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MT 2 Flashcards

1
Q

Leukemia

A

Neoplastic proliferation of WBC. Usually high WBCC.

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2
Q

Myeloblastic Leukemia

A

Can occur in all ages but more common with older

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3
Q

Lymphoblastic Leukemia

A

Normally occurs in those under 10

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4
Q

Leukemia Systemic Signs

A

Fatigue, weakness, anorexia, hemmorahges, fever, pallor, lymphadenopathy, hepatosplenomegaly, skin and mucous membrane ecchymoses (discoloration of skin due to bleeding)

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5
Q

Ocular findings with leukemia of active vs. chronic

A

Acute has 4 times the ocular findings

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6
Q

Ocular findings with leukemia

A

Venous dilation and tortuosity (early), retinal hemorrhages, exudates (leukemic cells), cotton wool spots, optic nerve infiltration, (all above late). Roth spots (hemorrhage with WBCs and fibrin), pre-retinal hemorrhages, Perivascular infiltration (WBCs around the BV). Basically WBCs and bleeding.

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7
Q

Waldenstrom’s Macroglobuilemia

A

Cancer involving increased IGM of plasma.

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8
Q

Onset of Waldenstrom’s

A

Usually over age 50

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9
Q

Clinical Findings with Waldenstrom’s

A

Weakness, weight loss, recurrent infections, retinal hemorrhages, blurred vision.

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10
Q

What are the clinical symptoms of Waldenstrom’s similar to?

A

Multiple Myeloma

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11
Q

Retinal findings with Waldenstrom’s

A

Dilated tortuous retinal veins, retinal hemorrhages, roth spots (similar to other anemias so must do case history)

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12
Q

Lipemia Retinalis

A

Greatly increases triglyceride levels. Family trait or secondary to systemic disease that affects fat metabolism. Patient are normally asymptomatic.

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13
Q

Fasting glucose in those with lipemia Retinalis

A

Fasting glucose >200 (normal is 120)

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14
Q

Total serum chol. level in those with lipemia retinalis

A

> 1,000. Normal is 120-220

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15
Q

Triglyceride level in those with lipedemia retinalis

A

> 10,000. Normal is 50-149.

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16
Q

When do retinal findings in lepemia retinal is typically occur

A

When triglyceride level reaches 2,500.

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17
Q

Retinal findings with lipedmia retinalis

A

Retinal vessels are salmon pink to ivory in color. This is diagnostic and just need blood test to confirm. Rest of retinal normal and Va’s not affected

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18
Q

What is age range for lepedmia retinalis

A

10-40

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19
Q

Treatment for lipedmia retinalis

A

Intensive diet and meds to reduce triglyceride. Control any systemic condition.

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20
Q

Behcet’s Disease

A

Systemic occlusive vasculitis (thought to be an immune complex disorder). Remissions and exacerbations.

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21
Q

Who is affected by Behcet’s

A

Young adults (18-40) most often in Japan and Mediterranean area. More sever in younger men.

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22
Q

Triad for Behcet’s

A

Aphthous stomatitis-ulcer in mouth, genital ulcers, recurrent hypopyon iritis (usually bilateral with posterior involvement. Uveitis too). Will also have joint pain, eye swelling inflammation and pain.

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23
Q

Early Retinal involvement with Behcet’s

A

Disc hyperamia, CME, Ischemic vascultis, deep retinal exudation. Will see diffuse vascular leakage with FA.

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24
Q

late Retinal involvement with Behcet’s

A

Will see sclerosed blood vessels and chorioretinal atrophy.

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25
Q

Tx for behcet’s

A

Topical and periocular steroids for uveitis, possible oral steroid and immunosuppresion (chlorambucil or cyclosprine), photocagulation for retinal neovascularation. Systmic consult with collagen vascular specialist.

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26
Q

Prognosis with Behcet’s

A

Poor. Uveitis is chronic, bilateral, and recurrent. Retinitis and vascultis may destroy the retina or optic nerve.

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27
Q

Sarcoidosis

A

Mostly affects lungs and lymph nodes. Granulomas form. Etiology is unknown (abnormal immune response)

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28
Q

Sarcoidosis incidence

A

Young black females

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29
Q

Test for Sarcoidosis

A

ACE

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30
Q

Systemic symptoms of Sarcoidosis

A

Persistent dry cough, fatigue, SOB. Some have no symptoms. Onset and progression of symptoms differ for everyone.

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31
Q

Diagnosis of sarcoidosis

A

Chest radiograph with see granulomas, pulmonary function tests, ACE (68% have), abnormal calcium metabolism (63% hypercalcemia), biopsy of the granuloma, consider gallium scan.

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32
Q

Ocular involvement with sarcoidosis

A

25-50% of patients. Enlargement of lacrimal gland, granulomatous anterior uveitis, conj lesions, vitrifies or string of pearls vitreous opacities, periphlebitis (inflammation of retinal vessels) with candle wax drippings, RVO, hemorrhages, optic disc edema, optic nerve granulomas.

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33
Q

Enlargement of lacrimal gland with sarcoid

A

S shaped upper lid. Seconary dry eye.

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34
Q

Granulomatous uveitis in sarcoid

A

bilateral. Mutton fat Kp’s. Iris nodules.

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35
Q

What conditions do candle wax drippings occur in?

A

Sarcoid and lupus

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36
Q

ONH swelling with sarcoid

A

ONH granuloma. Local edema. Orbital granuloma causes compression of ONH. Raised ICP

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37
Q

MGMT of sarcoid ocular complications

A

Manage dry eye, watch for cataracts from uveitis and steroid use, control anterior uveitis (topical steroids, oral steroid, immunosuppresent therapy). Watch for secondary glaucoma. Tx oral steroid or immunosupprsent for vision threatening retinopathy or optic disc edema.

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38
Q

Prognosis of Sarcoid

A

Disease appears briefly and then disappear. 20-30 permanent lung damage, 10-15 chronic, 5-10 fatal

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39
Q

Systemic Lupus Erythematosus

A

Chronic inflammatory disease affecting multiple organs (especially skin, joints, blood, and kidneys). Autoimmune disease. Can be mild-serious and life threatening disease.

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40
Q

Epidemiology of Lupus

A

Females, 20-40, black, indian, Asian

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41
Q

Criteria to dx lupus

A

malor rash over cheeks, discoid rash, photosensitivity resulting in sun rash, oral ulcers usually painless, arthritis involving two or more peripheral joints, serositis-pleuritis or pericarditis. Renal disorder (excessive protein in urine) Seizure or psychosis, hemolytic anemia or leukopenia.

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42
Q

Tests for Lupus

A

ANA (95). Possitive anti-DNA, anti-Sm

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43
Q

Lupus retina

A

Diffuse arteriolar occlusive vasculitis. See cotton wool spots, retinal hemorrhages, roth spots, swollen optic nerve head

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44
Q

Lupus tx

A

NSAIDs, acetominophen, steroids, antimalrials (chloroquine, hydroxyquine), Immunomodulating drugs (azathoprine, cyclophosphamide, methotrexate, cyclosporine), anticoagulants

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45
Q

AMD is the most common cause of vision loss in the elderly in the _______ world

A

Developed

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46
Q

AMD is the result of

A

oxidative stress, inflammation, metabolic end product deposition.

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47
Q

What does AMD affect?

A

RPE, Bruch’s membrane, choriocapillaris, photoreceptors.

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48
Q

Vision loss with AMD

A

Damage to the macular result in loss of central vision. The peripheral is spared.

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49
Q

AMD is directly related to_____

A

age

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50
Q

AMD is most common in what race

A

white

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51
Q

Non modifiable AMD risk factors

A

Age, F, Caucasian, light ocular pigmentation

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52
Q

How much of AMD risk is attributed to genetics

A

70%. ARMS and CFH

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53
Q

Modifiable AMD risk factors

A

smoking, Photoxicity (short waves), previous cataract surgery (controversial), obesity, HTN, Cardiovascular, Alcohol consumption (J shaped), Asprin daily use? MPOD,

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54
Q

J shape with alcohol consumption

A

A little alcohol will decrease and then drastically increase

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55
Q

AMD and quality of life

A

increased depression, decreased daily activities, frequent falls, social problems

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56
Q

Foveal avascular zone

A

Receives nutrition from choriocapillaris.

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57
Q

Early AMD

A

medium sized drusen, Vas usually not affected

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58
Q

Intermediate AMD

A

Larger drusen, RPE hyperplasia and hypertrophy, PED, Vas maybe affected (depends where drusen is)

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59
Q

Advanced AMD categories

A

Dry or Wet

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60
Q

Dry advanced AMD

A

20%. Geographic atrophy

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61
Q

Wet advanced AMD

A

80%. Choroidal neovascaulrization. Hemorrhagic RPE or sensory detachment, viterous hemorrhaging, disciform scarring if not treated.

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62
Q

RPE changes with AMD

A

Mottling of pigment epithelium and focal areas of hyper pigmentation. More often seen in eyes with soft or large drusen. If present then high risk of CN V.

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63
Q

RPE degeneration causes

A

damage of overlying photoreceptors and underlying choroidal perfusion suggesting chronic disease process.

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64
Q

RPE Degeneration FA

A

HypOflourescene in ares of clumping. HypeRflourescences in areas of hypopigmentation

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65
Q

Drusen

A

Extracellular deposits that lie between the BM of the RPE and inner collagen zone of bruch’s

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66
Q

Drusen Features

A

Often bilaterally symmetrical, clustered in the macular region, and tend to increase in number with age.

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67
Q

Drusen composition

A

Extracelllar material derived from RPE. Includes proteins, vitronectin, amyloid, inflammatory components, immunologically products.

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68
Q

What is drusen due to

A

Presence of inflammation in sub retinal space.

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69
Q

Small Hard Drusen

A

Small

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70
Q

Intermediate soft drusen

A

intermediate drusen (63-124). Tend to be fluffier. Pale yellow, dome shaped, deep with indistinct borders. Can vary in size and shape. Clnically may appear like RPE detachments. Associated with diffuse RPE dysfunction.

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71
Q

Large soft drusen

A

Large (greater than 125-width of large veins at disc margin). Same location as all drusen. Poorest prognosis of all drusen types. May become confluent and create a RPE detachments (PED)

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72
Q

Prevalence of large soft drusen is related to _____

A

age

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73
Q

Presence of large soft drusen has an increase risk of developing

A

RPE abnormalities, geographic atrophy, CNV

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74
Q

______ is sufficient to make AMD diagnosis

A

large soft drusen

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75
Q

FA of soft drusen

A

Soft drusen HYPERfluoresce early and either fade or stain later. Some drusen HYPO. Degree of fluorescence related to quality of pigment in overlying RPE and lipid content

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76
Q

Familial Drusen

A

AKA dominant drusen. Autosomal dominant pattern. + family hx. Metabolic defect in RPE. Present earlier in life. 20-30s. Bilateral, multiple, radiating, deep, and symmetrical. Pt may be symptomatic. May loose vision earlier in life.

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77
Q

Signs of familiar drusen

A

Elongated, radiating drusen in the macula bilaterally. May extend beyond the arcade, nasal to the dic, in a peripaillary patten, or on the disc margin. RPE degeneration and macula atrophy. Some patients may develop CNV. Usually periphery remains free of lesion.

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78
Q

Familial Drusen Symptoms

A

Often asymptomatic at first. In third or first generation may notice decreased VA, metamorphosis, paracentral scotoma.

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79
Q

Calcified Drusen

A

Long standing soft drusen that have aged and became crystalline in nature. Leave multifocal patches of atrophy and calcium deposits. Glistening appearance secondary to calcification.

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80
Q

AMD PED

A

Serous detachment of the RPE is common in AMD. Drusen develops and leads to loosening of adherence between RPE BM and inner collagenous portion of bruch’s (can lead to PED). There is no practical difference between a serous PED and soft drusen formation.

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81
Q

Causes of PED

A

serous fluid, hemorrhage, drusen coalescence or fibrovascular tissue

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82
Q

PED characteristics

A

Sharply demarcated, dome shaped, round oval elevation of the RPE, may have a smooth and homogenous surface.

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83
Q

PED characteristics

A

Overlying pigment clumping may be present. Can remain stable for several years. Collapses cause RPE or geographic atrophy

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84
Q

When does PED indicate possible CNV

A

If overlying sensory RD is present

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85
Q

Prognosis with PED

A

Depends on underlying z process.

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86
Q

PED and CNV

A

1/3-1/2 chance of CNV in older patient. Larger size increases chance.

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87
Q

PED FA

A

Gradual and uniform staining of the sub-RPE material

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88
Q

Symptoms of PED

A

Reduced vision and metamorphopsia

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89
Q

Nonexudative AMD

A

Same as dry. Most common form of AMD. 10-20 progress wo wet form. May lead to geographic AMD (advanced form)

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90
Q

Exudative AMD

A

Wet. Least common form. Most common cause of AMD.

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91
Q

AMD stages

A

When you first have AMD=dry (intermediate or large drusen) This is 80-90% of people. 10-20 progress to late stage AMD. Of the late stages 80% will have wet and 10-20 will have GA (dry). 10-20 of GA may become wet due to CNV.

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92
Q

Nonexudative AMD complaints

A

Maybe none, gradual mild to moderate vision impairment, vision loss more noticeable with near tasks, vision fluctuation, changes with night vision or changing light conditions.

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93
Q

Nonexudative Objective findings

A

Depigmentation of RPE, hyper pigmentation of RPE, granular clumping of RPE, VA rarely reduced to legal blindness, metamorphosis is rarely present early. Central vision is often spared initially (due to xanthophyll pigment). Fovea eventually involved. Over time areas may coalesce into geographic patterns (late)

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94
Q

Early Nonexudative

A

ID by several small drusen or a few medium. No obvious symptoms or VL

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95
Q

Intermediate nonexudative

A

ID by many medium sized drusen or one or more large, soft drusen. Symptoms may included blurred vision, blind spot, metamorphophsia, decreased contrast sensitivity, may be asymptomatic

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96
Q

Advanced nonexudative

A

ID by drusen as described above, plus a breakdown of photoreceptor cells and surrounding tissues in the macula. Blind spots may become larger and metamorphosis more severe. May eventually encompass the entire center field making detail vision impossible.

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97
Q

Follow Up with Nonexududative AMD within minimal RPE changes

A

1 year

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98
Q

Follow UP with nonexudative AMD as RPE disruption worsens

A

6 months

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99
Q

Follow up with nonexudative AMD with high risk confluent drusen and/or pigment degeneration

A

4-6 months

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100
Q

What else should you consider with with dry AMD followup

A

Consider risk factors.

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101
Q

Late AMD geographic atrophy

A

The most advanced form of dry AMD. Long standing traditional dry AMD can lead to geographic AMD. Often bilateral, symmetrical disease. May have a different rate of onset and progression. Areas of atrophy continue to enlarge over time.

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102
Q

What causes Late AMD Geographic atrophy

A

Unclear but may be due to areas of confluent large, soft drusen that have undergone regression, accumulation of lipofuscin and A2E, multiple areas of hyper or hypo pigmentation which may progress to large area of GA, spontaneous flattening of a PED

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103
Q

What occurs with late AMD geographic atrophy

A

Gradual loss of RPE, choriocapillaris, and photoreceptor layer. Outer plexiform layer is thinned and vacuoles.

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104
Q

In late AMD will CNV occur within atrophic zone

A

NO! Only 10-20% of eye may develop CNV at the margins of the atrophy.

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105
Q

Late Dry AMD complaints

A

Vision impairment, vision loss more noticeable with near, decreased contrast

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106
Q

Objective findings with late dry AMD

A

Choroidal atrophy (due to a reduction in nutritional demands), larger choroidal vessels become more prominent.

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107
Q

Test to run on a pt with late geographic atrophy

A

Retinal exam, color fundus photo, amsler grid, OCT, photostress test, color vision, central 10 automated perimetry, FA

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108
Q

Tx for geographic atrophy

A

No pratical effective treatment is available. Nutrietion education

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109
Q

Follow up for geographic atrophy

A

6-12 months depending on extent

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110
Q

Wet AMD

A

Due to CNV. Main cause of vision loss in AMD (10-20% VL(

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111
Q

What is the hallmark of wet AMD

A

Formation of neovascularization. CNV grow through a break in bruch’s.

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112
Q

Neovascularization in Wet AMD

A

Occurs due to a break in RPE/Bruch. New vessels from choriocapillaris grow up. CNV leak creating an RPE or sensory retinal detachment and lips exudation. CNV may hemorrhage created a sub-RPE or sub-retinal hemorrhage or form a disci form scar.

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113
Q

Sub RPE Neovascularization

A

Grow from choriocapillaries to just below RPE. Break between chorio and RPE

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114
Q

Sub-retinal Neovascularization

A

Grow from choriocapillaris to just below sensory retina. Sensory retina break from chorio.

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115
Q

Neovascular vessels are prone to _____

A

leakage. Leakage can lead to serous detachment of RPE, lipid exudation, hemorrhages, RPE tears

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116
Q

Complaints with Wet AMD

A

Reduced vision, distorted vision, color distortion.

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117
Q

When to think CNV

A
  1. grey-green membrane discoloration under the retina and may be w/ a pigmented ring which incircles the membrane
  2. Sensory retinal detachment
  3. Subretinal or sub RPE hemorrhage
  4. Hard exudates
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118
Q

Objective findings with neovasclarization

A

Slightly elevated sub retinal lesions of variable sizes, pale pink or yellow-white if broken into sub retinal space, associated with serous retinal elevation, sub retinal blood, or sub retinal lipid.

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119
Q

When do you want to diagnose someone with wet AMD

A

Early. By the time symptoms has occurred it is too late.

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120
Q

How much does a CNV grow a day

A

10-18 microns

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121
Q

Special emphasis on testing with choroidal neovascularization

A

FA

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122
Q

Foresee PHP

A

Designed to monitor progression of AMD from dry to wet.

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123
Q

Home Foresee PHP

A

Can have pt. take it home and monitor it. Helps with early detection.

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124
Q

Types of CNV membranes on FAs

A

Classic, minimally classic, occult

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125
Q

Classic CNV

A

13% of CNV. Has well-defined borders, fills with dye in lacy pattern, fluoresces brightly then leaks into sub retinal space around the CNVM.

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126
Q

Occult CNV

A

87%. Poorly defined membranes.

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127
Q

Minimally Classic

A

A mixture of the two. Has both characteristics.

128
Q

DX of Wet AMD

A

OCT in office, Fa to determine if tx if appropriate is a must, timely intervention is essential.

129
Q

If CNV is left untreated…

A

hemorrhage RPE detachment, hemorrhagic sensory detachment, viterous hemorrhage, disciform scaring, massive exudation. All of these lead to severe and permanent vision loss

130
Q

Hemorrhagic RPE detachment

A

Results from rupture of blood vessels. Initially appearance is very dark red and elevated.

131
Q

Hemorrhagic RPE FA

A

HYPERfluorescence corresponding to the RPE detachment with HYPOfluorescene with the hemorrhage

132
Q

Hemmorrhage Sensory Detachment

A

Develops as blood breaks through to the sub retinal space. Hemmohage is a bright red color. FA shows HYPOfluorescenec due to blockage of background cordial fluorescence.

133
Q

Disciform Scaring

A

Follows a hemorrhagic episode. Fibrous scar at the fovea. Can take on many shapes and sizes. Permanent loss of central vision.

134
Q

Massive Exudation

A

Results from chronic leakage from CNV. Can lead to exudative retinal detachment.

135
Q

Antioxidants

A

Can quench free radicals by donating extra electron without becoming a free radical. Vitamin E, C, beta-carotene.

136
Q

AREDs

A

Vitamine to prophylatically prevent against macula degeneration

137
Q

What should Smokers not take

A

Beta Carotene. (Vitamine A)

138
Q

When is ARED recommended

A

Extensive intermediate size drusen, I large drusen, non-central geographic atrophy, Advanced AMD or vision loss in 1 eye.

139
Q

Carotenoids

A

Macular pigments made of lutein and zeaxanthin. Protect from blue eye.

140
Q

Where is zeaxanthin more prevelent

A

The very center of the macula.

141
Q

Where is lutenin more prevelent

A

The peripheral macula

142
Q

Macula risk test

A

Commercially available. Can bill insurance

143
Q

Hard Exudates

A

Discrete white yellow lipid deposits in post pole. May present as large confluent exudation. Macular star patten. Ring pattern around leakage.

144
Q

Hard exudates vs. drusen

A

hard exudates are more anterior (between inner plexiform and inner nuclear layers). May have a distinct pattern, yellow waxy appearance.

145
Q

CWS

A

Fluffy areas of NFL edema. Caused by focal ischemia.

146
Q

AREDS II

A

Addes letein, zeaxanthin and fatty acids and deletion of Beta carotene and zinc.

147
Q

Which patients are strongly recommended to use AREDs

A

With intermediate or advanced in one eye

148
Q

Findings with AREDS II study

A

No reduction in progress with additional of fatty acids

149
Q

Treatment for dry AMD

A

No practical treatment available currently

150
Q

Rheopheresis

A

Look at treating dry AMD with this. Use double filtration plasmapheresis

151
Q

Antioxidant Eye drops for geographic atrophy

A

Well tolerated. Can possibly maintain Vas. Limited efficacy.

152
Q

Fenretinide

A

Looking at using for dry AMD. Well tolerated but many SE. Stops the conversion to wet. Very promising but currently no trials.

153
Q

Laser photocogulation

A

Thermal laser is used to destroy abnormal BVs. Decrease VAs but stop further deterioration.

154
Q

Do you do photocogulation to subfoveal and juxtafoveal CNVM

A

If small and if patient is willing

155
Q

AMD and nutrition

A

Intake of grain and whit meat may protect against AMD

156
Q

Visudyne (verteprofin)

A

Allows chemical obliteration of CNV without destroying overlying retinal tissue. Very $$$$. Visudyne targets abnormal tissue and non-thermal light directed at Visudyne.

157
Q

Who does photocoagulation work best in?

A

Classic AMD.

158
Q

Who does visudyne work best in?

A

Occult AMD

159
Q

Photocogulation and other therapies

A

Can be effective if used with other therapies

160
Q

What two drugs does genentech make

A

lucentis and avastin

161
Q

Macugen

A

only delayed progression of CNV. Vas still decrease with time.

162
Q

Lucentis (Ramizumaub)

A

First time that an increase in Vas was seen!

163
Q

Lucentis treatment

A

Will give every month for 3 months and then accordingly dependent on OCT

164
Q

Avastin (bevacizuma)

A

Used off label for AMD. Most commonly used drug.

165
Q

Does Avastin blind people

A

No! It is the formulating companies.

166
Q

Regeneron (VEGF trap-Eye)

A

Longer duration compared to conventional treatment.

167
Q

Pericytes

A

NV vessels mature with the help of tip cels. Tip cells produce PDGF -> attract pericytes. Pericytes create an Anti-VEGF armor

168
Q

Fovista

A

Stops pericytes from coming so the vessels are more vulnerable to VEGF

169
Q

_____ is the 2nd most prevalent retinal vascular disease seen

A

Branch retinal vein occlusion

170
Q

Categories of BRVO

A
  1. Major= 5+DD of retina
  2. Primary = involves 2-5 DD retina
  3. Secondary=
171
Q

BRVO an systemic disease

A

HTN, Cardiovascular disease, diabetes, glaucoma

172
Q

BRVO Complaints

A

Sudden, unilateral, painless VA loss suddenly over 24-48 hour period. Relative loss of part of the VF. VA may improve over time. Sometimes VA changes with postural changes.

173
Q

BRVO signs

A

Dilated, tortuous veins with retinal hemes and CWS in a wedge shape from AV crosses. Usually a superotemporal AV crossing. Lipid infiltrated near occlusion site later. Possible macular edema. Collatorals may form.

174
Q

Bonnet’s sign

A

Banking of vein (dilated) distal to crossing.

175
Q

Complications with BRVO

A

chronic macular edema and neovascularization

176
Q

Workup for BRVO

A

OCT, FA, DFE, DFE, VF, Fundus. Check BP. Fasting blood glucose, CBC, prothrombin time, ESR, ANA, CXR and ACE, RF. Cardiovascular workup.

177
Q

TX for BRVO

A

FA if threat of edema to macular or if neo indicated, home ambler, refer to retinologist, topical antigenic meds, possible anticoagulants, laser photocogulation.

178
Q

When to use laser with BRVO

A

Chronic ME reducing VA below 20/40 or retinal neovascularization

179
Q

Ozurdex

A

Dexamethasone implant used in patient with ME.

180
Q

Ranibizumab (lucentis)

A

Can use with BRVO

181
Q

CRVO epidemiology

A

Usually after 50. Associated with carotid artery disease. Men more often. Usually unilateral. Glaucoma can occur.

182
Q

CRVO complaints

A

Sudden, unilateral, painless vision loss.

183
Q

CRVO Signs

A

Diffuse retinal hemorrahge in all four quadrants of the retina with dilated, tortuous retinal veins. Possible CWS. Swollen ONH, Neo of ONH, retina, or iris,. Macular Edema. Possible APD.

184
Q

Nonischemic CRVO

A

75% cases. Can be 20/20-20/200. An incomplete CRVO with blood sliding. Milder funds changes. Young to middle age patient. No APD. Good prognosis depending on ME

185
Q

Ischemic CRVO

A

Total CRVO closure. Extensive retinal hemes. Mulitple CWS. Marked CME. Elderly pt. APD seen.

186
Q

Will CRVO have collaterals?

A

NO

187
Q

MGMT for CRVO

A

FA, D/C or change meds, reduce IOP, refer, consider ASA, laser photocogulation, Anti-VEGF, steroids.

188
Q

PRP for nonischemic CRVO

A

not very effective. Did not prevent the development of NVI. Wait until development for tx

189
Q

When to perform PRP

A

If neo of iris, retina, or optic nerve.

190
Q

Follow up for CRVO

A

Nonischemic: Q4 weeks for the first 6 m
Ischemic: Q3-4weeks after tx for the first week.

191
Q

VEGF and VO

A

Anti-VEGF approved for VO.

192
Q

BRAO

A

Disruption of vascular perfusion. Due to embolism (cholosterol, calcifications, platelet-fibrin, septic). Occurs in elderly and unilateral.

193
Q

Ischemia in inferior portion of retina

A

Indicates it is artery

194
Q

Association of BRAO and systemic dz

A

HTN, hypercoagulation, caratid occlusive disese, diabetes

195
Q

What causes VO typically

A

Hyperlipidemia of the blood. Not an emboli like with AO

196
Q

BRAO

A

unilateral, painless, abrupt loss of partial VF. May have HX TIA. Focal wedge shaped area of retinal whitening. Superior temporal arteries normally affected. Retinal edema. Possible CWS

197
Q

TX for BRA

A

Rapid TX required: massage to move embolic. Paracentesis if devastating to vision (remove aqueous), breath into a paper bag, FA to determine type of damage, CAIs po or IV, topical glaucoma meds.

198
Q

BRAO tests

A

ESR if elderly. CBC. ANA, RF, FTA. Drug screen for younger pt.

199
Q

BRAO mgmt

A

Cardiology consult, FA, Followup 3-6m to monitor

200
Q

CRAO

A

Disruption of vascular perfusion. Occurs in elderly and unilateral. Unilateral, acute vision loss (CF to LP) occurring over seconds. May have Hx of TIA.

201
Q

CRAO signs

A

Narrow arteries, superficial retinal whitening in posterior pole, cherry red spot of macula, +APD, boxcar ring of veins, neovacularization

202
Q

CRAO TX

A

Rapid tx: digital massage in supine, Paracentesis, Fa to determine damage, CAIs PO option, topical beta blockers, Hospital!

203
Q

CRAO lab

A

Immediate ESR to R/O GCA. Check BP. FB, CBV, ANA, RF, etc.

204
Q

CRAO workup

A

cardiology consult, FA, follow up Q1-4 weeks

205
Q

Hypertensive Retinopathy

A

Secondary to HTN. Patients usually asymptomatic.

206
Q

Chronic hypertensive retinopathy findings

A

Usually more subtle retinal findings, AV crossing changes, narrowing of arterioles, atheriosclerosis, CES, flame hemes, macro aneurysms, Possible central or branch occlusion of artery or veins. Venous tortuosity.

207
Q

Acute hypertensive retinopathy

A

Also called malignant hypertensive retinopathy. Much more pronouced retinal changes. Exudate in macular star. Exudates around optic nerve. Retinal edema. CWSs, flame, Swelling of ONH

208
Q

Hallmark of malignant hypertensive retinopathy

A

Swelling ONH

209
Q

Workup for hypertensive retinopathy

A

Mhx, check BP, complete ocular exam

210
Q

FU for hypertensive retinopathy

A

Refer to cardiologist, retinal consult if threat of CSME or hypoxia, RTC q 2-3m initially then q6-12

211
Q

Cerebral thromboembolism

A

Blood clot of artery that is likely damaged by atherosclerosis

212
Q

Cerebral embolism

A

embolisum travels to cerebral circulation to lodge in an artery

213
Q

Ocular Ischemic Syndrome

A

Ocular signs attributable to severe carotid artery obstruction or other ischemic coronary artery disease. Under-reported. Elderly men. usually unilateral.

214
Q

OIS complains

A

Mild loss of vision, pain, possible TIA. Afterimage of prolonged vision recovery after exposure to bright light

215
Q

OIS signs

A

RED EYE, narrowed retinal arteries, dilated but not tortuous retinal veins, mid peripheral heme, Neovascular, uveitis.

216
Q

OIS workup

A

MHx, ocular exam, FA, palpation of carotid, Lab test, refer to cardiologist, refer to neovascular surgeon, internist, stop smoking, manage glaucoma

217
Q

Retinopathy of prematurity

A

Proliferative retinopathy which affects pre termed infants exposed to high oxygen concentration. Have faso-proliferative stage once rerun to air. Then cicatrices stage-dragged retina

218
Q

Follow up for retinopathy of prematurity

A

Complete retinal exam q2w for all patient under 2 lbs 12 oz (unital 14 weeks). If no initial sign of ROP repeat exam at age 12-14 wks.

219
Q

Central serous retinopathy

A

Small break in RPE leads to serous retinal detachment under the macula. Detachement between RPE and rest of retina.

220
Q

Epidemiology of central serous retinopathy

A

Men between 20-40 years of age, type A, stress

221
Q

Complaints with central serous retinopathy

A

Fairly sudden onset of blurred vision in one eye, relative scotoma, metamorphosis, micropsia. Shallow round or oval elevation of the sensory retina. Borders outlined by glistening reflex.

222
Q

FA with central serous retinopathy

A

Hyperfluorescent spot of small RPE detachment. Smoke stake with FA, umbrella (mushroom)-spread dye laterally OR hyperfluorescenet spot of small RPE detachment and spot stays intense but gets slightly larger with time.

223
Q

Central serous retinopathy prognosis

A

80-90% have spontanous resolution within 1-6m. Mild metamorphosis may remain much longer.

224
Q

Tx for central serous retinopathy

A

No tx required. Argon laser photocoagulation of the leak considered when visual defect from recurrent attacks, vision in other eye is impaired, no resolution in 4-6m. Direct laser photocoagulation to leakage site shortens duration by 2 m but has no effect on final acuity

225
Q

Macular hole

A

Retinal hole in the fovea. Idiopathic. Trauma is rare

226
Q

Macular hole epidemiology

A

Agre related. Women. 60-80. CME, post surgical, postinflam are higher risk.

227
Q

Macular hole symptoms

A

decreased vision

228
Q

Macular Hole Mechanism

A

Posterior hyaloid is often attached to macula. As vitreous ages it become more liquid and the posterior hyaloid moves forward. This creates traction on the macula and a circular piece of the retina can be pulled free

229
Q

Operculum

A

The piece of the retina pulled free

230
Q

Macula Hole Signs

A

Full thickness hole, yellow deposits at level of RPE, Cuff os sub retinal fluid, operculum, positive watzke’s (subjective interruption of slit beam on slump)

231
Q

Macular Hole TX

A

No tx for stage 1 holes. Vitrectomy, membrane peel, gas fluid exchange, and gase injection. Use of adjuvant agents controversial.

232
Q

Macular hole prognosis

A

Good for recent onsets (less than 1 year). Poor for holes greater than 1 year.

233
Q

Myopic Degeneration

A

Progressive retinal degeneration seen in high myopes (>6D or >26.5) and pathological myopia (32.5mm). Sclera is stretched and thinned.

234
Q

Myopic degeneration damage

A

Most common area of damage is a myopic crescent (retina does not cover choroid) and ouch’s spot (dark spots of RPE hyperplasia) Choriorteinal atrophy, CNM

235
Q

Lacquer cracks

A

Yellow streaks. Breaks in bruchs. Occurs with myopic degeneration

236
Q

Posterior staphyloma

A

IOP pushes the thinned scleral outward.

237
Q

Circumpapillary Staphyloma

A

Straightening of bv. Myopic degeneration.

238
Q

Angioid Streaks

A

Breaks in calcified thickened Bruch’s membrane.

239
Q

Angoid streaks etiology

A

idiopathic or associated with systemic disease (pseudoxanthoma elasticum, pager’s, sickle cell)

240
Q

Symptoms with angioid streaks

A

asymptomatic, decreased vision, metamorphosis if choroidal neovascularization

241
Q

Angioid Streaks Signs

A

Irregular, deep, dark red-brown streaks radiating from the optic disc in a spoke like pattern.

242
Q

Angioid neovascularization

A

Can get neovascularization because bruch’s is damaged

243
Q

Angioid Streaks TX

A

Treat similar to ARMD. Polycarbonate safety glasses as trauma can cause hemorrhages.

244
Q

Angioid Streaks Px

A

Good unless CNM develops

245
Q

DX diabetes off of fasting blood sugar

A

over 126

246
Q

2 hour glucose tolerance done

A

Fasting glucose. Drink 75 gram glucose. Blood drawn 2 hours late. Over 200 problems

247
Q

HBA1C

A

look at glucose level of 3 months

248
Q

Numbers for prediabetes

A

100-126, 140-199, 5.7-6.4

249
Q

Type 1

A

Due to genes, immunological, and enviormental. Autoimmune destruction of pancreatic B cells. Usually acute polydipsia and polyuria. Patients hyperglycemic and symptomatic and 40% B cell loss.

250
Q

Pregnancy and Type 1

A

Must control levels before carrying.

251
Q

Complications with diabetes

A

Kidney, heart

252
Q

HBA1C for peds

A

lower than 7.5%

253
Q

HBA1C for adults

A

7

254
Q

HBA1C for older and long standing

A

8

255
Q

Type 2 diabetes

A

Failure of pancreatic B cells to secret enough insulin. Insulin resistance at cellular level. Strong genetic predisposition.

256
Q

Which type of DM has the stronger genetic predeposition

A

Type 2

257
Q

how much of DM population has type 2

A

90%

258
Q

What do most people die of with type 2

A

CV complications

259
Q

ClearPath DS-120 Lens fluorescence biomicroscope

A

A 6 second test that measure autofluroescence of lens. Predicated to diagnose types 2 diabetes

260
Q

Hypoglycemia

A

plasma glucose less than 3.9

261
Q

Symptoms of hypoglycemia

A

Sweating, blurry vision, dizziness, anxiety, hunger, irritability, shakiness, fast heartbeat, HA, weakness

262
Q

what do do with hypoglycemia during an eye exam

A

Give patient a rapid acting carb

263
Q

Recommendation for mgmt of DM

A

A: A1c

264
Q

A1c to mean plasma glucose

A

(A1C*35.6)-77.3

265
Q

DM 1.5

A

Type 1 that slows progression to insulin dedpenence. An autoimmune condition unlike type 2. Treated like type 2.

266
Q

Pregnancy and eye exams

A

Should have an eye exam proper to pregnancy or during the first trimester with follow ups every trimster

267
Q

Gestational DM

A

2/3 trimester. Lower in whites. Risk with obesity and family history of type 2.

268
Q

Is gestational DM associated with retinopathy

A

NO!

269
Q

TX during pregnancy

A

Type 2 switch from oral meds-insulin. Type 1 continues with insulin. Watch BP.

270
Q

Ocular and gestational diabetes

A

increased risk of development or progression of diabetic retinopathy. Usually mild and regresses. Increased risk of macula edema.

271
Q

Do you do high plus with those with diabetes

A

NO! Should be dilated

272
Q

Why gonio with DM

A

don’t want to miss neo in the angle.

273
Q

Tests for DM

A

Color vision (BY vision), contrast, macular function test, ultrasonography if vitreous heme, FANG for determining tx area

274
Q

Xanthelasmas

A

Occur with elevated serum lipid levels and reflect poor DM control.

275
Q

Macular dystophy

A

Macular is AR and granular is AD. Spaces between dots get hazy so need PK

276
Q

EBMD

A

Will get RCE first thing in the morning

277
Q

Avellino Drystophy

A

combo of lattice and granular

278
Q

EOM and DM

A

Due to occlusion of blood supply to the n. Commonly 3 and 6 but can 4th as well.

279
Q

Likely most common n affects

A

6th nerve! Will get horizontal diplopia in primary gaze and when looking to effectived side. Fresnel prism can be used to tx.

280
Q

Third n. palsy

A

Unable to elevate eye, depress, and eye down and out.

281
Q

Cornea and DM

A

Those with DM have decreased corneal sensitivity

282
Q

neuotrophic ulcers

A

common with DM. Due to patient not getting signal to blink so eye dries out

283
Q

DM and wound healing

A

very poor. Cl wear needs to be evaluated closely.

284
Q

Iris neovasclarization

A

Develops at pupillary frill or the anterior angle. Can block angle.

285
Q

How to tell if iris neovasclarization

A

will run over the TM and not with it.

286
Q

Pupils and DM

A

Pupil reactivity is sluggish. Excessive miosis or failure to dilate normally in the dark. Poor reaction to mydriatic agents.

287
Q

What to do if need more drops and patient responding to light

A

tropicamide

288
Q

What to do if need more drops and patient not responding to light

A

phenylephrine

289
Q

Viterous and DM

A

Increased liquefaction.

290
Q

Lenticular changes with DM

A

Changes in the hale of the lens and RE. Sorbital pathway causes lens to swell. Myopic shifts are most common with increasing blood sugar.

291
Q

CME Complain

A

Complain is decreased vision. Occur after cataract surgery commonly

292
Q

CME Signs

A

Irregularity and blurring and FLR, foveal thickening with small intraretinal cyst. FA often shows early leakage and late macular staining.

293
Q

CME TX

A

Most resolve spontneously in 6 m. Topical NSAIDS for 6 weeks (allegro or prolensa), Diamox daily

294
Q

Patient with DM and surgery

A

Pre-tx with Illevro or prolensa

295
Q

Diabetic Retinopathy

A

Closely related to duration of DM.

296
Q

What sex does DR more often affect?

A

Females

297
Q

Dr in type 1 vs type 2

A

type 1 more likely to get. Type 2 comes in more often with bad DR on diagnosis

298
Q

After 20 years how many of those with DM will have DR

A

80%

299
Q

Pathogensis of DR

A

Cell to cell communication. Changes due to hyperglycemia. Another major cause is leukocytes at the walls that damages them.

300
Q

DR signs

A

microaneurysms, retinal edema, hard exudates, CWS, IRMA, viterous heme, neovascularization

301
Q

IRMA

A

Shunt vessels appear. Very difficult to see. Stimulated by hypoxia.

302
Q

Types of DR

A

Nonproliferative and proliferative. Nonproliferative has mild, moderate, and severe

303
Q

Chance of going from NP to P

A

Mild 5-10, moderate 20-30, severe 50

304
Q

Mild NPDR

A

At leaf one retinal microaneuyrsm

305
Q

Moderate NPDR

A

hemorrhage/microaneurysm greater than or equal to 2A in 1-3 quadrants and/or soft exudates, venous needing, and IRMA

306
Q

Severe NPDR

A

4:2:1 rule. hemorrhage/microoaneurysm in all 4 quadrants. Venous needing in at least 2 quadrants. Irma in 1 quadrant

307
Q

CSME

A

AKA DME. Signs: Hard exuates with associated thickening with 1/3 DD of fovea, Edema within 1/3rd DD of center of fovea, Edema of 1DD within 1DD of fovea

308
Q

TX for CSME

A

Treat with intravitreal anti-VEGF with focal laser coagulation. Can also use kelalog injections or implantable lluvien or ozurdex.

309
Q

When to refer for a pt with DM in 2-4 weeks

A

macular edema, severe NPDR with may be treated if risk factors, early PDR

310
Q

When to refer a pt with DM in 24-48 hours

A

High risk PDR or vitreous heme.

311
Q

PDR

A

hallmark sign is neovasculariation. Commonly patient complains of blurry vision, Concern of tractional retinal Detachment secondary to fibrotic proliferation.

312
Q

TX for PDR

A

Retinal concsult, vitrectomy and new VEGF injections. PDR>

313
Q

High risk PDR

A

NVD>1/4 to 1/3 disc area, Any NVD with a pre retinal or vitreous hemorrhage, moderate to severe NVE with a vitreous or pre retinal hemorrhage, Any NVI.

314
Q

When to use PRP with PDR

A

High risk PDR, reubosis, widespread retinal ischemia.

315
Q

Lucentis

A

Can be used to treat DR> not standard of choice yet though

316
Q

Diabetic papillopathy

A

This can occur. Rare. VA only slightly changed. Often seen with macular edema. If bilateral then not pailledema.

317
Q

TX for diabetic papillopathy

A

No tx

OPT 633 (1 decks)

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