Chapter 3 - Acute and Chonic Inflammation; Tissue Repair Flashcards
Response of vascularized tissues to infections and tissue damage
Inflammation
Mediators of defense
Phagocytic leokocytes, antibodies, and complement proteins
Inflammatory reaction steps
- Offending agent recognized by host cells
- Leukocytes and plasma proteins are recruited to the site of the offending agent
- Eliminate the offending agent
- Reaction controlled and terminated
- Repair
Main characteristics of acute inflammation
Edema
Emigration of leukocytes predominantly neutrophils
Cells that detect presence of infection
Macrophage
Dendritic cells
Mast cells
T/F: Inflammatory mediators are also produced by plasma proteins
True
External manifestations or cardnal signs of inflammation
Swelling (tumor) Pain (dolor) Heat (calor) Redness (rubor) Loss of function (functio laesa)
Father of modern pathology
Rudolf Virchow
also discovered functio laesa
Causes of Inflammation
Infections
Tissue necrosis
Foreign bodies
Immune reactions
Toll like receptor
Located in plasma membrane and endosomes
Detect microbes
Recognize motifs called pathogen-associated molecular patterns (PAMP)
Receptors that recognize molecules which are liberated or altered as a consequence of cell damage or DAMP
Cytosolic receptors
Cytosolic receptors activate a complex called
Inflammasome
Inflammasome induces production of
Cytokine interleukin-1 (IL-1)
What is IL-1
Activated by inflammasomes
Induces inflammation by recruiting leukocytes
Circulating protein that recognized microbial sugars, promotes ingestion of microbes and activates complement system
Mannose-binding lectin
Circulating proteins that bind to microbes and promote phagocytosis
Collectins among others
Three major components of inflammation
Dilation of small vessels: increased blood flow
Increase permeability of microvasculature
Emigration of the leukocytes
Vascular reactions of acute inflammation
Changes in blood flow
Permeability of vessels
Escape of fluid, protein, and blood cells from the vascular system to the interstitial tissues
Exudation
Extravascular fluid that has high protein concentration and contains cellular debris
Exudate
Fluid with low protein content, little or no cellular material, low specific gravity
Transudate
What does an exudate indicates?
Increase in permeability of small blood vessels
What does a transudate indicate?
Ultrafiltrate of blood plasma
Result of osmotic or hydrostatic imbalance across vessels with normal permeability
Denotes excess of fluid in the interstitial tissue
Edema
Exudate rich in leukocytes, debris of dead cells, and microbe
Pus
TF: Vasodilation may be preceded by vasoconstriction
True
Vasodilation involves what blood vessels
Arterioles the opening of capillary beds
Vasodilation is followed by
Increased permeability of the microvasculature and outpouring of exudate
Acute Inflammation: Loss of fluid and increased vessel diameter lead to
Slower blood flow
Conentration of red cells in small vessels
Increased viscosity
Which then results to:
Stasis of blood
Vascular congestion
Erythema
AI: Mechanisms responsible for increased vascular permeability
Retraction of endothelial cells
Endothelial injury
Transocytosis
AI: Retraction of endothelial cells after exposure occur within how many minutes
15 - 30mins
AI: referred to as the immediate transient response
Retraction if endothelial cells
AI: main site for rapid increase in vascular permeability
Postcapillary venules
