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41 Cards in this Set
- Front
- Back
?- white cell assume a peripheral position along the endothelial surface |
Margination |
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- leukocytes tumble slowly along the endothelium and adhere transiently
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Rolling |
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- the endothelium is lined firmly by white cells ( resembling pebbles over which a stream runs without disturbing them ) |
Pavementing |
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in most forms of acute inflammation, neutrophils predominatein the inflammatory infiltrate during the first 6-24 hours, then are replaced by monocytes in 24-28 hours
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Leukocyte Adhesion & Transmigration- |
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- in most forms of acute inflammation, neutrophils predominatein the inflammatory infiltrate during the first 6-24 hours, then are replaced by monocytes in 24-28 hours
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Leukocyte Adhesion & Transmigration- |
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Why ? first? → they are more numerous in the blood → they respond more rapidly to chemokines → they attach more firmly to the adhesion molecules |
neutrophils |
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certain infxns have different pattern of cellular exudation |
Leukocyte Adhesion & Transmigration- |
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- neutrophils predominate over 2-4 days |
Pseudomonas infxn |
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- lymphocytes first |
Viral infxns |
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some hypersensitivity reaction - ? are the main cell type |
eosinophils |
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- after extravasation, leukocytes emigrate in tissues toward thesite of injury by a process called |
CHEMOTAXIS |
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defined as locomotion oriented along a chemical gradient |
CHEMOTAXIS |
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- the chemoattractants could be exogenous or endogenous |
CHEMOTAXIS |
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• Exogenous chemoattractants • Endogenous chemoattractants |
CHEMOTAXIS |
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- bacterial products most common |
Exogenous chemoattractants |
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1. components of the complement system, particularly C5a 2. products of the lipooxygenase pathway, mainly leukotriene B4 (LTB4) 3. cytokines |
Endogenous chemoattractants |
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- the efficiency of phagocytosis is greatly enhanced when microbesare opsonized by specific proteins (opsonins) for w/c thephagocytes express high-affinity receptors |
Phagocytosis |
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the major opsonins are : IgG antibodies the C3b breakdown products plasma lectins |
Phagocytosis |
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the 2 most important are: Mast cells Tissue macrophages |
Phagocytosis |
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- complement proteins- kinins |
Plasma-derived mediators |
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are normally sequestered in intracellular granulesthat need to be secreted (e.g. histamine in mast cells) |
Cell-derived mediators |
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or are synthesized de novo (e.g. prostaglandins, cytokines) in response to a stimulus |
Cell-derived mediators |
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- is marked by the outpouring of a thin fluid |
SEROUS INFLAMMATION |
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- is derived from either the plasma or the secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities (called effusion) |
SEROUS INFLAMMATION |
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- the skin blister resulting from a burn or viral infection represents a large accumulation of serous fluid |
SEROUS INFLAMMATION |
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- w/ more severe injuries & the resulting greater vascular permeability larger molecules such as fibrinogen pass the vascular barrier |
FIBRINOUS INFLAMMATION |
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- & fibrin is formed & deposited in the extracellular space |
FIBRINOUS INFLAMMATION |
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-is charac. of inflammation in the lining of body cavities, such as the meninges, pericardium & pleura |
FIBRINOUS INFLAMMATION |
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- charac. by the production of large amounts of pus or purulent exudate consisting ofcertain bacteria (e.g. staphylococci) produce this localized suppuration
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SUPPURATIVE OR PURULENT INFLAMMATION |
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- are localized collections of purulent inflammatory tissue caused by suppuration buried in a tissue / organ |
ACUTE AND CHRONIC INFLAMMATIONABSCESS |
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- is a local defect, or excavation, of the surface of an organ or tissue that is produced by sloughing (shedding) of inflammatory necrotic tissue |
ULCERS |
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- occur only when tissue necrosis exist on or near a surface |
ULCERS |
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- commonly encountered in: mucosa of the mouth, GIT & genitourinary tract subcutaneous tissue |
ULCERS |
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- is an inflammation of prolonged duration (weeks or months) in w/c active inflammation tissue destruction attempts at repair are proceeding simultaneosly |
CHRONIC INFLAMMATION |
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- arise in the following settings (causes): • Persistent infections • Prolonged exposure to potentially toxic agents (exogenous or endogenous) • Autoimmunity |
CHRONIC INFLAMMATION |
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- Morphologic features are: infiltration with mononuclear cells |
CHRONIC INFLAMMATION |
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- Morphologic features are: tissue destruction, induced by persistent offending agentor by the inflammatory cells |
CHRONIC INFLAMMATION |
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- Morphologic features are: attempts at healing by connective tissue replacement of damaged tissue, accomplished by proliferation of small bld vessels (angiogenesis) &, in particular, fibrosis |
CHRONIC INFLAMMATION |
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- the dominant cellular player in chronic inflammation |
Macrophage |
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- derived from blood monocyte |
Macrophage |
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- secrete a variety of biologically active products |
Macrophage |