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Mike > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

<p>What two structures make up the ciliary body?</p>

A

<p>Pars plana and pars plicata</p>

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2
Q

<p>How wide are the pars plana and pars plicata respectively?</p>

A

<p>4mm (pars plana)2mm (pars plicata)</p>

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3
Q

<p>What 3 structures make up the pars plicata?</p>

A

<p>ciliary muscles, ciliary vessels, ciliary processes</p>

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4
Q

<p>What are the 3 types of muscles that make up the ciliary muscle?</p>

A

<p>Longitudinal, radial and circular</p>

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5
Q

<p>Where do longitudinal muscles insert?</p>

A

<p>scleral spur</p>

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6
Q

<p>How does the longitudinal muscle affect IOP?</p>

A

<p>affects outflow facility (contraction of muscle increases outflow)</p>

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7
Q

<p>Which muscle fibers of the ciliary body are responsible for accommodation?</p>

A

<p>Circular</p>

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8
Q

<p>What is the blood supply of the ciliary body?</p>

A

<p>Anastomosis between branches of anterior and long posterior ciliary arteries</p>

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9
Q

<p>How many ciliary processes?</p>

A

<p>70</p>

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10
Q

<p>Name 5 functions of the ciliary body:</p>

A

<p>1. Suspends and alters shape of lens2. Produces aqueous3. Affects aqueous outflow4. Makes acid mucopolysaccharide component of vitreous5. Maintains blood aqueous barrier </p>

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11
Q

<p>Contraction of the longitudinal muscle creates what change in the lens?</p>

A

<p>shifts the lens forward and shallows the AC (DOES NOT CHANGE LENS SHAPE)</p>

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12
Q

<p>Contraction of the circular muscle creates what change in the lens? What refractive change?</p>

A

<p>relaxes the zonules making the lens more round with more refractive power (accommodation)</p>

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13
Q

<p>Relaxation of the circular muscle creates what change in the lens? What refractive change?</p>

A

<p>tightens the zonules making the lens flatter with less refractive power </p>

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14
Q

<p>By what method is aqueous humor produced?</p>

A

<p>Active secretion via Na+/K+ pump and carbonic anhydrase </p>

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15
Q

<p>How does glucose enter aqueous humor?</p>

A

<p>passive diffusion</p>

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16
Q

<p>What is the rate of aqueous production?</p>

A

<p>2-3microliters/min</p>

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17
Q

<p>What is the anterior chamber and posterior chamber volumes respectively?</p>

A

<p>250 microliters, 60 microliters</p>

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18
Q

<p>What is the rate of aqueous humor turnover?</p>

A

<p>1% per minute</p>

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19
Q

<p>What is fluorophotometry? What is it used for?</p>

A

<p>direct optical measurement of decreasing fluorescein concentration. Used to measure the rate of aqueous production.</p>

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20
Q

<p>How does the production of aqueous change daily and over a lifetime?</p>

A

<p>Decreases about 45% with sleep.Decreases about 2%/decade (counterbalanced by decrease outflow with increasing age)</p>

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21
Q

<p>What is the pH of aqueous?</p>

A

<p>7.2</p>

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22
Q

<p>Vitamin C concentration in aqueous is higher or lower than in plasma??</p>

A

<p>Much higher! 15x higher</p>

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23
Q

<p>Protein concentration in aqueous is higher or lower than in plasma??</p>

A

<p>Lower (provides optical clarity)</p>

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24
Q

<p>Name 3 functions of the aqueous?</p>

A

<p>1. Maintains IOP2. Provides nutrition to the lens/cornea3. removes metabolic waste</p>

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25
Q

<p>Blood/aqueous barrier is maintained by what cells in the ciliary body?</p>

A

<p>outer pigmented epitheliuminner non pigmented epithelium</p>

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26
Q

<p>Outer pigmented epithelium is continuous with what structure posteriorly?</p>

A

<p>RPE (basal lamina continuous with Bruch's)</p>

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27
Q

<p>Inner nonpigmented epithelium is continuous with what structure posteriorly?</p>

A

<p>neurosensory retina (basal lamina continuous with ILM) Site of active secretion</p>

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28
Q

<p>How do the inner and outer pigmented epithelium relate to each other?</p>

A

<p>Apex to apex</p>

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29
Q

<p>What is flare in the AC?</p>

A

<p>increase in concentration of protein</p>

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30
Q

<p>How does atropine decrease flare?</p>

A

<p>By closing tight junctions of the blood/aqueous barrier</p>

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31
Q

<p>What is the traditional aqueous outflow pathway? What percentage of aqueous outflow is via the traditional pathway?</p>

A

<p>Outflow via the TM80-85%</p>

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32
Q

<p>Give the structural pathway of the traditional aqueous outflow path. </p>

A

<p>uveoscleral meshwork -> corneoscleral meshwork-> juxtacanalicular connective tissue -> scheme's canal -> collector channels -> aqueous veins -> episcleral and conj veins -> anterior ciliary and superior ophthalmic veins -> cavernous sinus</p>

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33
Q

<p>What structure provides the greatest resistance to aqueous outflow?</p>

A

<p>Juxtacanalicular tissue (4-7micrometer pore size)</p>

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34
Q

<p>How many collector channels are there from Schlemm's canal?</p>

A

<p>30</p>

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35
Q

<p>Uveoscleral outflow accounts for how much of the total aqueous outflow?</p>

A

<p>15-20%</p>

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36
Q

<p>Aqueous passes through what angle structure in the uveoscleral outflow tract?</p>

A

<p>CB -> suprachoroidal space -> CB veins, choroidal veins and scleral veins</p>

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37
Q

<p>A cyclodialysis cleft increases aqueous outflow through what mechanism?</p>

A

<p>increase uveoscleral outflow</p>

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38
Q

<p>What affect do cycloplegics have on aqueous outflow? </p>

A

<p>increase uveoscleral outflow</p>

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39
Q

<p>What affect do miotic agents have on aqueous outflow?</p>

A

<p>Decrease uveoscleral outflowIncrease TM outflow</p>

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40
Q

<p>Why are angle structures only visible on gonioscopy?</p>

A

<p>total internal reflection of the air/cornea</p>

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41
Q

<p>Anatomically, Schwalbe's line is...</p>

A

<p>Termination of Descemet's membrane</p>

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42
Q

<p>Name causes of increased pigmentation of TM.</p>

A

<p>Pseudoexfoliation syndrome, pigment dispersion syndrome, uveitis, melanoma, trauma, hyphema, darkly pigmented patients, age</p>

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43
Q

<p>Ddx of blood in Schlemm's canal</p>

A

<p>elevated episcleral venous pressure, oculodermal melanocytosis, hypotony, congenital ectropion uvea, neurofibromatosis</p>

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44
Q

<p>Name 7 cases of PAS</p>

A

<p>1. angle closure2. uveitis3. NVA4. flat AC5. ICE syndrome6. ciliary body tumors7. mesodermal dysgenesis</p>

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45
Q

<p>How do you tell a normal angle vessel from an abnormal angle vessel?</p>

A

<p>abnormal angle vessels cross scleral spur</p>

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46
Q

<p>DDx for abnormal vessels in the angle?</p>

A

<p>1. Neovascularization2. Iris neoplasm3. Fuch's heterochromic iridocyclitis (Amsler sign)</p>

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47
Q

<p>Angle recession is disinsertion of what two structures?</p>

A

<p>tear between longitudinal and circular fibers of the ciliary muscle</p>

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48
Q

<p>What percentage of patients with traumatic hyphema have angle recession?</p>

A

<p>60-90%</p>

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49
Q

<p>What percentage of patient's with angle recession have glaucoma?</p>

A

<p>5%</p>

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50
Q

<p>A cyclodialysis cleft is separation of what 2 structures?</p>

A

<p>ciliary body and scleral spurDIRECT COMMUNICATION BETWEEN AC AND SUPRACHOROIDAL SPACE</p>

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51
Q

<p>How are cyclodialysis clefts treated?</p>

A

<p>cycloplegics to relax ciliary body, argon laser, cryotherapy, suture CBB to SS, intravitreal air bubble to close superior cleft</p>

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52
Q

<p>Iridodialysis is....</p>

A

<p>disinsertion of the iris root</p>

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53
Q

<p>How many axons make up the adult optic nerve?</p>

A

<p>1.2 million</p>

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54
Q

<p>Retinal nerve fiber layer blood supply?</p>

A

<p>Central retinal artery</p>

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55
Q

<p>Prelaminar and laminar optic nerve blood supply?</p>

A

<p>Short posterior ciliary arteries</p>

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56
Q

<p>What is the Goldmann Fick equation?</p>

A

<p>IOP= F/C +EVPF is rate of aqueous formationC is facility of outflowEVP is episcleral venous pressure</p>

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57
Q

<p>Facility of outflow is measured by what?</p>

A

<p>tonography</p>

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58
Q

<p>Facility of outflow increases or decreases with age?</p>

A

<p>Decreases</p>

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59
Q

<p>What is normal EVP?</p>

A

<p>8-12 mmHg</p>

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60
Q

<p>What can cause EVP to increase?</p>

A

<p>venous obstruction, AV shunt</p>

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61
Q

<p>How do you measure EVP?</p>

A

<p>manometry</p>

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62
Q

<p>What is the distribution of IOP?</p>

A

<p>Non gaussian, skewed towards higher IOP</p>

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63
Q

<p>What is a normal range of diurnal variation of IOP?</p>

A

<p>2-6mmHg</p>

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64
Q

<p>How does season affect IOP?</p>

A

<p>IOP is higher in winter than in summer</p>

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65
Q

<p>How does posture affect IOP?</p>

A

<p>IOP is higher when you are laying down compared to sitting up</p>

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66
Q

<p>How does refractive error affect IOP?</p>

A

<p>IOP is typically higher in myopes</p>

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67
Q

<p>Name 3 types of tonometry.</p>

A

<p>1. Applanation2. non-contact3. indentation</p>

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68
Q

<p>What is a Schiotz tonometer?</p>

A

<p>A known weight indents the cornea and displaces a volume of fluid within the eye. Amount of indentation determines pressure.Falsely low with eyes with low rigidity: high myopia, retinal detachments, intraocular gasFalsely high with scleral rigidity and hyperopia</p>

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69
Q

<p>What is the Imbert Fick principle and what is it used for?</p>

A

<p>P = F/Afor an ideal thin-walled sphere, pressure inside sphere equals force necessary to flatten its surface divided by area of flattening</p>

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70
Q

<p>What is the diameter of the application tip?Why?</p>

A

<p>3.06mmAt this diameter corneal rigidity and tear meniscus pull of tonometer cancel each other out</p>

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71
Q

<p>Thick corneas overestimate IOP by about how much? </p>

A

<p>5mmHg per 70micrometersSame is true for thin corneas</p>

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72
Q

<p>If the patient has astigmatism, what changes need to be made with application?</p>

A

<p>if >1.5D of astigmatism, must align red mark with axis of MINUS cylinder</p>

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73
Q

<p>What is a Perkin's tonometer?</p>

A

<p>Portable form of a Goldmann tonometer</p>

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74
Q

<p>What is a Mackay-Marg tonometer? What are some examples?</p>

A

<p>Applanates a small area so good for corneal scars. Ex: tonopen and pneumotonometer</p>

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75
Q

<p>What is the Scheie classification for gonioscopy?</p>

A

<p>Grade 1- wide open (CBB)Grade 2- SS visibleGrade 3- only ATM visibleGrade 4- closed</p>

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76
Q

<p>What is the Schaffer classification system for gonioscopy?</p>

A

<p>Grade 1- 10% open Grade 2- 20% open Grade 3- 30% open Grade 4- 40% open</p>

<p></p>

<p></p>

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77
Q

<p>What is the first element of the Spaeth classification system for gonioscopy? </p>

A

<p>First element is a CAPITAL LETTERA- anterior to TMB- at TMC- at SSD- CBB visibleE- large CBB with indentation gonioscopy, put first impression then indent and write actual insertion in (_)</p>

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78
Q

<p>What is the 2nd element of the Spaeth classification for gonioscopy?</p>

A

<p>iridocorneal angle width in degrees from 5-45</p>

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79
Q

<p>What is the 3rd element of the Spaeth classification for gonioscopy?</p>

A

<p>Peripheral iris configurationr= regular (flat)s= steep (convex)q= queer (concave)</p>

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80
Q

<p>What is the 4th element of the Spaeth classification for gonioscopy?</p>

A

<p>Amount of pigmentation graded from 0 to 4</p>

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81
Q

<p>Which gonioscopy lens gives a direct view of the angle?</p>

A

<p>Koeppe</p>

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82
Q

<p>Which lenses can perform indentation gonioscopy?</p>

A

<p>Zeiss, Posner, Sussman</p>

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83
Q

<p>Which indirect viewing lens CANNOT perform indentation gonioscopy?</p>

A

<p>Goldmann (too big)</p>

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84
Q

<p>What is the degree or extent a person with normal visual fields can see in all directions?</p>

A

<p>Nasal- 60Superior- 60Inferior 70-75Temporal 100-110</p>

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85
Q

<p>Define fixation loss. </p>

A

<p>patient responds to target that is displayed in the blind spot</p>

86
Q

<p>Define false positive</p>

A

<p>patient responds when there is no stimulus</p>

87
Q

<p>Define false negative</p>

A

<p>patient does not respond to a super threshold stimulus at a spot that was previously responded to (lack of attention, cloverleaf)</p>

88
Q

<p>What is mean deviation?</p>

A

<p>the average departure of each test point from the age-adjusted normal value</p>

89
Q

<p>what is the background illumination for HVF?</p>

A

<p>31.5 apostilbs</p>

90
Q

<p>what is the stimulus duration for HVF? </p>

A

<p>0.2s</p>

91
Q

<p>What is the technical name for a nasal step?</p>

A

<p>Nasal step of Ronne</p>

92
Q

<p>What is a seidel scotoma?</p>

A

<p>Small scotoma connected to the blind spot.</p>

93
Q

<p>When performing direct ophthalmoscopy and looking at the RNFL, what is the best setting/light to visualize the RNFL?</p>

A

<p>red free</p>

94
Q

<p>What cells die in glaucoma?</p>

A

<p>ganglion cells, amacrine and muller</p>

95
Q

<p>Where do you find the earliest histological changes in glaucoma?</p>

A

<p>lamina cribrosa</p>

96
Q

<p>What is Schnabels Cavernous Optic Atrophy? What causes it?</p>

A

<p>atrophy of neural element of the optic nerve and replacement with hyaluronic acid.</p>

<p>Glaucoma or atherosclerotic disease and normal IOP</p>

97
Q

<p>Schnabels Cavernous Optic Atrophy stains classically \_\_\_\_\_\_\_\_\_\_ with \_\_\_\_\_\_\_\_\_\_\_.</p>

A

<p>Hyalouronic acid (mucopolysaccharide)with colloidal iron (blue)</p>

98
Q

<p>Glaucoma is the \_\_\_\_\_\_\_ leading cause of blindness in the US.</p>

<p>(first, second, third or fourth)</p>

A

<p>Second</p>

99
Q

<p>Steroid responders have \_\_% chance of developing glaucoma in the next 5 years.</p>

A

<p>31%</p>

100
Q

<p>If a patient has glaucomatous damage in one eye, what is the risk of developing glaucoma in the fellow eye in 5 years?</p>

A

<p>29%</p>

101
Q

<p>What is the most common genetic cause of POAG?</p>

A

<p>OPTN (optineurin) mutation</p>

102
Q

<p>JOAG has been mapped to what gene?</p>

A

<p>MYOC/TIGR on chromosome 1q21-q31</p>

103
Q

<p>Name 6risk factors for glaucoma</p>

A

<p>1. age</p>

<p>2. increased C/D</p>

<p>3. thin CCT (<550)</p>

<p>4. family hx (6x increase in 1st degree relatives)</p>

<p>5. increased IOP</p>

<p>6. race (6x increased risk in African Americans)</p>

<p>7. Possibly DM, HTN, migraines??</p>

104
Q

<p>Decrease in what two colors is the first to occur with glaucomatous damage?</p>

A

<p>blue - yellow</p>

105
Q

<p>Name 5 causes of secondary open angle glaucoma.</p>

A

<p>1. clogging of TM (RBCs, macrophages, neoplastic cells, pigment, lens proteins, photoreceptor outer segments, visco)</p>

<p>2. Toxic/medication (steroids, siderosis, chalcosis)</p>

<p>3. Inflammation (uveitis, interstitial keratitis)</p>

<p>4. Increased EVP</p>

<p>5. Trauma (angle recession, chemical injury)</p>

106
Q

<p>\_\_\_\_\_\_\_% risk of glaucoma is hyphema is more than 50% the AC volume</p>

<p>\_\_\_\_\_\_\_\_\_% risk of glaucoma with total hyphema</p>

A

<p>27%, 52%</p>

107
Q

<p>What class of medication should be avoided in patients with sickle cell and hyphema?</p>

A

<p>Carbronic anhydrase inhibitors.</p>

<p>increase vitamin C in AC (decreases pH) and increases sickling</p>

108
Q

<p>Non-clearing VHcauses what type of glaucoma?</p>

A

<p>Ghost cell, khaki colored degenerated RBCs</p>

109
Q

<p>What does "lytic" mean when referring to glaucoma?</p>

A

<p>macrophages filled with something are obstructing the TM</p>

<p>Hemolytic (hemosiderin)</p>

<p>Phacolytic (lens proteins)</p>

<p>Melanomalytic (melanin from malignant glaucoma)</p>

<p>Melanocytomalytic (melanin from necrotic melanocytoma)</p>

<p></p>

110
Q

<p>What is phacolytic glaucoma? What cause it?</p>

A

<p>When lens proteins leak through the capsule in the setting of a hypermature cataract, macrophages engulf lens proteins and then become stuck in TM</p>

111
Q

<p>Who is your typical patient with pigmentary glaucoma?</p>

A

<p>young myopic male</p>

112
Q

<p>What percentage of patient with pigment dispersion develop pigmentary glaucoma?</p>

A

<p>50%</p>

113
Q

<p>How is pigment dispersion syndrome inherited?</p>

A

<p>AD</p>

114
Q

<p>What is the mechanism of pigment dispersion?</p>

A

<p>Reverse pupillary block. Iris bows back wards and there is mechanical rub against the pigmented posterior iris</p>

115
Q

<p>What corneal abnormalities can be present in PDS?</p>

A

<p>Kruckenberg spindle (endothelium metabolizes released melanin)</p>

116
Q

<p>Describe the TIDs of PDS.</p>

A

<p>Midperipheral, spoke like, radial</p>

117
Q

<p>Patients with PDS have a higher liklihood of having what 2 retinal pathologies?</p>

A

<p>Lattice (20%), RD (5%)</p>

118
Q

<p>What is the treatment for PDS?</p>

A

<p>miotics, excellent response to SLT</p>

119
Q

<p>True or False: SLT is recommended in patients with PDS.</p>

A

<p>True! respond very well to SLT</p>

120
Q

<p>What is the gene for pseudoexfoliation?</p>

A

<p>LOXL1</p>

121
Q

<p>What percentage of patients with Pseudoexfoliation Syndrome have secondary glaucoma?</p>

A

<p>50%</p>

122
Q

<p>True/False: PXE is a systemic disease.</p>

A

<p>True!</p>

123
Q

<p>What finding on gonioscopy is typical of PXE?</p>

A

<p>Sampaolesi's line</p>

<p>(band of pigment anterior to schwalbe's line)</p>

124
Q

<p>PXE is most common in what ethnic group?</p>

A

<p>Scandinavians</p>

125
Q

<p>In PXE, what changes can you see in the iris?</p>

A

<p>1. blood-aqueous barrier defect</p>

<p>2. pseudouveitis</p>

<p>3. iris rigidity</p>

<p>4. posterior synechiae</p>

<p>5. poor dilation</p>

126
Q

<p>In PXE, what changes can you see in the cornea?</p>

A

<p>1. Reduced endothelial cell count (interesting huh?)</p>

<p>2. endothelial decompensation</p>

<p>3. endothelial proliferation over TM</p>

127
Q

<p>True/False: PXE can cause both open and closed angle glaucoma.</p>

A

<p>True! weak zolunes can allow anterior movement of the lens and can cause intermittent angle closure glaucoma</p>

128
Q

<p>Treatment for PXE?</p>

A

<p>usually have a very good response to laser trabeculopasty</p>

<p>usually have higher initial IOP and more difficult to control IOP with medical treatment alone compared to POAG</p>

129
Q

<p>What is Schwartz's syndrome?</p>

A

<p>high IOP associated with RRD</p>

130
Q

<p>What material blocks TM outflow in Schwartz syndrome?</p>

A

<p>photoreceptor outer segments and pigment release from RPE</p>

131
Q

<p>What is the treatment for Schwartz syndrome?</p>

A

<p>repair RRD</p>

132
Q

<p>What is lens particle glaucoma?</p>

A

<p>lens particles block TM following trauma or cataract surgery (retained lens fragments). Greater inflammation than with phacolytic glaucoma</p>

133
Q

<p>What are some typical findings of lens particle glaucoma?</p>

A

<p>very high IOP, PAS, posterior synechiae and inflammatory membranes</p>

134
Q

<p>What is alpha-chymotrypsin?</p>

<p>How does it induce glaucoma?</p>

A

<p>An enzyme used to melt the zonules in intracapsular cataract extraction (ICCE)</p>

<p>Zonular fragments accumulate in TM, alpha-chymotrypsin itself does not cause damage</p>

135
Q

<p>Who gets steroid induced glaucoma?</p>

A

<p>1. Patients with POAG</p>

<p>2. Patients with Fam Hx</p>

<p>3. Older patients</p>

<p>4. High myopes</p>

<p>5. DM</p>

136
Q

<p>True or False: Oral steroids raise IOP more than topical steroids.</p>

A

<p>FALSE</p>

137
Q

<p>Siderosis (iron) and chalcosis (copper) cause glaucoma how?</p>

A

<p>TM toxicity and scarring from IOFB</p>

138
Q

<p>Name 4 types of non-infectious uveitis that are notorious for causing glaucoma.</p>

A

<p>1. JRA (20% develop glaucoma)</p>

<p>2. Posner Schlossman syndrome (episodic trabeculitis)</p>

<p>3. Fuch's heterochromic iridocyclitis (60% develop high IOP, glaucoma more common in those with spontaneous hyphema and bilateral disease)</p>

<p>4. UGH</p>

139
Q

<p>Glaucoma develops in \_\_\_% of patients that have >180 degrees of angle recession.</p>

A

<p>10%</p>

140
Q

<p>True or False: Acidic burns cause scarring of the TM more commonly than basic burns.</p>

A

<p>FALSE</p>

141
Q

<p>A patient with TAO is in your clinic and you notice that in upgaze the patients IOP in about 5mmHg higher than in primary gaze. Why?</p>

A

<p>calse elevation of IOP caused by IR fibrosis and resistance to upgaze</p>

142
Q

<p>What are some etiologies of elevated episcleral venous pressure?</p>

A

<p>CC fistula, cavernous sinus thrombosis, Sturge-Weber, NF, orbital mass, TAO, superior vena cava obstruction, mediastinal tumors and syndromes</p>

143
Q

<p>Elevated episcleral venous pressure can cause what finding on gonioscopy?</p>

A

<p>blood in Schlemms canal</p>

144
Q

<p>What is the mechanism of pupillary block?</p>

A

<p>In susceptible patients, iridolenticular touch causes resistance of aqueous flow from posterior to anterior chamber causing increased posterior pressure. When pupil in <strong>MID-DILATED</strong> (stress, low ambient light, sympathomimetric or anticholinergic meds), elevated posterior chamber pressure causes peripheral iris to bow forward and occlude angle</p>

145
Q

<p>What ethnic group comes to mind that is particularly known for having <strong>ACUTE </strong>angle closure?</p>

A

<p>Eskimos and Asians</p>

146
Q

<p>What racialgroup comes to mind that more commonly has CHRONIC angle closure?</p>

A

<p>African Americans more than asians</p>

147
Q

<p>At what age is a patient at highest risk for angle closure?</p>

A

<p>55-65 years old</p>

<p>5% of patients over age 60 have angles that can be occluded and 0.5% of those patients with occludable angles will develop angle closure</p>

148
Q

<p>Is angle closure glaucoma usually unilateral or bilateral?</p>

A

<p>Bilateral. 75% risk of untreated fellow eye in 5 years</p>

149
Q

<p>What anatomic features predispose to angle closure?</p>

A

<p>1. small anterior segment (hyperopia, nanophthalmos, microcornea, microphthalmos)</p>

<p>2. Hereditary narrow angle</p>

<p>3. anterior iris insertion (eskimos, asians and AA)</p>

<p>4. Shallow AC (large lens, plateau iris, loose or dislocated lens)</p>

150
Q

<p>You decide to treat a patient that you suspect is in acute angle closure with glycerin. What co-morbidity do you need to check the patients chart for before administering glycerin?</p>

A

<p>DM</p>

151
Q

<p>True or False: Acute angle closure glaucoma can cause optic nerve edema.</p>

A

<p>True</p>

152
Q

<p>After an episode of acute angle closure, what are some findings you may see in the lens? Iris?</p>

A

<p>Lens- glaukomflecken</p>

<p>Iris- atrophy from focal iris stromal necrosis, dilated irregular pupil from sphincter necrosis</p>

153
Q

<p>What do you call focal anterior lens epithelial necrosis after an episode of acute angle closure?</p>

A

<p>Glaukomflecken</p>

154
Q

<p>If you suspect a patient may be susceptible to angle closure, what are some in office tests you may consider?</p>

A

<p>Prone test</p>

<p>Darkroom test</p>

<p>Prone darkroom test</p>

<p>pharmacologic pupillary dilation</p>

155
Q

<p>You suspect a patient may be suseptible to angle closure so you decide to put them in a dark room, prone in your office. After 1 hour you check the IOP and it has risen by 6mmHg from baseline. Is this a positive or negative test?</p>

A

<p>Negative. IOP has to rise >8mmHg to be positive</p>

156
Q

<p>You suspect a patient is in acute angle closure and decide to give IV mannitol. What adverse events could possibly occur?</p>

A

<p>cardiovascular</p>

157
Q

<p>You give a patient with acute angle closure pilocarpine and nothing happens. Why?</p>

<p>You give a patient with acute angle closure pilocarpine and the IOP goes up. Why?</p>

A

<p>1. sphincter ischemia</p>

<p>2. iris lens diaphram moves forward and worsens pupillary block</p>

158
Q

<p>What is the difinitive treatment of angle closure?</p>

A

<p>PI</p>

159
Q

<p>You suspect a patient is in angle closure. Besides drops and lasers, what other treatment options do you have?</p>

A

<p>compression gonioscopy. Can force aqueous through block and open angle</p>

160
Q

<p>In a patient with angle closure glaucoma... if the iris is in \_\_\_\_\_\_\_\_ position, an LPI will not be aseffective treatment of a treatment. Instead you should try what type of laser?</p>

A

<p>Plateau iris.</p>

<p>Laser iridoplasty</p>

161
Q

<p>What is a potential serious adverse reaction to IV mannitol?</p>

A

<p>cardiovascular adverse effects</p>

162
Q

<p>In a patient in acute angle closure in one eye, what is the chance of ACG in the other eye in the next 5 years?</p>

A

<p>75%</p>

163
Q

<p>Name 2 exam findings you could see in a patient with a history of previous AACG or intermittent angle closure glaucoma.</p>

A

<p>PAS and glaukomflecken</p>

164
Q

<p>What is glaukomflecken?</p>

A

<p>gray-white epithelial and anterior cortical lens opacities that occur following an episode of markedly elevated IOP. Histopathologically, glaukomflecken are composed of necrotic lens epithelial cells and degenerated subepithelial cortex.</p>

165
Q

<p>Name a few causes on Secondary Angle-Closure glaucoma WITH PUPILLARY BLCOK.</p>

A

<p>Phacomorphic</p>

<p>dislocated lens</p>

<p>seclusio pupillae</p>

<p>nanophthalmos</p>

<p>SO</p>

<p>microspherophakia</p>

166
Q

<p>Name a few causes of Secondary Angle Closure WITHOUT PUPILLARY BLOCK and with posterior pushing mechanism.</p>

A

<p>Posterior pushing:</p>

<p>1. Anterior rotation of CB:</p>

<p> inflammation (scleritis, uveitis, s/p PRP)</p>

<p> choroidal effusion (uveal effusion, hypotony)</p>

<p> suprachoroidal hemorrhage</p>

<p>2. Aqueous misdirection (AKA Malignant glaucoma)</p>

<p>3. Pressure from posterior segment</p>

<p> tumor, expansive gas, exudative RD</p>

<p>4. Contracture of retrolental tissue</p>

<p> PHFV, ROP</p>

167
Q

<p>Name a few causes of Secondary Angle Closure WITHOUT PUPILLARY BLOCK with anterior pulling mechanism.</p>

A

<p>1. Epithelial downgrowth</p>

<p>2. endothelial downgrowth (ICE syndrome, PPMD)</p>

<p>3. NVG</p>

<p>4. adhesion from prior trauma</p>

168
Q

<p>Define nanophthalmos:</p>

<p>Hyperopia of....</p>

<p>axial length of....</p>

<p>corneal diameter of....</p>

A

<p>Hyperopia of >10D</p>

<p>axial length of <20mm</p>

<p>corneal diameter of <10.5mm</p>

169
Q

<p>Name some risk factors for development of malignant glaucoma.</p>

A

<p>uveitis</p>

<p>angle closure</p>

<p>nanophthalmos</p>

<p>hyperopia</p>

<p>s/p laser or incisional surgery in patients with PAS or CACG</p>

170
Q

<p>What clinical findings do you see in malignant glaucoma?</p>

A

<p>entire AC is shallow (vs with angle closure only the periphery is shallow)</p>

<p>IOP higher than expected</p>

<p>patent iridectomy</p>

<p>no suprachoroidal fluid or blood</p>

171
Q

<p>On POD1 after glaucoma surgery you do a Bscan on a patient and are concerned for a choroidal detachment. What patient SYMPTOM would be more indicative of a choroidal hemorrhage than a choroidal effusion? What CLINICAL FINDING?</p>

A

<p>Symptom: Pain more indicative of suprachoroidal hemorrhage. No pain with choroidal effusion.</p>

<p></p>

<p>Exam Finding: IOP elevated with suprachoroidal hemorrhage and low with effusion.</p>

172
Q

<p>What percentrage of cases of malignant glaucoma resolve with medical therapy alone?</p>

A

<p>50%</p>

173
Q

<p>Name 3 different laser/surgical options for management of malignant glaucoma.</p>

A

<p>1. Argon to ciliary process (shrink them?)</p>

<p>2. YAG to anterior hyaloid face</p>

<p>3. PPV with disruption of anterior hyaloid face</p>

174
Q

<p>What is the most common mechanism by which an intraocularmalignant melanoma produces glaucoma?</p>

A

<p>Direct invasion of the TM (can induce NVA and melanin laden macrophages can obstruct the TM (malanomalytis)</p>

175
Q

<p>What is melanomalytic glaucoma?</p>

A

<p>Secondary open angle glaucoma caused by obstruction of TM with melanin laden macrophages (intraocular malignant melanoma of uveal tract)</p>

176
Q

<p>This endothelial dystrophy looks like "snail tracks" and causes glaucoma by what mechanism?</p>

<p>BONUS:How is it inherited?</p>

A

<p>Posterior Polymorphous Corneal Dystrophy (PPMD) (don't think about the letters too hard)</p>

<p>Abnormal corneal endothelial cells migrate into angle</p>

<p></p>

<p>Autosomal dominant</p>

<p></p>

177
Q

<p>Name 4 proposed mechanisms of NTG.</p>

A

<p>Nocturnal hypotension (compromised blood supply to nerve)</p>

<p>Autoimmune (increased incidence of proteinemia and autoantibodies)</p>

<p>Vasospasm</p>

<p>Previous hemodynamic crisis (excessive blood loss)</p>

178
Q

<p>What <strong>exam</strong> finding is more commong in patients with NTG than POAG and can be a sign that IOP is not adequately controlled?</p>

A

<p>optic nerve splinter hemorrhages</p>

179
Q

<p>In NTG, visual fields differ from POAG in what way?</p>

A

<p>deeper defects, closer to fixation</p>

180
Q

<p>In ALT, what are the settings?</p>

<p>Power?</p>

<p>spot size?</p>

<p>Duration?</p>

<p># of spots over what area?</p>

A

<p>400-1200mW power</p>

<p>50micrometers spot size</p>

<p>duration 0.1s</p>

<p>50 spots over 180 degrees</p>

181
Q

<p>On average, ALT reduces IOP by what percentage?</p>

A

<p>30%</p>

182
Q

<p>If a burn is placed too posterior with ALT, what is a risk?</p>

A

<p>PAS</p>

183
Q

<p>ALT is successful most often in what type of glaucoma?</p>

A

<p>PXG (best) > PG > POAG > NTG > aphakic (worst)</p>

184
Q

<p>On gonioscopy, the more\_\_\_\_\_\_\_\_\_, the more likely ALT is to lower IOP.</p>

A

<p>pigment</p>

185
Q

<p>ALT may worsen IOP in what conditions?</p>

A

<p>uveitic glaucoma, angle recession, ACG, congenital glaucoma, steroids glaucoma</p>

186
Q

<p>The majority of glaucoma is inherited in a \_\_\_\_\_\_\_\_\_ fashion. The exception is \_\_\_\_\_\_\_\_\_\_\_ glaucoma, which is inherited \_\_\_\_\_\_\_\_\_\_.</p>

A

<p>The majority of glaucoma is inherited in an autosomal dominatefashion. The exception is congenital glaucoma, which is inherited autosomal recessive.</p>

187
Q

<p>SLT parameters:</p>

<p>spot size?</p>

<p>power?</p>

<p>number of shots over what degree?</p>

A

<p>400 micrometer spot size</p>

<p>power 0.6-0.9mJ</p>

<p>50 shots over 180 degrees</p>

188
Q

<p>You can do an LPI with either YAG or Argon laser (or both). What is the benefit and risk of each?</p>

A

<p>YAG bleed more but close less</p>

<p>Argon bleeds less, more pronounced iritis</p>

189
Q

<p>What are the laser settings for iridoplasty?</p>

<p>power?</p>

<p>spot size?</p>

<p>duration?</p>

A

<p>200-400 mW power</p>

<p>500 micrometer spot size</p>

<p>duration 0.5-1.0 seconds</p>

190
Q

<p>What patients are at higher risk of bleb failure with trabeculectomy?</p>

A

<p>previous surgical failure, darker skin, hx of keloid, younger, intraocular inflammation, scarred conjunctiva, hyperopia, shallow AC</p>

191
Q

<p>Mitomycin C is an antibiotic isolated from \_\_\_\_\_\_\_\_\_.</p>

A

<p>streptomyces caespitosus</p>

192
Q

<p>What is MMC mechanism of action?</p>

A

<p>intercalates with DNA and prevents replication, suppresses fibrosis and vascular ingrowth after exposure to the filtation site. Toxic to fibroblast in all stages of cell cycle, 100x more potent than 5-FU</p>

193
Q

<p>What happens if MMC gets in the eye?</p>

A

<p>corneal decompensation due to endothelial damage</p>

<p>AC inflammation</p>

<p>necrosis of CB</p>

<p>retinal toxicity</p>

194
Q

<p>What is 5-FUs mechanism of action?</p>

A

<p>affects the S-phase of the cell cycle</p>

195
Q

<p>What happens if 5-FU gets in the eye?</p>

A

<p>nothing at normal concentrations</p>

196
Q

<p>If IOP is high post operatively after trabeculectomy, what do you do?</p>

A

<p>laser suturelysis or digital massage</p>

197
Q

<p>POD1 trabeculectomy.</p>

<p>Bleb high, IOP low.</p>

<p>What is DDx and Tx?</p>

A

<p>DDx: overfiltration</p>

<p>Tx: revision</p>

198
Q

<p>POD1 trabeculectomy.</p>

<p>Bleb flat, IOP low.</p>

<p>What is DDx and Tx?</p>

A

<p>DDx: choroidal detachment</p>

<p>Tx: cycloplegics, steroids and +/- drainage</p>

<p></p>

<p>DDx: bleb leak</p>

<p>Tx: Antibiotis, IOP suppressants, stop steroid, reform AC, pressure patch, glue, surgery?</p>

199
Q

<p>POD1 trabeculectomy.</p>

<p>Bleb flat, IOP elevated.</p>

<p>What is DDx and Tx?</p>

A

<p>DDx: suprachoroidal hemorrhage.... Tx: Drainage</p>

<p>DDx: pupillary block.... Tx: cycloplegics, steroid, PI</p>

<p>DDx: malignant glaucoma..... Tx: cycloplegics, aqueous suppressants, PI, YAG to anterior hyaloid, PPV</p>

<p></p>

200
Q

<p>POD1 trabeculectomy.</p>

<p>Bleb high, IOP high.</p>

<p>What is DDx and Tx?</p>

A

<p>Dx: encapsulated bleb</p>

<p>Tx: needling, aqueous suppressants, bleb revision</p>

201
Q

<p>Most common organism to cause blebitis?</p>

A

<p>Staphylococcus</p>

202
Q

<p>Treatment of blebitis?</p>

A

<p>aggressive topical antibiotics, observe daily for endophthalmitis</p>

203
Q

<p>Bacteria most commonly associated with bleb associated endophthalmitis?</p>

A

<p>streptococcus or H flu</p>

204
Q

<p>Bleeding of this vessel causes a suprachoroidal hemorrhage after trab.</p>

A

<p>long posterior ciliary artery stretches until it ruptures</p>

205
Q

<p>What are risk factors for suprachoroidal hemorrhage after trabeculectomy?</p>

A

<p>increased age, HTN, CAD, aphakia</p>

206
Q

<p>What was the main conclusion of the Advanced Glaucoma Intervention Study? (AGIS)</p>

A

<p>African Americans: ATT</p>

<p>(ALT then trab then trab)</p>

<p>Caucasians: TAT</p>

<p>(trab first)</p>

207
Q

<p>What was the main conclusion from the Ocular Hypertension Treatment Study? (OHTS)</p>

A

<p>At 5 years, the risk of development of POAG in a patient with ocular HTN decreases from 9.5% to 4.4% with treatment of ocular hypertension.</p>

208
Q

<p>What was the main conclusion from the Collaborative Initial Glaucoma Treatment study (CIGTS)?</p>

A

<p>Initial treat of POAG with surgery or medical therapy results in similar VFs at 5 years.</p>

<p>VA loss was initially worse in the surgical group, but evened out by 5 year follow up.</p>

209
Q

<p>What was the main conclusion of the Early Manifest Glaucoma Trial?</p>

A

<p>Each 1mmHg of IOP suppression resulted in 10% decreased risk of progression.</p>

<p>Treatment of early glaucoma halves the chance of progression</p>

210
Q

<p>What was the main conclusion of the Glaucoma Laser Trial? (GLT)</p>

A

<p>initial treatment with ALT is at least as good as initial treatment with timoptic</p>

211
Q

<p>What was the main outcome of the Collaborative Normal Tension Glaucoma Study?</p>

A

<p>IOP is a factor the pathogenesis of NTG and lowering IOP by 30% is beneficial.</p>

212
Q

<p>In NTG, what are the factors that increase the rate of progression?</p>

A

<p>female gender, hx of migrains, disc hemorrhages</p>

Mike (6 decks)

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