Immune system Flashcards
Most common clinical manifestations of SLE
Hematologic
Fatigue
Arthritis, arthralgia or myalgia
Skin
Renal
“SOAP BRAIN, MD” mnemonic for SLE criteria
Serositis
Oral ulcers
Arthritis
Photosensitivity
Blood disorders
Renal involvement
ANAs
Immuno. (andi-dsDNA, anti-Sm, antiphospholipid antibodies)
Neurological disorders
Malar or Discoid rash
Genes that create genetic predisposition to SLE
HLA-DRA2 & HLA-DRA3
Most widely used method for detection of ANAs
Indirect immunofluorescence
Complement proteins deficient in SLE
C1q, C2 and C4
Common triggers of SLE, have not been proved as a cause for the disease.
UV light and EBV
Air particles or substances that increase the risk of developing SLE.
Cigarette smoking and silica
Type of hypersensitivity causing systemic lesions in SLE.
Type III hypersensitivity
Mechanism through which blood vessels are damaged in lupus.
Increased vascular permeability, complement activation and accuulation of PMNs that secrete enzymes.
Most dangerous clinical manifestation in SLE because of its high morbidity and mortality.
Renal involvement
Parts of the kidney where immune complexes deposit in SLE.
Glomerular basement membrane, mesangium and sometimes in the glomerulus.
Most common glomerular disease pattern in SLE.
Class IV
Class 1 is the least common
Types of class IV SLE kidney disease (diffuse lupus nephritis)
50% or more glomeruli with lesions:
IV-S: Lesions involving <half of glomerular tuft.
IV-G: Lesions involving >half of glomerular tuft.
Classes with which membranous lupus nephritis (V) can occur
III and IV
SLE nephritis in which 90% or more of the flomeruli are globally sclerosed.
VI. Advanced sclerotic lupus nephritis.
These deposits may cause the thickening of the capillary wall of the glomerulous, forming the wire loops structures on class IV SLE nephtropaty.
Subendothelial immune complex
Diffuse thickening of the glomerulous capillary walls.
Membranous lupus nephritis class V
Sclerosis of more than 90% of the glomeruli in SLE.
Advanced sclerosing lupus nephritis class VI
Findings in HE stained skin in SLE
Vacuolar degeneration of the basal layer of the epidermis.
Variable edema and perivascular inflammation in the dermis.
SLE skin finding with IF
Deposition of Ig and complement in the dermoepidermal junction.
Type of joint involvement in SLE
Non-erosive synovitis with little deformity
Histopathologic finding of the spleen in SLE
Perioarteriolar fibrosis (onion skinning)
Concentric intimal and smooth muscle cell hyperplasia
Histopathologic finding of the bone marrow in SLE
LE or hematoxylin bodies
Histopathologic skin findings in chronic discoid lupus erythematosus
Follicular plug (carpet tack)
Liquefaction degeneration
Thick basement membrane
Type of lupus with predominant skin involvement, initial widespread superficial and non-scarring rash and no genetic association, with extreme photosensitivity.
Subacute cutaneous lupus erythematosus
Drugs that may cause drug-induced LSE
Hydralazine, procainamide, isoniazid and D-penicillamine