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Rheumatology > SLE > Flashcards

SLE Flashcards

1
Q

Diff hypersensitivity rxns and examples?

A
  • type I: immediate (anaphalytic, atopic)
  • type II: cytotoxic: target cell receptors, platelet-thrombocytopenia, target fixed tissue ag; good pastures, MG
  • type III: immune complex; vasculitis, SLE
  • Type IV: cell mediated
    a) tuberculin rxn
    b) cytotoxic cells destroy target cells - allograft rej
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2
Q

What is SLE?

A
  • multisystem autoimmune disorder of unknown cause and is strongly assoc w/ various autoabs
  • deposition of ag-ab complexes along vascular and tissue basement membranes
  • is sometimes referred to as the great imitator because it affects many diff body systems
  • skin, its, serosal surfaces, muscles, kidneys, heart, lung, CNS, RBCs, and platelets
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3
Q

Incidence and prevalence of SLE?

A
  • 50-70 new cases/1 million/year
  • prevalence: 500/million
  • women:men = 9:1
  • occurs in childbearing yrs 20-40
  • higher incidence in blacks, Native Americans, Puerto Ricans, Chinese
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4
Q

Factors for SLE?

A

influenced by combo of following:
- genetic: x’some 6: HLA-DR3 and linked specificities DR2 and DQw1 increase risk by a factors of 3
- enviro:
UV light (rash)
bacterial and viral infections
drugs
abnormal stimulation of immune system
- endocrine: sex hormes - most cases develop after menarche and b/f menopause
- drug induced:
lupus like syndrome - MC: procainamide, hydralazine

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5
Q

Pathogenesis of SLE?

A
  • b-lymphocyte hyperactivity w/ exaggerated ab production
  • ag-ab complexes deposited along basement membranes of vasculature and tissue
  • localized inflammator responses:
    complement
    neutrophil migration
    cell-mediated tissue injury
  • onset may be insidious or acute (more devastating)
  • course is characterized by exacerbations and remissions
  • as in other autoimmune disorders - immune system attacks body cells and tissues, result is inflammation and tissue damage
  • type III autoimmune rxn caused by ab- immune complex formation
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6
Q

MC sxs of SLE?

A
  • systemic: low grade fever, photosensitivity
  • mouth and nose: ulcers
  • jts: arthritis
  • muscles: aches
  • psych: fatigue, loss of appetite
  • face: butterfly rash
  • pleura: inflammation
  • pericardium: inflammation
  • fingers and toes: poor circultation
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7
Q

Clinical manifestations of SLE?

A

constitutional:
- fatigue
- fever
- wt loss
- malaise
- anorexia
skin:
- butterfly rash (malar)
systemic: polyarthritis, arthralgias, jt pain (polyarthritis is symmetrical, but doesn’t not involve articular destruction)
- alopecia
- fingertip lesions
- periungual erythema
- nail fold infarcts
- splinter hemorrhages
- raynaud’s phenomen (about 20% of pts)

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8
Q

How common is renal involvement in SLE? Presentation? What can be prognostic?

A
  • occurs in approx 50% of pts
  • lupus nephritis:
    glomerulonephrits
    nephrotic syndrome: proteinuria, hyaline casts
  • HTN
  • renal bx can be prognostic:
    glomerular sclerosis
    fibrous crescents
    interstitial fibrosis
    tubular atrophy = poor outcome
  • chronic renal failure more common than acute
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9
Q

Ocular features of SLE?

A
  • conjunctivitis
  • photophobia
  • transient or permanent monocular blindness
  • blurred vision
  • cotton wool spots on retina
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10
Q

MSK features of SLE?

A

transient polyarthritis w/ symmetric involvement:
- small and large jts
- no signs of inflammation on exam of jts
- 10% develop rheumatoid like hand deformities
- bony erosions not present
osteonecrosis of the hips
fibromyalgia often present

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11
Q

Pulm features of SLE?

A
  • occurs in 40-50% of pts
  • transient basilar pneumonic infiltrates = lupus pneumonitis:
    nonproductive cough
    dyspnea
    hypoxemia
  • pleural effusions
  • pleuritis
  • bronchopneumonia
  • restrictive lung disease
  • rare: alveolar hemorrhage w/ massive hemoptysis, death
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12
Q

Cardiac features of SLE?

A
  • occurs in 30-40% of pts
  • pericarditis
  • myocarditis
    tachycardia
    ventricular arrhythmia
    conduction problems
    CHF, cardiomyopathy
  • increased muscle enzymes:
    MB or CPK
  • libman sacks endocarditis:
    V. surface vegetations on valves
    vegetation breakoff may allow colonizations
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13
Q

Serositis of SLE?

A
  • pleuritis
  • pericarditis
  • peritonitis
  • fluid less than 3000 WBC/mm3 = monocytes and lymphocytes
  • reduced complement
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14
Q

Vascular features of SLE?

A
  • raynaud’s phenomenon
  • arterial or venous thrombosis
  • lupus vasculitis: palpable purpuric lesions on the shins in a pt w/ lupus and necrotizing vasculitis of the skin, kidney, and brain
  • livedo reticularis: pt has antiphospholipid abs - can result in ulcer formation
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15
Q

GI sxs of SLE?

A
  • transient, nonspecific abdominal pain
  • increased incidence of primary biliary cirrhosis w/ SLE
  • vasculitis of mesentery can cause infarction or perforation of bowel w/ high mortality
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16
Q

What are CNS features of SLE?

A
  • occurs in 30-75% of pts
  • confusion, memory deficits, disorientation, hypomania, delirium, and schizophrenia
  • grand mal seizures, temporal lobe seizures
  • severe HAs, MC neuropsych sx, sometimes w/ scotomata like migraines
  • stroke: anti-phospholipid abs
  • ACR recognizes 19 neuropsych syndromes in SLE
17
Q

MC of death in SLE pts?

A
  • those due to nephritis - usually occur w/in first 5 yrs of sx onset
  • CV disease and malignancy which may be related to chronic inflammation and cytotoxic therapies, and common etiologies of late mortality
  • infectious complications related to active SLE and immunosuppressive tx are now the most common COD in early active SLE
18
Q

CBC findings in SLE? ESR, CRP, UA?

A
  • anemia:
    normocytic, normochromic, hemolytic
  • leukopenia: lymphocytopenia common, indicative of disease activity
  • thrombocytopenia: 50-100k
  • prolonged PTT:
    from antiphospholipid abs, false positive tests for syphilis
  • ESR and CRP: both be elevated
  • UA:
    proteinuria
    RBCs/WBCs
    cellular or hyaline casts
19
Q

Rheum lab findings in SLE?

A
  • ANA (esp rim, cartwheel or peripheral): sensitivity 99%, specificity 49%
  • anti dsDNA
  • anti ssDNA
  • anti ENA: anti SM, anti RNP
  • elevated nonspecific IgG, IgM levels
  • reduced complement levels (C3, C4)
  • decreased IgA levels
  • can have false positive for syphilis
  • anti-histone: drug induced - ANA abs often this type
20
Q

DDx for SLE?

A
  • antiphospholipid syndrome
  • FM
  • hep C
  • lyme disease
  • lymphoma, B cell
  • mixed CT disease
  • polyarteritis nodosa
  • rheumatic fever
  • rheumatic arthritis
  • scleroderma
  • serum sickness
  • TTP
21
Q

How do you dx SLE?

A
  • clinical
  • no one test or feature is fully dx
  • criteria for classification of SLE
22
Q

What is the criteria for dx SLE?

A
  • characteristic rash across cheek
  • discoid lesion rash
  • photosensitivity
  • oral ulcers
  • arthritis
  • inflammation of membranes of the lungs, heart or abdomen
  • evidence of kidney disease
  • evidence of severe neuro disease
  • blood disorders, including low red and white blood cell and platelet counts
  • immunologic abnormalities
  • positive ANA
  • pt must experience 4 of the criteria b/f a doctor can classify the condition as SLE, these criteria proposed by ACR are not to be relied upon solely for dx however
23
Q

Physical and lab findings in SLE?

A
  • butterfly (malar rash)
  • hypertension
  • alopecia
  • discoid lesions
  • ANA (particularly cartwheel, rim or peripheral)
  • dsDNA
  • anti Sm ribonuclear protein
  • hypocomplementemia
  • UA:
    WBC
    RBC
    proteinuria
    hyaline casts
24
Q

Tx of SLE?

A 
incurable but tx
tx aimed at:
- reducing inflammation
- suppressing immune system 
- closely follow pts clinically to ID disease features as early as possible 
- pt education and prevention of disease flares:
sunscreen and protective clothing
protective, warm clothes
avoidance of vasoconstrictive drugs
psych support
routine immunization 
- pharm tx:
glucocorticoids
antimalarials
immunosuppressants
IV immunoglobulin
plasmapheresis (Lupus nephritis)
Belimumab - fully human monoclonal ab (benlysta)
25
Q

Survival rate for SLE pts?

A
  • 95% at 5 yrs
  • 90% at 10 yrs
  • 78% at 20 yrs
26
Q

Presentation of drug induced lupus?

A
  • sex ratio nearly equal
  • primarily msk, pulm, polyserositic sxs
  • renal and neuro disease uncommon
  • abs themselves not harmful
  • no hypocomplementemia
  • anti-nuclear abs present, but return to normal w/ withdrawal of drug
  • reversal w/ d/c of drug
  • procainamide and hydralazine MC culprits
27
Q

Drugs that can cause drug induced lupus syndromes?

A 
- antihypertensives:
hydralazine
methyldopa
- antiarrhythmics:
procainamide
quinidine
- anticonvulsants:
dilantin
zarontin
primidone
tegretol 
- misc:
INH
sulfanamides
PCN
thorazine
PTU
tagamet
levodopa
BBlockers
28
Q

What is discoid lupus?

A
  • chronic cutaneous lupus
  • involves plaque like lesions of head, scalp, and neck
  • first appear as red, swollen patches or skin
  • later scarring, depigmentation, plugging of hair follicles
  • 90% of discoid lupus pts have disease that involves skin
  • probably occurs in genetically predisposed individuals, but the exact genetic connection hasn’t been determined
  • pathophys of DLE isn’t well understood
29
Q

DDx for discoid lupus?

A
  • actinic keratosis
  • dermatomyositis
  • keratocathomas
  • granuloma annulare
  • lichen planus
  • subacute cutaneous lupus
  • psoriasis
  • rosacea
  • sarcoidosis
  • squamous cell carcinoma
  • syphilis
  • warts
30
Q

Tx for discoid lupus?

A
  • goals of management are to improve pt’s appearance, to control existing lesions and limit scarring and to prevent the development of further lesions
  • therapy w/ sunscreens, topical corticosteroids and antimalarial agents is usually effective

Rheumatology (8 decks)

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