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BOARDS > Ocular Disease:posterior > Flashcards

Ocular Disease:posterior Flashcards

1
Q

Hruby Lens

A

◦ Indications: nonctonact examination of the optic disc, macula, posterior pole, and central vitreous
◦ Interpretation: provides a stereoscopic, erect, and magnified image

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2
Q

Three mirror lens indication

A

examination of the retina extending from the optic disc to the ora seratta. Performed in patients with peripheral retinal concerns such as peripheral vascular disease, history of blunt trauma, and those at risk or with symptoms of a retinal detachment

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3
Q

3 mirror lens interpretation

A

provides a stereoscopic, reversed, and magnified image of the retina 180 degrees away from he position of the mirror.

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4
Q

Trapezoid mirror on 3 mirror

A

73 degrees

Evaluate equator

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5
Q

Square mirror on three mirror

A

67 degrees

Used to eval the area between the anterior equator and the ora

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6
Q

Bullet mirror on 3 mirror

A

59 degrees

Anteiror chamber angle and the ora

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7
Q

Are 3 mirror views displaced laterally?

A

No

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8
Q

Indications of 78/90D lens

A

routine posterior segment evaluations. Easier to use than the Hruby lens and the three mirror. Image magnification and FOV are directly proportional to the pupil diameter and the dioptric power of the lens

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9
Q

Image in 78/90D

A

real, inverted, and reversed magnified image

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10
Q

Indications of BIO

A

routine comprehensive evaluation and similar indications as three mirror evaluation

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11
Q

Image in BIO

A

provides a real image that is magnified, reversed L-R, inverted top to bottom, and located between the examiner and the condensing lens

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12
Q

Red free filter

A

‣ The green filter (red free) allows easier differentiated of the nerve fiber layer, choroidal lesions, and retinal vasculature. A red free filter will cause a choroidal nevus to become more difficult to visualize or disappear

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13
Q

Scleral depression

A

◦ Indications: similar indications as a three mirror evaluation. Scleral depression allows oblique viewing of retinal tissue, which increases contrast and allows easier identification of abnormalities
◦ Scleral depression should NOT be performed on patients with recent intraocular surgery or patients with penetrating ocular injury, hyphema, or ruptured globe

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14
Q

Asteroid hyalosis

A
  • epidemiology/Hx: associated with aging; occurs in 0.5% of the population over 60 years of age
  • Symptoms: asymptomatic-does not interfere with vision or cause floaters
  • Signs: numerous small, yellow-white, refractile particles (calcium phosphate soaps) attached to collagen fibrils in an essentially normal vitreous; unilateral in 75% of the cases
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15
Q

Synchysis scintillans

A
  • pathophysiology/Dx: rare conditio nthat occurs after chronic uveitits, vitreous hemorrhage, and/or trauma
  • Signs: unilateral, golden-brown, refractile cholesterol crystals that are freely mobile in the vitreous cavity (often settle inferiorly)
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16
Q

Who gets PVDs

A

more common in females. Prevalence appx age after 50 years old (50% in 50 year old, 60% in 60 year old, etc)
◦ PVDs occur an average of 20 years earlier in myopes than in emmetropes
◦ Other risk factors include diabetes, intraocular surgery, intraocular inflammation, vitreous hemorrhage, and trauma

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17
Q

Pathophysiology of PVD

A

the HA-collagen complex in the vitreous is disrupted with age, causing the collagen to clump up in bundles. Liberated collagen can contract within the complex, causing the posterior hyaloid to detach from the retina. Pockets of liquefaction (syneresis) can travel through the hole in the posterior hyaloid and cause separation between the vitreous and the retina. The PVD can be localized, partial, or total

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18
Q

Symptoms of PVD

A

acute onset floaters, flashes of light, and decreased vision

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19
Q

Photopsia in eyes with acute PVDs

A

Thought to result from traction at the site of the vitreoretinal adhesions

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20
Q

Signs of PVD

A

Weiss ring (black or grey ring shaped vitreous opacity over the optic nerve) and anteiror displacement of the posterior hyaloid; may also see vitreous pigment cells (tobacco dust/Shaffer sign) and a vitreous hemorrhage

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21
Q

Vitreous traction during a PVD

A

can result in ERM, macular holes, vVMT, vitreous and retinal hemorrhages, and retinal breaks. 10-15% of patients with an acute symptomatic PVD will have a retinal break; this risk increases 70% if a vitreous hemorrhage is present. Retinal pigment epithelium can be released into the vitreous (Shaffer’s sign) after a retinal tear, which can aid in the diagnosis

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22
Q

Epidemiology of preretinal/vitreous hemorrhage

A

ask about trauma and pertinent ocular and systemic diseases, especially DM and HTN

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23
Q

Pathophysiology of preretinal/vitreous hemorrhage

A

preretinal and victory’s hemorrhages result from trauma or from conditions that cause retinal neo. These include the following
◦ diabetic retinopathy, retinal vein occlusion, sickle cell retinopathy, ROP, and ocular ischemic syndrome
◦ In each of these cases, the neo is preretinal in location and the newly formed vessels lack endothelial tight junctions. The location (preretinal) and strength (leaky) of these vessels created a situation where vitreous traction can cause shearing of the vessels, resulting in hemorrhage formation

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24
Q

Symptoms of preretinal hemorrhage

A

usually does not cause symptoms unless it involves part of the macula (results in sudden loss of vision or part of the visual field)

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25
Q

Symptoms of vitreous hemorrhage

A

usually causes painless vision loss and/or black spots that can have corresponding flashing lights

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26
Q

Signs of preretinal hemorrhage

A

located between the retina and an intact posterior vitreous face; appears very red and often has a keel shape

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27
Q

Signs of a vitreous hemorrhage

A

located within the vitreous (anterior to the posterior vitreous face). A mild vitreous hemorrhage will be characterized by blood that obscures only part of the fundus. Severe hemorrhages will completely obscure the view of the fundus. Chronic cases will appear yellow
‣ A B scan is indicated if the fundus cannot be viewed throught the vitreous hemorrhage

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28
Q

Types of neo

A

Preretinal and chorodial

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29
Q

Preretinal neo

A

leads to preretinal or vitreous hemorrhage and/or tractional retinal detachement. Remember DR VOS for preretinal neo

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30
Q

Chorodial neo

A

within the subretinal space (CNVM) that results in a subretinal and/or subREP heme, pigment epithelial detachment, and serous retinal detachment. Remember CHBALA for choroidal neo

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31
Q

Epidemiology/Hx of CRVO

A

prevalence 0.1-0.4%. CRVOs are the 3rd most common vascular cause of vision loss (DR is the second most common). An estimated 7% of patients will have a CRVO in the fellow eye

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32
Q

Risk factors for CRVO

A

HTN, DM, cardiovascular disease, and open angle glaucoma

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33
Q

Glaucoma and CRVO

A

◦ Glaucoma is the ocular disease that is most commonly assocaited with CRVOs; up to 40-60% of patients with CRVO have POAG

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34
Q

CRVO in young patients

A

oral contraceptive pills, protein S/C/antithrombin III deficiency, factor XII deficiency, antiphospholipid Ab syndrome, collagen vascular disease, and AIDs

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35
Q

Pathophysiology/Dx of CRVO

A

result from compression of an artery on a vein; this leads to turbulent blood flow, venous vessel wall damage, and thrombus formation. CRVOs are usually caused by a thrombus at or near the lamina cribrosa

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36
Q

Symptoms of CRVO

A

characterized by a sudden, unilateral, painless visions loss in an elderly patient. (90% of patients with a CRVO are > 50 years old)

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37
Q

Signs of CRVO

A

thrombus formation leads to ischemia and release of VEGF which characteristic retinal findings including retinal hemorrhages in all 4 quadrants, collaterals, dilated torturous retinal veins, CWS, and optic disc edema

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38
Q

Collateral veins in CRVO

A

‣ Collateral veins become visible over several weeks to months; they are often on the disc and permit blood flow between the retina and chorodial circulations, helping to accelerate drainage of excessive fluid (Retinal edema) into the choroidal circulation after a CRVO

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39
Q

Vision threatening complications of CRVO

A

◦ Vision threatening complications include macular disease and complication from neo. VEGF stimulates neo of the posterior and anterior segment and has been prove to cause capillary leakage leading to macular edema
‣ 1. Macular disease-macular ischemia, macular edema, and intramacular hemes
‣ 2. Neo-neovascular glaucoma, preretinal/vitreous hemorrhage, and tractional RD

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40
Q

Neovascular glaucoma and CRVO

A

◦ Neovascular glaucoma is a major concern in patients with a CRVO and is most likely to develop within the 1st 3 months of Dx (90 day glaucoma). 60% of ischemic cases develop iris neo and up to 33% develop neo glaucoma. 6% of non ischemic cases develop rubeosis or angle neo

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41
Q

Leading cause of vision loss in both ischemic and non ischemic CRVO

A

Macular edema

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42
Q

Ischemic vs nonischemic CRVOs

A

‣ Ischemic CRVO is defined as 10 disc diameters or more of non-perfusion on FA. 90% of cases present with 20/200 vision or worse, and the prognosis is poor. 16% of nonischemic cases progress to ischemic CRVOs

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43
Q

Epidemiology of BRVO

A

BRVOs are by far the most common retinal vascular occlusive disease; patients have a similar health history as patients with CRVOs

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44
Q

Most common vascular occlusive disease

A

BRVO

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45
Q

Risk factors for BRVO

A

HTN, cardiovascular disease, increased body mass index at 20 years old, and open angle glaucoma

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46
Q

Pathophysiolgoy/Dx

A

BRVOs are usually caused by a thrombus after compression of an artery on a vein at an AV crossing. 60% occur at an AV crossing within the superior/temporal quadrant

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47
Q

BRVOs that do not occur at AV crossings

A

• BRVOs that do not occur at an AV crossing should be evaluated with vasculitis. Remember that retinal arteries and veins share a common adventitia at AV crossings; this allows a thickened artery to compress the vein

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48
Q

Symptoms of BRVO

A

BRVOs are characterized by sudden, unilateral, painless visual field loss, blurred vision or no symptoms (if the macula is spared)

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49
Q

Signs of BRVO

A

retinal signs occur in the area of the distribution of the occluded vessel and include dilated torturous retinal veins, CWS, collateral vessels, and intraretinal hemorrhages

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50
Q

Vision threatening complications of BRVO

A

◦ Vision threatening complications include macular disease and complications from neo
‣ 1. Macular disease-macular ischemia, macular edema, and intramacular hemorrhage
‣ 2. Neo complications-preretinal/vitreous hemorrhage

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51
Q

Epidemiology/Hx of CRAO

A

ask about transient loss of vision (amaurosis Fugax). Commonly occurs in elderly patients. Patietns have a 10% risk of CRAO occurring in the fellow eye

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52
Q

Risk factors for CRAO

A

HTN, DM, carotid occlusive disease, cardiac valve disease

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53
Q

CRAO in young patients

A

IV drug usage and BC

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54
Q

Pathophysiology/Dx of CRAO

A

CRAOs most commonly arise from heart and/or carotid artery emboli
‣ Calcific emboli-large dangerous emboli from calcified heart valves often located in the CRA near the optic nerve
‣ Carotid Emboli-smaller cholesterol plaques (hollenhorst plaques)

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55
Q

Worst kind of emboli

A

Calcific

Usually from heart valves

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56
Q

Things that can cause CRAO

A

◦ Although retinal emboli are by far the most common etiolgoy for arterial occlusions, there are several other culprits to consider, including GCA, acute elevation in IOP, collagen vascular diseases, IV drug use, oral BC, sickle cell disease, and syphilis

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57
Q

Symptoms of CRAO

A

acute, profound vision loss (often 20/400 or worse). Unless a cilioretinal artery is present to spare the macula. If VA is LP or worse, strongly consider an ophthalmic artery occlusion

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58
Q

Cilioretinal artery in CRAO

A

‣ A cilioretinal artery branches form the SPCAs of the choroid and allows the macula to remain functional in a CRAO. It is present in 15-30% of patients

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59
Q

Signs of CRAO

A

superficial whitening of the inner retinal layers (returns to the normal color after perfusion is restored but does not regain function!), narrowed arterial vasculature, a cherry red spot in the foveola, and an afferent pupillary defect r(secondary to optic disc pallor from orthograde degeneration of RGC axons). Hollenhurst plaques or other emboli are also noted in 20-40% of cases

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60
Q

Neo glaucoma and CRAO

A

Rare

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61
Q

Epidemiology/Hx of BRAO

A

similar risk factors to CRAOs

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62
Q

Pathophysiology/Dx of BRAO

A

90% of cases are caused bu retinal emboli (hollenhurst plaques (most common), calcium, fibrin, and platelet emboli)

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63
Q

Symptoms of BRAO

A

often asymptomatic; may complain of a VF defect or sudden unilateral painless vision loss if the area of occlusion is close to or involving the macula

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64
Q

Signs of BRAO

A

superficial whitening of the retina in the distribution of the affected vessels due to retinal infarction and edema; hollenhurst plaques or other emboli are found within the area of occlusion in 62% of cases. The edem and retinal whitening eventually resolves within weeks, but the retinal tissue remains non functional and the patient with have permanent VF defect

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65
Q

Myelinated nerve fibers

A

are congential, benign, white patches in the superficial retina with feathery edges that represent abnormally myelination of ganglion cell axons anterior the lamina cribrosa. Myelination follows the distribution of the axons, can obscure the retinal vessels, and is typically located near the optic nerve. Differential diagnosis include BRAO and CWS

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66
Q

Indications for a diabetic retinal exam for type I DM

A

Within 3-5 years of diagnosis

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67
Q

Indications for a diabetic retinal exam for type II DM

A

At the time of diagnosis

For patietns with no diabetic retinopathy, repeat exams every year

For patients with mild to moderate retinopathy, repeat exams every 6-12 months

For patietns with severe NODR or PDR, repeat examinations every 2-4 months

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68
Q

Leading cause of new cases of blindness in the US for adults 20-74

A

diabetic retinopathy

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69
Q

Most important risk factors for development of DR

A

Duration of disease

	‣ Patients who are dx with DM before age 30 have a 2% risk per year for developing DR; after 7 years-50%, after 25 years-90% with have DR
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70
Q

Pathophysiology/Dx of DR

A

DR occurs because of a loss of pericytes and damage to the retinal capillary BM, resulting in a breakdown of the blood retinal barrier. DR can be divided into non proliferative DR (NPDR or background DR) and proliferative DR (PDR)

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71
Q

NPDR

A

Can be divided into mild, moderate, severe, and very severe

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72
Q

Mild NPDR risk of progression

A

5% in 1 year

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73
Q

Moderate NPDR risk of progression to PDR

A

15% in 1 year

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74
Q

Severe NPRD risk of progression to PDR

A

52% risk in 1 year

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75
Q

Risk of progression for very severe NPRD

A

75% in 1 year

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76
Q

When is the diagnosis of very severe NPDR made

A

When two or more criteria are met within the 4-2-1 rule

  1. Severe retinal hemorrhages in 4 quadrants
  2. Venous beading in 2 quadrants
  3. IRMA in 1 quadrant
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77
Q

The diagnosis of NPDR is made when

A

The patient meets one criteria from the 4-2-1 rule

  1. Severe retinal hemorrhages in 4 quadrants
  2. Venous beading in 2 quadrants
  3. IRMA in 1 quadrant
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78
Q

4-2-1 rule

A
  1. Severe retinal hemorrhages in 4 quadrants
  2. Venous beading in 2 quadrants
  3. IRMA in 1 quadrant
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79
Q

PDR

A

occurs in 5% of patients with DR and is diagnosed based on the presence of neovascularization. If left untreated, PDR can progress to devastating outcomes. Patients with PDR who are most at risk for visions loss have high risk characteristics (HRCs)

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80
Q

High risk characteristics of PDR

A
  1. Neovascularization of the disc (NVD) greater than 1/4 DD within 1DD of the optic nerve
  2. Any NVD or NVE with an associated vitreous or preretinal hemorrhage
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81
Q

Symptoms of PDR

A

patietns are often asymptomatic or May experience vision and metamorphopsia

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82
Q

Signs of PDR

A

although there are numerous signs of DR, the most important threats to vision include macular disease and neovascularization

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83
Q

Macular disease in PDR

A

Macular ischemia

Macular edema

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84
Q

Macualr ischemia in PDR

A

may look normal or thickened; a FA can be used to differentiate macular ischemia from macular edema (macular ischemia will appear as an enlarged fovea avascular zone (hypofluoresce))

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85
Q

Macular edema in PDR

A

it can occur at ant stage of DR. CSME is based not he following 3 criteria (based on the presence of retinal thickening within the fovea)
• A. Retinal thickening within 500um (1/3DD) of the fovea center
• B. Hard exudates within 500um of the fovea center with adjacent retinal thickening
• C. Retinal thickening of at least 1DD within 1DD of the fovea center

The patient only needs to have one of the three to be diagnosed with CSME

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86
Q

CSME in PDR

A
  • A. Retinal thickening within 500um (1/3DD) of the fovea center
  • B. Hard exudates within 500um of the fovea center with adjacent retinal thickening
  • C. Retinal thickening of at least 1DD within 1DD of the fovea center

The patient only needs to have one of the three to be diagnosed with CSME

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87
Q

Neovascularization in PDR

A

Threats to vision from neo include the following
‣ 1. Preretinal/vitreous hemorrhages
‣ 2. Neovascular glaucoma
‣ 3. Tractional RD

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88
Q

Epidemiology/Hx of HTN retinopathy

A

60 million Americans over the age of 18 years of age have HTN; more prevalent in AA. Essential HTN accounts for 95% of all cases of HTN and is defined as elevated blood pressure with no known cause

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89
Q

Pathophysiology/dx of HTN retinopathy

A

recall that retinal arteries are able to auto regulate their vessel diameter based on changes in blood pressure; autoregulation is altered at extremely high or chonrically elevated systolic pressures and retinopathy results. Systemic blood pressure must typically be at least 140/110 for the latter stages of HR to occur

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90
Q

Symptoms of HTN retinopathy

A

commonly asymptomatic. Vision is typically unaffected unless vascular changes cause macular edema (macular star), papilledema, a serous retinal detachement, or a vein occlusion

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91
Q

Stages of HTN retinopathy

A

1-4, 4 being the worst

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92
Q

Stage 1 HTN retinopathy

A

mild to moderate diffuse narrowing of the retinal arteries (but no focal constriction)

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93
Q

Stage 2 HTN retinopathy

A

stage 1 plus focal constriction of the retinal vasculature (AV nicking) and exaggerating of the arterial light reflex

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94
Q

Stage 3 HTN retinopathy

A

stage 2 plus retinal hemorrhages, CWS, hard exudates (likely in a star configuration within the OPL radiating away from the fovea), and retinal edema

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95
Q

Stage 4 HTN retinopathy

A

stage 3 plus papilledema (malignant HTN). Patients with malignant HTN must be hospitalized immediately due to high risk of stroke. BP at this stages is usually 220/120.

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96
Q

HTN retinopathy is associated with numerous secondary conditions that can lead to vision loss, including

A

vascular occlusion, retinal macroaneurysms, NAION, ocular motor palsies, and worsening of DM.

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97
Q

Elschnig spots

A

choroidal infarcts that occur in severe HR

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98
Q

Epidemiology/Hx of retinal macroaneurysms

A

more common in elderly women (7th decade) with HTN or atherosclerosis

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99
Q

Symptoms of retinal artery macroaneurysms

A

usually asymptomatic, but can have gradual vision loss from macular edema or sudden vision loss from a vitreous hemorrhage

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100
Q

Signs of retinal artery macroaneurysms

A

unilateral focal area of dilation in a retinal artery (100-250um in diameter) with multi-level hemorrhages (subretinal, intraretinal, preretinal, and/or vitreous hemorrhage) from a ruptured aneurysm with surrounding circulate exudates; often located at an AV crossing

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101
Q

Description of the hemorrhages in retinal artery macroaneurysms

A

multi-level hemorrhages (subretinal, intraretinal, preretinal, and/or vitreous hemorrhage)

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102
Q

Epidemiology/Hx of venous stasis retinopathy?OIS

A

Men

Ages 50-80

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103
Q

Pathophysiology/Dx of venous stasis retinopathy/OIS

A

caused by occlusion of the ICA and/or ophthalmic artery (less common), usually secondary to atherosclerosis; may also occur as a result of GCA

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104
Q

Symptoms of venous stasis retinopathy/OIS

A

common symptoms include gradual vision loss, dull periorbital pain or HA, and amaurosis fugax

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105
Q

Signs of venous stasis retinopathy/OIS

A

unilateral (80%) dot/blot hemorrhages of the midperipheral fundus, dilated non-tortuous retinal veins, narrowed retinal arteries, and possible neo of the disc and/or anterior segment (67% of patients with OIS have NVI/NVA at the time of diagnosis)

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106
Q

Difference between OIS and venous stasis retinopathy

A

‣ If a patient has these retinal findings and carotid artery obstruction, but no anterior segment signs, the condition is called venous stasis retinopathy
‣ The presence of both posterior and anterior segment signs and symptoms is referred to as OIS. OIS is most common in male patients 50-70 years old

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107
Q

OIS is commonly associated with

A

systemic HTN, DM, and cardiac disease; the latter is most common cause of a 40% 5 year mortality rate in these patients

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108
Q

Amaurosis fugax

A

type of TIA characterized by transient monocular vision loss that typically lasts seconds to minutes; vision returns to normal after the ischemic event. A carotid artery embolus is the most common cause of amaurosis fugax

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109
Q

TIA vs stroke

A

characterized by temporal neurological defects due to transient loss of blood flow to the brain. Perfusion is always resorted in less than 24 hours (usually less than 15 minutes), resulting in complete resolution of the patient’s symptoms without any permanent damage. In contrast, a stroke is characterized by permanent neurological deficits due to prolonged loss of blood flows that results in irreversible damage to the brain

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110
Q

Things that cause pre retinal neo

A 
Proliferative Neo 
DRVOS
-DM
-ROP
-Vein occlusions 
-OIS
-Sickle cell
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111
Q

What are the main problems with preretinal neo

A

Proliferative, DRVOS

  1. Preretinal/vit heme
  2. Tractional RD (vit pulls on neo)
  3. VEGF=NVG
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112
Q

Number one cause of all occlusions

A
  • HTN

- Plaques from the heart

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113
Q

A clot that stays where it formed

A

Thrombus

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114
Q

Which causes vein occlusions, thrombus or embolus

A

Thrombus

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115
Q

Which causes artery occlusions, thrombus or embolus

A

Embolus

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116
Q

Why do we get thrombus

A
  1. HTN/DM (artery prob)
  2. Artery compressing vein
  3. Bad/turbulent blood flow
  4. Thrombus formed
  5. VEGF released
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117
Q

Which is worse, ischemic or non ischemic CRVOs

A

Ischemic

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118
Q

What layers of the retina are damage in CRAO

A

OPL-> ILM

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119
Q

VF loss in BRAO

A

Respects horizontal midline, Mimics glaucoma

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120
Q

5 most important things in DM

A
  1. Preretinal/vit heme
  2. Tract RD
  3. VEGF-NVG
  4. Ischemic macula
  5. Macular edema
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121
Q

Damage to pericytes in DM

A
  • autoregulation problem
  • ONH
  • retinal vessels

Break down of BRB

  • between RPE cells
  • retinal BV
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122
Q

Swelling in ischemia

A

Ischemia is decreased O2, it initally swells and then thins

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123
Q

Primary HTN ret findings

A 
Mac star (3 or 4)
Papilledems (4)
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124
Q

Findings secondary to HTN (other than HTN retinopathy)

A 
CRAO, BRAO, CRVO, BRVO
NAION
EOM palsy
Worsening DM
Macroaneurysms
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125
Q

Things that cause NAION

A

Viagra
Imitrix
Amiodarone
SPCA not doing its job

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126
Q

What should be ordered for someone with OIS

A

Carotid Doppler

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127
Q

Pathophysiology/Dx of hyperviscosity retinopathy

A

an increase in resistance to blood flow secondary to elevated levels of proteins, RBCs, and/or WBCs, resulting in impaired circulation of blood flow and oxygen though the microvasculature. As blood flow decreases, blood vessel walls become damaged, causing leakage of fluid and retinal ischemia

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128
Q

The most common cause hyperviscocity retinopathy

A

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

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129
Q

Signs of hyperviscocity retinopathy

A

retinal venous dilation, retinal hemorrhages, CWS, and exudates. Central retinal vein occlusion may also occur and is bilateral in 10% of patients

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130
Q

HIV retinopathy

A

◦ The most common ocular manifestation of HIV/AIDS. Signs include CWS and retinal hemorrhages, similar appearance to DR and early CMV retinitis
◦ Patients are typically asymptomatic. The condition is non infectious in origin

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131
Q

Interferon retinopathy

A

◦ Patients on interferon therapy can develop retinal findings similar to DR, including CWS and retinal hemorrhages within the posterior pole.
◦ Retinopathy typically occurs within 3-5 months after interferon is started, and tends to resolve without treatment after interferon has been discontinued

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132
Q

How often should patients on interferon retinopathy be followed

A

◦ Patients on interferon therapy without retinopathy should be followed every 4-6 months; if retinopathy is present, follow ups should occur more frequently

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133
Q

Talc retinopathy

A

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

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134
Q

Periphlebitis

A

Sarcoidosis
-lac gland, CN VII, OHN, vessels, vitreous

AA female
Hard exudates that leak
Vasculitis=inflammation

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135
Q

An inflammatory condition characterized by exudates around the vessels (seen as white cuffing of the vessels). Retinal edema, ischemia, and hemorrhaging may also occur. Vessel walls will stain on FA

A

Vascualr sheathing/periphlebitis

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136
Q

Most common causes of vascular sheathing/periphlebitis

A

syphilis, sarcoidosis (known as candle wax drippings), pars planitis, and sickle cell disease

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137
Q

Testing for vascular sheathing/periphlebitis

A

◦ Diagnostic systemic lab testing should be done based on the revive of systems and case history to determine the systemic cause of the vascular sheathing

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138
Q

Are bilateral retinoblastoma hereditary or non hereditary

A

All bilateral=hereditary

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139
Q

Are unilateral RBs hereditary or non

A

Most of them are nonhereditary

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140
Q

Pathophysiology/Dx of idiopathic juxtafoveolar telangiectasia

A

abnormal perifovea capillaries present within the juxtafoveal region. IJXT is divided into three categories

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141
Q

Unilateral congenital idiopathic juxtafoveolar retinal telangiectasia

A

occurs in men in the 4th decade; results in 20/25-20/40 vision

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142
Q

Unilateral idiopathic form of idiopathic juxtafoveolar retinal telangiectasia

A

occurs in middle aged men; reuslts in 20/25 or better acuity

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143
Q

Bilateral acquired form of idiopathic juxtafoveolar retinal telangiectasia

A

equal sex distribution in the 5th or 6th decade. Poor visual prognosis

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144
Q

Symptoms of idiopathic juxtafoveolar retinal telangiectasia

A

Decreased vision

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145
Q

Signs of idiopathic juxtafoveolar retinal telangiectasia

A

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

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146
Q

Epidemiology/Hx of Coat’s disease

A

peak incidence in males less than 20 years old; 2/3 of cases present prior to age 10. Progression is more rapid in children under 4 years old, simulating retinoblastoma

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147
Q

Pathophysiology of Coat’s disease

A

idiopathic peripheral vascular disease. If left untreated, coats disease will gradually progress to a total exudative RD

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148
Q

Symptoms of Coats

A

decreased vision, strab, leukocoria

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149
Q

Signs of Coats

A

unilateral, telangiectatic dilated vessels that display a characteristic “lightbulb” appearance. Progression of the disease can lead to marked hard exudates (classic for coats), intraretinal hemorrhagehs, exudative retinal detachement, and NVG (results in red painful eye and potentially blind eye)

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150
Q

How does Coats lead to NVG

A

A chronic extensive serous detachment in coats disease results in retinal ischemia, which leads to the development of anterior segment neovascularization similar in pathology to the DR VOS conditions. NVA and NVI result in NVG

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151
Q

Epidemiology/Hx of ROP

A

occurs in premature infants (less than 32 weeks) or low birth weight infants (<1500g) who have received oxygen therapy

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152
Q

Pathophysiology of ROP

A

immature blood vessels vasoconstriction and stop developing in response to high oxygen concentration, leading to proliferative retinopathy. Threatens to vision include preretinal/vitreous hemorrhages, and tractional RDs

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153
Q

Signs of ROP

A

leukocoria, strab, vitreoretinal traction, preretinal/vitreous hemorrhages, and tractional RDs

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154
Q

Leukocoria and ROP

A

white pupillary reflex that resutls from fibrovascular scarring secondary to a tractional RD in cases of ROP

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155
Q

Which part of the retina matures last?

A

The anterior temporal retina is the last area of the retina to achieve mature vascular development during the 9th month of gestation. This area is most susceptible to neovascularization and subsequent tractional RDs in pre term infants with ROP

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156
Q

Epidemiology/Hx of RB

A

the most common intraocular malignancy in kids and the second most common of all age groups (choroidal melanoma is the most common). 95% of cases are diagnosed by 5 years of age. No gender or race predilection

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157
Q

The smog common intraocular malignancy in kids

A

RB

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158
Q

The second most common intraocular malignancy in all age groups

A

choroidal melanoma

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159
Q

Pathophysiology/ Dx of RB

A

tumor derived from cells in the developing retina (retinoblasts) as a result of mutations in the Rb tumor suppressor gene

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160
Q

Heritable RB

A

40%
all bilateral cases and about 10-20% of unilateral cases. However, only 6% of these have a positive family Hx of the condition because the tumor has such a high spontaneous mutation rate. Bilateral affected patients have a 50% chance of passing the disease on to each offspring

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161
Q

Non-heritable RB

A

60%

85% of all unilateral cases of RB are non heritable. Affected pateitns will not pass the disease on to their offspring

162
Q

Signs and symptoms of RB

A

leukocoria, strab, intraocular inflammation, and decreased vision

163
Q

Differentials for leukocoria

A

Coat’s disease, toxocariasis, RB, and ROP

164
Q

Epidemiology/Hx for CHRPE

A

the lesions are thought to be congenital with no race or sex predilection

165
Q

Signs of CHRPE

A

benign, pigmented (brown to black), non-progressive lesions with sharp borders and central hypopigmetned lacunae.
‣ CHRPEs are typically unilateral and solitary, measuring 1-6mm in diameter. Bilateral multifocal (4 or more) CHRPEs are assocaited with Gardner’s Syndrome-colonoscopy needed

166
Q

Epidemiology/Hx for choroidal nevus

A

common condition that occurs in 1-6% of the population and is most commonly in whites

167
Q

Pathophysiology/Dx of choroidal nevus

A

common benign focal accumulation of melanocytes within the choroid. Choroidal nevi are thought to be present at birth and are typically non progressive

168
Q

Growth of a nevus

A

‣ Growth during puberty is not unusual, but any growth in an adult should raise concern for conversion to malignant melanoma
‣ 10% of suspicious nevi progress to malignant melanoma

169
Q

The most common risk factors for transformation of a choroidal nevus into a chorodial melanoma are

A

To Find Small Ocular Melanomas, Use Helpful Hints”
• T=thickness (elevation >2mm)
• F=fluid (subretinal)
• S=symptoms (blurred vision and floaters)
• O=orange pigment (lipofuscin on surface of lesion)
• M=margins (irregular borders)
• UH=ultrasonographic hollowness (acoustically hollow with low internal reflectivity)
• H=halo absence
• The nevus should also around suspicion if it has a large diameter (>4DD or 6mm) or if its close proximity to the ONH

170
Q

Signs of choroidal nevus

A

the lesion is typically flat or slightly elevated, less than 5mm in size, and often contain overlying drusen

171
Q

Most common primary intraocular malignancy

A

Choroidal melanoma

172
Q

Things that cause subretinal neo

A

CHBALA

  • Choroidal rupture
  • Histo
  • Bests
  • Angioid streaks
  • Lacquer cracks
  • ARMD

Problems with Burch’s

173
Q

Two types of CNVM

A

Plasma

  • clear
  • dont treat
  • small break
  • detachment (PED)

RBCs

  • red
  • treat
  • large break
  • hemorrhage
  • looks grey/green
174
Q

Wet vs dry ARMD: PED

A

Wet PED
=break in bruchs

Dry PED
-drusenoid PED, no break in bruchs

175
Q

Where is drusen located

A

Inner collagenous zone of bruchs

176
Q

Main concerns in dry ARMD

A
  1. Drusenoid PED
  2. GA
  3. Progression to wet
177
Q

Macular degeneration is a progressive disease of the

A

RPE
Bruchs membrane
Choriocapillaris

178
Q

Who gets AMD

A

most common in patients over the age of 50. It is the second leading cause of blindness for patients 45-64 (DM number 1); exudative ARMD is the chief cause of vision loss in patients over the age of 50

179
Q

Risk factors fro ARMD

A

increasing age (esp >75), ethnicity (whites), positive family history, light iris color, cigarette smoking, hyperopia, HTN, HLD, female gender, and cardiovascular disease

Nutritional factors and light toxicity play roles

180
Q

Hyperopia and ARMD

A

Hyperopia greater than 0.75D is assocaited with a 2.5X increased risk of exudative ARMD. 10-20% of patients with ARMD have at least one first degree family member with vision loss from ARMD.

181
Q

Smoking and ARMD

A

Current smokers are 2.5x more likely to develop ARMD and 1.7-2.2x more likely to have recurrence of CNV compared to those who have never smoked

182
Q

What is the most common form of ARMD

A

No exudative (Dry)

183
Q

Characteristics of dry ARMD

A

presence of drusen (hallmark); assocaited RPE abnormalities (mottling, granularity, focal hyperpigmentation) may also be present

184
Q

Symptoms of dry ARMD

A

Most patients with dry ARMD do not have severe vision loss; metamorphopsia, gradual vision loss (over months to years), and blurred visions are common complaints

185
Q

4 main risk factors that increase the progression from dry to wet ARMD

A
  1. Multiple soft drusen (especially if confluent)
  2. Focal hyperpigmentation
  3. HTN
  4. Smoking
186
Q

Most of legal blindness is attributed to

A

Wet ARMD

187
Q

Symptoms of exudative ARMD

A

metamorphopsia, central scotoma, and rapid vision loss

188
Q

Signs of exudative ARMD

A

drusen that are associated with signs of a CNVM. CNVMs can leak blood or plasma into two potential places: 1. Sub-RPE space or 2. Subretinal space.

189
Q

What are the potential presentations of wet ARMD

A

CNVMs can either leak blood or plasma into two potential spaces; 1) subRPE, 2) subretinal space. This creates 4 potential presentations of wet ARMD

  1. Subretinal hemorrhage (blood under retina)
  2. SubRPE hemorrhage (blood under RPE
  3. Subretinal detachment (plasma under the retina, AKA serous retinal detachment)
  4. SubRPE detachment (plasma under the RPE, AKA pigmented epithelial detachement (PED))
190
Q

Another name for a subretinal detachment

A

Serous retinal detachement

191
Q

Another name for a subRPE detachment

A

Pigmented epithelial detachment (PED)

192
Q

PEDs in dry ARMD

A

can also occur with dry AMD due to a build up a confluent soft drusen on Bruch’s membrane, creating a space between the RPE and the choroid. This type of sub-RPE detachment is called a drusenoid pigment epithelial detachement. CNVMs can develop over time within drusenoid PEDs

193
Q

Classic vs occult CNVM

A

FA can be used to detail exact ares of leakage and classify them as occult or classic
• Classic CNVMs are characterized by a well defined membrane that fills will dye during the early stages of FA
• Occult CNVMs are characterized by a poorly-defined membrane with late appearing and less intense leakage
• Most patients with wet ARMD have a CNVM with a combination of classic and occult features. The term “predominantly classic” means that over 50% of the entire lesion is composed of a classic CNVM

194
Q

Incidence of involvement of the fellow eye in wet ARMD

A

incidence of involvement of the fellow eye with wet ARMD is estimated to be 28-36% during the first 2 years; the annual rate of bilaterality is about 6-12% per year for the next 5 years. The overall 5 year risk ranges from 40-85%

195
Q

Epidemiology/Hx of CSCR

A

commonly occurs in young to middle aged men (20-50) with a type A personality; associated with stress, pregnancy, steroid use, hypochondriasis, and HTN. A history of similar episodes is common-recurrences occurs in as high as 50% of cases

196
Q

Pathophysiology of CSCR

A

unknown etiology. CSR results in RPE and/or choroidal dysfunctions, with resulting accumulation of submacular serous fluid

197
Q

Symptoms of CSCR

A

unilateral sudden onset of blurred visions (20/20-2/200); metamorphopsia and a relative scotoma may also occur. Patients may have symptoms even if acuity is 20/20

198
Q

Signs of CSCR

A

localized macular serous detachment; 3% of cases will have an RPE detachment as well. FA will reveal a gradual pooling of Fl into a pigmented epithelial detachment or a “smokestack appearance”. OCT can also be used to dx and monitor the condition (now used more frequently than FA). Patietns may also have a hyperopic shift and loss of the foveal light reflex

199
Q

Permanent changes in CSCR

A

Patients often have permanent residual RPE changes within the macula after resolution of the condition.

200
Q

In CSCR, most people improve without treatment in

A

1-3months

201
Q

Prognosis of CSCR

A

Most patients improve without treatemtn by 1-3 months; 94% of patients will regain >20/30 acuity. 66% of patients achieve 20/20 acuity

202
Q

Vitritis in histoplasmosis

A

There is NONE!

This is a choroiditis, not a retinitis

203
Q

Worst case scenario for histoplasmosis

A

Break in bruchs membrane

-can get the 4 different types of nets

204
Q

Triad of histoplasmosis

A

Bilateral choroiditis with

  1. Peripapillary atrophy
  2. Peripheral histo spots
  3. Maculopathy
205
Q

Difference between histo and toxo

A

Toxo

  • parasite
  • retinitis=breakdown in BRB=vitritis
  • one eye
  • one lesion

Histo

  • fungus
  • choroiditis
  • BRB fine, no vitritis
  • both eyes
  • multiple lesions
206
Q

Difference between lacquer cracks and angioid streaks

A

Lacquer cracks

  • young males
  • yellow
  • coming from macula

Angioid streaks

  • always from the disk
  • PXE, ED
  • PEPSI
  • dont want streak across macula
  • red in appearance
207
Q

Glial cells and ERM

A

Glial cells on the ILM

  1. From vitreous
  2. From within the retina
208
Q

Epidemiology/Hx of histoplasmosis

A

rare in AA, most comm in the Ohio-Mississippi-river valley.

209
Q

Pathophysiology/Dx of histoplasmosis

A

infection caused by histoplasmosis capsulatum, a fungus that grows in soil and material contaiminted with bird or bat droppings.
‣ Recurrences of histo (30% of cases) occur through preexistent histo spots
‣ If spots are present in the disc or macular area, the chance of a symptomatic recurrence is appx 20% over 3 years

210
Q

Symptoms of histoplasmosis

A

asymptomatic unless maculopathy develops; the earliest symptom is metamorphopsia

211
Q

Signs of histoplasmosis

A

characterized by bilateral choroiditis and the clinical triad of bilateral peripapillary atrophy of the optic nerve, multifocal leasions in the periphery, and maculopathy (including CNVM). The vitreous is always clear in histoplasmosis!
‣ CNVM is a late manifestation: if it occurs, it is most likely to happen between the ages of 20 and 45

212
Q

Differences between histo and toxoplasmosis

A

Although toxoplasmosis and histoplasmosis are both types of posterior uveitis, they are characterized by very different etiologies and presentations
• Toxoplasmosis is caused by a parasite that results in retinitis, which is characterized by WBCs in the vitreous due to a breakdown in the blood retinal barrier. Remember ONE EYE, ONE LESION
• Histoplasmosis is caused by a fungus that leads to choroiditis; it does NOT cause a breakdown in the blood retinal barrier and does NOT present with a vitritis! Remember BOTH EYES and MULTIPLE LESIONS

213
Q

Epidemiology/Hx of pathological myopia

A

pathological myopia has a genetic predisposition, with elongation of the globe beginning in early childhood. Occurs in 2% of the population, most commonly in women during young adulthood. The condition is also referred to as myopic degeneration

214
Q

Pathophysiology/Dx of pathological myopia

A

defined as a refractive error >-6.00D spherical equivalent and/or axial length >26.5mm. Axial lengthening in the anterior-posterior direction results in scleral thinning and choroidal atrophy

215
Q

What refractive error and axial length define pathological myopia

A

> -6.00D

>26.5mm

216
Q

Symptoms of pathological myopia

A

patient may be asymptomatic or complain of decreased vision and metamorphopsia

217
Q

Macular and posterior pole signs of pathological myopia

A
  • Posterior staphyloma (the hallmark of pathological myopia): posterior bulging of the weakened sclera
  • Oblique insertion of the optic nerve
  • Fuch’s spots (focal subretinal hyperpigmentation secondary to scarring or CNVM
  • Lacquer cracks
  • Macular holes
218
Q

Peripheral signs of pathological myopia

A
  • Lattice degeneration
  • Snail track degeneration
  • Pavingstone degeneration
  • Retinal breaks
  • Retinal detachments
219
Q

Non retinal signs of pathological myopia

A
  • Premature cataracts (NS and esp PSC)
  • Extensive vitreous syneresis
  • PVD
220
Q

Lacquer cracks in pathological myopia

A

occur in about 5% of high myopes. They appear as fine yellow irregular lines that represent large breaks in Bruch’s membrane. Choroidal neo can result and lead to severe vision loss. Lacquer cracks frequently present in young males and may be one of the earliest findings in pathological myopia

221
Q

Pavingstone degeneration

A

discrete, circular areas of yellow-white chorioretinal atrophy in the retinal periphery. Also referred to as cobblestone degeneration. This condition is not a predisposing factor for a RD and has no clinical importance

222
Q

Epidemiology/Hx of ERM

A

more common in females. Prevalence increases with age; occurs in 2% of patients older than 50, and 20% of patietns older than 75
‣ The condition is often idiopathic but may be caused by PVDs, retinal breaks, cataract or other intraocular surgeries, and trauma

223
Q

Pathophysiology of ERM

A

ERMS result from glial cell proliferation on the ILM. Vitreous traction can result in residual glial cells from the posterior hyaloid (back of the viteous) on the ILM, or can cause small pores to develop in the ILM; this allows intraretinal glial cells to gain access to the anterior side of the ILM for proliferation

224
Q

Symptoms of ERM

A

may be asymptomatic or complain of decreased vision and/or metamorphopsia

225
Q

Signs of ERM

A

mild ERMS are characterized by fine, glistening membrane (cellophane maculopathy). Advanced ERMS appear as thick, gray-white membranes with associated retinal folds (macular pucker)

226
Q

Most patients with ERM have

A

A PVD

227
Q

Epidemiology/Hx of macular hole

A

83% of cases are associated with aging; women are more commonly affected

228
Q

Pathophysiology/Dx of macular hole

A

results from posterior vitreous traction on the macula. Most commonly idiopathic (senile), but may also develop after trauma, surgery, CME, or inflammation. The condition has a bilateral onset in 25-30% of cases. The risk of developing a macular hole in the fellow eye varies from 5-16% (there is no risk of a PVD has occurred)

229
Q

Symptoms of macula holes

A

decreased vision and/or metamorphopsia. Full thickness macular holes are assocaited with 20/200 or worse vision

230
Q

Signs of macula hole

A

condition is characterized by a round, red, well delineated spot in the macula.

231
Q

Stage 1 macula hole

A

impending hole with loss of the foveal depression and a yellow spot or ring at the fovea

232
Q

Stage 2 macular hole

A

round, small, full-thickness hole with a pseudo-operculum

233
Q

Stage 3 macular hole

A

large, full thickness hole with an operculum. Patients will report a positive Watzke-Allen sign

234
Q

Stage 4 macula hole

A

stage 3 plus a PVD

235
Q

Positive Watzke Allen test

A

characterized by a complete break in the middle of a thin line of light projected within the macula

236
Q

Macular photostress test

A

determine the patients BCVA prior to starting the test. Howl a bright light 2cm from the patient’s eye and instruct the patient to look at the light for 10s. Measure the time it takes for the patient to read one line less than his/her BCVA. Norma recovery time is less than 60s.

237
Q

Choroidal folds

A

Waves within the choroid, Bruchs membranes, and RPE that develop secondary to mechanical stress on or within the choroid. Characterized bu alternating light and dark striations within the fundus. Macular involvement may lead to symptoms of metamorphopsia and reduced VA

238
Q

What causes choroidal folds

A

◦ Commonly the result of ocular or systemic conditions that cause mechanical stress on the choroid, including choroidal, optic nerve, or orbital tumors, posterior scleritis, choroidal detachment, choroidal inflammation, orbital pseudotumor, TED, orbital myositis, hypotony, and intracranial HTN

239
Q

Pathophysiology/Dx of albinism

A

group of disorders characterized by a mutation in the genes responsible for the production of melanin. Albinism may affect the skin and eyes (oculocutaneous) or the eyes only (ocular albinism)

240
Q

Signs of albinism

A

characterized by hypopigmetnation of the skin and fundus, it is translucency, foveal hypoplasia, ON hypoplasia, icrocornea, nystagmus, strab, and mis-routing of the temporal optic nerve fibers through the optic chiasm

241
Q

Symptoms of albinism

A

photophobia and reduced VA

242
Q

Systemic conditions associated with albinism

A

Hermanksy-Pudlak and Chediak-Higashi syndromes.

243
Q

Number one cause of RRDs

A

Myopia

244
Q

Epidemiology/Hx of RP

A

the most common retinal dystrophy and can be non-heritable or heritable (most commonly AD), or in association with uncommon systemic disorders; Ushers syndrome (5% of RP patients) is the most common associated systemic condition. The average age of diagnosis is 9-19.

245
Q

Systemic disease assocaited with RP

A

Ushers

  • AR
  • hearing loss
246
Q

Pathophysiology/Dx of RP

A

generic term given to a group of hereditary conditions (29 loci associated with various phenotypes) characterized by a progressive loss of PR and RPE function. Although rods and cones are involved, rod damage is more dominant. There is tremendous variability in presentations, which correlates with the mode of inheritance

247
Q

Symptoms of RP

A

night blindness (most common symptom) and peripheral vision loss (only in dim light in early stages). It often takes years to decades for symptoms to develop; by 30 years of age, over 75% of patients are symptomatic

248
Q

Signs of RP

A

classic triad of retinal bone spicule pigmentation (pigment clumping in the mid-periphery), arteriolar attenuation, and waxy optic nerve pallor
‣ Other signs include PSC, optic disc drusen, macular changes (atrophy, CME, ERMs), keratoconnus, myopia, and progressive contraction of the VF

249
Q

ERG and RP

A

can be utilized for dx; in the early stages of RP, the scotopic ERG is reduced, and the photopic ERG is relatively normal.

250
Q

Epidemiology/Hx of Stargardts

A

Stargardts disease is the most common hereditary macular dystrophy. The onset is typically in the first Ir second decade of life, most commonly between the ages of 6 and 20. The inheritance is typically AR. There is no sex predilection

251
Q

What inheritance is stargardts

A

AR

252
Q

Pathophysiology of Stargardts

A

most often due to a mutation in the ABCA4 transmembrane protein that is responsible for moving all-trans retinal from the photoreceptor disc lumen to the cytoplasm. This results in a toxic accumulation of all-trans retinal within the PR discs, leading to degeneration of the PRs and the RPE. Fundus flavimaculatus and stargardts disease are considered variants of the same disorder

253
Q

Fundus flavimaculatus

A

diagnosis is reserved for patients WITHOUT macular dystrophy signs; it often presents later in life. Patients are commonly asymptomatic, although vision loss can still occur if fleck like lesions involve the macula

254
Q

Symptoms of stargardts disease

A

rapid vision loss and color vision abnormalities. The level of decreased vision is often out of proportion with the fundus appearance in the early stages of the disease. Acuity is typically 20/200 bu the third decade and is stable or slowly progressive thereafter

255
Q

Signs of Stargardts

A

early stages are characterized by bilateral yellow flecks scattered in a pisciform configuration throughout the posterior pole and mid-periphery. Non-specific RPE mottling of the macula May also be apparent. Later stages are characterized by a classic “beaten bronze” macular appearance (“bulls eye maculopathy”) and “salt and pepper” pigmentary changes in the periphery.

256
Q

ERG and stargardts

A

ERG is normal in the early stages of the disease, but becomes abnormal as the condition progresses

257
Q

Epidemiology/Hx of choroideremia

A

inheritance is X linked recessive, so only males are affected and all daughters are carriers. Onset is typically within the 1st decade

258
Q

Pathophysiology/Dx of choroidermia

A

due to deficiency in rab geranyl-geranyl transferase, an enzyme utilized in membrane metabolism

259
Q

Symptoms of choroideremia

A

night-blindness and peripheral vision loss. Night blindness occurs early in life in males and progresses to total night-blindness within a period of 10 years. Most patients have good visions until 50-60 years of age. In females, the condition is benign and non-progressive.

260
Q

Signs of choroidermemia

A

progressive, bilateral, diffuse atrophy of the ROE and choriocapillaris, causing exposure of the underlying sclera. The macula is often spared until late stages of the disease. The optic disc and retinal blood vessels are often unaffected

261
Q

DiffDx for night blindness

A

gyrate atrophy, choroidermia, and RP

262
Q

Epidemiology/Hx for cone dystrophy

A

onset within 1-3rd decade. Inheritance is variable, but most commonly AD

263
Q

Symptoms of cone dystrophy

A

slowly progressive decrease in central vision, severe photophobia, and severe color vision loss; symptoms are worse during the day. Cone dystrophy has a poor prognosis, with vision deteriorating to 20/400 by the 4th decade

264
Q

Signs of cone dystrophy

A

‣ Early-normal fundus appearance by abnormal cone function on the ERG
‣ Late-central GA of the RPE with a bulls eye macular appearance, vessel attenuation, and temporal pallor of the optic nerve (similar to RP) with severe deutan-tritan color defects, an abnormal photopic ERG, and fine nystagmus

265
Q

DiffDx for bulls eye maculopathy

A

stargardts disease, progressive cone dystrophy, chloroquine and hydroxychloroquine toxicity, and thioridazine toxicity

266
Q

Epidemiology/Hx for bests

A

uncommon condition. Inheritance is AD. The age of onset varies but the condition classically presents in early childhood

267
Q

Pathophysiology of bests

A

due to abnormal accumulation of material (posibly lipofuscin) in the RPE

268
Q

Symptoms of bests

A

the majority of cases are detected with little or no patient symptoms (75% better than 20/40). Patients eventually complain of decreased vision

269
Q

Signs of bests

A

characterized by a bilateral, yellow, round, subfoveal (“egg yolk”) lesion

270
Q

Egg yolk in bests

A

thought to be an abnormal accumulation of lipofuscin within the RPE cells. The egg-yolk can remain stable for years with only a mild reduction in VA (20/30-20/50) into midlife

271
Q

Stage 1 bests

A

previtelliform): characterized by an abnornal EOG (Arden ratio < 1.8) with a normal fundus in an asymptomatic patient

272
Q

Stage 2 bests

A

vitelliform): egg-yolk macular lesion appears; this is most likely to occur between the ages of 3-15

273
Q

Stage 3 best

A

pseudohypopyon): the entire lesion can become absorbed with little to no affect on vision.

274
Q

Stage 4 bests

A

vitelliruptive): the egg yolk starts to break up (scrambled egg), mild VA loss is expected at this stage

275
Q

Stage 5 bests

A

(end stage): characterized by moderate to severe vision loss due to choroidal neovascularization, hemorrhage, atrophy, and/or macular scarring

276
Q

ERG and bests

A

normal ERG but abnormal EOG (even prior to vision loss or fundus signs)

277
Q

Adult foveomacular vitelliform dystrophy vs bests

A

present in patients aged 30-50. Although similar signs to Bests, overall prognosis is better with minimal metamorphopsia, mild VA loss, normal EOG and ERG and slight tritan color defect.

278
Q

Gyrate atrophy epidemiology/Hx

A

inheritance is AR, symptoms are prevalent in most patients by age 10

279
Q

Pathophysiolgoy of gyrate atrophy

A

bilateral chororetinal degeneration due to a deficiency in the mitochondrial enzyme ornithine aminotransferase. Ornithine blood plasma levels will be high and can help in the dx if the clincal picture is unclear

280
Q

Symptoms of gyrate atrophy

A

nyctalopia (night blindness), decreased vision, constricted VF

281
Q

Signs of gyrate atrophy

A

multiple, well-defined, scalloped areas of peripheral chorioretinal atrophy; the lesions being in the midperiphery during childhood and then coalesce to engulf most of the posterior pole, with the macula being spared until the 4th or 7th decade. Associated with PSC, high myopia, and astigmatism

282
Q

Epidemiology/Hx of RRDs

A

occur more often in males, typically over the age of 45 years old. Risk factors for RRD include
‣ Previous ocular surgery. Pseudophakic RDs often reuslts from small retinal holes at the vitreous base
‣ PVD: 10-15% of patients with an acute symptomatic PVD will have a retinal break
‣ Trauma
‣ Family history of RRD or previous occurrence of RRD. Both eyes are eventually involved in about 10% of cases.
‣ Myopia: 40% of all RDs occur in myopic eyes
‣ Lattice degeneration

283
Q

Pathophysiology of RRDs

A

result from retinal breaks (full thickness retinal defects) that allow vitreous into the subretinal space, leading to separation of the sensory retina from the underlying RPE. Breaks include atrophic holes and vitreo-retinal traction tears

284
Q

A break in the retina

A

The term BREAK=atrophic HOLES and traction TEARS. Thus an RRD refers to a retinal detachment that was caused by a hole or a tear

285
Q

Atrophic holes and RRDs

A

round, often small, full-thickness defects that are NOT associated with vitreoretinal traction and therefore have a low risk for subsequent detachment. Holes are caused by chronic atrophy of the sensory retina and are most likely to be located in the temporal retina (superior > inferior quadrant)

286
Q

Retinal tears and RRDs

A

caused by vitreous traction. Types of retinal tears include flap (horseshoe) takers and operculated tears

287
Q

Flap tears

A

more serious)-the flap is present because of uneven vitreous traction; vitreoretinal traction often persists in these cases (vitreous stays attached to the flap), increasing the risk of a retinal detachment compared to operculated tears

288
Q

Operculated tears

A

the initial vitreoretinal traction resutls in an even, symmetric tear. After forming the tear, the vitreous pulls away and vitreoretinal traction no longer persists, reducing the risk for a RD

289
Q

Which is more serious, flap or operculated tears

A

Flap

290
Q

Symptoms of RRDs

A

classic symptoms include vitreous floaters, flashing lights (photopsia), a curtain or veil over the vision, and decreased acuity

291
Q

In RRDs, is it helpful to know what quadrant the flashes and floaters are?

A

The quadrant location in which a patient reports flashes of lights is of no value in predicting the location of a the primary retinal break; however, the quadrant location for VF defects is often valid. For example, if the field defect is reported in the inferior nasal quadrant, a superior temporal retinal break is expected

292
Q

Signs of an acute RRD

A

convex undulating retina with clear subretinal fluid that does not shift with body position; Shafer’s sign (pigment cells in AC) may or may not be present. Additional signs may include a mild iritis and lower IOP in the affected eye

293
Q

Signs of a chronic RRD

A

pigment demarcation line will be present (3 months or longer). Additional signs include intraretinal cysts, fixed folds, and/or subretinal precipitates

294
Q

Most likely location for a retinal break in patients with RRD

A

the ST quadrant is the most likely location for a retinal break in patients with and RRD. 50% of eyes with an RRD will have more than one retinal break; in most of these cases the breaks are located within 90 degrees of one another.

295
Q

Lattice degeneration

A

◦ Lattice is present in 6-10% of patients; 20-33% of patients with RRDs will have lattice degeneration; however only 1% of patients with lattice degeneration develop RRDS
◦ Lattice is an area of peripheral retinal thinning that is typically circumferential and concentric with the ora serrata.
◦ The inner portion of the lesion is atrophic (thin), while the outer margins of the lesions have a firm adhesion to the vitreous. The majority of lesions DO NOT contain the criss cross pattern of white sclerosed vessels; only 12% of patients have this classic appearance

296
Q

Location of lattice

A

often bilateral and mor commonly located temporally and superiority

297
Q

What systemic diseases can have lattice like lesions in the retina

A

Patients with Marfans syndrome, Sticklers syndrome, and Ehlers Danlos syndrome can have lattice like lesions (atypical lattice) that increase the risk of RD

298
Q

Vitreoretinal tufts

A

small, focal areas of vitreous traction located in the retinal periphery. They occur in 5% of the population and are the second most common peripheral retinal lesion associated with RD (lattice is first); less than 1% of patients with vitreoretinal tufts develop a RD

299
Q

Types of non RRDs

A

Serous

Tractional

300
Q

Serous RD (exudative)

A

result from subretinal disorders that damage the RPE and a,low fluid accumulation under the retina. Examples include ARMD, inflammatory conditions, vascular conditions, neoplasms, and miscellaneous causes. Patients with exudative RDs are typically asymptomatic, unless the detachment involves the macula

301
Q

Tractional RD

A

most commonly caused by PDR, ROP, and proliferative sickle cell retinopathy. Patients with TRDs usually do not have complaints of flashes and floaters and may be completely asymptomatic. Possible symptoms include decreased vision or progressive VF defects

302
Q

Epidemiology/Hx of age related degenerative retinoschisis

A

occurs in 4-7% of the general population; more common in patietns 40 years or older

303
Q

Pathophysiology/Dx of age related degenerative retinoschisis

A

degenerative process that results from a splitting of the OPL and the INL, resulting in elevation of the inner retina that mimics a RD

304
Q

Symptoms of age related degenerative retinoschisis

A

typically asymptomatic; vision loss is rare

305
Q

Signs of age related degenerative retinoschisis

A

dome shaped bullous elevation most commonly located inferiorly/temporally. Unlike a RD, the retina i immobile, bilateral findgins are common, and an absolute VF defect will correspond to the area of elevation
‣ 70% of patietns are hyperopic
‣ “Snowflake” or “frosting” and sheathed retinal vessels occur in the elevated retinal layer of the retinoschisis
‣ Inner wall breaks and outer wall breaks can occur in a retinoschisis. Outer wall breaks are more dangerous- they are required to cause a retinoschisis-associated RD. Outer wall breaks will appear “pock marked” on scleral depression. They can be surrounded with laser treatment to prevent an RD

306
Q

Inner and outer wall breaks in age related degenerative retinoschisis

A

‣ Inner wall breaks and outer wall breaks can occur in a retinoschisis. Outer wall breaks are more dangerous- they are required to cause a retinoschisis-associated RD. Outer wall breaks will appear “pock marked” on scleral depression. They can be surrounded with laser treatment to prevent an RD

307
Q

Pathophysiology/Dx of angioid streaks

A

large breaks in Bruch’s membrane that result from damage to the elastic core of Bruch’s membrane. 50% of cases are idiopathic; the remaining cases are caused by systemic disease

308
Q

Most common condition associated with angioid streaks

A

Remember PEPSI for the most common causes of angioid streak: PXE (by far the most common cause), Ehlers Danlos Syndrome, Paget’s disease, Sickle-cell disease, and idiopathic

309
Q

Symptoms of angioid streaks

A

may be asymptomatic or have profound vision loss from CNVM. 70% of patients will eventually have some form of vision loss

310
Q

Signs of angioid streaks

A

spoke like (around the disc), linear, well-demarcated red/orange or brown lines within the elastic core of Bruch’s membrane

311
Q

Toxocariasis pathophysiology/Dx

A

caused by toxocara canis or cati, which is the intestinal nematode in dogs or cats

312
Q

Symptoms of toxocariais

A

patients may complain of floaters and blurred vision

313
Q

Signs of toxocariass

A

ocular infection causes a significant unilateral inflammation response, resulting in optic nerve edema, RD, vitritis, endophthalmitis, and subretinal granulomas. large, white chorioretinal scars are present after the active infection has resolved

314
Q

Chororetinitis

A

form of posterior uveitis that is characterized by inflammation of the choroid and retina. Examples include toxoplasmosis, toxocariasis, sarcoidosis, syphilis, CMV, serpiginous choroidopathy, birdshot, TB, and onchocerciasis

315
Q

Acute posterior multifocal placoid pigment epitheliopathy

A

◦ Occurs acutely in young adults, typically after a viral illness. Characterized by bilateral, yellowish, flat, subretinal lesions. Disc edema and RD may also occur
◦ Usually resolves without treatment after a few weeks

316
Q

Central areolar choroidal dsytriphy

A

◦ An AD condition characterized by bialteral large areas of GA in the macula. Will cause vision loss in the 4-5th decade. Poor prognosis

317
Q

Senile choroidal atrophy

A

results from choroidal thinning and may cause an exaggerated tigroid fundus appearance due to increased visibility of the choroidal vasculature

318
Q

What kind of RD in DRVOS

A

Tractional

319
Q

What kind of RD in CHBALA

A

Serous

320
Q

Glaucoma

A

the most likely source of an optic neuropathy. It is a leading cause of irreversible blindness worldwide. In the US, it is estimated that 2.79mill people have POAG, and this number is expected to increase in the future. The following will focus on subjects related to glaucoma

321
Q

What is the most likely source of optic neuropathy

A

Glaucoma

322
Q

an IOP greater than 21 (IOP>24 per the OHTT) on consecutive visit is in a patient with an open angle and without glaucomatous optic neuropathy

A

Ocular HTN

323
Q

Risk factors for conversions of OHTN to POAG

A

◦ IOP-the only risk factor we can control!
◦ Race-AA-4-5x more likely to develop glaucoma
◦ Family Hx:overall proportion of POAG related to genetics is around 16%. Having a first degree relative (parent, sibling, child) with glaucoma is associated with a 3 to 4 fold increase risk of POAG
◦ Age-greater than 90% of those with glaucoma are over the age of 55
◦ Thin corneas

324
Q

What is the only risk factor we can control for converion of OHTN to POAG

A

IOP

325
Q

CCT readings and risk of glaucoma

A
  • <555um=higher risk
  • 555-588um=no change of risk based on CCT
  • > 588um=lower risk
326
Q

What CCT should we be worried about in glaucoma

A

<555

327
Q

the most common type of glaucoma that occurs in 0.5-2.1% of those over age 40. It is defined as glaucomatous optic nerve damage with corresponding VF loss that occurs with IOPs greater than 21mmHg with an open angle on gonio. The exact cause of the increased IOP is not known

A

POAG

328
Q

Signs for detection of POAG

A

damage to the optic nerve. Larger C/Ds, asymmetry between the optic nerves, focal vertical thinning or notching, nerve fiber bundle defects, and vascular signs (baring, hemorrhages) are important clinical signs. Recall that the larger the optic disc, the larger the expected cup size

329
Q

ISNT rule in glaucoma

A

suggests that normal optic nerves should have the most rim tissue in the inferior quadrant, then superior, nasal, and the temporal quadrant (thinnest). However, glaucoma may initially damage the inferior OR superior rim

330
Q

VF loss in POAG

A

◦ Initial field loss is variable, but nasal steps are the most common. Paracentral and arcuate defects are also relatively common

331
Q

Symptoms of POAG

A

usually asymptomatic until later stages when significant peripheral or central vision is lost

332
Q

Port wine stains and glaucoma

A

vascular birthmarks that have a high association with ipsilateral glaucoma (45% of cases). It is rarely associated with systemic disorders-most notably Sturge-Weber syndrome (5% of cases)

333
Q

Pseudoexfoliation syndrome and glaucoma

A

age related systemic condition that is most commonly in caucasians, especially those of Scandinavian decent. PXE is the most common identifiable cause of elevated IOP and resultant glaucoma

334
Q

Most common identifiable cause of elevated IOP and resultant glaucoma

A

Pseudoexfoliation syndrome

335
Q

Characteristics of Pseudoexfoliation syndrome

A

characterized by abnormal, white, flaky despots whose exact compilation and cause of formation remain unknown. The flaky deposits are found throughout the body and may have systemic implications
◦ In the eye, these deposits can be found on the pupillary margin, on the lens capsule in a bulls eye pattern, on the lens zonules, and in the TM
◦ Gonio often reveals a Sampoalesi’s line due to the accumulation of pigment that is releases as the deposits rub against the posterior iris epithelium.

336
Q

Sampaolesi’s line

A

increased pigmentation anterior to Schwalbes line; it is assocaited with PES and PDS

337
Q

What is Pseudoexfoliation syndrome associated with

A

poor pupil dilation and an increased risk of lens subluxation and cataract surgery complications due to weak lens zonules

338
Q

Patient presentation of pseudoexfoliation syndrome

A

majority of patients present with unilateral or bilateral asymmetric pseudoexfoliative glaucoma. The risk of developing glaucoma is 15% within 10 years

339
Q

Pigmentary dispersion syndrome

A

Condition that is usually bilateral, more common in caucasians, and presents in young patients. The condition is more common in myopes and males.
‣ Pigmentary dispersion Syndrome is thought to resutls from higher anterior chamber pressure that causes excessive bowing of the iris posteriorly, resulting in more contact between the iris and lens zonules; this leads to pigment shedding off the posterior edge of the iris

340
Q

Symptoms of PDS

A

often asymptomatic, but may have blurred vision and halos around lights after exercising or pupil dilation

341
Q

Signs of PDS

A

TIDs, Krukenburg’s spindle (vertically oriented line of pigment on the corneal endo), pigment on the anterior capsule of the lens and the iris surface, and TM hyperpigmentation

342
Q

Prognosis of PDS

A

Pigment dispersion syndrome may burn out over time as the lens thickens, resulting in less contact between the posterior iris epithelium and lens zonules

343
Q

Risk of glaucoma and PDS

A

risk of glaucoma at 5 years is 10% and 15 years is 15%

344
Q

Angle recession glaucoma

A

characterized by a wide open angle with a recessed iris and widened ciliary body band. It is most often unilateral and results from blunt trauma. Although the angle appears wide open, the TM is damaged, resulting in an increased risk of glaucoma over time. 10% of patietns with angle recession involving at least 2/3 of the angle will develop glaucoma

345
Q

Considered a type of POAG in which the NFL damage occurs at lower pressures; most define the condition as IOP less than 21mmHg with an open angle on gonio and glaucomatous ON damage with corresponding VF loss.

A

NTG

346
Q

Who is at risk of NTG

A

Females are at a greater risk and the condition has the highest prevalence among Japanese patients. Additional risk factors include vascular disorders such as Raynaud’s phenomenon or migraines, low blood pressure, sleep apnea, hypercoagulation, and taking BP meds before bedtime (may decrease ocular perfusion pressure)

347
Q

What must you do before Dx NTG

A

Before dx NTG, it is important to take diurnal IOP readings to ensure the diagnosis is truly NTG rather than POAG. This who develop NTG typically have IOPs in the high teens.

348
Q

Signs of NTG

A

similar to those of POAG, but Drance hemorrhages are more common in NTG. Initial VF defects in NTG are usually more focal (but more dense) and closer to fixation because the temporal and interotemporal rim tissue is more commonly affects first (compared to POAG)

349
Q

Other causes of optic neuropathy and NTG

A

Since IOP is within the normal range in NTG, it is important to rule out other possible sources of the optic neuropathy, especially cases of suspected unilateral NTG. Consider asking about a history of hemorrhagic shock, myocardial infarction, anemia, syphilis, and vasculitis

350
Q

Primary angle closure glaucoma

A

• can be acute or intermittent (sub acute) and occurs as a result of the posterior pressure in the posterior chamber pushing the peripheral iris anteirorly into contact with the TM, blocking part or all of the TM and impeding aqueous outflow. The pupil may or may not be blocked in angle closure glaucoma

351
Q

What are the two main causes of primary acute angle closure glaucoma

A

Pupillary block

PI

352
Q

Pupillary block

A

occurs in patients with anatomically narrow angles (hyperopes) when the aqueous flow through the pupil is blocked (usually by the lens but can also be the vitreous). Patients are most at risk for angle closure when the pupil reaches the mid position after coming down from dilation, as this is the point of greatest iris-lens contact

353
Q

Risk factors for pupillary block related angle closure

A

hyperopes, advancing cataracts, Asians and eskimos, and lens subluxation

354
Q

Plateau iris

A

characterized by anteriorly positioned ciliary processes that push the peripheral iris forward into contact with the TM. Slit lamp and gonio reveals a flat iris plane, a normal central anterior chamber depth, but a convex peripheral iris.

355
Q

What can be done to differentiate plateau iris and pupillary block

A

peripheral iridotomy or iridectomy can be performed to differentiate pupillary block from plateau iris configuration; in the latter, the peripheral iris proximity to angle structures will be unchanged after the procedure.

356
Q

Sub acute or chronic angle closure

A

occurs when part of the angle closes, causing episodes of elevated IOP without patient symptoms. Subacute angle closure is more common than acute angle closure. Chronic angle closure should be expected in patients with occludable angles and any of the following signs
‣ PAS or pigment splotching the TM
‣ Progressive optic nerve damage with corresponding VF loss

357
Q

Acute angle closure

A

defined as angle closure (no TM visible with gonio) causing an acute IOP spike (50-100mmHg) and patient symptoms. Signs and symptoms include:
‣ Vomiting, intense ocular pain, HA, halos, nausea, and progressive vision loss.
‣ Prominent signs include a 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 a peripheral iridotomy

358
Q

Glaucomflecken

A

anterior subcapsular opacities that resutls from lens epithelial cell ischemia and necrosis secondary to high pressures

359
Q

What is the greatest threat to vision in acute angle closure

A

CRAO

occurs when IOP is higher than the prefusuion pressure of the CRA

360
Q

Topamax and glaucoma

A

used for treating migraines, weight loss, epilepsy, can cause acute secondary angle closure. It causes supraciliary effusion, which moves the lens and iris forward into contact with the TM, resulting in angle closure. This typically occurs within the first month of use or if the dosage is increased

361
Q

Patients with a history of angle closure are at higher risk of

A

higher risk for developing open angle component of glaucoma due to TM and ONH damage. Will manifest as high IOP with ON damage with an open angle on gonio, and may be immediate or years later. Pts with narrow angle AND open angle component of glaucoma have mixed mechanism glaucoma

362
Q

Mixed mechanism glaucoma

A

Pts with narrow angle AND open angle component of glaucoma have mixed mechanism glaucoma

363
Q

serious condition that frequently results in severe vision loss and a painful eye. Neovascular glaucoma most commonly occurs with condition that results in severe retinal ischemia

A

NVG

364
Q

Most common cause of NVG

A

CRVO

-followed by PDR, OIS, and RD. Carotid artery disease and CRAO are less common causes

365
Q

Most important sign to recognize in NVG

A

rubeosis of the iris. The pupillary margin should be examined closely for capillary tufts or early signs of neo.

366
Q

Progression of rubeosis of the iris can cause secondary angle closure via what mechanisms

A

‣ Neo of the angle is always accompanies by fibrous tissue that forms a membrane over the TM, preventing aqueous outflow. A significant fibrous membrane can develop even with only 1-2 vessels on the angle
‣ The fibrovascular membrane can stick to the iris, pulling it into contact with the TM and causing secondary angle closure. This is known as “zippering of the angle”

367
Q

Occurs as a result of a PAS and PS formation in uveitis. Remember that uveitis causes the iris to become inflamed and sticky. The iris can stick to the lens or the TM

A

Uveitic glaucoma

368
Q

PS and uveitic glaucoma

A

will only cause an elevation in IOP when there is 360 degrees of attachment between the iris and the lens. This results in iris bombe and pupillary block, which moves the iris anteriorly into contact with the TM

369
Q

PAS and uveitic glaucoma

A

PAS will cause varying degrees of IOP elevation depending on the extent of angle involvement

370
Q

Importance in managing uveitis aggressively

A

very important to manage uveitis aggressively to prevent the formation of PS and PAS. If PS occur during the current epidose of inflammation, every effort should be made to break them. Once the current uveitis episode resolves, PS can only be removed surgically

371
Q

Congenital glaucoma

A

◦ Onset is typically birth to 3 months of age; the condition is most often bilateral and is more common in males. Congenital glaucoma results from a developmental abnormality in the AC that impedes aqueous outflow

372
Q

an enlarged eye with a corneal diameter >12mm that occurs by one year of age in patients with congenital glaucoma as a result of elevated IOP

A

Buphthalmos

373
Q

Group of disorders characterized by abnormal corneal endothelium that grows onto the iris or in the angle, increasing the risk for glaucoma. Signs include corneal edema, iris atrophy, PAS, and angle closure. These syndromes are more common in females and patients 20-50;

A

ICE syndromes

374
Q

What are the ICE syndromes

A

‣ Essential Iris atrophy-iris thinning with resultant heterochromia, polycorea, corectopia, and ectropion uvea
‣ Chandler’s syndrome-the corneal endothelium will have a”Beaten metal” appearance with corneal edema and corectopia
‣ Iris-Nevus-Syndrome (Cogan-Reese Syndrome)-Nodules will be present on the anterior iris surface

375
Q

What are the inflammatory glaucoma’s

A
  • glaucomatocyclitic crisis (Posner-Schlossman syndrome)
  • Fuch’s Heterochromic iridocyclitis
  • Phacolytic glaucoma
376
Q

Characterized by acute trabeculitis that results in an acute elevation of IOP (40-60mmHg). There will be few cells and flare in the AC, and gonio will reveal an open angle. The condition occurs most often to young to middle aged patients and is characterized by recurrent unilateral episodes that often burn out over time

A

• Glaucomatocyclitic Crisis: AKA Posner-Schlossman syndrome

377
Q

chronic, non-granulomatous, low grade anterior uveitits with stellate KPs. Additional signs include iris heterochromia and iris/angle neo. Patients have an increased risk of glaucoma (due to chronic TM damage) and cataracts due to chronic inflammation

A

Fuchs heterochromic iridocyclitis

378
Q

results from a hyper mature cataract that leaks lens material into the AC, resulting in blockage of the aqueous outflow through TM. Cells, flare, and iridescent lens particles will be present within the AC

A

Pahcolytic glaucoma

379
Q

RNFL and glaucoma

A

glaucoma is characterized by retinal ganglion cell death and corresponding RNFL loss. Upon clinical exam, the RNFL loss can be difficult to see, especially if it is early or mild. In an effort to detect structural optic nerve damage earlier, computerized instruments have been developed to detect mild changes in the RNFL. They may also be helpful to detect progression

380
Q

Imaging for the RNFL

A

‣ GDx uses scanning laser polarizer to detect thinning of the RNFL
‣ OCT uses optical coherence tomography
‣ HRT uses confocal scanning laser ophthalmoscopy for a topographical evaluation of the ONH and peripapillary rim

381
Q

OCT and glaucoma

A

• The OCT Stratus (zeiss) is a time domain system and the Spectralis (Heidelberg) and Cirrus (zeiss) are spectral domain systems. Spectral domain results in better resolution and is faster and more sensitive. Swept source, the newest technology, is even better than spectral domain because if higher sensitivity and speed

382
Q

Macular evaluation in glaucoma

A

the retinal ganglion cells are densest in the macula; studies have shown that patients with glaucoma show thinner areas in the macula that correspond with VF loss. There are 3 instruments that are capable of analyzing macular ganglion cell thickness: RTVue Ganglion Cell Complex Analyzer (optovue), Spectralis Posterior Pole Asymmetry Analyzer (Heidelberg), and CIrrus Ganglion Cell Analysis (Zeiss)

383
Q

Macular evaluation instruments for glaucoma

A

‣ RTVue measures the three innermost macular layers and compares the patients data to a normative database
‣ The spectralis does NOT have a normative database but allows for inter and intra-eye asymmetry results
‣ The cirrus measures only the ganglion cell-IPL complex and compares resutls to a normative database

384
Q

When to do gonio

A

performed in order to Dx the appropriate type of glaucoma. Additional indications include narrow angles on Van Herick, signs of PDS (TIDs and Kruckenberg spindle), iris neo, suspicious iris lesion, Hx of ocular trauma, or when following a CRVO

385
Q

Documentation of gonio

A

performed in order to Dx the appropriate type of glaucoma. Additional indications include narrow angles on Van Herick, signs of PDS (TIDs and Kruckenberg spindle), iris neo, suspicious iris lesion, Hx of ocular trauma, or when following a CRVO

386
Q

AC angle structures from posterior to anterior

A

: I Can See The Stupid Line=iris, CB, scleral spur, TM, Schwalbes line

387
Q

‣ Static automated perimetry (SAP)

A

the Humphrey VF is the most popular SAP threshold used

388
Q

‣ Short Wavelength Automated Perimetry (SWAP)

A

uses a yellow background with blue stimuli to detect early glaucomatous damage that is not detected with SAP

389
Q

Frequency Doubling Technology (FDT)

A

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

390
Q

Extent of normal VF

A

100 degrees temporal, 60 degrees nasal and superior, and 70 degrees inferior. The blind spot is located 15 degrees temporal and 7.5 degrees in diameter

391
Q

Reliability indices

A

fixation loses, FP, FN, and short term fluctuations (STF)

392
Q

Short term fluctuations on VF

A

determined by randomly retesting certain points. Poor performance on STFs could indicate poor reliability of early glaucoma

393
Q

Fixation losses > ____ will be flagged on VF

A

20%

394
Q

FP/FN errors > ___ will be flagged on VF

A

33%

395
Q

Grayscale on VF

A

this is a gross representation of the VF. The darker areas indicate reduced sensitivity. This can be used for patient education purposes but has minimal value in interpretation

396
Q

Total deviation on VF

A

compares how well the patient did compared to the database of healthy, age-matched samples
• A zero indicates the patient scored the same as the normative database. A positive number means the patient performed better than expected. A negative number means the patient performed worse than expected
• The darker the probability box on the total deviation probability plot, the greater the patients response deviated from the expected response

397
Q

Pattern deviation

A

filters out diffuse loss (cataracts) to show only focal areas of deviation that are more typical in glaucoma

398
Q

Glaucoma hemifield test

A

compares sensitivity levels between the upper and lower hemifields. Remember that glaucoma often causes asymmetric ONH damage, resulting in an asymmetric field loss above and below the horizontal midline. The GHT will state WNL, borderline, ONL, or reduced sensitivity

399
Q

Visual field indies (VFI)

A

this gives a measure of the rate of visual field loss over time and is given as a % of normal. 100% means no loss of the VF, 0% means total blindness

400
Q

Mean deviation on VF

A

Mean deviation (MD): the average of the differences between the patients overall sensitivity and the overall sensitivity of the normative database. MD is an indication of diffuse loss; the more negative the MD, the more general depression in the VF

401
Q

Pattern standard deviations on VF

A

compares the patients shape of the hill of vision to the shape of the hill of vision of the normative database. PSD indicates focal areas of depression that are typical in glaucoma. It is always an absolute value; higher PSD means greater focal VF loss.

BOARDS (14 decks)

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