M1: Acute & Chronic Inflammation Flashcards
Cell death
Necrosis
Protective response to rid the initial cause of cell injury. Complex reactions of both blood vessels and leukocytes.
Inflammation
Fluid portion of the blood
Plasma
Body’s principal defenders against foreign invaders
Plasma proteins, Circulating leukocytes & Tissue phagocytes “PCT”
Protein is primarily synthesized in what organ
Liver
Triggers the vascular & cellular reaction
Soluble factors
Blood component, polymorphonuclear cell, responsible for Acute Inflammation.
Neutrophil
Blood component responsible for Chronic Inflammation
Macrophage & Leukocyte
Primarily from B Lymphocytes
Plasma cells
Elimination of offending agent is achieved by
Termination of Inflammation
Blood component that has a short lifespan in tissues
Leukocytes
Repair of damage tissue/cell. Example is abrasion of skin.
Regeneration
Filling of the defect with fibrous tissue
Scarring
Produce by fibroblast
Collagen
Hardening of the blood vessels
Atherosclerosis
Cardinal signs of an Infection
Rubor, Tumor, Calor, Dolor & Functio Laesa
Cardinal sign: redness
Rubor
Cardinal sign: pain
Dolor
Cardinal sign: loss of function
Functio Laesa
Cardinal sign: heat
Calor
Cardinal sign: swelling
Tumor
Rapid host response that serves to deliver leukocytes and plasma proteins. Early onset, involving fluid exudation and polymorphonuclear cell immigration.
Acute Inflammation
Two main components of Inflammation
Vascular wall response & Inflammatory response
Later onset and longer duration involving lymphocytes and macrophages, with blood vessels proliferation and fibrosis.
Chronic Inflammation
Calor is due to
Vascular dilatation
Rubor is due to
Vascular dilatation & Congestion
Tumor is due to
Increased vascular permeability
Dolor is due to
Mediator release
Functio laesa is due to
Pain, Edema, Tissue injury or scar
Three major components of Acute Inflammation: 1. Alterations in _____________, leading to increased blood flow.
Vascular caliber
Three major components of Acute Inflammation: Structural changes in the ________, permitting plasma proteins and leukocytes to leave the circulation to produce inflammatory ________.
Microvasculature. Exudates.
Three major components of Acute Inflammation: ___________ from blood vessels and accumulation of the site of injury with activation.
Leukocyte emigration
Stimuli for Acute Inflammation
Tissue necrosis, Infection & Microbial toxin “TIM”
Detects bacteria
Toll-like Receptors
Tissue necrosis is due to
Ischemia
Produced by cells deprived of O2 & activates transcription of many genes involved in inflammation
Hif 1A
Reactions of Blood Vessels in Acute Inflammation
BV, Leukocytes & Termination “BLT”
Pathological term for leaky
Vascular Permeability
Is excess fluid in interstitial tissue or body cavities
Edema
Is an inflammatory, extravascular fluid with cellular debris and high protein concentration. Specific gravity of 1.020 or more.
Exudate
Is excess, extravascular fluid with low protein content. It is essentially an ultrafiltrate of blood plasma resulting from elevated fluid pressures or diminished plasma osmotic forces. Specific gravity of 1.012 or less.
Transudate
Is a purulent inflammatory exudate rich in neutrophils and cell debris
Pus
Normal fluid exchange in vascular beds depends on an intact
Endothelium
Normal fluid exchange are modulated by two opposing factors
Hydrostatic pressure & Plasma colloid osmotic pressure
Causes fluid to move into the capillaries
Plasma colloid osmotic pressure
Causes fluid to move out of the circulation
Hydrostatic pressure
Yellowish & Turbid. Escape of fluid, CHONs & cells from the vascular system into the interstitial tissue or body cavities. Inflammatory edema. Increase protein with cellular materials.
Exudate
Increase HP & Decrease OP causing transudate
Edema
Clear, less hazy & cloudy. Non inflammatory edema. Decreased protein. Little or non cellular material. An ultrafiltrate plasma.
Transudate
One of the earliest manifestations of Acute Inflammation. Increase blood flow. Followed by Increase permeability of the microvasculature.
Vasodilation
Mediates Vasodilation
Histamine & Nitric Oxide
Lining of a vessel
Endothelium
Increases when there is vasodilation
Hydrostatic pressure
Combination of vascular dilation and fluid loss leads to
Increased blood viscosity & concentration of RBCs
Slow movement of erythrocytes
Stasis