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60 Cards in this Set
- Front
- Back
5 cardinal signs of inflammation and explaination |
1. heat/hot: ↑ blood flow in affected area 2. redness 3. swell: ↑ bulk (gel-like) 4. pain: ↑ tension tissue 5. loss of function |
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healthy, physiological outcomes of inflammation |
-can be a defense mechanism -evolutionary term, inflammation is a protective system |
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How can inflammation can be harmful |
-life threatening: fill up of air spaces in lung -mechanical trauma: cutting/crushing -chemical injuries: produced by acid |
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Acute inflammation |
-onset: fast -cells: neutrophils -tissue: limited -physical sign: obvious |
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Chronic inflammation |
-onset: slow -cells: macrophages & lymphs -tissue: progessive -physical sign: subtle
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2 main components of inflammation: |
1. cellular: (leukocytes) accumulation of leukocytes at site of injury (migration) 2. vascular: vasodiliation, ↑ vascular permeability |
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Exudate |
↑ vascular permeability -mass of cell & fluid that has speed out of blood vessels or organs especially in inflammation |
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Transudate |
↑ hydrostatic pressure ↓ colloid osmotic pressure |
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6 types of exudate: |
1. serous exudate 2. fibrinous exudate 3. haemorrhagic 4. purulent 5. catarrhal 6. membrane & pseudomembranous |
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serous exudate |
↓ in protein fluid in blister |
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fibrinous exudate |
↓ volume & ↑ protein, -two surface covered in fibrin stick together to build bridge = scar tissue form = loss of function |
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Haemorrhagic exudate |
occur where small blood vessel severely damage that allow the escape of red cells from lumen into extravascular space. |
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Purulent exudate |
-neutrophil dominant -large # cells -liquefaction of dead tissue (fluid material pus)
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Catarrhal exudate |
occur when mucous membrane is inflammed |
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Membrane/Pseudomembranous exudate |
consist dead epithelial cells (fibrin+neutrophils) |
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Major cells in inflammation |
white cells, endothelial cells, neutrophils, eosinophils, basophils (mast cells) |
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mast cells release |
histamine |
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which cells control adhesion/migration of inflammation cells |
endothelial cells |
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neutrophils |
most # of cells that migrate to injured area in early stages of acute inflammation |
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eosinphils |
-promote inflammation -benefical when isolating/controlling disease site and ongoing inflammation |
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basophils |
release histamine, chemotactics factors, cytokins |
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Explain leukocyte recruitment (out of blood vessels into inflamed) |
1. injured/inflammed tissue 2. release chemicals 3. endothelial cells produce adhesion mol. in response to chemicals 4. white cells moving in blood 5. tether/roll 6. adhere 7. immune cell exit the blood vessel |
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Leukocyte |
white blood cells that fight of bacteria |
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3 steps in phagocytosis |
1. opsonization 2. engulfment 3. lysosomal fusion°ranulation |
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Opsonization |
-coat microbes & target them for opsonins -the microbes bind to phagocyte receptor - two proteins: IgG & C3b |
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Egulfment |
phagocyte membrane zips up around microbe |
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Lysosomal fusion & degranulation |
break down |
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phagocytosis |
it keeps bacteria foreign bodies away from other parts of cell and packs it up then kill it |
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Vasoactive amines |
-histamine -serotonin |
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Histamine: |
-↑ vascular premeability = swelling -↑ inflammatory responses -hot, red, swollen = cause small blood vessels in -tissue to expand/dilate/leak -allow protective blood proteins + WBCs to leave vessels & start repair. |
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Serotonin: |
↑ blood pressure = constriction blood vessels (vasoconstriction) |
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Complement system: |
-opsinzation -w/infection system activated, lead sequence of events on surface of pathogen and destroy/eliminate infection. |
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4 major functions of inflammation in complement system: |
C3a and C5a - mast cell release histamine C3b - bind to cells to tag phagocytosis C3a - recruit/activate WBCs C5b-C9 - forms MACS & lyses microbes |
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Kinin System: |
-serious of enzymes leading to conversion of plasma precursors into active polypeptides -dilation of blood vessels -bradykinin agent produce vascular dilation, ↑ vascular permeability |
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Coagulation system: |
-thrombin: fibrin clots + endothelial activation |
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products of arachidonic acid breakdown: |
-mediate inflammatory reactions -fatty acid (responsible for inflammation in muscle tissue)
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Arachidonic acid breakdown example |
working out, muscle damage, certain enzymes flock toward affected area and free ARA from membrane. |
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acute phase proteins: |
-↑ conc. in plasma during inflammation -iron-storage protein that measure iron status -plasma protein |
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IL-8: (protein mediator) |
some attract neuclophils that attact monocytes |
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chemokine alpa: |
produced by monocytes, some T lymphocytes, endothelial cells, platelets |
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IL1: (protein mediator) |
-induce fever -↓ blood pressure
-release prostagladins -collagenas -acute phase proteins |
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TNF alpha: (protein mediator) |
-fambam of ligands -host defense against infections -a cytokine produced in greatest amount by stimulated macrophages
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process of mast cell in tissue to be released |
1. surface coated with receptors 2. cytoplasm loaded with granules containing mediators of inflammation 3. receptor outside bind w/ligand & trigger exocytosis of granules (move outside of mast cell) |
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key players in initiation of inflammation: |
mast cells |
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what activates recruiting: it recruits what? |
-mediators
-neutrophils, lymphocytes (B T cells), eosinophils |
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TNF alpha cause:
lead to:
what kind of protein is it: |
-excessive inflammation
-lead to pain and tissue damage
-signaling protein |
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chemokines with adhesion molecules cause what in inflammatory: |
directional migration of leukocytes in inflammatory |
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Reactive Oxygen Species (ROS) produced by: |
activated phagocytes: neutrophils + macrophages |
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ROS lead to:
damages: |
-tissue injury
-other molecules and cell structure they're part of |
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3 examples of ROS molecules: |
1. hydrogen peroxide ions 2. hydroxyl radicals 3. superoxide (anion + ion) |
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ROS are good too because: |
the macrophages and neutrophils must generate to kill bacteria engulfed by phagocytosis (and they're released during macro+neu activated). |
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3 roles of exudate: |
1. dilution 2. bacterial killing by antibody and complement 3. localization |
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Bradykinin relaxes: |
smooth muscle walls of arterioles |
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Bradykinin ↑ and ↓ what:
Bradykinin is like: |
- blood flow to tissue (make red/swollen)
-blood pressure
-histamine |
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precursor: |
compound that participate in chem rxn that makes another compound. |
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how do hageman factor make bradykinin: |
1. HF circulate blood inactive precursor 2. tissue damage, blood escape into tissue space 3. HF contact collagens inside space = actived 4. HF start cleaving prekillikrein into killinkrein 5. kallikrein cleaves kininogen forming bradykinin |
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acute inflammation responds by (3): |
1. isolating damaged area 2. mobilizing effector cells/mols to site even if later 3. promote healing |
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Abcess formation: |
1. center: liquefied dead tissue mixed with remain of dead neutrophils 2. fibrin & living neutrophils present 3. healthy part, proliferating fibroblasts, young collagen fibers (repair process) |
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in abcess, what's good about the outer layer: |
this zone is a barrier so no more inflammation spreads |
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ulcers: |
-local defect in epithelial surface cause by shedding of dead epithelial cells |