Inflammation Flashcards
There are two types of inflammation: Acute & Chronic.
What are the four phases of Acute Inflammation?
a) Vascular phase – momentary vasoconstriction of the blood vessels in the affected area (this is transient phase lasting only a few seconds); this is as a result of a smooth muscle response. This transient phase is followed immediately by dilation of the blood vessels (which can last from minutes to days). This comes about as a result of chemical mediators.
* NB: the arterioles and venules both become dilated as a result the capillary channels are also dilated and as a result the blood 7low through the area slows leading to the exudative phase*
b) Exudative phase – exudate fluid escapes from the endothelial cells.
c) Migration of leukocytes – mainly neutrophils, although eosinophils & basophils can also be involved, but more so in allergic responses.
d) Pyrexia – fever; which is produced by neutrophils
There are several types of chronic inflammation? What are they?
a) Granulotamous – usually caused by organisms of low virulence but great persistence
b) Lymphocytic/plasmacytic – a diffuse, ongoing inflammation usually seen in diseases of CNS, the GIT, respiratory tract and urogenital tract.
* NB: necrosis and fluid accumulation (exudate) tend to more be associated with ACUTE inflammation; while fibrosis and accumulation is more CHRONIC.*
What are the vascular changes that happen during ACUTE inflammation?
The arterioles and venules both become dilated and as a result the capillary channels are also dilated. As a result the blood flow through the area slows leading to the exudative phase. This phase is largely mediated by mast cells. They release histamine which causes endothelial cell contraction and therefore increased vascular permeability.
NB: endothelial cell contraction causes the tight junctions to come apart and then the protein rich fluid inside the blood will leak out into the tissue
What are the cellular changes gthat occur during ACUTE inflammation?
Neutrophils begin to marginate (go towards the edges of the blood vessels in preparation to leave) usually in venules and capillaries. They will either move through tight junctions which are open or will force themselves through some of them. They will travel to the site of damage and will degranulate releasing their cellular fluid, proteins and enzymes.
What are the main agents that induce acute inflammation?
MAST CELLS:
Degranulate, releasing histamines & cytokines, which are chemotactic for other phagocytic cells & cause synthesis of inflammatory mediators in surrounding tissue:
The molecules thus released into the extracellular environment include:
Preformed mediators (from the granules):
serine proteases, such as tryptase
histamine
serotonin
proteoglycans, mainly heparin (active as anticoagulant)
newly formed lipid mediators (eicosanoids):
thromboxane
prostaglandin D2
leukotriene C4
platelet-activating factor
cytokines:
Eosinophil chemotactic factor
NEUTROPHILS:
Pyrogenic - fever-inducing
Pyogenic - pus-forming
Chemotactic, phagocytic, degranulating
- anti-microbial properties in granules released into tissue that increase permeability
- collagenases, proteases, defensins, lysozymes
Histamines are released from mast cells that degranulate. What are histamines’ effects in allergy?
Histamine
- dilates post capillary venules
- activates the endothelium
- increases blood vessel permeability
This leads to local edema (swelling), warmth, redness, and the attraction of other inflammatory cells to the site of release. It also irritates nerve endings (leading to itching or pain). Cutaneous signs of histamine release are the “flare and wheal”-reaction. The bump and redness immediately following a mosquito bite are a good example of this reaction, which occurs seconds after challenge of the mast cell by an allergen.
What are the cells involved in chronic inflammation?
- Lymphocytes - T-cells & B cells
- Plasma cells
- Macrophages
- Fibroblasts
- Vascular endothelium
What is the role of lymphocytes - T & B cells – in chronic inflammation?
T-cells & B-cells circulate between the blood tissues and lymphatic system to seek out & destroy/neutralise antigen. They are more long lived than neutrophils, which only survive a few hours.
What is the role of plasma cells in chronic inflammation?
Their presence in a tissue indicates the body is producing a humoral response (antibodies) against an antigen.
What is the role of macrophages in chronic inflammation?
Derived from circulating monocytes, which leave the blood vessels and enter the tissue.
Effects:
Phagocytosis
Antigen presentation
Stimulation of fibroplasia and fibrosis - macrophages play a key role in repair since they stimulate cytokines, growth factors and TIMPs which lead to: increased collagen synthesis, increased fibroblast proliferation and decreased matrix metalloproteinase activity respectively. All of these factors together regulate the production of collagen.
What role do fibroblasts play in chronic inflammation?
Derived from local connective tissue cells, they are involved in the organization of damaged tissue (fibroplasia) into granulation tissue.
What role do vascular endothelial cells play in chronic inflammation?
in conjunction with fibroblasts undergoing fibroplasia, vascular endothelial cells also proliferate into the organizing tissue (granulation tissue).
How does inflammatory effusion help in the healing/repair process of an infection?
Inflammatory effusion, ie., the accumulation of fluid in tissues:
I. Dilutes the toxic agent
II. May contain contain antibodies that will attack or coat
(opsonize) the irritantand therefore facilitate phagocytosis by neutrophils and macrophages
III. May contain fibrin which immobilizes the irritant
IV. Is chemotactic to neutrophils so it brings more of these cells into the injured area
V. Will wash away the irritant if on the surface (as in some body systems – e.g. skin and alimentary tract)
VI. Will facilitate further processing or antigen presentation by bringing the irritant to the local lymph nodes.
How does CONNECTIVE TISSUE aid repair in chronic inflammation?
I. Removal of necrotic debris - inflammatory effusion
II. Ingrowth of immature blood vessels (granulation tissue) – forms at sites of skin injury if large areas of epithelium have been lost
III. Production of immature scar tissue (fibroplasia)
IV. Production of mature scar tissue (fibrosis)
NB: eventually granulation tissue will be replaced first by immature then mature fibrous tissue
What are the differences between labile, stable & permanent in terms of the nature of tissue that undergoes acute inflammation?
Labile:
Has the greatest capacity for regeneration. Constantly replenishes throughout life (e.g. skin and mucous membranes)
Stable:
Only limited ability to replace itself, although this tissue retains the capacity to replace cells that have undergone necrosis (e.g. liver, renal tubular epithelium etc). Stable tissue also has the ability to respond to greater need (e.g. bone, skeletal and smooth muscle)
Permanent:
Has poor or no regenerative capacity (e.g. neuronal cell bodies, cardiac muscle myofibres)
In acute inflammation, are precapillary sphincters open or closed?
Open.
Capillaries become engorged with drug; blood flow through capillary channels slows down because there are more capillaries open through which blood can flow

