Inflammation and repair has several phases. Each phase involves different biochemical mediators and cells that function together to capture and remove injurious agents from the inflammatory site(Huether & McCance 2000). Inflammation is nonspecific, meaning it has no memory like the immune system with antigen-specific. So inflammation stimulus occurs in the same manner even on the second exposure to the same stimulus. Acute inflammation is self-limiting and continues only until the threat to the host is eliminated which usually takes 8-10 days from onset to healing. If it takes longer than two weeks then it's consider as chronic inflammation (Huether & McCance 2000).
Acute Inflammatory Response:
Acute inflammatory response begins after cellular injury from trauma, oxygen or nutrient deprivation, genetic or immune defects, chemical agents, microorganisms, extreme temperature, and ionizing radiation. The vascular effects of inflammation are immediate unlike immune response which takes days to develop (Huether & McCance 2000). The University of Western Sydney 'Acute & Chronic Inflammation' handout (2010) explains that vasodilation occurs in vascular response where arteriolar dilates increasing hydrostatic pressure and contraction of endothelial cells which widen the junctions between endothelial cells. Then permeability of blood vessels increases, exudates plasma and blood cells into tissues where proteins leaks out and causing plasma moving into tissues resulting oedema (tumour & dolor). This raised blood viscosity in the vascular compartment.
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There are four stages of cellular response of acute inflammation: margination and pavementing of white blood cells, emigration, chemotaxis, and phagocytosis. Margination and pavementing is where leukocytes marginate to the vessel periphery, tumble on the endothelial surface, and transiently sticking along the way and rolling. Then leukocytes adhere to certain adhesion molecules before crawling between cells and through endothelial basement membrane into extravascular space (emigration). After leukocytes adehered, it moves towards the site of injury and anchor themselves to extracellular matrix (ECM) and pull the remainder of the cell. Neutorphils and macrophages normally circulate in the bloodstream and are stimulated by inflammation to migrate through vessel walls near an inflammatory lesion. Neutrophils predominate early in infection and marcophages originate from monocytes, leaves the blood, enter infected tissue, and develop into phagocytic cells. Phagocytes are chemically attracted to the site of infection, chemotaxin. Plasma membrane of phagocyte attaches to the surface of pathogen or foreign material also known as adherence. Then opsonization happens where the coating invader with opsonins that facilitates attachment. The plasma membrane of phagocytes extends projections (pseudopods) which engulf the microbe. Microbe is enclosed in a sac called phagosome. Finally, digestion occurs inside the cell, phagosome fuses with lysosome to form a phagolysosome. Lysozyme destroys th cell wall peptidoglycan. After digestion, residual body with undigestable material is discharged.
There are systemic effects of acute inflammation such as fever, Interleukiin-1 (IL-1), released from neutrophils, macrophages, and other cells of inflammation. IL-1 acts directly on the hypothalamus which controls the body's thermostat. Its release occurs after phagocytosis or after exposure of the cell to bacterial endotoxin or to antigen-antibody complexes (Huether & McCance 2000). Anorexia, pain in head, muscle, and joint, general malaise, increase erythrocyte sedimentation rate (ESR), C reactive protein (CRP), and leukocytes are other systmeic effects of acute inflammation (University of Western Sydney 2010).
Chronic inflammation is characterized by infiltration with mononuclear cells, tissue destruction and repair, and fibrosis. It is a prolong duration which may follow acute inflammation. It usually arises in persistent infection by microorganisms, treponema pallidum fungi, viruses, and a prolonged exposure to potentially toxic agents (University of Western Sydney 2010).
Marchopahges, T lymphocytes, plasma cells, and eosinophils are chronic inflammatory cells. Marchopages has the ability to kill ingested organisms and some tumour cells which are responsible for tissue destruction, angiogenesis, and fibrosis. T lymphocytes has close relationship with marchopahges. It is activated by interaction with APC producing a variety of cytokines (IFN-g, IL-1). Plasma cells are antibodies that fight against antigens and eosinophils are parasitic infections, or in immune reactions mediated by IgE (University of Western Sydney 2010).
The University of Western Sydney 'Acute & Chronic Inflammation' hand out (2010) explained that there are two types of chronic inflammation: inflammation 1 and inflammation 2. Type 1 inflammation has three other types of inflammation; granulomatous inflammation, fibrinous inflammation, and ulcerative inflammation. Granulomatous inflammation is characterized by the formation of granulomas when some macrophages differentiate into large epithlioid cells, which cannot phagocytose but can take up debris and other small particles (Huether & McCance 2000). An example of this would be tuberculosis, leprosy and syphilis. Fibrinous inflammation is an increase in vascular permeability where fibrin accumulates. This is commonly seen in serous cavities, where the conversion of fibrinous exudates into a scar can occur between serous membranes, and limiting their function. Ulcreative inflammation is inflammation occurring near epithelium resulting necrotic loss of tissue exposing lower layers and causing ulcer. Type 2 inflammation include purulent inflammation and serous inflammation. Inflammation resulting in large amount of pus, (neutrophils, dead cells, and fluid) caused by pyogenic bacteria (staphylococci). A large localized collection of pus is call abscesses. This process is called purulent inflammation. Serous inflammation increases effusion of non-viscous serous fluid by mesothelial cells of serous memberanes or blood plasma causing skin blisters (University of Western Sydney 2010).
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Healing and repairmen of tissue occurs after inflammation. There are first and second intentions of healing. First intention minimizes tissue loss and no granulation formation. Second intention healing has a significant of tissue loss, tissue granulation, slow healing, and scar tissue (Huether & McCance 2000). All the healing and regeneration depends on the tissue type. Labile cells are more capable of lifelong regeneration. Stable cells can regenerate when stimulated. Permanent cells have no ability to regenerate (University of Western Sydney 2010).