ocular phys final

  1. how is aqueous humor related to glaucoma?
    glaucoma is too much aqueous due to blockage of trabecular meshwork outflow or uveoscleral outflow
  2. where is AH secreted into normally?
    posterior chamber
  3. what does AH resemble?
  4. what is the measurement of AH?
  5. what's AH's composition?
    • 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
  6. what is the most important risk factor for glaucoma development?
    increase IOP
  7. what ocular structure does AH supply?
    cornea and lens, as well as their waste carried by AH
  8. how is AH different from blood?
    • 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)
  9. how is AH formed?
    • diffusion
    • ultrafiltration
    • active secretion (main way)
  10. what enzymes does non-pigmented epithelium have?
    • Na/K-APTase
    • carbonic anhydrase
  11. what do the enzymes in NPE do?
    they push the ions (Na, K, and Cl) so water can follow
  12. what does acetazolamide do?
    • there are aqueous suppression drugs that inhibit carbonic anhydrase
    • then bicarbonate can't leave so, acetazolamide decreases aqueous production
  13. are there neurostimulation of NPE to produce aqueous humor?
  14. how is neurostimulation done?
    • 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.
  15. when id AH made the least?
    asleep b/c sympathetic nervous system is not stimulated
  16. what are the factors that are associated with decreased AH secretion?
    • 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
  17. what must happen for aqueous outflow?
    production = drainage
  18. how is aqueous outflow regulated?
    • 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
  19. what does pilocarpine do?
    • "tugs on scleral spur" in order to shrink pupil and stretch out meshwork to allow more fluid to flow through ->
    • decrease IOP
  20. what does trabecular meshwork to?
    • 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
  21. what cells are trabecular endothelial cells derived from?
    • 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
  22. what does the canal of schlemm do?
    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
  23. what does the uveoscleral outflow do for aqueous outflow?
    • pressure INdependent
    • same rate of flow no matter what the system blood presure or IOP is
  24. what does the Episcleral Venous Pressure do for aqueous outflow?
    • EVP directly affects outflow
    • IOP increases when EVP increases
  25. advantages of Schiotz
    • reliable
    • cheap
    • easy calibration
    • use on restricted parties
  26. distadvantages of Schiotz
    • anesthesia required
    • good patient cooperation
    • possible injury
    • must clean after each use
    • displaces aqueous when measure
  27. advantages of Goldman
    • standard for accuracy
    • no caliberation needed
    • compact
    • cheap
    • hand held & slit lamp models available
    • displaces little aqueous
    • no electronics
    • little maintenance
  28. disadvantages of Goldman
    • anesthesia required
    • poor result with edematous cornea
    • calibration at factory
    • hard to delegate
    • influenced by external pressure
    • injury possible
  29. advantages of Non-Contact (air puff)
    • reduce infection
    • accurate
    • no anesthetic require
    • displaces little aqueous
    • quick
    • can be delegated
    • no epithelial damage
    • measure thru CL
  30. disadvantages of Non-Contact (air puff)
    • patient apprehensive
    • expensive
    • large instrument
    • factory calibrated
    • multiple readings necessary
  31. advantages of tonopen
    • most accurate method for scarred/edematous corneas
    • quick
    • min corneal disruption
    • can use on restricted patients
    • portable, lightweight
  32. disadvantage of tonopen
    • not very accurate
    • factory calibrated
    • expensive
    • displaces significant aqueous
  33. factors the increase IOP
    • 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)
  34. what the main cause of IOP increase in glaucoma?
    outflow resistance
  35. when is IOP highest?
    in the morning
  36. what is the normal IOP daily variation?
    5mmHg or less
  37. what's the normal range of IOP?
  38. what is considered as glaucoma?
    22mmHg and up and greater than 5mmHg daily variation
  39. what's the normla difference of IOP between two eyes?
  40. can corneal curvature affect IOP?
    • yes
    • the flatter (hyperopia) the cornea, the lower the measured pressure (underestimate)
    • the steeper (myopia) the cornea, the higher the measured pressure (overestimates)
  41. can biomechanics affect IOP?
    • yes
    • the stiffer the cornea, the greater the measured pressure
    • the softer the cornea, the lower the measured pressure
  42. can corneal thickness affect IOP?
    • yes
    • the thicker the cornea, the higher the measured pressure
    • the thinner the cornea, the lower the measured pressure
  43. what alteration will LASIK have on IOP?
    cornea is thinner after lasik therefore IOP is underestimated
  44. what is special about the lesn?
    no nerves or blood supply as well as no cellular contact with other tissues
  45. what happens to lens when accommodating?
    • when accommodation occurs, the ciliary muscle contracts and zonules relax.
    • this allow the lens to get thicker
    • acoommodation doesn't affect IOP
  46. what's special about the lens capsule?
    • 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
  47. how does the lens epithelium make new cells?
    • the lens epithelium is MITOTIC at Pre-Equator, but is NON-MITOTIC in center.
    • the mitotic pre-equator secrets new cells into lens capsule
  48. what's special about the lens fibers?
    • 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
  49. what's special about lens metabolism?
    • 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
  50. what type of glycolysis does lens epithelium use?
    • AEROBIC (like normal cell)
    • the lens epithelium divides to makes lens fibers, secrete lens capsule and maintain Na/K pump
  51. what doe HMP shunt do?
    • 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)
  52. what does glutathione do?
    • #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
  53. where is the Na/K pump located?
    • 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
  54. what's the summary of lens?
    • 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
  55. how do prevent cataract?
    • 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
  56. what is cataractogenesis?
    • 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
  57. whats the most common cause of cataracts?
    • age
    • other include UV exposure, poor nutrition, sorbitol accumulation/diabetes, smoking, alcohol consumption, injury, steroids, long term medication use and genetics
  58. what's in a diabetic lens?
    • 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
  59. what are the symptoms of cataracts?
    blurriness, dimness, color fading, sensitivity to light/glare, double vision, change in refraction such as a myopic shift
  60. what is nuclear cataract?
    • 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
  61. what is posterior subcapsular cataract?
    • 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
  62. what is cortical cataract?
    • 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
  63. what does the vitreous do?
    80% of total globe volume and is made of 99% water
  64. what is the composition of vitreous
    a GEL composition due to the COLLAGEN and GAG crosslinking within the collagen that perfectly spaces the substance for the trasmitting of light
  65. what is hyaluronic acid?
    it stabilizes gel structure and conformation of collagen fibrils so it is "gel" and not "watery"
  66. what is syneresis?
    shrinkage of the vitreous
  67. what is synchysis?
    liquefacation of vitreous
  68. what's the strongest to weakest vitreal attachment?
    • 1. ora serrata (vitreous base)
    • 2. optic disc
    • 3 macula
    • 4 Weiger's ligament (back of lens)
  69. what is Posterior Vitreal Detachment (PVD)?
    • 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
  70. what is floaters?
    a floater is an aggregated piece of the vitreous
  71. what can vitreal detachment lead to?
    • 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
  72. what is vitreal heme?
    • 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%
  73. what is Tobacco Dust (aka Shafer's Sign)?
    • 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
  74. summary of PVD
    • 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.
  75. how does the RPE get rid of waste?
    via phagocytosis to get rid of waste products of photoreceptors OUTER segments
  76. what else does the RPE do?
    • 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
  77. what's going on in the retina when it's dark?
    signal being released all the time (glutamate)
  78. what's going on in the retina when it's light?
    phototransduction: hits photoreceptors -> Na channels close, K opens and glutamate STOPPED being released
  79. what is retinitis pigmentosa?
    • this is when the RPE does not phagocytize the ROD outer segments, when it should
    • since rods are more peripheral, RP is peripheral disease
  80. what's the blood supply to the retina?
    choriocapillaris supplies the outer retina, RPE and photoreceptors (has blood retinal barrior)
  81. what supplies the INNER retina?
    central retinal artery
  82. what's going on around the fovea?
    • avascular and a capillary free zone
    • this allows light to hit photoreceptors
    • the photoreceptors, themselves, are avascular and are nourished by the choroid
  83. what does the choroid do?
    • 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
  84. what is Congential Hypertrophy Retinal Pigmented Epithelium? (CHRPE)
    just extra pigmentation of RPE in which there are bigger and darker cells
  85. how is vein occlusion formed?
    from thrombis (occluded at spot where obstacle formed)
  86. what does atery occlusion form?
    an embolus (piece that broke off from obstacles and traveled to get caught and block blood supply)
  87. what is autoregulation do?
    local blood pressure. it is regulated by the SYMPATHETIC nervous system
  88. what is ischemia and what causes it?
    • disease that cause decrease in blood flow:
    • 1. ARMD: (drusen = lipofuscin). no TX for Dry ARMD
    • 2. Glaucoma
    • 3. Hypertension
    • 4. Myopia
  89. what else can cause neovascularization?
    • 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
  90. explain optic nerve
    • ganglion cells compose 90% of optic nerve
    • the eye has a blind spot, which is a result of NO photoreceptors
  91. what happens to the retina if you smoke and have high blood pressure?
    blood vessels in retina bcecome "tortuous"
  92. what causes retinal pathology?
    blood vessel occlusion or leakage
  93. Blood vessel Occlusion
    • ischemia/no O2
    • 1. cotton wool spots: "explosion of nerve"
    • 2. New BV (neovascularization): VEG-F and leaky BV
  94. Blood Vessel leakage
    • 1. hemorrhage: everything getting out
    • 2. edema: just fluid/plasma getting out
    • 3. exudates: lpid, proteins, solids seeping out/building up (no blood cells)
  95. what does laser phtocoagulation treatment do?
    • used in diabetics
    • kills new BV growth, decreases VEG-F and decreases O2 demand
  96. what is Central Retinal Vitreous Occlusion? (CRVO)
    • 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
  97. what is Branch Retinal Vein Occlusion? (BRVO)
    • 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
  98. what is Central Retinal Artery Occlusion? (CRAO)
    • 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
  99. what is Branch Retinal Artery Occlusion? (BRAO)
    • ischemia is more localized to a specific area in the retina
    • this is caused by an embolus, not crushing, like ain BRVO
  100. what's so critical about artery occlusion?
    In a retinal ARTERY occlusion, have 100min before start dying!!
  101. what is retinal detachment?
    detachment between phtoreceptros and RPE
  102. what is pigment epithelium detachment?
    detachment between RPE and Bruch's membrane
Card Set
ocular phys final
ocular phys final