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35 Cards in this Set
- Front
- Back
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3 components of inflammation
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Vascular changes
Migration and activation of leukocytes Systemic reactions |
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Unique feature of inflammation
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Reaction of blood vessels leading to accumulation of fluid and leukocytes in extravascular tissues
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Two main components of inflammation
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Vascular and cellular response
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Describe acute inflammation
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Rapid in onset
Short duration Exudation of fluid and plasma proteins (edema) Emigration of leukocytes (neutrophils) |
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Describe chronic inflammation
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Long in duration
Presence of macrophages and lymphocytes |
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3 major components of acute inflammation
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1. Vasodilation which leads to increased blood flow
2. Increased vascular permeability that allows plasma proteins and leukocytes to leave circulation 3. Emigration, accumulation and activation of leukocytes |
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Exudate vs transudate
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Exudate - high protein
Transudate - low protein |
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Pus
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Purulent exudate - high in neutrophils, debris of dead cells, microbes
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Stimuli for acute inflammation
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-Infections
-Trauma (blunt and penetrating) -Physical and chemical agents -Tissue necrosis -Foreign bodies -Immune reactions |
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Describe changes in vascular flow
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First, transient constriction of arterioles (few seconds)
Vasodilation first involves arterioles only, then opening of new capillary beds - heat and redness |
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Stasis
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Slower blood flow
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Most common mechanism of vascular leakage
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Formation of endothelial gaps in venules, caused by chemical mediators (histamine, bradykinin) - immediate transient response
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Name mechanisms of vascular permiablity
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1. Contraction of endothelial cells - increasing gaps
VENULES only 2. Direct injury - arterioles, capillaries and venules, toxins, burns, chemicals, fast but may last longer 3. Leukocyte dependent injury - leukocytes adhere to endothelium, release ROS - venules + pulmonary capillaries 4. Delayed prolonged leakage - appears after delay and lasts longer - late appearing sunburn 5. Increased transcytosis - venules only - VEGF 6. Leakage from new blood vessels |
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Sequence of events for leukocyte extravasation
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1. In lumen - margination, rolling, adhesion to endothelium
2. Transmigration across endothelium - DIAPEDESIS 3. Migration in interstitial tissue toward chemotactic factor |
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Describe exogenous and endogenous chemoattractants
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Endogenous - C5a, LTB4, cytokines
Exogenous - bacterial products |
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3 steps of phagocytosis
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-Recognition and attachment
-Engulfment -Killing |
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Defects in leukocyte adhesion
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LAD1 - recurrent bacterial infections and delayed wound healing
LAD2 - milder form of LAD 1 |
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Chediak Higashi syndrome
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Defect in phagolysosome function
Neutropenia Defective degranulation Delayed microbial killing |
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Most frequent cause of leukocyte deficit
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Bone marrow suppression
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Name two vasoactive amines
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Histamine and serotonin
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What produces histamine
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Mast cells (also basophils and platelets)
Histamine is preformed and released from mast cells in response to physical injury (cold, heat), immune reactions, anaphylotoxins (C3a and C5a), neuropeptides and cytokines |
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Main action of histamine
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Dilate arterioles
Increase permeability of venules Constricts large arteries |
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Serotonin is released from
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platelets
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Which complement is powerful chemotactic agent
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C5a
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C5-C9
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MAC - membrane attack complex
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Anaphylotoxins
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C3a + C5a
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Opsonin
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C3b
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Action of bradykinin
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Vascular permeability
Smooth muscle contraction Dilation of blood vessels Pain |
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Eicosanoids produced by
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Cyclooxygenase - prostaglandin + thromboxane
Lipooxygenase - leukotrienes + lipoxins |
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What inhibits cyclooxygenase
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Aspirin
NSAID |
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Two major cytokines
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TNF + IL1
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3 outcomes of acute inflammation
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1. Complete regeneration
2. Healing by fibrosis 3. Chronic inflammation |
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Morphological patterns of inflammation
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Serous
Fibrinous Purulent Ulcers |
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Best example of purulent inflammation
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Appendicitis
Abscess |
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Prototype of granulomatous disease
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TB (central caseous necrosis)
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