Glossary of Mechanisms of Disease - Inflammation
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- a protective response whose purpose is to eliminate the cause of cell injury and the necrotic cells resulting from the injury
- What are some examples of harmful or potentially fatal inflammatory responses?
- Asthma, atherosclerosis, anaphylaxis, pericarditis, RA
- What are the characteristics of acute inflammation?
- lasts minutes to days, fluid and protein from blood seep into tissue, neutrophils infiltrate the tissue, inflammation resolves with minimal or no damage
- What are the characteristics of chronic inflammation?
- lasts days to years, lymphocytes and macrophages infiltrate the tissue, they cause tissue destruction, tissue repair is by fibrosis and neovascularization.
- A critical function of the acute inflammatory response is to deliver ___________ to the site of cell injury.
- Neutrophils may prolong inflammation and induce tissue damage by releasing _________.
- enzymes, chemical mediators, and free radicals
- What causes local hyperemia in acute inflammation?
- local arteriolar vasodilation, the site becomes red and warm. There is an increase in RBC's and neutrophils There is an increase in flow volume but a decrease in flow velocity.
- What causes vascular permeability in acute inflammation?
- Structural changes in local microvasculature permit leakage of water, plasma proteins, and neutrophils. The site becomes swollen and painful.
- What else can cause "leakiness"?
- direct injury from mechanical impact, burn or bacterial toxins, or endogenous factors like ischemia/hypoxia.
- What else can injury to a cell cause besides "leakiness"?
- release of histamines, bradykinin, leukotrienes, IL-1, TNF, all of which aggrevate the leakiness.
- What occurs in leukocyte emigration?
- as blood flow slows, laminar flow decreases, neutrophils have increased contact with epithelial cells, stick, roll along the endo. and finally adhere and emigrate by diapedesis.
- Binding of _____ factors enhances the neutrophils' mobility and initiates new neutrophil tricks.
- What happens when chemotactic factors activate leukocytes?
- Arachidonic acid ->
1)cyclooxygenase -> prostaglandins
2)5-lipoxygenase -> Leukotrienes
- What are the chemical mediators of inflammation?
- histamine, found in mast cells
eicosanoids (prostaglandins, leukotrienes)
cytokines, Nitric oxide, lysosomal enzymes
- What do NSAID's do?
- block the cyclooxygenase pathway that produces prostaglandins
- What diagnostic tools are used to detect inflammation?
- C-reactive protein (will be high)
esr, which will increase because of the increase in fibrinogen.
- What are the outcomes of acute inflammation?
- complete resolution, scarring, abscess formation, progression to chronic inflammation.
- When is chronic inflammation seen?
- persistent infections, like syphilis and tuberculosis, prolonged exposure to toxic agents, autoimmune diseases, sarcoidosis
- What type of cells are involved in chronic inflammation?
- macrophages, lymphocytes, plasma cells, eosinophils
- This is a distinctive form of chronic inflammation, characterized by aggregation of activated macros that develop a squamous
- granulomatous inflammation
- What is the role of the lymphatics during inflammation?
- They remove inflammatory fluid and debris from the interstitial space.
- What is the Blood brain barrier and what is its use?
- The BBB is made up of capillaries with tighter epithelial cell junctions, making it harder for certain dangerous and helpful substances to get through.
- What are the morphologic patterns in acute and chronic inflammation?
- serus - i.e. skin blister
fibrinous - leads to scarring
suppurative - exudate forms with an abcess
ulceration - epit. surface becomes inflammed, necrotic, and eroded.
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