2. Acute Inflammation

Question 1

What is inflammation?

Answer 1

The response of living tissue to injury.

Question 2

Why is inflammation needed?

Answer 2

To limit tissue damage.

Question 3

What are some key features of acute inflammation?

Answer 3

Innate, immediate and early, stereotyped. Short duration: minutes/hours/a few days.

Question 4

What are some causes of acute inflammation?

Answer 4

Microbial infections, hypersensitivity reactions, physical agents, chemicals and tissue necrosis.

Question 5

What are the clinical features of acute inflammation?

Answer 5

Rubor (redness), tumor (swelling), calor (heat), dolor (pain_. Leads to loss of function, protective mechanism.

Question 6

How does acute inflammation change tissues?

Answer 6

Changes in blood flow, exudation of fluid into tissues, infiltration of inflammatory cells.

Question 7

How does blood flow change in acute inflammation?

Answer 7

Transient vasoconstriction of arterioles, then vasodilatation of arterioles then capillaries - increases blood flow causing calor and rubor. Blood vessels get more permeable so there’s exudation of fluid into tissues and slowing of circulation from swelling.

Question 8

What chemical mediators are present in the immediate early response?

Answer 8

Histamine, released from mast cells, basophils and platelets. Response to many stimuli.

Question 9

What does histamine cause?

Answer 9

Vascular dilatation, transient increase in vascular permeability, and pain.

Question 10

What is Starlings Law of fluid loss?

Answer 10

Fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid.
Increased hydrostatic pressure -> increased fluid flow out of vessel.
Increased osmotic pressure of interstitium -> increase fluid flow out of vessel.

Question 11

How does acute inflammation cause oedema?

Answer 11

Arteriolar dilatation leads to increased hydrostatic pressure, increased permeability of vessel walls leads to loss of protein into interstitium. So net flow of fluid is out of the vessel.

Question 12

What is oedema?

Answer 12

Excess of fluid in interstitium.

Question 13

What is the difference between oedema in exudate and transudate?

Answer 13

Fluid loss in inflammation is exudate, high protein content. Fluid loss due to hydrostatic pressure imbalance only is transudate, low protein content.

Question 14

What are the mechanisms of vascular leakage?

Answer 14

Endothelial contraction -> gaps
Cytoskeletal reorgansation -> gaps
Direct injury, leukocyte depend injury, increased transcytosis.

Question 15

What is the key cell type involved in acute inflammation?

Answer 15

Neutrophils.

Question 16

How do neutrophils infiltrate in acute inflammation?

Answer 16

Margination - line up at the edge of the bleed vessels along the endothelium.
Rolling - roll along endothelium, stick to it intermittently,
Adhesion - stick more avidly.
Emigration - through blood vessel wall.

Question 17

How do neutrophils escape from vessels?

Answer 17

Relaxation of inter-endothelial cell junctions, digestion of vascular basement membrane and movement.

Question 18

What is chemotaxis?

Answer 18

Movement along concentration gradients of chemoattractants.

Question 19

What is the role of neutrophils in acute inflammation?

Answer 19

Phagocytosis. Contact, recognise and internalise the debris.

Question 20

What is neutrophil action facilitated by?

Answer 20

Opsonins.

Question 21

What are the two types of killing mechanisms?

Answer 21

O2 dependent - produce superoxide and hydrogen peroxide.

O2 independent - lysozyme and hydrolases.

Question 22

What are some chemical mediators of acute inflammation?

Answer 22

Proteases - plasma proteins, produced in the liver.
Prostaglandins/leukotrienes - metabolites of arachidonic acid, increases blood flow.
Cytokines/chemokines - many and varied.

Question 23

How does exudation of fluid combat injury?

Answer 23

Delivers plasma proteins to area of injury (immunoglobulins, inflammatory mediators, and fibrinogen), dilutes toxins, increases lymphatic drainage (delivers micro-organisms to phagocytes and antigens to immune system).

Question 24

How does infiltration of cells combat injury?

Answer 24

Removes pathogenic organisms, necrotic debris.

Question 25

How does vasodilatation combat injury?

Answer 25

Increases delivery, increases temperature.

Question 26

How does pain and loss of function combat injury?

Answer 26

Enforces rest, reduces chance of further traumatic damage.

Question 27

What are some local complications of acute inflammation?

Answer 27

Swelling - blocks tubes. Exudate - compression and serositis. Loss of fluid, pain and loss of function.

Question 28

What are some systemic effects of acute inflammation?

Answer 28

Fever, leukocytosis, acute phase response (loss of appetite, raised pulse rate etc.), and acute phase proteins concentration rise.

Question 29

What is shock?

Answer 29

When the body is overwhelmed by acute inflammation?

Question 30

What are the possible results of acute inflammation?

Answer 30

Complete resolution, continues acute inflammation with chronic inflammation (abscess), chronic inflammation and fibrous repair, death.

Question 31

What happens in resolution of acute inflammation morphologically?

Answer 31

Changes gradually reverse, and vascular changes stop.

Question 32

What happens to cell mediators of acute inflammation in resolution?

Answer 32

Mediators have short half-lives. May be inactivated by degradation, inhibitors can binds. May be unstable or diluted. Specific inhibitors of acute inflammatory changes.

Question 33

What are some disorders of acute inflammation?

Answer 33

Herediatry angio-oedma, alpha 1-antitrypsin deficiency, inherited complement deficiences, defects in neutrophil function, defects in neutrophil numbers.