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Inflammation.
Acute inflammation
| Question | Answer |
|---|---|
| Whats is inflammation? | A. Allows inflammatory cells, plasma proteins (e.g., complement), and fluid to exit blood vessels and enter the interstitial space B. Divided into acute and chronic inflammation |
| What is acute inflamation when does it take place | Characterized by the presence of edema and neutrophils in tissue B, Arises in response to infection (to eliminate pathogen) or tissue necrosis (to clear necrotic debris) C, Immediate response with limited specificity (innate immunity). |
| What is innate immunity? | includes epithelium mucus- protect against infection complement product- inactivated protien mass cells-activates immune response macrophages- killer cells neutrophill, eosinophils, basophils. spefic immunity- lymphocytes, antibodies Tcells |
| Factors effecting innate immunity | TLR, Arachidonic acid, mast cells,complement, illegamen factor. |
| What are Toll like receptors and how do they work? | TLR are on innate immunity cells. recofnize PAMP on pathogens CD14 (a TLR) on macrophages recognizes LPS lipo polysaccharide (PAMP) on outer membrane of gram-negative bacteria TLR activation= upregulation of NF-kB,(nuclear transcription factor.)=respons |
| What is arachidonic acid? | released from phospholipid cell membrane by phospholipase A2, and then acted upon by: i. Cyclooxygenase ii. 5-lipoxygenase |
| how doees Arachidonic acid relate to Cyclooxygenase for immunity? | AA is acted upon by cyclooxygenase i. Cyclooxygenase produces prostaglandins (PG). a. PGI2, PGD2 and PGE2 mediate vasodilation(arteriole) and increased vascular permeability(post capilary venule). b. PGE2 also mediates pain and Feeeever. |
| how doees Arachidonic acid relate to 5-lipoxygenase for immunity? | 5-lipoxygenase produces leukotrienes (LT). a. LTB4, attracts and activates neutrophils. b. LTC4 LTD4, and LTE4 (slow reacting substances of anaphylaxis) mediate vasoconstriction, broncho spasm, and increased vascular permeability |
| What are the four things that attract neutrophils? | LTB4, C5A Il8, bacterial products! |
| How do mast cells help with immunity ? | distributed thru connective tissue Activated by tissue trauma, complement proteins C3a and C5a, or cross-linking of cell-surface IgE by antigen release of preformed histamine granules =vasodilation of arterioles and increased vascular permeability. |
| How to activate complement? | inactive precursors; activation- Classical path-—it binds IgG or IgM that is bound to antigen. Alternative pathway—Microbial products directly activate it Mannose-binding lectin (MBL) pathway—MBL binds to mannose on microorganisms and activates comple |
| The complement pathway | LOOK IT UP Classical path Alternate pathway Lectin pathway C3a and C5a (anaphylatoxins)—trigger mast cell degranulation, resulting in histamine reaction C5a—chemotactic for neutrophils Ob—opsonin for phagocytosis MAC—creating a hole in the cell m |
| What is the Hageman factor? | Inactive proinflammatory protein produced in liver Activated exposure to tissue collagen in turn, activates iCoagulation iiComplement iii. Kinin cleaves high-molecular-weight kininogen (HMYVK) to bradykinin --> histamine like response and pain |
| Signs of inflamation | Redness and warm- vasodilation,results in increased blood flow 2. Occurs via relaxation of arteriolar smooth muscle; key mediators are histamine, prostaglandins, and bradvkinin. B. Swelling (tumor) 1. Due to leakage of fluid from postcapillary venules |
| how is fever developed? | 1. Pyrogens (e.g., LPS from bacteria) cause macrophages to release IL-1 and TNF, which increase cyclooxygenase activity in perivascular cells of the hypothalamus,->PGE2 2. Increased PGR, raises temperature set point. |
| Steps for neutrophil arrival and function- Step 1 | Step 1—Marginatum 1. Vasodilation slows blood flow in postcapillary venules. 2. Cells marginate from center of flow to the periphery. |
| Acute inflammation time line | there are three phases - fluid phase - immediate- edema - neutrophil phase - 24hours - macrophages phase - 2-3 days |
| Steps for neutrophil arrival and function- Step 2 | 1. Select in "speed bumps" are upregulaled on endothelial cells. 2. Selectins bind sialyl Lewis X on leukocytes. 3. Interaction results in rolling of leukocytes along vessel wall, |
| describe the selectins one the edothelium surface | i. P-seleclin release from Weibel Patade bodies is mediated by histamine. ii. E-selectin is induced by TNF and IL-1. |
| Steps for neutrophil arrival and function- Step 3 | Cellular adhesion molecules upregulated on endothelium by TNF & IL-1 Integrins are upregulated on leukocytes by C5a & LTB4. (same as the one that activate neutrophiles) 3. This results in firm adhesion of leukocytes to the vessel wall |
| what is Leukocyte adhesion deficiency? | Leukocyte adhesion deficiency is due to an autosomal recessive defect of integrins (CD18 suhunit). Clinically: delayed separation of the umbilical cord, increased circulating neutrophils (due to impaired adhesion , and recurrent bacterial infections. |
| Steps for neutrophil arrival and function- Step 4 | Step 4—Transmigration and Chemotaxis 1. Leukocytes transmigrate across the endothelium of'postcapillary venules and move toward chemical attractants (chemotaxis). 2. Neutrophils are attracted by bacterial products, IL-8, CSa, and LTB.. |
| Steps for neutrophil arrival and function- Step 5 | Step 5—Phagocytosis 1. Consumption of pathogens or necrotic tissue; phagocytosis is enhanced by opsonins (IgG and C3a). 2. Pseudopods extend from leukocytes to form phagosomes, which are internalized and merge with lysosomes to produce phagolysosomes. |
| describe Chediak-Higashi syndrome | a protein trafficking defect(broken track!) (autosomal recessive) impaired phagolysosome formation pyogenic infections risk Neutropenia Giant granules in leukocytes (fusion of granules arising from Golgi) dense granules in platelets Albinism |
| Steps for neutrophil arrival and function- Step 6 | Step 6—Destruction of phagocytosed material 1. O,-DEPENDENT killing is the most effective mechanism. 2. HOCL generated by oxidative burst in phagolysosomes destroys phagocytosed microbes. O,-independent is less effective & uses enzymes from lysozymes |
| myloperoxidase deficiecy syndrome | MPO deficiency results in defective conversion of H2o2 to HOCL'. i. Increased risk for Candida infections; however, most patients are asymptomatic. ii. NBT is normal; |
| What is Chronic granulomatous disease? | NADPH oxidase defect- cant make bleach-Leads to recurrent infection and granuloma formation with catalase-positive organisms, particularly Staphylococcus aureus, Pseudpmonas cepacia, Serratia marcescens, Nocardia, & Aspergillus Nitrobiue tetrazolium t |
| What is the Nitrobiue tetrazolium test? | iii. Nitrobiue tetrazolium test is used to screen for CGD. Leukocytes are incubated with NBT dye, which turns blue if NADPH oxidase can convert 02, to o2-, but remains colorless if NADPH oxidase is detective. |
| Why do patients with Chromic granulomatous disease have recurrent infection and granuloma formation with catalase-positive organisms? | (in the pathway from o2->o2- ->H2o2->HOCL)NadPH oxidase is defective. Most bacteria produce H2o2 which is converted to HOCL. But catalase positive bacteria hydrolyze the H2o2= no HOCL=infection |
| Steps for neutrophil arrival and function- Step 7 | Step 7—Resolution 1, Neutrophils undergo apoptosis and disappear within 24 hours after resolution of the inflammatory stimulus. pus!!! |
| What happens after neutrophils have done the work? | Monocyte derived Macrophages - peak 2-3 days after inflammation. Entery same way as neutrophils Ingest organisms via phagocytosis (augmented by opsonins) and destroy phagocytosed material(e.g., lysozyme) in secondary granules (02 independent killing) |
| What do macrophages do ? | antiinflamatory process- IL10 and TGF beta Continued acute inflamatory - IL8(Macrophages call more neutrophils)more PUS Abscess- fibrosis around the walled off area of actue inflammation. Chronic inflammation- MHC2- CD4 helper T cells. |
Created by:
atayal
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