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Systemic Disease (Wolfe) > Orbital Disease > Flashcards

Orbital Disease Flashcards

1
Q

Average female PD

A

53-65

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2
Q

What is it called if PD is greater than average?

A

hypertelorism

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3
Q

What are Hertel exophthalmometry norms?

A

12-21 white, around 24 AA; >2mm difference b/w eyes is significant

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4
Q

What does pulsatile proptosis tell us?

A

vascular

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5
Q

What does resistance to retropulsion tell us?

A

there is something blocking the orbit

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6
Q

What is MRD 1?

A

UL to corneal reflex

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7
Q

What is MRD 2?

A

LL to corneal reflex

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8
Q

What is total palpebral width?

A

MR1 + MR2

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9
Q

Why might a goldmann VF be preferred?

A

goes out further which is good for neurological defects

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10
Q

What might be a reason not to run a HVF?

A

reduced acuity, may not see target

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11
Q

What is the brightest stimulus on Goldmann?

A

V4e

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12
Q

What is a ceco-central scotoma?

A

scotoma that involves the blindspot

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13
Q

What indicates true ON defect due to papillomacular bundle involvement?

A

ceco-central scotoma

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14
Q

What is the pneumonic for optic atrophy differentials?

A

VIN DITTCH, MD

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15
Q

What are the differentials for optic atrophy?

A

vascular, infectious/inflammatory, neoplastic, demyelinating, idiopathic, toxic/nutritional, traumatic, congenital, hereditary, metabolic/endocrine, degenerative

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16
Q

What are infectious etiologies of orbital disease?

A

orbital abscess/cellulitis/mucormycosis, syphilis (leuitic), TB

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17
Q

What are endocrine/metabolic etiologies of orbital disease?

A

thyroid

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18
Q

What are inflammatory etiologies of orbital disease?

A

sarcoid, orbital inflammatory pseudotumor, tolosa-hunt, granulomatosis with polyangitis

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19
Q

What are space occupying etiologies of orbital disease?

A

meningioma, mucocele

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20
Q

What are neoplastic etiologies of orbital disease?

A

orbital rhabdomyosarcoma, lymphoma, metastatic CA

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21
Q

What are vascular etiologies of orbital disease?

A

carotid cavernous fistula

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22
Q

What causes a carotid cavernous fistula?

A

rupture of the wall of the carotid artery, or one of its branches, into the cavernous sinus

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23
Q

What alters the hemodynamic state of the cavernous sinus and its venous exits in a CCF?

A

exposure to arterial pressure

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24
Q

What is the major orbital communication of the cavernous sinus?

A

superior ophthalmic vein

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25
Q

If the superior ophthalmic vein expands tremendously, what may occur subsequently?

A

engorgement of all orbital and conjunctival veins; veins become arterialized producing signs and symptoms of venous congestion

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26
Q

What are s/s of CCF?

A

pulsating exophthalmos, ocular bruit, diplopia, HA, conj chemosis, increased ICP, dilated conj vessels and visual decrease

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27
Q

Why is there some degree of bilateral orbital involvement of CCF?

A

normally occurring venous communications between the cavernous sinuses

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28
Q

What is the management of CCF?

A

typically resolves on it’s own but need to watch them

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29
Q

Orbital cellulitis/abscess can be secondary to infections in what locations?

A

paranasal air sinuses, ethmoid, puncture wound, bug bite, hordeolum

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30
Q

What is orbital cellulitis caused by?

A

gram positive staph and strep

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31
Q

What should you expect with orbital cellulitis?

A

fever

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32
Q

What is mucormycosis?

A

aggressive opportunistic fungal infection, humans are exposed often with soil and decaying vegetation but infection rarely occurs with intact immune system because macrophages phagocytize the spores

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33
Q

How does mucormycosis get to the orbit?

A

from the paranasal sinus mucosa

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34
Q

T/F the mortality rate of mucormycosis is low

A

false, high mortality rate; rapidly progressing infection with late diagnosis due to nonspecific symptoms

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35
Q

What patient populations are at risk for mucormycosis?

A

diabetes (especially ketoacidosis), people who receive multiple blood transfusions, immunocompromised patients with severe neutropenia, those on chronic steroids

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36
Q

What happens if mucormycosis leads to orbital apex syndrome?

A

ON involvement and vision loss, involvement of nerves III, IV, VI, V1 and V2

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37
Q

What is the cause of syphilis?

A

treponema pallidum, spiral shaped gram negative highly mobile bacterium

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38
Q

What are ocular findings of syphilis?

A

focal gummas (soft, non-cancerous growth) along nerves or orbital fissure syndrome

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39
Q

What is the cause of TB?

A

mycobacterium tuberculosis, small aerobic, nonmotile bacillus `

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40
Q

What are most common presentations of TB?

A

proptosis, nontender or mildly painful orbital/lid swelling, sinus formation, involvement of bony orbit and lacrimal gland with soft tissue inflammatory mass/abscess formation

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41
Q

Orbital tuberculosis presents with…

A

destruction of bone with or without sclerosis, extraconal inflammation/abscess formation, extension into the infratemporal fossa or intracranial extension, lacrimal gland involvement

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42
Q

What is the pathogenesis of TED?

A

antibodies bind antigenic receptor sites, T lymphocytes migrate to orbital tissues, cytokine cascade, GAG secretion and fibroblast proliferation

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43
Q

What does GAG secretion and fibroblast proliferation in TED result in?

A

swelling/inflammation/fibrosis; if chronic, fatty infiltration of muscles

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44
Q

Why can you have TED at any thyroid state?

A

it’s an autoimmune condition, Abs to TSH receptor

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45
Q

What is special about hyaluronic acid?

A

super hyperosmotic, 1 molecule attracts 4 molecules of water

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46
Q

What 3 main things plump the orbit?

A

adipogenesis (via increased Leptin), HA synthesis, myofibroblast differentiation and proliferation

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47
Q

How does Tepezza work?

A

blocks the IGF-1R-TSHR complex to prevent orbital edema and adipogenesis from ever starting; shown to reverse the effects of TED

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48
Q

What stage can you use Tepezza in?

A

active and chronic phases

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49
Q

What is elevated in hyperthyroid?

A

T3 and T4

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50
Q

What is elevated in hypothyroid?

A

TSH

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51
Q

What does euthyroid mean?

A

normal T3, T4, and TSH

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52
Q

What is Grave’s?

A

hyperthyroid + orbitopathy

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53
Q

What are categories of thyroid disease?

A

primary hyper, central hyper, primary hypo, secondary hypo

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54
Q

What is primary hyperthyroidism?

A

thyrotoxicosis and goiter

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55
Q

What is central hyperthyroidism?

A

secretory pituitary tumor

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56
Q

What is secondary hypothyroidism?

A

following radiation or resection

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57
Q

Why may a patient be on thyroxine?

A

hypothyroid initially due to involutional changes or hypothyroid following correction of hyperthyroidism

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58
Q

What are primary causes of thyroid changes?

A

autoimmune, nodule/tumor, previous radioactive iodine tx, iodine deficiency, medications, pregnancy

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59
Q

What is the central cause of hyperthyroidism?

A

pituitary gland tumor

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60
Q

What is the treatment of hyperthyroidism?

A

surgery, radioactive iodine treatment, anti-thyroid medication

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61
Q

What is more likely to cause TED following the procedure, radioactive iodine or surgical resection

A

radioactive iodine

62
Q

What is active TED?

A

inflammatory phase, 6 months to 5 years, average 2 years

63
Q

What is inactive TED?

A

fibrotic phase, becomes permanent damage

64
Q

What are risk factors of TED?

A

smoking and radioactive iodine treatment

65
Q

What is NO SPECS?

A

no s/s, only signs, soft tissue involvement, proptosis, EOM infiltration and fibrosis, corneal changes, sight loss

66
Q

What are corneal changes in TED?

A

exposure keratopathy

67
Q

What causes vision loss in TED?

A

optic nerve involvement

68
Q

What is the coca-cola bottle sign?

A

appearance of the muscles of the orbit in thyroid eye disease; belly of muscle enlarges with tendinous insertions spared

69
Q

Which muscles are affected first in TED?

A

IMSLO

70
Q

When are tendons involved in disease?

A

in orbital pseudotumor, not TED

71
Q

Where is IOP highest in TED?

A

in upgaze because IR presses on the globe

72
Q

What are TED treatments?

A

palliative, rescue and rehabilitation

73
Q

Which TED treatments are done in active phase?

A

palliative and rescue therapy

74
Q

Which TED treatment is done in inactive phase?

A

rehabilitation

75
Q

What is palliative/supportive therapy for TED?

A

ocular lubricants and ointments, eye masks/lid tape

76
Q

What is rescue therapy for TED?

A

corticosteroid tx IV and orbital radiation

77
Q

What is rehabilitation therapy for TED?

A

orbital decompression, strabismus, eyelid repositioning/blepharoplasty

78
Q

What comes after orbital decompression surgery?

A

orbital decompression then strabismus surgery then blepharoplasty

79
Q

T/F after orbital decompression surgery, EOMs are still swollen

A

true

80
Q

What kind of disease is orbital inflammatory pseduotumor?

A

non-specific orbital inflammatory disease

81
Q

What are other names for orbital inflammatory pseudotumor?

A

idiopathic orbital inflammation, orbital inflammatory syndrome

82
Q

What is the most common cause of painful orbital mass in adults?

A

orbital inflammatory pseudotumor

83
Q

When localized, what does orbital inflammatory pseudotumor involve?

A

EOMs, lacrimal gland, sclera, uvea, superior orbital fissure, cavernous sinus

84
Q

When diffuse, what does orbital inflammatory pseudotumor involve?

A

orbital fatty tissues

85
Q

What are the 3 most common orbital diseases in order?

A

TED, orbital lymphoma and non-specific orbital inflammatory disease

86
Q

T/F non-specific orbital inflammatory disease is a diagnosis of exclusion

A

true

87
Q

What is Tolosa Hunt?

A

episodic orbital pain associated with paralysis of one or more of CN 3, 4, or 6 which resolves spontaneously but can relapse and remit

88
Q

What are diagnostic criteria for Tolosa-Hunt?

A

one or more episodes of unilateral orbital pain persisting for weeks if untreated, paresis of one ore more CNs and/or demonstration of cavernous sinus granuloma by MRI or biopsy, paresis coincides with the onset of pain or follows it within 2 weeks, pain and paresis resolves within 72 hours when treated adequately with corticosteroids

89
Q

What did biopsied cases of tolosa hunt show?

A

the syndrome has been caused by granulomatous material in the cavernous sinus, SOF or orbit

90
Q

What is lagophthalmos?

A

incomplete closure of the lids

91
Q

What does sarcoid show on histology?

A

non-caseating epithelioid granuloma

92
Q

How is sarcoid diagnosed?

A

elevated angiotensin-converting enzyme levels

93
Q

How often does sarcoidosis involve the eye?

A

1/2 of the time

94
Q

What does ocular involvement of sarcoid involve?

A

uveitis, periphlebitis, multifocal choroditis, papillitis, papilledema, lacrimal gland enlargement and dry eye

95
Q

What is granulomatous with polyangiitis?

A

Wegner’s, granulomatous and sometimes necrotizing vasculitis targeting the respiratory tract and kidneys

96
Q

How often is there orbital involvement in granulomatous?

A

60% of patients; frequently the first or only clinical presentation

97
Q

What is treatment of granulomatous with polyangiitis?

A

corticosteroids

98
Q

What highly suggests GPA (granulomatous)?

A

proptosis + respiratory disease

99
Q

What can aid in diagnosis of GPA?

A

positive ANCA

100
Q

What is the diagnostic criteria for GPA?

A

nasal or oral inflammation, respiratory radiographic abnormalities consistent with respiratory tissue destruction, microhematuria or RBC casts on urinary sediment analysis, granulomatous inflammation on biopsy for pathology

101
Q

When 2 of 4 diagnostic criteria for GPA are met, sensitivity and specificity of diagnosis are..

A

88.2 and 92%

102
Q

T/F positive ANCA is conclusive for GPA

A

false

103
Q

What is the common demographic for GPA?

A

men in 5th decade

104
Q

What is a meningioma?

A

benign growth often > 50 year old male

105
Q

Where are meningiomas often located in the head?

A

40% skull base and 20% sphenoid wing (greater propensity for greater wing)

106
Q

What systemic condition can meningioma be associated with?

A

NF2

107
Q

What is a mucocele?

A

mucus filled cyst, slow growing

108
Q

What does a mucocele cause?

A

bone erosion

109
Q

What is the most common primary orbital malignancy in children?

A

rhabdomyosarcoma?

110
Q

Where are rhabdomyosarcoma’s typically located?

A

superior and superior nasal orbit leading to proptosis and inferior/inferior temporal displacement of the globe

111
Q

What age group does rhabdomyosarcoma affect?

A

90% occur before the age of 16, mean 5-7 years old

112
Q

What tissue type is rhabdomyosarcoma composed of?

A

mixed tissue type originates directly from striated muscle

113
Q

What are two differentials for rhabdomyosarcoma?

A

orbital cellulitis and concomitant sinus/URT infection

114
Q

What are s/s of rhabdomyosarcoma?

A

pain, visual loss, rapidly progressive course

115
Q

What produces insidiously progressive exophthalmos?

A

most orbital neoplasms in adults (exception metastatic tumor)

116
Q

Who is lymphoma more common in?

A

female population

117
Q

What is the most common site of lymphoma malignancy?

A

orbit 46-74%, conj 20-33%, eyelid 5-20%

118
Q

What percent of adult malignant orbital tumors does lymphoma make up?

A

55%

119
Q

What is the survival rate of lymphoma if isolated and treated promptly?

A

90-94%

120
Q

What is treatment of lymphoma?

A

surgical excision, radiotherapy or external beam irradiation

121
Q

What is the most common primary OAL?

A

low-grade malignant extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue

122
Q

What indicates Hodgkin’s lymphoma?

A

reed-sternberg cells

123
Q

What indicates Hodgkin’s lymphoma?

A

reed-sternberg cells

124
Q

What is a salmon colored lesion on the conj?

A

likely conjunctival lymphoma

125
Q

What are common presentations of primary metastatic cancer of the orbit?

A

proptosis and visual loss

126
Q

What are common presentations of orbital metastases?

A

diplopia and pain

127
Q

What are the most common tumors to metastasize to the orbit?

A

breast, lung, prostate

128
Q

What are some examples of congenital hypertelorism causes?

A

Crouzon syndrome, Waardenburg syndrome, cri du chat syndrome

129
Q

What is Crouzon?

A

autosomal dominant genetic disorder known as a branchial arch syndrome

130
Q

What branchial arch does Crouzon affect?

A

first aka pharyngeal, which is a precursor of the maxilla and mandible

131
Q

What can Crouzon’s cause?

A

premature fusion of certain skull bones

132
Q

What are important HPIs for orbital disease?

A

medical history, family history, onset, symptoms, progression

133
Q

What is pathognomonic for a fungal tumor on MRI?

A

lesion gets darker from t1 to t2

134
Q

What lights up on a T2 MRI?

A

water

135
Q

What is an osteotomy?

A

removal of bone

136
Q

What are 3 stages of visual field recovery following resection of compressive lesion?

A

initial fast, delayed slower, late mild

137
Q

What is the cause of initial fast recovery of visual field?

A

restoration of signal conduction along retinal ganglion cell axons

138
Q

What is the cause of delayed slower recovery of the VF?

A

restoration of axoplasmic transport and remyelination of the decompressed optic nerve

139
Q

What is aspergillus?

A

saprophytic fungus found in soil and decaying vegetation

140
Q

What is the most common organism form to contaminate paranasal sinus and orbit in the US?

A

aspergillus fumigatus, commonly in immunocompromised host

141
Q

What kind of environment does aspergillus prefer?

A

hypoxic (anaerobic sinus)

142
Q

What is invasive aspergillosis?

A

damage caused by necrosis and/or infiltration; granulomatous inflammation and necrotic fibrosis or fulminate diffuse vascular invasion, thrombosis and tissue necrosis

143
Q

What is non-invasive aspergillosis?

A

damage caused by mechanical pressure, does not invade bloodstream; fungus ball, chronic erosive fungal, allergic fungal

144
Q

Always get an MRI before prescribing…

A

steroids for orbital pseudotumor, you can kill your patient

145
Q

T/F Memphis is #6 on the list for Aspergillosis

A

true

146
Q

How is CT useful in fungal infection?

A

shows calcifications that are common in fungal sinusitis, rare in bacterial sinusitis and tumors; shows bony erosion

147
Q

How is MRI useful in fungal infection?

A

more important in the invasive form; characteristic very low signal on the T2 weighted image due to mineralization of the fungal tissue with iron and manganese

148
Q

What is the only way to definitively diagnose aspergillosis?

A

histological examination

149
Q

What is the treatment of aspergillosis?

A

debridement and debulk of invasive form; amphotericin B 0.5 mg/kg/day (toxic SE) and -azole antifungals

150
Q

How does Fluconazole work?

A

binds cytochrome P-450; less side effects than amphotericin B

151
Q

What is the new standard of care treatment of Aspergillosis?

A

Voriconazole, 96% bioavailability, transient blurred vision and light sensitivity

152
Q

Why may many children have facial asymmetry?

A

They are still growing

Systemic Disease (Wolfe) (10 decks)

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