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199 Cards in this Set
- Front
- Back
2 common chronic injury cell type changes
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smoker:ciliated epithelium - stratified squamous. Cervix - glandular to squamous epithelium
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4 systems in cell vulnerable to injury
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membrane pump, genetic apparatus, aerobic respiration, structural-enzymatic proteins
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4 mediators - cell death
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02 and 02 free radicals, intracellular Ca+, ATP depletion, membrane permeability defects
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2 energy mechs affected in cell injury
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aerobic respiration (oxydative phosphorylation), glycolysis (anaerobic respiration)
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result when each energy mech. injured
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aerobic - ATP production lost. glycolysis - depletion of glucogen, byproducts and acidity
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byproducts - glycolysis
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lactic acid, reduces intercellular pH
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4 mechanisms free radical injury
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peroxidation of membrane lipids, DNA breaks, X-linking of proteins destroys function, damage to mitochondria.
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6 free radical injuries
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reperfusion/hypoxia, aging, radiation, 02 toxicity, chemical injury, INFLAMMATION
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2 mechanisms chemical injury
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direct (chemotherapy), toxic reactive metabolite reaction (in liver)
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2 methods necrotic cell removal
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denaturation, enzymatic digestion
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nuclear shrinkage
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pyknosis
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many cytoplasmic proteins denature - result?
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cytoplasmic eosinophilia (incr. staining)
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markers of infarct in brain
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cyst, tissue debris, fluid, inflamm. cells, bacteria
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normally seen in caseous necrosis
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granulomatous inflammatory border with giant cells, epitheloid histiocytes
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2 conditions assoc. w apoptosis
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viral infections, radiation injury
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fast necrosis dev. in organs with?
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high met. rate (int. mucosa), cytolytic enzymes(pancreas), vital organs - high O2 (brain, heart, lungs)
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physiologic hyperplasia 2 types, examples
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compensatory (liver regen) hormonal (breast/uterus - pregnancy)
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inflammation mediators
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chemicals derived from host
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inflammatory changes occur where
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terminal vascular bed, blood, conn. tissue
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main cells involved in inflammation
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monocytes, neutrophils, macrophages
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purpose of inflammation
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eliminate injurious agent and initiate repair, restoring continuity if not function
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characteristics acute inflam.
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short duration, fluid exudate, plasma proteins (edema), neutrophil and leukocytes to tissue, then macrophages.
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chronic inflam. char.
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long duration, lymphocytes, plasma cells, macrophages, vascularization, fibroblasts.
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following vascular chgs
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blood tissue barrier chgs - widen endothelial gaps - histamine reaction - edema
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swelling of inflammation bc of
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capillary leakage - blood plasma and leukocytes to tissue
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inflammatory exudate
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cellular debris, plasma proteins, fluid
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cellular events of inflamm
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margination, pavementing w/in vessel wall, emigration from vessel to interstitium, chemotaxis-site, phagocytosis
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inflamm cell types
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Neutrophils first 24 hrs, then monocytes 24-48 hrs
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5 host derived main mediators inflammation
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vasoactive amines, plasma proteases, cytokines, adhesion molecules, arachiodonic acid metabolites
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2 vasoactive amines
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histamine, seratonin
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purpose, origin vasoactive amines
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vascular chgs inflammation
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what produces vasoactive amines
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mast cells, platelets
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3 systems of plasma proteases
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kinin, clotting, complement systems
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cytokine, peptide source
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macrophages
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cytokine purposes
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inflammatory mediators (IL1, TNF), activate polymorphs, macrophages to incr. killing, incr. vasc. permeability
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ICAM1 def
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cytokine - initiated production by endothelium
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ICAM1 purpose
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facilitates inflam cell binding to vessel endothelium
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AA metabolites are?
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arachiodonic acid - degraded phospholipids of cell membranes
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AA’s cause?
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inflammation - vasodilation, chemotaxis, increase vasc. permeability
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aspirin function
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blocks prostaglandin synthesis
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prostaglandin function
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pathogenesis of pain and fever - hyperalgesic
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steroid function
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blocks prostaglandin, leukotrines
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leukotrines
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chemotactic, activate neutrophil aggregation, adhesion
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chronic inflam cells
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MNL, lymphocytes, plasma cells
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main processes, chronic inflam
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healing and repair and tissue destruction cycle
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define granuloma
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form of chronic inflam w/ lots of histiocytes, giant cells, LANGHANS cells
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granuloma forms bc
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bacterial or fungal infection, foreign materials
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3 examples persistent infections causing chronic inflam
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tuberculosis, syphilis, fungi
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2 autoimmune disorders assoc w chronic nflamm
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rheumatoid arthritis, thyroiditis
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chronic inflammation: granuloma histology
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activated macrophages, large squamous cell epitheloid appearance
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pyogenic organism example
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staphlococcus
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3 systemic effects inflam
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fever, elevated WBC count, neutrophylia, lymphocytosis
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exudate with RBCs
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hemorrhagic
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inflammation is
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response of VASCULARIZED tissue to injury
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inflammation designed to
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bring plasma proteins to site of injury in fastest poss.time
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main chgs in inflammation
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blood flow changes, formation of fluid and cellular exudates
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3 functions fluid exudate
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bring plasma proteins, dilute toxins, loosen conn. tissue to allow diffus-migration of cells to injury site
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cell type assoc w/ parasitic infection
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EOSINOPHILS
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PMN
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polymorphonuclear leukocytes: NEUTROPHILS
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chemical attractants at injury site
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host factors - plasma proteins, and infectious agents
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protein expressed on infectious agent
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OPSONIN - labels agent for phagocytic destruction
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3 conditions lysosomal enzymes released inadvert. during inflamm.
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during phagocytosis, trying to digest on flat surface (frustrated phagocytosis), cytotoxic release
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system: removes AgAb complexes in spleen, liver, bone marrow
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reticulo-endothelial system
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tissue destruction from cytotoxic release
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GOUT
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4 agents of chronic inflammation
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microorganisms, foreign bodies, toxins, auto-immune reactions
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chronic inflam main events
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cellular infiltrate, tissue destruction, repair by scar
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granuloma
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chronic infection, macrophages differentiate - epitheloid cells, cluster
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4 disorders assoc w granulomatous inflam
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tuberculosis, syphilis, leprosy, crohns
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2 modes of destruction AbAg complex
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direct lysis, complement activation
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cells with FC receptors
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macrophages, NK cells, eosinophils, neutrophils
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direct lysis of AgAb complexes how
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cell with FC receptor engages FC fragment, releases lysosomes - destroys complex
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2 basics of complement system
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hydrolytic enzymes directly lyse infectious agents or chemical mediators initiate acute inflammation, attract neutrophils to phagocytose
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2 main classes Tlymphocytes
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CD4s assist others, CD8s kill directly
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3 types of antigen presenting cells
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dendritic(skin), macrophages, langerhans
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distinguish self from non-self
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major histocompatibility protein (MHP)
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two types of MHP & locations
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Class I - all cells, Class II - ONLY antigen-pres. cells
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MHC protein recognition
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CD4s recognize class II, CD8s only class I
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cytokine, source activates Bcells
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interleukin produced by Type2 CD4s
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cytokine source - activates macrophages
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Interferon Gamma, produced by Type1 CD4s
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macrophage activation results
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increased size, lysosomal enzymes, ability to digest/kill, secretion of growth factors(endothelial cells, fibroblasts), hydrolytic enzymes
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macrophages kill what and how
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TB, parasites, fungi, tumour cells, organ trans. direct lysis or phagocytosis
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CD8s kill antigens how
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proteolytic enzymes -- osmotic lysis
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CD8s mostly kill
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virus infected cells, tumour cells, organ trans (non-self)
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stimulates scar repair in chronic inflam
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activated macrophages secrete growth factors
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Type I hypersensitivity mediated by Ig?
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IgE
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2 cell types central to Type I hypersensitivity
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mast cells and basophils
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mast cells - what and where
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from marrow, wide dist. in body, esp. around nerves, vessels, subepithelial where Type I reacts occur
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Mast cells/basophils activated how?
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crosslinking IgE receptors
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diff btwn mast cells and basophils
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basophils in blood, small numbers
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type of helper cell assoc. w Type I hypersens
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Type 2 CD4s
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What is produced by Type 2 CD4s
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Interleukins 4 and 5
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genetic predisposition to type 1 hypersensitivity called
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atopic disease (allergy) IgE diseases
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other IgE mediated diseases
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asthma, dermatitis, gastrointestinal food allergy
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released upon exposure to allergen?
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histamines, leukotrines
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SRS-A
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slow-reacting substance of anaphylaxis
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ECF-A
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eosinophil chemotactic factor of anaphylaxis
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type 1 mediators act on what?
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vessels, sm. musc, secretory glands
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Type 1 mediators cause what?
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edema, cellular infiltrate, clinical features of allergy
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IL4 is what
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IgE switch factor, produced by Th2, activates Bcells
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HDN example of what type hypersensitivity
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Type II
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produced in mother in HDN following second child?
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IgG antibodies, which cross placenta
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problem with IgG crossing placenta?
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attack fetal erythrocytes - hemolytic anemia
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natural antibodies reactive with AB blood groups
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IgM - can’t cross placenta
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2 examples of Type II hypersensitivity
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organ rejection, myasthenia gravis
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define RA (rheumatoid arthritis)
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chronic systemic inflamm.autoimmune disease - joints
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what histocompatibility complex assoc. with rheum arth
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HLA-D4, and HLA- DR4
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what are rheumatoid factors
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immunoglobulins specific for FC fragment of IgG - an antibody against ones own antibody Immunoglobulin
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2 examples Type III hypersensitivity
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serum sickness, arthus phenomenon
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inflammatory factors associated with rheumatoid arthritis
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histamine release, cytokine production (neutrophils, monocytes), white cells to synovial space
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define pannus
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vascular mass of lymphocytes around area of necrosis where bone and cartilage have degraded
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cause of tuberculosis
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mycobacterium tuberculosis (or mycobac.T.bovine)
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TB inflammation type
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focal granulomatous with central caseous necrosis
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tuberculosis vaccine
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BCG - bacille Camette Geurin
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Test for TB
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PPD purified protein derivative
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endogenous infection
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from interior - ones own flora attacking system
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how well an organism can produce symptoms
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pathogenicity
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how severe symptoms are that are prod. by organism
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virulence
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poisons secreted by bacteria
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exotoxins
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examples of 3 exotoxins
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diptheria, tetanus, enterotoxin
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diptheria pathology
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sore throat - death. destroys epithelium and mucous memb, leaving fibrous necrotic tissue, esp. in throat.
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tetanus pathology
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neurotoxin, interrupts motor nerve signals, causes spasm
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enterotoxin
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food poisoning - staphylococcus
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endotoxins released when
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when bacteria destroyed
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3 bacterial metabolic examples - contrib. to disease
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hyaluronidase, streptokinase, coagulase
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metabolite - dissolves conn. tissue
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hyaluronidase
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metabolite - demineralizes tooth enamel
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plaque acid
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metabolite - breaks down fibrin
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streptokinase
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metabolite, breaks down DNA
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streptoadornase
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3 examples where foreign organisms multiply - prod. inflammation
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shigellosis(dysentry), Salmonella Typhi (Typhoid Fever), Spirochete(necrotizing ulcerative gingivitis)
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organism in bloodstream from infection called
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bacteremia
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another name for blood poisoning
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sepsis
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3 main factors - infection resistance
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patient factors(immunity, nutrition, biochem, secretions), organism virulence, site of infection, level of blood supp.
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atrophy caused by plasma protein deposition in tissue
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amyloidosis
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autoimmune disease where antibodies clog acetylcholine receptors
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myasthenia gravis - causes generalized muscular weakness
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chronic rheumatic fever can lead to risk of
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infective endocarditis - heart valve deformity, incompetency
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asthma
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mast cell histamine release-mucous hypersecretion-more goblet cells - bsmt. memb. thickening-sm. vessel constriction
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5 HIV related infections
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fungus in meninges, cytomegalovirus - gigantic langhans cell, lung yeast infection, carposis sarcoma, lymphoma
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proteins that regulate cell cycle
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cyclins
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continuously regenerating cells
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labile, from stem cells, eg: marrow, epithelia
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cells which can but don’t normally divide
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stable- divide if injured, eg: liver, fibroblasts, sm. musc
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cycle stage cells at
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G0 - resting(quiescent)
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matrix btwn cells - origin, composition
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interstitial matrix:fibroblasts-amorphous gel, collagen, elastin, proteoglycan, glycoproteins
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bsmt membrane composition
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platelike mesh, type IV collagen, glycoproteins
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extracellular matrix active in tissue repair how
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mech support, determine orientation, control regulate growth and differentiation, pres: regulatory molecules
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collagen - describe
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fibrous structure proteins from fibroblasts Xlink by VitC in triple helix
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source of cell growth factors
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activated macrophages
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3 examples growth factors
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epidermal, fibroblast, cytokines
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basic substrate extracell. matrix forms on and timing
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granulation tissue at abt. 3 days
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char. of first intention healing
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more epithelial regen than fibrosis
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1st intention - process
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neutrophils, mitosis; epithelial migration, new bsmt memb.; macrophages, granulation tissue, collagen fibres; epidermis - collagen fibre bridge
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char. of 2nd intention healing
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fibrosis rather than epithelial regen
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example 2nd intention
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ulcer (eg Diabetes)
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process 2nd intention
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big inflamm. reaction, lots of granulation tissue, wound CONTRACTS
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3RD intention
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delayed closure to allow some natural disinfection
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exuberant collagen production in 1st intention wound
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keloid
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types of factors effecting healing
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local(infection, foreign body, blood supp, temp.) Systemic(immunosup.,vasc.disease, nutrition, alcohol)
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key characteristics neoplasia
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autonomous cell division persisting post cessation of initiating stimuli
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2 components of tumours
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parenchyma (prolif. neoplastic cells) stroma (conn. tiss & vessels)
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benign tumour of epithelial origin
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papilloma (eg squamous or transitional)
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malignant tumour of epithelium
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carcinoma
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benign tumour of glandular origin
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adenoma
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malignant tumour of glandular origin
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adenocarcinoma
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age effected carcinoma versus sarcoma
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carcinoma 55+, sarcoma usually children
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3 categories of hereditary cancers
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mutant gene inheritance (autosomal dominant - eg:retinoblastoma), familial (uncommon CA type, prevolent in family), autosomal recessive (need both parental alleles)
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well differentiated versus poorly differentiated
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Grade I (less agress) - Grade III(v.aggress)
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highly UNDIFFERENTIATED tumour cells called
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ANAPLASIA
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variation in size and shape of tumour cells called
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pleomorphism
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tumour cell nuclei with lots of DNA - dark staining
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hyperchromasia
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6 morphologic chgs in anaplasia
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pleomorphism, hyperchromasia, lg nuclei, incr. mitosis, giant cells, disturbed orientation
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disorderly growth type that doesn’t nec. lead to CA
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dysplasia
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type of benign tumour not well defined
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hemangioma (tum. of blood vessels)
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spread through blood
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hematogenous - usually sarcomas
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tumour (benign or malig) effects depend on what 6?
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location, impingement; functional activity; bleeding; 2ndary infections; ulcerations; initiation of acute symptoms: rupture or infarct
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example of local effect of benign tumour
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adenoma of pituitary destroying pit. function, causing endocrinopathy
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hormonal effect example - benign tumour
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pancreatic islet tumour, overproduction of insulin, causes deadly hypoglycemia
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wasting syndrome associated with cancer
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cachexia - usually a result of cytokines
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example of substance imbalance assoc. w cancer
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cushings syndrome - lung or pancreatic CA producing ACTH
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histologic features, squam. cell CA
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sheets or solid nests “mosaic” pattern, intercellular bridges, sometimes keratinized
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term: sm. muscle
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leiomyo
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examples of acquired pre-neoplastic disorders
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chronic wound - cell regeneration, so potential for cancer; smokers - chronic bronchial dysplasia; chronic gastritis (pernicious enemia) - all can become malignant
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risk factor for oral CA
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leukoplakia - incr. risk squamous cell CA
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risk for colorectal CA
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villous adenoma (glandular)
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basis of carcinogenesis
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non-lethal genetic damage (chem, radiation, viral)
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targets of genetic dmg in cells
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genes: promote or inhibit growth, or apop.regulators
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growth promoting gene
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proto-oncogene
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oncogene is what
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a mutant allele of a proto-oncogene
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oncogene does what
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promotes autonomous cell growth
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example tumour supressor gene
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Rb gene - usually prevents cell cycle which otherwise causes retinoblastoma
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Most common genetic disorder in cancer
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TP53 gene - regulates apoptosis, senses DNA damage and initiates repair
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HER2 gene does what
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protooncogene - produces growth factor. commonly damaged in 20 - 30% of breast cancer cases.
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Type I hypersensitivity
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mast cells, basophiles release vasoactive amines, provoke an immediate (anaphylactic) response - eg food allergy, hay fever - IgE antibodies
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Type II hypersensitivity
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mediated by humoral antibodies which predispose cells to phagocytosis, lysis - complement mediated cytotoxicity - (hemolytic disease of newborn, transfusion reactions) - IgG antibodies
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Type III hypersensitivity
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Immune complex mediated (rheumatoid arthritis, serum sickness) --acute inflammatory response initiated, causing cell injury (in Rheum - fc fragment of IgG antibody)
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type IV hypersensitivity
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cell mediated (delayed hypersensitivity reaction) TCells rather than antibodies. eg tuberculosis.
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what might accompany a type II transfusion reaction
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hemolysis
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what is the last stage in wound healing?
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remodelling
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what type of cancer is xeroderma pigmentosum
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autosomal recessive CA-probs w genetic repair mechs
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in what vessels does the exudate occur
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post-capillary venules
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what percentage of patients have paraneoplastic syndromes associated with cancer
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10%
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