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35 Cards in this Set

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