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Integrative Analysis II > Inflammation, Thyroid, Cornea > Flashcards

Inflammation, Thyroid, Cornea Flashcards

1
Q

What does intermediate uveitis entail?

A

peripheral retina, pars plana, vitreous

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2
Q

What are mutton fat KPs?

A

dense, oily appearance of epitheliod cells and macrophages in granulomatous uveitis

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3
Q

What are fine KPs?

A

fine debris, keratic precipitates of lymphocytes, non-granulomatous

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4
Q

What are koeppe iris nodules?

A

granulomatous or non-granulomatous at pupillary border

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5
Q

What are bussaca iris nodules?

A

found on iris surface (midperiphery) in granulomatous uveitis

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6
Q

Iris atrophy

A

diffuse in simplex and sectoral in zoster

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7
Q

Fuch’s uveitis and iris changes

A

heterochromia due to chronic inflammation

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8
Q

IOP in uveitis

A

initially decreased due to inflammation and poor function of ciliary body, later increased due to trabeculitis and synechiae

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9
Q

What grading scale does anterior chamber cells/flare use?

A

SUN (using 1 mm slit lamp beam)

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10
Q

What is an approximate grading for cells?

A

0 <1// 1+ 6-15// 2+ 16-25// 3+ 26-50// 4+ >50

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11
Q

Should you see cells if you see flare?

A

ideally yes because of molecular weight but that does not always apply clinically

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12
Q

What is an approximate grading for flare?

A

0 none// 1+ faint// 2+ moderate aka iris details clear// 3+ marked// 4+ intense fibrin and plastic aqueous

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13
Q

What diseases are associated with nongranulomatous uveitis?

A

HLAb27, juvenile idiopathic arthritis, trauma, glaucomacyclitic crisis

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14
Q

What diseases are associated with granulomatous uveitis?

A

sarcoid, syphilis, TB, lens induced, sympathetic ophthalmia, VKH

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15
Q

When should you order a work up after uveitis?

A

bilateral, granulomatous, recurrent, children, panuveitis, posterior uveitis/retinal vasculitis, necrotizing retinitis

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16
Q

Treatment of uveitis?

A

aggressive corticosteroid treatment

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17
Q

What are topical corticosteroids?

A

prednisolone acetate, dexamethasone, difluprednate, loteprednol, fluorometholone

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18
Q

What are injectable corticosteroids?

A

triamcinolone acetonide, methylprednisone, betamethasone

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19
Q

What are oral corticosteroids?

A

prednisone, methylprednsione packs

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20
Q

What healthcare individuals might you consult in uveitis?

A

rheumatology, infectious disease, retina/ophthalmology

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21
Q

What is the most common orbital disorder in adults?

A

graves orbitopathy

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22
Q

What is the most common cause for proptosis

A

graves orbitopathy

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23
Q

What is the female male ratio of graves orbitopathy?

A

9 to 1

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24
Q

What are risk factors for ocular complications of thyroid disease

A

increased age at onset, smoking, use of radioactive iodine therapy

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25
Q

TED pathophysiology

A

development of autoantibodies stimulate thyroid gland which can lead to goiter, t-cell mediated response in orbit; t-cell response affects orbital fibroblasts

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26
Q

How do tcells and orbital fibroblasts interact?

A

adipogenesis, accumulation of GAGs and resultant tissue edema, infiltration of lymphocytes and mast cells, fibrosis of extraocular muscles

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27
Q

What are the two phases of TED?

A

active and inactive/latent

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28
Q

What is the active phase of TED?

A

active inflammatory process: periorbital edema and erythema, conjunctival injection and edema, eyelid retraction, ptosis, diplopia, lasts longer in smokers

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29
Q

What is the inactive/latent fibrotic stage of TED?

A

plateau of active inflammation: reduced chemosis/injection/edema and persistent proptosis/lid retraction/diplopia

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30
Q

What are clinical features of TED?

A

lid retraction, lid lag on down gaze (von graefe), lid edema, exophthalmos, EOM changes, ON changes

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31
Q

What EOM changes occur in TED?

A

upgaze and abduction especially, inferior>medial>superior>lateral recti>obliques

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32
Q

Explain lid retraction

A

lid retraction occurs in 82% of patients may be due to increased sympathetic tone, overaction of the levator and superior rectus muscles to compensate for inferior rectus restriction or inflammation and scarring of the levator complex

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33
Q

What are secondary effects of TED?

A

exposure keratoconjunctivitis/lagophthalmos, diplopia due to EOM involvement/strabismus, APD due to ONH compression, increased IOP from compression effects

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34
Q

Where may IOP be higher in TED?

A

in upgaze because of compression

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35
Q

What is NOSPECS

A

no signs or symptoms, only signs and no symptoms, soft tissue involvement with signs and symptoms, proptosis, EOM involvement, corneal involvement, sight loss

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36
Q

What is VISA?

A

vision/optic neuropathy, inflammation/orbital congestion, strabismus, appearance/exposure

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37
Q

What is EUGOGO?

A

breaks down graves orbitopathy into activity (severity of inflammation) and severity (impact on QOL/risk of vision loss)– clinical activity score: pain, redness, warmth, swelling, impaired function; severity assessment: eyelid measures, proptosis, EOMs, corneal integrity, neuropathy

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38
Q

Systemic symptoms of thyroid dysfunction

A

hair loss, heat or cold intolerance, weight loss/change, skin changes, memory difficulties, mood changes

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39
Q

What labs do you run for TED?

A

serum TSH (sensitive thyrotropin), free thyroxine T3 T4, thyroid related antibodies and thyroid peroxidase antibodies + anti-microsomal and anti-TSH

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40
Q

Orbital imaging

A

MRI for muscle bellies, CT for bone with decompression surgery

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41
Q

Management of TED

A

smoking cessation, lubricants, lid taping, short term fresnel, orbital decompression, orbital steroids, steroid sparing agents, orbital irradiation, glaucoma meds

42
Q

What is tepezza?

A

inhibits insulin like growth factor-1 which plays a role in upregulating fibroblastic activity

43
Q

How does tepezza work?

A

infusion every few weeks for 8 total treatments, reduces proptosis and associated exposure symptoms, reduced diplopia

44
Q

What are the anterior corneal dystrophies?

A

epithelial basement membrane dystrophy, meesman dystrophy, reis-bucklers/thiel-behnke

45
Q

Which corneal dystrophies are in Bowmans?

A

reis-bucklers and thiel-behnke

46
Q

What are the stromal corneal dystrophies?

A

lattice, granular, macular

47
Q

What are endothelial corneal dystrophies?

A

fuchs

48
Q

What is the most common anterior corneal dystrophy?

A

epithelial basement membrane dystrophy

49
Q

What improper developments of the basement membrane occur in EBMD?

A

thickened and misdirected development into the epithelium, intraepithelial microcysts degenerating epithelial cells, fibrillary material between descemets and bowmans

50
Q

What are symptoms of EBMD?

A

dry eye, fluctuating vision, pain association with RCE, blur from irregular astigmatism

51
Q

What are signs of EBMD?

A

intraepithelial lesions-gray, map patches, dots, fingerprint, whorls, best seen on retro illumination

52
Q

What is the treatment of EBMD?

A

debridement, pressure patch, bandage CL for RCE, anterior stromal puncture for RCE, phototherpeutic keratectomy, superficial keratectomy, chronic hypertonic solution and ointment

53
Q

What are hypertonic solutions

A

Muro 128 and freshkote

54
Q

How does freshkote work?

A

polyvinyl pyrrolidone and polyvinyl alcohol create oncotic gradient for freshkote to reduce microcystic edema

55
Q

What are signs of meesmann dystrophy?

A

diffuse intraepithelial cysts especially intrapalpebral, visualized well on retro illlumination

56
Q

When does Meesmann present?

A

as young as age 1 but symptomatic in adult years

57
Q

What are symptoms of meesmann?

A

mild irritation, DES, pain with ruptured cysts

58
Q

What happens with cysts in Meesmann?

A

cysts may rupture like small bullae, ruptured cysts may scar

59
Q

What are treatments of Meesmann?

A

bandage CL, superficial keratectomy

60
Q

What are signs of reis bucklers?

A

sub-epithelial, reticular opacities in central cornea; may eventually have central opacification with irregular astigmatism

61
Q

What are symptoms of reis bucklers?

A

reduced VA, pain from recurrent erosions

62
Q

What are the treatments of reis bucklers?

A

bandage CLs for RCE, various keratoplasties (lamellar, penetration)

63
Q

What dystrophy often occurs in a graft

A

reis bucklers, lattice, macular

64
Q

What are signs of lattice dystrophy?

A

refractile lines in anterior stroma become more dense, opaque

65
Q

What are symptoms of lattice dystrophy?

A

decreased VA, pain from RCE

66
Q

What are treatments for lattice dystrophy?

A

bandage CL for RCE, PKP

67
Q

What are signs of granular dystrophy?

A

dense, white clumps of opacities in anterior stroma, central with clear spaces between opactities that progress into hazy areas

68
Q

What are symptoms of granular dystrophy?

A

erosions are rare, opacities progress and intervening space becomes haze reducing VA

69
Q

What are treatments of granular dystorphy?

A

PKP when VA is reduced, possibly PTK

70
Q

What makes macular dystrophy rare?

A

autosomal recessive inheritance

71
Q

What are signs of macular dystophy?

A

hazy, gray stomal lesion extending to limbus

72
Q

What are symptoms of macular dystophy?

A

PKP when VA is reduced

73
Q

What are signs of Fuch’s?

A

guttata formation indicating abnormal endothelial cell function resulting in corneal edema

74
Q

What are symptoms of fuch’s?

A

blur, glare, colored haloes worse in am, pain from ruptured bullae

75
Q

What are treatments for fuchs?

A

hypertonic solutions, PKO, descemet’s stripping automated endothelial keratoplasty

76
Q

What is keratoconus?

A

a corneal ectasia

77
Q

What are symptoms of keratoconus?

A

decrease vision, distortion, pain form hydrops, vision changes starting in teens

78
Q

What are signs of keratoconus?

A

irregular astigmatism, apical thinning, steepening cornea, vogt stria, fleischer ring, munson sign, central corneal scarring

79
Q

What are treatments of keratoconus?

A

rigid CLs, intacs, DALK, PKP, collagen crosslinking

80
Q

RPR/VDRL

A

syphilis

81
Q

ACE

A

sarcoidosis, TB

82
Q

FTA-ABS/MHA-TP

A

syphilis

83
Q

ANCA

A

autoimmune vasculitis (Wegeners)

84
Q

Chest xray

A

TB, sarcoid, SLE

85
Q

Hertel norms

A

white 12-20 mm and AA 12-24 mm

86
Q

What is normal critical flicker fusion frequency?

A

33 dB, lower is decreased sensitivity

87
Q

Lenses for keratoconus

A

Jupiter-sclera, rose K-RGP, synergeyes-RGP/hydrogel hybrid, accukone-RGP, SO2-scleral multifocal, Centracone-RGP

88
Q

At what endothelial cell count do pumps struggle to function?

A

<500 cells/mm^2

89
Q

What technique helps evaluate endothelial cells?

A

specular microscopy

90
Q

Polymegetheism

A

change in cell size

91
Q

Pleomorphism

A

change in cell shape

92
Q

Guttata

A

focal clumping of excess abnormal basement membrane on descemets that has a beaten metal appearance especially on retro illumination

93
Q

What is descemet’s stripping automated endothelial keratoplasty DSAEK

A

partial thickness corneal transplant corneal layer, exchange patient’s damaged endothelium and descemets membrane with donor tissue with healthy posterior stroma/descemet/endo

94
Q

Advantages of keratopasty (PKP)

A

faster healing, quicker visual improvement, less surgery induced astigmatism, predictable and minimal change in anterior surface topography, sutures not necessary, decrease risk of wound dehiscence, decrease risk intra-operative expulsive suprachoroidal hemorrhage

95
Q

Episcleritis treatment

A

palliative therapy with AT and FML, clinically Pred Forte with possible oral NSAID

96
Q

Etiologies of episcleritis

A

idiopathic, collagen vascular disease, gout, infectious

97
Q

What percent of RCE patients have EBMD?

A

50%

98
Q

What demonstrates negative staining

A

EBMD

99
Q

What is a RCE treatment?

A

anterior stromal puncture (creates scar and thus adhesion to anterior stromal bed, avoid visual axis) or phototherapeutic keratectomy which is a excimer laser to bowmans that increases collaged and hemidesmosome activity

100
Q

Dalrymple’s sign

A

lid retraction/ scleral show superiorly

Integrative Analysis II (5 decks)

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