NURS 165 Study Guide - Final Guide: Complement System, Worker Bee, Reperfusion Injury
Inflammation Notes
• Endogenous - from inside body
• Exogenous - from outside body
• Body wants to neutralize the invasion --> inflammation
• Injury occurs at cell level, and cells have ability to respond
• Blood vessel dilation --> blood/immune factors swelling in -->
inflammation
• Innate vs. Adaptive immunity
- innate is quicker but doesn't last as long
• Injury --> tissues damaged, release cells
- Bacteria accumulate
• Cardinal signs of inflammation: pain, heat, redness, swelling
• 5th: loss of function
• Suffix: -itis
- usually refers to significant inflammation
• Outcomes of Acute Inflammation
- Ideally, resolution
- Bad outcomes
- abscess (pus)
- fistula (abnormal communication)
- ulcers or scars form
- chronic inflammation
• Cells and Mediators of Inflammation
- Different WBCs
▪ Macrophages
▪ Neutrophils
▪ Basophils
▪ Eosinophils
▪ Monocytes
- Platelets
• Sequence of Events
find more resources at oneclass.com
find more resources at oneclass.com
1.) Precipitating event
a. Tissue damage, bacterial invasion
2.) Activation of local inflammatory cells
a. Macrophages, mast cells
3.) Recruitment of neutrophils, plasma proteins
a. At same time, capillaries are leaking – spilling out
fluids into vascular space → causes swelling
4.) Generation of local mediators
a. Prostaglandins, leukotrienes, etc.
b. These help pain sensation
5.) Functional consequences
a. Vasodilation, inc. vascular permeability
b. Neutrophils drawn to area
6.) Resolution of acute inflammation
a. Once resolved, neutrophils have to get out
(apoptosis)
b. New tissue growth w/ help of fibroblasts
• Pluripotent stem cells
o Come from bone marrow
o Two types
▪ Lymphoid
• Lymphocytes, natural killer cells
• T cells, B cells (come from bone marrow,
develop in thymus)
▪ Myeloid
• Granulocytes, monocytes, erythrocytes, etc.
• Myeloid
o Granulocytes
▪ WBCs with granules w/ enzymes to destroy bacteria
▪ Include neutrophils, basophils, eosinophils
• Neutrophils most numerous, constantly in/out of
circulation
• Worker bee neutrophils in damaged tissues
may spill over into secondary tissues →
reperfusion injury
• Chemotaxis, phagocytosis, etc.
o Leukocytosis
▪ Colony-stimulating factor: substance increasing rate of
WBC production
• Some immature cells may end up in
bloodstream
o Shift to the left
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Bacteria accumulate: cardinal signs of inflammation: pain, heat, redness, swelling, 5th: loss of function, suffix: -itis. Usually refers to significant inflammation: outcomes of acute inflammation. Chronic inflammation fistula (abnormal communication: cells and mediators of inflammation. Different wbcs: macrophages, neutrophils, basophils, eosinophils, monocytes. Activation of local inflammatory cells: macrophages, mast cells. Recruitment of neutrophils, plasma proteins: at same time, capillaries are leaking spilling out fluids into vascular space causes swelling. Generation of local mediators: prostaglandins, leukotrienes, etc, these help pain sensation. Functional consequences: vasodilation, inc. vascular permeability, neutrophils drawn to area. Coxs: cox prostaglandin vasodilation, other mediators: cytokines, association with macrophages and lymphocytes, alter wbc activity, mediators (cytokines) can stimulate liver to produce proteins that will help inflammatory response, increase in these proteins (ex. Complement system: decrease in other proteins (ex. Albumin: bradykinin transduces signal for pain, atherosclerosis, = artery inflammation, can be widespread or limited to just heart/a blood vessel, fibrosis = loss of function.
