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19 Cards in this Set
- Front
- Back
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What type of disease is lupus? what are the important cells that mediate it? what are some possible problems that lead to it?
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type III autoimmune.
neutrophils and complement are the main things that screw up normal tissues. no evidence that central "slippage" of clonal deletion causes it - probably peripheral. Maybe failure of the FAS-ligand apoptosis sytem, maybe failure of T suppressor cells, infectious agents may mimic self antigens and get everything started, release of sequestered antigen, EBV. Note that ANA is found in a lot of SLE pts, but there's no direct role for it in cytotoxcisity. |
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what factors are implicated in SLE?
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genetics - 24% of twins have it.
changing native antigen some drugs heavy exposure to sunlight, makbe from IL1 production. general immune disfunction - too many B cells activated, not enough suppressor T cells, HERV's. |
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hormones involved?
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just know that androgens are protective.
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what drugs are implicated?
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hydralazine = antihypertensive.
also, antiarrhythmics like procainamdide and practolo. Chelating agents too. |
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clinical presentation?
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major diagnostic criteria include:
allopecia, photosensitivity, psychosis, pleuritis/pericarditis, chronic falst positive tests for syphillis, ANTI-DNA antibodies, arthritis without deformity, reynaud's, BUTTERFLY RASH, focal erythemia. |
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what are some blood tests that might suggest SLE?
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ANA seen in most patients.
Anemia. also, low WBC's. probably 'cause they're all out in the tissues messing up life. also, thrombocytopenia.' anti-nuclear double-stranded DNA antibodies and smith antibodies - SLE. |
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morphology: talk about vessels, skin, histology findings, organs.
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Haematoxylin Body = pathognomonic for SLE.
see SWOLLEN GROUND SUBSTANCE. see fibrinous deposits in blood vessels. see 85% of patients with skin abnormalities. |
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other forms of lupus?
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discoid - affecting skin, serious scarring and depigmentation - rarely progresses to SLE.
also, subacute lupus - again, mostly skin involvement, non scarring, mild systemic disease. Interface dermititis. |
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is the kidney involved?
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big time. get several different kinds of nephritis, leading to nephrotic syndrome, weird urine sediment, some patients present with renal disfunction, 55% end up with serious renal disease.
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what about lungs and heart? liver? skeletal?
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both yes. See recurrent pleuritis, effusions, pheumonitis.
also, see CHF, peripheral vasculitis (reynaud's phenomenom). verrucous endocarditis. do see hepatomegaly. skeletal - morning stiffness. |
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what about eyes? lymph nodes?
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"cotton wool retinal exudates = cytoid bodies).
see necrosis in lymph nodes. |
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what organs can onset be seen in?
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any organ in the body! usually skin, kidneys, serosal membrane,s joints, and heart.
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demographcs at risk?
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9:1 female to male. remember that androgens are protective.
blacks at higher risk. remember child-bearing age. |
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genetics?
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high concordence between identical twins, also some between family members. HLA II muts in whites are seen.
also, some have weird mutations in complement components. |
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non-genetics?
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UV exposure.
also, see lupus like disease in people on procamide and hydralazine. |
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what type of autoimmune disease is this?
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mostly type III - specific tissue damage, like in the kidneys, comes from complexes that end up in the nucleus.
but also type II - autoantibodies are made against circulating blood cells and they get lysed/phagocytosed. this is why you see diminished blood counts in SLE patients. |
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slices of kidney - what can you see?
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wire loops, diffuse, or focal proliveration.
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describe the typical presentation:
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young black woman of child bearing age with butterfly rash.
fever joint pain pleuretic chest pain, photosensitivity. |
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course?
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course is extremely variable. some can die within months, especially if there's early kidney involvement.
some have only skin problems their whole lives. most live a remitting/relapsing course, with acute flareups treated with steroids and such. 80% ten year survival. 90% five year survival. |
