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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
"epithelioid" appearance.
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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