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40 Cards in this Set
- Front
- Back
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Inflammation |
It's a protective response to remove the source of injury |
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What are indicators of inflammation? |
Redness (erythema) Increased blood flow (hyperaemia) Swelling (edema) Pain Loss of Function |
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What is anaphylaxis? |
It is when an otherwise harmless agent causes a toxic (inflammatory) response |
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What tissue damage makes it more susceptible to infection? |
Ulceration, which is where the top layer of epithelia has rubbed off |
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What are the stages of the inflammatory response? |
Vasodilation Fluid and protein exudation White blood cell infiltration |
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What are the forms of exudate? |
Serous: watery Fibrous: contains fibrin (if too much of this exudate forms our clotting ability decreases) Purulent: Pus containing |
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All Immune cells and class they fall under |
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What is the process by which neutrophils line the vascular wall called and how do they attach? |
Margination (and they attach by selectins) |
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What is the process by which neutrophils migrate into the tissue called? |
Diapedesis |
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What are the threes phases in neutrophil-pathogen interaction? |
1) Attachment 2) Engulfment 3) Digestion |
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How is attachment expedited in neutrophils? |
Neutrophils interact with opsonins on the pathogen surface (including antibodies, complement etc.) |
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How does degradation occur in the phagosome? |
It occurs by free radicals Oxygen molecules can react with NADPH to become reduced into act oxygen radicals Alternatively myeloperoxidase can produce OCl radicals that are similar to bleach |
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What is the order of innate immune processes? |
First is edema (almost instant), followed by neutrophils (24-48hrs.) and finally macrophages (post 48hrs.) |
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What are two important chemical mediators of inflammation? |
Histamine and Complement |
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What cells secrete histamine and what triggers its release? |
Mast cells and basophils that release it in response to IgE or complement binding |
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What are the effects of histamine release? |
Bronchoconstriction, vasodilation, and edema (swelling and leaky vessels) |
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Where is complement manufactured? |
In the liver |
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What are the roles of individual complement, how about several complement? |
Individual: chemotaxis, opsonins, vascular permeability Several: Membrane attack complex |
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What is a major product of arachidonic acid? |
Prostaglandins |
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What is arachidonic acid formed from? |
Linoleic acid |
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How are arachidonic acids produced and what inhibits the process? |
Phospholipase A2 releases them from membrane lipids Process can be inhibited by cortisol |
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What two enzymes act on arachidonic acids? |
Lipoxygenase and cyclooxygenase |
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Lipoxygenase produce _____ |
leukotrienes |
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Cyclooxygenase produces _____________ |
prostaglandins prostacyclines thromboxanes |
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What drugs inhibit cyclooxygenase? |
NSAIDS and aspirin |
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What cells can regulate leukotriene production? |
Mast cells bind to IgEs and can trigger the production of leukotrienes |
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What do leukotrienes do? |
Increase vascular permeability, vasodilation, bronchoconstriction, chemotaxis |
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What do prostaglandins do and what do they mediate? |
promote vasodilation and edema development Mediate fever and pain |
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Why do treatments for headaches target prostaglandin synthesis? |
Prostaglandins are important mediators of pain and by preventing their synthesis you can control the pain associated with a headache
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Where are thromboxanes formed? |
Platelets |
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What is the function of thromboxane? |
To promote platelet aggregation and vasoconstriction |
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Where are prostacyclins formed? |
In the endothelia |
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What is the function of prostacyclins? |
to cause vasodilation and inhibit platelet aggregation |
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What two arachidonic acid metabolites have antagonistic activity? |
Thromboxanes (promote platelet aggregation and vasoconstriction=clot formation) and Prostacyclins (prevent platelet aggregation and promote vasodilation=clot prevention) |
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Cytokines |
Activate lymphocytes and promote interactions Also promote chemotaxis |
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Interleukin 1 |
pro-inflammatory and activates T-cells |
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TNF-a |
Pro-inflammatory and triggers release of proteolytic enzymes Can trigger cells to go through apoptosis |
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Systemic indicators of inflammation |
Increase in ESR and C-reactive protein (acute phase opsonin) |
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What is a systemic indicator of chronic inflammation? |
Increase in lymphocytes (called differential count, because more innate cells during acute infection) |
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eosinophilia |
occurs during parasites or allergies |
