Wahedra1.txt

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emm64
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Wahedra1.txt
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2011-12-03 15:35:47
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F2 Acute Wahedra
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F2 Acute Wahedra
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  1. Acute
    • - short duration (minutes-days)
    • - Emigration of fluids (edema) and leukocytes into site of injury
  2. Chronic
    • - longer duration (months, years)
    • - presence of lymphocytes, macrophages
    • - proliferation of blood vessels
    • - fibrosis and tissue necrosis.
  3. Inflammation
    • complex reaction in tissues that consists mainly of responses of blood vessels and leukocytes.
    • Principal defenders
    • plasma proteins
    • circulating leukocytes (white blood cells),
    • phagocytes neutrophils, mast cells, monocytes and macrophages
    • inflammatory response coordinates the reactions of vessels, leukocytes, and plasma proteins to achieve this goal.
  4. cytokines vs chemokines
    • chemokines are a type of cytokine;
    • cytokines elicit a reaction in a cell,
    • chemokines act specifically to localize cells
  5. 5 stages of Inflammation
    • PRISH = Pain, Redness, Immobility (Loss of Function), Swelling, Heat
    • PAIN: local production of substances that stimulate pain
    • REDNESS: capillary vasodilation & leakage of red blood cells into tissues
    • IMMOBILITY (loss of function): Due to pain, swelling or tissue destruction
    • SWELLING: Leakage of fluid from capillaries and venules into tissue
    • HEAT: increased local blood flow
    • fever = reset hypothalamic thermostat
    • PUS PRODUCTION Influx of leukocytes into tissue
  6. STIMULI FOR ACUTE INFLAMMATION
    • Infections
    • Tissue necrosis
    • Foreign bodies
    • Immune reactions ( hypersensitivity reactions) are reactions in which the normally protective immune system damages the individual's own tissues.
  7. hypersensitivity reactions
    normally protective immune system damages the individual's own tissues.
  8. Inflammation Triggers
    • soluble factors = cytokines, chemokines, released either by pathogens or necrotic cells
    • They quickly decay (e.g., arachidonic acid metabolites)
    • inactivated by enzymes (e.g., kininase inactivates bradykinin)
    • scavenged (e.g., antioxidants scavenge toxic oxygen metabolites)
    • inhibited (e.g., complement regulatory proteins break up and degrade activated complement components).
    • System of checks and balances that regulates mediator actions.
    • -for acute inflammation, resident monocytes/macrophages turn into mast cells
  9. mesenchymal cells
    (endothelium, smooth muscle, fibroblasts) and most epithelia
  10. summary of acute response
    • LPS (bacterial component) elicits response from mast cells/macrophages,
    • which secrete cytokines/chemokines
    • that change the blood vessel;
    • these changes then allow substances in blood (macrophages, neutrophils), to enter the site of infection
  11. Inflammatory Paracrines
    • macrophages/lymphocytes secrete IL-1 and TNF-alpha, which have powerful, widespread effects.
    • mast cells- found under epithelia filled with large vesicles containing histamine and other inflammatory paracrines
    • arachidonic acid derivatives- break down into prostaglandins and leukotrienes, both important in eliciting inflammatory response (asprin and NSAIDs)
    • C3a C5a complement peptides
  12. secondary mediators
    • may have the same actions as the initial mediators but may also have different and even opposing activities. Such cascades provide mechanisms for amplifying-or, in certain instances, counteracting-the initial action of a mediator.
    • Once activated and released from the cell, most of these mediators are short-lived
  13. Acute inflammation steps
    • 1. Vasodilation, increase blood flow
    • 2. Changes in microvasculature -plasma proteins and leukocytes leave circulation
    • 3. Emigration of leukocytes from microcirculation to site of injury
  14. Vasodilation
    • balance between hydrostatic pressure & outside pressure (colloid/osmotic pressure)
    • usually, very little passes between the two; when there is inflammation, there are 2 big changesk
    • increase in Blood Flow, heat and redness (erythema), vascular permiability
  15. Exudate
    • occurs via vasodilation and statis, as well as increased interendothelial spaces
    • an extravascular fluid that has a high protein concentration, contains cellular debris, and has a high specific gravity.
    • Its presence implies an increase in the normal permeability of small blood vessels in an area of injury and, therefore, an inflammatory reaction.
  16. Transudate
    • Increased hydrostatic pressure, decreased osmotic pressure
    • a fluid with low protein content (most of which is albumin), little or no cellular material, and low specific gravity.
    • It is essentially an ultrafiltrate of blood plasma that results from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability.
  17. edema
    denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an exudate or a transudate.
  18. Pus
    • purulent exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils), the debris of dead
    • cells and, in many cases, microbes
  19. Extravasation:
    • journey of leukocytes from the vessel lumen to the interstitial tissue
    • 1. In the lumen: margination, rolling, and adhesion to endothelium. Vascular endothelium in its normal, unactivated state does not bind circulating cells or impede their passage. In inflammation the endothelium is activated and can bind leukocytes, as a prelude to their exit from the blood vessels.
    • 2. Transmigration: Migration across the endothelium and vessel wall
    • 3. Migration in the tissues toward a chemotactic stimulus
  20. Early Rolling
    • adhesion mediated by selectin family:
    • E-selectin (endothelium),
    • P-selectin (platelets, endothelium),
    • L-selectin (leukocytes) bind other surface molecules (i.e.,CD34, Sialyl-Lewis X-modified GP)
    • Upregulated on endothelium by cytokines (TNF, IL-1) at injury sites
  21. Adhesion
    • Rolling comes to a stop and adhesion results
    • INTEGRINS
    • Other sets of adhesion molecules participate:
    • Endothelial: ICAM-1, VCAM-1
    • Leukocyte: LFA-1, Mac-1, VLA-4
    • (ICAM-1 binds LFA-1/Mac-1, VCAM-1 binds VLA-4)
    • Ordinarily down-regulated or in an inactive conformation, but inflammation alters this
  22. Integrins
    • key to adhesion (stop rolling)
    • leukocytes express different integrins, which are all low affinity until cytokines are released;
    • cytokines change leukocytes to express high-affinity integrins
  23. VEGF
    induces increased transcytosis (vascular permeability for vessel endothelium)
  24. What leaves with vasodilatioin?
    • edema-escape of a protein-rich exudate into the extravascular tissue
    • -Fluid contains salts, high conc. of protein (incl. immunoglobulins)
    • -Neutrophils From WBCs population
    • -Macrophages Phagocytes; derived from monocytes
    • -Lymphocytes Few
  25. Acute Inflammation Hallmark
    • Neutrophils
    • Main effector cells to mediate effects of acute inflammation
    • Important cause of neutrophilia
    • (increased neutrophils in the blood)
    • -bacterial infections
    • -infarctions
    • Short lived so have to be rapidly replaced
  26. Neutrophils
    • More numerous in the blood,
    • Respond more rapidly to chemokines,
    • Attach more firmly to the adhesion molecules that are rapidly induced on endothelial cells, such as P- and E-selectins.
    • After entering tissues, neutrophils are short-lived; they undergo apoptosis and disappear after 24 to 48 hours.
    • Monocytes not only survive longer but may proliferate in the tissues, and thus become the dominant population in chronic inflammatory reactions
    • -a characteristic way that a pathologist can diagnose/differentiate btw chronic & acute inflammation: initially, there is edema (fluid entering site of infection),
    • then neutrophils;
    • if infection isn’t cleared, then macrophages/monocytes are recruited
  27. Leukocytes
    • 1. recognition of the offending agents, which deliver signals that
    • 2. activate the leukocytes to ingest and destroy the offending agents and amplify the inflammatory reaction
    • once activated, cannot distinguish between host and offender
    • amplify
    • adhesion & migration
    • kill microbes
  28. Leukocytes at injury site
    • Recognize and attach
    • Engulf (form phagocytic vacuole)
    • Kill (degrade)
  29. Oxidative burst
    • Reactive oxygen species formed through oxidative burst that includes:
    • Formation of superoxide ion
    • 2O2 + NADPH  2O2-rad + NADP+ + H+ (NADPH oxidase)
    • O2 + 2H+  H2O2 (dismutase)
    • Hydrogen peroxide alone insufficient
    • Therefore, PMNs can kill by halogenation, or lipid/protein peroxidation
  30. Degradation
    • Limit/contain the immune response
    • Reactive end-products only active within phagolysosome
    • Hydrogen peroxide broken down to water and oxygen by catalase
    • Dead microorganisms degraded by lysosomal acid hydrolases
  31. Inflammatory response and repair
    • same time as inflammation destroys, dilutes, and walls off the injurious agent, it sets into motion a series of events that try to heal the damaged tissue.
    • Repair:
    • regeneration of native parenchymal cells
    • by filling of the defect with fibrous tissue (scarring)
    • most commonly, by a combination of these two processes
  32. Acute Inflammation Outcomes
    • Resolution-restoration
    • Suppuration/Abscess Formation Pus, combo of living and dying and cellular debris
    • Fibrosis-scar
    • Chronic inflammation-pathogen not removed
  33. Acute inflammation diagnosis
    • Clinical indications
    • -Generalize malaise
    • -Fever
    • -Pain often localized to the inflamed area
    • -Rapid pulse rate
    • Lab values
    • -Raised neutrophil count in the peripheral blood
    • -Increased erythrocyte sedimentation rate
    • -Increased acute phase proteins in the blood
    • Increase greatly in acute inflammation
    • Induced by IL-1 and produced by the liver
    • C-reactive protein (liver) is the most comon
    • -Used to monitor patients with acute myocardial infarction
  34. Abscess Formation

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