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Oc Dz 3 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Glaucoma is the ___ world leading cause of blindness

A

3rd

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2
Q

Glaucoma is the ___ world leading cause of blindness

A

3rd

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3
Q

Glaucoma Epidemology

A

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

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4
Q

Ocular glaucoma risk factor with RE

A

Myopia (especially greater than 6D)

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5
Q

Visual acuity and glaucoma

A

Normally only affected late in the dz

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6
Q

Pupils and glaucoma

A

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

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7
Q

Steamy cornea with perilimbal injection

A

Acute angle closure glaucoma

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8
Q

Krukenberg spindle

A

Pigment. May be pigment dispersion glaucoma

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9
Q

Glaucomfleckin

A

This is opacification of the lens from high IOP.

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10
Q

Normal IOP

A

10-21 mmhg.

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11
Q

What IOP pressure alone is enough to start tx?

A

30 mmhg

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12
Q

Normal corneal thickness

A

555 nm

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13
Q

____ Corneas underestimate IOP

A

Thin

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14
Q

____ Corneas overestimate IOP

A

Thick

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15
Q

Corneal thickness at a high risk

A
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16
Q

Corneal thickness at a lower risk

A

> 588

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17
Q

Progressive thinning of _____ is pathonogmonic for glaucoma

A

Neural rim

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18
Q

Disk size of myopes vs. hyperopes

A

Myopes have a bigger disc.

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19
Q

As C/D reaches ____ glaucoma risk increases

A

.6

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20
Q

Is asymmetrical optic discs normal?

A

NO! Any difference of .1 is abnormal

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21
Q

Glaucoma Epidemology

A

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

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22
Q

Ocular glaucoma risk factor with RE

A

Myopia (especially greater than 6D)

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23
Q

Visual acuity and glaucoma

A

Normally only affected late in the dz

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24
Q

Pupils and glaucoma

A

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

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25
Q

Steamy cornea with perilimbal injection

A

Acute angle closure glaucoma

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26
Q

Krukenberg spindle

A

Pigment. May be pigment dispersion glaucoma

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27
Q

Glaucomfleckin

A

This is opacification of the lens from high IOP.

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28
Q

Normal IOP

A

10-21 mmhg.

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29
Q

What IOP pressure alone is enough to start tx?

A

30 mmhg

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30
Q

Normal corneal thickness

A

555 nm

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31
Q

____ Corneas underestimate IOP

A

Thin

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32
Q

____ Corneas overestimate IOP

A

Thick

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33
Q

Corneal thickness at a high risk

A
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34
Q

Corneal thickness at a lower risk

A

> 588

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35
Q

Progressive thinning of _____ is pathonogmonic for glaucoma

A

Neural rim

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36
Q

Disk size of myopes vs. hyperopes

A

Myopes have a bigger disc.

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37
Q

As C/D reaches ____ glaucoma risk increases

A

.6

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38
Q

Is asymmetrical optic discs normal?

A

NO! Any difference of .1 is abnormal

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39
Q

ONH red flags for glaucoma

A

Vertical elongation or vertical notching.

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40
Q

Rim thinning in glaucoma

A

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

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41
Q

Vasculature in glaucoma

A

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

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42
Q

___ of individuals with PDS go on to develop glaucoma

A

30-50% (closer to 35%)

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43
Q

Glaucomatous VF defects

A

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

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44
Q

PG and PDS epidemilogy

A

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.

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45
Q

GDx nerve fiber layer analyzer

A

Use polarization of NFL. Looks at thickness of NFL.

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46
Q

TSNIT curves

A

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

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47
Q

Ganglion Cell complex

A

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

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48
Q

Reichert Ocular Response Analyzer

A

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

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49
Q

Color testing in glaucoma

A

Red cap. Only affects very late

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50
Q

Common Denominator in glaucoma

A

An acquired, progressive optic neuropathy.

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51
Q

Primary open angle glaucoma

A

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

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52
Q

Secondary glaucoma

A

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

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53
Q

Developmental glaucoma

A

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

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54
Q

Most common form of adult glaucoma

A

Open angle glaucoma. No obstruction by iris root

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55
Q

Psudoexfoliation material

A

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.

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56
Q

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

A

OCT and Fundus photos. Bring them back.

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57
Q

Pigment glaucoma and pigment dispersion syndrome

A

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

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58
Q

Is the ciliary body normally pigmented?

A

YES

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59
Q

Pig. disperion syndrome vs. Pigmentary glaucoma

A

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

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60
Q

Types of PDS

A
  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)
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61
Q

___ of individuals with PDS go on to develop glaucoma

A

30-50%

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62
Q

Pathophysiology of PDS

A
  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
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63
Q

PG and PDS epidemilogy

A

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

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64
Q

IS PDS and PG bilateral?

A

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

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65
Q

Symptoms of PG or PDS

A

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

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66
Q

PG or PDS and exercise

A

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

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67
Q

Classic triad with PG

A
  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)
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68
Q

Kruckenberg spindle

A

Vertical pigment accumulation in the endothelium

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69
Q

Less common signs of PG

A

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

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70
Q

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

A

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

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71
Q

Tx and Mgmt for PG

A

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

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72
Q

Pseudoexfoliative glaucoma vs. pseduoexfoliation syndrome.

A

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

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73
Q

PXS/PXE characteristics

A

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.

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74
Q

Psudoexfoliation material

A

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.

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75
Q

PEX and kruckenberg

A

Can also cause kruckenberg. Do not automatically assume PDG.

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76
Q

Pseudoexfoliative glaucoma

A

Occurs when the material is carried to the TM.

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77
Q

PXG prevelance

A

.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.

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78
Q

____ of patients with PXS develop glaucoma afte 10 years

A

15%

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79
Q

Psuedoexfoliation begins most commonly as a ____ conditions

A

Monocular. Increases bilaterally with age

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80
Q

What conditions is Pseudoexfoliation linked with?

A

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

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81
Q

Clinical features of Pseudoexfoliation on the lens

A
  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)
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82
Q

Pseudoexfoliation of the iris and pupil

A

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.

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83
Q

Lens subluxation and Pseudoexfoliation

A

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

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84
Q

Cataracts and PXS

A

33% of cat. pt. also had PXS.

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85
Q

Cornea and PXS

A

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

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86
Q

Classifications of angle closure glaucoma

A

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)
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87
Q

Pigment and PXS

A

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

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88
Q

Medical TX for PXG

A

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

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89
Q

Surgical TX for PXG

A

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

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90
Q

Diet and PXG

A

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

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91
Q

Neovascular Glaucoma

A

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.

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92
Q

Key to neovascular glaucoma tx

A

early detection

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93
Q

Pathophysiology of Neovascular glaucoma

A

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.

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94
Q

Most common cause of neovascular glaucoma

A

CRVO (36%) Ischemic most common.

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95
Q

Other causes of neovascular glaucoma

A

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

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96
Q

Disorders that predispose patients to neovascular glaucoma

A

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

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97
Q

Early phase signs of neovascular glaucoma

A

Small vessels at the pupillary margin are the earliest sign.

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98
Q

Middle phase of neovascular glaucoma

A

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

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99
Q

Late Phase Neovascular glaucoma

A

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

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100
Q

Clinical features of neovascular glaucoma

A

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

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101
Q

TX of neovascular glaucoma

A

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.

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102
Q

Last step tx for neovascular glaucoma

A

Cyclodestruction, retrobulbar alcohol injection or enucleation.

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103
Q

Angle closure glaucoma cause

A

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

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104
Q

Symptoms and signs to diagnose angle closure glaucoma

A

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)

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105
Q

Pupillary block AACG

A

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.

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106
Q

Risk factors of AACG

A

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

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107
Q

Enviormental stimulus causing AACG

A

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

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108
Q

Features of AACG

A

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

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109
Q

Dark room provocative test

A

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

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110
Q

AACG without pupillary block (plateau iris)

A

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.

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111
Q

Plateau Iris Epidemiology

A

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.

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112
Q

TX for plateau iris

A

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)

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113
Q

Phacomorphic glaucoma

A

Due to lens swelling.

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114
Q

Malignant glaucoma

A

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

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115
Q

Glaucoma treatment flow

A

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

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116
Q

Theories of glaucoma damage

A 
Direct mechanical theory (ocular pressure blocks axoplasmic flow)
Ischemic theory (ocular pressure blocks circulation to n)
Apoptosis (programmed cel death mediators involved. Genetic predisposition)
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117
Q

Main glaucoma tx mechanisms

A

Reduce aqueous production,
Increase aqueous outflow,
Neuroprotections.

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118
Q

Drugs that reduce aqueous protection

A

Adrenergic antagonists (beta blockers), CAI (Amide)

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119
Q

Beta blockers

A

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

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120
Q

Betaxolol

A

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

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121
Q

Dosing with beta blockers

A

Normal dosing is BID.

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122
Q

Carteolol

A

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

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123
Q

CAI

A

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

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124
Q

Systemic CAI

A

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

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125
Q

CAI SE

A

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.

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126
Q

Drugs that increase outflow

A

Adrenergic agonist, Miotics, Prostaglandins, Hyperosmotics. Docasonoids?

127
Q

Dipivefrin

A

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

128
Q

Apraclonidine

A

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

129
Q

Brimonidine

A

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

130
Q

Combigan

A

Brimonidine and timol. More $$. Very effective.

131
Q

Simbrinza

A

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

132
Q

Pilocarpine

A

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

133
Q

Carbachol

A

Miotic.

134
Q

Prostaglandins

A

Prost

135
Q

Latanoprost

A

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

136
Q

Travaprost

A

Prostaglandin.

137
Q

Bimatoprost

A

Decreased concentration due to increased benzochloride (preservatives)

138
Q

Tafluprost

A

First preservative free prostaglandin.

139
Q

Things to know with prostaglandins

A

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

140
Q

Uniprostone

A

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

141
Q

Hyperosmotics

A

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

142
Q

Gene therapy for glaucoma

A

TIGR/MYOC mt- incorporate a gene into TM.

143
Q

Steroids and glaucoma

A

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

144
Q

What meds should you NOT use with uveitic glaucoma

A

Pilocarpine or prostoglandins.

145
Q

Laster treatment

A

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

146
Q

Incisional Surgical Glaucoma Tx

A

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

147
Q

Micro-invasive glaucoma surgery

A

Little microscopic pipes put into the eyes to increase outflow.

148
Q

Cyclocryotherapy and transcleral YAG laser cryophtocoagulatin

A

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

149
Q

What is ON surrounded by

A

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

150
Q

Inferior nasal fibers

A

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

151
Q

Blood supply to ON

A

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

152
Q

Optic Neuropathy includes…

A
  1. ION
  2. Optic neuritis
  3. Papilledema
153
Q

Things you will see with optic neuropathy

A

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

154
Q

Bow Tie Atrophy

A

Have temporal VF loss. Affect more of the nasal fibers

155
Q

Temporal atrophy

A

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

156
Q

Superior/inferior atrophy

A

Ischemic

157
Q

Band or bow tie atrophy

A

chiasm or optic tract

158
Q

Macula vs. ON problems

A

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

159
Q

Does pallor of optic rim occur with glaucoma

A

NO

160
Q

what is the most common optic neuropathy?

A

Glaucoma.

161
Q

Malinserted disc

A

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

162
Q

Tilted Disc

A

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

163
Q

Megalopappilla

A

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

164
Q

Small scleral canal

A

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

165
Q

Optic nerve hypoplasia

A

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
Q

Morning glory disc anomaly

A

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

167
Q

Colobomatous optic disc

A

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

168
Q

Optic Pit

A

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

169
Q

Myelinated NFL

A

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

170
Q

Disc Drusen

A

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
Q

Standard for dx of Drusen

A

B scan. Drusen will also light up with autofluroscents.

172
Q

Drusen on OCT

A

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

173
Q

Vessels and Drusen

A

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

174
Q

Drusen vs. disc edema

A

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

175
Q

Pseudopapilledema

A

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

176
Q

Papilledema

A

Disc edema due to raised ICP

177
Q

Idiopathic Intracranial Hypertension

A

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

178
Q

Spinal fluid cycle

A

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

179
Q

Papilledema and brain tumors

A

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

180
Q

Who gets IIH

A

Obese women of child bearing age.

181
Q

Pseudotumor cerebri

A

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
Q

Papilledema characteristics

A

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

183
Q

Does absense of spontaneous venous pulsation=papilledema

A

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

184
Q

MRI with papilledema

A

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

185
Q

What do you need to remember about puncture

A

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

186
Q

Treatment for papilledema and IIH

A

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
Q

Surgical treatment for IIH and papilledema

A

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
Q

Most common ON problem in those under 40

A

Optic neuritis

189
Q

Demyelinating optic neuritis

A

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

190
Q

Progression of optic neuritis

A

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
Q

Anterior vs. posterior optic neuritis

A

Anterior=NH involved

Post=no NH involvement

192
Q

Demyelinating Optic Neuritis Symptoms

A

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
Q

Prevelence of different demylinating neuritis

A

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

194
Q

Dx of optic neuritis

A

Send for MRI to look for plaques for MS.

195
Q

TX for optic neuritis

A

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
Q

Prognosis after topic neuritis

A

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
Q

MS risks with ON

A

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

198
Q

ON problems in those over 40

A

Anterior Ischemic Optic neuropathy

199
Q

Anterior ischemic optic neuropathy

A

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

200
Q

Posterior Ischemic optic Neuropathy

A

Arteritic (same char was AAION but can’t see)

Non-arteritic (only if pt. had long surgery with lots of blood loss)

201
Q

Diabetic papillopathy

A

Normally bilateral

202
Q

Non-arteritic anterior ischemic optic neuropathy

A

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
Q

VA with NAION

A

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

204
Q

NAION investigation

A

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

205
Q

Toxic/Metabolic Optic Neuropathy causes

A

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

206
Q

Prognosis with NAION

A

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
Q

Arteritic anterior ischemic optic neuropathy systemic symptoms

A

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

208
Q

Arteritic anterior ischemic optic neuropathy ocular symptoms.

A

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
Q

Testing for AAION

A

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

210
Q

AAION TX

A
  1. IV methylprednisone then oral prednison. Very slow taper. Consider calcium, vitamin D supplements, and peptic ulcer prophylaxis. Low dose aspirin.
211
Q

AAION prognosis

A

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
Q

Compressive optic neuropathy causes

A

Tumor, infection, inflammation, thyroid eye disease

213
Q

Compressive optic neuropathy

A

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
Q

Tx for compressive optic neuropathy

A

Observation. Radiotherapy, chemotherapy, surgical resection

215
Q

Thyroid optic neuropathy

A

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
Q

MGMT of thyroid optic neuropathy

A

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

217
Q

Astrocytichamartoma

A

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

218
Q

Myelanocytosis

A

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

219
Q

Inflammatory ON

A

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

220
Q

Infectious ON due to syphilis

A

Treponema pallidum. Tx: penicillin

221
Q

Infectious ON due to Cat-scratch disease

A

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

222
Q

Infectious ON due to Lyme disease

A

Transmitted through a tick bite. TX: ceftriaxone

223
Q

Toxic/Metabolic Optic Neuropathy causes

A

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

224
Q

Toxic/Metabolic ON symptoms

A

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

225
Q

Autosomal Dominant Optic Atrophy Epidemiology

A

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

226
Q

LHON (Leber’s hereditary optic neuritis)

A

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.

227
Q

Traumatic Optic Neuropathy

A

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

228
Q

What cells are most likely affected with bad genes?

A

RPE. Could also be retina or choroidal though

229
Q

Direct gene therapy

A

Using vectors to replace the missing genes

230
Q

Many hereditary conditions are _____

A

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

231
Q

Signs and symptoms of hereditary retinal disease when rods are involved

A

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

232
Q

Signs and symptoms of hereditary retinal disease when cones are involved

A

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

233
Q

What is the most common hereditary retinal dystrophy

A

Retinintisis Pigmentosa

234
Q

Inheritance types of RP

A

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.

235
Q

_____ of RP cases are part of a systemic syndrome

A

30-40

236
Q

RP symptoms

A

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

237
Q

RP signs

A

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.

238
Q

RP and ERG

A

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.

239
Q

Retinitis Sine Pigmento

A

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

240
Q

Sector RP

A

Inferior quadrants only

241
Q

Increased AF

A

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

242
Q

Retinitis Punctata Albescenes

A

Varient of RP. Has white things instead of bone spicules

243
Q

Usher Syndrome

A

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

244
Q

RP Tx

A

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.

245
Q

Leber’s Congenital Amaurosis

A

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.

246
Q

Gene therapy for LCA

A

Use for people carrying RPE65 gene.

247
Q

Sensory (afferent) congenital nystagmus

A

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

248
Q

Motor (efferent) congenital nystagmus

A

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

249
Q

Congenital stationary Night blindness

A

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

250
Q

Oguchi’s disease

A

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

251
Q

Cone-Rod Dystrophies

A

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.

252
Q

Gyrate Dystrophy

A

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

253
Q

Gyrate dystrophy tx

A

B6 supplement, diet low in protein

254
Q

Choroideremia

A

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.

255
Q

Most common Juvenile hereditary macular dystrophy

A

Stargardt’s macular dystrophy

256
Q

Stargardt’s Macular Dystrophy

A

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

257
Q

Stargardt’s signs

A

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

258
Q

Fundus Flavimaculatus

A

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

259
Q

Vitelliform Dystrophy (best’s dz)

A

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.

260
Q

Best’s TX

A

Anti-VEGF therapy can improve.

261
Q

Diagnosisng stargardt

A

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

262
Q

Achromatopsia

A

Congenital absesnse of cone function.

263
Q

Types of achromatopsia

A
  1. Rod monochromatism-AR

2. Blue cone monochromatism-X linked

264
Q

Signs of achromatopsia

A

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

265
Q

Tx for achromatopsia

A

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

266
Q

Progressive Cone Dystrophy

A

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.

267
Q

How is progressive cone dystrophy different from achromatopsia

A

Not congenital and there will be no nystagmus.

268
Q

Central Areolar Choroidal Dystrophy

A

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

269
Q

Albinism

A

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

270
Q

Oculocutaneous Albinism

A

Systemic, skin, hair, and eyes affected

271
Q

Ocular Albinism

A

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

272
Q

Albinism signs

A

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.

273
Q

Retinal aneurysm

A

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

274
Q

Choridal flush

A

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

275
Q

Arterial phase

A

10-15s. Arteries are bright

276
Q

Arterial venous phase

A

20-23. Veins begin to fill.

277
Q

Venous phase

A

Early venous: laminar flow of v. a. still bright.

Venous phase: v and a. fully bright

278
Q

Late phase

A

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

279
Q

OCT and vascular dz

A

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

280
Q

Intraretinal cystoid changes

A

Fluid between IPL and ONL. Type A males normally

281
Q

Retroviterous hemorrhage

A

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.

282
Q

Intraviterous

A

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

283
Q

Superficial/flame shaped hemorrhage

A

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

284
Q

Drance Heme

A

Flame heme at edge of optic nerve

285
Q

Splinter heme

A

Fame heme at edge of optic nerve with swollen ONH.

286
Q

Dot blot hemorrhage

A

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

287
Q

Sub-retinal hemorrhages

A

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

288
Q

Subretinal hemorrhage (above RPE)

A

Red color

289
Q

Sub-RPE

A

Grey-green color.

290
Q

Roth spot

A

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

291
Q

Microaneuyrsms

A

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

292
Q

Which will hyper. Micro or dot blot

A

micro

293
Q

Macroaneurysm

A

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

294
Q

Hard Exudates

A

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.

295
Q

Cotton Wool Spot

A

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

296
Q

Neovascularization

A

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.

297
Q

Disease associated with neovascularization

A

Branch retinal vein occlusion, DM, retinopathy of prematurity

298
Q

Intra-Retinal Microvascular Anomalies

A

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

299
Q

Collaterals

A

New BV that gives AA or VV communication

300
Q

Shunt

A

New BV that gives AV or VA communication.

301
Q

Retinal vascular tortuosity Congenital

A

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

302
Q

Acquired vascular turosity

A

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

303
Q

Venous bleeding

A

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.

304
Q

Non-arteritic Anterior Ischemia Optic N.

A

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

305
Q

Hematocrit

A

Percentage of RBC in whole blood.

306
Q

Hematologic DZ and retinal problems

A

partial or total occlusion of bv can occur

307
Q

Anemia

A

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

308
Q

Iron Deficiency Anemia

A

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

309
Q

Pernicious Anemia

A

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

310
Q

Hemolytic Anemia

A

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

311
Q

Aplastic Anemia

A

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

312
Q

Sickle Cell Dz

A

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

313
Q

Polycythemia

A

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)

314
Q

Sickle cell dz tx for neovascularization

A

Laser photogoagulation

Oc Dz 3 (3 decks)

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