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Fichas por Afronewtzz, actualizado hace más de 1 año
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Creado por Afronewtzz
hace más de 9 años
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| Pregunta | Respuesta |
| How does acute inflammation of meningitis appear? | Thick exudate - Creamy appearance due to accumulation of neutrophils beneath the arachnoid membrane. |
| What are the 3 membranes that line the skull and vertebral canal called? Under which of these 3 membranes do neutrophils recruit to during meningitis? | - Dura mata - Arachnoid* (middle) - Pia mater |
| What is meant by 'local' chemical mediators of inflammation? | - Mediated by cells at the site of inflammation. - Resident or recruited. - Active over a short range. |
| What is meant by 'systemic' chemical mediators of inflammation? | - Synthesised by the liver and enter the circulation. - e.g. plasma proteins |
| What 3 components make up the storage granules in mast cells? | - Histamine - Serotonin - Lysosomal enzymes |
| What 5 mediators of inflammation are synthesised by the ER in a mast cell before release at sites of infection? | - IL- 8 - Prostaglandins - Leukotrienes - Oxygen radicals - Nitrogen radicals |
| What is histamine? | Chemical released by cells which causes contraction of smooth muscle and dilation of capillaries. |
| What is Serotonin? | - Released from platelets following their aggregation. - Causes vasoconstriction during clotting. |
| What is the purpose of lysosomal enzymes in mast cells? | To help in the breaking down/ degranulation of mast cells. |
| What is the purpose of IL8 ? | - Interleukin-8 is a member of the CXC chemokine family. - Small heparin- binding proteins (pro-inflammatory) - mediate activation of neutrophils into tissue from peripheral blood. |
| What is the purpose of prostaglandins? | Metabolic products of phospholipids. Induce pain and fever during inflammation. |
| What are leukotrienes? | Biologically-active compounds - orginally isolated from leukocytes. |
| What is the purpose of the release of oxygen/ nitrogen radicals? | Free radicals exert their actions via activation of nuclear factors which induce the synthesis of cytokines; promoting synthesis of inflammatory mediator. > Exert their toxic effect at site of inflammation. |
| Name 4 systems which are systemic mediators of inflammation. | - Complement system - Clotting system - Kinin system - Fibrinolysis system |
| What enzyme catalyses the conversion of fibrinogen (soluble in blood) into fibrin (insoluble)? | Thrombin |
| What is the purpose of fibrin (formed from fibrinogen)? | Forms a fibrous mesh that impedes the flow of blood. |
| Name 2 vasoactive amines. | Histamine Serotonin |
| Name 5 factors which can induce the release of histamine from mast cells. | - Physical injury (trauma, heat) - IgE cross-linking with antigens - C3a and C5a - Neuropeptides (substance P) - IL-1 and IL-8 |
| What are the purpose of IL-1 and IL-8? | - IL-1 = Cytokine = Activation of vascular endothelium. - IL-8 = Cytokine = Mediates the activation and migration of neutrophils into tissue from the blood. |
| What is chemotaxis? | Movement of an organism in response to chemical stimuli. |
| Name 3 cell-derived mediators which are recruited to endothelial cells (post-degranulation of mast cells) during inflammation.. | - Bradykinin - Thrombin - Histamine |
| When histamine, bradykinin and thrombin are released from mast cells and recruited to endothelial cells during inflammation, what does this induce? | - Causes an increase in Ca2+ conc. - Causing the synthesis of Nitric oxide by Nitric oxide synthase... - Causing the synthesis of Prostaglandin PG12 via Cyclooxygenase... - These cell-derived mediators are secreted... - Induces vasodilation and smooth muscle cell relaxation. - Heat generation. |
| Describe the formation of prostaglandins. | - Stimulation = Bradykinin, C5a and other cell-derived mediators activate Phospholipase A2/ PLA2 at the plasma membrane. - Phospholipid is cleaved from membrane by PLA2 as Arachidonic acid & Lysophospholipids. - Products are divided by enzymes: - Lipoxygenases cleave off Leukotrienes. - Cyclooxygenases/ Cox cleave off prostaglandins. |
| Other than Prostaglandins, Leukotrienes are also produced from the metabolism of phospholipids, what do they do? | Leukotrienes, specifically LTB4, is chemotactic for neutrophils. Able to induce the adhesion and activation of leukocytes. |
| During the metabolism of Arachidonic acid, what 4 prostaglandins can be generated from the cyclooxygenase pathway? | - PGE2 - PGD2 - PGF2-alpha - PGI2 |
| What is the purpose of the prostaglandin PGI2 produced using the cyclooxygenase pathway of arachidonic acid metabolism? | Potent vasodilator and inhibitor of platelet aggregation. |
| What is 5-lipoxgenase enzyme? | A major Arachidonic acid metabolizing enzyme in neutrophils. |
| What leukotrienes are mainly made my neutrophils during the metabolism of Arachidonic acid? | LTB4 |
| What is the Leukotriene, LTB4? | A potent chemotactic agent produced by neutrophils during the metabolism of Arachidonic acid (used in positive feedback). |
| What leukotrienes are mainly made my mast cells during the metabolism of Arachidonic acid? | LTD4 E4 |
| What are the leukotrienes, LTD4 and E4? | Leukotrienes produced by mast cells during the metabolism of Arachidonic acid. Cause broncho-constriction and vascular permeability - hence difficulty in breathing (asthma). |
| What do steroids do as an anti-inflammatory? | Steroids block the pathway which converts Phospholipids into Arachidonic acid & Lysophospholipids by inhibiting Phospholipase A2. |
| Why are NSAIDs drugs used to control the anti-inflammatory process? | NSAIDs block the conversion of Arachidonic acid into Prostaglandins via inhibiting Cyclooxygenases / Cox. Thus, preventing pain and fever. |
| Why pathway do NSAIDs NOT block when used as a drug to control inflammation? | NSAIDs do not block the break down of lysophospholipids into leukotrienes as they cannot inhibit the lipoxygenases. |
| What are 2 cyclooxygenase enzymes targetted by NSAIDs which go on to inhibit the production of prostaglandins? What is the difference? | - Cox-1 and Cox-2 - Cox-1 catalyses the production of mucosal prostaglandins responsible for acid-induced damage in the GI tract. - Cox-2 catalyses the production of prostaglandins responsible for pathogenesis, pain, fever and inflammation. |
| Why are Pharmaceutical companies trying to develop drugs which only target Cox-1 cycooxygenase? | Because it has been found that targetting Cox-2 cyclooxygenase can have serious thrombatic cardiovascular consequences on the patient. |
| Name 2 cyclooxygenase inhibitor drugs which have been used in anti-inflammation. | - Aspirin - Indomethacin |
| When the body is not undergoing inflammation, are systemic mediators active? | No. |
| What complement from the Complement cascade inserts itself into the membrane of bacteria to puncture their cells? What is this process called? | - C6C7C8C9 - Membrane Attack Complex/ MAC |
| How is the Complement Cascade initiated? | When an antigen-antibody complex forms. |
| When C3a and C5a (?) are produced in the complement cascade, what function do they perform? | - Anaphylatoxins: - Induce mast cells to release histamine. - Act directly on blood vessels to increase vascular permeability. - C5a is chemotactic for neutrophils. - C5a also causes a conformational change in integrins. |
| Explain how anaphylatoxins help to control the adhesion of leukocytes to the vascular endothelium. | - C3a and C5a - Alter the conformation of the integrins which allows adhesion to perform. |
| What is the purpose of Fibrin? | Traps platelets and induces clot formation. |
| What is the purpose of fibrinopeptide released from fibrinogen during the formation of fibrin? | - Increases vascular permeability. - Chemotactic for WBC. |
| What is Bradykinin? | - Similar to histamine. - Causes contraction of smooth muscle and vasodilation. - Rapidly inactivated. |
| What is the purpose of the systemic mediator, the kinin cascade? | Generate bradykinin |
| What is the purpose of the fibrinolytic cascade (systemic mediator)? | - Assist in de-coagulation - without fibrinolysis, any injury would result in irreversible clotting.. |
| How is plasmin formed in the fibrinolytic pathway and what does it do? | - Plasminogen is converted to plasmin via Kallikrein (from kinin cascade). - Plasmin destroys blood clots by attacking fibrin. - Plasmin also activates C3 > C3a to induce mast degranulation. |
| How is thrombin formed and what is its function in the clotting cascade? | - Thrombin is one of the final products of the clotting cascade. - Thrombin converts fibrinogen to fibrin. - Thus, initiates clotting. |
| Other than phagocytosis, what else do neutrophils do kill invading pathogens? | Produce reactive oxygen radicals. |
| By what process is phagocytosis of microorganisms facilitated by? By what? | Opsonisation Opsonins |
| Define opsonins. | - Serum proteins that bind to the surface of microorganisms - i.e. Immunoglobulins, IgG - i.e. Complement component, C3b |
| Describe the process of phagocytosis using Opsonins (opsonisation). | - IgG and C3b opsonins (on bacteria) bind to Fc receptor and C3b receptors (on phagocyte) respectively. - Phagocytes engulf opsonent pathogen. - Phagosome and lysosome bind. - Lysosomes promote reduction of toxic mediators inside the cell therefore the phagosomes do not do damage to the phagocyte or surrounding cells. |
| Describe the role of fMet- Leu - Phe receptors in the phagocytosis of pathogens. | - Opsonins on pathogens bind to opsonin receptors on phagocytes. - fMLP receptors on the surface of the phagocytes recognise fMet-Leu-Phe peptides from the same pathogen. - This activates Rac2 - Bacteria are taken up in vesicles. |
| Describe how phagolysosomes are generated/ activated to degrade its components. | - Phagosome fuses with primary and secondary granules. - Rac2 makes NADPH oxidase in the phagolysosome membrane; leading to production of oxygen radicals/ O2-. - Ion influx/ Acidification. - Granule proteases released from matrix. - Degradation of microbial components. |
| Name some oxygen-dependent anti-microbial mechanisms (7). | - O* (Superoxide) - OH* (Hydroxyl radical) - H2O2 (Peroxide) - ClO- (Hypochlorite) - NO (Nitric oxide) - NO2 (Nitrogen dioxide) - HNO2 (Nitrous acid) |
| Name some oxygen-independent anti-microbial mechanisms (7). | - Defensins - Lysozyme - Hydrolytic enzymes |
| What major mediators of acute inflammation initiate the following effects? - Vasodilation - Increased vascular permeability - Chemotaxis - Fever - Pain | - Vasodilation = Prostaglandins & Nitric oxide. - Increased vascular permeability = Amines, C3a, C5a, Bradykinin & Leukotrienes. - Chemotaxis = C5a, Leukotriene B4, Bacterial products & Chemokines (e.g. IL-8). - Fever = IL-8, IL-6, TNF & Prostaglandins. - Pain = Prostaglandins & Bradykinin. |
| What 3 products of acute inflammation cause tissue injury? | - Reactive oxygen species - Lysosomal enzymes - Metabolic products of arachidonic acid (leukotrienes). |
| What are 3 main outcomes of Acute Inflammation? | - Resolution - Scarring or fibrosis (abscess formation inevitably leads to this) - Inability to clear damage or eradicate infectious agent > Chronic Inflammation. |
| What are 3 common features of Chronic inflammation? | - Mononuclear cells - Tissue destruction - Angiogenesis & Fibrosis |
| What is Angiogenesis? | Development of new blood vessels. |
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