Inflammation in Response to Injury Flashcards
What are the cellular responses to stress + noxious stimuli?
- Hyperplasia = increase in no. cells
- Hypertrophy =. increase in size of cells
- Atrophy = cells shrink + loose function
- Metaplasia = one cell type replaced by another
What are the 2 mechanisms of cell death?
- Necrosis - cells liquify, always pathogenic
- Apoptosis - programmed cell depth, normal functions
Name causes of cell injury
- oxygen deprivation
- hypoxia
- ischaemia
- physical agents
- chemical agents + drugs
- infectious agents
- immunologic reactions
- genetics derangements
- nutritional imbalances
What is the aim of inflammation?
Neutralise offending agents + start repair
What are the main characteristics of acute inflammation?
- fluid exudation
- exudation of plasma proteins
- emigration of WBC’s
How is acute inflammation terminated?
Offending agent eliminated, secreted mediators broken down, anti-inflam mechanisms
- short half-life of mediators
- short neutrophil life span
- stop signals = LIPOXIN generated
- anti-inflam cytokines
What are the major components of inflammation?
- Vascular changes
- Cellular changes
- Cells of acute inflam = NEUTROPHIL, platelets, mast cells
- Cell of chronic inflam = MACROPHAGE, lymphocytes, plasma cells
Describe the vascular changes that take place in inflammation
- Transient vasoconstriction (prevent blood loss) followed by vasodilation (histamine, NO)
- Increased permeability = protein leakage = WBCs allowed through
- Stasis + concentrations of RBCs - slows blood flow
- Causes neutrophil margination
- Dilation = more space for blood so it slows down = WBC’s come to edges of BV
What is the function of histamine and NO in vascular changes?
Cause endothelial retraction + formation of gap junctions = space for WBC’s to exit
What cellular changes take place in inflammation?
Phagocytosis + Leukocyte extravasation
Describe the process of Leukocyte extravasation
- ROLLING due to selectins = presented on CS when histamine present
- ADHESION due to integrins
- TRANSMIGRATION across endothelium by cellular adhesion molecules
- > migration towards chemotactic stimulus = bacterial products + endogenous chemoactractant
What us the function of TNF and IL1?
Cause generation of adhesion molecules
What are the chemical factors of inflammation?
Plasma derived
= clotting pathway + complement system = causes of fibrin split products = increased vasc perm
Cell derived
- mast cells/basophil produce histamine
- platelets produce serotonin
- inflam cells (neutrophils) produce platelet activating factor, prostaglandins, leukotrienes
- endothelium produces NO, platelet activating factor, prostaglandins + leukotrienes
Endpoint = increased vasc. perm so cells can move out = oedema…
What are anaphylatoxins and what is their role?
Vasoactive mediators, part of complement, responsible for allergic reaction
Role:
- Activation of tissues = cycloxygenase + lipoxygenase products
- Mast cell stimulation = histamine release + leukotriene synthesis (= increased vasc perm)
1 + 2 = smooth muscle contraction (constriction)
What are the 2 types of inflammatory mediators?
- Vasoactive = histamine, serotonin, bradykinin, leukotrienes, PG’s + anaphylatoxins
- Chemotactic = C5a, lipoxygenase products, chemokines
