ocular phys final

glaucoma is too much aqueous due to blockage of trabecular meshwork outflow or uveoscleral outflow

posterior chamber

CSF

IOP

• more glucose in AH than blood
• more ascorbic acid in AH than blood
• more lactic acid in AH than blood
• LESS protein in AH than blood plasma
• AH is more HYPERTONIC than blood

increase IOP

cornea and lens, as well as their waste carried by AH

• due to 2 physical characteristics of anterior segment:
• 1. there's a BAB (blood aqueous barrier) (at ciliary epithelium and endothelium)
• 2. active transport of substances by ciliary epithelium (the NPE of ciliary body actively secretes the aqueous humor)

• diffusion
• ultrafiltration
• active secretion (main way)

• Na/K-APTase
• carbonic anhydrase

they push the ions (Na, K, and Cl) so water can follow

• there are aqueous suppression drugs that inhibit carbonic anhydrase
• then bicarbonate can't leave so, acetazolamide decreases aqueous production

yes

• alpha 2 and beta 1 receptors.
• the sympathetic nervous system and parasympathetic nervous system are both involved in stimulating howflow but sympathetic nervous system has more of an impact-> this is why beta blockers and alpha2-agonists are good Tx for glaucoma b/c they inhibit aqueous production.

asleep b/c sympathetic nervous system is not stimulated

• increased age
• diurnal (less secretion when sleeping)
• short term secretion decrease when exercise
• decrease in BP
• hypothermia
• acidosis
• general anesthesia
• uveitis
• increase in IOP by aqueous secretion (body will counteract)
• retinal detachment
• retrobulbar anesthesia
• choroidal detachment
• Note: AH production does NOT change from stystem BP change! This is b/c AH production is an ACTIVE process and can only go so fast as its enzymes and channels permit

production = drainage

• 1. trabecular meshwork (drainage #1, main) - pressure dependent
• 2. uveoscleral pathway (drainage #2) - pressure independent
• 3. episcleral venous pressure (what AH drain into) -> all AH drains into EVP so if raise pressure in episcleral veins, it will be harder for AH to drain into them

• "tugs on scleral spur" in order to shrink pupil and stretch out meshwork to allow more fluid to flow through ->
• decrease IOP

• main site of AH outflow
• phagocytic cells/macrophages located here to clean out the meshwork
• flow is unidirectional and pressure dependent
• the higher the IOP, the more fluid through the trabecular meshwork

• corneal endotheliual -> so can't divide and once they're gone, they're gone.
• So as age increase, the # of cells decreases because can't divide

blood isn't seen in canal unless IOP falls below that of episcleral venous pressure. The blood will never get into aqueous because of the blood aqueous barrier

• pressure INdependent
• same rate of flow no matter what the system blood presure or IOP is

• EVP directly affects outflow
• IOP increases when EVP increases

• reliable
• cheap
• easy calibration
• use on restricted parties

• anesthesia required
• good patient cooperation
• possible injury
• must clean after each use
• displaces aqueous when measure

• standard for accuracy
• no caliberation needed
• compact
• cheap
• hand held & slit lamp models available
• displaces little aqueous
• no electronics
• little maintenance

• anesthesia required
• poor result with edematous cornea
• calibration at factory
• hard to delegate
• influenced by external pressure
• injury possible

• reduce infection
• accurate
• no anesthetic require
• displaces little aqueous
• quick
• can be delegated
• no epithelial damage
• measure thru CL

• patient apprehensive
• expensive
• large instrument
• factory calibrated
• multiple readings necessary

• most accurate method for scarred/edematous corneas
• quick
• min corneal disruption
• can use on restricted patients
• portable, lightweight

• not very accurate
• factory calibrated
• expensive
• displaces significant aqueous

• increased EVP
• drugs: caffeine, nicotine, steriods
• hyperventilation
• TIGR gene presence [TIGR effects outflow in glaucoma. it makes mucin. mucin will get stuck in meshwork causing a decrease in outflow]
• hypertension
• high water consumption
• reclining/laying down posture (increase venous pressure in the head)
• hard/forced blinking
• increased in age increases IOP
• EOM contraction involving eyes
• intraorbital congestions or anything pressing on orbit
• valsalva
• sneezing, coughing, lifting
• diurnal (higest in morning)

outflow resistance

in the morning

5mmHg or less

15-21mmHg

22mmHg and up and greater than 5mmHg daily variation

3mmHg

• yes
• the flatter (hyperopia) the cornea, the lower the measured pressure (underestimate)
• the steeper (myopia) the cornea, the higher the measured pressure (overestimates)

• yes
• the stiffer the cornea, the greater the measured pressure
• the softer the cornea, the lower the measured pressure

• yes
• the thicker the cornea, the higher the measured pressure
• the thinner the cornea, the lower the measured pressure

cornea is thinner after lasik therefore IOP is underestimated

no nerves or blood supply as well as no cellular contact with other tissues

• when accommodation occurs, the ciliary muscle contracts and zonules relax.
• this allow the lens to get thicker
• acoommodation doesn't affect IOP

• a diabetic's lens capsule is much more fragile
• capsule seals off the lens early in development so the lens proteins are antigenic
• the body will attack the lens as a foreign invader if the lens capsule ruptures!
• if the lens ruptures, there is a major immune response. the immune system will attack the cells within the lens capsule because the body recognizes the lens cells as invaders

• the lens epithelium is MITOTIC at Pre-Equator, but is NON-MITOTIC in center.
• the mitotic pre-equator secrets new cells into lens capsule

• has NO organelles, NO mitochondria, NO nucleus, but in a VERY REGULAR arrangement.
• they are just filled with crystalline protein. the main protein in the lens fivers is crystalline.
• Crystalline is WATER SOLUBLE (85%) and slight water insoluble (15%). As lens ages, the amount of water soluble proteins increase
• the lens fibers have NO membrane bound organelles (including mitochondria) so using ANAEROBIC glycolysis for energy.
• lens fibers have nothing but crystalline in them

• lens epithelium, cornea, and ciliary epithelium all contain Na/K pumps for dehydration purposes so water doesn't build up in lens
• Na - increase with age; increases with CORTICAL cataracts
• Cl - low inside lens
• K - constant with age; decrease in CORTICAL cataracts
• Ca - don't want Ca in lens, because don't want to "calcify" lens into a cataract (need the right amount b/c if too much or too little will cause cataract)
• Ascorbic acid (vit C) - high in AH than plasma because the lens needs it; ascorbic acid is an anti-oxidant that rids free radicals

• AEROBIC (like normal cell)
• the lens epithelium divides to makes lens fibers, secrete lens capsule and maintain Na/K pump

• the principle source for NADPH and materials for DNA/RNA.
• the HMP shunt then goes to sorbitol pathway
• this wayway creates cataracts and sorbitol.
• fluid is then pulled into lens (a cataract occurs when sortibol builds up. in diabetes, sorbitol accumulates and can't diffuse out because excess glucose enters the sorbitol pathway)

• #1 anti-oxidant in lens that scavenges free radicals.
• Glutathione is desired in its reduced form in order to accept oxygen/free radicals
• as get older there are less reduced forms around and more free radicals can cause damage -> cataract formation

• 1. anterior part of lens
• 2. cornea endothelium (deturgescence)
• 3. lens epithelium (deturgescence)
• 4. ciliary epithelium (for aqueous production along wtih carbonic anhydrase)
• 5. lacimal gland has Na/K pump as well

• the lens has a capsule and fibers of cystalline protein that are water soluble
• the main antioxidant is reduced glutathione
• there are reduced and oxidized forms but as get older, there is more of the oxidized form around.
• possible scenario: if too much glucose (diabetic) -> convert to sorbitol -> conver to FRUCTOSE

• protein must be preserved from photo-oxidation and aggregation
• oxygen must be lowered in lens center
• anti-oxidants must be made and present
• molecular chaperones must be preserving proteins from aggregating and precipitating
• and, constant internal circulation of water, ions, and metabolites must be occuring

• formation of cataract
• catatactogenesis is associated with intralenticular increase in water, sodium and calcium, as well as decrease in pottasium, reduced glutathione, ATP, and altered membrane permeability

• age
• other include UV exposure, poor nutrition, sorbitol accumulation/diabetes, smoking, alcohol consumption, injury, steroids, long term medication use and genetics

• more glucose, so it is converted to sorbitol -> fructose -> CATARACT
• the sorbitol will bring water into the lens, so there will also be a decrease in vision before conversion

blurriness, dimness, color fading, sensitivity to light/glare, double vision, change in refraction such as a myopic shift

• 2nd sight may occur
• this is myopic shift with lens hardening
• more light may also give better vision because allow more light to reach retina
• there is increased oxidative damage to lens proteins and lipids
• mostly due to age
• age onset: 60-70
• symptoms: myopic shift, blurred vision, loss of B-Y color

• this thas the most affect on VA
• there is a flat to steep change of the lens
• can occur from diabetes or steriod use
• age of onset: 40-60
• Symptoms: glare, diminishing reading, monocular diplopia

• these are mostly UV induced
• the damage starts out on the edges, so more of a hyperopic shift in vision occurs
• Age onset: 40-60
• Symptoms: glare, monocular diplopia

80% of total globe volume and is made of 99% water

a GEL composition due to the COLLAGEN and GAG crosslinking within the collagen that perfectly spaces the substance for the trasmitting of light

it stabilizes gel structure and conformation of collagen fibrils so it is "gel" and not "watery"

shrinkage of the vitreous

liquefacation of vitreous

• 1. ora serrata (vitreous base)
• 2. optic disc
• 3 macula
• 4 Weiger's ligament (back of lens)

• there is detachment from the vitreous from the optic disc.
• a shadow called a Weiss ring is apparent in a PVD only.
• this was the previous connection of vitreous to the optic nerve
• a PVD can cause a macular hole
• symptoms of PVD include lightning streaks because of the vitreous is tugging on the retina

a floater is an aggregated piece of the vitreous

• it can cause a tear in the retina, which can lead to water getting in where the vitreous detached
• this can then lead to retinal detachment which is much more serious

• it's when there is blood in the vitreous
• if there is a PVD with a Heme then there is a 70% chance that there will be a retinal tear
• if there is a PVD without a heme then the chances for a retinal tear are much lower, around 2-4%

• this pigment in anterior vitreous indicates a heme is present.
• the pigment seen is actually blood cells in anterior vitreous
• these pigmented spots indicate that a retinal tear has occured
• the pigment is coming from the RPE in the retinal tear

• sympthoms of a PVD include: shafer's sign, tobacco dust, retinal tear, vitreal heme, weiss ring
• Note: everyone with PVD does NOT get PD or retinal tear! you are 70% more likely to get a retinal tear with a vitreal heme.

via phagocytosis to get rid of waste products of photoreceptors OUTER segments

• also transports and stores vitamin A. it reduced scatter by its pigmentation. it also regulated fluid levels between photoreceptors and RPE
• its blood supply comes from the choriocapillaris from fenestrated capillaries

signal being released all the time (glutamate)

phototransduction: hits photoreceptors -> Na channels close, K opens and glutamate STOPPED being released

• this is when the RPE does not phagocytize the ROD outer segments, when it should
• since rods are more peripheral, RP is peripheral disease

choriocapillaris supplies the outer retina, RPE and photoreceptors (has blood retinal barrior)

central retinal artery

• avascular and a capillary free zone
• this allows light to hit photoreceptors
• the photoreceptors, themselves, are avascular and are nourished by the choroid

• choroid has fenestrated capillaries that make a "bed of plasma fluid". the retina has tight junctions to keep fluid contained
• the sclera is on the other side of theis "bed of plasma fluid" to keep it contained
• the choroid is not stiff, but spongy, and non-dense to allow this gathering of lfuid
• it supplies nutrients to the toher 1/3 of retina

just extra pigmentation of RPE in which there are bigger and darker cells

from thrombis (occluded at spot where obstacle formed)

an embolus (piece that broke off from obstacles and traveled to get caught and block blood supply)

local blood pressure. it is regulated by the SYMPATHETIC nervous system

• disease that cause decrease in blood flow:
• 1. ARMD: (drusen = lipofuscin). no TX for Dry ARMD
• 2. Glaucoma
• 3. Hypertension
• 4. Myopia

• if you have a tumor, then there is a high demand of blood
• this cause neovascularization to the tumor/growth itself.
• Tumor increase blood flood

• ganglion cells compose 90% of optic nerve
• the eye has a blind spot, which is a result of NO photoreceptors

blood vessels in retina bcecome "tortuous"

blood vessel occlusion or leakage

• ischemia/no O2
• 1. cotton wool spots: "explosion of nerve"
• 2. New BV (neovascularization): VEG-F and leaky BV

• 1. hemorrhage: everything getting out
• 2. edema: just fluid/plasma getting out
• 3. exudates: lpid, proteins, solids seeping out/building up (no blood cells)

• used in diabetics
• kills new BV growth, decreases VEG-F and decreases O2 demand

• here blood has already been brought to retina by the artery and is IN the retina
• now it can't get out! main risk factor is arterial hypertension
• will have thrombosis
• the CRVO occurs where veins leaves the optic disc - the blood backs up and spills everywhere!
• will see cotton wool spots, tortuosity, venous dilation, macular edema, neovascularization and macular ischemia

• occurs from crushing of the retinal vein in an A/V crossing
• the vein becomes occluded
• a BRVO is not as bad as CRVO because doesn't affect entire retina, just 1-2 quadrants
• just effects retina in area where blood coming from
• can get ischemia, but more indirect
• other symptoms include edema, exudates, macular edema, macular ischemia, and leaky BV

• an embolus gets caught in artery at optic disc
• the blood supply can't get IN to retina
• the retina turns white in color and the ENTIRE RETINA becomes ischemic
• APD shows up in pupil testing

• ischemia is more localized to a specific area in the retina
• this is caused by an embolus, not crushing, like ain BRVO

In a retinal ARTERY occlusion, have 100min before start dying!!

detachment between phtoreceptros and RPE

detachment between RPE and Bruch's membrane