ACUTE INFLAMMATION
– Acute inflammation is rapid in onset and of short duration, lasting from a few minutes to as long as a few days,
– characterized by fluid and plasma protein exudation
– And a predominantly neutrophils leukocyte accumulation.
Components Of Acute Inflammation
Vascular changes
– Vasodilation
– increased vascular permeability
Cellular events
– cellular recruitment (emigration of leukocytes to injury).
– (polymorphic nuclear leukocytes) Neutrophils (1st responder)
Stimuli for Acute Inflammation
– Infections (bacterial, viral, fungal, parasitic)
– Trauma (blunt and penetrating) and various physical and chemical agents
– Tissue necrosis including ischemia and physical and chemical injury
– Foreign bodies (splinters, dirt, sutures, crystal deposits)
– Immune reactions (also called hypersensitivity reactions) against environmental substances or against “self” tissues.
Recognition of Microbes, Necrotic Cells, and Foreign Substances
– Phagocytes, dendritic cells (cells in connective tissue and organs that capture microbes and initiate responses to them), and many other cells, such as epithelial cells, express receptors that are designed to sense the presence of infectious pathogens and substances released from dead cells. These receptors have been called “pattern recognition receptors” because they recognize structures (i.e., molecular patterns) that are common to many microbes or to dead cells.
– The two most important families of these receptors are the following
– Toll-like receptors (TLR) are microbial sensors that are named for the founding member called Toll, which was discovered in Drosophila.
– The inflammatory is a multi-protein cytoplasmic complex that recognizes products of dead cells, such as uric acid and extracellular ATP, as well as crystals and some microbial products.
Vascular Changes
Vascular Changes
– The main vascular reactions of acute inflammation are
– increased blood flow secondary to vasodilation and increased vascular permeability,
– both designed to bring blood cells and proteins to sites of infection or injury.
Changes in Vascular Caliber and Flow
– After transient vasoconstriction (lasting only for seconds),
– arterioles vasodilation, resulting in locally increased blood flow and engorgement of the down-stream capillary beds, causing the redness (erythema) and warmness.
– The micro vasculature becomes more permeable,
– protein-rich fluid moves into the extra vascular tissues, causes the red cells in the flowing blood to become concentrated, thereby increasing blood viscosity and slowing the circulation, called stasis.
– After stasis develops,
– Leukocytes begin to accumulate along the vascular endothelial Surface, called marination.
Increased Vascular Permeability
– Endothelial cell contraction leading to intercellular gaps in post capillary values
– (short-lived, 15 to 30 minutes after binding of histamine, Brady kin in, prolonged retraction from changes in the cytoskeleton, induced by cytokines i.e. (TNF) and interleukin-1 (IL-1) persisting for 24 hours)
– Endothelial injury results in vascular leakage by causing endothelial cell necrosis and detachment.
– Increased Endocytosis of proteins by way of an intracellular vesicular pathway augments annular permeability, especially after exposure to certain mediators such as (VEG F).
– Leakage from new blood vessels. These vessel sprouts remain leaky until proliferating endothelial cells mature sufficiently to form
– intercellular junctions. Also having increased expression of receptors for vocative mediators, (e.g., VEG F).
Responses of Lymphatic Vessels
– Lymph flow is increased and helps drain edema fluid, leukocytes, and cell debris from the extra vascular space.
– The lymphatics may become secondarily inflamed, as may the draining lymph nodes.
– Inflamed lymph nodes are often enlarged because of hyperplasia of the lymphoid follicles and increased numbers of lymphocytes and Phagocytes cells
– lining the sinuses of the lymph nodes
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