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108 Cards in this Set
- Front
- Back
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1. What is inflammation?
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Protective response of living, vascularized CT intended to eliminate the initial cause of cell injury and cell/tissue necrosis resulting from the original insult
**Insult is commonly bacteria **Also get rid of damaged cells and tissues as well |
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2. What do the histological and clinical characteristics of the inflammatory response depend upon?
(two things) What are the five major components in the inflammatory response? What type of response is inflammation? |
1. Extent of injury
2. Nature of injurious agent 1. Plasma 2. Circulating blood cells 3. Blood vessels 4. Cells of ECM (mast cell, macrophages, fibroblasts) 5. Macromolecules of ECM Connective tissue response |
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3. How is acute inflammation?
What is it characterized by? |
Rapid onset and short duration
Accumulation of... -fluid -plasma proteins -leukocytes (neutrophils) |
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4. How is chronic inflammation?
What is it characterized by? |
Less predictable phase of inflammation in terms of severity and duration
**usually longer than acute 1. Accumulation of leukocytes and macrophages 2. Vascular proliferation 3. Fibrosis |
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5. What sets repair in motion?
How is repair accomplished? When does repair begin? When is repair completed? |
Set in motion by inflammation
Accomplished by the regeneration of original parenchymal cells and/or formation of fibrous scar Begins during inflammation **repair and inflammation co-exist at certain points Completed after injurious agent is removed |
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6. How do chemical mediators govern the evolution and strength of the inflammatory response?
What is infection? |
Combination of mediators produces, the sequence of their appearance, and the amount produced
Invasion and multiplication of microorganism in body tissue **cause of inflammation |
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7. What is acute inflammation?
What are the two major components of acute inflammation? What is the hallmark cell type of acute inflammation? |
Rapid response the injurious agents designed to deliver pre-formed defensive elements of blood to the extravascular site of injury
1. Vascular changes 2. Cellular events *emigration of neutrophils, activation and accumulation at site of injury Neutrophils |
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8. What vascular changes does a neural reflex cause during acute inflammation?
What much more important vascular change occurs during acute inflammation? What does this engorging of the capillary beds result in? (two things) Due to vasodilation of arterioles what clinical signs can be observed regarding the area? (two things) |
Inconstant and transient vasoconstriction of arterioles
**lasts a few seconds Vasodilation of arterioles 1. Increased blood flow (hyperemia) 2. Increased local intravascular hydrostatic pressure 1. Warm (calor) 2. Red (rubor --> erythema) |
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9. What happens to the vascular permeability of microvasculature during acute inflammation?
What does an outpouring of protein-rich fluid due to increase vascular permeability result in? (three things) |
Increase in vascular permeability
1. Intravascular hemoconcentration in venous return 2. Increased viscosity of blood 3. Stasis *slowing of blood flow in capillary bed and post-capillary venules |
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10. What does stasis permit?
(two things) What is the hallmark of acute inflammation? What are the four cardinal signs of inflammation? |
1. Migration of neutrophils along endothelium
2. Firm adherence of neutrophils to endothelium to permit transmigration to extravascular spaces Increased vascular permeability 1. Red (rubor) 2. Warm (calor) 3. Swollen 4. Pain |
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11. What is a transudate?
How is the permeability of vessels when transudate occurs? |
When arteriolar vasodialtion w/ increased blood flow initially causes increased hydrostatic pressure in the capillaries and an increased push of fluid into the CT
Permeability of vessels is still normal |
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12. What is exudate?
What is exudate a result of? What do the escaped proteins from exudate do? (two things) |
Escape of fluid as well as large molecules (proteins) from the microvasculature
**occurs after transudate Increase in vascular permeability through the action of chemical mediators 1. Participate in the inflammatory response 2. Enhance fluid loss from vessels by osmosis |
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13. What do both a transudate and an inflammatory exudate cause?
(two things) What are seven mechanisms of increased vascular permeability? |
1. Fluid accumulation in extravascular space (edema)
2. Tissue swelling (tumor) 1. Endothelial cell contraction 2. Endothelia cell retraction 3. Increased transcytosis 4. Direct endothelial injury 5. Delayed prolonged leakage 6. Leuokocyte-meditaed endothelial injury 7. Leakage from regenerating capillaries |
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14. What is the most common mechanism of increased vascular permability?
What does this cause? What is it caused by? What type of venules it is limited to? What else it it called and why? |
Endothelial cell contraction
Causes intracellular gaps Caused by binding to endothelialc cell surface receptors of: -histamine -bradykinin -leukocytes Post-capillary venules "Immediate, transient response" **b/c short-lived and reversible |
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15. How does endothelial cell retraction occur?
What change takes place? How are the effects? |
Occurs via reorganization of cytoskeleton
Complex cellular change where the intra-cellular gaps in post-capillary venules are widened Effects last 24+ hrs and are reversible |
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16. How does increased transcytosis of fluid/protein occurs?
What is it induced by? |
Occurs through venule walls near cell junctions via the vesiculovacuolar organelle system
VEGF enhances this normal mechanism |
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17. What is direct endothelail injury?
What can directy endothelial injury affect? When does it usually occur? How is leakage during direct endothelial injury? When does leakage end? (two scenarios) |
Increased permebaility due to endothelial necrosis and detachment
Affects any/all levels of microcirculation After severe injuries -burns Leakages is immediate and sustained 1. Damaged vessels are thrombosed 2. Damaged vessels are repaired w/ new endothelium |
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18. When does delayed prolonged leakage of venules and capillaries occur?
By what mechanisms does it work? |
Occurs following more mild thermal injury, sunburn and some bacterial toxins
Mechanism is unclear but delayed cell damage occurs **some damage to epithelium but it appears normal |
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19. What causes leukocyte-mediated endothelial injury?
Where is this restricted to? |
Caused by leukocytes releasing toxic substances while adherent to or in close proximity to endothelium
*neutrophils releasing potent enzymes too close to venule or capillary Restricted to sites where leukocytes adhere to endothelium **venules at sites of inflammation, pulmonary capillaries |
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20. When does leakage from regenerating capillaries occur?
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During angiogensis repair process
This leakage occurs following an injury severe enough to induce repair **leakage of new vessels |
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21. What permits leukocytes to move from central column of blood flow to periphery in large numbers?
What is this process termed? What do surface selectins allow leukocytes to do? What are two examples of selectins? When are they expressed? |
Slowing of blood flow (stasis)
Margination Selectins allow leukocytes to adhere to the endothelium through transiently weak interactions CD62-E and CD62-P Not expressed by normal endothelium but are up-regulated to cell surface by inflammatory mediators |
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22. Where is the selectin CD62-L found?
What do the selectins on endothelium bind? Where is the molecule found? |
On leukocytes
Bind a specific oligosaccharide on a mucin like glycoprotein Expressed on the neutrophil cell surface **selectins on neutrophils bind a similar glycoprotein on endothelium |
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23. What breaks the weak interaction between leukocytes and selectins?
What is meant by the term rolling? |
Blood flow
The quick reformation of the leukocyte-selectin bond downstream so the neutrophils tumble/roll over the endothelial surface in a breaking action |
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24. After neutrophils have been slowing by rolling what happens?
What is meant by pavementing? |
1. Integrins on neutrophil cell surface undergo conformation change by inflammatory mediators
**increased binding affinity 2. Integrins bind to up-regulated molecules of the immunoglobulin superfamily on endothelial cell surface Stronger interaction that causes firm adhesion of neutrophils and they begin to flatten on endothelial surface |
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25. What is diapedesis?
What cell(s) express CD31(PECAM)? What does CD31 function as? What does it do? |
Transmigration of leukoctyes through the blood vessel wall that also occurs at intercellular junctions of endothelium mainly in post-capillary venules
Neutrophils and endothelial cells near intercellular gaps express it Serves as both receptor and ligand Signals location of interceullar gap |
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36. What cells are predominate in the early phase of acute inflammation?
What cells become numerous in 24-48 hours? What will be the predominant cell type of the pyogenic bacteria (pus) cannot be removed)? Where are neutrophils more numerous? How do neutrophils respond to chemotatic factors? How do neutrophils attach to adhesion molecules initially expressed by endothelium? How does the lifespan of neutrophils and monocytes compare? |
Neutrophils
Monocytes Neutrophils continue to be predominant More numerous in the blood Respond more rapidly Attach more firmly Neutrophils: -short lived -die by apoptosis Monocytes/Macrophages: -live longer (days) |
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27. What is chemotaxis?
What are the two general types of chemotactic agents? An influx of what ion is triggered via the complex, energy-dependent process w/ cell surface/chemotaxin interaction? What does an influx of this ion trigger? (two things) |
Unidirectional migrationof cells up a chemical gradient towards increasing concentrations of chemotactic agents
**towards site of injury 1. Exogenous -bacterial products -various lipids 2. Endogenous -leukotriene B4 -cytokines/chemokines Influx of Ca++ ions 1. Triggers assembly of contractile elements (actin) 2. Formation of pseudopods and movement |
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28. Once leukocytes are in the area of injury what happens to them?
What happens to leukocytes once they are activated? (three things) Can leukocyte activation be harmful? |
Activated by various chemicals
**important step in inflammation 1. Increase synthetic activity 2. Become more phagocytic 3. Increase release of chemical mediators -lysosomal enzymes, free radicals Can be harmful if occurs too close to site of damage b/c can damage vessel and make it leaky |
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29. How is leukocyte activation accomplished?
What special receptor do leukocytes have that help accomplish leukocyte activation? What do these receptors do? |
Accomplished via cell surface receptors for mediators
Have Toll-like receptors (TLRs) TLRs recognize a number of bacterial and viral products |
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30. What is phagocytosis?
What are the principal phagocytes? What are the three steps in the process? |
Engulfment and interanlization of microbs, cell debris, foreign particulate material
Neutrophils, macrophages, monocytes 1. Recognition and attachment 2. Engulfment 3. Killing/Degradation |
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31. How can the efficiency of phagocytosis be greatly increased?
How does this process work? |
Binding of the targeted material to the phagocyte cell surface
Microbes can be coated w/ IgG, C3b or plasma collectins and leukocytes have cell surface receptors fro each type of molecule |
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32. What are opsonins?
What are examples of opsonins? What is opsonization? |
Opsonins are bridges
Examples: IgG C3b Collectins Enhanced binding to the cell surface for phagocytosis |
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33. What triggers engulfment?
How is a phagosome created? How is a phagolysosome generated? What doe lysosomal enzymes released into phagolysosomes aid in? |
Triggered by binding of ospsonized particles to cell surface receptors
Phagosome -pesudopods surrounding and enclosing attached particles Phagolysosome -internalized phagosome fuse w/ cytoplasmic lysosome Aid in killing and digestion of microbe/particle |
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34. What is the principal and most potent mechanism in killing and degradation?
What is the burst in oxygen consumption associated w/ phagocytosis due to? What does NADPH oxidase do? |
It is oxygen-dependent
Activation of NADPH oxidase Generates free radical **superoxide anion |
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35. Once generated by NADPH oxidase what happens to the superoxide anion?
What converts the H2O2 to the free radical HOCl? How does HOCl kill microbes? If a cell cannot make HOCl b/c they are deficient in MPO how do they kill microbes? |
Spontaneously dismutates to hydrogen peroxide w/in the lysosome
Myeloperoxidase Kills by halogenation or lipid peroxidation Via superoxide hydroxyl radical |
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36. How do non-oxygen dependent mechanisms of bacterial killing occur?
What are four examples? |
Via other molecules and enzymes present
1. Lysozyme 2. Major basic protein (eosinophils) 3. Defensins 4. Bactericidal permeability increasing protein |
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37. What are defensins?
Following killing what completes the degradation of bacteria? |
Cationic peptides cytotoxic for microbes and cells
**rich in arginine Lysosomal acid hydralases |
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38. What problematic thing can leukocyte activation and phagocytosis result in?
Why is this problematic? What are four mechanisms for release of leukocyte products and leukocyte induced tissue injury? |
Can result of lysosomal products
**ROS into extracellular spaces If potentially toxic lysosomal component release is persistant and unchecked, leukocyte infiltrate itself becomes the offender **cause collateral tissue damage 1. Regurgitation during feeding 2. Frustrated phagocytosis 3. Cytotoxic release 4. Direct secretion (exocytosis) |
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39. What is regurgitation during feeding?
What is frustrated phagocytosis? What is cytotoxic release? |
Lysosomal components are released into forming phagolysosomes before the phagolysosome completely closes at the cell surface
Release of enzymes w/o phagocytosis of particle on flat surface Release of enzymes when pahgocyte ingests membranolytic substance like urate crystals |
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40. What do defects in leukocyte function lead to?
What are examples of defects in leukocyte function? |
Increased susceptibility to recurrent infection
1. Leukocyte adhesion defect (LAD) 2. Chediak-Higashi syndrome 3. Chronic granulomatous disease 4. Acquired diseases |
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41. What is type 1 LAD?
What is type 2 LAD? What is leukocyte adhesion defect associated w/ in the dental world? |
Genetic defect in structure of integrins causing defective firm adhesion and phagocytosis
Defect in structure of oligosaccharide component of mucin-like glycoprotein on leukocytes **disrupt interaction w/ endothelial secretin "Pre-pubertal periodontitis" |
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42. What three things characterize Chediak-Higashi syndrome?
What is the problem with this syndrome? What happens in phagocytes? |
1. Neutropenia
2. Defective degranulation 3. Defective microbial killing Problem is defect in membrane associated protein responsible for docking and fusion of intracellular vacuoles in all cells Phagosomes do not fuse w/ lysosomes |
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43. What does chronic granulomatous disease result from?
What are the most common variants of it? Generally what is chronic granulomatous disease associated with? |
Inherited defects on components of NADPH oxidase and lack of production of superoxide radical
X-linked and autosomal recessive **in males Childhood disease of recurrent bacterial infections |
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44. What are examples of acquired diseases the disrupt leukocyte chemotaxis?
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1. Diabetes
-also affect adhesion 2. Sepsis 3. Malignancy 4. Immunodeficiencies |
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45. What are generally the three outcomes of acute inflammation?
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1. Complete resolution
-occurs when injury is limited, no or minimal tissue framwork damage and dead cells can be easily replaced 2. Progression to chronic inflammation 3. Healing by CT replacement (scarring and fibrosis) -if have considerable tissue damage or inflammation in tissue that do not regenerate -also occurs when fibrin is abundant in exudage and not adequately resorbed |
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46. What three things can modify the morphology of acute inflammation?
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1. Severity of the reaction
2. Specific cause 3. Particular tissue and site involved |
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47. What is serous inflammation?
What does serous inflammation create? Is there increased vascular permeability in serous inflammation? |
Water, protein poor fluid derived from serum or mesothelial secretions in body cavities
Creates an effusion Increased vascular permeability is minimum |
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48. What happens in fibrinous inflammation?
What type of injury is associated w/ fibrinous inflammation? How is the vascular permeability? Where does fibrinous inflammation occur? What happens? |
Have a greater outflow of protein into extravascular space
More severe injury Greater vascular permeability **larger molecules Occurs in.. -pleural cavities -pericardial cavities -peritoneal cavities Sticky fibrin-rich exudate fills the space causing both sides of the cavity to stick together |
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49. What happens if the fibrin in fibrinous inflammation is not removed promptly?
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Ingrowth of fibroblasts and blood vessels occurs forming granulation tissue
**eventually a scar or fibrosis forms resulting in fibrous adhesions |
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50. What characterizes suppurative (purulent) inflammation?
Microscopically what characterizes it? What bacteria induce this type of inflammation? |
Large mounts of pus
Acute inflammatory exudate of edema, protein and neutrophils Pyogenic bacteria |
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51. What is an abscess?
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Localized collections of purulent inflammation in a tissue, organ or confined space
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52. What is an ulcer?
Where are ulcers most commonly found? |
Local defect of the surface of an organ/tissue produced by sloughing of inflamed necrotic tissue
GI tract, mouth & skin of lower limbs |
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53. Where do chemical mediators of inflammation arise from?
Two places.. What can be induced to synthesize mediators? |
1. Plasma precursors
-must be activated by proteolytic cleavage 2. Cells -may be preformed & stored in vacoules -may be synthesized de nove **major cellular sources: -neutrophils -mast cells -platelets -endothelium -monocyte/macrophages Mesenchymal cells and most epithelia |
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54. How do most mediators operate?
How do mediators amplify or modulate the response? How regulation of mediators? What is the life span of mediators? How are mediators eliminated? (four ways) |
Operate by binding to specific cell-surface receptors on target cells
Stimulate release of secondary mediators or other molecules from target cells Tight regulation **some can cause harmful effects Short-lived 1. Spontaneous decay 2. Enzymatically destroyed 3. Scavenged by antioxidants 4. Bound by inhibitors |
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55. What are examples of chemical mediators?
(nine) What are examples of vasoactive amines? |
1. Vasoactive amines
2. Arachidonic acid metabolites 3. Platelet-activating factor 4. Cytokines 5. ROS 6. Nitric oxide 7. Lysosomal constituents of leukocytes 8. Neuropeptides 9. Plasma protein derived mediators 1. Histamine 2. Serotonin |
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56. How and where is histamine stored?
What causes the release of histamine? Six stimuli.... |
In granules in perivascular mast cells
Degranulation of mast cells cause by... 1. Physical injury 2. Immune reactions (IgE) 3. Binding of C3a or C5a 4. Cytokines 5. Neuropeptides (substance P) 6. Histamine releasing proteins from leukocytes |
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57. What does histamine cause?
What is histamine the main mediator of? How does histamine do this? What inactivates histamine |
Causes dilation of arterioles
Main mediator of immediate phase of increased vascular permeability of venules Via endothelial cell contraction Histaminase |
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58. Where is serotonin mainly present?
(two places) What is serotonin released in response to? What are the effects of serotonin similar to? |
1. Platelets
2. Enterochromaffin cells Platelet aggregation in response to contact w/ collagen, ADP, antigen-antibody complex Histamine |
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59. What are arachidonic acid metabolites?
What is arachidonic acid? How is arachidonic acid released from phospholipids? |
Eiocosanoids that produce results locally and then decay spontaneously or destroyed enzymatically
**short-ranged hormones formed de novo FA normally incorporated in cell membrane phospholipids Phospholipase A2 |
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60. How is phospholipase A2 activated?
By what two enzymatic pathways are arachidonic acid metabolites produced? |
Mechanical, chemical, physical stimuli or various mediators (C5s)
1 Cyclooxygenase pathway -synthesis of prostaglandins (produce pain) 2. Lipoxygenase pathway -synthesis of leukotrienes |
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61. What does the cyclooxygenase pathway produce?
Three things... |
1. PGI2 (prostacyclin)
2. TXA2 (thromboxane) 3. PGD2, PGE2, PGF2 |
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62. What cell produces PGI2?
What does prostacyclin do? (three things) |
Endothelial cells
1. Inhibitor of platelet aggregation 2. Potent vasodilator 3. Opposes effects of thromboxane |
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63. What cell produces TXA2?
What two things does thromboxane do? |
Platelets
1. Potent platelet aggregator 2. Vascoconstrictor |
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64. What do prostaglandins D2, E2, and F2 cause?
(four things) What do COX-2 inhibitors do? Why do COX-2 inhibitors cause a greater risk of acute ischemic events in the heart? |
1. Vasodilation
2. Fever 3. Pain 4. Potentiate edema Selectively block the inflammatory effects of prostaglandins w/o inhibiting COX-1 which is expressed in gastric mucosa Inhibit PGI more than TXA creating a prothrombotic state |
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65. What does the lipoxygenase pathway produce?
Three things... |
1. 5-HETE
**chemotactic for neutrophils 2. LTB4 3. LTC4, LTD4, LTE4 **leukotrienes |
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66. What cells produces LTB4?
What does it do? |
Neutrophils and macrophages
Potent chemotactic agent fro neutrophils **like 5-HETE |
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67. What cell produces LTC4, LTD4, and LTE4?
What two things do these leukotrienes cause? |
Mainly in mast cells
1. Bronchospasms 2. Increased vascular permeability in venules |
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68. What function do lipoxins mainly serve?
What is transcellular biosynthesis? |
Inhibitors of inflammation by inhibiting chemotaxis and adhesion to endothelium
When neutrophils "pass" leukotriene intermeidates to platelets which complete the synthesis of lipoxins |
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69. What are glucocorticoids?
How do they act? |
Powerful anti-inflammatory agents
Act in part by inhibiting activity of phospholipase A2 **arachidonic acid isn't released from phospolipid bilayer so neither cyclooxgenase nor lipoxygenase pathway can occur |
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70. What is platelet-activating factor?
What are the pro-inflammatory effects of platelet-activating factor? How does it compare do histamine in terms of vasodilation and increased vascular permeability? How does it affect leukocytes? How doe s it effect other chemical mediators? |
Long chain FA released from cell phospholipid membranes by phospolipase A2
Cause platelet aggregation and degranulation, bronchoconstriction, & vasoconstriction 100x more potent Modulates leukocyte adhesion, enhances activation and chemotaxis Boosts their synthesis **esp. eicosanoids |
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71. What are cytokines?
What are cytokines important in? What are two examples of cytokines? |
Polypetides secreted by one cell type to modulate the differentiation or function of another cell type
Inflammation and immune response 1. IL-1 (interleukin-1) 2. TNF (tumor necrosis factor) **both share many biologic properities |
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72. How do IL-1 and TNF exert their effects?
What is their principal source? What stimulates the secretion of IL-1 and TNF? (three things) |
Autocrine, paracrine and endocrine mechanisms
Activated macrophages 1. Microbial products 2. Immune complexes 3. T cells during active immune resposne |
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73. In inflammation what is the most important action of cytokines?
What does this do? (five things) |
Activation of endothelial cells
1. Stimulate expression of adhesion molecules 2. Increase leukocyte recruitment 3. Enhance production of chemokines and eiocsanoids 4. Increase thrombogenicity of endothleium 5. Activate neutrophils |
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74. What in particular does IL-1 do?
Via endocrine actions what do cytokines such as IL-1 and TNF do? |
Activates fibroblasts w/ production and turnover of ECM (healing)
Cause systemic acute-phase response: -fever -loss of appetite -lethargy **TNF plays role in hemodynamic changes of septic shock |
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75. What are chemokines?
What do a unique combination of chemokines do? What are two major groups of chemokines and what do they do? |
Cytokines w/ chemotactic properties
Recruit particular cell populations to sites of inflammation 1. CXC -> acute inflammation -act primarily on neutrophils 2. CC -> chronic inflammation -attract monocytes, macrophages, eosinophils, etc. |
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76. What do reactive oxygen species aid in when formed in phagolysosomes?
What can extracellular release of low levels of free radicals do? What happens when free radicals are released at higher levels? What does the extent of tissue damage depend upon? |
Aid destruction of ingested microbes
Pro-inflammatory **increase expression of other inflammation mediators Higher levels --> cause tissue injury Based on balance between free radicals and antioxidants in tissues |
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77. What is nitric oxide (NO)?
How are the affects of NO and why? How is endothelial NOS (eNOS)? |
Soluble free radical gas synthesized by nitric oxide synthetase (NOS)
Short range (only nearby cells) b/c half-life is in seconds Constantly producing low amounts of NO that relaxes smooth muscle causing vasodilation |
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78. Where is inducible NOS (iNOS) present?
What is iNOS used for? What does NO released during inflammation cause? What does it inhibit? |
Present in macrophages
-also endothelium & various other cells Use it as microbiocidal agent Causes vasodilation Inhibits all stages of platelet activation and reduces leukocyte recruitment to injured areas |
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79. When are lysosomal constituents (enzymes and bactericidal factors) of leukocytes released?
Where do acid proteases operate? What are neutral proteases capable of doing? (three things) What do serum and tissue fluids contain to keep these enzymes in check? What does tissue damage result from? |
Released during phagocytosis and cell death
Operate in phagolysosomes at low pH 1. Breakdown ECM 2. Cleave C3 & C5 directly to form C3a & C5a 3. Cleave high MW kinigen to bradykinin Antiproteases Imbalance between proteases and anti-proteases |
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80. What do neuropeptides do?
What are examples of neuorpeptides? What does the substance P contained in nerve fibers in the lung and GI tract do? |
Initiate inflammatory response
Substance P & neurokinin A 1. Transmits pain signals 2. Regulate vessel tone 3. Modulate vascular permeability |
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81. What pathways activate the complement system?
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1. Classical pathway
-antigen-antibody complexes 2. Alternate pathways -microbial endotoxins -aggregated IgA -complex polysaccharides 3. Lectin pathway -involves collectins and C1 components |
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82. What does each pathway generate?
What does this do? How are complement components controlled? |
C3 convertase
Cleaves C3 to C3a & C3b Factors regulate C3 and C5 convertases |
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83. What does C3b do?
(two things) What does C5b do? |
1. Bind to cell or microbe surface
*opsonization & phagocytosis 2. Couple w/ C3 convertase to make C5 convertase Combines w/ remaining complement components to produce membrane attack complex (MAC) **MAC causes target cell lysis |
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84. What role does C5a in have inflammation?
(five things) What role dose C3a have in inflammation? (two things) |
1. Leukocyte adhesion
2. Chemotaxis 3. Leukocyte activation 4. Increased vascular permeability 5. Vasodilation 1. Increased vascular permeability 2. Vasodilation |
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85. What does Hageman factor (XII) convert?
What does kallikrein release? What else does kallikrein do? (three things) |
Prekallikrein in plasma to enzyme kallikrein
Bradykinin **from high MW kininogen 1. Activates XII 2. Splits C5 to form C5a 3. Chemotaxic |
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86. What does bradykinin cause?
(four things) What inactivates it? |
1. Vasodilation
2. Increased vascular permeability 3. Smooth muscle contraction 4. Pain (dalor) Kininase (locally) or angiotensin-converting enzyme (circulating) |
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87. What does the clotting system consist of?
What does thrombin bind to? What does thrombin cause? (two things) What does fibrin cleave fibrinogen into? (two things) |
Intrinsic and extrinsic pathways culminating in formation of thrombin and cleavage of fibrinogin to fibrin
Bind to protease-activated receptors 1. Increased leukocyte adhesion 2. Fibroblast proliferation 1. Fibrin 2. Fibrinopeptides **increase vascular permeability **chemotactic for leukocytes |
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88. What does factor Xa cause?
(two things) When the fibrinolytic system is activated during clotting what does it generate? When plasmin lyses fibrin clots what does it produce? What do these products induce? Besides splitting fibrin clots what can plasmin do? (two things) |
1. Increased vascular permeability
2. Exudation of leukocytes Plasmin Produce fibrin split product Induce increased vascular permeability 1. Activate factor XII 2. Split C3 to C3a & C3b |
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89. What does XIIa initiate?
(four systems involved in inflammation) What amplifies this process by further activation of factor XII? |
1. Kinin system
2. Clotting system 3. Fibrinolytic system 4. Complement system Kallikrein and plasmin |
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90. During chronic inflammation what three processes occur simultaneously?
How does chronic inflammation frequently begin? |
1. Active inflammation
2. Tissue destruction 3. Healing Insidiously and asymptomatically |
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91. Under what setting will chronic inflammation arise as the primary process?
Four situations |
1. Viral infections
2. Persistent infections -evoke delayed-type hypersensitivity 3. Prolonged exposure to exogenous or endogenous potentially toxic agents 4. Immune-mediated inflammatory diseases |
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92. Microscopically how is chronic inflammation characterized?
What is tissue destruction largely due to? What is the key feature of chronic inflammation? What is the dominant cell type in chronic inflammation? |
Mononuclear cell infiltrate
-lymphocytes -plasma cells -macrophages Due to inflammatory products secreted by the cells Persistence Macrophages |
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93. What system are macrophages a part of?
From the blood macrophages migrate into tissue and become what? How do these compare to regular macrophages? (three differences) Where is emigration of macrophages enhanced? |
Body wide mononuclear phagocyte system (MPS)
Resident macrophages 1. Larger (more active metabolism) 2. More phagocytic 3. Longer lifespan At sites rich in specific inflammatory mediators (C5a, PDGF, IL-8, tissue breakdown products) |
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94. At the site of inflammation what chemical agent from T cells activates emigrating macrophages?
If inflammation persists by what means do macrophages continues to accumulate? (three means) |
IFN-gamma
1. Recruitment of monocytes from blood via inflammatory mediators 2. Local proliferation of macrophages 3. Immobilization of macrophages by certain cytokines |
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95. What can IFN-gamma secreted by T cells do?
What do macrophages secrete? How are macrophages involved in the repair process (pro-repair)? |
Cause macrophages to fuse into mulit-nucleated giant cells
Wide variety of biologically active substances Secrete various growth factors that cause... -fibroblast proliferation -angiogenesis -repair |
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96. What hallmark of chronic inflammation is a by-product of macrophage products?
If lymphocytes (B & T) recognize an antigen what do they do? How do macrophages affect T cells? |
Tissue destruction of parenchyma and supporting stromal network
Differentiate and secrete factors (T cells) that stimulate an immune response as well as macrophages that promote inflammation Products activate T cells |
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97. What are plasma cells?
Eosinophils accumulate at sites of immune reactions mediated by what two things? What do eosinophils secrete? How is MBP? |
Differentiated B cells at site of inflammation that produce antibodies
IgE (allergies) & parasitic infections Major basic protein (MBP) Highly cationic and toxic to mammalian and parasitic cells |
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98. Where are mast cells located?
What type of inflammation do mast cells participate in? What else are mast cells important in? What do they secrete? |
Widely distributed in CT throughout the body
Both acute and chronic Type I hypersensitivity reactions w/ IgE Secrete a # of things (very active) |
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99. What is the predominant cell in granulomatous inflammation?
What is a granuloma? Where may multinucleated giant cells form? What is it called when the nuclei are at the cell periphery in a ring? |
Epithelioid macrophages
**activated macrophage resembling epithelial cell Aggregate of epithelioid macrophages surrounded by a collar of lymphocytes and plasma cells In center or periphery of granuloma Langhans-type giant cells **common in TB |
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100. What chronic immune and infectious diseases are granulomatous inflammation found in?
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1. TB
2. Leprosy 3. Lymphogranuloma inguinale 4. Deep fungal infections 5. Cat scratch disease 6. Suphilis 7. Sarcoidosis 8. Crohn's disease |
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101. In TB what is the granuloma referred to as?
What does the granuloma often exhibit? |
Tubercle
Exhibits central caseous necrosis |
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102. What do lymphatic do?
What are immunologic tissue in lymph nodes and the spleen? |
Drain areas of inflammation reducing edema and carrying away cellular debris
Secondary lines of defense |
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103. What is lymphangitis and lympadenitis?
What happens if lymphatics are overwhelmed? |
When lymphatics become secondarily inflamed
Bacteria gain access to blood as bacteremia **In massive infections bacteria can cause endocarditis, meinigitis, septic arthritis, renal abscesses, etc. |
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104. What is acute-phase reaction?
What is it principally mediated by? |
Collection of systemic effects brought on by more widespread inflammation
TNF, IL-1, and IL-6 |
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105. What are manifestations of acute-phase reaction?
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1. Fever
2. Elevated plasma levels of acute phase proteins 3. Other manifestations -increased heart rates -increased blood pressure -decreased sweating -shivering/chills |
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106. How is the set point in the hypothalamus elevated to cause fever?
What are the elevated plasma levels of acute phase proteins mostly synthesized by? Severe bacterial infections (sepsis) can result in large quantities of what in the blood stream? |
LPS, TNF and IL-1 act as pyrogens that stimulate PGE synthesis
Live after stimulation by IL-6 TNF, IL-12, and IL-1 |
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107. What is luekocytosis?
It is a common feature of inflammatory reactions caused by what? In leukocytosis what do IL-1 and TNF initially do? |
Increased white cell count in blood
Bacterial infections which produce neutrophilia Induce increased release of cells from bone marrow |
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108. What is leukopenia?
What can cause leukopenia? (three things) |
Reduced white cell count in blood
1. Infections from some viruses 2. Rickettsiae 3. Certain protozoa |
