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Clinical Med I > MSK/Rheumatology - Rheumatology- Exam 3 > Flashcards

MSK/Rheumatology - Rheumatology- Exam 3 Flashcards

1
Q

What is SLE?

A

Chronic multi-organ autoimmune disorder, targets young adult females

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2
Q

What are the clinical manifestations of SLE mediated by?

A

Antibody formation and creation of immune complexes that deposit in damage tissue

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3
Q

Although the SLE etiology remains unknown, what are the main contributors?

A

Genetic, hormonal, immunologic, environmental changes that promote production of antinuclear antibodies (ANA)

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4
Q

What are the general clinical presentations of SLE?

A

Fatigue*, fever, LAD, weight loss

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5
Q

What are the skin clinical presentations of SLE?

A 
Malar "butterfly" rash
Discoid (keratotic, photosensitivity)
Mucocutaneous - painless ulcers
Alopecia
Raynaud phenomenon
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6
Q

What is the Raynaud phenomenon that occurs in 30% of patients?

A

Vasospastic disease of extremities with cold temps/ stress; bicentennial disease: red, white, and blue

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7
Q

What is the treatment for the Raynaud phenomenon?

A

Calcium channel blocker

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8
Q

What is discoid?

A

Erythematous patches with keratitis scaling in sun exposed areas

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9
Q

What heart related risk is increased in SLE patients?

A

MI - accelerated atherosclerosis

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10
Q

How can SLE affect the kidney?

A

Nephritis with proteinuria

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11
Q

Besides systemic involvement, what other clinical manifestations are affected by SLE?

A

Ophthalmologic involvement, hematologic abnormalities, antiphospholipid syndrome

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12
Q

What drugs are most commonly associated with drug-induced lupus?

A

Drugs that trigger specific immune response- procainamide, isoniazid, hydralazine

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13
Q

What do patients with drug-induced lupus present with in terms of blood work?

A

Positive antihistone antibody

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14
Q

What is the treatment for drug-induced lupus?

A

Stop the offending drug

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15
Q

What diagnostic lab testing is performed for SLE?

A

Antinuclear antibody (ANA) = cardinal feature
-reported in 2 parts: titer of antibodies with serial dilution and staining pattern of antibodies
Anti-DNA
Anti-Sm
Antiphospholipid Ab

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16
Q

What is a homogeneous staining pattern?

A

Entire nucleus stained

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17
Q

What is a speckled staining pattern?

A

Fine or course speckles through nucleus

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18
Q

What is a centromere staining pattern?

A

30-60 uniform speckles, localize to chromosomes in dividing cells

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19
Q

What is a nucleolar staining pattern?

A

Homogeneous or speckled staining of nucleolus

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20
Q

What are some nonpharmacologic treatments for SLE?

A 
Sun protection
Diet/ nutrition
Exercise
Smoking cessation
Immunizations
Treatment of comorbid conditions
Pregnancy/ contraception
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21
Q

What is the first line treatment for SLE?

A

Antimalarials = long-term daily Hydroxychloroquine (Plaquenil) with regular ophthalmologic f/u

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22
Q

What meds may be added to antimalarials for the treatment for SLE?

A

NSAIDS, corticosteroids (systemic), immunosuppressive agents

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23
Q

How many of the 11 criteria for SLE (based on the 1997 ACR criteria) do patients usually present with?

A

4+

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24
Q

What are the leading causes of death in patients with SLE?

A

Active disease (renal and CNS)
Infections
CV disease

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25
Q

What is polymyositis?

A

Idiopathic progressive, inflammatory condition causing symmetric proximal muscle weakness, multisystem disorder

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26
Q

What are common complaints of a patient with polymyositis?

A

Weakness with deltoid and hip flexors
“Difficulty getting up from a chair”
“Trouble carrying groceries”

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27
Q

What is the clinical presentation of polymyositis?

A 
Progressive symmetric muscle weakness of proximal extremities*
Lungs (interstitial lung disease)*
Esophageal disease
Cardiac disease
Raynaud phenomenon
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28
Q

What is dermatomyositis?

A

Polymyositis + cutaneous manifestations

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29
Q

What cutaneous eruptions are seen with dermatomyositis?

A

Heliotrope rash, Gottron’s papules, Shawl sign

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30
Q

The link between inflammatory myopathy and what is greater in patients with dermatomyositis compared to patients with polymyositis?

A

Occult malignancy

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31
Q

What is the clinical presentation of a heliotrope rash?

A

Erythematous to violaceous eruption on the upper lids

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32
Q

What is the clinical presentation of Gottron’s papules?

A

Erythematous/ violaceous papules on the dorsal aspect of PIP, DIP, and MCP

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33
Q

What is Shawl sign?

A

Widespread, flat, reddened area that appears on the upper back, shoulders, and back of the neck

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34
Q

What muscle enzymes are elevated in patients with PM and DM?

A

CK and aldolase

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35
Q

What is the 1st line of treatment of PM and DM, and what else may be added?

A

1st line: glucocorticoids

May add: steroid-sparing immunosuppressive agents (azathioprine, methotrexate)

36
Q

What is Sjogren’s syndrome (SS)?

A

Systemic, chronic autoimmune inflammatory disorder with exocrine gland and extraglandular features, idiopathic

37
Q

What other diseases are sometimes associated with Sjogren’s syndrome?

A

SLE, RA, systemic sclerosis

38
Q

What glands are affected by Sjogren’s syndrome and what is this complex called?

A

Lacrimal and salivary glands = “sicca complex” = combo of xerophthalmia (dry eyes) and xerostomia (dry mouth)

39
Q

What is the clinical presentation of Sjogren’s syndrome?

A 
Constitutional (fatigue)
Keratoconjunctivitis sicca- dry eyes
Xerostomia- dry mouth
Dryness of other surfaces
Disease spectrum- extraglandular effects
40
Q

Although there is no single diagnostic test for SS, what test may be used?

A

Schirmer test- test of tear production

41
Q

What labs/ tests are performed for SS besides the Schirmer test?

A

Labs- ANA subtypes = Anti-Ro and Anti-La

Salivary gland biopsy

42
Q

What is the treatment for dry eyes in SS?

A 
Artificial tears
Ophthalmic lubricating ointments
Cyclosporine drops (Restasis)
43
Q

What is the treatment for xerostomia in SS?

A

Artificial saliva
Frequent sips of water
Sugarless candy

44
Q

What is the treatment for the extraglandular manifestations in SS?

A

NSAIDS and acetaminophen

Steroids and immunosuppressive medications for severe cases

45
Q

What is polyarteritis nodosa (PAN)?

A

Systemic necrotizing vasculitis

46
Q

What are the manifestations of PAN?

A

Transmural inflammation of muscular arteries = narrowing of lumen
Results in thrombosis, ischemia, or infarct

47
Q

What are not affected by PAN?

A

Veins

48
Q

Aside from general systemic effects such as fever, weight loss, malaise, and weakness, how does PAN present clinically?

A

Arthralgia/ myalgia

Cutaneous effects = tender nodules, ulcers, purpura

49
Q

What will a biopsy of skin lesions reveal with PAN?

A

Leukocytoclastic vasculitis

50
Q

What is the most common systemic involvement of PAN?

A

Renal manifestations - infarctions and hypertension

Can also see sensory and motor polyneuropathy

51
Q

Although there is no diagnostic lab test for PAN, what will be elevated in blood tests?

A

ESR and CRP

52
Q

What will be negative in a blood test for PAN?

A

Antineutrophil cytoplasmic antibodies (ANCA)

53
Q

What is the treatment for PAN if it is mild or cutaneous only?

A

Glucocorticoids

54
Q

What is the treatment for PAN if it is moderate to severe?

A

Glucocorticoids + immunosuppressive medications

55
Q

What is the treatment for PAN if it is associated with Hep B or C?

A

Primarily antivirals +/- glucocorticoids depending on severity

56
Q

What is the treatment for PAN if it is associated with HTN?

A

ACE-I or ARB

57
Q

Does PAN represent a spectrum of disease or a single entity?

A

Spectrum of disease

58
Q

What is systemic sclerosis?

A

An autoimmune disorder that causes diffuse fibrosis (tightening and thickening) of the skin and internal organs

59
Q

What vascular changes are associated with systemic sclerosis?

A

Narrowing of small blood vessels

60
Q

Although the etiology of systemic sclerosis is unknown, what is it thought to be caused by?

A

Immunologic mechanisms leading to vascular endothelial damage and activation of fibroblasts

61
Q

What score on the 2013 classification criteria for systemic sclerosis classifies a patient as having the definite disease?

A

9+

62
Q

What does CREST stand for?

A 
Calcinosis- calcium deposits in skin
Raynaud's phenomenon
Esophageal dysfunction
Sclerodactyly
Telangiectasias
63
Q

What are the characteristics of limited cutaneous SS?

A

CREST syndrome
Skin changes limited to hands, forearm, face, neck
Better prognosis

64
Q

What are the characteristics of diffuse cutaneous SS?

A

Limited + trunk and proximal extremities (chest, abdomen, arms, shoulders)
Increased risk of internal organ involvement
Rapid development

65
Q

What is sclerodactyly

A

Localized thickening/ tightening of skin (fingers, hands and toes)

66
Q

What does shiny skin suggest?

A

Impending skin thickening

67
Q

What is a common initial presentation of sclerodactyly

A

Diffusely puffy hands

68
Q

What labs are performed for systemic sclerosis?

A

ANA (+)
ACA (limited)
Anti-Scl-70 (diffuse)
Anti-RNA polymerase III (rapidly progressive diffuse)

69
Q

What is the treatment for SS?

A

Patient education
Symptomatic/ supportive care
Renal and HTN: ACE-inhibitors

70
Q

What treatment is given for Raynaud and esophageal disease for SS?

A

Raynaud- nifedipine (calcium channel blocker)

Esophageal disease- proton pump inhibitors and small, more frequent meals

71
Q

What is included in patient education in treatment for SS?

A

Warm clothing, smoking cessation

72
Q

If you see the buzz words: multi-organ, autoimmune dz, ANA, anti-dsDNA, Anti-Sm, malar rash, discoid rash, and hydroxychloroquine, what should you think of?

A

SLE

73
Q

If you see the buzz words: peocainamide, isoniazid, hydralazine, anti-histone Ab, what should you think of?

A

Drug induced lupus

74
Q

If you see the buzz words: progressive muscle weakness proximal UE, LE, +/- ILD, what should you think of?

A

Polymyositis

75
Q

If you see the buzz words: transmural artery inflammation, ANCA (-), what should you think of?

A

Polyarteritis nodosa

76
Q

If you see the buzz words: diffuse fibrosis, limited vs. diffuse, ACA, anti=SCL (anti-topoisomerase) Ab, and CREST, what should you think of?

A

Systemic sclerosis

77
Q

If you see the buzz words: vasospasm of extremities, worsens with cold, and CCB, what should you think of?

A

Raynaud phenomenon

78
Q

Does a + ANA automatically mean a patient has SLE?

A

No

79
Q

What is pharmacologic treatment based on for SLE?

A

Disease severity

80
Q

What is the prognosis for SLE?

A

Varies based on severity

81
Q

What is the onset of polymyositis?

A

Gradual onset over weeks to months

82
Q

What are other complications that a patient with polymyositis might present with?

A

Dysphagia, myocarditis, aspiration pneumonia

83
Q

What is the major goal of treatment of PM and DM?

A

Improve muscle strength and avoid complications

84
Q

What are general treatment recommendations for SS?

A

Regular f/u with dentist, ophthalmologist, rheumatologist

85
Q

When PAN is triggered, what is the most typical trigger?

A

HBV

86
Q

What is Anti-RNA polymerase III antibody associated with?

A

Rapidly progressive diffuse SSc, and increased risk of renal crisis

Clinical Med I (24 decks)

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