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KMK > Ocular disease Pt 2 > Flashcards

Ocular disease Pt 2 Flashcards

1
Q

Asteroid hyalosis

What is it made up of?

A

associated with aging over 60 yo

made with calcium soaps

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2
Q

What are the signs and symptoms of asteroid hyalosis?

A

Sx: asymptomatic, no floaters

signs: numerous small, yellow-white refractile particles attached to collagen fibrils in a normal vitreous, unilateral in 75% of cases

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3
Q

Synchysis Scintillans

A

usually found AFTER a anterior chronic uveitis, vitreous heme or trauma

made up of cholesterol crystals, unilateral golden brown, refractile that are freely mobile in the vitreous cavity and often settle inferiorly?

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4
Q

What’s the difference between asteroid hyalosis and synchysis scintillans?

A

Asteroid hyalosis - calcium soaps, occurs w/ normal aging

Synchysis scintillans - cholesterol crystal, settle inferiorly, occurs w/ chronic anterior uveitis/vit heme/trauma

BOTH UNILATERAL

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5
Q

PVD

A
  • more common in females
  • prevalence ~50 yo (50% by age 50 and 65% by age 65)
  • can occur 20 years earlier in myopes
  • collagen clumps causing the liberated collagens to contract –> causing PVD. Pockets of liquefaction (syneresis) can travel through the hole in the posterior hyaloid causing separation between the vitreous and the retina
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6
Q

What signs can aid in detecting a RD/break after a PVD?

A

schafer’s sign (tobacco dust) and vitreous heme (70% increase risk of a break)

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7
Q

What are risk factors for PVD?

A

diabetes, myopia, age, surgery, inflammation, vitreous heme, trauma

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8
Q

What are the signs and symptoms of a PVD?

A

Sx: acute floaters, decreased vision, flashes of light

Sign: Weiss ring, anterior displacement of the posterior hyaloid, pigmented cells (shafer’s sign), vit heme

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9
Q

What else can PVD result in?

A

erm, macular hole, VMT, vitreous and retinal heme, retinal breaks

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10
Q

If you see vitreous heme, what should you ask about?

A

trauma, diabetes, HTN

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11
Q

What can cause a vitreous heme?

A

trauma, DR VOS

Diabetes
ROP
Vein occlusion
OIS (ocular ischemic syndrome)
Sickle cell

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12
Q

What are the signs and symptoms of a Vitreous heme/pre-retinal heme ?

A

Pre-retinal heme: asymptomatic unless the macula is involved, sudden vision loss or VF loss

Vitreous heme can cause sudden, painless vision loss and/or black spots that have corresponding flashing lights

Signs:
Preretinal heme: located between the retina and posterior vitreous, very red and keel shape

Vitreous heme: anterior to the posterior vitreous face (within the vitreous). mild vitreous heme will be characterized by blood that obscures only part of the fundus, severe heme will completely obscure the view of the fundus chronic cases will appear yellow

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13
Q

Whats the most common cause of a spontaneous vitreous heme?

A

DR (31-54% of cases)

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14
Q

What test should you order if you have a difficult time seeing the fundus through the vit heme

A

B-scan

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15
Q

What are the 2 types of neo? What causes each of them?

A
  1. Preretinal - DR VOS
  2. Choroidal - CHBALA
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16
Q

CRVO

A
  • 3rd most common vascular cause of vision loss, DR is the most common
  • compression of an artery on a vein leading to turbulent blood flow
  • venous vessel walla damage, thrombus formation, thrombus at or near lamina cribosa
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17
Q

What are the risk factors for CRVO

A

HTN, diabetes, cardiovascular dz, open-angle glc

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18
Q

what’s the ocular dz that’s most commonly associated with CRVO?

A

Glaucoma/POAG (40-60%)

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19
Q

What are the causes of CRVO or BRVO in a young patient?

A

a young pt with clotting issues

oral contraceptive, protein S/ protein C/ antithrombin III deficiency, factor XII deficiency, antiphospholipid antibody syndrome, collagen vascular dz, and AIDS

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20
Q

What are the signs and symptoms of a CRVO?

A

sudden, unilateral, painless vision loss in an elderly pt ( 90% of pts are >50 yo)

signs:
thrombus formation leads to ischemia and release of VEGF with characteristic signs including retinal heme in all 4 quads, collaterals, dilated tortuous retinal veins, CWS, optic disc edema

** remember veins drain blood from the retina**

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21
Q

Collateral veins

A

visible over several weeks to months, often on the disc and permits blood flow between the retina and choroidal circulations
helping to accelerate drainage of excessive fluid (retinal edema) into the choroidal circulation after a CRVO

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22
Q

What are some vision-threatening complications that CRVO can cause?

A
  1. Macular edema, macular ischemia, intramacular hemes
  2. Neo (BAD!!),
  3. 90-day glaucoma (within first 3 months of diagnosis of CRVO)

ischemic CRVO
-60% of ischemic cases develop iris neo and 30% develop neo glaucoma
- higher risk of neo glaucoma

non-ischemic CRVO
6% of nonischemic cases develop rubeosis or angle neo

ALWAYS DO GONIO

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23
Q

What is the leading cause of vision loss in ischemic and non-ischemic CRVO?

A

macular edema

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24
Q

What defines ischemic CRVO?

A

10DD or more of nonperfusion on FA
- 90% of cases are 20/200 or worse
- poor prognosis, final VA CF

16% of nonischemic cases become ischemic

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25
Q

BRVO

A

most common retinal vascular occlusive dz, pts have similar health hx as pts with CRVO
- caused by thrombus after compression of an artery on a vein (AV crossing)
- 60% occur at an AV crossing within the sup/temporal quad

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26
Q

What are the risk factors for BRVO?

A

HTN, cardiovascular dz, increased body mass index at 20 years, open angle glc

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27
Q

Where does most AV crossing occur in a BRVO?

A

S/T quad

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28
Q

What if the BRVO does not occur at an AV crossing? What should you suspect?

A

evaluate for vasculitis

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29
Q

What are the signs and symptoms for a BRVO?

A

sx: sudden, unilateral, painless VF loss , blurred or no sx

signs:
usually occur at the occluded area, dilated tortuous, retinal veins, CWS, collateral vessels, and intraretinal heme

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30
Q

What are vision-threatening complications for BRVO?

A
  1. macular disease - ishcemia, edema, heme
  2. Neo complications - pre-retinal/vitreous heme
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31
Q

CRAO

A
  • amaurosis fugax (transient vision loss)
  • common in elderly pts
  • 10% risk of CRAO in the fellow eye
  • commonly arise from the heart and/or carotid artery emboli

“Big APD , 70 yo M”

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32
Q

What are the risk factors for CRAO?

A

HTN, DM, carotid occlusive dz, cardiac valve dz

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33
Q

What should you consider if you see a CRAO in a younger pt?

A

drug use and BC

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34
Q

Which one is more dangerous?

calcific emboli or carotid emboli?

A

calcific emboli is more dangerous, large, from calcified heart valves and often located in the CRA. near the optic nerve

carotid emboli = smaller cholesterol plaques (hollenhorst plaques) = MOST COMMON CAUSE

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35
Q

What tests would you recommend for a pt with a retinal emboli?

A

evaluate for carotid artery and cardiac dz with carotid doppler and EKG/Echo

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36
Q

What are causes for CRAO?

A

retinal emboli is the most common cause

other culprits include GCA, acute elevation in IOP, collagen vascular dz, IV drug use, oral contraceptives, sickle cell and syphilis

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37
Q

What are the signs and symptoms for CRAO?

A

Sx: transient vision loss
acute profound vision losss (often 20/400 or worse), unless cilioretinal artery is present to spare the macula, VA is LP or worse, strongly consider opthalmic artery occlusion

Signs: superficial whitening of the inner retinal layers (color is restored after perfusion but does not regain function), narrowed arterial vasculature, cherry red spots inthe foveola, APD, hollenhorst plaque (40% of cases)

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38
Q

What does the cilioretinal artery branch from?

A

SPCAs of the choroidal, allows the macula to remain functional in a CRAO (present in 15-30%)

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39
Q

T or F Neovascular glaucoma is rare in CRAO

A

T, because the retina dies too fast

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40
Q

What’s the most common cause of BRAO?

A

retinal emboli

other causes are calciium, fibrin, and platelet

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41
Q

What are the signs and sx of BRAO?

A

Sx: asymptomatic, VFdefect or sudden unilateral painless vision loss if the area of occlusion is close to or involving the macula

Signs: superficial whitening of the affected vessels (90% are temporal vessels) due to infarction and edema, hollenhorst plaques or other emboli found in the area of occlusion 62% of cases, edema/retinal whitening resolves within weeks but tissue remains nonfunctional and pts will have permanent VF defect

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42
Q

What’s the difference between CRAO and BRAO?

A

BRAO only affects area of the occluded vessel vs CRAO is all 4 quad

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43
Q

Indications for a diabetic retinal examination

A

initial examination should be done within 3-5 years after diagnosis

  • pts w/ no DR, repeat exam every year
  • pts w/ mild to mod retinopathy, repeat every 6-12 months
  • pts with severe NPDR or PDR, repeat examinations every 2-4 months
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44
Q

Myelinated nerve fiber

A

congenital, benign, white patches in the superficial retina with feathery edges that represent abnormal myelination of GC axons anterior to the lamina cribosa

  • can obscure retinal vessels and located near the optic nerve usually
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45
Q

what’s the leading cause of blindness in the US?

A

DR

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46
Q

What’s the most important risk factor for the development of DR?

A

duration

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47
Q

DR

A
  • occurs b/c loss of pericytes and damage to the retinal capillary BM causing breakdown of the BRB
  • DR can be broken down into NPDR and PDR
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48
Q

What’s the diagnosis for a severe NPDR?

A

when a pt meets one of the three criteria 4-2-1 rule

HVI
- retinal heme in all 4 quads
- 2 quads of venous beading
- 1 quad of irma

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49
Q

What’s the diagnosis for very severe NPDR?

A

2 or more criteria is met within the 4-2-1 rule

HVI
- retinal heme in all 4 quads
- 2 quads of venous beading
- 1 quad of irma

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50
Q

PDR

A
  • dx based on the presence of neo in a pt w/ DR

High risk characteristics:
-NVD: neo of the disc greater than 1/4 disc diameter within 1DD of ON
-NVD or NVE w/ associated vitreous or preretinal heme

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51
Q

What are the signs and sx of PDR?

A

sx: asymptomatic, may experience blurred vision, metamorphopsia

signs: numerous signs of DR, most important threats to vision include macular dz and neo

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52
Q

What are the threats to vision from a macular dz?

A
  1. Macular ischemia - may look normal or thickened, HYPOfl on FA
  2. Macular edema - can occur at any stage of DR CSME

** FA can differentiate between macular ischemia vs edema**

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53
Q

What’s the criteria for dx DR CSME

A
  1. retinal thickening within 500um (1/3 DD) of the foveal center
  2. Hard exudates within 500um of the foveal center with adjacent retinal thickening
  3. Retinal thickening of 1DD within the foveal center
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54
Q

Threats to vision from neo include the following

A
  1. Preretinal/vitreous heme
  2. Neovascular glc
  3. Tractional retinal detachment
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55
Q

HTN retinopathy

A
  • BP must typically be at least 140/110 for the latter stages of HR to occur
  • autoregulation is altered at extremely high or chronically elevated systolic pressures and retinopathy results
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56
Q

What are the signs and symptoms of HR

A

sx: asymptomatic, unless there is presence of ME (macular star), papilledema, serous retinal detachment or vein occlusion

signs: bilateral but asymmetric

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57
Q

What are the signs and symptoms of OIS?

A

Sx: gradual vision loss, dull periorbital pain or headache, amaurosis fugax

signs: unilateral, dot/blot heme of the mid-peripheral fundus, dilated, narrowed retinal arteries and possible neo of the disc and/or ant seg (67% of pts with OIS have NVI/NVA at the time of diagnosis)

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58
Q

What if a pt had HR retinal findings AND a carotid artery obstruction what would the condition be called?

A

venous stasis retinopathy

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59
Q

What if pt had presence of both posterior and anterior segment signs of HR what would the condition be called?

A

OIS, common in male 50-70yo

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60
Q

What is OIS commonly associated with?

A

HTN, DM, cardiac dz; the latter is most common cause of 40% of a 5 yr mortality rate

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61
Q

Amaurosis fugax

A

TIA characterized by monocular vision loss that typically lasts seconds to minutes; vision returns to normal after an ischemic event

most common cause is a carotid artery embolus

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62
Q

TIA

A

characterized by temporary neurologic deficit due to transient loss of blood flow to the brain. Perfusion is always restored in less than 24 hours, resulting in complete resolution of the pts sx without any permanent damage

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63
Q

stroke

A

characterized by a permanent neurologic deficit due to prolonged loss of blood flow that results in irreversible damage to the brain

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64
Q

Hyperviscosity retinopathy

A
  • increase resistance to blood flow 2’ to elevated levels of plasma proteins, RBC, and/or WBC, resulting in impaired circulation of blood flow causing damage to walls of the vessels, leaking of fluid, and retinal ischemia
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65
Q

What is the most common cause of hyperviscosity retinopathy? What else is it associated with?

A

hyperglobulinemia - a condition found in waldenstrom’s macroglobulinemia, multiple myeloma, serum positive RA, SLE, HIV infection

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66
Q

What are the signs of hyperviscosity?

A

Retinal venous dilation, retinal heme, CWS and exudates, CRV may also occur and is bilateral in 10% of pts

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67
Q

HIV retinopathy

signs/sx?

A

most common ocular manifestation of HIV/AIDS

Signs: CWS and retinal heme, similar to DR and early CMV retintitis
Sx: asymptomatic, non-infectious

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68
Q

Interferon Retinopathy

A
  • Pts on interferon therapy can develop retinal findings similar to DR, CWS, and retinal heme in the posterior pole
  • retinopathy occurs 3-5 months after interferon is started and tends to resolve w/o tx after interferon has been discontinued
  • Pts on interferon therapy without retinopathy should be followed every 4-6 months; if retinopathy is present, f/us should occur more frequently
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69
Q

Talc retinopathy

A
  • Presents bilaterally in IV drug users who use talc as a filler
  • talc gets caught in the retinal capillaries and will appear as multiple, yellow, refractile deposits that tend to be clustered near the macula
  • talc may cause capillary occlusion and retinal ischemia
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70
Q

Vascular sheathing/periphlebitis

A
  • inflammatory condition by exudates around the vessels (seen as white cuffing of the vessels
  • retinal edema, ischemia, and heme
  • vessel walls will stain on FA
  • most common in syphilis, sarcoidosis (candle wax dripping), pars planitis, and sickle cell dz
  • testing should be done and case hx
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71
Q

Describe stage 1-4 for HR

A

Stage 1: arterial attenuation
Stage 2: Stage 1 + AV nicking and exaggeration of arterial light reflex
Stage 3: Stage 2 + color. CWS, hard exudates (likely star config) within the OPL radiating away from the fovea, retinal edema
Stage 4: Stage 3 + papilledema (malignant HTN), send to ER IMMEDIATELY, HIGH RISK OF STROKE. BP at this stage is usually 220/120

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72
Q

HTN is associated with which 2’ conditions that can lead to vision loss?

A

NAION, retinal macroaneurysm, vascular occlusion, ocular motor nerve palsies, Worsening of diabetes

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73
Q

Elschnig spots vs Elschnig pearls

A

spots = choroidal infarcts that occurs with HR

pearl = post cataract sx, usually tx w/ Nd:Yag

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74
Q

Which drug is associated with an NAION?

A

Viagara

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75
Q

Retinal artery Macroaneurysm (RAM)

signs/sx

A
  • more common in elderly W, 7th decade
  • asymptomatic but can have gradual vision loss from ME or sudden vision loss from vit heme
  • unilateral focal area of dilation in the retinal artery (100-250um in diameter) with multi-level hemorrhage (subretinal, intraretinal, preretinal and/or vit heme) from a ruptured aneurysm with surrounding circinate exudates, often located at AV crossing
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76
Q

OIS/venous stasis retinopathy

A
  • more common in men, ages 50-80
  • occclusion of the ICA and/or ophthalmic artery (less common), usually 2’ to atherosclerosis; may occur as a result of GCA
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77
Q

Idiopathic Juxtafoveolar Retinal Telangiectasia (IJXT)

A

abnormal perifoveal capillaries present within the juxtafoveal region (1-199um from the center of the fovea)

Divided into 3 categories
1. Unilateral congenital form - 40 yo M, 20-25-20/40 VA
2. Unilateral idiopathic form - middle aged men; 20/25 or better VA
3. Bilateral acquired form - M&F 5th-6th decade, poor visual prognosis

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78
Q

What are the signs and sx of IJXT

A

sx: decreased vision

sign: right angle venules and dilated tortuous vessels, hemes, varying degrees of exudate (moderate to none at all) within or nearby the fovea, macular edema, and or CNVM

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79
Q

Coat’s dz

A
  • Male less than 20 yo
  • 2/3 of cases present prior to 10yo
  • progression is more rapid under 4yo, stimulating retinblastoma
  • idiopathic peripheral vascular dz, if left untreated will gradually progress to total exudative detachment
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80
Q

What are the signs/symptoms of coats dz

A

sx: decreased vision, strabismus, leukocoria

signs: Unilateral, telangiectatic dilated vessels that display a characteristic “light bulb” appearance
- progression can lead to marked hard exudates (classic for coat’s)
- intraretinal heme, exudative retinal detachment, NVG ( results in red, painful, blind eye)

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81
Q

A chronic extensive serous detachment in Coat’s dz results in?

A

Retinal ischemia –> which leads to devel. of ant seg neo

  • similar to DR VOS conditions
  • NVA and NVI result in NVG
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82
Q

Retinopathy of prematurity (Retrolental fibroplasia)

A
  • occurs in premature infants (less than 32 weeks)
  • low birth weight infants (<1500) who have recieved oxygen therapy
  • Immature blood vessels vasoconstrict and stop developing in response to high concentration, leading to proliferative retinopathy.
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83
Q

What are the threats to vision with ROP

A

pretinal vitreous heme and tractional retinal detachment

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84
Q

What are the signs for ROP?

A

leukocoria, strabismus, vitreoretinal traction, preretinal/vitreous heme, and TRD

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85
Q

Leukocoria

A

white pupillary reflex that results from fibrovascular scarring 2’ to TRD and in cases of ROP

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86
Q

What’s the LAST area to achieve mature vascular developement during 9th month of gestation?

A

anterior temporal retina

this area is most susceptible to neo and subsequent TRD in pre-term infants with ROP

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87
Q

What’s the area that’s most susceptible to neo and TRD in pre-term infants with ROP?

A

anterior temporal retina

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88
Q

What’s the most common intraocular malignancy in children?

A

Retinoblastoma

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89
Q

What’s the 2nd most common intraocular malignancy tumor of all age groups?

A

choroidal melanoma

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90
Q

Retinoblastoma

A
  • most common intraocular malignancy in chidlren
  • 95% of cases dx by the age of 5
  • no gender or race predilection
  • tumor derived from cells in developing retina (retinoblast) as a result of mutations to the retinoblastoma (Rb) tumor supressor gene

Bilateral = heretable retinoblastoma (40%)
Unilateral = non-heritiable (60%)

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91
Q

What are the signs and sx of retinoblastoma

A
  • leukocoria, strabismus, intraocular inflammation, decreased vision (depending on tumor size and location)
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92
Q

Differentials for leukocoria

A
  • Coats dz, Rb, toxocariasis, ROP
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93
Q

Congenital Hypertrophy of the retinal pigmented epithelium (CHRPE)

signs:

A
  • congenital w/ no race or sex predilection

Signs;
- benign, pigmented (brown to black), non-progressive lesions with sharp borders and central hypopigmented lacunae
- unilateral and solitary, measuring 1-6mm in diameter (aka bear tracks)
- Atypical CHRPE; bilateral, multifocal (4 or more), tear shaped, with a hypopigmented border on one end

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94
Q

What is an atypical CHRPE associated with?

A

Gardner’s syndrome

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94
Q

Choroidal nevus

A
  • most common in whites
  • benign focal accumulation of melanocytes within the choroid
  • thought to be present at. birth and are typically non-progressive
  • ANY growth should cause concern for malignant melanoma, 10% of suspicious nevi progress to malignant melanoma
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95
Q

What are the most significant risk factors for transformation into choroidal melanoma?

A

“To find small ocular melanomas, use helpful hints”
T = thickness (elevation >2mm)
F = fluid (subretinal)
S = symptoms (blurred vision, floaters)
O = orange pigment (lipofuscin on the surface of the lesion)
M = margins (irregular borders)
UH = ultrasonographic hollowness (acoustically hollow with low internal reflectivity)
H = halo absence

nevus should be sus if it has a large diameter >4DD or 6mm and close proximity to the ON and often contains overlying drusen

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95
Q

What are the signs of choroidal nevi

A

lesion is flat or slightly elevated, less than 5mm in size, contains overlying drusen

96
Q

What’s the most common primary intraocular malignancy?

A

choroidal melanoma

97
Q

ARMD

A
  • retinal dz of the RPE, bruch’s and choriocapillaris
  • common in pts >50 yo, 2nd leading cause of blindness for pts 45-64 yo
  • exudative ARMD is the chief cause of vision loss over age 50
98
Q

What’s the first and second common cause of blindness?

A
  1. diabetes
  2. ARMD
99
Q

What are the risk factors for ARMD?

A
  • increasing age (75 yo and older)
  • ethnicity (caucasians most at risk)
    • fam hx
  • light iris color
  • smoking
  • hyperopia, HTN, hypercholesterolemia
  • female gender
  • cardiovascular dz
  • nutritional factors and light toxicity
100
Q

what’s the HIGHEST risk factors for ARMD?

A
  • hyperopia >0.75D
  • current smokers
  • Choroial neo

about 2.5X increased risk for all of the above

101
Q

Nonexudative ARMD

A
  • 85-90% cases of ARMD
  • characterized by the presence of drusen (hallmark), RPE abnormalities (mottling, granularity, focal hyperpigmentation) may also be present
  • most do not have severe vision loss, metamorphopsia, gradual vision loss (over months to years), and blurred vision are common complaints
  • 12% of all dry ARMD will develop severe vision loss (defined of loss >6 lines); majority of this is due to GA
102
Q

What are the risk factors that increase the risk of progression from dry to wet ARMD?

A

Multiple soft drusen (esp if it’s confluent)
Focal hyperpigmentation
HTN
Smoking

103
Q

Exudative ARMD (wet ARMD)

A
  • 10-15% of cases of ARMD
  • 88% of legal blindness is attributed to wet ARMD
  • common sx of wet ARMD include metamorphopsia, central scotoma, and rapid vision loss
  • characterized by drusen that are associated with signs of a CNVM can leak blood or plasma into 2 potential places: sub RPE or subretinal
104
Q

What are the 4 potential presentations of wet AMD?

A
  1. subretinal heme (blood under retina)
  2. sub RPE heme (blood under RPE)
  3. subretinal detachment (plasma under retina)
  4. sub RPE detachment (plasma under RPE) AKA PED
105
Q

T/F PED can occur with dry ARMD

A

T

aka drusenoid pigment epithelial detachment, CNVMS can occur overtime with drusenoid PEDs

106
Q

FA can be used to detail exact area of leakage:
what’s the difference between classic and occult leakage?

A

Classic CNVMs = well-defined membrane that fills with dye during the early phases of FA

Occult CNVMs = poorly-defined membrane with late-appearing and less intense leakage

107
Q

What does predominantly classic mean?

A

Most pts with wet AMD have both classic and occult CNVMS

this means that over 50% of the entire lesion is composed of classic CNVM

108
Q

involvment of the fellow eye with wet AMD is what percent for overall 5 year risk range?

A

overall 5 year risk ranges from 40-80%

109
Q

Central Serous Chorioretinopathy (CSCR)

A
  • middle-aged men with type A personality
  • associated with stress, pregnancy, steroid use, hypochondriasis, and HTN
  • recurrences occur in as high as 50% of cases
  • unknown etiology
  • CSR results in RPE or choroidal dysfunction, accumulation of submacular serous fluid
110
Q

What are the signs and symptoms of CSR

A

symptoms;
- unilateral w. sudden onset of blurred vision (20/20 to 20/200)
- metamorphopsia, or scotoma

signs:
- localized macular serous detachment, 3% will have RPE detachment
- FA will show smokestack appearance
- hyperopic shift
- loss of fovea light reflex
- pts often permanent residual RPE changes within the macula after resolution of condition
- will improves without tx 1 to 3 months

111
Q

Histoplasmosis

A
  • Rare in AA, most common in the Ohio-Mississippi river valley
  • Infection caused by Histoplasma capsulatum, a fungus that grows in the soil and material contaminated with bird or bat droppings
  • Recurrences of histo (30%) occur through preexistent histo spots
  • If spots are present on the disc or macula, the chance of a sx recurrence is approx 20% over 3 years
112
Q

What are the s/s of histo?

A

Asymptomatic unless maculopathy develops, earliest sx is metamorphopsia

Signs: bilateral choroiditis and the clinical triad of bilateral peripapillary atrophy of the ON, multifocal lesions in the periphery and maculopathy (including CNVM)
- the vitreous is always clear in histoplasmosis **
- CNMV is a late manifestation, 20-45 yo

113
Q

Toxoplasmosis vs histoplasmosis

A

Toxo
- parasite causing retinitis
- WBCs in the vitreous due to break down of BRB
- ONE EYE ONE LESION

Histo
- vitreous is always clear!!
- caused by a fungus that leads to choroiditis
- BOTH EYES MULTIPLE LESION

114
Q

What’s the histoplasmosis triad?

A
  • bilateral peripapillary atrophy of the ON
  • multifocal lesions in the periphery
  • Maculopathy
115
Q

Pathological myopia

A
  • genetic predisposition with globe elongation in early childhood
  • mostly in women in young adulthood
  • aka myopic degeneration
  • refractive error >-6.00
  • spherical equivalent and/or on an axial length >26.5mm
  • axial lengthening in the antero-posterior direction results in scleral thinning and choroidal atrophy
116
Q

What are the signs and symptoms of myopia degeneration

A

sx:
asymptomatic, decreased vision, metamorphopsia

Signs:
- Macular and posterior pole: posterior staphyloma (hallmark), posterior bulging of weakened sclera, oblique insertion of the ON, fuch’s spots (focal subretinal hperpigmentation 2’ scarring or CNVM) , lacquer cracks, macular holes
-peripheral signs: lattice degeneration, snail track degeneration, paving stone degen, retinal breaks, retinal detachment
- non-retinal signs: NS and especially PSC, extensive vitreous syneresis, PVD

117
Q

Signs of mac degen on the mac/posterior pole

A

posterior staphyloma (hallmark), posterior bulging of weakened sclera, oblique insertion of the ON, fuch’s spots (focal subretinal hperpigmentation 2’ scarring or CNVM) , lacquer cracks, macular holes

118
Q

Signs of mac degen in the peripheral retina?

A

lattice degeneration, snail track degeneration, paving stone degen, retinal breaks, retinal detachment

119
Q

Signs of mac degen that is non-retinal

A

NS and especially PSC, extensive vitreous syneresis, PVD

120
Q

Lacquer cracks

A
  • occur in about 5% in myopes
  • fine yellow irregular lines that represent a large break in bruchs
  • CNV can lead to severe vision loss
  • lacquer cracks present in young males and may be one of the earliest findings in pathological myopia
121
Q

Pavingstone degeneration

A
  • discrete, circular areas of yellow-white chorioretinal atrophy in the retinal periphery
  • aka cobble stone degen
  • no clinical importance
122
Q

ERM

A
  • F older than 50
  • may be caused by PVDs, retinal breaks, cataract or other intraocular surgeries, and trauma
  • the result of glial cell proliferation, escapes from a small hole of ILM
123
Q

What are the signs and symptoms of ERM?

A

sx: blurred vision, metamorphopsia

signs: mild ERMS are characterized by fine, glistening membranes (cellophane maculopathy), advanced ERMs appear as thick, gray-white membranes with assoc. membrane folds (macular pucker)

** most pts with ERM have PVDs**

124
Q

Macular hole

A
  • 85% of cases are assoc with aging
  • mostly F
  • results from VT on the macula, most commonly idiopathic (senile), trauma, sx, trauma, or inflammation
  • bilateral onset of 25-30%
  • risk of developing hole in the fellow eye 5-16%
125
Q

What are the signs and sx of a macular hole

A

sx: decreased vision, metamorphopsia

signs: round, red, well-delineated spot in the macula

126
Q

Describe the 4 stages of a macular hole

A

Stage 1: yellow spot or ring at the fovea

Stage 2: round, small, FT hole w/ pseudo-operculum

Stage 3: Large FT hole w/ operculum. Positive watkze allen sign

Stage 4: stage 3 plus PVD

127
Q

A positive watzke-allen sign means what?

A

complete break of a thin light on the macula = stage 3 (large FT hole w/ operculum)

128
Q

Macular Photostress test

A
  1. Measure BCVA
  2. shine a light 2cm from the pt for 10 sec
  3. time the amt of time it takes for the pt to read one line less than the BCVA

normal recovery is less than 60 seconds

129
Q

Choroidal folds

A
  • folds within the choroid, RPE, and bruchs
  • dark and light striations due to mechanic stress on or within the choroid
  • may lead to reduced VA and metamorphopsia
130
Q

What causes choroidal folds?

A

systemic conditions that causes stress on the choroid - choroidal, optic nerve, or orbital tumor
- posterior scleritis, choroidal inflammation, choroidal detachment
- Thyroid-related ophthalmopathy
- orbital myositis
- hypotony
- intracranial HTN

131
Q

Albinism

A
  • mutation in gene responsible for melanin
  • may affect the skin and eyes (oculocutaneous albinism) or eyes only (ocular albinism)
132
Q

What are the s/s of ocular albinism

A

sx: hypopigmentation of skin and fundus, iris translucency, foveal hypoplasia, ON hypoplasia, microcornea, nstagmus, strab, misrouting of ON fibers through the optic chiasm

signs:
- photophobia and reduced VA
- severity depends on degree of iris/fundus hypopigmentation and foveal hypoplasia

133
Q

What condition is associated with Hermansky-Puldak and Chediak-Higashi syndromes?

A

Albinism

134
Q

RP

A
  • most common retina dystrophy
  • AD, non-heritable or heritable
  • associated w. usher’s syndrome
  • avg age of dx 9-19
  • progressive loss of PR and RPE function
  • rod damage is more dominant compared to cones
135
Q

What’s the most common retinal dystrophy?

A

RP

136
Q

What condition is associated with usher’s syndrome

A

RP

137
Q

Usher’s syndrome

A
  • AR
  • congenital hearing loss
138
Q

What are the s/s of RP

A

sx: night blindness, peripehral vision loss (only dim in early stages), takes years for zx to develop; by 30yo, over 75% of pts are symptomatic

signs: retinal bone spicules pigmentation, arteriolar attenuation, waxy optic disc pallor, PSC, ERM, CME

other signs = keratoconus, myopia, progressive contraction of VF, annular scotomas that may progress to central vision loss in the late stages of RP

139
Q

What are the central findings for RP?

A

PSC, ERM, CME

140
Q

What can be used for early dx of RP?

A

scotopic ERG will be reduced, photopic ERG will be normal

141
Q

Stargardt’s dz

A
  • most common hereditary macular dystrohy
  • onset 1st-2nd decade of life betw ages 6-20
  • AR
  • no sex predilection
  • mutation of ABCA4 transmembrane protein that’s responsible for moving all-trans retinal from the PR disc lumen to the cytoplasm causing toxic accumulation of all trans-retinal within the PR disc, leading to degen of PR and RPE
  • same as fundus flavimaculatus
142
Q

Funuds flavimaculatus

A
  • same as stargardt’s dz but reserved for pts WITHOUT macular dystrophy signs
  • presents later in life 4th-5th decade
  • asymptomatic
  • vision loss can still occur if fleck lesions involve the macula
143
Q

What are the s/s of stargardts?

A
  • rapid vision loss and color vision abnormalities
  • level of vision decr is often out of proportion with fundus appearance in the early stages of dz
  • acuity is 20/200 by third decade and is stable or slowly progressive thereafter

signs:
- early stages: bilateral yellow flecks, pisciform config throughout post pole and mid-periphery, non specific RPE mottling of macula may also be apparent
- Late stages: beaten bronze macular appearance (bulls eyes maculopathy) and salt and pepper pigmentary changes in the periphery
- ERG is normal in early stages of d but becomes abnormal as the condition progresses

144
Q

Choroiderma

A
  • X-linked = only affects male, females are carriers
  • onset first decade
  • deficiency of rab geranyl-geranyl (enzyme for membrane metabolism)
145
Q

What are the signs and symptoms of choroiderma?

A
  • night blindness and peripheral vision loss
  • men will be affected first 10 years = total night blindness
  • Females are benign and non-progressive
  • most have good vision until 50-60 yo

signs:
- macular is spared until end stage
- progressive, bilateral atrophy of the RPE and choriocapillaris, exposure of underlying sclera

146
Q

What are other conditions that can cause night blindness?

A

RP, choroiderma, gyrate atrophy (non-exhaustive list)

147
Q

Cone dystrophy

A
  • AD
  • 1st-3rd decade
148
Q

What are the s/s of cone dystrophy

A
  • worst during the day
  • severe color vision loss
  • photophobia
  • vision deteriorating to 20/400 by 4th decade

Signs:
- abnormal ERG, cone function
- late: vessel attenuation, geographic atrophy w/ bulls eye macular appearance, temporal pallor, severe deutan-tritan color defects, an abnormal photopic ERG, fine nystagmus

149
Q

differential dx for bulls eye maculopathy

A

stargardt’s, progressive cone dystrophy, chloroquine, hydroxychloroquine toxicity and thioridazine

150
Q

Gyrate atrophy

A
  • AD
  • deficiency in mitochondrial ornithine aminotransferase
  • ornithine blood plasma is high (helps with dx)
151
Q

What are the s/s of gyrate atrophy?

A
  • nyctalopia, decreased vision, constricted VF

signs:
- scalloped areas of peripheral chorioretinal atrophy
- lesions begin in the mid periphery in childhood during childhood and then coalesce to engulf most of the posterior pole, with the macula being spared until the 4th to 7th decade
- assoc with posterior subcapsular cataracts, high myopia, astig

152
Q

Best’s dz

A
  • AD
  • onset early childhood 5-10 years
153
Q

What are the s/s of best dz?

A
  • little to no sx until the age of 50 (75% better than 20/40)
  • eventually will complain about decreased vision

signs:
- accumulation of lipofuscin = egg yolk appearance (subfoveal)
- can remain stable until mid-age
- bilateral, yellow, subfoveal egg yolk lesion.

154
Q

Describe the 5 stages of best dz

A
  1. Previtelliform: abnormal EOG (Arden ratio <1.8), usually asymptomatic
  2. Vitelliform: egg yolk appearance at the macula btw ages 3-15 yo
  3. Pseudohypopyon = egg yolk blister under the retina causing a cyst under the retina
  4. Vitelliruptive: scrambled egg appearance = visual loss expected at this stage
  5. End stage: CNVM, heme, atrophy, macular/scarring = moderate to severe vision loss
155
Q

What would testing looking like for best dz?

A

abnormal EGO but normal ERG in early stages

156
Q

Adult foveomacular vitelliform dystrophy

A
  • ages 30-50 yo
  • looks similar to best dz
  • overall prognosis is better with minimal metamorphopsia, mild acuity loss, normal EOG and ERG and slight tritan color defect
157
Q

Rhegmatogenous RD

A
  • caused by an atrophic hole or tractional tear
  • M older than 45 yo
  • # 1 cause myopia
  • other causes: lattice degeneration, PVD, ocular sx, trauma
  • retinal breaks that allows vitreous to enter the subretinal space (separation of sensory retina and RPE)

BREAK = atrophic holes and tractional tears

158
Q

Atrophic holes

A

round, small, full-thickness defects that are NOT associated with vitreoretinal traction and therefore have low risk for subsequent detachment
- located S/T
- chronic atrophy of sensory retina

159
Q

Retinal tears

A
  • flap and operculated tears
160
Q

Horshoe tear

A

uneven VT
- vitreous stays attached to the flap

161
Q

Operculated tears

A

even, symmetric tear
- vitreous pulls away from the tear, VT no longer exist

162
Q

Lattice degeneration

A
  • can cause RRD 6-10%
  • peripheral retinal thinning (cigar-shaped and concentric with the ora serrata)
  • not everyone will have a crisscross pattern
  • bilateral, S/T
  • contain an atrophic hole 25%
  • thinned retina
  • retina tears can result from VT on the atrophic, thinned retina
163
Q

What are the s/s of RRD

A
  • vitreous flashes, floaters, curtain veiling and decreased VA
  • we don’t care about the location of the flash only the VF defect
  • if the field defect is reported in the inferior nasal quadrant, a superior temporal retinal break is expected

signs:
- vary in acute and chronic RDs
- Acute RD: Shafer’s sign, mild iritis, lower IOP
- Chronic RD: pigment demarcation line (takes 3 months or longer to form), intraretinal cyst (1 year to develop), fixed folds, subretinal precipitates

164
Q

most likely location for a retinal break in pts with RRD

A

S/T, 50% of eyes will have more than 1 retinal break (usually located 90 degrees from one another)

165
Q

Which systemic conditions can present with lattice-like lesions (atypical lattice) that incr the pts risk of an RD

A
  • Marfan’s
  • stickler sydnrome
    -ehlers danlos
166
Q

Vitreoretinal tufts

A
  • small, focal areas of vitreous traction located in the retinal periphery
  • occur in 5% of the population and are the 2nd most common peripheral retinal lesion assoc w/ RD
  • less than 1% of pts with vitreoretinal tufts develop a RD
167
Q

What can cause a nonrheg RD?

A
  • serous (exudative) RDs and traction RDS
  • DRVOS (traction RD)
    -CHBALA (Exudative)
168
Q

Exudative RDs

A
  • CHBALA
  • damage to the RPE allowing fluid to accumulate under the retina
  • ARMD, scleritis, coat’s dz, choroidal melanoma, coloboma
  • usually asymptomatic unless the detachment involves the macula
169
Q

Traction RDs

A
  • caused by PDR, ROP and proliferative sickle cell retinopathy
  • may be asymptomatic
  • decreased vision or progressive VF defects (may remain stationary for years)
170
Q

Age- Related Degenerative Retinoschisis

A
  • more common in 40 yo or older
  • splitting of the OPL and INL, resulting in the inner retina that mimics retinal detachment
171
Q

s/s of Age-related degenerative Retinoschisis

A
  • usually asymptomatic, vision loss is rare

signs:
- dome-shaped bullous elevation most commonly located inf/temporal
- immobile, bilateral findings common
- absolute VF defect will correspond to the area of elevation
- 70% hyperopic
- snowflake or frosting and sheathed retinal vessels occur in the elevated retinal layer of retinoschisis

172
Q

Which one is more dangerous outer wall breaks or inner wall breaks of retinoschisis?

A

outer wall breaks are more dangerous - the are required to cause a retinoschisis-associated RD
- will appear “pock-marked” on scleral depression

172
Q

Angioid streak

A
  • Large break in bruchs, damage elastic core of bruch’s membrane
  • 50% are idiopathic
  • PEPSI common cause of angioid streaks
173
Q

PEPSI

A
  • causes of angioid streaks
  • pseudoxanthoma elastic
  • ehlers danlos
  • Paget’s
  • sickle cell
  • idiopathic
173
Q

s/s of angioid streak

A
  • asymptomatic, or profound vision loss, CNVM, 70% will eventually have vision loss

signs: spoke-like (around optic disc), linear, well-demarcated red/orange or brown lines (depending on amt of pigment involved), within the elastic core of bruch’s

174
Q

Toxocariasis

A
  • caused by toxocara canis or cati, nematode in dogs or cats
  • most common in children and young adult eating dirt or infected food/water, direct contact with infected puppies or kittens
175
Q

s/s of toxocariasis

A

sx; floaters and blurred vision

sign: unilateral inflammatory response, ON edema, Rd, vitritis, endophthalmitis, subretinal granulomas, chorioretinal scars present after active infection has resolved

176
Q

Chorioretinitis

A

form of posterior uveitis that is characterized by inflammation of the choroid and retina
- caused by toxoplasmosis, toxocariasis, sarcoid, syphilis, CMV, serpiginous chorioretinopathy, TB, onchocerciasis

177
Q

Acute posterior multifocal placoid pigment epitheliopathy

s/s?

A
  • young adults, typically after viral illness
  • bilateral, yellowish, flat subretinal lesions
  • disc edema and RD may occur
  • resolves without tx for a few weeks
178
Q

Central Areola Choroidal Dystrophy

A
  • AD
  • bilateral large areas of GA in the macula
  • will cause vision loss in 4th-5th decade
    poor prognosis
179
Q

Senile choroidal atrophy

A
  • results in choroidal thinning and may cause an exaggerated tigroid fundus appearance due to increased visibility of the choroidal vasculature
180
Q

Mostly likely source of of an optic neuropathy

A

glaucoma

181
Q

Ocular HTN

A

IOP > 21 mmHg
- open angle without glaucomatous optic neuropathy
- risk factor for conversion into POAG - IOP, AA, fmhx, age >55 yo, thin corneas < 555

182
Q

normal CCT?

A

555um

183
Q

POAG

A
  • glaucomatous ON damage** w/ corresponding VF defect, IOP>21, open angle on gonio
  • Large C/Ds, asymmetry btw ON, focal vertical thinning or notching, NF bundle defects, vascular signs (baring, heme), the larger the optic disc, the larger the expected cup size
  • doesn’t follow ISNT rule
  • nasal step, paracentra, and arcuate most common VF defect
  • asymptomatic until later stages when peripheral or central vision is lost
184
Q

Port-Wine Stain

A

vascular birthmarks that hive high association w/ ipsilateral glc
- mostly assoc w/ sturgers web syndrome

185
Q

Pseudoexfoliation OAG

A
  • caucasians esp scandanavians descent
  • abnormal, white, flaky deposits
  • flaky deposits are found throughout the body and mya have systemic implications
  • can be found on pupillary margin, lens capsule in a bulls eye pattern, on lens zonules, and TM
  • gonio reveals sampaolesi’s line (pigmented schwalbe’s)
  • accumulation of pigment rub against the posterior iris epithelium releasing pigment
  • assoc with poor pupil dilation and increased risk of lens subluxation and cat sx complications due to weak zonules
  • unilat or bilat, risk of devel glc in 15% within 10 years
186
Q

Sampaolesi’s line

A

increased pigmentation anterior to schwalbe’s line, associated with PXF and PDS

187
Q

Pigment dispersion glaucoma

A
  • bilateral, caucasians, young pts (30-40s), more common in myope males
  • PDS result from higher AC that causes excessive bowing of the iris posteriorly, resulting in more contact between iris and lens zonules causing shedding of pigment off the posterior edge of the iris
  • asymptomatic, blurred vision, halos around lights after exercising or pupil dilation
  • TID, krukenberg spindle, pigment on ant capsule/lens/iris surface, and TM hyperpigmentation
  • risk of glc 5 years is 10%, risk for 15 years is 15%
188
Q

Angle recession glc

A
  • wide open angle with recessed iris and widened CBB
  • unilateral from blunt trauma
  • TM is damaged resulting in increased risk of glc over time
189
Q

NTG

A
  • type of POAG
  • NFL damage occurs at lower pressures w/ IOP <21mmHg
  • open angle and glaucomatous ON damage w/ corresponding VF
  • Japanese F, vascular disorders (Raynaud’s phenomenon or migraines), low BP, sleep apnea, hypercoagulation, taking BP meds before bedtime (may decrease ocular perfusion pressure)
  • important to take diurnal IOP readings to ensure the pt has NTG
  • drance heme more common in NTG
  • more focal but more dense and closer to fixation b/c the temporal and inferotemporal rim tissue is more commonly affected first
190
Q

If pt has NTG, what important health hx should you ask about?

A
  • hemorrhagic shock, myocardial infarction, anemia, syphilis, vasculitis

important to rule out other sources of optic neuropathy

191
Q

Primary angle closure glc

A
  • can be acute or intermittent
  • results from PC pushing on peripheral iris anteriorly into contact with TM. blocking part or all TM and flow of Aqueous outflow
192
Q

What are the 2 causes of ACG

A

pupillary block (more common) and plateau iris syndrome

  • pupillary block is anatomically narrow angles, more often in hyperopes, post DFE (mid position after coming down from DFE) - point of greatest iris-lens contact, advancing cataracts, asians/eskimos, lens sublux
  • Pleateau iris characterized by anteriorly position ciliary processes that push iris forward into contact with TM, flat iris plane, normal AC, convex peripheral iris
  • tx LPI or iridectomy
193
Q

sub-acute angle closre or chronic angle closure

A
  • occurs when part of the angle closes causing episodes of elevated IOP w/o sx
  • more common than acute angle closures
  • chronic angle closure should be expected in pts with occludable angles and any of the following signs : PAS or pigment splotching on TM, progressive ON damage with corresponding VF losss
194
Q

Acute angle closure

A
  • angle closure (No TM visible w/ gonio)
  • acute elevation in IOP 50-100mmHg and pt sx
  • vomiting, intense ocular pain, HAs, haloes, nausea, and progressive vision loss
  • prominent signs include hazy cornea, mid-dilated pupil that responds poorly to light, ciliary flush, and glaucomflecken
  • IOP must be quickly lowered so that corneal edema will resolve, allowing for peripheral iridotomy
195
Q

Glaucomflecken

A
  • anterior subcapsular opacities that result from lens epithithelal cell ischemia and necrosis 2’ to high IOP
196
Q

the greatest threat to vision in an acute angle closure

A

CRAO (IOP is higher than the perfusion pressure)

197
Q

Topamax (topiramate)

A
  • treat migraines, weight loss, and epilepsy, can cause 2’ acute angle closure
  • causes supraciliary effusion which causes lens and iris to push forward into contact with the TM
  • occurs within the first month of use or if the dosage is increased
198
Q

T/F pts with angle closure are more prone to developing POAG

A

T b/c it causes damage to the TM and ON
- will cause elevated IOP with optic nerve damage with open angle and may occur immediately or years later after tx of angle closure
- pts with open-angle and narrow-angle have mixed-mechanism (combined) glc

199
Q

What are the most common causes of NVG?

A

1 cause CRVO

2nd PDR
- OIS
- RD

Less common: CRAO, carotid dz

200
Q

NVG

A
  • rubeosis of the iris, ciliary tufts or early sign of neo
  • progression into the AC can cause 2’ angle closure
  • neo of the angle is always accompanied by fibrous tissue that forms over the TM, preventing aqueous outflow
  • a significant fibrovascular membrane can develop even with only 1-2 vessels in the angle
  • fibrovascular membrane can stick to the iris, pulling it into contact with the TM causing 2’ angle closure aka “zippering of the angle”
201
Q

Uveitic glaucoma

A
  • result of PAS and PS formation in uveitis
  • uveitis causes the iris to become inflamed/sticky
  • iris can stick to the lens (PS) or the TM (PAS)
  • PAS will only cause IOP elevation if its 360 deg of attachment between the iris and lens = iris bombe, moving iris anteriorly into contact with the TM
  • PAS will cause varying IOP elevation depending on extent of angel involvement
  • TREAT AGRESSIVELY & IMMEDIATELY
202
Q

Congenital glc

A
  • onset from birth - 3months
  • M, bilateral
  • developmental abnormality of the AC that impedes aqueous outflow
203
Q

Bupthalmos

A

enlarged eye w/ corneal diamter >12mm that occurs by 1 yo with congenital glc as a result of elevated IOP

204
Q

Iridocorneal endothelial syndrome (ICE)

A
  • abnormal corneal endothelium that grows onto the iris or angle increasing risk for glc
  • corneal edema, iris atrophy, PAS, angle closure
  • F age 20-50
  • includes essential iris atrohy, chandler’s syndrome, iris-nevus syndrome
205
Q

Essential iris atrophy

A

iris thinning with resulting heterochromia, polycoria, corectopia, ectropion uveae

206
Q

Chandler’s syndrome

A

corneal endothelium will have a beaten metal appearance with corneal edema and corectopia

207
Q

Iris-nevus syndrome (Cogan-Reese syndrome)

A

Nodules will be present on the anterior iris surface

208
Q

list types of inflammatory glaucoma

A
  • Glaucomatocyclicitic crisis
  • Fuchs heterochromic irdocycltitis
  • Phacolytic glaucoma
209
Q

Glaucomatocyclitic crisis (Posner-schlossman syndrome)

A
  • acute trabeculitis
  • acute elevation of IOP 40-60mmHg
  • few cells in the AC, open angle glc
  • recurrent unilateral episodes that often burn out over time
210
Q

Fuch’s Heterochromic Irdocyclitis

A

chronic, non-granulomatous, low grade ant uveitis w/ stellate keratic precipitates
- iris heterochromia and iris/angle neo
- incr risk of glc due to TM damage, cataracts due to chronic inflammation

211
Q

GDx

A

uses scanning laser polarimetry to detect thinning of RNLF

211
Q

Phacolytics glaucoma

A

results from hypermature cat that lakes material into the AC, resulting in blockage of the aqueous outflow thorugh the TM
- cells, flare, iridescent lens particles will be present within the AC

211
Q

Glaucoma

A
  • characterized by ganglion cell death and corresponding RNFL loss
212
Q

OCT

A

optical coherence tomography

213
Q

HRT

A

uses confocal scanning laser ophthalmology for a topographical eval of the ON and peripapillary retina

214
Q

OCT stratus

A

time domain system

215
Q

Spectralis (Heidelberg) and Cirrus

A

spectral domain system
- better resolution, faster, more sensitive

216
Q

swept source

A
  • newer
  • better than spectral domain b/c of higher sensitivity and speed
217
Q

Instruments that evaluates ganglion cell

A
  • RTVue ganglion cell complex analysis (optovue) = measures 3 innermost macular layers and compares them to the normative database
  • Spectrailis posterior pole asymmetry analysis (Heidelberg) = inter and intra-eye asymmetry analysis
  • Cirrus ganglion cell analysis (Zeiss) = measures ganglion cell IPL complex and compares results to a normative database
218
Q

Gonio

A
  • structure is seen 180 deg away
  • document iris insertion in relation to the TM (steep/flat/concave), neo, PAS, pigmentation, angle recession, iris processes
219
Q

Structure of the angle (posterior to anterior)

A

I CAN SEE THE STUPID LINE

220
Q

Static automated perimetry (SAP)

A

threshold test

221
Q

Short wavelength automated perimetry (SWAP)

A

yellow background with blue stimuli helps detect early glaucoma damage not detected with SAP

222
Q

Frequency doubling technology (FDT)

A

fast (90 sec per eye) screening that uses sinusoidal gratings as the stimulus

223
Q

What is the normal VF for the following

Superior
nasal
temporal
inferior

A

Superior and nasal = 60 deg
temporal = 100 deg
inf = 70 degree

224
Q

Where is the blind spot located? diameter of the blind spot?

A

15-degree temporal, 7.5 degrees in diameter

225
Q

Reliability indices

A
  • include fixation losses, false negative, false positive, short term fluctuations (STF)
226
Q

STF for VF

A
  • determined by retesting certain points
  • poor reliability or early glaucoma
227
Q

fixation loss and false negative is deemed reliable at what percentage for VF?

A

fixation loss >20%

false negative errors >33%

flagged as abnormally high sensitivity or reduced reliability

228
Q

Grayscale of VF

A
  • gross representation of the VF
  • darker areas = reduced sensitivity
  • has minimal value in interpretation
229
Q

Total deviation of VF

A

compares how well the pt performed compared to database of healthy, age-matched samples
- 0 = scored the same as normative database
- (+) = pt did better than expected
- (-) = pt did worse than expected
- the darker the probability box on total deviation probability plot = the greater the pts response deviated from expected response

230
Q

Pattern deviation

A
  • filters out diffuse loss (ex cataracts)
231
Q

Glaucoma hemifield test

A
  • compares sensitivity levels btw upper and lower hemifeilds
  • glc is asymmetric ONH dammage
  • GHT will state WNL, borderline, ONL, or reduced sensitivity
232
Q

VFI - visual field index

A
  • measure rate of VF loss over time is given as a % of the normal
    100% = no vision loss
    0% = total blindness
233
Q

Mean deviation (MD)

A

represents avg of differences between pts overall sensitivity and overall sensitivity of the normative database
- MD is an indication of diffuse loss
- the more negative = the more general depression in the VF

234
Q

Pattern standard deviation (PSD)

A
  • compares pt shape of hill to the normative database
  • indicates focal areas of depression that are typical in glc
  • always shows an absolute value; higher PSD = greater VF loss

KMK (18 decks)

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