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Inflammation. Etiology. Vascular Changes. Cellular Events in Inflammation. Acute Inflammation. Morphologic Patterns
Inflammation. Etiology. Vascular Changes. Cellular Events in Inflammation. Acute Inflammation. Morphologic Patterns
Inflammation. Etiology. Vascular Changes. Cellular Events in Inflammation. Acute Inflammation. Morphologic Patterns
Acute inflammation.
Morphologic patterns.
Questions
Inflammation. Definition. Basis. Etiology
and pathogenesis. Nomenclature.
Acute inflammation: tissue response.
Mediators in acute inflammation.
Type of cells in the focus of acute
inflammation. Consequences of acute
inflammation.
Patterns of acute inflammation.
Inflammation
A protective response intended to eliminate
the initial cause of cell injury as well as the
necrotic cells and tissues resulting from the
original insult.
Exudates
increased vascular permeability allows
plasma proteins and leukocytes to enter
sites of infection or tissue damage;
fluid leak through blood vessels results in
edema.
Exudates v/s transudates
Exudate - in inflammation because of
increased vascular permeability as a
result of increased interendothelial
spaces.
Transudates - when fluid leaks out
because of increased hydrostatic
pressure or decreased osmotic pressure.
Responses of Lymphatic Vessels
C1q (collectins).
Leukocyte Activation
Stimuli for activation
microbes, products of necrotic cells, and several
mediators
Leu express on their surface different kinds of receptors and
engagement of these receptors by microbial products or by
various mediators of inflammation induces leukocyte activation
Leukocyte functions:
Phagocytosis of particles
an early step in the elimination of harmful substances.
Production of substances that destroy phagocytosed
microbes and remove dead tissues
lysosomal enzymes and reactive oxygen and nitrogen species.
Production of mediators that amplify the inflammatory
reaction- arachidonic acid metabolites, cytokines.
Leukocyte Effector Mechanisms
5HT, 5-Hydroxy-
Tryptamine)
Platelets and
Enterochromaffin Cells
Vasoactive mediator, with
effects similar to those of
histamine
Evokes NO synthetase
Arachidonic Acid (AA) Metabolites
(EICOSANOIDS)
Affect a variety of biologic processes, including
inflammation and hemostasis.
Leukocytes, mast cells, endothelial cells, and platelets are the
major sources of AA metabolites in inflammation.
= Products derived from the metabolism of AA
AA is a 20-carbon polyunsaturated fatty acid, a component
of cell membrane phospholipids.
It is released from these phospholipids via cellular phospholipases,
activated by mechanical, chemical, or physical stimuli, or by
inflammatory mediators (C5a).
AA metabolism - 2 enzymatic pathways:
Cyclooxygenase ⇒ prostaglandins and thromboxanes,
lipoxygenase ⇒ leukotrienes and lipoxins
Metabolites
(EICOSANOIDS)
Effects
Prostaglandins, thromboxanes
Pain, fever, clotting
Leukotrienes
Chemotaxis, vasoconstriction, increased
Permeability
Lipoxins
Inhibit chemotaxis, vasodilatation, counteract
actions of leukotrienes
Platelet-Activating Factor (PAF)
Lysozyme (Bact.)
Acid Hydrolases
Lactoferrin
Lysozyme
Alkaline Phosphatase
Coagulation proteins
Activated factor XII triggers the clotting, kinin and
complement cascades, and activates the fibrinolytic
system, production of fibrin
Kinins (bradykinin)
Produced by proteolytic cleavage of precursors;
increased permeability, Smooth muscle contraction
(non vascular), pain
COMPLEMENT SYSTEM
>20 components, in circulating plasma
Plays an important role in host defense
(immunity) and inflammation
Upon activation, different
extensive “cascade”
Outcomes of acute
inflammation
Resolution,
Healing by scarring
(fibrosis),
Chronic
inflammation
Outcomes of acute
inflammation
Resolution of inflammation
when the injury is limited or short-lived and
there has been no or minimal tissue damage,
when the tissue is capable of replacing any
irreversibly injured cells
Termination of the acute inflammatory
response involves:
neutralization, decay or enzymatic degradation
of the various chemical mediators, normalization
of vascular permeability, cessation of leukocyte
emigration, death (by apoptosis) of extravasated
neutrophils.
leukocytes produce mediators that inhibit
inflammation and thus limit the reaction
lymphatic drainage and macrophage ingestion of
necrotic debris lead to the clearance of the
edema fluid, inflammatory cells, and detritus
Outcomes of Acute Inflammation