Flashcards
Inflammation & Chronic Inflammation L1
Cards in this deck (49)
- 1InflammationThe biological response of vascular tissues to harmful stimuli such as pathogens, injury, or irritation.
- 2Characteristics of Inflammation (5)Swelling, redness and heat arising from increased blood flow, pain, oedema, and 'infiltration' of the cells of the immune system.
- 3OedemaMedical term for fluid retention in the body.
- 4Diseases involving InflammationInflammation is a symptom of almost all major diseases: cancer, cardiovascular diseases, Alzeimers, diabetes II, arthritis, auto immune diseases, neurological diseases, pulmonary diseases etc.
- 5Hallmark features of Inflammation (5)Tumor (swelling), Rubor (redness), Calor (heat), Dolor (pain), and an associated loss of activity/function on the inflamed area.
- 6i1 Inflammatory ResponseInitiated by tissue damage caused by endogenous or exogenous factors: physical, chemical, biological (infectious), immunological injury.
Initiation requires utilisation of both the innate and adaptive immune system components. - 7EndogenousSubstances or processes originating from within an organism, tissue or cell.
- 8ExogenousAny material that is present and active in an individual organism or living cell but that originated outside that organism, as opposed to an endogenous factor.
- 9i2 Inflammatory ResponseInflammation begins rapidly with local release of inflammatory mediators by damaged tissue.
These trigger local vasodilation, which produces rubor and calor.
Fluid leaks out through the vessel walls, resulting in oedema (tumor), which produces localised pressure on nerve endings causing pain (dolor). - 10Effects of Local VasodilationIf the blood vessel is dilated, this increases the blood flow and enhances the capillary permeability.
- 11i3 Inflammatory ResponsePhagocytic cells (principally neutrophils) accumulate within 30-60 minutes and begin the process of phagocytosis and the release of inflammatory cytoplasmic granules to destroy invading microorganisms.
- 12Respiratory BurstRelease of toxic neutrophil granules accompanied by a transient increase in their oxygen consumption.
- 13i4 Inflammatory ResponseInflammatory mediators activate the endothelium to produce adhesion molecules such as E-selectin to facilitate neutrophil binding.
Inflammatory mediators also stimulate the production of complementary molecules on the surface of monocytes and neutrophils to facilitate their binding & entering into the damaged/infected region. - 14What role does oedema serve?Oedema facilitates the release of leukocytes into the injured area, which secrete chemotactic factors that promote migration and recruitment of more leukocytes to bind to the endothelium, and then undergo diapedesis to move into the injured/inflamed area.
- 15ExtravasationProcess of leukocyte migration out of blood capillaries into the tissues.
- 16ii1 Process of ExtravasationLeukocyte is slowed by interaction with adhesion molecules expressed on the blood vessel wall, such as E-selectin, which enables the cells to "roll" along the endothelial cell wall.
- 17ii2 Process of ExtravasationBinding of the phagocyte to the endothelium is increased via engagement of receptors, notably to proteins up-regulated by the locally released inflammatory mediators.
- 18ii3 Process of ExtravasationLeukocyte squeezes between neighbouring endothelial cells, a process termed diapedesis.
- 19EndotheliumIt is a thin layer of simple squamous cells called endothelial cells in blood or lymph vessels.
- 20ii4 Process of ExtravasationLeukocyte migration to the site of injury/infection (chemotaxis) driven by a locally produced chemoattractant such as IL-8.
- 21i5 Inflammatory ResponseIf inflammation persists, within 5-6 hours there will be an infiltration of more mononuclear cells; macrophages and lymphocytes.
- 22Benefits of Macrophages in InfiltrationMacrophages will provide further phagocytic activity and antigen presentation for activation of lymphocytes, to initiate the adaptive immune response.
- 23Innate Immune SystemCells and proteins that are always present and ready to mobilize and fight microbes at the site of infection. The main components of the innate immune system are 1) physical epithelial barriers, 2) phagocytic leukocytes, 3) dendritic cells, 4) natural killer T-cell, and 5) circulating plasma proteins.
- 24Adaptive Immune SystemThere are two types of adaptive immune responses: humoral immunity, mediated by antibodies produced by B lymphocytes, and cell-mediated immunity, mediated by T lymphocytes.
- 25Complement SystemThe complement system helps or “complements” the ability of antibodies and phagocytic cells to clear pathogens from an organism. It is part of the innate immune system.
- 26Antibody dependent/independent Branches of Complement CascadeAntibody dependent and independent branches of the complement cascade triggered facilitating micro-organism targeting and clearance. Producing further release of local inflammatory mediators and chemotactic factors that facilitate vessel wall permeability and leukocyte recruitment.
- 27Promotion of Tissue RepairTumour necrosis factor-a (TNFa) stimulates platelet-activating factor (PAF) to trigger a blood clot at the site of injury, restricts loss of plasma and provides a barrier against further infection.
- 28HeamostasisThe stoppage of bleeding.
- 29iii1 Process of Heamostasis: Vascular SpasmVascular Spasm: Contraction on the smooth muscle produces the vasoconstriction.
- 30iii2 Process of Heomstasis: Formation of the Platelet PlugFormation of the Platelet Plug: Lesion of the endothelium exposes the collagen fibers; platelet adhesion is triggered.
Plateletes release mediators which further favourise platelet aggregation; the plug is formed. - 31iii3 Process of Heamostasis: The CoagulationThe Coagulation: Fibrin filaments polymerise; red and white blood cells become enmeshed in fibrin threads and the blood clot is formed.
- 32i6 Inflammatory ResponseCellular rebuilding/repair mechanisms ensue during the course of the insult, resulting in a restorating of the damaged area to its normal state or scar tissue formation.
- 33Mediators of InflammationMacrophages secrete a number of cytokines; interleukins, e.g. local and systemic increase in interleukin-1 (IL-1) & tumour necrosis factor-a (TNF-a), which are pro-inflammatory cytokines.
IL-1 and interferon-g are components of the pyrogens released from macrophages which result in fever. - 34NecrosisThe premature death of cells and living tissue, caused by external factors, such as infection or trauma. It is ATP independent.
- 35IL-10 and TGF-bClassic anti-inflammatory cytokines. IL-10 is produced primarily from monocytes and to a lesser extent lymphocytes, and it is capable of inhibiting synthesis of pro-inflammatory cytokines.
- 36JAK-STATJAK = Janus Finase
STAT = Signal Transducer and Activator of Transcription
Ligands that include certain cytokines utilise the JAK-STAT signalling pathway. - 37JAK-STAT Signalling PathwayExtracellular binding.
Activation of JAKs & receptor tyrosine phosphorylation, STATs bind activated receptors & in turn are phosphorylated & activated.
Homo and hetero STAT dimers migrate to nucleus to alter gene transcription. - 38JAK-STAT Signalling Pathway (Image)
- 39Interferon-gActivated CD4+Th1, CD8+T and NK cells synthesise IFN-g. Which activates NK T-cells, NK cells, and macrophages.
IFN-g induces the expression of MHC class II molecules on many cell types. - 40Interferon-a & -bThey are secreted as a response to viral infection as they inhibit the spread.
- 41How Interferon-a & -b Inhibit the Spread of Viral Infection (3)Activation of genes that limit viral replication.
Stimulate the expression of MHC class I molecules to facilitate viral protein expression on infected cells and their destruction by cytotoxic T-cells.
Activate NK cells to further initiate direct infected cell death and maintain immunosurveillance. - 42ChemokinesFamily of cytokines that posses chemoattractant properties, and includes IL-8.
Function to recruit leukocytes to a site of injury/infection.
Secreted by a variety of cell types, classically separated based upon the position of cysteine residues within amino acid consensus sequences: thereby divided into CXC, CC, C, CXXXC. - 43Structure of Chemokine Classes
- 44Acute Phase ResponseAcute infection results in activation of macrophages and secretion of the pro-inflammatory cytokines IL-1, TNFa, IL-6, and IL-8.
Stimulate up or down regulation of a number of circulatory proteins from the liver, termed the acute phase response. - 45Circulatory proteins from Liver in Acute Phase Response: C-reactive Protein (CRP)Levels increase as inflammatory response. CRP acts as an opsonin, on bacterial and fungal cell surfaces.
For bacteria this stimulates C1q initiating the classical complement pathway, which results in phagocytosis and cell lysis. - 46Circulatory proteins from Liver in Acute Phase Response: Mannose-binding Protein (MBP)Binds pathogen surfaces and activates MBP-associated serine protease (MASP) that initiates the lectin-mediated complement pathway.
Results in phagocytosis and cell lysis.
MBP and likewise complement C3 are upregulated as an inflammatory response. - 47Circulatory proteins from Liver in Acute Phase Response: Serum Amyloid AUpregulated by inflammation.
Multi-functional including recruitment of immune cells to site of inflammation. - 48Circulatory proteins from Liver in Acute Phase Response: FibrinogenConverted by thrombin into fibrin during blood coagulation.
Fibrin in turn is then cross-linked by factor XIII to form a blood clot. - 49Circulatory proteins from Liver in Acute Phase Response: HaptoglobulinBinds haemoglobin.
Haptoglobulin upregulation possibly inhibits microbe uptake of free iron.
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- Bachelors Degree Infection and Defence Flashcards on Inflammation & Chronic Inflammation L1, created by rosiewilkinson35 on 07/11/2015.
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- rosiewilkinson35 · Nov 2015
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- Feb 19, 2016
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