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30 Cards in this Set
- Front
- Back
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what's wescott aldrich syndrome?
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eczema, thrombocytopenia, immunodeficiency. x linked.
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systemic sclerosis?
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see topoisomerase I antibodies. can be diffuse or limited (crest), which improves.
activation of fibroblasts. weird tough skin, trouble swallowing. nearly all get reynaud's phenomenon. |
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dermatomyositus?
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see heliotrope rash, weakness in the proximal muscles. trouble getting up.
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mixed connective tissue disease?
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antibodies against RNP.
kinda looks like SLE and systemic sclerosis. |
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sjogren's syndrome?
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dry mouth. positive SSA and SSB antibodies. autoimmune targeting of the lacrimal and paritod glands.
note that there's a 40X increase in the risk of B cell lymphoma. |
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what's erythema nodosum?
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paniculitis. neutrophils and then lymphocytes later on. weird reddish nodules on legs.
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in the milk-filled breast or uteturs, what's going on in terms of cellular growht/proliferation?
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in the breast, it's mostly lobular hyperplasia.
in the uterus, it's also mostly hyperplasia. so at the end of a cycle, there's lots of apoptosis (not atrophy) |
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what do you find with dermatitis herpitiformis?
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granular deposits of IgA against the tips of the dermal papilae. Eventually get PMN's up athere, making blisters. Giladin from gluten is the primary antigen.
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What happens to people with IgA deficiency?
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if you transfuse them, even if typed right, they'll react badly because they don't have any IgA normally, so they produce anti-IgA antibodies. also, recurrent nose/GI infections.
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describe the difference between CREST and systemic sclerosis:
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crest is a milder form, and you're more likely to see anti-centromere antibodies.
in full scleroderma, more likely to see anti-topoisomerase antibodies (SCL-70) |
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we know that SLE involves anit-nuclear DNA. What's RA against?
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RA is also a type III autoimmune disorder involving Anti IgM-FC region, using IgG's.
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What do you see that's different in drug-induced lupus?
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anti-histone antibodies. done by hydralazine and procanimade.
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what separates mixed tissue disease from scleroderma?
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no renal involvement (so normal urine analysis), and they have anti-ribonuclear antibodies in mixed tissue disease.
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what autoimmune diseases are linked with cancer?
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shogruns's has a much higher risk of lymphoma, and dermatomyositus is connected with lung cancer.
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what are our B-cell disorders?
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a gamma globulin anemia - have a RTK that doesn't work, don't get B cells turning into plasma cells.
IgA deficiency - trouble making IgA plasma cells. Common variable immunodeficiency - seen at all ages, problems with getting B cells turned into plasma cells. |
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severe combined immuno deficiency involves problems with what and is caused by what?
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B and T cell development (combined).
ADA can cause it. note that bone marrow transplants help and it's good 'cause you don't reject allografts. |
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if you give someone repeated blood transfusions, what do you expect to build up in them? bilirubin or hemosiderin?
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hemosiderin - iron's really hard to get rid of, while bilirubin has a whole method of excretion in the bile. see lots of kupfer cells and macrophages full of iron.
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what kind of nercosis is typically seen in GVHD?
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apoptosis - the donor's T cells attack the host and induce apoptosis.
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what's the difference between the menstrual cycle and the preggers uterus?
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menstruation and the buildup of the endometrium is about cell number - hyperplasia of the endometrium followed by apoptosis.
preggers = smooth muscle (myometrium) hypertrophy (need to buff up to squeeze out baby) followed by atrophy. |
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tissue regeneration - what are labile, stabile, and permanent cells?
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labile and stabile cells are capable of dividing and can regenerate (parenchymal cell regeneration). labile cells are stem cells, stabile cells are things like fibroblasts.
permanent cells can't replicate. |
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what's the difference between primary and secondary intention wound healing?
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primary is for smaller wounds, usually. involves lots of granulation tissue. get deposition of type III collagen, followed by type I collagen (metaloprotineases do this).
secondary involves WOUND CONTRACTION BY MYOFIBROBLASTS. |
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WBC rolling/margination happens before WBC sticking and diapedesis. what is the main mediator of this?
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selectins on both the WBC and endothelial cell are required for this. Then, sticking is mediated by integrins. Integration took awhile.
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what does myeloperoxidase do?
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it's in the macrophages and produces HOCl-, a powerful antimicrobial and radical.
think that muscle activity makes acid, and myelo sounds likem uscle |
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what can TGF-beta do?
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big thing is turn up fibroblast activity to make collagen. also considered anti-inflammatory.
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what determines if a liver can regenerate?
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if you screw with the connective tissue architecture, it can't.
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why do clucocorticoids make healing not go well?
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they inhibit collagen synthesis.
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what skin disorders involve Ig's against skin parts?
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Pemphigus Vulgaris - IgG's against desmosomes, show bullae on epidermis especially around the mouth.
Bullous pemphigous - IgG against the basement membrane. Lesions are below the skin. Dermatitis herpitiformis - IgA against the dermal papilae tips. Actually complexes. Seen with celiac's disease (think that IgA is involved in the gut). |
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what causes psoriasis?
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unregulated proliferation of keratinocytes.
often shows up on the glans. |
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erythema nodosum?
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seen on the anterior side of the shins. panniculitis.
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if you see dark staining on the armpits/skin of the neck?
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anthacosis nigrans - this is an indication of cancer elsewhere, especially in the GI tract.
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