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70 Cards in this Set
- Front
- Back
- 3rd side (hint)
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two types of of acquired hypofunction of immune system
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iatrogenic and infectious
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type IV is mediated by what two cells
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type of hypersensitivity mediated by T-lymphocytes and Macrophages
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Asthma, Hay Fever, and Insect Bites are examples of what kind of hypersensitivity
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localized type I
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Insect stings are an example of what kind of hypersensitivty
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type I systemic
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drug allergies, hives, and some food allergies are examples of what kind of hypersensitivity
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type I
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what are the two components of complement which are known as anaphylatoxins
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C3a and C5a
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what happens in the two phases of Type I (anaphylactic reactions)
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Immediate: IgE on mast cell surface - degranulation of preformed mediators
Delayed: tissue infiltration by eosinophils, basophils, neutrophils, and some T cells; tissue injury, mucosal damage and remodeling |
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The initial response in type I reaction last how long and results in what kind at kind of tissue response
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5 minutes to I hour -
vasodilation, vascular leakage, smooth muscle contraction, glandular secretion |
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The secondary response of type 1 hypersensitivty can last up to 2 hours or days and is characterized by what
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tissue infiltrate by eosinophils, basohils, PMNs, and some T cells. tissue injury, mucosal damage and remodeling
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biogenic amines (e.g histimine), chemotactic mediator, enzymes, and proteoglycans are all what kind of mediators
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primary
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leukotrienes, protaglandins, PAF, and cytokines are what kind of mediators
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secondary
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how do eosinophils ctntribute to Type I hypersensitivity damage
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MBP feeds back and self amplifys the response. causes epithelial damage and mast cell degranulation.
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Severe urticaria
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caused by cold or hot. puffiness, facial edema, redening of skin. Not IgE mediated but does result from mast cell degranulation.
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atopic keratoconjunctivitis is an example of what kind of reactoin
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type one hypersensitivity. it results in puffy cornea
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how might the smooth muscle change in someone with chronic asthma
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sm muscle will replicate and hypertorophy. each time bronchoconstriction gets worse. also mucous glands get worse
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which cells are key in the change in tissue seen in pts with chronic asthma
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DCs -
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In addition to changes in muscle and mucous glands in a patient with chronic asthma - what might happen to the epithelium
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epithelial cell shedding
and BM pseudo-thickening also see Edema epithelial damage due to eosinophils |
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hemolysis is what type of reaction
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type II
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what is the difference between Acute and Delayed Hemolysis
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Acute hemolysis requires pre-existant Ab and leads to rapid intravascular hemolysis. Delayed hemolysis involves a low/rising titer to Ab over 1-2 weeks and results in slow extravascular hemolysis
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intravascular vs. extravascular
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erythroblastosis fetalis is what kind of hypersensitivity reaction
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Type II - RH incompatibility
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in erythroblastosis fetalis youwould see RBC where in the liver
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in Kupfer cells - broken down
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what cells would you see alot of inthe liver which might be abnormal in a baby with erythroblastosis fetalis
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tiny red cells - erythroblasts - may be in any organ - baby cant keep up with loosing reds
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a disease which involves making Antibody against Type IV collagen (BM)
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Goodpasture's disease (type II hypersensitivity)
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what might you see in lung w/ goodspastures (rare)
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hemmorrhage into lung
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what type of hypersensitvity - rheumatic fever
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type II
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Cross reacting antibodies in strep infections has hyaluronidase which targets what and might lead to what
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cartilage - lead to arthritis
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Cross reacting antibodies in strep infections has Group A Carbohydrates which is an Ag similar to those found on heart valves which would cause
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endocarditis
think fish mouth! |
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fish mouth deformity of the aortic valve might be seen in what kind of disease and what kind of hypersensitivity is this
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rheumatic fever. type II
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aschoff bodies are seen in what disease
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seen in rheumatic heart disease due to inflammatory reaction. they are moncytes some have merged to form giant cells. looser organization than granulome (not a nodule)
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Antibody has natural ligan activity on TSH receptor
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Graves - leads to activaiton
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Ab against AcH receptor - blocked
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myasthenia gravis
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key cell in type III reacation
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PMNs (but MO also involved)
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systemic type III reactions include what three diseases - mechanisms
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serum sickness, SLE, drug interactions
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arthus reaciton, vasculaitis, glomerulonephritis, arthritis is what kind of type III reaction
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localized
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why do PMNs lead to most of the tissue damage seen in type III reactions
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enzymes that digest pretty much everything
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post-streptococcal glomerulonephritis is what kind of reaciton
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localized type III reaction
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what kind of infiltrate are you likely to see in glomerulonephritis
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PMNs
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the lumpy bumpy pattern seen in a glomeruli would be an indication of what kind of reaction
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type III
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The inflammatory phase and necrotic phase of vasculitis is often due to what kind of reaction
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type III -
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small vessel vasculits caused by a type III reaction is often due to
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drug
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what two cells mediate the tuberculin reaction and the granulomatous reactions
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CD4+ and macrophages
(delayed type) |
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what cells are primarily involved in reactions to tumors, viruses and allogenic cells
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CD8+ (T cell mediated cytotoxicity
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what two cells are involved in rejection of transplanted organ
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Both CD4 and CD 8 (but B cells/Antibodies may be involved
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what are the three microglial and monocyte cell products that are beneficial
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TGFBeta
Growth and Trophic Factors GM-CSF |
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What three cells are abolutely essential for Delayed Type hypersensitivity
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T lymphocytes, APCs, Macrophages
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what is injected with the tuberculin reaction
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Purified Protein Derivitive (PPD) - last 2/3 dayrs
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what are the two cells seen in the tuberculin reaction
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T cells and macrophages
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what causes the endothelium to become sticky for circulating leukocytes
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T cells release cytokines which activate endothelial cells
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what kind of graft rejection results in rapid thrombosis of vessels and involves preformed antibodies
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hyperacute
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what kind of graft rejection happens weeks to months afterward and may involve a cellular or humoral reaction
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acute rejection
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what kind of acute graft rejection involves lymphocyte and macrophage infiltrates
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acute cellular
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graft reaction inolves the possibility of vasculitis, thrombosis, endothelial proliferation
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acute
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what kind of rejection involves intimal fibrosis, obliteration of lumen, organ ischemia, interstial mononulcear cell infiltrate, organ atrophy, and chronic vasculitis
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chronic rejection
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what is the difference between the direct and indirect pathway in a graft rejection
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direct inolves APCs w/in graft and Indirect involves recipients APCs with sample of graft
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in what kind of rejection might you see graft arteriosclerosis and tubular atrophy
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chronic
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both the direct and indirect pathway in a graft reaction stimulate Th1 which secret IFN-gamma which activate what cells
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macrophages
(IFN-gamma also increases vascular permeability and endothelial injury) |
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what histological change might you observe in the myocardial fibers if a pt has rheumatic fever
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increased size of nuclei and hypertrophy of myocardium.
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crescents are hallmarks of relatively severe glomerular injury and consist of
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proliferating parietal epithelial cells as well as monocytes from the blood stream. With time they are organized into fibrous tissue which may or may not obliterate the glomerulus
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cytokine produced by macrophages and DCS which are critical for induction of TH1
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IL-12
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Key mediator (cytokine) of DTH
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IFN-gamma(powerful activator of MO)
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autocrine and paracrine proliferation of T cells
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IL-2
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effects on endothelial cells. - all changes facilitate extravasation of lymphocytes and monocytes at site of DTH
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TNF
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activates eosinophils
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IL-5
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stimulates differentiation to the TH2 pathway
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IL-4
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two cytokines which down regulates immune system
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IL10 and TGFbeta
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two major components of granuloma in Type IV
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epithoid cells surrounded by lympocytes
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a common B cell deficiency which is mostly asymptomatic with some recurren tinfections and occurs 1/ 700 people
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IgA Deficiency
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cause of herediatry angioedma
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C1 inhibitor deficiency - C proceeds unchecked - mast cells degranulated - vessel leaks etc...
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what kind of immunity is effected in the follwoing diseases: hodgkins, tb, sarcoidosis, leprosy, measles
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cellular immunity affected
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chemotherapy and radiation are what kind of immunodeficiencies
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iatrogenic (secondary)
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