1. Abscess: a walled pocket of infection; can result from dysfunctional wound healing
2. Adhesion: how well cells are able to stick to one another
3. Angiogenesis: ability to make own blood vessels
4. Atherosclerosis: artery thickens because of accumulation of fatty materials, plaque formation
in main arteries
5. Bradykinin: produced by kinin cascade; causes pain, vasodilation, and vascular permeability
6. C-reactive protein: increases to neutralize inflammatory chemicals; indicates inflammation
7. Calor: heat
8. CBC: complete blood count
9. Cellular response: chemotactic factors attract neutrophils to marginate, emigrate, migrate,
and phagocytosis
10. Chemotaxis: movement of an organism or entity in response to a chemical stimulus
11. Cicatrization: maturation
12. Collagen: lattice which wound can heal on
13. Complement: primary effector system for innate and adaptive immune systems
14. Cytokines: endogenous pyrogens that cause fever
15. Dolor: pain caused by bradykinin
16. Emigrate: chemotactic factors attract neutrophils to squeeze through capillary walls
17. ESR – erythrocyte sedimentation rate: increased plasma proteins; indicates inflammation
18. First intention wound healing: must be clean, able to approximate wound edges, fast and
preferred (surgery)
19. Fistula: opening within the tissues as a result of dysfunctional collagen synthesis
20. HDL – high density lipoprotein: good cholesterol – higher is better
-<40 low, >60 high
21. Hernia:
22. Histamine: potent vasodilator released by mast cells in the complement cascade
23. Homocysteine: elevated in reduces folate levels, B vitamins, and riboflavin <15 ; systemic
marker of inflammation
24. Inflammation: usually lasts 1-2 days
25. Interferons:
26. Keloid: overfilling of a tissue
27. LDL – low density lipoprotein: bad cholesterol – lower is better
Optimal <100 mg/dL
28. Leukocytosis: increased WBC > 11,000 and in infection a “left shift ratio”
29. Leukotrienes: produce the Type 1 hypersensitivity response
30. Lymphokines:
31. Mast cells: immune cells that contain histamine
32. Marginate: chemotactic factors attract neutrophils to move to the capillary walls (capillary
walls are now permeable)
33. MMP (matrix metalloproteinases): remodel collagen and fibrin
34. Monocyte – Macrophage: dissolve clots, clear debris and add growth factors (TGF-B,
VEGF, MMP)
35. Neutropenia: deficiency of neutrophils (WBC)
36. Neutrophils: involved in cellular response
37. Opsonin: bind to foreign substances making them more susceptible to phagocytosis
38. Phagocytosis: facilitated by opsonization; gets rid of infectious substances
39. Purulent: pus (suppurative); not normal  infection)
40. Recognition: communication among cells (ability to distinguish on cell from another)
41. Rubor: redness due to increased blood at area of inflammation
42. Sanguinous: bloody
43. Second intention wound healing: used in contaminated wounds, large amount of tissue lost,
very slow, large scar
44. Sero-sanguinous: clear, pink, blood-tinged (thinner)
45. Serous: watery, like plasma (straw color)
46. Stricture: narrowing of a lumen or structure
47. TGF-B (transforming growth factor beta): stimulates collagen precursor to procollagen
48. Third intention wound healing: rarely used, to close large wounds that are clean enough
(skin grafting)
49. Triglycerides: usually elevated in DM, increased ETOH, sugar
<150 mg/dL = normal
50. Tumor: swelling
51. Vascular response: histamine and bradykinin stimulate vasodilation
52. VEGF (vascular endothelial growth factor): stimulates angiogenesis
53. WBC with differential: provides information about the types and amounts of white blood
cells in a person's blood.
54. Septicemia: infection of the blood; high mortality rate
55. Anaplastic: poorly differentiated cells (hallmark sign of cancer cells)
56. Neoplastic: altered growth an differentiation
57. Malignant: anaplasia (poorly differentiated cells), poor cellular recognition, inadequate
cellular adhesion (causing tissue friability), poor intracellular communication
58. Benign: well differentiated (easily identified), cellular recognition, normal cellular adhesion,
intracellular communication, controlled rate of mitosis, apoptosis (normal cell death)
59. Metaplastic: a cell begins to look different (reversible change in one adult cell type is
replaced by another cell type
Pathophysiology Vocabulary/Nursing Role: 5-10%
Genetics: 5 -10%
Cellular Alterations and Cancers: 5 -10%
Fluids, Electrolytes, Acid-Base, CHF, HTN, Renal Failure, MI, Diabetes, Hyper –thyroid and
hypothyroid: 15 -25%:
Inflammation, Infection, Normal and Abnormal Wound Healing: 20 – 25%
Normal and Abnormal Immunity: 15-20%
Hematologic: 5-10%
Study Questions:
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What stimuli could trigger the inflammatory response from cells?
What is meant by the Vascular or Hyperemic response? How does it occur?
Describe the chemicals that are released from cells when they are damaged to form the
chemotaxic gradient. Be able to name them and describe what they do.
What is meant by the Cellular Response? Describe the process with the proper
vocabulary.
What are the local signs of inflammation? Use both sets of terms.
What are the systemic signs of inflammation?
How does the nurse distinguish between inflammation and infection? What blood tests
could be done to help?
What is a normal white blood cell count? What does it mean to obtain a “differential?”
What does a “shift-to-the-left” indicate?
What factors are needed for adequate wound healing? What factors would slow or
interfere with wound healing?
Describe the wound healing process. What role do the WBC’s play? Describe
angiogenesis, granulation tissue, hypertrophic scar tissue, and cicatrization.
Describe the three main methods of wound healing. Under what circumstances would
one be indicated over the others?
How long does wound healing usually take? What recommendations could the nurse
make to the patient to facilitate adequate wound healing?
Describe at least 5 complications of wound healing.
Why is atherosclerosis an inflammatory disease? What risk factors contribute to the
development of atherosclerosis? What blood tests for inflammation can be done to
assess a person’s risk for developing atherosclerosis? Why is it important to control the
buildup of atherosclerosis?
Name at least one other disease that has inflammation as a major component.
Define septicemia, what are the risk factors for it?
Chronic Kidney Disease/Injury versus Acute Kidney disease/Injury
Pre-renal, intra-renal, post-renal
Describe different types of angina. Risk factors for MI, Stroke, HTN.
Endocrine disorders- DM, hyper and hypothyroid.