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What are the three causes of hypersensitivity diseases?
1.) autoimmunity 2.) rxn against microbes (maybe prolonged exposure to something 3.) rxn against enviromental antigens (all of us are exposed to these but only some people react to them, they are usually harmless antigens ex. Pollin)
Type I hypersensitivity is mediated by ____ directed against specific antigens (allergens)
immunoglobulin E (IgE)
Primary mediators of type I hypersensitivity include ___, ___, ___ and ____.
histamine, adenosine, heparin and proteases
Secondary mediators of type I hypersensitivity include ____, ___, ____ and ____.
leukotrienes (which are 10x more potent than histamine), prostaglandin D2, platelet-activating factor, and cytokines
Anaphylaxis, allergies, and bronchial asthma are all prototype disorders of type ___ hypersensitivity
In type I hypersensitivity, both primary and secondary mediators cause ___, ____ and ____.
vascular permeability, smooth muscle contraction, and prolonged inflammation
Hypersensitivity can cause ___ and ___ reactions
local (ex. Bee sting) and systemic (ex. Anaphylactic response)
With Type II hypersensitivity, antibodies are directed against target antigens on the surface of cells or orther tissue components. This leads to _____.
What are the three kinds of Type II hypersensitivity?
1.) complement-dependent reactions 2.) antibody-dependent cell-mediated cytotoxicity 3.) antibody-mediated cellular dysfunciton
List the five reactions of complement-dependent Type II reactions.
1.) transfusion rxns 2.) erythroblastosis fetalis 3.)autoimmune hemolytic anemia, agranulocytosis or thrombocytopenia 4.) drug rxns 5.) pemphigus vulgaris
What are the three mechanisms of Type III hypersensitivity?
1.) antigen-antibody complexes 2.) activates complement in tissues at site of trapping of complexes 3.) accumulation of polymorphonuclear leukocytes
What are the three phases of type III hypersensitivity?
1.) complex formed btw antigen and antibody 2.) complex deposits in tissue 3.) this triggers recruitment of PMNs (inflammatory rxn)
TB (and other mycobacteria), fungi, protozoa, parasites, sarcoidosis, contact skin sensitivity and transplant rxns can all cause type ___ hypersensitivity.
What are the two types of Type IV hypersensitivity?
1.) delayed-type hypersensitivity 2.) direct cell cytotoxicity
In delayed-type hypersensitivity, CD4 T cells are activated and then differentiate into _____.
Th 1 (T-helper) cells
Delayed-type hypersensitivity activates ____ and ____
macrophages and TNF (which add more to the inflammation process ex. PPD test, contact dermatitis)
If delayed-type hypersensitivity is not resolved it can cause _____.
chornic inflammation--> multinucleated giant cells
______ is when perivascular CD4 T-cells infiltrate is replaced by macrophages over a 2-3 week time period and turn into epithelioid cells (large, flat, eosinophilic -> multinucleated giant cells)
granulomatous inflammation (ex. Poison ivy)
reactions to transfusion, Rh incompatibility and Hashimoto's thyroditis are examples of
Type II (cytotoxic antibody reaction)
Type III hypersensitivity should be associated with_____
antigen-antibody complex deposits in tissue
What is the role of MHC?
Once a pathogen is engulfed and broken down into peptides the MHC is activated and results in antigen presentation so the T-cell can recognize infected cells
________reactions to _________is the cause of certain human disease
immune; self-antigens (presence of antigens alone is not pathologic)
describe the general process of tissue injury due to autoimmune disease
The individual has self-reactive lymphocytes which binds to their own cells activating APC's thus causing an increase of lymphocytes into tissue which leads to tissue injury
what are the 11 criteria for classification of SLE
malar rash, discoid rash, photsensitivty, oral ulcers, arthritis, serosis, renal disorder, neurologic disorder (seizures or psychosis), hematologic disorder, immunologic disorder or antinuclear antibody
A 16-year-old black female presents to her primary care physician with symptoms of fatigue, musculoskeletal pain, and a facial rash. On examination she is noted to be thin with malar skin changes. No other abnormality is found
A 52-year-old woman presents with a 2-month history of bilateral hand and wrist pain, and swelling in her fingers. She has also recently noted similar pain in the balls of her feet. She finds it hard to get going in the morning and feels stiff for hours after waking up. She also complains of increasing fatigue and is unable to turn on and off faucets or use a keyboard at work without a significant amount of pain in her hands.She also presents with leg ulcers that have been chronic and has ulnar deviation of the hands bilaterally. She denies any infections before or since her symptoms started
pathologic changes that begin in ligmentous attachments to bone; frequently involves SI joints
A 45-year-old woman presents with fatigue and a history of positive anti-nuclear antibodies. She has had recurrent sensation of sand/gravel in eyes and dry mouth every day for more than 3 months.
skin involvment is confined to fingers/face, visceral involvement occurs late, presents with CREST
limited scleroderma SS
Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and telangiectasia
what is the next step in the immune response after mast cells and macrophages are recruited
release of fibroblast growth and chemotactic factors or endothelial cell injury
characterized by decreased antibodies, T/B-cells, phagocytes or complements
characterized by old age, chronic malnutrition, widespread malignancy, metabolic (DM, liver failure...), drugs, splenectomy or HIV
Name some high risk groups of HIV
risky sex, IV drug users, homosexual, transfusion pts, and hyperphiliacs
AIDS defining diseases include (6)
toxoplasmosis, candidiasis, salmonella, kaposi's sarcoma, non-hodgkin's lymphoma, TB
Nonspecific complaints of amyloidosis
weakness, fatigue, initial weight loss, renal involvement (proteinuria-nephrotic syndrome), hepatomegaly, splenomegaly, cardiac abnormalities (arrhythmias
Catagorized as "systemic amyloidosis" (5)
Immunocyte dyscrasias (primary), reactive systemic (secondary), hemodialysis, hereditary (familial mediterranean fever or familial amyloidotic neuropathies), systemic senile
catagorized as "localized amyloidosis" (3)
Senile cerebral, endocrine (medullary carcinoma of thyroid, islet of langerhans), isolated atrial amyloidosis
disease associated with immunocyte dyscrasias with amyloidosis
multiple myeloma and other monoclonal B-cell proliferations
Carcinogen-----monoclonal B lymphocyte proliferation----plasma cells-----immunoglobulin light chains (limited proteolysis)
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