Acute Inflammation

Question 1

Define acute inflammation

Answer 1

Rapid response to injury that resolves quickly

Question 2

What are the 3 main processes involved in acute inflammation?

Answer 2

• vascular changes + formation of exudate
• activation of endothelial cells and release of mediators
• cellular changes including activation of neutrophils

Question 3

Describe the clinical features of acute inflammation

Answer 3

• redness due to dilatation of small blood vessels
• heat due to increased blood flow and fever
• swelling due to accumulation of fluid in ECM
• pain due to stretching of tissues from oedema and mediators such as bradykinin and serotonin stimulating pain receptors
• loss of function (movement) due to pain and swelling which can immobilise the inflamed area

Question 4

Describe the vascular changes that occur in acute inflammation

Answer 4

• vasodilation (transient vasoconstriction then vasodilation): starts in arterioles and increases blood flow to affected area as a result of histamine and NO on vascular smooth muscle
• increased vascular permeability due to contraction of endothelial cells: permits escaped protein rich exudate into extra vascular tissue leading to oedema. Mediated by histamine, bradykinin and substance P. Increased inter-endothelial space which allows passage of fluid into ECM
• vascular congestion (stasis): slower flow of blood leading to increased concentration of chemical mediators at site
• endothelial cells activated by mediators produced during inflammation and increased levels of adhesion molecule expression

Question 5

Describe the cellular process that occurs in acute inflammation

Answer 5

• neutrophil polymorphs migrate to site of inflammation.
• marination occurs where white cells sit more peripherally in blood vessels due to stasis of slow
• cells then roll with white cells sticking and detaching from the vessel wall mediated by selectins
• can be upregulated by IL-1 and TNF
• adhesion then occurs (mediated by integrins and chemokines and stimulated by IL-1 and TNF)

Question 6

How can the acute response be terminated?

Answer 6

• removal of stimulus
• neutrophils have a short half-life
• variation in cytokine stimuli
• neural impulses

Question 7

Where are mediators of inflammation synthesised?

Answer 7

In the liver and are activated at the site of inflammation

Question 8

What forms exudate and its purpose

Answer 8

• water
• proteins (eg. Fibrin)
• inflammatory cells
• allows delivery of nutrients, dilution of toxins and entry of antibodies to stimulate the immune response

Question 9

List the types of exudate

Answer 9

• fibrinous: rich in fibrin, on serosal surfaces eg. Meninges
• suppurative: pus forming, rich in neutrophil polymorphs eg. Abscesses
• haemorrhagic: severe vascular injury or depletion of coagulation factors
• membranous: epithelium is coated in membrane of fibrin, epithelial cells and inflammatory cells
• pseudomembranous (ulceration): surface exudate on mucosal/epithelial sites eg. C.diff colitis
• necrotising (gangrenous): high tissue pressure leading to vascular occlusion and thrombosis

Question 10

What are the cells involved in the acute inflammatory response?

Answer 10

• neutrophil polymorphs (phagocytose bacteria)
• macrophages (contain lysosomes, present antigens, phagocytose, synthesise IL-1,6 and TNF)
• complement cascade
• plasma factors (eg. Kinin system, coagulation and fibrinolytic system)

Question 11

What are the benefits of acute inflammation?

Answer 11

• dilution of toxins by oedema fluid
• increased entry of antibodies and drug transport
• fibrin traps microorganisms
• delivery of nutrients
• stimulation of immune response

Question 12

What are the detrimental effects of acute inflammation?

Answer 12

• digestion of normal tissue
• swelling (can be life threatening in some locations)
• inappropriate responses

Question 13

How can infection spread?

Answer 13

• stays local at initial site or may spread to local lymph nodes by draining lymphatics
• haematogenous: through blood/lymph
• can be tracked through tissue to form abscesses/infections elsewhere

Question 14

What are the clinical signs of acute infection spread?

Answer 14

• increased resp rate
• increased HR
• high or low temp
• high or low WBC count
• check for sepsis/septic shock

Question 15

What are the possible outcomes of acute inflammation?

Answer 15

• resolution: complete restoration of normal tissue (if minimal damage, in a tissue with regenerative capacity or if cause is rapidly removed/good vascular drainage)
• healing by fibrosis/scarring (if substantial damage to tissue, incapable of regeneration, or abundant fibrin exudate)
• progression to chronic inflammation (if persistent stimulus or tissue destruction leading to ongoing inflammation)