MoD 3 Acute Inflammation Flashcards Preview

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Flashcards in MoD 3 Acute Inflammation Deck (26):

What is acute inflammation?

Response of living tissue to injury, initiated to limit tissue damage.
Innate, immediate and early, stereotyped, short duration (mins/hrs/few days)


What can cause acute inflammation?

Microbial infections (e.g pyogenic organisms)
Hypersensitivity reactions (acute phase)
Physical agents
Tissue necrosis


What are the main clinical signs of acute inflammation?

& loss of function


What changes in tissues occur?

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


What are the changes in blood flow?

transient vasoconstriction of arterioles (few secs)
Vasodilatation fo arterioles then capillaries -> inc blood flow(heat then redness)
Increased permeability of blood vessels ->protein rich exudation and slowing circulation (swelling)
inc RBC conc in small vessel and increased viscosity can lead to stasis


What are the microscopic steps in acute inflammation?

1. Vasodilation
2. Gaps form in endothelium
3. Exudation
4. Margination and emigration- neutrophils adhere to swollen endothelial cells and migrate through vessel basement membrane
5. Marcrophages and lymphocytes migrate in a similar way to neutrophils


What chemical mediators cause vasodilation?

Histamine, prostaglandins, C3a, C5a


What chemical mediators cause increased vascular permeability?

Histamine, prostaglandins, Kinins


What chemical mediators cause emigration of leukocytes?

Leukotrienes, IL-8, C5a


Discuss the actions of neutrophils

phagocytose organisms by making contact, recognising and internalising them then fusing with lysosomes to destroy the contents.
Neutrophils move to the site of injury by chemotaxis.
Activated neutrophils may also release toxic metabolites and enzymes causing damage to host tissue


What are the systemic consequences of acute inflammation?

Acute phase response


What occurs in acute phase response?

Decreased appetite, raised heart rate, altered sleep patterns and changes in plasma conc of acute phase proteins e.g C-Reactive Proteins (CRP), fibrinogen and a1-antitrypsin
Spread of microorganisms and toxins may lead to shock, a clinical syndrome of circulatory failure


What endogenous pyrogens are produced?

IL-1, TNFalpha, and prostaglandin


What is fluid flow across vessel walls determined by?

Balance between hydrostatic and colloid osmotic pressure in the plasma and interstitial fluid.
Increasing hydrostatic inside or colloid osmotic pressure outside increases flow out of the vessel


What may happen after the development of acute inflammation?

Complete resolution
Continued acute inflammation with chronic inflammation(abscess)
Chronic inflammation and fibrous repair, probably with tissue regeneration


How does resolution occur?

All mediators of acute inflammation have short half lives and may be inactivated by degradation, dilution in exudate or inhibition
Gradually all changes reverse and vascular changes stop. Neutrophils no longer marginate, vessel permeability returns to normal and exudate drains via lymphatics


When is complete resolution not possible?

If the collagen framework/tissue architecture has been destroyed


Describe some complications of acute inflammation?

Swelling- Blockage of tubes e.g. bile duct, intestine
Exudate-Compression e.g cardiac tamponade, serositis
Loss of fluid e.g burns
Pain and loss of function- especially if prolonged


Describe skin blisters

Caused by heat, sunlight, chemicals
pain and profuse exudate
Collection of fluid strips of overlying epithelium
Relatively few inflammatory cells so exudate clear
Resolution or scarring


Describe Abscesses

Solid tissues
Inflammatory exudate forces tissue apart
Liquefactive necrosis in centre
May cause high pressure and so pain
May cause tissue damage and squash adjacent structures


Describe Pericarditis

Inflammation of serous cavity
Pericardium becomes inflamed and increases pressure on heart


Give examples of inherited disorders of the acute inflammatory process

alpha1 anti-trypsin deficiency
Inherited complement deficiencies e.g Hereditary Angio-Oedema
Defects in neutrophil function e.g Chronic Granulomatous Disease
Defects in neutrophil number


What is Hereditary Angio-Oedema?

Caused by a deficiency of C1 inhibitor so C1 cleaves C2 and C4 to form C3
The C1 inhibitor usually inhibits Bradykinin too and uninhibited bradykinin increases endothelial permeability causing oedema.


How is Hereditary Angio-Oedema treated?

C1 inhibitor infusion or fresh frozen plasma


What is alpha1 anti-trypsin deficiency?

alpha1 anti-trypsin inhibits elastase
Without inhibition elastase breaks down lung and liver tissue causing emphysema and liver sclerosis


What is Chronic Granulomatous Disease?

Recessive sex linked
Immune phagocytes can't form ROS
Cant kill some bacteria without ROS
Granulomas form in attempt to contain the bacteria