Rheumatology II Flashcards

1
Q

What is Systemic Lupus Erythematous?

Who is it most common in?

A

Chronic inflammation affecting almost every organ
Autoantibodies to nuclear antigens

Ages 15-40
Women
Black women

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2
Q

What is the most common symptoms you’ll see with SLE?

What skin lesion is most commonly associated with SLE

A

FATIGUE

Butterfly rash

Due to Photosensitivity

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3
Q

Diagnostic Criteria for SLE?

A

Requires 4 or more criteria

Malor rash
Discoid rash
Photosensitivity 
Oral ulcer
Arthritis 
Serosistis (pleuritis/pericardisits)
Kidney disease (hematuria, proteinuria)
Neurologic disease (seizures, psychosis)
Hematologic disorders
Immunoligic abnormalities 
Positive ANA
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4
Q

Which lab is most indicative of SLE?

A

+ANA

Also more specifically

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5
Q

If you have a positive ANA what reflex test must be done?

Which finding will have the highest sensitivity and specificity

A

Anti-dsDNA** (high specificity and sensitivity)

Anti-Sm (high specificity)

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6
Q

Treatments for SLE

A
Sun protection, exercise
NSAIDS
Antimalarials
Hydroxycholorquine, chloroquine – helpful for MSK and skin manifestations [remember eye exams]
Corticosteroids
Methotrexate for arthritis
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7
Q

What 3 things can characterise Acute Cutaneous Lupus Erythematous (ACLE)

A

Facial eruption, generalized eruption, or TEN

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8
Q

What things characterize Subacute Cutaneous Lupus?

A

scaly papules that evolve into psoriasiform plaques

Usually shoulders, forearms, neck, upper torso

Photosensitivity

Positive antinuclear antibodies

Arthralgias

Oral ulcers

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9
Q

Clinical Presentation of Discoid Lupus

A

Erythematous, mildly indurated plaques, covered with a scale

Inflammation and scarring lesions

Face, neck, scalp, ears

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10
Q

What complications can occur with SLE and pregnancy?

A

Higher rates of spontaneous abortion
Risk of preterm birth, IUGR
Acquired autoimmunity

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11
Q

What complications can be seen in Neonatal Lupus

A

Congenital heart block

Cutaneous involvement

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12
Q

What is Antiphospholipid Antibody Syndrome

A

Autoimmune, multisystem disrder
Hypercoagulability syndrome
Recurrent thromboses in venous or arterial circulation

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13
Q

What is the difference between Primary and Secondary Antiphospholipid Syndrome?

A

Primary
In the absence of other disease

Secondary
Occurs with other autoimmune disease
SLE

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14
Q

Clinical Presentation of Antiphospholipid Antibody Syndrome?

A

Asymptomatic until they experience:

Recurrent pregnancy loss
Unexplained fetal death after first trimester
1 or more premature births before 34 weeks due to eclampsia or preeclampsia

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15
Q

How is Antiphospholipid Antibody Syndrome diagnosed?

A

One clinical event + positive antibody blood test(s)

Anti-cardiolipin antibodies

Can produce false-positive test for syphilis

Antibodies to beta-2-glycoprotein

Lupus anticoagulant antibody

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16
Q

Antiphospholipid Antibody Syndrome treatment?

A

Anticoagulation for life - warfarin to maintain an INR of 2-3

17
Q

What is Raynaud Phenomenon?

How is it caused?

A

Syndrome of paroxysmal digital ischemia

Initial phase: excessive vasoconstriction
Recovery phase: vasodilation

18
Q

Clinical presentation of Raynaud Phenomenon?

A

Initial phase: demarcated digital pallor or cyanosis
Numbness, stiffness, pain decreased sensation

Recovery phase: intense hyperemia and rubor
Intense throbbing, paresthesia, pain

Primarily affects fingers

Resolves with warm temps or putting extremity in warm water

19
Q

1st Line Treatment for Raynaud Phenomenon?

A

Calcium channel blockers - first line

Nifedipine, amlodipine, felodipine

20
Q

What is Scleroderma?

What is the pathophysiology behind this?

A

Diffuse fibrosis of skin and internal organs

Deposition of collagen in skin, kidney, heart, lungs, stomach
Results in fibrosis of skin and organs

21
Q

Clinical Presentation of Scleroderma: CREST

A
Calcinosis cutis
Raynaud phenomenon
Esophageal dysfunction
Sclerodactyly
Telangiectasias
22
Q

slide 42

A

slide 42

23
Q

Labs for Scleroderma?

A

+ ANA in 90% of patients with diffuse scleroderma

+ anti centromere antibody in CREST syndrome (more specific)

24
Q

Treatment for Scleroderma?

A

No cure

Monitor for HTN, as it signals kidney involvement

25
Q

What is Polymyositis & Dermatomyositis (P&D)

A

Inflammation of striated muscle
Proximal skeletal muscle weakness
Dermatomyositis – skin manifestations

26
Q

Clincal presentation of polymyositis and Dermatomyositis?

A

Insidious, painless muscle weakness around neck, shoulders, hips

SOB

Dysphagia
Choking while eating, aspiration

27
Q

What 4 skin rashes are associated with Polymyositis and Dermatomyositis

A

Malar
Heliotrope
Gottron’s papules
Shawl sign

28
Q

What labs can help diagnose Polymyositis and Dermatomyositis?

What is the most definitive diagnostic test?

A

Labs:
Elevated muscle enzymes
Creatine kinase (CK)
Aldolase

Muscle biopsy**

29
Q

What is the pathophysiology of Sjӧgren Syndrome

A

Auto antibodies destroy salivary and lacrimal glands

Decreased production of saliva and tears

30
Q

What is a definitive diagnostic test used to idenfity Sjogren Syndrome

A

Lip biopsy to evaluate for gland fibrosis

31
Q

Treatment for Sjogren Syndrome

A

Avoid medications with anticholinergic and antihistamine effects

Keep mucosa moist

Pilocarpine can increase salivary flow (muscarinic agonists, secretagogue)

Cyclosporine can improve eye symptoms

32
Q

Clinical presentation of Sjogren syndrome?

A

Xerostomia (dry mouth)
Xerophthalmia (dry eyes)
Enlarged parotid glands

33
Q

What labs are used to diagnose Sjogren syndrome

Which are going to be most specific

A

ANA (95%)

Anti-Ro (ant-SSA)
Anti-La (ant-SSB)

34
Q

What is a positive Shirmer test when it comes to Sjogren?

A

Wetting less than 5mm of filter paper in 5 minutes is positive for Sjogren