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Lines of defense:
1st line – mechanical and chemical barriers
Cellular response
o phagocytosis by:
neutrophils
monocytes
macrophages
2nd line – non-specific (inflammation and phagocytosis)
vascular response
o Increased capillary permeability
Vasodilation
3rd line – specific immunity (humoral and cell-mediated immunity)
humoral immunity
o B cells and Ab’s
Cell mediated
o T cells
Inflammation
Local effects:
Redness (rubor or erythema), heat, swelling, pain (vascular)
- Redness and warmth are caused by increased flow into the damaged area
- Edema is caused by the shift of protein and fluid into the interstitial space
- Pain is from increased pressure
Systemic effects: (cellular)
Mild fever, malaise, fatigue, headache, and anorexia
Differentiation (specialization)
- Cells vary in their degree of development depending on differentiation required for a
particular cells function
Cancer
Risk factors (carcinogen):
- Genetic factors: oncogenes that regulate all growth
- Viruses: oncogenic viruses alter host cell DNA
- Radiation: UV rays (sun), x-rays, gamma rays, and radioactive chemicals cause cumulative
chromosomal damage in cells
- Chemicals: exposure to both natural and synthetic products in excess can be dangerous; the
effects of carcinogenic agents depend on the amount and duration of exposure
- Biological factors: chronic irritation and inflammation with increased mitosis
- Age: increasing
- Diet: natural substances, additives, or processing methods
- Hormones
Etiology:
- Carcinogenesis is the process by which normal cells are transformed into cancer cells
Pathogenesis:
Spread of cancer:
In situ: cell growth and reproduction, such as cancer, remaining at the original site, not invasive or
spreading
Invasive: local spread
Metastasis: spread of the cancer cells to distant sites by the blood or lymphatic’s; secondary
malignant tumor
Seeding: refers to the spread of cancer cells in the body fluids or along membranes, usually in body
cavities
Primary tumor:
Secondary tumor: