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Flashcards in Inflammation Deck (25)
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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?


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
proteoglycans, mainly heparin (active as anticoagulant)

newly formed lipid mediators (eicosanoids):
prostaglandin D2
leukotriene C4
platelet-activating factor

Eosinophil chemotactic factor


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?


- 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?

1. Lymphocytes - T-cells & B cells

2. Plasma cells

3. Macrophages

4. Fibroblasts

5. 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.



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 irritant
and 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?


Has the greatest capacity for regeneration. Constantly replenishes  throughout life (e.g. skin and mucous membranes)


 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)


Has poor or no regenerative capacity (e.g. neuronal cell bodies, cardiac muscle myofibres)


What is the danger of excess fibrosis that occurs as a result of acute inflammation?

Can lead to the progressive destruction of the
tissue due to further injury to adjacent normal tissue.

Eg., In liver, the loss of vascularization can occur as normal tissue is replaced by scar tissue (e.g. liver in cirrhosis and kidney in chronic renal failure)


What are the FIVE CARDINAL SIGNS of inflammation? 

1. heat - increased blood flow: the temperature of the inflamed portion approximates to internal body temperature

2. pain - due to chemical mediators released into damaged tissue, and by local pressure on nerve endings from the exudate

3. redness -  increased blood flow to the area (hyperaemia due to dilation of previously inconspicuous capillaries)

4. swelling - exudation of fluid from dilated blood vessels into the inflamed tissue

5. loss of function - reluctance to use the inflamed portion


What are the possible consequences of ACUTE INFLAMMATION?

1. Death - cytokine & chemokine-related

2. Resolve by regeneration-  in association with host defence mechanisms, (which may be assisted by therapeutic measures)

3. Repair by fibrosis -ie., scar tissue

4. Become chronic (goes through a subacute -- transition between acute & chronic -- phase first), depending on persistence of agent & amount of damage


In acute inflammation, are precapillary sphincters open or closed?


Capillaries become engorged with drug; blood flow through capillary channels slows down because there are more capillaries open through which blood can flow


Where do mast cells migrate from to reach damaged tissue? 

They don't migrate from anywhere. They're already located in tissue.


What are the six different classifications of inflammation by fluid type (effusion), from least to most severe?

1. Serous

Due to mild vascular injury in an organ or in vessels underlying a surface
- a clear to cloudy fluid with little protein present
- vesicles of the skin produce a serous fluid; many inflammations in joints are serous

2. Catarrhal

Mild form & occurs in mucous membranes
- varies from watery to gelatinous in consistency and cloudy to pinkish in colour
- essentially a shedding of epithelium containing many mucous cells, neutrophils, some RBCs & flecks of fibrin
- common in mild forms of rhinitis, tracheitis, bronchitis, gastritis and enteritis

3. Fibrinous

"tipping point" of inflammation
Due to more severe endothelial injury resulting in the escape of fibrinogen from the blood and conversion to fibrin (just like a blood clot)
• yellowish coagulum on surface of a tissue or within its substance
• common in lungs and on serous surfaces (e.g. thoracic, pericardial and peritoneal)
• in hollow organs, it may coagulate within the lumen, forming a cast
• it will peel off from the underlying tissue

- may also if the fibrin is digested by macrophages

4. Diphtheritic

A more severe form of fibrinous exudate in which there is considerable necrosis of underlying tissues
- firmly adherent to the underlying tissue: attempts at removal cause tearing of this
tissue ie., cannot peel exudate away
- commonly seen with internal surface fungal infections

5. Haemorrhagic

A severe acute to peracute inflammation in which
haemorrhage is the main component
- seen in the lymph nodes, lungs and intestine 
- sometimes occurring in all tissues
- if widespread, is most commonly associated with acute deaths.

6. Purulent (suppurative) & abscess formation

Where pus (an admixture of dead and dying neutrophils with necrotic cells and a pyogenic agent) is the predominant feature;
- proteolytic enzymes released by the dying neutrophils lyse tissue cells producing a fluid
- colour varies - white, yellow, green, brown - depending upon the agent


What is a "giant cell" in terms of inflammatory immune response?

It is a macrophage subtype. 

Multinucleated (several hundred) cells formed by the fusion of macrophages or epithelioid cells.


What is an epithelioid cell & what is its role in chronic inflammatory immune response?

It's a macrophage subtype (along with Giant Cell).

- microscopically epithelioid macrophage celss look like squamous epithelial cells with a pink cytoplasm and indistinct borders

- may be binucleate

- primarily secretory rather than phagocytic


What is the microscopic structure of a granuloma? 

a. Central core containing agent or irritant

b.  Surrounding chronic inflammatory cells:

- macrophages (often as 'epithelioid' cells), lymphocytes and plasma cells
eosinophils in parasitic granulomas
-  necrosis in mycobacterial and fungal granulomas
calcification in mycobacterial granulomas in some species

c. Outer fibrous capsule


What is an example of an infection that causes granulamatous inflammation in veterinary species?

Actinomyces bovis (lumpy jaw)

Bacterial colonies seen as "tissue grains" in h

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