SLE Pathology

MD SOAP BRAIN
MD SOAP BRAIN

Malar rash – butterfly rash, sparing of nasolabial folds
Discoid rash – basement membrane involved, may cause scarring
Serositis – pleuritis/pericarditis
Oral ulcers
Antinuclear antibody (ANA) – very sensitive test
Photosensitivity – skin rash to sunlight
Blood – haemolytic anaemia, leukopaenia, thrombocytopaenia
Renal disorder – proteinuria and cell casts
Arthritis – symmetrical, involving 2+ small or large peripheral joints
Immunological disorder – anti-dsDNA
Neurological – seizures, psychosis

Skin
Skin
Vascular degeneration of the epidermal basal layer
Dermal edema
Perivascular inflammation
Vasculitis with prominent fibrinoid necrosis

Joint pathology
Non erosive synovitis with little deformity
Contrasts with RA-which is rather destructive

CNS pathology
Not as evidence based:
Neuropsychiatric symptoms caused by:
-Antibodies against a synaptic membrane protein?
Acute vasculitis?
-Studies show frank vasculitis is rare
Non-inflammatory occlusion of small vessels by intimal proliferation
-Endothelial damage by antiphospholipid antibodies?

Cardiovascular
-Pericardial involvement*** in up to 50% of patients
-Myocarditis, mononuclear cell infiltration-less common and less severe
-Valvular abnormalities
-Mitral and Aortic most commonly
-Diffuse leaflet thickening

Libman-Sacks endocarditis
Warty deposits on both side of the valve (above and below), chordae thickening, starts off as a sterile deposit, in the case of a bacteremia they may serve as a nidus for colonization.

Coronary atherosclerosis
Particularly in young patients with long standing disease, especially those treated with corticosteroids

Renal disease
Major mechanism of injury?
Detail of ^ based on etiology?
Probably the most common cause of death in Lupus pts, tied with infection.

Affects ~50% of SLE patients
Major mechanism of injury: immune complex deposition

DNA/anti-DNA, others histone/anti- histones (from drug induced SLE)

Thrombi in glomerular vasculature
Often associated with anti-phospholipid antibodies

Formed in situ or from circulation

Thrombi in glomerular vasculature
Often associated with anti-phospholipid antibodies

Mesangial lupus glomerulonephritis I & II
Class I
Minimal mesangial lupus nephritis
Little to no increase in the mesangial matrix and the number of measangial cells

Class II
Mesangial proliferative lupus nephritis
Moderate increase in the mesangial matrix and the number of measangial cells
Granular mesangial deposits of immunoglobulin and complement are always present

Focal proliferative glomerulonephritis III
FN,Crs,thrm,prlf,lkc,esp
Focal proliferative glomerulonephritis III
FN,Crs,thrm,prlf,lkc,esp
Class III
Less than 50% of the glomeruli are involved
Lesions may be segmental (affecting only a region of the glomerulus) or global (affecting the entire glomerulus)

Characterized by:
Crescent formation
Fibrinoid necrosis
Thrombi in the Glomerulus
Proliferation of endothelial and mesangial cells
Infiltrating leukocytes
Eosinophilia

Diffuse proliferative glomerulonephritis (Class IV)
Diffuse proliferative glomerulonephritis (Class IV)
Most severe, most common form of lupus nephritis
Pathologic changes may be identical to Class III lesions, but affect greater than 50% of glomeruli
Patients are usually symptomatic
Hematuria
Proteinuria
Hypertension
Mild to severe renal insufficiency

Membraneous glomerulonephritis (Class V)
Characterized by diffuse thickening of the glomerular walls
Severe proteinuria
Nephrotic syndrome
May occur concurrently with focal or diffuse lupus nephritis

Granular deposits of antibody and complement
Granular deposits of antibody and complement
Can be detected by immunofluorescence

-Mesangial (a characteristic of all classes)
-Intramembraneous
-Subepithelial
Predominant in Class V
-Between the basement membrane and visceral epithelial cells
-Subendothelial
-Seen in proliferative types (II and IV)
-When prominent, cause wire loop lesions, a diffuse thickening of the capillary wall

Minute 59 Picture Detail

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