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30 Cards in this Set

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Immflammation
Response to tissue injury by:
Endogenous agents (Produced or originating from within a cell or organism.)
Exogenous agents (Originating outside an organ or part)
Mechanisms of prevention:
Intact skin
Inflammation & nonspecific mechanisms if immunity.
Specific immune response
Atrophy
Reduction in cell or organ size.
Hypertrophy
Increase in cell or organ size due to increase in work load.
There are 3 types:
Physiologic
Compensatory
Pathologic
Hyperplasia
Increase in the # of cells caused by increased workload, hormonal stimulation or decreased tissue density. May be physiologic, compensatory, or pathologic.
Dysplasia
Abnormal differentiation of dividing cells, abnormal size shape or appearance.
Can be cancerous.
Metaplasia
Replacement of one cell type with another.
Can be physiologic & pathologic.
Redness (rubor)
An acutely inflamed tissue appears red, for example skin affected by sunburn, cellulitis due to bacterial infection or acute conjunctivitis. This is due to dilatation of small blood vessels within the damaged area.
Heat (calor)
Increase in temperature is seen only in peripheral parts of the body, such as the skin. It is due to increased blood flow (hyperaemia) through the region, resulting in vascular dilatation and the delivery of warm blood to the area. Systemic fever, which results from some of the chemical mediators of inflammation, also contributes to the local temperature.
Swelling (tumor)
From oedema, the accumulation of fluid in the extra vascular space as part of the fluid exudate, and to a much lesser extent, from the physical mass of the inflammatory cells migrating into the area.
Pain (dolor)
Results partly from the stretching and distortion of tissues due to inflammatory oedema and, in particular, from pus under pressure in an abscess cavity. Some of the chemical mediators of acute inflammation, including bradykinin, the prostaglandins and serotonin, are known to induce pain.
Loss of function
Movement of an inflamed area is consciously and reflexly inhibited by pain, while severe swelling may physically immobilise the tissues.
4 Phases of cellular response
Margination (Adherence of leukocytes to blood vessels during the 1st stages of inflammation)
Pavementing (leukocytes adhere to the capillary lining.
Immigration (passage of leukocytes through the capillaries to the damaged tissue.
Chemotaxis (directional movement of leukocytes to the injured area)
Pavementing
Cardinal Effects
Redness (rubor)
Heat (calor)
Swelling (tumor)
Pain (dolor)
Loss of function
Systemic (entire body) effects
(Fever) Pyrexia (low grade or mild)
Fatigue
Malaise
Headache
Anorexia
How is chronic inflammation different than acute inflammation?
Less swelling
More Lymphocytes
More Macrophages
More fibroblasts
More collagen production (more fibrous scar tissue formation)
Granulomas may develop.
More tissue destruction
Granuloma
Inflammatory response that results when macrophages are unable to destroy foreign substances that have entered or invaded body tissues. Large numbers of macrophages are drawn to the affected area over 7 to 10 days, surround the target, and enclose it. They in turn are surrounded by polymorphonuclear leukocytes, other immune cells, and fibroblasts.
In what ways do cells adapt?
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
Dysplasia
Deranged cellular growth
is not considered a true cellular adaptation but Atypical hyperplasia.
Susceptibility of neurons to ischemic necrosis
High * 3-5 min
Susceptibility of Myocardium, Hepatocytes & Renal tissue to ischemic necrosis
Intermediate * 30-120min
Susceptibility of Fibroblast, Skeletal Muscles & epidermis to ischemic necrosis
Low * many hours.
Primary biochemical target of hypoxia?
Oxidative phosphorylation
The critical event in lethal cell injury?
Cell membrane damage.
Compenbsatory Hyperplasia
Adaptive mechanism that enables certain organs to regenerate.
Hormonal Hyperplasia
Occurs chiefly in estrogen dependent organs, such as the uterus & breast. (enlargement during pregnancy)
Pathologic hyperplasia
The abnormal proliferation of normal cells. (Pathologic endometrial hyperplasia-causes excessive menstrual bleeding)
Hypoxia
lack of sufficient oxygen, is the single most common cause of cellular injury.
Ischemia
Reduced blood supply, the most common cause of hypoxia.
Anoxia
Total lack of oxygen.