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Systemic Disease (Wolfe) > Autoimmune-- Collagen-Vascular > Flashcards

Autoimmune-- Collagen-Vascular Flashcards

1
Q

List autoimmune collagen-vascular diseases

A

rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, sjogren’s, ankylosing spondylitis, reactive arthritis, scleroderma

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2
Q

List vascular autoimmune diseases

A

granulomatosis with polyangiitis (wegener’s), temporal arteritis

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3
Q

What is the most common ocular manifestation of autoimmune disease?

A

dry eye

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4
Q

What is a collagen-vascular disease?

A

development of an immune response by the organisms against the host tissue

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5
Q

What is the etiology of collagen-vascular disease?

A

idiopathic or secondary to trauma, infection, or exposure to environmental antigens or cross-reactivity between medications

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6
Q

What happens in a collagen-vascular disease?

A

deposition of fibrin and diffuse inflammatory damage to connective tissue and vascular system (targets collagen and elastin) disseminated throughout the body

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7
Q

What is the etiology of rheumatoid arthritis?

A

unknown, environmental or viral factors may initiate disease in susceptible individuals

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8
Q

What is the demographic of RA?

A

W>M 25-50 year onset

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9
Q

What is the MOA of RA?

A

production of abnormal IgG causes autoantibody production (rheumatoid factors RF then attack the IgG); process attracts inflammatory cells to synovial fluid causing red, painful, swollen joints

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10
Q

What is testing for RA?

A

80% of patients are positive for rheumatoid factor

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11
Q

What are systemic manifestations of RA?

A

gradual onset over weeks to months affecting hands and feet first; other organs affected include heart, lungs, CNS, skin and GI tract; physical impairment and deformity affects quality of life

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12
Q

What are early systemic symptoms of RA?

A

fatigue, anorexia, morning stiffness, multi-joint involvement, symmetric joint swelling with associated warmth, swelling, tenderness, pain

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13
Q

What are rheumatoid nodules?

A

cutaneous nodules– firm, round, subcutaneous masses on the extensor surface of the forearms or near affected joint

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14
Q

What are ocular manifestations of RA?

A

DRY EYE, episcleritis, anterior scleritis, scleromalacia perforans, posterior scleritis, uveitis, glaucoma

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15
Q

What is scleromalacia perforans?

A

painless thinning of the sclera in RA patients

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16
Q

What are s/s of posterior scleritis?

A

pain, decreased VA, redness, diplopia, proptosis, choroidal folds, retinal striae, dis edema, macular edema, RD; important to look for injection of sclera deep into fornix

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17
Q

What is the sign of posterior scleritis on B scan?

A

T sign, depicts fluid behind globe

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18
Q

Does every case of scleritis necessitate a systemic work up?

A

yes, high prevalence for systemic disease w/ scleritis

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19
Q

What is keratopathy secondary to RA?

A

sclerosing keratitis, acute stromal keratitis, furrowing, sterile peripheral ulcerative keratitis

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20
Q

What is sclerosing keratitis?

A

associated with anterior scleritis at level of stroma, peripheral infiltrates, vascularization, lipid deposition, scarring, grayish opacification of stroma

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21
Q

What is sterile peripheral ulcerative keratitis?

A

secondary to scleral inflammation, leads to thinning and perforation; systemic treatment required

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22
Q

T/F PUK in the course of systemic connective tissue disorder may reflect the presence of a potentially lethal systemic vasculitis?

A

true

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23
Q

RA diagnosis

A

(+)RF 80%, (+)ANA 20%, elevated ESR, RA confirmed by synovial fluid analysis, X-rays

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24
Q

What is (+) RF?

A

not specific for RA, (+) with Lupus, Sjogren, sarcoid, scleroderma, polymyositis, infectious disease

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25
Q

What is prognostic for the course and severity of RA?

A

elevated ESR (and CRP)

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26
Q

What do x-rays show?

A

narrowed joint spaces, loss of cartilage; more helpful later in the disease

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27
Q

What is RA medical treatment?

A

NSAIDS and analgesics, oral and intra-articular glucocorticoids, and DMARDS

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28
Q

What are NSAIDS and analgesics for in RA tx?

A

control pain and inflammation, GI upset (rx w/ H2 blocker), platelet and liver dysfunction

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29
Q

Describe oral and intra-articular glucocorticoids for RA tx?

A

5-10 mg daily, weight gain, DM, osteoporosis, infection, cataract, IOP

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30
Q

What is DMARDS?

A

disease modifying rheumatic drugs

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31
Q

What are examples of DMARDS?

A

hydroxychloroquine (plaquenil), gold salts, methotrexate, TNF inhibitors

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32
Q

What is HCQ?

A

antimalarial, 1-6 months for maximum therapeutics

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33
Q

HCQ ocular side effects

A

whorl keratopathy, toxic maculopathy

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34
Q

What are gold salts?

A

IM or oral, 3-6 months to reach maximum therapeutic benefit

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35
Q

What are gold salt ocular side effects?

A

corneal or conjunctival deposits, lens deposits, K ulcer, iritis, conjunctivitis

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36
Q

What is methotrexate?

A

IM or oral, immunosuppressive agent/chemotherapy drug, patients should also take folic acid supplements

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37
Q

What are methotrexate ocular side effects?

A

punctate keratitis, periorbital edema, blepharitis, conjunctival hyperemia, photophobia

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38
Q

What are TNF inhibitors?

A

subcutaneous injections 2x/week; remicade, humira, enbrel

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39
Q

What are ocular side effects of TNF inhibitors?

A

optic neuritis

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40
Q

HCQ AAO screening guidelines risk factors for toxic retinopathy

A

HCQ >5.0 mg/kg real weight and CQ >2.3 mg/kg real weight; duration of use > 5 years; subnormal GFR; concomitant tamoxifen use; macular disease

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41
Q

HCQ AAO screening guideline clinical examination techniques

A

automated VF (24-2 and 10-2 in Asian population due to maculopathy being further out), spectral domain OCT

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42
Q

What is no longer recommended for HCQ clinical examination?

A

fundus exam, time-domain OCT, fluorescein angiography, full-field ERG, amsler, color testing, EOG

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43
Q

What is the most common connective tissue disease in children?

A

juvenile rheumatoid arthritis

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44
Q

What is the most common etiology of uveitis in children?

A

juvenile rheumatoid arthritis

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45
Q

What are the 3 forms of JRA (JIA)?

A

Pauciarticular, polyarticular, systemic

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46
Q

What is pauciarticular JIA?

A

1-4 joints affected

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47
Q

What is polyarticular JIA?

A

5 or greater joints

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48
Q

What is systemic JIA?

A

Still’s disease, high spiking fevers (104+), lymphadenopathy, evanescent (transient) salmon-colored rash

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49
Q

What is onset of JIA?

A

all forms <5 years old, no complaint of pain but avoids limb use

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50
Q

JIA etiology

A

girls>boys 4:1; precipitating factors: trauma, URI, hereditary components; most RF (-)

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51
Q

What is the most common form of JIA?

A

60% of all JIA is pauciarticular

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52
Q

What form of JIA is most likely to develop uveitis?

A

pauciarticular

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53
Q

What are 3 JRA ocular manifestations?

A

cataract, band keratopathy, glaucoma

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54
Q

Cataracts and JIA

A

50% of eyes with chronic anterior uveitis secondary to steroid use and inflammation

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55
Q

Band keratopathy and JIA

A

77% of eyes with chronic anterior uveitis, not calcium related, VA loss when visual axis affected

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56
Q

Glaucoma and JIA

A

15-45% with uveitis, secondary to steroid use and inflammation

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57
Q

T/F treatment of JIA is systemic steroids

A

false, oral steroids should be avoided in children with JIA related uveitis because these drugs have overwhelming effect on bone growth

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58
Q

What is systemic treatment of JIA?

A

intra-articular prednisolone or triamcinolone, physical therapy, NSAIDS, DMARDS

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59
Q

What is systemic lupus erythematosus?

A

idiopathic, chronic, multi-system inflammatory disease characterized by pathogenic antibodies that attack cells and tissues throughout the body; exacerbations and remissions

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60
Q

Etiology of systemic lupus erythematosus

A

genetic predisposition, environmental influence triggers immune response

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61
Q

Dx of autoimmune lupus

A

(+) ANA in 90%

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62
Q

What are forms of lupus?

A

auto-immune, discoid lupus erythematosus, drug induced

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63
Q

What is discoid lupus erythematosus?

A

dermatologic condition (cutaneous form) (-) ANA

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64
Q

What is drug induced lupus?

A

(+) ANA, chlorpromazine, hydralazine, phenytoin, isoniazid, methyldopa, quinidine

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65
Q

T/F ocular severity of lupus relates to systemic severity

A

true, if you see ocular signs, you can assume they are not doing well

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66
Q

Demographics of lupus

A

females 90% > males, AA and hispanics most effected, 1st-4th decades of life

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67
Q

Age of onset for lupus?

A

average age 30 years old

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68
Q

What cancers does lupus increase the risk of?

A

lymphoma and cervical cancer

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69
Q

What is the most common presenting symptom of lupus?

A

non-erosive, non-deforming, symmetrical arthropathy

70
Q

What 3 systemic side effects of lupus were emphasized?

A

discoid lesions, butterfly rash, and raynuad’s phenomenon

71
Q

What are constitutional side effects of lupus?

A

90%; fever, fatigue, weight loss

72
Q

What are musculoskeletal side effects of lupus?

A

90%; arthritis, myalgia, arthralgia, joint deformities

73
Q

What are cutaneous lesion side effects of lupus?

A

80%; discoid lupus erythematosus, butterfly rash (40%), alopecia, photosensitivity, oral ulcers

74
Q

What are hematologic side effects of lupus?

A

80%; anemia, vasculitis, thrombosis (15%) venous, arterial; associated with antiphospholipid syndrome

75
Q

What are neurologic side effects of lupus?

A

50%; HA, anxiety, depression, mood swings, Bell’s palsy

76
Q

What are cardiac side effects of lupus?

A

50%; accelerated atherosclerosis, carditis

77
Q

What are pulmonary side effects of lupus?

A

pleural effusions

78
Q

What are renal disease side effects of lupus?

A

50%; proteinuria, nephrotic syndrome, renal failure

79
Q

What are GI side effects of lupus?

A

45%; mild pain, diarrhea, abnormal liver enzymes, colitis

80
Q

What percent fetal loss is associated with lupus?

A

30%

81
Q

SLE lab testing

A

(+) ANA 95%, anti-native double stranded DNA very specific for SLE

82
Q

Rheumatology criteria for SLE

A

4 of 11 symptoms (none ocular); anemia, pericarditis, diarrhea, cognitive dysfunction, vascular thrombosis, musculoskeletal arthralgia and myalgia, proteinuria, malar rash

83
Q

Why might you see madarosis in SLE?

A

madarosis secondary to scarring of the hair follicle from the discoid lesion

84
Q

SLE corneal effects

A

k-sicca, stromal infiltrates, ulcer, vascularization, SPK, pannus, furrowing

85
Q

SLE conjunctival effects

A

nonspecific conjunctivitis: bulbar and palpebral

86
Q

SLE sclera effects

A

scleritis, diffuse or nodular

87
Q

SLE uvea effects

A

non-granulomatous uveitis, choroidopathy causes damage to overlying RPE and can lead to serous detachment of RPE

88
Q

SLE periorbital effects

A

skin lesions: discoid lupus, edema

89
Q

SLE EOM effects

A

myositis

90
Q

SLE vitreal effects

A

hemorrhage from NVD, NVE

91
Q

SLE retina effects

A

CWS, vasculitis induced proliferative retinopathy > hemorrhages > R; vascular occlusion arterial >venous

92
Q

T/F 88% of those with lupus retinopathy have active systemic disease

A

true, retinopathy parallels systemic disease activity

93
Q

SLE ON effects

A

optic neuritis, AION, atrophy

94
Q

SLE neuro-ophthalmic effects

A

CN palsies (diplopia), transient ptosis, pupil abnormalities, VF loss, cortical blindness, INO, nystagmus, papilledema

95
Q

SLE tx

A

rest, avoidance of stress and UV light, NSAIDS, HCQ, corticosteroids, cytotoxic agents

96
Q

What are examples of cytotoxic agents (immunosuppressants)?

A

azathioprine, mycophenolate mofetil, cyclosporine, methotrexate, leflunomide, cyclophosphamide, chlorambucil, nitrogen mustard

97
Q

What is management for SLE?

A

refer to rheumatologist

98
Q

What is the prognosis of SLE?

A

if only cutaneous and musculoskeletal: good; if brain, lungs, hearts, or kidney: poor

99
Q

What is the survival rate of SLE?

A

10 years 90%; >20 years 63-75%

100
Q

What is cause of death with SLE?

A

cardiovascular disease, infection, renal failure

101
Q

T/F organismal invasion is more likely to cause a granulomatous uveitis

A

true

102
Q

What is sjogren’s syndrome?

A

autoimmune disorder with progressive loss of lacrimal and salivary exocrine glands

103
Q

What is the demographic for sjogren’s?

A

women age 50, no race or ethnic predilection

104
Q

What is primary sjogren’s?

A

more aggressive form of disease process, must rule out lymphoma (5%)

105
Q

What is sjogren’s secondary to?

A

RA, SLE, scleroderma, polymyositis

106
Q

What are oral manifestations of sjogren’s?

A

painful fissures in corners of mouth/tongue, periodontal disease, oral yeast infections, aphagia, enlarged parotid glands “chipmunk cheeks”

107
Q

What are systemic manifestations (xerosis)?

A

skin, gynecological complications

108
Q

What sjogren’s systemic manifestations were emphasized?

A

Raynaud’s phenomenon, trigeminal nerve involvement (facial pain and numbness), joint pain, myalgia, fatigue, and high risk for lymphoma

109
Q

What are minor systemic manifestations of sjogren’s?

A

respiratory tract: nosebleeds, alteration of smell and taste, difficulty speaking, chronic cough, bronchitis; GI: chronic gastritis, reduced exocrine secretion in the GI tract can lead to gastritis and pancreatitis; kidney and liver: interstitial inflammation of kidney

110
Q

What are ocular manifestations of sjogren’s?

A

aqueous layer of tear film diminished, mucous strands/filamentary keratitis, injection, corneal opacification, pannus, ulceration

111
Q

Ocular diagnosis of sjogren’s

A

K sicca, (+) lip biopsy confirming lymphocytes, confirmed connective tissue or autoimmune disorder

112
Q

K sicca in sjogren’s

A

schirmer test or phenol red thread test, decreased TBUT, decreased tear meniscus, corneal staining

113
Q

What does NaFl “stain”?

A

devoid epithelium, dryness

114
Q

What does Rose Bengal stain?

A

devitalized cells

115
Q

What are sjogren’s antibody tests?

A

antiSS-A (RO), antiSS-B (LA), and antiSS-C; detect antinuclear antibodies and confrims diagnosis

116
Q

What blood testing is completed for sjogren’s?

A

check ANA, RF, and ESR

117
Q

Tx of oral sjogren’s symptoms

A

saliva substitutes, dental hygiene, rinses, anti-fungal tablets and creams, frequent liquid consumption, humidifiers, nasal sprays, oral pilocarpine, cevimeline

118
Q

What is cevimeline for?

A

stimulates exocrine glands

119
Q

Tx of systemic sjogren’s symptoms

A

skin creams, NSAIDS for myalgia and arthralgia, systemic steroids

120
Q

Tx of ocular sjogren’s symptoms

A

reduce symptoms, prevent complications, copious ATs, topical cyclosporin A, punctal occlusion, oral flax seed oil and omega 3 fish oil capsules, lateral tarsorrhaphy, moisture goggles, spectacle side shields

121
Q

What is filamentary keratitis tx?

A

lubrication, NaCl drops and ung, acetylcysteine 10% to break up mucous, debride filaments, bandage CL

122
Q

What does topical cyclosporinA (Restasis) do?

A

stimulates tear production by suppressing inflammation

123
Q

What are examples of spondyloarthropaties?

A

ankylosing spondylitis, psoriatic arthritis, reiter’s syndrome, inflammatory bowel disease

124
Q

What is consistent between spondyloarthropaties?

A

inflammatory disorders (-) RF and (+) HLA-b27 involving the central or axial skeleton and resulting in non-granulomatous anterior uveitis

125
Q

What is the demographic for ankylosing spondylitis?

A

young men

126
Q

What ocular involvement is present before systemic ankylosing spondylitis symptoms (initial presentation of disease)?

A

acute, unilateral non-granulomatous uveitis

127
Q

T/F non-granulomatous uveitis is related to systemic severity of ankylosing spondylitis

A

false, not related to systemic severity of disease, completely resolves in between occurrences

128
Q

What are signs of acute, unilateral non-granulomatous uveitis?

A

painful and confined to the AC, a lot of fibrin in AC, pupil may become occluded with a fibrous membrane, hypopyon

129
Q

What is ankylosing spondylitis characterized by?

A

inflammation of distal joints and central skeleton; produces lesions at the site of the attachment of the ligament to bone (most commonly around the pelvis and spine); lower back pain

130
Q

Why is early diagnosis of ankylosing spondylitis important?

A

early dx and tx is essential to prevent permanent spinal deformity aka bamboo spine

131
Q

How is ankylosing spondylitis diagnosed?

A

(+) family history, (+) HLA-B27, (-) RF and ANA, elevated EST and C-reactive protein, elevated alkaline phosphatase, X-ray reveals sacroilitis and other joint involvement

132
Q

What is ankylosing spondylitis systemic treatment?

A

relieve pain and stiffness via exercise and physical therapy, oral NSAIDS (indomethacin + H2 blocker), glucocorticoid injection, antirheumatic drugs

133
Q

What is ankylosing spondylitis ocular treatment?

A

topical steroids and cycloplegics, topical phenylephrine for breaking PS, monitor for side effects like cataracts of increased IOP, educate pt on s/s of uveitis and FU q6-12 months

134
Q

What is psoriatic arthritis?

A

psoriatic skin and nail disease with arthritis of the spine

135
Q

What is psoriasis?

A

mild to moderate itching, discrete erythematous lesions with scaling and flaking; nail involvement parallels arthritis severity

136
Q

What is nail involvement in psoriatic arthritis?

A

discolored, thickened, cracked, pitted nails

137
Q

What are the demographics of psoriatic arthritis?

A

males=females, peak age of onset is 4th or 5th decade; periods of exacerbations and remissions

138
Q

What is the diagnosis of psoriatic arthritis?

A

(-) RF (-) ANA (+) HLA, clinical s/s, (+) family history,

139
Q

What are ocular complications of psoriatic arthritis?

A

conjunctiviits and uveitis

140
Q

What is tx of conjunctivitis from psoriatic arthritis?

A

supportive therapy, cold compresses, vasoconstricots, lubricants

141
Q

What is tx of uveitis from psoriatic arthritis?

A

cycloplegics, topical steroids

142
Q

What is systemic treatment for psoriatic arthritis?

A

antirheumatic meds, topical retinoid gels/corticosteroid creams and UV light therapy for skin lesions, steroid injections for synovitis

143
Q

What is reactive arthritis?

A

acute arthritis associated with an antecedent infection ex: chlamydial; characterized by distal joint inflammation (large weight bearing joings)

144
Q

What is the reactive arthritis triad?

A

arthritis, urethritis, conjunctivitis; if all 3 are not present= incomplete form of the disease

145
Q

The majority of reactive arthritis infections follow which 2 types of infection?

A

sexually acquired infection usually chlamydia or enteric infection usually salmonella

146
Q

What percent of reactive arthritis from STI causes ocular involvement and what is the demographic?

A

50% w/ males 5x > females

147
Q

What percent of reactive arthritis from enteric infection causes ocular involvement and what is the demographic?

A

70% w/ males = females

148
Q

Which is a more common reactive arthritis infection, enteric or STI?

A

enteric

149
Q

What are ocular concerns of reactive arthritis?

A

unilateral or bilateral conjunctivitis and acute nongranulomatous uveitis

150
Q

Describe the unilateral or bilateral conjunctivitis from reactive arthritis

A

initial symptom, develops within days of systemic infection; non-infectious and self limiting (non-purulent w/ SPK)

151
Q

Describe the acute nongranulomatous uveitis from reactive arthritis

A

recurrent, unilateral, KPs lead to synechia

152
Q

What is the diagnosis of reactive arthritis?

A

history and physical exam, (+) HLA-B27 75% of the time, elevated ESR and CRP, (-) ANA, CBC w/ mild anemia, radiographic confirmation of joint involvement

153
Q

What is systemic treatment of reactive arthritis?

A

pain relief, exercise encouraged, NSAIDS, glucocorticoids avoided unless pt is confined to bed, if chlamydial then oral azithromycin

154
Q

What is ocular treatment of reactive arthritis?

A

vasoconstictors/lubricant for conjunctivitis, topical steroids/cycloplegic/systemic steroids for uveitis, topical fluoroquinolone for keratitis or corneal ulceration, manage secondary glaucoma

155
Q

Scleroderma

A

read in textbook

156
Q

What is giant cell arteritis/temporal arteritis?

A

disease of the elderly average onset 70 years old

157
Q

What is systemic (autoimmune) vasculitis?

A

obliterative vasculitis, arterial walls become thickened by granulomatous deposition and giant cell formation results in luminal narrowing and ischemia of downstream tissues w/ predilection for cranial arteries

158
Q

What is vision loss from giant cell?

A

AION, ophthalmic artery involvement, severe and permanent, unilateral to bilateral in 1-10 days if no treatment 50-75%, TIAs with preceding photopsia and HA

159
Q

What is polymyalgia rheumatica (PMR)?

A

aching and stiffness in torso and proximal limbs, exclusive to the elderly, occurs with GCA, 15-30% of people with PMR get GCA

160
Q

GCA and PMR demographics

A

caucasians, females > males; about 50% of those with GCA get PMR

161
Q

What is the clinical presentation of GCA?

A

elderly patient with sudden LOV and HA + fever, malaise, night sweats, weight loss, anorexia, severe HA, neck pain, jaw claudication, lack of temporal pulse in 40%; 20% with no symptoms

162
Q

What are ocular manifestations of GCA?

A

amarosis fugax, AION, AAION, APD, altitudinal VF defect, CRAO, CN palsy, ischemia of A or P seg

163
Q

What is AAION?

A

sudden, painless, permanent vision loss, edematous disc, splinter hemes, CWS, (+) APD, altitudinal VF defect

164
Q

What does A seg ischemia lead to?

A

K edema, iritis, hypotony, cataract

165
Q

What does P seg ischemia lead to?

A

neovascular glaucoma

166
Q

What is the diagnosis of GCA?

A

age, s/s, elevated EST and C-reactive protein

167
Q

T/F you should wait for diagnostic evidence to treat GCA?

A

false, treat prior to results in enough clinical evidence

168
Q

What is a temporal artery biopsy for?

A

confirming GCA diagnosis, serial sectioning of the vessel so that inflamed areas are not missed; assess 25 mm length, 15% are biopsy negative

169
Q

What is normal ESR?

A

male age/2 and female (age +10)/2

170
Q

What is 100% sensitive for GCA?

A

CRP >2.45 mg/dL

171
Q

What is treatment for GCA?

A

refer to ER STAT; goal is to preserve vision in the fellow eye with oral or IV corticosteroids to decrease arterial inflammation and increase blood flow

172
Q

How are GCA and GPA (Wegner’s) different?

A

GCA= large to medium artery while GPA= small artery and/or vein

Systemic Disease (Wolfe) (10 decks)

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