| Question | Answer |
| Acute inflammation | Rapid onset
terminates quickly
chemical mediators orchestrate response |
| Three stages of acute inflammation | Increased vascular permeability - WBC platelets get through to inflammation (histamine)
Cellular Chemotaxis - movement
Systemic response |
| White Blood Response | 1st 6-24 hours
- Neutrophils
- Replaced by monocytes
24-48 hours
- monoctyes to macrophages
- macro predominate in persistant inflammation
- macro carry our phagocytosis
Viral infections
- lymphocytes dominate |
| Systemic responses in acute inflammation | Fever
lymphadenopathy
anorexia
sleepiness
lethargy
anemia
weight loss
chemical mediators - pyrogens, TNF-alpha, interleukins,
drugs to reduce inflammation target these ^^ |
| Fever | Pyrogens cause fever
WBCs and microorganisms release signals causing prostaglandins to reset temperature
anti-prost reduce fever
Fever onset - shivering to increase temp
Fever "breaks" - sweating to reduce temperature |
| Reyes syndrome | never give aspirin to children to reduce fever, cause swelling in brain |
| Outcomes of acute inflammation | Complete resolution
Healing by connective tissue
-regeneration of normal cells does not occur
-excessive proliferation of connective tissue, fibrous scar tissue formed
Chronic inflammation
-resolution does not occur
-extensive tissue damage occur |
| Chronic Inflammation | inflammation for weeks or months with no resolution or healing
persistant infection - tuberculosis, syphilis, viruses
hypersensitivity disorders - RA, SLE
Exposure toxic agents - coal dust - anthracosis (black lung)
Athersclerosis -chronic inflam. dis |
| Chronic differ from acute | Predominance of monocytes, lymphocytes, and macrophages
Continual secretion of cytokines damage healthy tissues stimulating further inflammation
Granuloma formation - macrophages aggregate and are transformed into epithelial like cells |
| C vs A | T and B lymphocytes amplify and perpetuate inflammatory signals
- autoimmune disorders
- EX: RA, Lupus |
