MT 2 Flashcards
(317 cards)
1
Q
Leukemia
A
Neoplastic proliferation of WBC. Usually high WBCC.
2
Q
Myeloblastic Leukemia
A
Can occur in all ages but more common with older
3
Q
Lymphoblastic Leukemia
A
Normally occurs in those under 10
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)
5
Q
Ocular findings with leukemia of active vs. chronic
A
Acute has 4 times the ocular findings
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.
7
Q
Waldenstrom’s Macroglobuilemia
A
Cancer involving increased IGM of plasma.
8
Q
Onset of Waldenstrom’s
A
Usually over age 50
9
Q
Clinical Findings with Waldenstrom’s
A
Weakness, weight loss, recurrent infections, retinal hemorrhages, blurred vision.
10
Q
What are the clinical symptoms of Waldenstrom’s similar to?
A
Multiple Myeloma
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)
12
Q
Lipemia Retinalis
A
Greatly increases triglyceride levels. Family trait or secondary to systemic disease that affects fat metabolism. Patient are normally asymptomatic.
13
Q
Fasting glucose in those with lipemia Retinalis
A
Fasting glucose >200 (normal is 120)
14
Q
Total serum chol. level in those with lipemia retinalis
A
> 1,000. Normal is 120-220
15
Q
Triglyceride level in those with lipedemia retinalis
A
> 10,000. Normal is 50-149.
16
Q
When do retinal findings in lepemia retinal is typically occur
A
When triglyceride level reaches 2,500.
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
18
Q
What is age range for lepedmia retinalis
A
10-40
19
Q
Treatment for lipedmia retinalis
A
Intensive diet and meds to reduce triglyceride. Control any systemic condition.
20
Q
Behcet’s Disease
A
Systemic occlusive vasculitis (thought to be an immune complex disorder). Remissions and exacerbations.
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.
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.
23
Q
Early Retinal involvement with Behcet’s
A
Disc hyperamia, CME, Ischemic vascultis, deep retinal exudation. Will see diffuse vascular leakage with FA.
24
Q
late Retinal involvement with Behcet’s
A
Will see sclerosed blood vessels and chorioretinal atrophy.
25
Tx for behcet's
Topical and periocular steroids for uveitis, possible oral steroid and immunosuppresion (chlorambucil or cyclosprine), photocagulation for retinal neovascularation. Systmic consult with collagen vascular specialist.
26
Prognosis with Behcet's
Poor. Uveitis is chronic, bilateral, and recurrent. Retinitis and vascultis may destroy the retina or optic nerve.
27
Sarcoidosis
Mostly affects lungs and lymph nodes. Granulomas form. Etiology is unknown (abnormal immune response)
28
Sarcoidosis incidence
Young black females
29
Test for Sarcoidosis
ACE
30
Systemic symptoms of Sarcoidosis
Persistent dry cough, fatigue, SOB. Some have no symptoms. Onset and progression of symptoms differ for everyone.
31
Diagnosis of sarcoidosis
Chest radiograph with see granulomas, pulmonary function tests, ACE (68% have), abnormal calcium metabolism (63% hypercalcemia), biopsy of the granuloma, consider gallium scan.
32
Ocular involvement with sarcoidosis
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.
33
Enlargement of lacrimal gland with sarcoid
S shaped upper lid. Seconary dry eye.
34
Granulomatous uveitis in sarcoid
bilateral. Mutton fat Kp's. Iris nodules.
35
What conditions do candle wax drippings occur in?
Sarcoid and lupus
36
ONH swelling with sarcoid
ONH granuloma. Local edema. Orbital granuloma causes compression of ONH. Raised ICP
37
MGMT of sarcoid ocular complications
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.
38
Prognosis of Sarcoid
Disease appears briefly and then disappear. 20-30 permanent lung damage, 10-15 chronic, 5-10 fatal
39
Systemic Lupus Erythematosus
Chronic inflammatory disease affecting multiple organs (especially skin, joints, blood, and kidneys). Autoimmune disease. Can be mild-serious and life threatening disease.
40
Epidemiology of Lupus
Females, 20-40, black, indian, Asian
41
Criteria to dx lupus
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.
42
Tests for Lupus
ANA (95). Possitive anti-DNA, anti-Sm
43
Lupus retina
Diffuse arteriolar occlusive vasculitis. See cotton wool spots, retinal hemorrhages, roth spots, swollen optic nerve head
44
Lupus tx
NSAIDs, acetominophen, steroids, antimalrials (chloroquine, hydroxyquine), Immunomodulating drugs (azathoprine, cyclophosphamide, methotrexate, cyclosporine), anticoagulants
45
AMD is the most common cause of vision loss in the elderly in the _______ world
Developed
46
AMD is the result of
oxidative stress, inflammation, metabolic end product deposition.
47
What does AMD affect?
RPE, Bruch's membrane, choriocapillaris, photoreceptors.
48
Vision loss with AMD
Damage to the macular result in loss of central vision. The peripheral is spared.
49
AMD is directly related to_____
age
50
AMD is most common in what race
white
51
Non modifiable AMD risk factors
Age, F, Caucasian, light ocular pigmentation
52
How much of AMD risk is attributed to genetics
70%. ARMS and CFH
53
Modifiable AMD risk factors
smoking, Photoxicity (short waves), previous cataract surgery (controversial), obesity, HTN, Cardiovascular, Alcohol consumption (J shaped), Asprin daily use? MPOD,
54
J shape with alcohol consumption
A little alcohol will decrease and then drastically increase
55
AMD and quality of life
increased depression, decreased daily activities, frequent falls, social problems
56
Foveal avascular zone
Receives nutrition from choriocapillaris.
57
Early AMD
medium sized drusen, Vas usually not affected
58
Intermediate AMD
Larger drusen, RPE hyperplasia and hypertrophy, PED, Vas maybe affected (depends where drusen is)
59
Advanced AMD categories
Dry or Wet
60
Dry advanced AMD
20%. Geographic atrophy
61
Wet advanced AMD
80%. Choroidal neovascaulrization. Hemorrhagic RPE or sensory detachment, viterous hemorrhaging, disciform scarring if not treated.
62
RPE changes with AMD
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.
63
RPE degeneration causes
damage of overlying photoreceptors and underlying choroidal perfusion suggesting chronic disease process.
64
RPE Degeneration FA
HypOflourescene in ares of clumping. HypeRflourescences in areas of hypopigmentation
65
Drusen
Extracellular deposits that lie between the BM of the RPE and inner collagen zone of bruch's
66
Drusen Features
Often bilaterally symmetrical, clustered in the macular region, and tend to increase in number with age.
67
Drusen composition
Extracelllar material derived from RPE. Includes proteins, vitronectin, amyloid, inflammatory components, immunologically products.
68
What is drusen due to
Presence of inflammation in sub retinal space.
69
Small Hard Drusen
Small
70
Intermediate soft drusen
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.
71
Large soft drusen
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)
72
Prevalence of large soft drusen is related to _____
age
73
Presence of large soft drusen has an increase risk of developing
RPE abnormalities, geographic atrophy, CNV
74
______ is sufficient to make AMD diagnosis
large soft drusen
75
FA of soft drusen
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
76
Familial Drusen
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.
77
Signs of familiar drusen
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.
78
Familial Drusen Symptoms
Often asymptomatic at first. In third or first generation may notice decreased VA, metamorphosis, paracentral scotoma.
79
Calcified Drusen
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.
80
AMD PED
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.
81
Causes of PED
serous fluid, hemorrhage, drusen coalescence or fibrovascular tissue
82
PED characteristics
Sharply demarcated, dome shaped, round oval elevation of the RPE, may have a smooth and homogenous surface.
83
PED characteristics
Overlying pigment clumping may be present. Can remain stable for several years. Collapses cause RPE or geographic atrophy
84
When does PED indicate possible CNV
If overlying sensory RD is present
85
Prognosis with PED
Depends on underlying z process.
86
PED and CNV
1/3-1/2 chance of CNV in older patient. Larger size increases chance.
87
PED FA
Gradual and uniform staining of the sub-RPE material
88
Symptoms of PED
Reduced vision and metamorphopsia
89
Nonexudative AMD
Same as dry. Most common form of AMD. 10-20 progress wo wet form. May lead to geographic AMD (advanced form)
90
Exudative AMD
Wet. Least common form. Most common cause of AMD.
91
AMD stages
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.
92
Nonexudative AMD complaints
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.
93
Nonexudative Objective findings
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)
94
Early Nonexudative
ID by several small drusen or a few medium. No obvious symptoms or VL
95
Intermediate nonexudative
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
96
Advanced nonexudative
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.
97
Follow Up with Nonexududative AMD within minimal RPE changes
1 year
98
Follow UP with nonexudative AMD as RPE disruption worsens
6 months
99
Follow up with nonexudative AMD with high risk confluent drusen and/or pigment degeneration
4-6 months
100
What else should you consider with with dry AMD followup
Consider risk factors.
101
Late AMD geographic atrophy
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.
102
What causes Late AMD Geographic atrophy
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
103
What occurs with late AMD geographic atrophy
Gradual loss of RPE, choriocapillaris, and photoreceptor layer. Outer plexiform layer is thinned and vacuoles.
104
In late AMD will CNV occur within atrophic zone
NO! Only 10-20% of eye may develop CNV at the margins of the atrophy.
105
Late Dry AMD complaints
Vision impairment, vision loss more noticeable with near, decreased contrast
106
Objective findings with late dry AMD
Choroidal atrophy (due to a reduction in nutritional demands), larger choroidal vessels become more prominent.
107
Test to run on a pt with late geographic atrophy
Retinal exam, color fundus photo, amsler grid, OCT, photostress test, color vision, central 10 automated perimetry, FA
108
Tx for geographic atrophy
No pratical effective treatment is available. Nutrietion education
109
Follow up for geographic atrophy
6-12 months depending on extent
110
Wet AMD
Due to CNV. Main cause of vision loss in AMD (10-20% VL(
111
What is the hallmark of wet AMD
Formation of neovascularization. CNV grow through a break in bruch's.
112
Neovascularization in Wet AMD
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.
113
Sub RPE Neovascularization
Grow from choriocapillaries to just below RPE. Break between chorio and RPE
114
Sub-retinal Neovascularization
Grow from choriocapillaris to just below sensory retina. Sensory retina break from chorio.
115
Neovascular vessels are prone to _____
leakage. Leakage can lead to serous detachment of RPE, lipid exudation, hemorrhages, RPE tears
116
Complaints with Wet AMD
Reduced vision, distorted vision, color distortion.
117
When to think CNV
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
118
Objective findings with neovasclarization
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.
119
When do you want to diagnose someone with wet AMD
Early. By the time symptoms has occurred it is too late.
120
How much does a CNV grow a day
10-18 microns
121
Special emphasis on testing with choroidal neovascularization
FA
122
Foresee PHP
Designed to monitor progression of AMD from dry to wet.
123
Home Foresee PHP
Can have pt. take it home and monitor it. Helps with early detection.
124
Types of CNV membranes on FAs
Classic, minimally classic, occult
125
Classic CNV
13% of CNV. Has well-defined borders, fills with dye in lacy pattern, fluoresces brightly then leaks into sub retinal space around the CNVM.
126
Occult CNV
87%. Poorly defined membranes.
127
Minimally Classic
A mixture of the two. Has both characteristics.
128
DX of Wet AMD
OCT in office, Fa to determine if tx if appropriate is a must, timely intervention is essential.
129
If CNV is left untreated...
hemorrhage RPE detachment, hemorrhagic sensory detachment, viterous hemorrhage, disciform scaring, massive exudation. All of these lead to severe and permanent vision loss
130
Hemorrhagic RPE detachment
Results from rupture of blood vessels. Initially appearance is very dark red and elevated.
131
Hemorrhagic RPE FA
HYPERfluorescence corresponding to the RPE detachment with HYPOfluorescene with the hemorrhage
132
Hemmorrhage Sensory Detachment
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
Disciform Scaring
Follows a hemorrhagic episode. Fibrous scar at the fovea. Can take on many shapes and sizes. Permanent loss of central vision.
134
Massive Exudation
Results from chronic leakage from CNV. Can lead to exudative retinal detachment.
135
Antioxidants
Can quench free radicals by donating extra electron without becoming a free radical. Vitamin E, C, beta-carotene.
136
AREDs
Vitamine to prophylatically prevent against macula degeneration
137
What should Smokers not take
Beta Carotene. (Vitamine A)
138
When is ARED recommended
Extensive intermediate size drusen, I large drusen, non-central geographic atrophy, Advanced AMD or vision loss in 1 eye.
139
Carotenoids
Macular pigments made of lutein and zeaxanthin. Protect from blue eye.
140
Where is zeaxanthin more prevelent
The very center of the macula.
141
Where is lutenin more prevelent
The peripheral macula
142
Macula risk test
Commercially available. Can bill insurance
143
Hard Exudates
Discrete white yellow lipid deposits in post pole. May present as large confluent exudation. Macular star patten. Ring pattern around leakage.
144
Hard exudates vs. drusen
hard exudates are more anterior (between inner plexiform and inner nuclear layers). May have a distinct pattern, yellow waxy appearance.
145
CWS
Fluffy areas of NFL edema. Caused by focal ischemia.
146
AREDS II
Addes letein, zeaxanthin and fatty acids and deletion of Beta carotene and zinc.
147
Which patients are strongly recommended to use AREDs
With intermediate or advanced in one eye
148
Findings with AREDS II study
No reduction in progress with additional of fatty acids
149
Treatment for dry AMD
No practical treatment available currently
150
Rheopheresis
Look at treating dry AMD with this. Use double filtration plasmapheresis
151
Antioxidant Eye drops for geographic atrophy
Well tolerated. Can possibly maintain Vas. Limited efficacy.
152
Fenretinide
Looking at using for dry AMD. Well tolerated but many SE. Stops the conversion to wet. Very promising but currently no trials.
153
Laser photocogulation
Thermal laser is used to destroy abnormal BVs. Decrease VAs but stop further deterioration.
154
Do you do photocogulation to subfoveal and juxtafoveal CNVM
If small and if patient is willing
155
AMD and nutrition
Intake of grain and whit meat may protect against AMD
156
Visudyne (verteprofin)
Allows chemical obliteration of CNV without destroying overlying retinal tissue. Very $$$$. Visudyne targets abnormal tissue and non-thermal light directed at Visudyne.
157
Who does photocoagulation work best in?
Classic AMD.
158
Who does visudyne work best in?
Occult AMD
159
Photocogulation and other therapies
Can be effective if used with other therapies
160
What two drugs does genentech make
lucentis and avastin
161
Macugen
only delayed progression of CNV. Vas still decrease with time.
162
Lucentis (Ramizumaub)
First time that an increase in Vas was seen!
163
Lucentis treatment
Will give every month for 3 months and then accordingly dependent on OCT
164
Avastin (bevacizuma)
Used off label for AMD. Most commonly used drug.
165
Does Avastin blind people
No! It is the formulating companies.
166
Regeneron (VEGF trap-Eye)
Longer duration compared to conventional treatment.
167
Pericytes
NV vessels mature with the help of tip cels. Tip cells produce PDGF -> attract pericytes. Pericytes create an Anti-VEGF armor
168
Fovista
Stops pericytes from coming so the vessels are more vulnerable to VEGF
169
_____ is the 2nd most prevalent retinal vascular disease seen
Branch retinal vein occlusion
170
Categories of BRVO
1. Major= 5+DD of retina
2. Primary = involves 2-5 DD retina
3. Secondary=
171
BRVO an systemic disease
HTN, Cardiovascular disease, diabetes, glaucoma
172
BRVO Complaints
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
BRVO signs
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
Bonnet's sign
Banking of vein (dilated) distal to crossing.
175
Complications with BRVO
chronic macular edema and neovascularization
176
Workup for BRVO
OCT, FA, DFE, DFE, VF, Fundus. Check BP. Fasting blood glucose, CBC, prothrombin time, ESR, ANA, CXR and ACE, RF. Cardiovascular workup.
177
TX for BRVO
FA if threat of edema to macular or if neo indicated, home ambler, refer to retinologist, topical antigenic meds, possible anticoagulants, laser photocogulation.
178
When to use laser with BRVO
Chronic ME reducing VA below 20/40 or retinal neovascularization
179
Ozurdex
Dexamethasone implant used in patient with ME.
180
Ranibizumab (lucentis)
Can use with BRVO
181
CRVO epidemiology
Usually after 50. Associated with carotid artery disease. Men more often. Usually unilateral. Glaucoma can occur.
182
CRVO complaints
Sudden, unilateral, painless vision loss.
183
CRVO Signs
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
Nonischemic CRVO
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
Ischemic CRVO
Total CRVO closure. Extensive retinal hemes. Mulitple CWS. Marked CME. Elderly pt. APD seen.
186
Will CRVO have collaterals?
NO
187
MGMT for CRVO
FA, D/C or change meds, reduce IOP, refer, consider ASA, laser photocogulation, Anti-VEGF, steroids.
188
PRP for nonischemic CRVO
not very effective. Did not prevent the development of NVI. Wait until development for tx
189
When to perform PRP
If neo of iris, retina, or optic nerve.
190
Follow up for CRVO
Nonischemic: Q4 weeks for the first 6 m
Ischemic: Q3-4weeks after tx for the first week.
191
VEGF and VO
Anti-VEGF approved for VO.
192
BRAO
Disruption of vascular perfusion. Due to embolism (cholosterol, calcifications, platelet-fibrin, septic). Occurs in elderly and unilateral.
193
Ischemia in inferior portion of retina
Indicates it is artery
194
Association of BRAO and systemic dz
HTN, hypercoagulation, caratid occlusive disese, diabetes
195
What causes VO typically
Hyperlipidemia of the blood. Not an emboli like with AO
196
BRAO
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
TX for BRA
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
BRAO tests
ESR if elderly. CBC. ANA, RF, FTA. Drug screen for younger pt.
199
BRAO mgmt
Cardiology consult, FA, Followup 3-6m to monitor
200
CRAO
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
CRAO signs
Narrow arteries, superficial retinal whitening in posterior pole, cherry red spot of macula, +APD, boxcar ring of veins, neovacularization
202
CRAO TX
Rapid tx: digital massage in supine, Paracentesis, Fa to determine damage, CAIs PO option, topical beta blockers, Hospital!
203
CRAO lab
Immediate ESR to R/O GCA. Check BP. FB, CBV, ANA, RF, etc.
204
CRAO workup
cardiology consult, FA, follow up Q1-4 weeks
205
Hypertensive Retinopathy
Secondary to HTN. Patients usually asymptomatic.
206
Chronic hypertensive retinopathy findings
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
Acute hypertensive retinopathy
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
Hallmark of malignant hypertensive retinopathy
Swelling ONH
209
Workup for hypertensive retinopathy
Mhx, check BP, complete ocular exam
210
FU for hypertensive retinopathy
Refer to cardiologist, retinal consult if threat of CSME or hypoxia, RTC q 2-3m initially then q6-12
211
Cerebral thromboembolism
Blood clot of artery that is likely damaged by atherosclerosis
212
Cerebral embolism
embolisum travels to cerebral circulation to lodge in an artery
213
Ocular Ischemic Syndrome
Ocular signs attributable to severe carotid artery obstruction or other ischemic coronary artery disease. Under-reported. Elderly men. usually unilateral.
214
OIS complains
Mild loss of vision, pain, possible TIA. Afterimage of prolonged vision recovery after exposure to bright light
215
OIS signs
RED EYE, narrowed retinal arteries, dilated but not tortuous retinal veins, mid peripheral heme, Neovascular, uveitis.
216
OIS workup
MHx, ocular exam, FA, palpation of carotid, Lab test, refer to cardiologist, refer to neovascular surgeon, internist, stop smoking, manage glaucoma
217
Retinopathy of prematurity
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
Follow up for retinopathy of prematurity
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
Central serous retinopathy
Small break in RPE leads to serous retinal detachment under the macula. Detachement between RPE and rest of retina.
220
Epidemiology of central serous retinopathy
Men between 20-40 years of age, type A, stress
221
Complaints with central serous retinopathy
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
FA with central serous retinopathy
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
Central serous retinopathy prognosis
80-90% have spontanous resolution within 1-6m. Mild metamorphosis may remain much longer.
224
Tx for central serous retinopathy
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
Macular hole
Retinal hole in the fovea. Idiopathic. Trauma is rare
226
Macular hole epidemiology
Agre related. Women. 60-80. CME, post surgical, postinflam are higher risk.
227
Macular hole symptoms
decreased vision
228
Macular Hole Mechanism
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
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Operculum
The piece of the retina pulled free
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Macula Hole Signs
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)
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Macular Hole TX
No tx for stage 1 holes. Vitrectomy, membrane peel, gas fluid exchange, and gase injection. Use of adjuvant agents controversial.
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Macular hole prognosis
Good for recent onsets (less than 1 year). Poor for holes greater than 1 year.
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Myopic Degeneration
Progressive retinal degeneration seen in high myopes (>6D or >26.5) and pathological myopia (32.5mm). Sclera is stretched and thinned.
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Myopic degeneration damage
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
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Lacquer cracks
Yellow streaks. Breaks in bruchs. Occurs with myopic degeneration
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Posterior staphyloma
IOP pushes the thinned scleral outward.
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Circumpapillary Staphyloma
Straightening of bv. Myopic degeneration.
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Angioid Streaks
Breaks in calcified thickened Bruch's membrane.
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Angoid streaks etiology
idiopathic or associated with systemic disease (pseudoxanthoma elasticum, pager's, sickle cell)
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Symptoms with angioid streaks
asymptomatic, decreased vision, metamorphosis if choroidal neovascularization
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Angioid Streaks Signs
Irregular, deep, dark red-brown streaks radiating from the optic disc in a spoke like pattern.
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Angioid neovascularization
Can get neovascularization because bruch's is damaged
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Angioid Streaks TX
Treat similar to ARMD. Polycarbonate safety glasses as trauma can cause hemorrhages.
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Angioid Streaks Px
Good unless CNM develops
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DX diabetes off of fasting blood sugar
over 126
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2 hour glucose tolerance done
Fasting glucose. Drink 75 gram glucose. Blood drawn 2 hours late. Over 200 problems
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HBA1C
look at glucose level of 3 months
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Numbers for prediabetes
100-126, 140-199, 5.7-6.4
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Type 1
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.
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Pregnancy and Type 1
Must control levels before carrying.
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Complications with diabetes
Kidney, heart
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HBA1C for peds
lower than 7.5%
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HBA1C for adults
7
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HBA1C for older and long standing
8
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Type 2 diabetes
Failure of pancreatic B cells to secret enough insulin. Insulin resistance at cellular level. Strong genetic predisposition.
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Which type of DM has the stronger genetic predeposition
Type 2
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how much of DM population has type 2
90%
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What do most people die of with type 2
CV complications
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ClearPath DS-120 Lens fluorescence biomicroscope
A 6 second test that measure autofluroescence of lens. Predicated to diagnose types 2 diabetes
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Hypoglycemia
plasma glucose less than 3.9
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Symptoms of hypoglycemia
Sweating, blurry vision, dizziness, anxiety, hunger, irritability, shakiness, fast heartbeat, HA, weakness
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what do do with hypoglycemia during an eye exam
Give patient a rapid acting carb
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Recommendation for mgmt of DM
A: A1c
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A1c to mean plasma glucose
(A1C*35.6)-77.3
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DM 1.5
Type 1 that slows progression to insulin dedpenence. An autoimmune condition unlike type 2. Treated like type 2.
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Pregnancy and eye exams
Should have an eye exam proper to pregnancy or during the first trimester with follow ups every trimster
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Gestational DM
2/3 trimester. Lower in whites. Risk with obesity and family history of type 2.
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Is gestational DM associated with retinopathy
NO!
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TX during pregnancy
Type 2 switch from oral meds-insulin. Type 1 continues with insulin. Watch BP.
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Ocular and gestational diabetes
increased risk of development or progression of diabetic retinopathy. Usually mild and regresses. Increased risk of macula edema.
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Do you do high plus with those with diabetes
NO! Should be dilated
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Why gonio with DM
don't want to miss neo in the angle.
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Tests for DM
Color vision (BY vision), contrast, macular function test, ultrasonography if vitreous heme, FANG for determining tx area
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Xanthelasmas
Occur with elevated serum lipid levels and reflect poor DM control.
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Macular dystophy
Macular is AR and granular is AD. Spaces between dots get hazy so need PK
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EBMD
Will get RCE first thing in the morning
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Avellino Drystophy
combo of lattice and granular
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EOM and DM
Due to occlusion of blood supply to the n. Commonly 3 and 6 but can 4th as well.
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Likely most common n affects
6th nerve! Will get horizontal diplopia in primary gaze and when looking to effectived side. Fresnel prism can be used to tx.
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Third n. palsy
Unable to elevate eye, depress, and eye down and out.
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Cornea and DM
Those with DM have decreased corneal sensitivity
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neuotrophic ulcers
common with DM. Due to patient not getting signal to blink so eye dries out
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DM and wound healing
very poor. Cl wear needs to be evaluated closely.
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Iris neovasclarization
Develops at pupillary frill or the anterior angle. Can block angle.
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How to tell if iris neovasclarization
will run over the TM and not with it.
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Pupils and DM
Pupil reactivity is sluggish. Excessive miosis or failure to dilate normally in the dark. Poor reaction to mydriatic agents.
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What to do if need more drops and patient responding to light
tropicamide
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What to do if need more drops and patient not responding to light
phenylephrine
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Viterous and DM
Increased liquefaction.
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Lenticular changes with DM
Changes in the hale of the lens and RE. Sorbital pathway causes lens to swell. Myopic shifts are most common with increasing blood sugar.
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CME Complain
Complain is decreased vision. Occur after cataract surgery commonly
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CME Signs
Irregularity and blurring and FLR, foveal thickening with small intraretinal cyst. FA often shows early leakage and late macular staining.
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CME TX
Most resolve spontneously in 6 m. Topical NSAIDS for 6 weeks (allegro or prolensa), Diamox daily
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Patient with DM and surgery
Pre-tx with Illevro or prolensa
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Diabetic Retinopathy
Closely related to duration of DM.
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What sex does DR more often affect?
Females
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Dr in type 1 vs type 2
type 1 more likely to get. Type 2 comes in more often with bad DR on diagnosis
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After 20 years how many of those with DM will have DR
80%
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Pathogensis of DR
Cell to cell communication. Changes due to hyperglycemia. Another major cause is leukocytes at the walls that damages them.
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DR signs
microaneurysms, retinal edema, hard exudates, CWS, IRMA, viterous heme, neovascularization
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IRMA
Shunt vessels appear. Very difficult to see. Stimulated by hypoxia.
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Types of DR
Nonproliferative and proliferative. Nonproliferative has mild, moderate, and severe
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Chance of going from NP to P
Mild 5-10, moderate 20-30, severe 50
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Mild NPDR
At leaf one retinal microaneuyrsm
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Moderate NPDR
hemorrhage/microaneurysm greater than or equal to 2A in 1-3 quadrants and/or soft exudates, venous needing, and IRMA
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Severe NPDR
4:2:1 rule. hemorrhage/microoaneurysm in all 4 quadrants. Venous needing in at least 2 quadrants. Irma in 1 quadrant
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CSME
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
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TX for CSME
Treat with intravitreal anti-VEGF with focal laser coagulation. Can also use kelalog injections or implantable lluvien or ozurdex.
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When to refer for a pt with DM in 2-4 weeks
macular edema, severe NPDR with may be treated if risk factors, early PDR
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When to refer a pt with DM in 24-48 hours
High risk PDR or vitreous heme.
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PDR
hallmark sign is neovasculariation. Commonly patient complains of blurry vision, Concern of tractional retinal Detachment secondary to fibrotic proliferation.
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TX for PDR
Retinal concsult, vitrectomy and new VEGF injections. PDR>
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High risk PDR
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.
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When to use PRP with PDR
High risk PDR, reubosis, widespread retinal ischemia.
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Lucentis
Can be used to treat DR> not standard of choice yet though
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Diabetic papillopathy
This can occur. Rare. VA only slightly changed. Often seen with macular edema. If bilateral then not pailledema.
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TX for diabetic papillopathy
No tx
