Acute Inflammation

Mind Map by , created over 6 years ago

Blood Science Mind Map on Acute Inflammation, created by maisie_oj on 04/29/2013.

Created by maisie_oj over 6 years ago
Haemostasis (part 1: primary haemostasis)
Haematopoietic System Malignancies 2
Bone marrow failure syndromes
Test Primer Parcial - Tecnologías de la Información I
Ing. José Luis A. Hernández Jiménez
salesforce Developer 1
Cell adaptations
Rheumatoid Arthritis
Acute inflammation
Sebastian Bassi
Blood transfusion and haematopoietic stem cell transplantation
Haemopoietic System Malignancies
Acute Inflammation
1 Definition
1.1 Complex reaction of vascularized tissue to injurious agents or necrotic tissue
1.1.1 Aims to get rid of irritants and prepare injured tissue for repair
1.1.2 Consists of vascular, cellular and systemic responses
1.2 Generally protective but can be harmful
1.2.1 Hypersensitivity (e.g. to insect bite)
1.2.2 Inflammatory diseases
1.2.3 Repair of cell damage leading to fibrosis
1.3 2 types
1.3.1 Acute Rapid onset Short duration (mins, hours, days)
1.3.2 Chronic Long duration (months, years) Different cell types and tissue responses
2 Causes
2.1 Infection - bacterial/parasitic
2.2 Trauma
2.3 Physical/Chemical agens - burns, irradiation
2.4 Tissue necrosis (by definition)
2.5 Foreign bodies (e.g. sutures)
2.6 Immune reaction
2.7 Some causes have distinct features but all produce fundamental features
3 Symptoms
3.1 Calor (hotness)
3.2 Rubor (redness)
3.3 Tumour (swelling)
3.4 Dolor (pain)
3.5 Laseofunctio (loss of function)
4 Vascular Changes
4.1 Alterations in vascular calibre cause changes in blood flow
4.1.1 Transient constriction then dilation of arterioles, capillaries and venules Increased blood flow to capillaries Increased permeability of capillaries
4.2 Structural changes in small blood vessels allow plasma proteins and cells to leave circulation
4.2.1 Increased vascular permeability Accumulation of fluid in interstitial tissue - oedema Protein-rich fluid = exudate Protein-low fluid = transudate
4.2.2 Migration of leukocytes into tissue
4.3 Loss of fluid causes blood to become more viscous - moves more slowly (stasis)
4.3.1 Allows cells to come into contact with blood vessel wall Leukocytes stick to endothelium and migrate out into tissues
4.4 Changes to Vascular Permeability
4.4.1 Formation of Endothelial Gaps Rapid, short duration - 30 mins Caused by histamine, leukotrienes, bradykinin Cause cell contraction TNF and IL-1 have similar effects but they are delayed (4-6-hours) Only affects venules
4.4.2 Direct Endothelial Cell Injury Rapid, long lasting Caused by necrotising injuries - burns Destruction of endothelial cells causes immediate, sustained vascular permeability Response can be delayed - sunburn
4.4.3 Leukocyte Mediated Endothelial Cell Injury Leukocytes activated as part of acute inflammatory response Release toxic oxygen species which kill endothelial cells
4.4.4 Increased Transcytosis Enhanced by VEGF and histamine Movement of interconnected vesicles across cytoplasm Vesicuvacuolar organelle
4.4.5 Angiogenesis Part of response to acute inflammation New blood vessels are leaky Prolonged
5 Cellular Changes
5.1 Leukocyte extravasation
5.1.1 Margination, rolling (transient adhesion) and firm adhesion to endothelium Transmigration across endothelium (diapedesis) Migration in the tissue towards chemotactic stimulus Accumulation in area of injury Activation to destroy and engulf injurious agent Margination - cells occupy periphery of blood vessel (due to stasis)
5.2 Leukocyte Adhesion and Transmigration
5.2.1 Selectins E-selectin - endothelial cells P-selectin - endothelial cells and platelets L-selectin - leukocytes Bind to sialyl-Lewis X-modified glycoprotein on leukocytes Mediate rolling
5.2.2 Immunoglobulins ICAM-1 - mediates adhesion, arrest and migration VCAM-1 - mediates adhesion Found on endothelial cells CD31 (PECAM) - mediates migration Ligands for integrins Transmembrane protein - alpha and beta subunit Beta2 integrins LFA-1 (CD11a/CD18) Mac-1 (CD11b/CD18)
5.3 Chemotaxis
5.3.1 Movement along a chemical gradient
5.3.2 Stimuli Endogenous Complement components (C5a) in plasma Products of the lipoxygenase pathway (LTB4) from damaged tissue Cytokines (IL-8) from activated macrophages/lymphocytes Exogenous Bacterial products
5.3.3 Chemotactic factors bind to 7 g-protein coupled receptors on leukocytes PLCg and PI3K activation Actin polymerisation Migration
5.4 Leukocyte Activation
5.4.1 Via 4 receptors on leukocytes 7 transmembrane G-protein coupled receptors Recognise microbes, C5a and bacterial products Initiates release of microbicidal factors Toll-like receptors Different TLRs recognise different microbes Bind to LPS and dsRNA (found in some viruses) Lead to production of cytokines and ROIs Mannose receptor Causes ingesting of microbes Binds terminal mannose/fucose residues on bacterial wall that aren't present in mammals Scavenger receptors Bind to modified LDL/bacterial wall
5.5 Phagocytosis
5.5.1 3 stages Recognition and attachment Microbes bind to specific receptors - aided by opsonisation (higher affinity) Opsonins IgG - Fc receptor C3 complement fragment - CR1 Fibrinogen - integrins Fibronectin - CR proteins Engulfment Cytoplasmicpseudopods flow around particle and form phagosome Fuses with lysosomal granule ieukocyte (phagolysosome) Killing and degradation Generally via RO species H2O2-MPO-Halide system Bacteriacidal permeability increasing protein (BPI) Lysozyme - hydrolysis of glycopeptides Lactoferrin Major basic protein - cytotoxic to parasites Defensins - cytotoxic to microbes

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