Inflammation Flashcards
Acute vs. Chronic: timing
Acute: immediate
Chronic: persistent
Acute vs. Chronic: onset
Acute: rapid
Chronic: slow
Acute vs. Chronic: type of immunity
Acute: innate
Chronic: cell-mediated
Acute vs. Chronic: cell predominance
Acute: neutrophils (PMNs)
Chronic: mononuclear cells; lymphocytes, plasma cells, monocytes
Acute vs. Chronic: duration
Acute: hours-weeks
Chronic: weeks-years
Acute vs. Chronic: vascular response
Acute: prominent
Chronic: less prominent
Causes of acute inflammation
- Microbial infections
- Tissue necrosis
- Physical agents
- Chemical irritants
- Immune-mediated hypersensitivity
Causes of chronic inflammation
- Persistent tissue injury and acute inflammation
- Microorganisms resistant to phagocytosis or intracellular killing
- Foreign bodies
- Autoimmune disorders
- Primary granulomatous diseases (Crohn’s disease)
Outcomes of inflammation
- localizes or eliminates cause of injury
- removes injured tissue components
- leads to repair
Classic Signs of Acute Inflammation
Rubor, Tumor, Calor, Dolor, Functio Laesa
Vasoactive Mediators of Edema: two categories
- Plasma derived
2. Cell-derived
Plasma-derived vasoactive mediators of edema
- Fibrin split products
- Kinins (bradykinins)
- C3a, C5a
Cell-derived vasoactive mediators of edema
- Histamine
- Serotonin
- platelet-activating factor, prostaglandins, leukotrienes (from inflammatory cells)
- Nitric oxide, platelet activating factor, prostaglandins (from endothelium)
Mechanism of phagocytosis and cell killing
- C3b and Fc on bacterium bind with receptors on PMN
- phagosome forms
- degranulation + NADPH oxidase activation
- Bacterial killing and digestion
Phagocytic Cell Respiratory or Oxidative Burst: Order of Events
- Molecular oxygen reduced by NADPH oxidase produces superoxide anion (O2-)
- Generation of hydrogen peroxide (H2O2) with superoxide dismutase (SOD)
- H202 produces HOCl or hydroxyl radical (attacks DNA)