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What is 'Acute inflammation'?

The response of living tissue to injury, initiated to limit the tissue damage

The mechanisms of acute inflammation are innate, immediate and of short duration (minutes to a few days)


What are some of the causes of acute inflammation?

Microbial infections (E.g. Pyogenic organisms)
Hypersensitivity reactions (acute phase)
Physical agents
Tissue necrosis


What are the macroscopic features of acute inflammation?

What are the microscopic hallmarks of acute inflammation?

Rubor - erytherma (redness)
Tumor - oedema (swelling)
Calor - heat
Dolor - pain
Loss of function

Exudate of fluid
Infiltrate of inflammatory cells


What are the major tissue changes present in acute inflammation and how are they controlled?

Changes in blood flow
Exudation of fluid into tissues
Infiltration of inflammatory cells

Inflammatory mediators control each step


Give description of how blood flow changes during acute inflammation

Mention how these changes result in a macroscopic clinical feature of acute inflammation

Transient vasoconstriction of arterioles (only lasts a few seconds)

Then vasodilation of arterioles then capillaries, leading to an increase in blood flow (erythrema)

High concentration of RBCs in small vessels and increased viscosity of blood leads to stasis (serious slowing or cessation of blood flow)


Describe how exudation of fluid into tissues comes about

What macroscopic feature of acute inflammation does this cause?

Increased permeability of blood vessels caused by histamine release in the tissue

Histamine causes endothelial cells to swell and retract, leaving gaps in the endothelium

This, along with arteriolar dilatation leads to exudation of protein rich fluid into tissues (oedema) and a slowing of the circulation

Macroscopically, this causes swelling


What determines fluid flow across a vessel wall?

How does this relate to acute inflammation?

Fluid flow across the vessel wall determined by the balance between hydrostatic and colloid osmotic pressures (Starling's Law)

Increased hydrostatic pressure = increase fluid flow out of the vessel
Increased colloid osmotic pressure = increased fluid flow into the vessel

In acute inflammation:

Arteriolar dilatation leads to increased hydrostatic pressure, fluid moves into the interstitium

Increased permeability of vessels leads to protein loss into interstitium

This leads to protein rich exudate in the tissues (oedema/excess fluid in interstitium)


What is the difference between exudate and transudate?

Which of these leads to oedema?

Exudate is protein rich fluid loss in inflammation

Transudate is fluid loss due to hydrostatic pressure only and is therefore low in protein

Oedema can result from both


Name a major consequence of oedema

Increased lymphatic drainage


What are some other mechanisms of vascular leakage seen in acute inflammation?

Include some of the possible causes for each mechanism

Cytoskeletal reorganisation leading to gaps in the endothelium:
- Cytokines, IL-1 and TNF

Direct injury:
- Toxic burns
- Chemicals

Leukocyte dependent injury:
-ROS damage
- Enzymes from leukocytes

Increased transcytosis across endothelial cells:


what is the most common cell type seen infiltrating into the tissues during acute inflammation?

What other types of cells infiltrate into acutely inflamed tissues?


Macrophages, Lymphocytes


Describe in basic terms how neutrophils infiltrate into tissues

Hint: 4 stages

Stasis causes neutrophils to line up along the endothelium

Neutrophils roll along the endothelium, sticking intermittently

Then stick more avidly

Neutrophils move through the cell wall


How is it that once neutrophils have adhered to the vessel walls they are able to move into tissues?

Relaxation of endothelial cell junctions

Digestion of the vascular basement membrane


What is a neutrophil? (TOB)

A white blood cell involved in inflammation

Polymorphonuclear leukocyte


List the actions of a neutrophil

Migrate to and infiltrate tissues by chemotaxis

Phagocytose microorganisms

May release toxic metabolites and enzymes that damage the host tissue


What is chemotaxis?

How do neutrophils perform chemotaxis?

Movement along a concentration gradient of chemoattractants

Neutrophils have cell surface receptors that bind to these chemoattractants and allow the neutrophil to direct its migration

Examples of neutrophil chemoattractants include:
- C5a (complement)
- Bacterial peptides
- IL-8


How do neutrophils perform phagocytosis?

Neutrophil must make contact with a cell coated in opsonins (C3b, Antibodies) that it then recognises with cell surface receptors

Cytoskeletal changes allow the neutrophil to internalise the cell forming a phagosome

A lysosome is fused with the phagosome to form a secondary lysosome and digest the internalised cell


By what mechanisms might neutrophils kill internalised cells?

Hint: 2 types of mechanism

O2 dependent mechanisms:
- Produces superoxide and H2O2
- H2O2-myeloperoxidase-halide system (produces HOCl)

O2 independent mechanisms:
- Lysozyme and hydrolases
- Bactericidal permeability increasing protein (BPI)
- Cationic proteins (Defensins)


List some of the chemical mediators of inflammation according to the process they mediate


Increased vascular permeability:

Bacterial peptides
Leukotrienes (leukocytes)



How does exudation of fluid into tissue combat injury?

Delivers plasma proteins to area of injury
For example:
Inflammatory mediators

Dilutes toxins

Increases lymphatic drainage delivers microorganisms to phagocytes and antigens in the immune system


How does infiltration of inflammatory cells help combat injury?

Removes pathogenic organisms and necrotic debris


How does vasodilatation help combat injury?

Increases delivery of blood to the area and increases temperature


How does pain and loss of function help combat injury?

Enforces rest
Reduces chance of further traumatic damage


What are the possible local complications of acute inflammation?

Swelling can cause the blockage of tubes, for example in the bile duct or intestine

Exudate into tissues can cause compression (as in cardiac tamponade) and serositis

Can lead to loss of fluid (E.g. In burns)

Can lead to pain and loss of function, especially when prolonged


List the systemic effects of acute inflammation

Acute phase response
Spread of microorganisms and toxins that can lead to shock


Why does acute inflammation lead to fever?

What can be done to reduce the fever?

Endogenous pyrogens produced:

Note: Pyrogens are compounds that cause fever

Prostaglandins also produced, therefore aspirin reduces fever


What is leukocytosis?

Why does acute inflammation lead to leukocytosis?

Leukocytosis is a white blood cell count of above normal range, a sign of inflammatory response

IL-1 and TNF-alpha produce an accelerated release of WBCs from the marrow

Macrophages produced as T-lymphocytes produce M-CSF (Macrophage colony stimulating factor)

In bacterial infections, neutrophils are produced

In viral infections, lymphocytes are produced


What is the acute phase response and what does it cause?

A class of proteins whose concentrations increase or decrease in response to inflammation

Decreased appetite
Raised pulse rate
Altered sleep patterns
Changes in plasma protein concentrations


List some proteins involved with the acute phase response

C-reactive protein (CRP)
Alpha-1 antitrypsin
Serum amyloid A protein


List the possible consequences of acute inflammation

Complete resolution

Continued acute inflammation with chronic inflammation = abscess

Chronic inflammation and fibrous repair, probably with tissue regeneration



In complete resolution of inflammation, what morphological changes are seen?

Changes gradually reverse

Vascular changes stop:
- Neutrophils no longer marginate
- Vessel permeability returns to normal
- Vessel calibre returns to normal


What is the result of the morphological changes seen during resolution of inflammation?

Exudate drains to lymphatics

Fibrin is degraded by plasmin and other proteases

Neutrophils die, break up and are carried away or phagocytosed

Damaged tissue might be able to regenerate


What determines whether tissue will be able to fully regenerate after acute inflammation?

If tissue architectures is damaged, full resolution is not possible

If intact, full resolution possible


By what mechanisms is acute inflammation resolved?

For each mechanism, give an example of an inflammatory mediator that is inactivated by it

All mediators of inflammation have short half lives and may be inactivated by:
- Degradation (E.g. Heparinase)
- Inhibitors may bind (E.g. Anti-proteases)
- May be unstable (E.g. Some arachidonic acid derivatives)
- Dilution in exudate (E.g. Fibrin degradation products)
- Specific inhibitors of inflammatory change (E.g. Lipoxin)


What is meningitis and what are two common features?

Acute inflammation of the meninges

Can cause:
- Vascular thrombosis
- Reduce cerebral perfusion


What might be observed in the alveoli during lobar pneumonia?

What does this cause and what is the causative organism?


Can lead to:
- Shortness of breath/difficulty breathing
- Worsening fever, prostration and hypoxaemia over a few days

Infection by streptococcus pneumoniae


What are the possible causes of a skin blister?

What are the predominant features?

How is it resolved?

Heat, sunlight, chemical

- Pain and profuse exudate
- Collection of exudate in tissue strips off epithelium
- Exudate clear due to relatively few inflammatory cells unless bacterial infection develops

Complete resolution or scarring can occur


What is an abscess?

What might an abscess cause?

Inflammatory response in solid tissues where the exudate forces tissues apart
Liquefactive necrosis then occurs in the centre

High pressure, therfore can cause pain
Can cause tissue damage and squash adjacent structures


What happens during acute inflammation of serous cavities?

Give some examples

Exudate pours into the serous cavity

Pleural or pericardial effusion


What is bread an butter pericarditis?

Pericarditis with fibrin deposition in the pericardium that results in a 'bread and butter' appearance


Give a few examples of disorders of acute inflammation

Hereditary angio-oedema
Alpha-1 anti-trypsin deficiency
Inherited complement deficiencies
Defects of neutrophil function or number


What happens following inhalation of streptococcus pneumonia (assuming it will result in inflammation)?

Follow this process to resolution

Inhalation and invasion of bacterium into tissue of the lungs (alveoli and bloodstream)

This stimulates the release and production of inflammatory mediators

This will lead to an inflammatory response

- Vasodilation (subsequent stasis),
- Exudation of fluid (increased hydrostatic pressure + increased vascular permeability)
- Infiltration of inflammatory cells (especially neutrophils)

Symptoms such as fever, pain, redness, swelling and loss of function may occur

Bacterial cells are phagocytosed by inflammatory cells such as neutrophils

Inflammatory mediators are inactivated after bacteria are cleared and inflammation is resolved