Chapter Three Flashcards

Terms Definitions
A steady yet dynamic state considered the body's "normal" range
Negative feedback
Opposes the body's deviation from the norm; most common homeostatic system in the body
Positive feedback
Response that enhances original stimulus
Primary prevention
Activities to improve general well being while also involving specific protection for selected diseases
Secondary protection
Early detection, diagnosis, and rapid initiation of treatment to stop the progress of disease processes
Tertiary prevention
Rehabilitation and return to a status of maximum usefulness with a minimum risk of reoccurrence
General Adaptation Syndrome (GAS)
Fight or flight response; temporary energy to run or confront
Epinephrine, norepenephrine
Adrenocortical steroid hormone
Polypeptides that act as the brain's natural opiates
Pro and anti inflammatory cytokines
Peptide hormones that act as communication links between immune and inflammatory response systems.
Local Adaptation Syndrome
Classic inflammatory response; includes redness, swelling, pain, movement limitations, sometimes drainage
Reversible cell injury
Cell withstands assault and returns to normal
Cellular adaptation
Potentially reversible; adapts to a persistent injury by changing structure or function
Cellular death
Due to severe and prolonged injury
Cellular atrophy
Shrinkage of individual cells
Cellular hypertrophy
Growth of individual cells
Cellular hyperplasia
Increased number of cells
Cellular metaplasia
Change of cell type but with ordered and controlled growth
Cellular dysplasia
AKA atypical hyperplasia. Cellular change results in disordered growth and change to less differentiable type and/or loss of growth restrictions.
Normal or pathologic. Cell shrinks and is consumed by neighbors without inflammation. Causes: environmental signals, survival signals.
Nonspecific immunity
1st line mechanical: intact epithelial barriers, tracheal mucus with cilia. 1st line chemical: acid in stomach, vagina and urine. 2nd line phagocytosis: WBC and macrophages
Plasma protein systems
Three cascades: complement, clotting and kinin. All are inactive proteins in blood that are activated by positive feedback.
Granular leukocytes
Neutrophils, eosinophils, basophils
Agranular leukocytes
Lymphocytes and monocytes
Systemic effects of inflammation
Circulating cytokines cause fever, chills, sweats, aches, malaise. Leukocytosis occurs. There is an increase in liver production of plasma proteins
Vascular effects of inflammation
Arteriole vasodilatation. Precapillary cells dilate for local blood flow. Postcapillary cells increase vessel permeability.
Cellular reaction to inflammation
WBC move into area. Platelets are drawn in by mast cells. Margination occurs. Damaged cells are phagocytized.
Mast cell response to inflammation
Degranulate during injury, complement activation, exposure to toxins. Histamine and other substances cause vasodilation.
Cellular mediators of inflammation
Complex interaction between many mediators. Balance of pro and anti inflammatories. Released by: WBC, mast cells, endothelial cells, platelets and liver. Manmade as antihistamines, NSAIDs, corticosteriods.
Main chemical mediator of inflammation, released by platelets, basophils and mast cells
Increases vascular permeability and allows adhesion of WBC to capillary
Activated in domino fashion (cascade) by foreign carbohydrate or binding to an antibody bound protein to: opsonize foreign substances, directly kill substances and give positive feedback to inflammatory response.
Increase blood flow and capillary permeability, stimulate pain receptors, cause fever, potentiate the effect of histamine
Polypeptides that increase blood flow and capillary permeability.
Inflammation associated messenger molecules. Role as a group is to activate, recruit, regulate defense cells, circulatory cells, etc, to eliminate threat and repair damage.
4 signs of inflammation
Redness, heat, swelling, pain
Stages of acute inflammatory response
Vascular and cellular
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