Inflammation Flashcards
What is inflammation
Inflammatory response’ encompasses a whole range of processes designed to limit tissue injury’.
Causes of inflammation
Cardinal signs of inflammation
- Redness - increased bloodflow to area
- Heat - dilated vessels
- swelling - signalling to WBC’s and immunoglobulins
- pain - chemical mediators
- loss of function
What is hyperaemia
Excess of blood
What is necrotising inflammation
When a virulent organism produces severe tissue damage and extensive cell death
Chronic inflammation can occur when…
The inciting injury is persistent or resurrect or when the inflammatory reaction is insufficient to completely degrade the agent.
Vascular phase of acute inflammation
Early transient vasoconstriction which is mediated by contraction of smooth muscle within arterioles, which leads to a short lived reduction in blood - response to inflammatory mediators i.e histamine, bradykinin etc and is short lived
Followed by vasodilation which is achieved by relaxation of the arteriolar smooth muscle and distension of capillaries within the injured site - increased blood flow so more neutrophils to area
What happens to permeability in inflammation
It increases
Transudate vs exudate
Transudate - low protein content, few cells
Exudate - high protein content and some red and white cells
What is an oedema
Presence of excess fluid within extra vascular space and body cavities - can be Transudate or exudate
What is pus
Type of exudate containing dead or dying bacteria and neutrophils
What happens in direct endothelial injury
Seen after some bacterial infection and burns Some delay from Time of injury and the leakage of exudate, to allow the development of the full process of cell death and detachment from the vessel wall
Vascular response in acute inflammation
- Protein passage - leak of proteins due to increased permeability
- Fluid movement - hyperaemia lead to increase in bp + loss of protein leads to decreased plasma osmotic pressure and increase in interstitial protein so increased filtration pressure forms an oedema
Cellular Phase of the Acute Inflammatory Response
The cellular phase of acute inflammation involves the movement of white blood cells, particularly neutrophils, from the circulation into the site of tissue damage where they act to limit the extent of injury
- Margination
As the blood flows slowly along the microcirculation, the white blood cells roll on the endothelial surface. This process is known as margination - Rolling
- Adhesion
This leukocyte endothelial adhesion is achieved by the expression on the surface of activated endothelial cells of a family of molecules known as selectins
How do Leukocytes migrate to the site of injury
Chemotaxis - directional migration in which the leukocytes sense and respond to a concentration gradient of chemotaxins
Steps of phagocytosis
(A) The microorganism is opsonised with antibody or complement.
(B) The opsonised particle becomes attached to neutrophil membrane receptors for the opsonin.
(C) Engulfment.
(D) The opsonized microorganism is internalised into a phagocytic vacuole (phagosome).
(E) Fusion of the lysosomes (primary granules) with the phagosome allows the discharge of lysosomal enzymes into the phagolysosome and triggers the respiratory burst, which results in bacterial killing.
(F) Lysosomal enzymes degrade the dead microorganism.
Sources and roles of inflammatory mediators
What is fibrinous inflammation
refers to a pattern of acute inflammation where the acute inflammatory exudate has a high plasma protein content
What is necrotising inflammation
when a virulent organism produces severe tissue damage and extensive cell death. Examples include necrotizing fasciitis and necrotizing pharyngitis
What is a granuloma
a collection of activated macrophages and is frequently surrounded by a rim of lymphocytes
Examples of granulomatous inflammation
Healing inflammatory phase
Initiated by microbial invasion, tissue damage, other exogenous or endogenous stressors. In some instances, pathogen-associated molecular patterns (PAMPs) are recognised by pattern recognition receptors (PRRs), usually by dendritic cells and tissue macrophages.
Inflammasomes form and release cytokines, which attract inflammatory cells and influence other cell types.
Damaged blood vessels/bleeding into tissues initiates coagulation.
Mediators released by cells and tissues attract neutrophils, tissue macrophages and other inflammatory cells. Cytokines, interferons and growth factors are secreted by the antigen-presenting cells (APCs) and inflammatory cells.
Neutrophil polymorphs and tissue macrophages undergo apoptosis when replete with phagocytosed material; no further recruitment.
Cellular content diminishes.
New type III collagen is replaced with type I as wound remodelling and further wound contraction occurs. Type I collagen cross-linking stabilises wound.
‘Restoration’ macrophages help to restore the inflammatory cell types and numbers in the tissues to normal levels.
healing proliferative phase
Epithelium proliferates to reunite breach, if present.
Endothelial proliferation from existing vessels generates and secretes collagen.
Fibroblasts mature into myofibroblasts, proliferate and secrete collagen.
Initial phase of wound contraction reduces the size of the injured site.
