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21 Cards in this Set
- Front
- Back
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What are the main morphological characteristics of acute inflammation?
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- Can be measure in minutes to days
- Main features are fluid exudation and neutrophil emigration |
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What are 5 initiators of inflammation?
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1. Infection
2. Injury 3. Foreign body 4. Neoplasm 5. Autoimmune |
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What vascular changes are observed in acute inflammation?
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1. Arteriolar vasodilation - swelling, increased blood flow
2. Increased permeability - becomes "leaky" 3. Stasis/congestion - blood slows down 4. Leukocyte margination - WBC's "line up" at periphery All designed to bring fluid and leukocytes to area of injury! |
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What is the main way that vessels become leaky during acute inflammation?
What mediators is it induced by? |
Endothelial cell contraction
- Induced to contract by chemical mediators such as HISTAMINE, BRADYKININ, and LEUKOTRIENES - Short lived response, <24hrs |
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What are the 5 ways that vessels can become leaky?
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1. Endothelial contraction
2. Direct injury 3. Injury mediated by inflammatory cells 4. Transcytosis 5. Leakage from new vessel formation |
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What factor mediates transcytosis (increased transport across membrane) and allows vessels to be more permeable?
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VEGF (vascular endothelial growth factor)
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What is an edema?
Effusion? |
Edema: accumulation of fluid within extravascular compartment or interstitial tissues
Effusion: Excess fluid in body cavities/potential space - Serous effusion: cell poor, clear/straw color - Serosanguinous effusion: serous, but with RBC's (red tinge) |
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What are the 2 types of effusions (not serous/serosanguinous)?
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1. Transudate - clear/less dense. Often seen in non-inflammatory conditions (ie not infected).
2. Exudate (pus) - thick/milkshake-like. Has presence of protein and even blood cells |
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What is serous inflammation characterized by?
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Characterized by the outpouring of thin fluid, relatively protein and cell poor.
- An example would be a BLISTER secondary to a mild burn - Often seen where vascular injury would be slight |
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What is fibrinous inflammation characterized by?
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- Larger molecules (fibrinogen) pass through injured endothelium
- Can resolve (removal of fibrin by macrophages) - Can organize (ingrowth or fibroblasts and vessels), may lead to scarring and organ dysfunction |
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What are the characteristics of suppurative (purulent/exudative) inflammation?
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- Pus (purulent exudate), composed or neutrophils, edema fluid, necrotic cells
- ABSCESS - focal collection of pus. Typically have central necrosis, surrounding zone of vascular and fibroblastic proliferation |
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What are the characteristics of an ulceration inflammation?
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- site of inflammation where an epithelial surface has become necrotic and eroded
- often associated with subepithelial acute and chronic inection |
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What are the 3 important cellular events in inflammation?
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1. Leukocyte emigration
2. Chemotaxis 3. Leukocyte activation |
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What are the 4 steps in emigration of leukocytes from the vasculature?
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1. Rolling - tumbling down endothelial surface
2. Adhesion - sticking firmly to endothelium 3. Transmigration - leaving vasculature 4. Chemotaxis - migrating toward chemoattractants |
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What chemical mediators aid in Rolling of leukocytes?
Firm Adhesion? |
Rolling: Selectins. E-selectins expressed by endothelium in response to inflammatory response. E-selectins bind leukocytes
Adhesion: Integrins |
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What are 4 major examples of chemoattractants for leukocytes after they exit the vasculature?
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1. N-formylmethionine (a bacterial wall product)
2. Complement component C5a 3. Leukotriene B4 4. Chemokines |
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What is an oxidative burst?
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The process in a phagocyte whereby oxygen gets converted to H2O2 and then MPO converts H2O2 to HOCl-
Done to kill engulfed pathogen |
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What are 3 oxygen independent pathways that leukocytes have to kill bacteria?
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BPIP (bactericidal permeability increasing protein) - increases bacterial membrane permeability
Lysozyme - degrades bacterial membrane Major Basic Protein - found in eosinphils, important in killing parasites |
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What is Chediak-Higashi syndrome?
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- Defect in phagolysosome formation
- See giant neutrophil granules - Patients have susceptibility to infections |
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What are 3 interrelated plasma derived mediators that play key roles in inflammation?
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1. Complement (C3a/C5a)
2. Clotting System 3. Kinins (Bradykinin- causes pain) |
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What is the role of C3a/C5a?
C3b? |
C3a/C5a = anaphylatoxins (act on mast cells) and chemotaxis
C3b = opsonin |
