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Musculoskeletal/Rheum > SLE > Flashcards

SLE Flashcards

1
Q

What are the 4 different types of lupus?

A
  • Systemic Lupus Erythematosus
  • Discoid Lupus Erythematosus
  • Drug-induced Lupus Erythematosus
  • Neonatal Lupus Erythematosus
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2
Q

What are the characteristics of Systemic Lupus Erythematosus?

A
  • Mulitsystem inflammatory disorder

- Autoantibodies to numberous self-antigens

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3
Q

What are the characteristics of Discoid Lupus Erythematosus?

A
  • Confined to the skin ONLY

- Discoid lesions can be seen in SLE

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4
Q

What are the characteristics of Drug-induced Lupus Erythematosus?

A
  • Less severe than SLE
  • Resolves once offending drug is removed
  • Nephritis is very uncommon unless with anti-TNF agents
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5
Q

What are the characteristics of Neonatal Lupus Erythematosus?

A
  • Newborns of mothers with lupus

- Skin rash and heart block

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6
Q

Do genes play in to the pathogenesis of lupus?

A

YES- highly!

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7
Q

What are the susceptibility genes in lupus?

A

HLA-DR2, DR-3 (weak), C4A (complement deficiency)

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8
Q

What ethnic groups get lupus?

A 
African Americans (3-6X more than whites)
Hispanic and Native americans (2-3X more than whites)
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9
Q

What are the abnormally functioning cells in SLE?

A

B-cells produce autoantibodies
T-cells are abnormal
pDC cells- interferon signature

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10
Q

What is an Interferon-signature?

A

Innate immune system does not turn off after containing infection. Alpha and beta-interferon causes pDC cells activates T cells to Th1/Th17 phenotype–get activation of B cells–> Lupus.

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11
Q

What causes tissue damage in lupus?

A
  • Immune complexes get deposited in tissues

- Pro-inflammatory molecules are activated (complement-medicated)

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12
Q

What are some predictors of lupus flare?

A
  • New evidence of complement consumption (drop in C3 and C4)
  • Rising anti-dsDNA titer
  • Increased ESR
  • New lymphopenia
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13
Q

What are factors associated with higher disease severity?

A
  • Abrupt onset of symptoms
  • Increased renal, neurologic, hematologic, and serosal involvement
  • Rapid accrual of damage (irreversible organ injury)
  • Men
  • Lower SES
  • Early age of onset
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14
Q

What is the leading causes of death in lupus?

A

heart disease
malignancy
infection

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15
Q

How do you test for ANA?

A

IFA

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16
Q

When is ANA presence helpful in diagnosing lupus?

A

if patient has high pretest probability for lupus

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17
Q

When is ANA absence helpful in ruling out lupus?

A

HIGH SENSITIVITY (if patient does not have it, they will not have lupus)

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18
Q

What other autoantibodies are common in SLE patients?

A

anti-dsDNA and anti-sm and antiphospholipid

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19
Q

Are anti-dsDNA and anti-sm sensitive or specific?

A

highly specific–almost always associated with lupus ONLY

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20
Q

What is anti-dsDNA clinically associated with?

A

lupus nephritis

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21
Q

What is antiphospholipid antibody clinically associated with?

A

clotting diathesis

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22
Q

What can be measured to see if the classical complement pathway is being activated?

A

C4

usually see decreased C3 and C4

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23
Q

What musculoskeletal abnormalities of the hand do you see in lupus?

A

periarthritis (with loosening of the ligaments) –> reducible hand deformities

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24
Q

What are factors associated with serositis?

A

pleuritic chest pain
pericardial abnormality (effusion)
peritoneal cavity fluid accumulation

25
Q

How does a baby get neonatal lupus?

A

-transplacental transfer of autoantibodies

26
Q

What are some obstetrical obstacles for patients with lupus?

A
  • fertility not affected
  • recurrent fetal loss (due to antiphospholipid antibodies)
  • babies small for gestational age
27
Q

What is a major cardiac problem that is found in patients with lupus?

A

extensive coronary atherosclerosis involving MAJOR CORONARY ARTERIES that can lead to an MI

28
Q

What are common autoantibodies found in Sjogren’s syndrome?

A

ANA (85%)
Anti-Ro (SSA)
Anti-La (SSB)

29
Q

What are the complement levels like with Sjogren’s syndrome?

A

Low blood levels of C3 and C4

30
Q

What is keratoconjunctivitis sicca?

A

keratitis caused by decreased lacrimal secretions

31
Q

How do you diagnose Sjogren’s syndrome?

A

Schirmer’s test

32
Q

What are oral symptoms of Sjogren’s syndrome?

A
  • Severe dry mouth
  • Multiple dental caries
  • Fissuring/ulceration of lips/tongue/buccal membranes
  • Parotid/submandibular salivary gland enlargement
33
Q

What is primary Sjogren’s syndrome v. secondary Sjogren’s syndrome?

A

Primary is without another autoimmune disease; Secondary Sjogren’s syndrome (complication of another autoimmune CT disease- RA nad SLE)

34
Q

If a patient has a swollen parotid gland, what should you do?

A

obtain a biopsy

35
Q

What cancer is associated with Sjogren’s syndrome?

A

Non-Hodgkin’s lymphoma

36
Q

What is the most common renal finding with Sjogren’s syndrome?

A

renal tubular acidosis

37
Q

What autoantibody is associated with limited SS?

A

Anti-centromere antibody

38
Q

What autoantibody is associated with diffuse SS?

A

Anti-topo1 (Scl70)

39
Q

What are the clinical associations with Anti-topo1?

A

pulmonary fibrosis

heart involvement

40
Q

What are the clinical associations with Anti-centromere antibody?

A

severe digital ischemia
PAH
sicca syndrome
calcinosis

41
Q

If someone with lupus has SS, what antibody would likely be found?

A

U1-RNP

42
Q

What are characteristics of diffuse scleroderma?

A

initial wide-spread skin involvement with rapid progression and early visceral involvement (better survival rate)

43
Q

What are characteristics of limited scleroderma?

A

relatively mild skin involvement (only fingers and face) with visceral involvement late (CREST SYNDROME)

44
Q

What is CREST syndrome?

A

calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia

45
Q

What is the underlying pathogenesis of scleroderma?

A

T cell mediated disease that attacks vasculature and stimulates fibroblasts

46
Q

How are B cells involved in scleroderma?

A

produce autoantibodies

47
Q

What are the earliest pathological changes in SS?

A

endothelial cell abnormalities (increased apoptosis, upregulation of MHC class II, and increased ICAM-1 expression on endothehlial cells)

48
Q

Why should you encourage your SS patients to stop smoking cigarettes?

A

digital artery occlusion occurs with SS (and is worsened by smoking)

49
Q

What are the color changes that occur with Raynaud’s phenomenon?

A

white–> blue –> red

50
Q

What are total body vasospastic attacks in response to cold called?

A

total body Raynaud’s

51
Q

What is Raynaud’s phenomenon?

A

condition that affects blood vessels in extremities (can be primary or secondary related to autoimmune diseases)

52
Q

What are characteristics of nail bed vasculature in Raynaud’s patients?

A
  • Drop out of capillary number

- Dilated capillary loops

53
Q

What is vitilgo-like changes in SS?

A

“salt and pepper” discoloration usually over places of fibrotic change

54
Q

What form of SS is PAH most associated with?

A

late limited form (strange)

55
Q

What is en coup de sabre SS?

A

Localized scleroderma that is usually in children–go down into muscles/bone and can affect brain development

56
Q

What is the autoantibody profile found in MCTD?

A

Elevated Anti-U1-RNP
Positive ANA
Negative anti-sm, anti-ro, and anti-la

57
Q

What is the largest cause of future morbidity and mortality in a patient with MCTD?

A

pulmonary hypertension

58
Q

What do the hands of a patient with MCTD look like?

A

puffy, edematous hands that ache

59
Q

What finding is seen in almost all patients with MCTD?

A

Raynaud’s phenomenon

Musculoskeletal/Rheum (12 decks)

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