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25 Cards in this Set
- Front
- Back
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What can cause inflammation |
Chemical damage Immune Infection Tissue damage |
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What is the purpose of inflammatory responde |
Eliminate the stimulus Produce healing and restore to normal physiological state |
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What happens if the acute inflammatory response fails to eliminate the stimulus or if the stimulus is self perpetuating |
Inflammation becomes chronic Major problem |
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Name some diseases associated with chronic inflammation |
Asthma, RA, skin disorders, MS, neurodegeneration, LUPUS, Colitis |
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Whats some signs of inflammation |
Heat pain, swelling, rednesss, loss of function |
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What do chemoattractants do |
Allow white blood cells to come in |
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Name the pathway from stimulus to tissue repair |
Stimulus- mediator release- vasodilation/cellular infiltration Stimulus- mediator release- increased vascular permeability-tissue damage-tissue repair |
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What are some mediators of inflammation |
Complement, Lysosomal enzymes, Kinins, histamine, superoxide,leukotrienes,thromboxane, prostaglandins, PAF, NO, cytokines |
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How does C3 get to cell lysis |
C3to C3bto C5b-9 to cell lysis |
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In C3 where does histamine get released |
C3 to C3a then histamine released |
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C3 to opsonisation |
C3 to C3b to opsonisation |
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C3b to C5a produces what |
Chemotaxis, histamine release, activates white blood cells |
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Cell membrane phospholipids to 12-HETE |
Cell membrane phospholipids to arachadonic acid by phospholipase A2 12-lipoxegenase to 12-HETE |
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Cell membrane phospholipid to PGD2, PGE2, PGF2a |
Cell membrane phospholipid to arachadonic acid by phospholipase a2 Through COX to cyclic endoperoxides(PGG2, PGH2) To PGI2, TXA, PGD2, PGE2, PGF2a |
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Arachadonic acid to LTB4-LTE4 |
Arachidonic acid through 5-lipoxygenase to 5-HPETE Then LTB4-LTE4 |
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what does kinins, PAF, histamine and LTD4 cause |
Vascular permeability |
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What does C5a, PAF, LTB4 and cytokines cause |
Cell migration |
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What does CGRP, PAF, histamine , kinins and PGs cause |
Vasodilation |
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What does kinins, PGs and paf cause |
Pain |
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How does stimulus get to inflammation and then get to chronic inflammation |
Stimulus- mediator release- inflammation- failure to eliminate noxious stimulus |
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How does stimulus get to resolution |
Stimulus, mediator release, inflammation, resolution Stimulus- mediator release- lipoxins, resolvins and IL-10 to resolution |
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What is rheumatoid arthritis |
Chronic inflammatory disease primarily affecting the joints butnwith other extra articular manifestations |
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What does RA effect |
Joints symmetrically, may only begin with a couple of joints and most frequently attacks wrists, hands, elbows shoulders knees and ankles |
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What happens in the joint in normal patient compared to RA |
Normal- nice space and covering of cells RA- rubbing of cartilage(cartilage loss), inflammation, bone loss and erosion |
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Who can get RA? And whats the pathway |
Genetic suceptibility Enviromental stimulus(smoking?) To get an immune response against autoantigens Then joint inflammation Formation of granulation tissue then erosion of bone and cartilage then joint destruction |
