Term
| 5 Cellular Responses to Injury |
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Definition
| 1. Adaptation; 2. Acute cell injury; 3. Chronic cell injury; 4. Metabolic derangements; 5. Pathologic calcification |
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Term
| Examples of Etiologic Agents of Cell Injury |
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Definition
| hypoxia/ischemia; physical agents; chemical agents, infectious agents, immunologic reactions, genetic derangements; nutritional imbalances |
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Term
| Physical Agents of Cell Injury |
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Definition
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Term
| Chemical Agents of Cell Injury |
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Definition
| oxygen, for example, at too high a concentration; salt; smoke; medications |
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Term
| Infectious Agents of Cell Injury |
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Definition
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Term
| Immunologic Reactions Causing Cell Injury |
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Definition
| inappropriate response; anaphylaxis; auto-immune response; for example, Lupus, etc. acting against self-antigens |
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Term
| Genetic Derangements Causing Cell Injury |
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Definition
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Term
| Nutritional Imbalances Causing Cell Injury |
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Definition
| for example, too much saturated fat, etc. |
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Term
| Hypoxia/Ischemia Causing Cell Injury |
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Definition
| ischemia causes cell injury faster b/c in hypoxic conditions blood can still flow just with reduced oxygen-carrying capacity |
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Term
| General Mechanisms of Cell Injury |
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Definition
| cell membrane attack (i.e. clostridia); aerobic respiration (i.e. cyanide); inhibition of protein synthesis; enzyme degradation; DNA disruption |
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Term
|
Definition
| the response of a cell to an injurious stimulus depends not only on the type of injury and its duration but on the adaptability of the cell itself |
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Term
| Oxygen Derived Free Radicals |
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Definition
| extremely reactive unstable molecules with single unpaired electron in outer orbital; attack cell membranes; attack DNA in mitotically active cells; may underlie aging |
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Term
| Free Radicals are formed from what? |
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Definition
| radiation; chemicals, inflammation; aging; reperfusion injury |
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Term
|
Definition
| 1. lipid peroxidation of membranes; 2. oxidative modification of proteins/enzymes; 3. DNA disruption |
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Term
| 3 Most Biologically Important Free Radicals |
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Definition
| 1. superoxide; 2. hydroxyl ion; 3. hydrogen peroxide |
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Term
| Ways to Inactivate Free Radicals |
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Definition
| endogenous antioxidants (i.e. albumin, transferrin, enzymes); exogenous antioxidants (i.e. vitamins E, A, C, etc.) |
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Term
| Increased Cytosolic Free Calcium activates: |
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Definition
| phospholipases; proteases; ATPases; endonucleases |
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Term
| Effects of Membrane Permeability Changes due to Free Radicals |
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Definition
| ATP-depletion- pump dysfunction; calcium fluxes; direct damage- toxins, organisms; complement activation; cytolytic lymphocytes; chemical agents |
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Term
| changes in mitochondrial function with free radicals |
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Definition
| mitochondrial permeability transition pore; pore in mitochondrial membrane; disrupts functions- ATP declines |
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Term
| reversible types of cell injury in an acute event |
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Definition
| hypoxia; ATP levels drop; lactate builds up; anaerobic glycolysis ensues |
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Term
| morphology of reversible cell injury leads to: |
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Definition
| clumped chromatin; cellular edema; fatty change; bleb formation; myelin figures; detachments of ribosomes; mitochondrial swellings |
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Term
| 2 most important results of irreversible cell inury |
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Definition
| 1. permanent mitochondrial dysfunction; 2. permanent membrane damage |
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Term
| Critical factor in cell death |
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Definition
| permanent membrane damage (mechanisms include ATP depletion, free radicals, Ca++ activation of proteases, Ca++ activation of phospholipases) |
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Term
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Definition
| 1. coagulative necrosis; 2. liquifactive necrosis; 3. gangrenous necrosis; 4. caseous necrosis; 5. enzymatic fat necrosis |
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Term
| histologic and gross changes of necrosis |
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Definition
| early stage: gross pallor, congestion; middle stage: cytoplasmic eosinophilia, vacuolization, loss of nuclear detail; late stage: loss of nucleus |
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Term
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Definition
| ischemic insult that causes irreversible damage; the body doesn't enzymatically digest cell; cells are denatured and become ghost-like remnants, eventually these cells will be lysed |
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Term
|
Definition
| cells are abruptly and intensely degraded by enzymes to become liquified |
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Term
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Definition
| may be physiologic or pathologic; does NOT elicit an inflammatory response; regulation by BCL-2 gene; morphology: cell shrinkage, chromatin condensation, nuclear fragmentation, intense cytoplasmic eosinophilia |
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Term
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Definition
| embryogenesis; hormonal independent involution; cell deletion in proliferating cell populations; |
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Term
|
Definition
| cytotoxic T cells in transplants; viral hepatitis; injurious stimuli like chemicals, chemo; atrophy in gland with blocked duct |
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Term
| the subcellular alterations of chronic cell injury |
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Definition
| lysosomal autophagy; cytoskeletal changes; lysosomal storage |
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Term
|
Definition
| damage in pre-keratin filaments which form eosin-bodies in hepatocytes |
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Term
| 3 types of intracellular accumulations |
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Definition
| 1. normal cell constituent (fatty liver); 2. abnormal endogenous substance (glycogen storage); 3. abnormal exogenous substance/ infectious particle (carbon, silica, virus) |
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Term
|
Definition
| found in liver, heart, muscle, or kidney; caused by triglyceride accumulation; and is a reversible form of cell injury; examples: alcohol decreases FA oxidation, anoxia inhibits FA oxidation, starvation increases TG synthesis |
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Term
|
Definition
| alcohol leads to decreased fatty acid oxidation; CCL4/protein malnutrition leads to decreased lipoprotein synthesis; anoxia inhibits fatty acid oxidation; starvation increases triglyceride synthesis |
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Term
| other causes of intracellular accumulations |
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Definition
| cholesterol and cholesterol esters (atherosclerosis, xanthomas, areas of necrosis); proteins; glycogen; pigments |
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Term
| 4 types of cellular adaptation |
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Definition
| 1. hyperplasia; 2. hypertrophy; 3. atrophy; 4. metaplasia |
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Term
|
Definition
| conversion of one benign cell type to another benign cell type |
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Term
|
Definition
| hyperplasia in the face of trauma (i.e. if a piece of the liver is cut out, most of it will grow back) |
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Term
|
Definition
| death of tissue due to loss of blood supply |
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Term
| what kind of necrosis do organ infarctions exhibit? |
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Definition
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|
Term
| what kind of necrosis do brain infarctions exhibit? |
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Definition
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Term
|
Definition
| necrosis: many cells, cell swelling, inflammation, mechanism- ATP depletion, membrane damage; apoptosis: single cells, chromatin condensation, no inflammation, cell shrinkage, mechanism- genes, endonucleases |
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Term
|
Definition
| low grade injury that doesn't kill the cell off, but alterations occur for survival |
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Term
|
Definition
| continuous injury to cells and organelles within injured cell, they are degraded and then phagocytosed |
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Term
|
Definition
| hormonal (female breast); compensatory (hepatectomy- liver can grow back); prostate if asymptomatic |
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Term
|
Definition
| endometrial hyperplasia (due to unopposed estrogenic stimulation); warts; prostate if symptomatic |
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Term
|
Definition
| increased mitosis leads to increased cell numbers |
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Term
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Definition
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Term
|
Definition
| uterus in pregnancy; weight lifter's muscles |
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Term
|
Definition
| decompensated heart in HTN |
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Term
|
Definition
| loss of cellular substance; cell shuts down; cell shrinks |
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Term
|
Definition
| gonads with decreased hormonal stimulation in age; sedentary lifestyle |
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Term
|
Definition
| muscle atrophy in nerve damage; vascular disease with chronic ischemia |
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Term
|
Definition
| 1. acute; 2. chronic; and then repair |
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Term
|
Definition
| short duration (hours to days); involves exudation of fluids from intravascular into extravascular as well as emigration og neutrophils from blood into tissues |
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Term
|
Definition
| long duration (days to weeks); mononuclear cells predominate |
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Term
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Definition
| involves angiogenesis/neovascularization and fibroblastic proliferation; areas where parenchymal cells cannot proliferate will be replaced solely with scar tissue of fibroblasts (i.e. heart) or with a mix if cells can proliferate (i.e. skin) |
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Term
| initiators of inflammation |
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Definition
| 1. chemical factors; 2. tissue injury; 3. antigenic cross-reactivity |
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Term
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Definition
| activated as a result of activation of agents associated with injury; itself activates plasminogen to plasmin which leads to fibrolysis and fibrin degradation products |
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Term
| two results of plasmin activation |
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Definition
| fibrin degradation products and complement activation which leads to anaphylatoxin |
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Term
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Definition
| results from activation of hageman factor, and leads to kinin generation |
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Term
| activation of coagulation system |
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Definition
| results from activation of hageman factor and leads to blood clotting |
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Term
| metabolites of arachadonic acid activated in inflammation |
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Definition
| 1. COX pathway- prostaglandins (vasodilators, bronchodilators); 2. Lipooxygenase pathway- leukotrienes (chemotactic for phagocytes, adherence, permeability) |
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Term
|
Definition
| leads to membrane attack complex, which causes cell lysis |
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Term
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Definition
| C5a, C3a: chemotactic, stimulate immune response, activate tissues to produce COX and Lipoc products, stimulate mast cells to release histamine and leukotrienes which increase vascular permeability and cause edema |
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Term
| 3 components of acute inflammation |
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Definition
| 1. increased blood flow (blood flow decreases and pressure increases); 2. increased vascular permeability (leads to fluid to flow out into vessels); 3. emigration of leukocytes |
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Term
|
Definition
| via prostaglandins, complement/anaphylatoxins, histamine (basophils/mast cells), platelet activating factor, bradykinin |
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Term
| increased vascular permeability |
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Definition
| via anaphylatoxins, leukotrienes (stimulated by C5a), histamine, platelet activating factor |
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Term
| phagocytosis that involves recognition of FC receptor and C3b |
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Definition
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|
Term
| phagocytosis that involves direct identification and destruction |
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Definition
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|
Term
| phagocytosis that involves H2O2-MPO-halide system, in which primary and secondary granules are activated |
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Definition
| superoxide and halogenation |
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Term
| cause of inflammation-induced tissue injury |
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Definition
| lysosomal enzymes; oxygen derived free radicals; prostaglandins/leukotrienes- perpetuate and amplify response; leukocyte-dependent tissue injury |
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Term
| clinicopathologic results of inflammation |
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Definition
| complete resolution; healing with fibrosis; abscess formation; progression to chronic inflammation |
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Term
| genetic defect in leukocyte formation |
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Definition
| defect in oxidative burst, microtubule formation, abset H2O2 |
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Term
| acquired defect in leukocyte function |
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Definition
| defect in chemotaxis, adhesion, and phagocytosis |
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Term
| chronic inflammation follows. . . |
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Definition
| acute inflammation or de novo low grade persistent response can be subclinical for months or years |
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Term
| pathogenesis of chronic inflammation |
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Definition
| lymphocytes; plasma cells; tissue macrophages; tissue destruction; angiogenesis |
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Term
| macrophages in chronic inflammation |
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Definition
| respond to C5a, IL8, chemoattractants, and lead to epitheloid cell formation and elaboration of multinucleated giant cells called granulomas |
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Term
| macrophage fate in inflammation |
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Definition
| short lived in acute, can be long lived in chronic |
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Term
| lymphocytes in inflammation |
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Definition
| recruitment and activation by cytokines |
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Term
| plasma cells in inflammation |
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Definition
| do not cause damage directly |
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Term
| eosinophils in inflammation |
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Definition
| secrete major basic protein which is toxic to self as well as can lead to tissue damage |
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Term
| neutrophils in inflammation |
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Definition
| a minority cell type in persistent low-grade infections; present in chronic active inflammation |
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Term
| common, inflammation product that walls off agent the host can't deal with, and lacks central necrosis within granuloma |
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Definition
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|
Term
| cheese-like, walls off agent host can't deal with, necrotic within |
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Definition
| caseating granuloma (Tb only) |
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Term
|
Definition
| produce angiogenesis or neovascularization |
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Term
| vascular endothelial growth factor |
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Definition
| produce angiogenesis or neovascularization |
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Term
| fibroblast growth factor; vascular endothelial growth factor |
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Definition
| components of angiogenesis |
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Term
| platelet derived growth factor; fibroblast growth factor; transforming growth factor- beta |
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Definition
| components of recruitment and activation of fibroblasts |
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Term
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Definition
| inflammatory process producing thin, watery fluid (transudate)- i.e. blister |
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Term
|
Definition
| acute inflammation produces large amounts of fibrin which flows out with edema fluid into tissues |
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Term
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Definition
| a result of fibrinous inflammation; exudate lies on pleura of lungs, outer surface of bowel; causes pleuritis, pericarditis, peritonitis, etc. |
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Term
|
Definition
| causes pain, pericardial friction rub; leads to scarring, fibrosis; can lead to adhesive pericarditis- where visceral/parietal pericardium stick together, and constrictive pericarditis- which limits the correct contraction of the heart |
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Term
|
Definition
| intense recruitment of macrophages, causes abscess formation and liquifactive necrosis |
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Term
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Definition
| localized area of surface necrosis that can lead to perforation to open cavity |
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Term
| acute systemic effects of acute inflammation |
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Definition
| fever, anorexia, hypotension, hypoproteinemia, acute phase reactants (IL-1, IL-6, TNF) which increase protein levels (C reactive protein, ferrenin) |
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Term
|
Definition
| increased leukocytes in peripheral blood; normal level is 5-10K/cc blood |
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Term
|
Definition
| cells shifted in peripheral blood toward left |
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Term
| wound healing facilitated by mediators |
|
Definition
| leading to monocyte chemotaxis, fibroblast proliferation, angiogenesis, collagen synthesis from fibroblasts |
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Term
|
Definition
| 1. primary union; 2. secondary union |
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Term
|
Definition
| clean, straight wound, day 5 tissue fill, day 7 fibroblast proliferation, increased collagen, day 28 scar |
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Term
|
Definition
| large tissue, gaping wound; necrotic debris; myofibroblasts lead to wound contraction after it heals, leaving a big scar that contracts and is wrinkled |
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Term
|
Definition
| presence of excess fluid in the interstitial spaces either focally or diffusely |
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Term
|
Definition
| high specific gravity of exudate with proteins |
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Term
|
Definition
| alteration of hydrostaic balance leads to net change in the distribution of fluid resulting in edema |
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Term
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Definition
| diffuse edema associated with rnal disease; net outflow into interstitial tissues |
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Term
| arteriolar dilation, increased venous pressue, hypervolemia (sodium retention, decreased renal function), heart failure lead to: |
|
Definition
| increased hydrostatic pressure |
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|
Term
| hypoproteinemia (malnutrition, cirrhosis), chronic liver or renal disease leads to: |
|
Definition
| decreased oncotic pressure |
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|
Term
| increased hydrostatic pressure leads to: |
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Definition
| outflow of blood from blood |
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|
Term
| decreased oncotic pressure leads to: |
|
Definition
| outflow of fluid from tissue to blood |
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|
Term
| increased capillary permeability leads to: |
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Definition
|
|
Term
| lymphatic obstruction leads to: |
|
Definition
| outflow of fluid from tissue to blood |
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|
Term
| 12 mL/min flows from artery to veins, 2 mL/min flow from artery to interstitial tissue |
|
Definition
| normal hydrostatic situation |
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Term
|
Definition
| subcutaneous- tissue has excess fluid; pulmonary- usually due to chronic heart failure; cerebral- multiple causes no place for expansion due to skull; effusions- pours into body cavities |
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|
Term
| pink material, acellular at high power (so, not fibrinous exudate of bronchopulmonary pneumonia; fibrin would be more brightly eosinophilic whereas this is frothy and not as bright pink) |
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Definition
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|
Term
| how does chronic heart failure lead to hepatosplenomegaly and pitting edema? |
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Definition
| heart dilates due to increased pressure in heart, which causes blood to back-up in the lungs, causing congestion in the lungs, which leads to pulmonary edema; if severe enough, pleural effusion results, leading to right-sided failure, and pressure backs up into the liver, causing congestion, necrosis, ascites, and eventually hepatosplenomegaly, causing a back up of blood and pitting edema |
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Term
|
Definition
| increased amount of blood in a certain area |
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|
Term
|
Definition
| inflammatory states, increased vascular permeability, heat, and redness due to inflammatory mediators |
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Term
|
Definition
| impaired venous drainage to the area or organ where pressues cause blood to back up into tissues leading to congestion; dark and blue-ish- cyanotic |
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Term
|
Definition
| bleeding into tissue, body cavity, or exterior |
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Term
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Definition
| general term for collection of blood, may be interchanged with ecchymosis |
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Term
|
Definition
| hematoma; collection of blood |
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Term
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Definition
| microhemmorhages in skin; minute, less than 1 mm. |
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Term
|
Definition
| microhemmorhage; small, >3 mm. |
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Term
| massive body cavity hemorrhage |
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Definition
| bleeding into pericardial sac (cardiac tampanade); hemothorax (thoracic cavity); hemoperitoneum (abdominal cavity) |
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Term
|
Definition
| central tear which leads to a split through the middle of the aorta which can rupture |
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Term
|
Definition
| massive edema which leads to acute hemorrhagic pancreatitis |
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Term
| predisposition to thrombosis |
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Definition
| endothelial injury; alterations in blood flow (stasis, turbulence around abnormal valve, aneurism, genetic/acquired hypercoagulability) |
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Term
| pieces of thrombi that break off and travel elsewhere in the body |
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Definition
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|
Term
| appearance of currant jelly and chicken fat |
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Definition
| post-mortem clot (random mixture of RBCs, WBCs, and platelets |
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Term
| Lines of Zahn (feature of thrombosis) |
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Definition
| organized pattern of RBCs and platelets with fibrin layered in lines; more apparent in larger arteries and heart |
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Term
| thrombi that is soft and bloody |
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Definition
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|
Term
| thrombi that is firm, lighter-colored, and partly stuck to the wall |
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Definition
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|
Term
| 5 possible fates of thrombi |
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Definition
| 1. dissolution & resolution; 2. organization & persistence, leading to bump of scar tissue; 3. recanalization to form new pathway through thrombis to restore blood flow; 4. embolization; 5. propagation, thrombus continues to get bigger and embolizes or blocks critical artery |
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Term
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Definition
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|
Term
|
Definition
| deep veins (95%) of lower extremity thrombose, and pieces or whole thing lodges in pulmonary artery |
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|
Term
|
Definition
| instant death due to pulmonary embolism |
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Term
|
Definition
| fracture of long bone causes fat to embolise, leading to venular rupture with large amount of fat, 2-3 day latency and respiratory failure, 10% fatal |
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Term
|
Definition
| cervical or umbilical venous rupture |
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Term
|
Definition
| anemic/white (solid organs); hemorrhagic/red (loose tissues- lung, dual vascular supply- lung, bowel, venous occlusion); septic (bacterial with necrosis leading to abscess formation); bland (no bacteria) |
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Term
|
Definition
| ischemic; usually coagulative necrosis due to hypoperfusion and resultant cellular anoxia; may be arterial or venous occlusion |
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Term
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Definition
| 0-24 hr. poorly defined area; 24-72 hr. sharply demarcated region due to ongoing coagulative necrosis |
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|
Term
| single vs. dual vascular supply and infarction |
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Definition
| single supply leads to white infarction, dual to red |
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Term
| rate of inclusion in infarction |
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Definition
| slowly leads to adaptation and collateral vessel formation |
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|
Term
| tissue vulnerability in infarction |
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Definition
| doesn't die quickly from ischemia- embolism blocks but breakdown by fibrinolysis works to remove embolus soon enough to prevent infarction |
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|
Term
| syndrome associated with various etiologies resulting from systemic hypoperfusion with resultant tissue and cellular hypoxia often culminating in multi-system organ failure and death |
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Definition
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|
Term
|
Definition
| poor tissue perfusion due to heart not pumping properly leading to cell and tissue death; can be due to MI, cardiac tamponade, arrhythmias, pulmonary embolism |
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Term
|
Definition
| poor tissue perfusion due to low blood volume leading to cell and tissue death |
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|
Term
|
Definition
| overwhelming bacterial infections: gram negative septicemia ("endotoxic shock"), or gram positive septicemia; peripheral vasodilation, pooling of blood, endothelial activation/injury |
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|
Term
| myocardial dysfunction, hypotension, endothelial injury, DIC, ARDS (adult respiratory distress syndrome), hepato-renal failure, widespread multi-system organ failure are symptoms of what? |
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Definition
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|
Term
|
Definition
| 1. non-progressive stage- early shock where patients are not very sick; 2. progressive- severe hypotension, signs of organ failure, still reversible; 3. irreversible- anoxia, cell damage, tissue damage, patient death |
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|
Term
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Definition
| mononuclear phagocyte system is largely responsible for the clinical syndrome of shock via its ability to secrete IL-1 and TNF-a thereby promoting intravascular coagulation and capillary thrombosis; they, in turn, activate other mediators causing vasodilation and hypotension |
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|
Term
| development of antibodies against our own aberrant cells |
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Definition
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|
Term
| cell mediated; reacts to foreign material by defense cells (NKs, macrophages, WBCs), not Abs |
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Definition
| cellular branch of immunity |
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Term
|
Definition
| family of proteins that respond to different antigens and activate NFkBwhich stimulates cytokines and phagocytes |
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Term
| Ab-mediated, B and T cells; cytokines |
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Definition
| humoral branch of immunity |
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Term
| class of T cell with delayed hypersensitivity, macrophage activation, synthesis of IgG2b Abs; inhibited by IL-10; if dominance, more macrophage activation and activity against i.e. TB/HIV |
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Definition
| Th1 subset of helper (CD4) T cells |
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Term
| class of T cell which aids synthesis of other classes of antibodies including IgE (allergy, anaphylaxis); inhibited by IFNg; more allergic responses if dominant |
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Definition
| Th2 subset of helpet (CD4) T cells |
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|
Term
| maintains self-tolerance by suppressing activation and expansion of self-reactive lymphocytes |
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Definition
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|
Term
|
Definition
| activates T helper cells (CD4); absence of costimulation results in T cell apoptosis or anergy |
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Term
|
Definition
| helper T cell interaction with B cell via CD40 ligand is essential for B cell maturation and secretion of antibodies |
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Term
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Definition
| gel-like matrix in the CT of most tissues; slows spread of many infectious agents |
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Term
|
Definition
| enzyme found in saliva, tears, saliva, nasal secretions that breaks down bacterial cell walls |
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Term
|
Definition
| causes cell lysis by interfering with the cell's ability to control intracellular Ca++ |
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Term
|
Definition
| transmigration of leukocytes through the endothelial cell wall |
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|
Term
| 4 steps of cell-mediated immunity |
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Definition
| 1. recognition; 2. proliferation and differentiation of activated T cells; 3. clone production; 4. elimination of pathogen |
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Term
|
Definition
| first encounter between an antigen and a naive lymphocyte |
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|
Term
| major initiators of adaptive immunity that actively migrate to the lymph nodes and secondary lymphoid organs and present antigen to T and B cells |
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Definition
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|
Term
|
Definition
| non-specific killers which respond to the lack of self-antigens; able to kill virus-infected body cells and some tumor cells by releasing various defense molecules (perforin)- NOT by phagoctosis |
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Term
|
Definition
| Transporter associated with Antigen Processing; load endogenous antigens onto MHCI in endoplasmic reticulum |
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Term
|
Definition
| stimulates B cells to produce Ig-E in hypersensitive response |
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|
Term
| TST; Tine Test; PPD Test; Mantoux Test |
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Definition
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|
Term
| 2 phases in the development of autoimmune disease |
|
Definition
| induction phase; effector phase |
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|
Term
| induction phase in the development of autoimmune disease |
|
Definition
| breakdown of self-tolerance |
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|
Term
| effector phase in the development of autoimmune disease |
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Definition
| tissue damage mediated by adaptive immune system |
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|
Term
| clonal deletion; clonal anergy; peripheral suppression of Ag |
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Definition
| 3 mechanisms of self-tolerance |
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|
Term
| leading cause of death in lupus patients |
|
Definition
| renal failure because of glomerulonephritis |
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|
Term
| disorganized but mature mesenchymal or epithelial tissues found in their normal anatomic location; represents an aberrant differentiation, not a true neoplasia |
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Definition
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|
Term
| normal mature tissue located at an ectopic site |
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Definition
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|
Term
| grossly visible nodule or mass projecting from a mucosal or epidermal surface; a hyperplasic response to chronic inflammation or irritation |
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Definition
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|
Term
| immortal; transformed; contact inhibition; need for solid support; requirement of growth factors and nutrition; can dislodge from cells and basement membranes; invasive capacity |
|
Definition
|
|
Term
|
Definition
| abnormal cell-form; disordered growth pattern (most often in relation to epithelium); loss of uniformity in individual cells; loss of architectural organization; nucleus/cytoplasm ratio- nucleus is larger |
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Term
|
Definition
| formation of the platelet plug. |
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Term
|
Definition
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|
Term
|
Definition
|
|
Term
|
Definition
| most potent platelet inhibitor |
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|
Term
|
Definition
| most potent platelet activator |
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|
Term
|
Definition
| Helps blood clot quickly; tissue fluid. |
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|
Term
|
Definition
| Hemophilia A - bleed like stink. |
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Term
|
Definition
|
|
Term
|
Definition
| activates factor 13, which will strengthen the fibrin-fibrin ionic bonds and strengthen the platelet plug. |
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|
Term
| Vitamin K dependent clotting factors |
|
Definition
|
|
Term
|
Definition
| red blood cells with strands of pink granular material streaking through the blood. These streaks are known as lines of Zahn and are seen in true thrombus materials |
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Term
| Atrophy can be caused by several different things. |
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Definition
a. Diminished blood flow
b. Decreased workload
c. Loss of innervation
d. Inadequate nutrition
e. Loss of endocrine stimulation/signaling
f. Aging
g. Pressure |
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Term
| Generalized Edema is also known as: |
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Definition
|
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Term
|
Definition
| has a low specific gravity. |
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Term
| Inflammatory edema is associated with: |
|
Definition
| vasoactive inflammatory cell products. |
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Term
| Passive hyperemia is associated with: |
|
Definition
| impaired venous drainage, pooled venous blood, congestive heart failure, and congestion of the tissues. |
|
|
Term
| pulmonary edema is associated with: |
|
Definition
| heavy, frothy lungs at autopsy; left heart failure; Extravasation of fluid across alveolar capillary walls; Intraalveolar fluid accumulation |
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Term
| The most serious consequence of body cavity hemorrhage is: |
|
Definition
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|
Term
| The Pathophysiology of SHOCK involves all of the following: |
|
Definition
| Vasodilatation and hypotension; Endothelial injury; Coagulation system activation; Multisystem organ failure |
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Term
| Inappropriate Antigenic cross reactivity with circulating or inhaled antigens has been postulated to be the triggering stimulus for the inflammatory destruction of tissues in what kind of diseases? |
|
Definition
| Autoimmune disorders, certain pneumonitides and some renal diseases |
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Term
| Type I Hypersensitivity reactions are orchestrated by: |
|
Definition
| Th2 type CD4+Helper T Cells |
|
|
Term
| Graves Diseases is a manifestation of: |
|
Definition
| Type II Hypersensitivity Reaction |
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|
Term
| Graft versus host disease is due to: |
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Definition
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Term
| A patient with known AIDS presents with dysphagia and multiple distal esophageal ulcers. Endoscopic biopsy shows squamous epithelial cells with "ground glass" and eosinophilic nuclear inclusions, and some multinucleated cells. This cytopathic effect is diagnostic of: |
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Definition
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Term
A couple has three children, one of whom was recently diagnosed with a rare autosomal recessive genetic disorder. Linkage analysis using RFLPs has yielded the following results:
Mother: 34 bp segment; 92 bp segment
Father: 34 bp segment; 92 bp segment
Son: 34 bp segment; 34 bp segment
Daughter 1: 34 bp segment; 92 bp segment
Daughter 2: 92 bp segment; 92 bp segment
If one of the daughters is affected, the clinical status of the other children is: |
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Definition
| The other daughter is a carrier, and the son is not a carrier and is not affected |
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Term
A 47-year-old smoker presents with cough, tachypnea, fever, and chest pain. Lab studies reveal
elevated white blood cell count (Leukocytosis) with a "left shift". Many Bands and scattered
metamyelocytes and some myelocytes are identified in the peripheral blood. What is the best explanation for this clinical scenario? |
|
Definition
| This is most likely a bacterial infection. Proceed to identify a source and consider antibiotic therapy once a source and organism are identified. |
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