Catriona McLean; Week 8 MED1011; Pathology
Acute inflammation is reaction to tissue injury. Vascular component is a dilation of vessels, exudative component is vascular leakage of protein rich fluid; neutrophils are recruited in the third stage. This leads to resolution, suppuration, organisation and progression to chronic inflammation. Causes of inflammation can be infection (pyogenic bacteria, viruses), physical agents (trauma, heat, cold, ionising radiation), chemicals (acids, corrosives, alkalis), tissue necrosis, ischaemic infarction, hypersensitivity reactions.
Macroscopic appearances are redness from dilated vessels, heat from increased blood flow and systemic fever, swelling, pain and loss of function. Early stages of acute inflammation include changes in vessel calibre and flow, increased permeability and formation of fluid (exudate). Formation of cellular exudate allows migration of neutrophils into the extravascular space.
Vessel calibre changes. Arteriole regulates flow from artery to venule, allows axial and plasmatic flow. There is a triple response to changes in microcirculation. Momentary white line is vasoconstriction, flush is capillary reaction secondary to relaxation of capillary sphincters, flare is irregular red zone around the area related to arteriolar dilation, lasts 15 minutes to hours. Wheal is a zone of oedema that develops around the site as a result of fluid exudation into extravascular space.
Small vessels act as microfilters, water and solutes move in by ultrafiltration and large molecules and cells do not move in. These move through the fenestrae. Fluid moves out at the arteriolar end of the capillary and fluid moves back in at the venous end of the capillary. Hydrostatic pressure controls the movement of blood in and out of the vessel, and oncotic pressure is controlled by plasma proteins. In acute inflammation capillary hydrostatic pressure increases, plasma proteins in extravascular space increases and lowers vessel oncotic pressure, outflow of proteins leads to exudate, larger molecules in the extravascular space such as immunoglobulins can change hydrostatic pressure.
Fenestrae are caused by actin filaments in cells, are increased or decreased from direct injury to endothelial cells, chemical mediators are released (effect is tissue dependant) which change permeability. Neutrophils play a large part in acute inflammation, margination occurs due to flow change, adhesion of neutrophils to endothelial walls and emigration into the extravascular space. Granules contain myeloperioxidase, alkaline phosphatase and lysozyme. Its role is chemomediated movement, adhesion, phagocytosis (aided by opsonisation and release of lysosymes), and killing of organisms (oxygen dependent with catalase and independent with lysosomes). Later stages of acute inflammation include chemotaxis of neutrophils, chemical mediators causing vasodilation, emigration of neutrophils, chemotaxis, increased vascular permeability and itching and pain.
Histamine has an immediate effect when released from mast cells, causes vasodilation and increased permeability; lysosomal compounds are from neutrophils, increase permeability and activation of complement. Prostaglandins cause permeability and platelet aggregation, leukotrienes are vasoactive, serotonin is a vasoconstrictor. Different types of chemokines attract leukocytes. Plasma factors controlling cascade systems also have an effect.
Acute inflammation can cause pericarditis (protein rich exudate eg of inflammation of peritoneal surface), suppurative inflammation is neutrophil rich eg abscess formation. Inflammation can cause dilute toxins, entry of effector cells, entry of antibodies, fibrin formation/trapping, delivery of nutrients, stimulation of immune response. Harmful effects are digestion of normal tissues, swelling, inappropriate reaction.
Sequelae can be resolution with minimal damage, suppuration (abscess formation), organisation (repair process), progression to acute inflammation.