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Inflammation 1 - Coggle Diagram
Inflammation 1
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Biochemical Mediators
The Kinin system
Biomedically mediates inflammation by causing dilation permeability of the blood vessels at the site of injury
Clotting Mechanism
Cause mast cells to release granules that contain histamine and other mediators into surrounding tissue
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Prostaglandins:
derived from cell membranes, cause increased vascular dilation, permeability, erythema and pain
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Endotoxins
Serve as chemotactic factor, active complement, and function as antigen and damage bone tissue.
Systemic clinical signs
Elevated C-Reactive Protein:
- A nonspecific protein produced in the liver and elevated in the circulating blood when inflammation is present in the body
- Used as early infection protection
Lymphadenopathy:
- Hyperplasia and hypertrophy of lymphocytes
- Hyperplasia: an increase in then number of cells
- Hypertrophy: enlargement of individual cells
Fever:
- Production of pyrogens affects the hypothalamus resulting in an increase in body temperature
- Pyrogens: produce fever by increasing the synthesis and release of prostaglandins in the hypothalamus
Leukocytosis:
- An increase in the number of WBC circulating in the blood
- Normal level count of 4,000 increased to 10,000/mm3
Types of inflammation
Acute inflammation: short and lasts only few days. The tissue may return to its original state, or repair of the tissue may begin immediately.
Granulomatous inflammation*: Neither acute nor chronic. Specific type of inflammation in response to specific stimuli.
Chronic inflammation: injury to the tissue continues, the inflammatory response is longer lasting. lasts weeks, months, or even indefinitely. Heals less readily.
Cells involved
Leukocytes (White Blood Cells)
WBC emigrate to the site of injury to begin the process of inflammation
Neutrophils
First type of WBC to site of injury
Most common during acute inflammation
Produced throughout life
Mobile
Die shortly after phagocytosis
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