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MSK/Rheum Exam- Clin Med > Connective Tissue Diseases > Flashcards

Connective Tissue Diseases Flashcards

1
Q

SLE pathophysiology

A

Precise mechanism unknown
Abnormal cell apoptosis resulting in cellular breakdown
Immune complex formation and deposition, resulting in complement-dependent inflammation of involved organs

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2
Q

SLE and race

A

3x more common in Afro-Americans than whites
More prevalent and severe in Asians, Afro Americans, Afro caribeans, and Hispanics

More common in urban areas

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3
Q

SLE: must have 4 out of 11 of these…

A 
Malar rash 
Discoid rash 
Photo sensitivity 
Oral or nasal ulcerations 
Arthritis in 2 or more joints 
Serositis (pleuritis or pericarditis)
Renal disorder 
Neurological disorder 
Hematologic disorder 
Immunologic disorder 
Antinuclear antibody
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4
Q

Nonspecific symptoms of SLE

A 
Raynauds
Unexplained fever 
Alopecia
Fatigue
Myalgias, arthalgias
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5
Q

Renal involvement in SLE

A

Nephritis
Nephrotic syndrome
Tubulointerstitial dz
IgG deposition*

  • *clinically look for persistent Proteinuria and cellular casts
  • *definitive diagnosis by biopsy
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6
Q

Neurological involvement in SLE

A

Seizures

Psychosis

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7
Q

Hematologic involvement in SLE

A

Hemolytic anemia
Leukopenia
Lymphopenia
Thrombocytopenia

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8
Q

Lupus general info

A

Multi system variable disease of unknown etiology
Hormones play a role!
Adult females to males are 7-15:1
Child females to males are 3:1

65% on onset between 16-55 yo

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9
Q

Immunologic disorder associated with SLE

A

Antiphospholipid syndrome- characterized by vascular thrombosis (arterial or venual)…pregnancy mortality
Pos anticardiolipin Abs
Abs to dsDNA

*false pos with syphilis

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10
Q

ANA patterns in SLE

A

Diffuse or homogenous- least specific. High titers seen in SLE
dsDNA- most specific..SPECKLED and NUCLEOLAR important

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11
Q

Histone ANA pattern

A

DRUG INDUCED LUPUS

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12
Q

Centromere patterns

A

THINK CREST SYNDROME

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13
Q

Drug induced lupus

A

Acts and looks like SLE but I’d reversible once offending drug is stopped

Hydralazine, procainimide, minocycline, chlorpromazine, isoniazid, penicillamine, methyldopa, interferon-alpha, infliximab

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14
Q

Discoid lupus

A

Subset of lupus limited to the skin
Diagnosis confirmed by skin biopsy
ANA often negative
Prognosis good..

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15
Q

Poor prognostic indicators for SLE

A 
Renal dz
CNS dz
Early or late age 
Males 
Non whites 
Overall disease activity
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16
Q

Late in SLE disease, complications/death more likely due to…

A

Thromboembolic disease

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17
Q

Labs in SLE patients

A 
BUN/Cr
UA
ANA (increased, watch patterns)
C3/C4 decreased 
CRP normal or increased 
ESR increased 
dsDNA present
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18
Q

If renal involvement in SLE suspected….

A

Tissue biopsy

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19
Q

SLE treatment for fatigue and skin rashes

A

hydroxychloroquine

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20
Q

SLE treatment for renal dz

A

High do corticosteroids and/or powerful immunosuppressants like Cyclophosphamide

21
Q

Azathioprine, mycophenalate, methotrexate

A

Immunosuppressants often considered “steroid sparing”

22
Q

Pregnancy and SLE

A

Very risky!
Effective birth control and family planning
Must have dz und excellent control before conception
Close monitoring during pregnancy

23
Q

Most important when diagnosing SLE

A

LISTEN TO THE PATIENT! Figure out which symptoms are there

Don’t rely too much in ANA to make or break dx

24
Q

Scleroderma

A

Thickening, hardened skin
2 forms:
Systemic sclerosis
CREST syndrome (limited)

*females>males
Peak onset 30-50 yo

25
Q

Scleroderma pathophysiology

A

Poorly understood

Deposition of collagen and other matrix proteins in affected tissues

26
Q

Clinical presentation of systemic scleroderma (ss)

A

Skin: raynauds, thickening of chest, abdomen, face, upper arms,
shoulders, hands, feet
Pulm: interstitial lung dz and fibrosis
GI: dysmotility, “watermelon stomach”
Renal: acute renal failure w abrupt onset HTN. Mild Proteinuria
MSKL: arthralgias, puffy hands early on, carpal tunnel

**speckled pattern ANA

27
Q

Nail fold microscopy

A

Can help determine if Raynauds is associated w other systemic dzs
(Ex SS)

28
Q

Systemic scleroderma treatment

A

Tx aimed at organs involved!

29
Q

Renal tx in SS

A

ACE inhibitors

30
Q

Raynauds tx in SS

A

Ca channel blockers

31
Q

GI tx in SS

A

Pro motility agents

32
Q

Pulmonary/lung tx in SS

A

Cyclophosphamide for lung dz

Viagra/Levitra and Bosantan for pHTN

33
Q

What tx to avoid in SS patients

A

High dose steroids!!!!!! Can lead to renal crisis**

34
Q

CREST syndrome

A

Limited scleroderma

Calcinosis
Raynauds
Esophageal dysmotility 
Sclerodactyly of fingers to the MCPs
Telangiectasia
35
Q

Complications of CREST

A
  • tends to be more benign than SS

complications. ..pulmonary HTN (must get annual pulm fx test)

36
Q

Polymyositis/dermatomyosits

A

Autoimmune inflammatory myopathy resulting in PAINLESS muscle weakness (sometimes a rash)

****DM IS OFTEN ASSOCIATED WITH MALIGNANCY IN ADULTS!!!
(But not children)

More common in females
Peak ages 40-60

37
Q

Clinical presentation of polymyositis/DM

A

PAINLESS* muscle weakness of proximal muscle groups with gradual onset
Pts complain of difficulty getting out of chair, climbing stairs, styling hair due to lack of power

Early on…no signs of fascinations or muscle atrophy

38
Q

Skin manifestations in DM

A

Heliotrope rash of eyelids (purple eyeshadow)
Gottrens papules on hands
Shawl sign (redness on shawl area of body)
Mechanic hands (Really dry, thick)
Periungal erythema (nailbeds)
Calcinosis cutis

39
Q

Manifestations (other than skin) in polymyositis/dermatomyosits

A

Pulmonary: interstitial lung disease, BOOP, diffuse alveolar damage
Esophagus: dysphasia, gagging
Misc: fever, polyarthritis, Raynauds

Pos ANA plus other autoantibodies
Elevated CPK!*
Aldolase, AST, ALT may also be elevated

40
Q

CPK in DM

A

Elevated

41
Q

Diagnostic tools in DM

A

*muscle biopsy!!!

Must examine for malignancy!!!!

42
Q

DM treatment

A

High dose corticosteroids
Methotrexate or Azathioprine
*IV Ig for refractory/severe cases

(DM will resolve if malignancy treated)

43
Q

Sjorgens syndrome general info

A

Autoimmune dz affecting exocrine glands causing dry eyes and dry mouth (sicca)
Unknown cause
Can be primary or secondary (often seen w RA or SLE)
Female to male 20:1
Peak age 30-40

44
Q

Sjorgens pathophysiology

A

Trigger unknown
Infiltration of lymphocytes to glands and are activated
Cytokines released which promote parotid swelling, destruction and
Localized inflammation
B cells produce autoantibodies (SSA, SSB) and over time can
transform from a benign polyclonal expansion to malignant
expansion lymphocytes resulting in lymphoma

45
Q

Sjorgens clinical presentation

A

Sicca symptoms: dry eyes, dry mouth. Ask pt to chew saltine
Parotid swelling
Rash less common..purpura of lower extremities

46
Q

Sjorgens complications

A

Lymphoma
Primary biliary cirrhosis
Accelerates dental caries , corneal atrophy and ulceration
Oral candiasis

47
Q

Sjorgens lab results

A

Rheumatoid factor and ANA >90%

Anti SSA 70-90% (antiSSB 50%)

48
Q

Schirmers test

A

Used to dx Sjorgens
Place strip of paper in corner of patients eye against cornea

*wetness at 5 minute should be >10mm

49
Q

Sjorgens treatment

A

Dry mouth..good hydration. Frequent dental visits (q3m), avoid
medications that make symptoms worse
(Salagen or Evoxac may be helpful)

Dry eyes..artificial tears, lacrimal duct plugs, restasis eye drops

MSK/Rheum Exam- Clin Med (7 decks)

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