Injury > Inflammation

Lindie Metz
Mind Map by Lindie Metz, updated more than 1 year ago
Lindie Metz
Created by Lindie Metz about 4 years ago
6
1

Description

? Pathology Mind Map on Injury > Inflammation, created by Lindie Metz on 03/02/2016.

Resource summary

Injury > Inflammation
1 PLASMA DERIVED MEIATORS
1.1 HAGERMAN FACTOR
1.1.1 XIIa
1.1.1.1 KININ
1.1.1.1.1 Bradikinin
1.1.1.1.1.1 ↑ Histamine, ↑ VascPermeability, ↑ Vasodilation, BronchoSpasm
1.1.1.1.2 FIBRINOLYTIC
1.1.1.1.2.1 Plasminogen
1.1.1.1.2.1.1 Plasmin
1.1.1.1.2.1.1.1 Fibrin
1.1.1.1.2.1.1.1.1 Fibrinogen
1.1.1.1.2.1.1.2 COMPLEMENT
1.1.1.1.2.1.1.2.1 ↑ VascPermeability, ↑ Leuk activation, adhesion, chemostaxis, Phagocytosis
1.1.1.1.2.2 Inactivates thrombin to limit clotting
1.1.1.2 CLOTTING
1.1.1.2.1 Prothrombin
1.1.1.2.1.1 Thrombin
1.1.1.2.1.1.1
1.1.1.2.1.1.2 Acute Inflammation
1.1.1.2.1.1.3 Cleaves fibrinogen > clot formation, binds to platelets and EN
1.1.2 BM, Collagen, Platelets
2 VASCULAR PHASE
2.1 ↑ VASODILATION
2.1.1 Red/hot/swollen
2.1.2 ↑ Blood to area > ↑ WBC
2.1.3 ↑ in hydrostatic P > Transudate
2.2 ↑ PERMEABILITY
2.2.1 ↓ Colloid Osmotic P > Exudate
2.2.2 ↑ WBC to tissue > Activated (mediators) > ↑ function and phagocytosis
3 ACUTE PHASE REACTION
3.1 VASCULAR CHANGES
3.1.1 1. Vasodilation
3.1.1.1 Mast cells > histamine > relax smooth muscle of vessels
3.1.1.2 ↑ hydrostatic P > Transudate
3.1.1.3 Slows bloodflow > marginalisation of leukocytes
3.1.2 2. Vascular permeability
3.1.2.1 Release mediators from cells (Histamine, Serotonin, Bradykinin, Leukotriens, NO)
3.1.2.2 Endothelial cell contraction > ↑ permeability
3.1.2.3 Fluid + protein into ECM > ↓ Colloid osmoric P > Exudate
3.1.2.4 ↑ sludging and marginalisation
3.1.3 3. Lyphatic vessels
3.1.3.1 Clears inflammation: oedema, inflammation cells, detritis
3.2 CELLULAR CHANGES
3.2.1 1. Leukocyte recruitment
3.2.1.1 (1) Adhesion (2) Transmigration (3) Chemotaxis
3.2.1.2 Chemotaxis stimulated by bacterial products, complement med, leukotriens
3.2.1.3 Chemotaxis of (1) Neutrophils (first responders) (2) Monocytes (replace neutrophils)
3.2.2 2. Leukocyte actication
3.2.2.1 Phogocytosis (1) Recognise and attach (2) Engulf (3) Kill
3.2.2.2 Opsonisation > engulfment
3.2.2.3 Produce lysosomal enzymes: destroy phagocytosed microbes and dead tissue
3.2.2.4 Produce mediators > amplify inflammation
3.2.3 3. Tissue injury
3.2.3.1 Leukocyte induced injury d/t tissue clearing and progression to AI dx
4 CELL DERIVED MEDIATORS
4.1 VASO ACTIVE AMINES
4.1.1 Histamine
4.1.1.1 ↑ Vasodilation, ↑ VascPermeability, BronchoSpasm (Mast)
4.1.2 Serotonin
4.1.2.1 Vasoconstriction (Pl)
4.2 ARACHADONIC ACID METABOLISM
4.2.1 Phospholipases
4.2.2 Lipoxygenase
4.2.2.1 Lipoxins
4.2.2.1.1 ↑ Vasodilation, ↓ Neutrophils, ↑ Monocytes
4.2.2.2 Leukotrienes
4.2.2.2.1 Vasoconstriction, ↑ VascPermeability, BronchoSpasm (Mast)
4.2.3 Cyclooxygenase
4.2.3.1 Prostacyclin
4.2.3.1.1 ↑ Vasodilation, ↓ Platelet aggregation (EC)
4.2.3.2 Thromboxane
4.2.3.2.1 Vasoconstriction, ↑ Platelet aggregation (Pl)
4.2.3.3 Prostaglandin
4.2.3.3.1 ↑ Vasodilation, Potentiate oedema (Pl, Leuk, EC)
4.3 PAF
4.3.1 ↑ Platelet aggregation, cause degranulation
4.4 CYTOKINES
4.4.1 TNF
4.4.1.1 ↑ EN thrombogenicity, ↑ Neutrophil aggregation and actrivation
4.4.2 IL-1
4.4.2.1 Activate tx fibrblasts, ↑ ECM proliferation
4.4.3 Fever, lethargy, cacexia, anorexia
4.5 CHEMOKINES
4.5.1 Chemo-attractants for leukocytes
4.6 REACTIVE OXYGEN SPECIES
4.6.1 Produced in lysosomes and released byNeutrophils and macrophages
4.6.2 Low: ↑ immune response
4.6.3 High: EN damage, protease activation, direct injury to cell
4.7 NITRIC OXIDE
4.7.1 ↑ Vasodilation, ↓ Platelet aggregation, ↓ lLeukocyte adhesion, Microbicidal in macrophages
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