
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what main thing does tear film provide to corneal epithelium via difusion
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oxygen
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tear film collects what that is washed away with blinking
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debris
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what antibacterials are located in the aqueous layer of tear film
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IgA
Lysozyme Lactoferrin |
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how does the tear film help provide corneal transparency
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pH
osmolarity |
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thinnest layer of tear film
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lipid <1%
|
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role of lipid layer
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prevent evaporation of aquoeus layer
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primary source of lipid secretion
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blinking
|
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thickest portion of tear film
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aqueous (60-70%)
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role of aqueous layer
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protection via proteins (antibacterials)
nutrition via glucose, water, gas exchange |
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aqueous contains what
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urea, inorganic salts, proteins, glucose, lactoferrin, lysozyme, IgA, inerleukins
|
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innervation of lacrimal gland
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parasympathetic
sympathetic sensory |
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most lacrimal gland secretions are what innervation
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parasympathetic
|
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reflex and emotional tearing come from
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lacrimal gland
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maintanance tearing comes from
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accessory (K/W) lacrimal glands
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what is the 2nd thickest layer of tear film
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mucin (30-40%)
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role of mucin layer
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provides medium for aqueous to cover corneal epithelium
|
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mucus secretion can be enhanced via
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parasympathetic mostly and sympathetic innervation which stimulate goblet cells
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how does the epthelium accept mucin and therefore aqueous layer
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corneal epithelim makes glycocalyx which absorbs mucus making it the epithelium HYDROPHILIC and thus able to accept the aqueous layer
|
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glycocalyx of corneal epithelium is important because
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it absorbs mucus making the epithelium hydrophilic and thereby allowing the aqueous layer to spread over cornea
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TBUT looks at what layer of tear film
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lipid layer
|
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lipids break down in TBUT because
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lipids migrate down to mucus layer and contaminates it
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average TBUT
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5-10sec
|
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what % of tears are lost to evaporation
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25%
|
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75% of tears are eliminated via
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NL system
|
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osmotic pressure of tears
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315 mOSm/kg
|
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what do CL do to tear film and thus osmotic pressure
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increases evaporation and thereby the osmotic pressure to 330
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pH of tears
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7.45
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what is special about the pH of tears
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excellent buffers (pH 3.5-10.5)
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eyedrops are mostly what type of soln
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weak bases
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corneal epithelium and endothelium are what
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hydrophobic, lipid soluble non-inonized thus that is why eye drops are non ionized weak bases
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junction found in K epithelium
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tight jxns - barrier
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K epithelium LS or WS
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lipid soluble/non ionized
doesnt like water/ionized |
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K stroma is LS or WS
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water soluble/ionized
doesnt like lipids |
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K endothelium is LS or WS
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lipid soluble/non ionized
doesnt like water |
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what is the main source of energy for K epithelium
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glucose from aqueous humor
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where does K epithelium get oxygen from
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diffusion from tears
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where does stroma get nutrients and oxygen from
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from AH via diffusion through endothelium
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where does K endothelium get glucose and oxygen from
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AH
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what happens to epithelium when there is hypoxia
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lactic acid builds up and cant cross the epithelium therefore doesnt reach stroma or endo causing edema
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what allows the cornea to have minimal light scattering
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spacing of collagen fibirls less the 1/2 wavelength apart to cause deconstructive interference
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what maintains stromal spacing
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proteoglycans (ground substance)
|
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what are the 2 pumps of the corneal epithelium
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Na/K
Na K Cl cotransporter |
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the Na/K pumps moves what where
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K into epithelium
Na into stroma |
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what does the contransporter do
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move K and Cl into epithelium
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the movement of what ion into AH stimulates the release of Cl into tears with water following causing dehydration of cornea
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K
|
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corneal thickness is altered by moving what ion into tears
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Cl then water follows
|
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K channel responds to what changes in cornea and does what
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pH
hypoxia moves more K into AH, moves Cl and water out to tears to restore natural thickness |
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what ion controls thickness
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K by moving itself into AH and CL/water out to tears
|
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what happens if the epithelial BM remains intact after trauma
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regeneration is fast
|
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what happens if BM is damaged
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takes months because hemidesmosomes have to be made
|
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what is the first thing to happen when the epithelium is injured
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stop basal cell mitosis
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describe the regeneration process in damaged BM
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basal cell mitosis stops - defected cells detach from BM and enlarge - make new hemidesmosomes btw migrated cells and BM
|
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changes in cornea with age
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ATR
increase light scatter Descemets thickens (D3) thinning of endothelium/density |
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what is autoregulation
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alter resistance of vessels in order to cause a change in blood flow
flow & R inv. related R and diameter of vessel inv related |
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what is responsible for autoregulation in the eye
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retinal vessels
|
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metabolic autoregulation occurs in response to what
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decrease in systemic arterial pressure
retina releases metabolites to dilate vessels |
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myogenic autoregulation occurs in response to
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transmural pressure
smooth m of bv either constrict or dilate |
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what structure performs autoregulation
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retina
|
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purpose of autoregulation
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means in which retinal vessels get oxygen despite high IOP
|
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critical closing pressure
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pressure at which vessels collapse and blood flow stops
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if IOP is too high what can happen
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CRA reaches critical closing pressure and shuts down
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what happens in acute angle closure attack
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arterial pressure decreases and IOP increases, critical closing pressure of CRA can be reached thereby causing a CRAO leading to hypoxia in the retina and vision loss
|
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sympathetic innervation
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vasoconstriction of uvea
does not innervate CRA past lamina cribosa |
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parasympathetic innervation
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vasodilation of anterior uvea
|
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IOP is what in relation to perfusion pressure of retinal and uveal arteries
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lower
|
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IOP is what in relation to extravascular pressure
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lower
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the majority of blood flow in eye is to what
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choriocapillaris
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where is PO2 highest
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in retina despite high blood flow in choroid
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is the choriocapillaris fenestrated or tight
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fenestrated to nourisg RPE and outer retina
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is MAC fenestrated or tight
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fenestrated
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is the CB capillaries fenestrated or tight
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fenestrated
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is the iris capillaries fenestrated or tight
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tight
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is the retinal capillaries fenestrated or tight
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tight
|
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what supplies inner retina
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CRA
|
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what supplies outer retina
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choroid
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where are the retinal capillaries must dense
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around fovea
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what regions of retina are avascular
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extreme periphery
center of fovea - FAZ |
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where does the FAZ get its blood supply
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choriocapillaris
|
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does the retina like blood
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No, TOXIC to retina
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name the 2 blood retinal barriers in the eye
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1. tight jxn btw endothelial cells linning the retinal bv
2. btw RPE cells keeping blood from choriocapillaris out |
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what type of secretion is meibomian gland
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holocrine
|
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what type of secretion is goblet cells
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apocrine
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what is bell's phenomenom
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forced eye closure causes eye to go up and out
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why do dry eye patients blink a lot
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to stimulate holocrine secretion of lipid from MG
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which part of cornea gets oxygen from the tear film
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epithelium
|
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where does the corneal epithelium get glucose from
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AH
|
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what layers of cornea get oxygen and glucose from AH
|
bowman's
stroma descemet's endothelium |
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when the eye is closed how does the cornea get oxygen
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lid capillaries
|
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what happens during sleep
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lid capillaries provide cornea with oxygen; corneal becomes tad hypoxic resulting in mild edema upon awakening
|
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what does Na/K pump of epthelium do
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pump Na into stroma
pump K into epithelium |
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what does Na/K/Cl cotransporter do
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pump K & Cl into epo
|
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K stimulates what when pH is low (acid)
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Cl into tears with water following
|
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what is 1st thing to happen after epithelial injury
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stop basal mitosis
|
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Goldmann Tonometry
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measures force needed to flatten cornea
assumes all corneas have same thickness overestimates IOP in thick corneas underestimates IOP in thin corneas |
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NCT
|
amount of time btw initiation of air and peak response of photocell
|
|
average IOP
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15.5
most ppl have >22 |
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when is IOP highest
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in morning and supine (laying on back)
|
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what do B blockers do
|
block AH production by NPCE
|
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what do alpha agonists do
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constrict CB bv limiting diffusion and ultrafiltration of plasma available for making AH
|
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what do CAI do
|
inhibits formation of bicarbonate
|
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what do PG do
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increase US outflow
|
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what does pilocarpine do
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increase TM outflow
|
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what is the only cardioselective B blocker for GLC
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betaxolol
|
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what can cause decreased IOP
|
-decrease bp limiting available plasma for active secretion
-acidosis -hyperosmolality -uveitis (sick CB) |
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inflow and outflow must be
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equal
|
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corneoscleral (TM) route of outflow
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-80%
-pressure dependent -the more IOP the more that is drained out |
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what happens when IOP is too high in corneoscleral route
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SC collapses and outflow into veins stops
|
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what drains SC
|
episcleral veins
|
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uveoscleral route of outflow
|
-20%
-pressure independent -constant amount leaves regardless of pressure |
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what causes a decrease in outflow
|
increased episcleral venous pressure
|
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does blood pressure affect IOP
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no unless its super high
|
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role of AH
|
nutrition to cornea, lens, anterior vitreous, TM
shape and protection |
|
what is AH compared to plasma/blood
|
hyperosmotic
hypertonic |
|
AH made where
|
NPCE
|
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how is AH made
|
diffusion
ultrafiltration active secretion |
|
difussion
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small LS particles get thru via CB fenestrations
|
|
ultrafiltration
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blood plasma gets into CB via increased hydrostatic pressure
|
|
active secretion
|
major mech accounts for 80-90%
large WS are actively transported using energy and 2 enzymes to move Na and bicarb into PC to make AH |
|
2 enzymes of active secretion
|
Na/KATPase
Carbonic Anhydrase |
|
Na/KATPase
|
uses ATP to pump Na into PC with water following
|
|
Carbonic anhydrase
|
makes bicarb
|
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what blocks Na/KATPase and CA
|
Na/KATPase - cardiac glycosides
CA- CAIs |
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what has more protein, AH or plasma
|
plasma
AH has very little protein |
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what has more ascorbate
|
AH
lens>AH>plasma |
|
what is ascorbate
|
antioxidant that protects against UV
|
|
what has more Cl/aa/lactate plasma or AH
|
AH
tears>plasma>AH |
|
name 3 locations of blood AH barrier
|
tight jnxs at:
iris vessels SC endothelium NPCE |
|
afferent pupil fibers travel where
|
pretectal nucleus
|
|
where do afferent pupil fibers project after synapsing and passing thru pretectal
|
to EW to go into tectotegmental tract
|
|
what controls pupillary constriction in near reflex
|
frontal eye fields -- EW
bypasses pretectal |
|
when do sympathetic fibers become postganglionic
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after synapsing in SCG
|
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what does a pancoast tumor destroy
|
preganglionic symp fibers that were on way to synapsing and becoming postgang at SCG
|
|
miosis when sleeping
|
sympathetic inhibits EW which always wants to make the pupils small, but when sleep EW is uninhibited and makes pupils small
|
|
what is lens made up of
|
water 2/3
protein 1/3 |
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where is n highest in lens
|
nucleus
|
|
why does lens have varying n's
|
protein content varies in each part of lens
|
|
crystallins
|
proteins found in cytoplasm of lens fiber cells
|
|
alpha crystallins
|
act as chaperones offering resistance of degradation to other crystallins
|
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what type of proteins are crystallins
|
water soluble
|
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what happens to crystallins with age
|
become water insoluble leading to cataracts
|
|
what protects lens from oxidative damage
|
glutathione
catalase ascorbate |
|
calcium in lens
|
< than aqueous
toxic to lens leads to cataracts |
|
blood supply of lens
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avascular
|
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where does lens get nutrients from
|
AH
|
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what does the lens epithelium contain
|
Na/K pump
|
|
what does Na/K pump in lens do
|
maintains lens dehydrated
|
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where does energy needed for Na/K pump come from
|
anaerobic glycolysis
|
|
enzyme that changes glucose into glucose 6 phosphate
|
hexokinase
|
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glucose is converted to sorbitol via what enzyme
|
aldose reductase
|
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when does glucose become sorbitol
|
when hexiokinase is absent
|
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what does excess sorbitol do to the lens
|
accumulates in lens fibers allowing water to move into lens fibers thus causing swelling and favoring cataract formation
|
|
where are crystallins found
|
lens cortex
|
|
crystallins that contribute to refractive index
|
gamma and betta
|
|
where are insoluble proteins in lens found
|
nucleus
|
|
primary protector against oxidative damage in lens; transports AH and is made in lens epithelial cells and fiber cells
|
glutathione
|
|
prevents lens from oxidative damage; has highest concentration in lens
|
ascorbic acid (vit C)
|
|
what helps keep lens transparent
|
lens fibers dont have organelles and ae packed close together
|
|
what nerves supply lens
|
NONE
|
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what happens to soluble and insoluble lens proteins with age
|
soluble decrease
insoluble increases |
|
what happens to glutathione with age
|
decreases
|
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what happens to Na, Ca, H2O with age
|
increases
|
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what happens to nuclear fibers with age
|
become yellow-brown in color
|
|
what does a small pupil provide
|
less spherical and chromatic abberations
increase depth of field |
|
fxn of CB
|
CM
makes AH ciliary stroma provides drainage space for AH via US router |
|
fxn of choroid
|
supplies outer retina
|
|
vitreous fxn
|
transparent unhindered medium for light passage that cushions eye and is a shock absorber
stores nutrients for retina and lens |
|
what is the most important fxn of vitreous
|
stores nutrients for retina and lens
|
|
what alters the bioavailability of drugs in PC
|
vitreous gel
|
|
vitreous composition
|
water
collagen hyaluronic acid |
|
what does hyaluronic acid do
|
provides spacing and support for collagen
|
|
floaters
|
aggregates of collagen with age
|
|
where is collagen least located in vitreous
|
center
|
|
semicircular canals detect what
|
angular head rotations causeing reflex eye movements -- VOR
|
|
2 otoliths of ear
|
utricle
sacculus |
|
what do the otoliths detect
|
linear head rotations causing reflex eye movemnts that are equal and opp to head motion --- linear VOR
|
|
rapid eye movemenths that maintain foveation
|
saccades
|
|
what controls saccades
|
contralateral FEF of frontal lobe
|
|
smooth tracking for slowly moving objects
|
pursuits
|
|
what controls pursuits
|
ipsilateral parietal lobe
|
|
stimulus that drives accommodation
|
retinal blurs
|
|
stimulus that drives vergence
|
retinal disparity
|
|
muscle in same eye that has secondary action that contribute to eye movement like that of agonist
|
synergist
|
|
muscle in same eye counteractive to agonist
|
antagonists
|
|
increased innervation to agonist is accompanied by corresponding decrease of innervation to antagonist
|
sherrington's law
|
|
what happens in primary gaze
|
all EOMS are contracting equally resulting in balanced centration
|
|
what happens if a muscle becomes inactive during primary gaze
|
eye is unbalanced and will shift in direction of antagonist
|
