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31 Cards in this Set
- Front
- Back
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When does inflammation occur? |
It is the early protective response to injury, and aids in removing pathogen/ insult. Also initiates cell repair and remove necrotic cells. |
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Acute inflammation: 1. Time 2. Triggers |
1. Minutes to hours 2. Infections (bacterial, viral, ectoparasites), tissue damage, ischemia, foreign bodies, burn/ chemical, primary immune reactions |
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Physical signs of inflammation? |
PRISH
Note: not all symptoms may be present - depends on location and pain receptor threshold |
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Explain how vasodilation occurs: |
Histamine and nitric oxide cause dilation Starts from arteriole > capillary > venule Stasis occurs when enlarged vessels pack with cells, to help leukocytes reach endothelium |
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Explain how vascular permeability occurs: |
Occurs for only 15-30 minutes. Mediated by histamine, leukotrienes, bradykinin, neuropeptide substance P to cause endothelial cell contractions (increase space between cells)
Antibodies and fribin (clotting) can move through endothelium into tissue. Edema is aused by increased fluid in tissues. |
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How can inflammation occur in the endothelium? (3) |
1. Immediately by physical injury 2. Delayed by chemical or irradiation 3. Leukocyte - cytotoxic degranulation |
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What are the symptoms of the triple Response of Lewis? |
It is a histamine based reaction.
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In acute inflammation, which leukocytes are recruited to the site of injury? |
6-24 hours post injury: neutrophils 24-48 hours post injury: monocytes, lymphocytes (sometimes eosinophils) |
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What are the steps involved in having leukocytes move from blood vessel to site of injury? (5) |
1. Margination (leukocytes move to endothelial surface) 2. Rolling (weak interactions and detachment) 3. Integrin activation and firm adhesion (ICAM and VCAM) 4. Transmigration (diapedesis) 5. Chemotaxis (to site of injury through IL-8, LTB4) |
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How is acute inflammation turned off? (3) |
1. Neutrophils die after 3 days 2. Chemical mediators degrade in body/ stopped production 3. Anti-inflammatory mediators produced (lipocins, IL-10, TGF-beta, resolvins and protectins from omega 3 fatty acids) |
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What is systemic inflammatory response syndrome (SIRS)? |
When a body infection leaves local tissue and enters circulation, systemic inflammation occurs and overwhelms the host + abnormal regulation by cytokines. This can result in organ dysfunction and failure. |
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What are characteristics for SIRS? (3) |
1. Fever pyrogens and generalized increase in prostaglandins (internal temperature threshold is reset) 2. Production of acute phase reactants (fibrinogen, c-reactive proteins, serum amyloid a, p) 3. Leukocytosis (increased leukocytes released from BM) |
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What are external and internal pyrogens? |
External : bacterial LPS Internal : IL-1, TNF |
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What are common symptoms of SIRS? (6)
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SMARTT
1. Tachycardia 2. Tachypnea 3. Rigors/ shivering 4. Anorexia 5. Somnolence 6. Malaise |
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When is SIRS diagnosed? |
When you have two or more of:
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Define: septicemia and bacteremia |
Sepsis caused by infection Septicemia - generic microoganism or toxins Bacteremia - by bacteria |
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Define: severe sepsis and septic shock |
Severe sepsis - sepsis with end organ damage Septic shock - severe sepsis with hypotension |
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What are outcomes of acute inflammation? (4) |
1. Resolution 2. Fibrosis - incomplete regeneration, result in scarring (no longer functional tissue) 3. Abscess formation (cavity containing pus) 4. Chronic inflammation (persistent, lasts days to years, dominated by macrophages in injured tissue with continuous release of cytotoxic compounds and tissue destruction) |
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How is chronic inflammation caused? (4) |
1. Prolonged infection (viruses, parasites, etc.) 2. Autoimmune disorders (rheumatoid arthritis) 3. Hypersensitivity reactions (asthma) 4. Toxic agents (silicosis, asbestosis) |
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What is the physiological responses of chronic inflammation? (4) |
1. Recruitment of innate and adaptive immune cells (monocytes, macrophages, lymphocytes, sometimes mast/ eosinophils) 2. Tissue degredation by cytotoxic immune cells 3. Fibrosis (scarring) 4. Angiogenesis (new blood vessels formed for help immune cell refruitment and tissue repair) |
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Function of eicosanoids? |
They are essential in inflammation and immunity.
*basically they do a lot of stuff, including vasodilation/ contriction, permeability, chemotaxis, etc |
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Types of acute phase proteins? |
Positive factors - increase during inflammation. Destroy/ inhibit microbes, negative feedback on inflammatory response, and increase clot production.
Negative factors - decrease during inflammation. Reserves/ saves amino acids for positive factor synthesis. |
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How are acute phase proteins produced? |
Produced in liver. Production stimulated by IL-1, 6, 8, and TNF-alpha. |
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How can you observe acute phase proteins? |
Positive factors - C-protein increase correlates with RBC sedimentation rate.
Negative factors - reduced serum albumun, transferrin, antithrombin |
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Function of the factor XII plasma mediator system? |
Factor XII (aka hageman factor) is a serine protease inactive during circulation.
Activates 3 plasma systems during inflammation:
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How is factor XII activated? |
But confirmational change by interactions with collagen, platelets, and basement membranes. |
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Define: granulomas inflammation |
Granulomas: defined lesions caused by persistent attempts to encapsulate infection or foreign bodies. Epitheloid cells - macrophage aggregation into epithelial like cells. |
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Define: fibrinous inflammation |
Scar formation by fibrinous exudate. Fibrin passes through large holes in permeable vessels, causing procoagulation signal - pseudomembrane sheets formed. |
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Define: purulent inflammation |
Inflammation caused by microorganisms make pus. May be found in abscesses. |
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Define: serous inflammation |
Collection of serous exudate causing blisters |
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Define: ulcerative inflammation |
Inflammation near epithelium, causing tissue loss from surface. Exposes dermis and is very painful due to exposed nerve endings. |
