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Flashcards in Midterm 1 Deck (314):
1

Glaucoma is the ___ world leading cause of blindness

3rd

2

Glaucoma is the ___ world leading cause of blindness

3rd

3

Glaucoma Epidemology

A.A., older, HTN, Hyperlipidemia, diabetes, systemic vascular dz, Raynauds, alchohol/smoking, FHx

4

Ocular glaucoma risk factor with RE

Myopia (especially greater than 6D)

5

Visual acuity and glaucoma

Normally only affected late in the dz

6

Pupils and glaucoma

Affected late in the disease but occur bilaterally so no relative defects

7

Steamy cornea with perilimbal injection

Acute angle closure glaucoma

8

Krukenberg spindle

Pigment. May be pigment dispersion glaucoma

9

Glaucomfleckin

This is opacification of the lens from high IOP.

10

Normal IOP

10-21 mmhg.

11

What IOP pressure alone is enough to start tx?

30 mmhg

12

Normal corneal thickness

555 nm

13

____ Corneas underestimate IOP

Thin

14

____ Corneas overestimate IOP

Thick

15

Corneal thickness at a high risk

16

Corneal thickness at a lower risk

>588

17

Progressive thinning of _____ is pathonogmonic for glaucoma

Neural rim

18

Disk size of myopes vs. hyperopes

Myopes have a bigger disc.

19

As C/D reaches ____ glaucoma risk increases

.6

20

Is asymmetrical optic discs normal?

NO! Any difference of .1 is abnormal

21

Glaucoma Epidemology

A.A., older, HTN, Hyperlipidemia, diabetes, systemic vascular dz, Raynauds, alchohol/smoking, FHx

22

Ocular glaucoma risk factor with RE

Myopia (especially greater than 6D)

23

Visual acuity and glaucoma

Normally only affected late in the dz

24

Pupils and glaucoma

Affected late in the disease but occur bilaterally so no relative defects

25

Steamy cornea with perilimbal injection

Acute angle closure glaucoma

26

Krukenberg spindle

Pigment. May be pigment dispersion glaucoma

27

Glaucomfleckin

This is opacification of the lens from high IOP.

28

Normal IOP

10-21 mmhg.

29

What IOP pressure alone is enough to start tx?

30 mmhg

30

Normal corneal thickness

555 nm

31

____ Corneas underestimate IOP

Thin

32

____ Corneas overestimate IOP

Thick

33

Corneal thickness at a high risk

34

Corneal thickness at a lower risk

>588

35

Progressive thinning of _____ is pathonogmonic for glaucoma

Neural rim

36

Disk size of myopes vs. hyperopes

Myopes have a bigger disc.

37

As C/D reaches ____ glaucoma risk increases

.6

38

Is asymmetrical optic discs normal?

NO! Any difference of .1 is abnormal

39

ONH red flags for glaucoma

Vertical elongation or vertical notching.

40

Rim thinning in glaucoma

Will go temporal-->superior and inferior-->nasal.

41

Vasculature in glaucoma

Vessel kinking at cup edge, nasal migration of vessels over time. Collateral shunt forming.

42

___ of individuals with PDS go on to develop glaucoma

30-50% (closer to 35%)

43

Glaucomatous VF defects

Paracentral scotoma first. Seidel scotoma (not connected to blind spot)-->accurate. Will obey horizontal raph.

44

PG and PDS epidemilogy

Occurs in younger age 20-40. PDS more common in Caucasians. PDS equal in M and W. PG more common in M. PDS can be inherited as autosomal dominant trait. More often in myopes and those with deep angles.

45

GDx nerve fiber layer analyzer

Use polarization of NFL. Looks at thickness of NFL.

46

TSNIT curves

Looks at temporal, superior, nasal, inferior, temporal doing a circle around the NFL. Shows how thickness compares.

47

Ganglion Cell complex

Measures thickness of 3 innermost layers affected by glaucoma. NFL, GCL, IPL.

48

Reichert Ocular Response Analyzer

Records to pressure values. The difference is the corneal hysteresis (lower CH in NTG pt)

49

Color testing in glaucoma

Red cap. Only affects very late

50

Common Denominator in glaucoma

An acquired, progressive optic neuropathy.

51

Primary open angle glaucoma

Can be high tension or normal. No associated disorder. The angle is open but aqueous outflow is reduced.

52

Secondary glaucoma

Caused by a variety of ocular and systemic disorders. Can be open or closed. Inherited or acquired and bilateral or unilateral

53

Developmental glaucoma

Due to abnormalities of the anterior chamber angle. Abnormalities occurring during gestation. Most forms are secondary type glaucoma or chronic.

54

Most common form of adult glaucoma

Open angle glaucoma. No obstruction by iris root

55

Psudoexfoliation material

Fibrilogranular material of a protein nature and it is amyloidlike. Is possibly secondary to disturbances in the biosynthesis of basement membranes in epithelial cells. Iris pigment epithelium, ciliary epithelium, and peripheral anterior lens epithelium are thought to create. Has a wide distribution throughout the body.

56

What two glaucoma workups can you not bill on the same day?

OCT and Fundus photos. Bring them back.

57

Pigment glaucoma and pigment dispersion syndrome

Occurs by pigment from iris depositing on anterior segment structures. Pigment in TM.

58

Is the ciliary body normally pigmented?

YES

59

Pig. disperion syndrome vs. Pigmentary glaucoma

Pigmentary glaucoma has pigment accumulation in TM resulting in ocular HTN WITH optic neuropathy. PDS does NOT have optic neuropathy.

60

Types of PDS

1. Classic 2. Long anterior zonule associated PDS (Long zonules inserted onto central lens capsule may cause mechanical disruption of pigment epithelium at the pupillary ruff and central iris. This leads to pigment dispersion)

61

___ of individuals with PDS go on to develop glaucoma

30-50%

62

Pathophysiology of PDS

1. Pigment release from iris pigment epithelium
2. Mechanical disruption-radial folds of iris pigment epithelium against lens capsule or zonular fibers. Occur in middle of iris. Think that a reverse pupillary block (between iris and lens) results in iris bowing back and making concave lips

63

PG and PDS epidemilogy

Occurs in younger age 20-40. PDS more common in Caucasians.

64

IS PDS and PG bilateral?

Yes. Can be asymmetrical though (the more myopic eye will be affected more)

65

Symptoms of PG or PDS

Asymptomatic or intermitten or rapid IOP elevation causing Pain, corneal edema, intermittent blurry vision, halos around lights.

66

PG or PDS and exercise

Often have symptoms after working out. Working our liberates more pigment. Can also occur with pupil dilation.

67

Classic triad with PG

1. Kruckenberg spindle (can happen with other dz)
2. Iris transillumination defects
3. Pigment deposition in the TM (homogenous and even). May see Sampaolesi's line (pigmented schwalbe's line)
4. Zentmeyer ring or Scheie's line (pigment accumulation at the zonular attachment of the lens)

68

Kruckenberg spindle

Vertical pigment accumulation in the endothelium

69

Less common signs of PG

Pigment on anterior iris, pigmentation of the lens zones and lens capsule. Also commonly find concavity of the mid peripheral iris.

70

What conditions are PG and PDS pt at a higher risk for?

Retinal detachment (6-7%) and lattice degeneration.

71

Tx and Mgmt for PG

Topical beta-adrenergic antagonist, alpha2 adrenergic agonistic, CAI, Prostaglandin analogues, Miotics, Laser peripheral iridotomy (may eliminate bowing) or Argon laster trabeculoplasty.

72

Pseudoexfoliative glaucoma vs. pseduoexfoliation syndrome.

Syndrome (PXE/PXS) is anterior segment changes without increased intraocular pressure and/or glaucomatous VF and optic nerve changes.

73

PXS/PXE characteristics

Characterized by gray-white flakes of granular material depositing through the surfaces of the anterior chamber structures. Associated with secondary open-angle glaucoma. It is a common ocular manifestion of a systemic disease.

74

Psudoexfoliation material

Fibrilogranular material of a protein nature and it is amyloidlike. Is possibly secondary to disturbances in the biosynthesis of basement membranes in epithelial cells. Iris pigment epithelium, ciliary epithelium, and peripheral anterior lens epithelium are thought to create.

75

PEX and kruckenberg

Can also cause kruckenberg. Do not automatically assume PDG.

76

Pseudoexfoliative glaucoma

Occurs when the material is carried to the TM.

77

PXG prevelance

.6% in 52-64
5% in 75-85 year olds. Predominate disorder of the elderly (60-80). Most studies more common in W. Men more likely to develop glaucoma. Common in scandinavians.

78

____ of patients with PXS develop glaucoma afte 10 years

15%

79

Psuedoexfoliation begins most commonly as a ____ conditions

Monocular. Increases bilaterally with age

80

What conditions is Pseudoexfoliation linked with?

Alzhimers, senile dementia, stroke, TIA, heart disease, hearing loss, higher homocystein levels (risk for cardiovascular dz)

81

Clinical features of Pseudoexfoliation on the lens

1. Grey-white deposits on anterior lens in a bull's eye pattern
2. Three identifiable zones with dilation. Central translucent zone, intermediate clear zone, peripheral granular zone. Clear zone due to rubbing (can cause PDS)

82

Pseudoexfoliation of the iris and pupil

Pseudoexfoliative material seen at the pupillary border. Pupillary ruff defects are seen. Iris transillumination shows a moth eaten pattern at the peripupillary and sphincter regions of the iris.

83

Lens subluxation and Pseudoexfoliation

PXM found on the CB and zonules early in the process. Resulting in degernation and lens sublaxation in 10-15%

84

Cataracts and PXS

33% of cat. pt. also had PXS.

85

Cornea and PXS

May see flakes or clumps on the endothelium (may have a kruckneberg spindle). Decreased endothelium cell count.

86

Classifications of angle closure glaucoma

Classified based on anatomical structure of force causing the iris apposition to the TM.
1. Pupillary block
2. Plataeu iris (level of CB)
3. Phacomorphic glaucoma (level of lens)
4. Malignant glaucoma (forces posterior to the lens)

87

Pigment and PXS

Will have increased pigment in the angle. Less dense than in PDS and more spotty.

88

Medical TX for PXG

Frequently more resistant to medical treatment. Topical beta-adrenergic antagonists, alpha2 adrenergic agonists, CAI, prostaglandin analogues, miotics

89

Surgical TX for PXG

Argon laster trabeculoplasty (earlier in tx), selective laster trabeculoplasty (repeatable), surgical trabeculectomy, combined surgery.

90

Diet and PXG

Pt. has increased homocystein concentration. The use of B-12 and folic acid supplements to decrease hyperhomocysteinemia in pt.

91

Neovascular Glaucoma

Increased IOP due to angle closure from fibrovascular membrane formation obstructing aqueous outflow. Can lead to glaucoma from a secondary open or closed angle mechanism.

92

Key to neovascular glaucoma tx

early detection

93

Pathophysiology of Neovascular glaucoma

Usually due to retinal hypoxia or ischemia. Hypoxic retina produces an angiogenic factor that stimulates neovasculerization. New blood vessels on iris (rubeosis iridies or NVI). VEGF.

94

Most common cause of neovascular glaucoma

CRVO (36%) Ischemic most common.

95

Other causes of neovascular glaucoma

Diabetic retinopathy (32%), Carotid artery disease (13%)

96

Disorders that predispose patients to neovascular glaucoma

CRAO (18%), Uveitis, long standing retinal detachment, intraocular tumors, carotid cavernous fistula.

97

Early phase signs of neovascular glaucoma

Small vessels at the pupillary margin are the earliest sign.

98

Middle phase of neovascular glaucoma

The angle becomes involved. Neovascularization toward the angle. Fibrovascular membrane can grow with NVA and obstructing the TM. Hyphema may occur.

99

Late Phase Neovascular glaucoma

Fibrovascular membrane in the AC contracts producing peripheral anterior synechia (PAS) Begins in one quadrant but can go 360

100

Clinical features of neovascular glaucoma

Cells and flare may be present due to vascular proliferation. Early in disease IOP is often normal. Contraction of the membrane pulls the peripheral iris over the TM resulting in acute angle closure

101

TX of neovascular glaucoma

Need early dx. Treat underlying disease. Topical steroid to treat inflammation. Anti-VEGF therapy. Control IOP. Panretinal photocogulation is a first line therapy. Panretinal cryotherapy is an alternative to PRP in eyes that have cloudy media and in eyes for which PRP failed. Can use anti-VEGF with PRP. Filtering surgery in neovascular glaucoma is used to prevent pressure-induced injury and to improve vascular perfusion.

102

Last step tx for neovascular glaucoma

Cyclodestruction, retrobulbar alcohol injection or enucleation.

103

Angle closure glaucoma cause

Caused by iris apposition to the TM due to abnormal relationships of the anterior segment structures. No aqueous reaches the TM.

104

Symptoms and signs to diagnose angle closure glaucoma

2 symptoms (ocular pain, N&V, history of intermittent blurring with halos) and must have 3 signs (IOP greater than 21, Conj injection, corneal epithelial edema, mid-dilated non-reactive pupil, shallow chamber in presence of occlusion)

105

Pupillary block AACG

Rapid increae in IOP. Triggered with mid-dilation. May occur in people with or without predisposing ocular char. Most attacks occur during the evening. Can also occur in the movies (dark and pupil dilates). Adherence between the back of the iris and the front of the lens, prevents aqueous to pass forward, increased in IOP behind the iris creates an Iris Bombe, the peripheral iris is pushed forward to adhere to the cornea or TM.

106

Risk factors of AACG

Females, hyperopes (shallower eye), caucasian, asian, positive family history, increased risk with age (until cataract surgery), increased lens thickness.

107

Enviormental stimulus causing AACG

Entering a dark room, mental and emotional stress, fatigue, trauma, respiratory infections

108

Features of AACG

Gonioscopy shows a 360 closed angle, possible peripheral anterior synechiae, possible posterior synechiae, glacomflecken. Iris torsion, patchy iris atrophy, disc edema, possible optic atrophy.

109

Dark room provocative test

Dilate or put in a dark room and see if angle closes.

110

AACG without pupillary block (plateau iris)

Plateau iris occurs. Caused by large ant. positiond ciliary processes. Pushes peripheral iris forward. Obstruction of aqueous outflow due to position of the ciliary processes against the TM crowding the angle. Last iris roll will be bunched and forced against the TM on pupil dilation.

111

Plateau Iris Epidemiology

Accounts for more than 50% of young pts with recurrent angle closure. Tends to occur in young patients and females. Suspect if narrow angle persists.

112

TX for plateau iris

Laser peripheral iridotomy is the first tx. Some patients have plateau iris syndrome (occluded angle even with LPI) Treat these patient with laser iridoplasty (laser burns at the peripheral iris to shrink the iris and pull it from the angle) May need to use conventional surgery to keep IOP down (tube shunt)

113

Phacomorphic glaucoma

Due to lens swelling.

114

Malignant glaucoma

Due to virtual pressure. Angle closure due to posterior forces pushing the lens iris diaphragm forward.

115

Glaucoma treatment flow

Medical-->laser treatment (laster trabeculoplastey-->surgery (filtration/bleb/trabeculectomy)

116

Theories of glaucoma damage

Direct mechanical theory (ocular pressure blocks axoplasmic flow)
Ischemic theory (ocular pressure blocks circulation to n)
Apoptosis (programmed cel death mediators involved. Genetic predisposition)

117

Main glaucoma tx mechanisms

Reduce aqueous production,
Increase aqueous outflow,
Neuroprotections.

118

Drugs that reduce aqueous protection

Adrenergic antagonists (beta blockers), CAI (Amide)

119

Beta blockers

Beta 1-the heart
Beta 2-the lungs
Used to be the drug of choice.
olol

120

Betaxolol

The only Beta 1 selective. May be more safe. Won't affect patients with asthma. May have neuroprotection.

121

Dosing with beta blockers

Normal dosing is BID.

122

Carteolol

Does not cross the BBB as much as the other drugs.

123

CAI

Inhibits Carbonic anhydrase E in ciliary epithelium from produced aqueous. Rarely used by itself. Amide.

124

Systemic CAI

Acetazolamide, methazolamide, dichlorphenamide. use in 911 situation. Use with above 40.

125

CAI SE

Bitter taste, sulfa allergies, HA, nausa, tinnitus. Don't use with such. Avoid with sulfa allergy, sick cell, blood dyscrasias, corneal surgery patient, or corneal endo cell disease.

126

Drugs that increase outflow

Adrenergic agonist, Miotics, Prostaglandins, Hyperosmotics. Docasonoids?

127

Dipivefrin

Adrenergic agonists. Converts to epinephrine. Raise pressure initially. First drop for glaucoma. Stimulates alpha and beta.

128

Apraclonidine

Stimulates alpha 2. used mainly for post op. Not used long term. Turns off tap and increases outflow (only drug with dual jobs)

129

Brimonidine

Stimulates alpha 2. Decreases aqueous production and increases uveoscleral outflow. The safest glaucoma drug for patients.

130

Combigan

Brimonidine and timol. More $$. Very effective.

131

Simbrinza

Brinzolamide and Brimonidine. Only combo drugs that doesn't have timolol.

132

Pilocarpine

Miotics. Causes accommodation and myopia to occur. Do not give to high myopes.

133

Carbachol

Miotic.

134

Prostaglandins

Prost

135

Latanoprost

Prostaglandin. Increase uveoscleral outflow. This is the 1st choice drug.

136

Travaprost

Prostaglandin.

137

Bimatoprost

Decreased concentration due to increased benzochloride (preservatives)

138

Tafluprost

First preservative free prostaglandin.

139

Things to know with prostaglandins

Irreversible iris darkening, lash thickening, periocular skin darkening, CME in aphakes/pseudophakes, uveitis, onset of herpes, simplex ocular infections

140

Uniprostone

Docasahexonic acid. Possible TM outflow mechanism. Safest systemic profile of all glaucoma meds.

141

Hyperosmotics

Temporary immediate use only. Indicated for very high IOP. Pulls water from tissues into bloodstream. Glycerol, Isosorbide, Mannitol, Urea.

142

Gene therapy for glaucoma

TIGR/MYOC mt- incorporate a gene into TM.

143

Steroids and glaucoma

Steroid increase IOP. May reduce IOP in certain inflammatory glaucoma conditions (uveitic or chemical burn glaucoma).

144

What meds should you NOT use with uveitic glaucoma

Pilocarpine or prostoglandins.

145

Laster treatment

Contracts collagen of TM and increases met activity. Initially IOP spike that drops later.
Argon are heat laster.
SLT: new laster. Can repeat.

146

Incisional Surgical Glaucoma Tx

Sclerostomy: full scleral channel, conj. flap
Trabeculectomy: partial scleral channel
Valve or tube implanation. Anti-metabolite (5-FU) used to prevent scars.

147

Micro-invasive glaucoma surgery

Little microscopic pipes put into the eyes to increase outflow.

148

Cyclocryotherapy and transcleral YAG laser cryophtocoagulatin

Destroy the CB epithelium. High rate of complication. Last resort.

149

What is ON surrounded by

Dura, pia, arachnoid. ON sheath is also connected to some EOM.

150

Inferior nasal fibers

Ill loop up. Superior nasal will cross but not loop up. Temporal straights back.

151

Blood supply to ON

All branches from opthalmic a. Include short posterior ciliary a, recurrent choroidal a., pial arterial network, central retinal artery. SRPC.

152

Optic Neuropathy includes...

1. ION
2. Optic neuritis
3. Papilledema

153

Things you will see with optic neuropathy

reduced VA, decreased color vision, relative afferent pupillary defect (most common) VF defect, optic disc swelling, pallor, cupping

154

Bow Tie Atrophy

Have temporal VF loss. Affect more of the nasal fibers

155

Temporal atrophy

Toxic and nutritional ON, autosomal dominanat ON, lebers hereditary ON, ON.

156

Superior/inferior atrophy

Ischemic

157

Band or bow tie atrophy

chiasm or optic tract

158

Macula vs. ON problems

ON will have RAPD, scotoma or cloud, vasoline over vision, reduced brightness, reduced color vision,

159

Does pallor of optic rim occur with glaucoma

NO

160

what is the most common optic neuropathy?

Glaucoma.

161

Malinserted disc

10% have this. Nasal disc is more raised and temp. is more flat

162

Tilted Disc

Temporal disc is more raised. Pt have an increased amount of astigmatism. Can have chasmal problems

163

Megalopappilla

Big optic disc. Looks like glaucoma but no notching or vertical elongation

164

Small scleral canal

NFL in small A. Looks like disc edema. However vessels are not obscured

165

Optic nerve hypoplasia

ON small because reduced axons going to the n. See ring sign (white ring around). Vision varies depending on amount of axons. All VF will be stable.

166

Morning glory disc anomaly

Disc is larger than average. Will have white tuft and look like bv are coming from the edge of the disc.

167

Colobomatous optic disc

VA can be fine in mild cases. Pt. has no rim.

168

Optic Pit

Typically at temp. edge of ON. Normal VA unless edema. VF defect looks like glaucoma (respects horizontal)

169

Myelinated NFL

Very common. Stable condition. Feather appearance and follows NFL.

170

Disc Drusen

Inheritied. Young looks like papilledema and then when 20/25 start to see nasal drusen and a decrease in height. Calcified axonal debris. Greater in women. Bilateral. Arcuate defects (inferior, inferior nasal). Can be buried or visible (must do VF). Have concentric constriction, enlarged blind spot.

171

Standard for dx of Drusen

B scan. Drusen will also light up with autofluroscents.

172

Drusen on OCT

Normally have no cup. Center is more raised. NFL keeps a normal thickness once you leave ON.

173

Vessels and Drusen

Will commonly have abnormal vessels. Will have trifercations of vessels and turosity

174

Drusen vs. disc edema

If average NFL over 116 more likely edema. If below more likely drusen.

175

Pseudopapilledema

Look like papilledema. High hyperopia, vitreopapillary traction, glial tissue over ON, scleral infiltration, optic disc drusen, hypo plastic ON, myelinated NFL, high hyperopia.

176

Papilledema

Disc edema due to raised ICP

177

Idiopathic Intracranial Hypertension

Increased ICP, normal CSF composition, no abnormality that causes increased ICP.

178

Spinal fluid cycle

Chroidal plexus continuously makes spinal fluid. Enters subarachnoid space and gets absorbed in veins and drains to jugular v. and out of head.

179

Papilledema and brain tumors

Occurs in 60-80% brain tumors. Pt. has severe HA and bilateral disc edema. High lumbar puncture so papilloedema. Cerebral venous sinus thrombosis.

180

Who gets IIH

Obese women of child bearing age.

181

Pseudotumor cerebri

Intracranial hypertension with a cause. Can be due to systemic conditions (pregnancy, anemia, HTN, sleep apnea, hypo or hyper thyroid) Medications: tetracycline, corticosteroids, retinoids, lithium.

182

Papilledema characteristics

Normal color vision and va, no RAPD, VF enlarged blind spot, bilateral disc edema, lack of spontaneous venous pulsation.

183

Does absense of spontaneous venous pulsation=papilledema

No because 20% don't have. If it is there though you know it is not papilledema.

184

MRI with papilledema

Empty sella (the pit. gland is flattened) ON sheath will be swollen. Flattening of globe

185

What do you need to remember about puncture

Must do imaging before puncture. Tumor can be pushing on globe and take out fluid and get compression of midbrain and death.

186

Treatment for papilledema and IIH

Eliminate secondary cause (decrease weight, tumor, etc) Alleviate symptoms, prevent vision loss. Decreasing ICP (Acetazolamide). Headache treatment (topiramate-also weight loss, NSAIDS), Anticoagulant therapy

187

Surgical treatment for IIH and papilledema

Optic n. sheath decompression (cut slits in ON sheath and allows cerebral spinal fluid to leave. Choose if main symptom is vision loss)
Ventriculoperitoneal or lumboperitoneal shunt: Shunt to peritoneal where it can drain. Often have to repeat.

188

Most common ON problem in those under 40

Optic neuritis

189

Demyelinating optic neuritis

Occurs in 50% MS pt. Presenting sign of MS in 20%. Females. 20-50.

190

Progression of optic neuritis

When eyes look normal and vision normal will have pain with eye movements and then loss of vision. Will have RAPD. Associated numbness in extremities that gets worse over 1-2 weeks, better in 1 week, then better (no prog. past 6 weeks)

191

Anterior vs. posterior optic neuritis

Anterior=NH involved
Post=no NH involvement

192

Demyelinating Optic Neuritis Symptoms

Acute vision loss in one eye, Pain behind the eye that is worse with movement, Photopsia, numbness, vertigo, loss of balance. VA 20/20 to NLP. Decreased color vision. Decreased contrast. RAPD. Decreased brightness sensation. Can get any type of VF loss.

193

Prevelence of different demylinating neuritis

Visible ON (33), retrobulbar ON (67). ON pallor after 4-6 wks.

194

Dx of optic neuritis

Send for MRI to look for plaques for MS.

195

TX for optic neuritis

Can use IV steroids to recover feaster. Benefit in 15 days. No oral steroids (will increase occurrence) Consider for pt. that are monocular, severe pain or vision loss, occupational requirements. Follow patient 2-4 weeks to assure vision improving. Refer to neurology.

196

Prognosis after topic neuritis

No progression of vision loss after 2 weeks. Rapid improvement in 4 weeks. 93% have at least 20/40. 74% have 20/20. Color vision and RAPD may persist.

197

MS risks with ON

1-2 lesions at 15 yrs-25%
2 lesions at 15 years: 50%
3 lesions at 15 years: 75%

198

ON problems in those over 40

Anterior Ischemic Optic neuropathy

199

Anterior ischemic optic neuropathy

Can see edema. Can be arthritic or non-arteritic.

200

Posterior Ischemic optic Neuropathy

Arteritic (same char was AAION but can't see)
Non-arteritic (only if pt. had long surgery with lots of blood loss)

201

Diabetic papillopathy

Normally bilateral

202

Non-arteritic anterior ischemic optic neuropathy

Mean age 61-66. Painless vision loss. Vasculopathic risk factors. Disc at risk (small and crossed disc). Common with papilledema, ONH drusen, increased IOP, radiation, acute hypotension, sleep apnea, amiodarone, erectile dysfunction meds.

203

VA with NAION

75 are better than 20/200. Reduced color vision. Inferior altitudinal visual filed defect.

204

NAION investigation

ESR and CRP (should be normal. Only do to rule out giant cell) Neuroimaging if atypical. OCT to monitor as it improves.

205

Toxic/Metabolic Optic Neuropathy causes

Vitamin B12 deficiency, alcohol, Medications (ethambutuol, amiodarone, ciprofloxacin, suflonamides, ergot, immunosuppresive, chemo agents)

206

Prognosis with NAION

Vision is typically stable. 40% recover at least 3 lines of snellen. Optic disc pallor within 4-6 weeks. No cupping. 15-19% have involvement of other eye in 5 years.

207

Arteritic anterior ischemic optic neuropathy systemic symptoms

Mean age 75-76. Symptoms: HA, pain on chewing, scalp tenderness. Malaise, fever.

208

Arteritic anterior ischemic optic neuropathy ocular symptoms.

vision loss over hours or days, usually unilateral but may be bilateral, transient visual obscuration, diplopia. 20% that go blind have no symptoms. Will have severe vision loss (mean 20/400). Decreased color vision, RAPD, VF (altitudinal defect) Low IOP, Firm temporal artery.

209

Testing for AAION

ASAP lab work. ESR (increased). CRP increased, platelet count is great. Do a temporal artery biopsy (5-11 have false neg)

210

AAION TX

911. IV methylprednisone then oral prednison. Very slow taper. Consider calcium, vitamin D supplements, and peptic ulcer prophylaxis. Low dose aspirin.

211

AAION prognosis

95% develop AAION of the fellow eye in hours or days without treatment. Recurrence in 10%. Systemic symptoms resolve within one week of steroid tx. Will not regain vision.

212

Compressive optic neuropathy causes

Tumor, infection, inflammation, thyroid eye disease

213

Compressive optic neuropathy

Progressing vision loss, HA, Diplopia, proptosis, transient vision loss (occurs when looking in 1 direction), decrease VA and color vision, RAPD, proptosis, EOM motility limitation, VF (any type), disc swelling or pallor, optic nerve cupping, chorioretinal striae, optocililary shunt vessels.

214

Tx for compressive optic neuropathy

Observation. Radiotherapy, chemotherapy, surgical resection

215

Thyroid optic neuropathy

Differs from tumor as it is bilateral and symmetric. 5-10% with thyroid eye dz. Swelling of muscle with spared tendon seen on CT.

216

MGMT of thyroid optic neuropathy

Spontaneous remission, immunosuppression, orbital decompression, control thyroid hormones, smoking cessation (much more common in pt. that smoke)

217

Astrocytichamartoma

Other optic nerve tumors. Glistening calcified tissue. Over ON.

218

Myelanocytosis

Pigment on ONH. Typically benign. Can be black. May grow very slightly.

219

Inflammatory ON

Sarcoidosis, lupus, behcet's, sjogrens, atopic dermatisis. Will often look very similar. Cannot decide on ON only. Sarcoid most common.

220

Infectious ON due to syphilis

Treponema pallidum. Tx: penicillin

221

Infectious ON due to Cat-scratch disease

Most common cause of neuroretinitis. Fever, malaise, HA. Conj. is most common ON problem. Starburst exudates.

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Infectious ON due to Lyme disease

Transmitted through a tick bite. TX: ceftriaxone

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Toxic/Metabolic Optic Neuropathy causes

Vitamin B12 deficiency, alcohol, Medications (ethambutuol, amiodarone, ciprofloxacin, suflonamides, ergot, immunosuppresive, chemo agents)

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Toxic/Metabolic ON symptoms

Painless bilateral vision loss (better than 20/400), decreased color vision, VF (central or cecocentral. Sparring of periphery) No RAPD. Perm. pallor.

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Autosomal Dominant Optic Atrophy Epidemiology

4-6 years average onset. OPA1 gene. VA 40% better than 20/60. VF (Central or cecocentral scotoma with sparing of the peripheral field)

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LHON (Leber's hereditary optic neuritis)

Vision loss between age 15-35. Males. Maternal inheritance pattern. Painless vision loss (usualy worse than 20/200. Bilateral and symmetric). Decreased color vision. VF: central or cecocentral sparring the peripheral VF.

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Traumatic Optic Neuropathy

Pt. will know trauma occurred. Must do case history.

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What cells are most likely affected with bad genes?

RPE. Could also be retina or choroidal though

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Direct gene therapy

Using vectors to replace the missing genes

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Many hereditary conditions are _____

polygenetic. The same phenotype occurs from many genotypes. Must start treatment early

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Signs and symptoms of hereditary retinal disease when rods are involved

Peripheral field loss, loss of night vision, ERG scotopic loss. Acuity and color vision affected late. Photosensitivity

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Signs and symptoms of hereditary retinal disease when cones are involved

Decreased acuity, central scotoma, ERG photopic loss, color vision loss, photosensitivity

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What is the most common hereditary retinal dystrophy

Retinintisis Pigmentosa

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Inheritance types of RP

Autosomal recessive (most common, most severe. Night vision and peripheral loss in early childhood. Central by adulthood) Autosomal dominant: least severe from with central vision intact util 40s and 50s. X-linked: similar to AR.

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_____ of RP cases are part of a systemic syndrome

30-40

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RP symptoms

Nigh blindness (nyctalopia), reduced mobility, some are asymptomatic, eventual central acuity loss.

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RP signs

Arterial attenuation (sometimes first sign), waxy looking optic nerve, classic bone spicule pigment pattern (begins in mid periphery. Ring scotoma). Cataracts develop in 50% of cases. Macular edema in late stages.

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RP and ERG

Scotopic ERG will be abnormal before signs. Relative loss of scotopic vs. photopic ERG clarifies which photo are involved. Often necessary for firm dx in early stages of dz, results can help determine the RP type and the prognosis.

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Retinitis Sine Pigmento

No or minimal pigmentary changes. May just be an early stage of dz. Waxy nerve and arterial attenuation are prominant

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Sector RP

Inferior quadrants only

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Increased AF

=areas of high lipofuscin. Decreased liopfuscin=RPE and photo death.

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Retinitis Punctata Albescenes

Varient of RP. Has white things instead of bone spicules

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Usher Syndrome

Congenital sensior-neural hearling loss and RP. 50% of blind and deaf people.

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RP Tx

Nutrient supplements: Vit A palmitate and omega 3 rich diet has slowed progression. Lutein shown to slow mid-peripheral loss. Oral 9-cis-B-Carotene has been shown to slow progression.
Short wavelength blocking tints: help with photo. Cataract removal. Treatment of CME.

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Leber's Congenital Amaurosis

Similar to RP but congenital. Usually AR. Visually unresponsive baby with nystagmus. Retina may look normal at first. ERG shows diminished or absent rod cone response. Molecular genetic testing is critical. Gene therapy trials for LCA are happening now for people caring RPE65 mutation.

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Gene therapy for LCA

Use for people carrying RPE65 gene.

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Sensory (afferent) congenital nystagmus

Secondary to disease disrupting the foveal pathway early in life. Bilateral retinal or optic nerve. disease that is congenital or develops in the first 2 years

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Motor (efferent) congenital nystagmus

Due to primary abnormality in the ocular-motor system. Usually hereditary pattern.

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Congenital stationary Night blindness

Nigh blindness is primary symptom. Mild acuity reduction (20/30-30/60). Normal to near normal retina. Nystagmus with severe. ERG pattern is dx.

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Oguchi's disease

Variant of CSNB found in japanese. The retina changes colors with light adaptation.

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Cone-Rod Dystrophies

Both rod and con function affected early in disease. Reduced acuity in childhood. Can have macula or perimacula lesions. Both photopic and scotopic ERG diminished.

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Gyrate Dystrophy

Hereditary choroidal dz. Very rare. Hyperornithinemia due to deficient enzyme activity (ornithine aminotransferase). high myopia early in life. Night blindness and RPE changes in 2nd decade. RPE and choroidal atrophy with a bar sclera. Pattern of vision loss similar to RP

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Gyrate dystrophy tx

B6 supplement, diet low in protein

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Choroideremia

X linked (Males only). Onset of night blindness first 5-10 years. Diffuse RPE mottling is early sign then large patches of RPE and choroidal atrophy in mid periphery leaving sclera bare. Corresponding peripheral field loss. Scotopic field loss becomes non-recordable.

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Most common Juvenile hereditary macular dystrophy

Stargardt's macular dystrophy

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Stargardt's Macular Dystrophy

AR inheritance. 8-16 years usual onset. Acuity loss may precede observable macular change!

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Stargardt's signs

FLV lost, atrophic RPE, beaten bronze appearance at end. Yellow pisciform flecks in surrounding posterior pole. Usually Vas stabilize by early 20s.

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Fundus Flavimaculatus

Variant of stargardt's with a later onset. Piscifiform lesions are primary presentation. Macula disease and acuity loss develop later.

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Vitelliform Dystrophy (best's dz)

AD inheritance. Usually begins in early childhood.
Previtelliform stage: abnormal EOG
Vitelliform stage: yellow spots coalesce into egg yolk macula appearance (Vas normal)
Psudohypopyon stage: lesions partially reabsorbs
Citelliruptive stage: Lesion breaks up in to scrambled egg. Va drop a ton.

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Best's TX

Anti-VEGF therapy can improve.

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Diagnosisng stargardt

FAF and OCT. Help you to diagnose. Lipofuscin starts to form at 2 years.

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Achromatopsia

Congenital absesnse of cone function.

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Types of achromatopsia

1. Rod monochromatism-AR
2. Blue cone monochromatism-X linked

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Signs of achromatopsia

photophbia, nystagmus, Va in 20/100-20/200 range. Normal fundus in young patients. No color vision. Photopic ERG diminished.

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Tx for achromatopsia

Red tens is good for achromatic. magenta tint for blue monochromat.

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Progressive Cone Dystrophy

Reduced Va (20/60-20/200 range by teens). Photophobia. Most common: bull's eye macular lesions. Poor color vision (not absent). Extremely diminished photopic ERG, normal scotopic ERG. VA stabilizes around 20/200.

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How is progressive cone dystrophy different from achromatopsia

Not congenital and there will be no nystagmus.

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Central Areolar Choroidal Dystrophy

Later onset, ofter 40. Atrophy involving choriocapillaris-->RPE-->retina. Normal electrodignostics. Abnormal color vision. Loss of central vision with acuity dropping below 20/200.

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Albinism

Very common form of congenital visual impairment. Varying degrees of a melanosis due to deficiency of tyrosinase. Anomalous wiring at the chasm limits binocularity.

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Oculocutaneous Albinism

Systemic, skin, hair, and eyes affected

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Ocular Albinism

X linked. Affected males show near normal skin and hair pigmentation but varying ocular depigmentation. Autosomal recessive form tends to be more severe.

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Albinism signs

Foveal hypoplasia (major factor affecting acuity)*, a melanosis of iris and retina, nystagmus (and ability to dampen with close object), strabismus and impaired BV, astigmatism.

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Retinal aneurysm

Abnormal widening or ballooning of a portion of an artery due to weakness in the wall of the BV. Microaneurysem (50-100). Macroaneurysm (-280)

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Choridal flush

Occurs in 10-12s. Fluid in choroid. If present ciliorteinal artery will fill.

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Arterial phase

10-15s. Arteries are bright

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Arterial venous phase

20-23. Veins begin to fill.

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Venous phase

Early venous: laminar flow of v. a. still bright.
Venous phase: v and a. fully bright

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Late phase

10 min post inj. A. and V. almost empty.

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OCT and vascular dz

Blood vessels create shadows. Excess blood, drusen, or exudate can created hyper reflectivity.

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Intraretinal cystoid changes

Fluid between IPL and ONL. Type A males normally

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Retroviterous hemorrhage

Red blood behind vitreous. Shifts with eye movement. Called subyloid hemorrhage and pre retinal hemorrhage. Usually in post. pole. Boat shaped. No compromise of visual function after resolution. Can get with valsalva. Boat like or blob like.

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Intraviterous

Varied appearance with vitreous. Clots quickly, settles into lacunae. Often visually devastating.

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Superficial/flame shaped hemorrhage

Follows NFL fibers. Parallel to retinal surface. Can have a white center (called a roth spot). Hypoflurescent. Lasts weeks and then reabsorbs. No compromise of VF after resolution

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Drance Heme

Flame heme at edge of optic nerve

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Splinter heme

Fame heme at edge of optic nerve with swollen ONH.

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Dot blot hemorrhage

INL, OPL, ONL. Common with diabetes and HTN.

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Sub-retinal hemorrhages

Between RPE and sensory retina. Large lobulated borders. Usually in posterior pole. Often visual devastating.

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Subretinal hemorrhage (above RPE)

Red color

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Sub-RPE

Grey-green color.

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Roth spot

Retinal hemorrhage surrounding a white center. White is WBC, CWS.

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Microaneuyrsms

From Inner retinal capillaries. Occurs with DM, HTN, blood dyscrasisas, leukemias. Hyperflurosce with FA.

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Which will hyper. Micro or dot blot

micro

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Macroaneurysm

50-80 year olds, F. Commonly seen in superior temporal. exudate and heme can occur

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Hard Exudates

Lipid deposits associated with deep retina edema. Debris from backed up drain (only get with edema). Dense, waxy. Diabetes is the number one cause. No tx if in periphery.

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Cotton Wool Spot

Area of NFL ischemia. White fluffy. Black on fang. Resolves in 5-7 weeks.

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Neovascularization

Response to hypoxia and release of VEGF. Associated with intra-retinal microvascular anomaly. Direct threat to vision. Neo of dic penetrates the vitreous body. If you see IRMA in one eye you need to refer.

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Disease associated with neovascularization

Branch retinal vein occlusion, DM, retinopathy of prematurity

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Intra-Retinal Microvascular Anomalies

An intra-retinal shunting system. Tortuous capillaries in areas of severe capillary non perfusion. IRMA does not leak or bleed.

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Collaterals

New BV that gives AA or VV communication

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Shunt

New BV that gives AV or VA communication.

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Retinal vascular tortuosity Congenital

All quadrants, symmetric OU. Can be linked with syndromes.

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Acquired vascular turosity

Previously documented normal. Sectoral involvement. Associated thickening and darkening of the BV column. Indicator of hypoxia.

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Venous bleeding

indicates widespread retinal ischemia. Looks like bulges in the wall of the veins. Results in slugging of venous blood. Often associated with DM-->risk for PDR.

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Non-arteritic Anterior Ischemia Optic N.

Small BV disease that affects the pre-laminar portion of disc. Due to hypo perfusion of the ONH commonly.

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Hematocrit

Percentage of RBC in whole blood.

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Hematologic DZ and retinal problems

partial or total occlusion of bv can occur

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Anemia

Reduction in the total number of blood cells or reduction in quantity of hemoglobin. Retinal Problem when hemoglobin levels at half. Can cause increased intracranial pressure

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Iron Deficiency Anemia

Most common in US. Cold feet, pale skin, SOB, tired. No retinal changes unless sever.

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Pernicious Anemia

Small intestine tract failure to absorb vitamin B12 due to lack of intrinsic factor. Treat with supplements.

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Hemolytic Anemia

RBCs destroyed prematurely. Body cannot replace them. Occurs with infections, meds, immune.

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Aplastic Anemia

Bone marrow damage-->inefficiency to make enough RBCs. During visit 50% will have hemorrhage of retina, skin, or mucous membrane

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Sickle Cell Dz

Mutation in hemogloblin. African americans. Recessive gene. Will see turtuosity. Will see a sea fan neovascularization.

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Polycythemia

Many types of blood cells. Primary (bone marrow overproduces) Seoncdary (kidney overproduces erythropoietin hormone that causes increased). Viscous blood. Can see deep or superficial retinal hemorrhage. Retinal v. occlusion. Can have amaurosis fugal (monocular blindness)

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Sickle cell dz tx for neovascularization

Laser photogoagulation