Sesson 3 - Acute Inflammation

Question 1

What is acute inflammation?

Answer 1

Response of living tissue to injury inititated to limit tissue damage

Question 2

Features of acute inflammation?

Answer 2

Innate, immediate and early, stereotyped, short duration

Question 3

Causes of acute inflammation? (5)

Answer 3

Microbial infections (pyogenic organisms)
Hypersensitivty reactions
Physical agents
Chemicals
Tissue necrosis

Question 4

Clinical features of acute inflammation? (5)

Answer 4

Rubor
Tumor
Calor
Dolor
Loss of function

Question 5

Changes in tissues during acute inflammation?

Answer 5

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

Question 6

What are the changes in blood flow associated with acute inflammation?

Answer 6

Transient vasoconstriction
Vasodilatation of arteries and then capillaries (increase in blood flow)
Increased permeability of blood vessels (exudation -> slowing circulation)
STASIS in small vessels (high viscosity of blood)

Question 7

Chemical mediators of acute inflammation?

Answer 7

Immediate - Histamine (mast cells, basophils and platelets)
Causes vascular dilatation, increased vascular permeability, pain
Persistent response - Leuktrienes, Bradykinin

Question 8

What stimuli causes histamine to be released

Answer 8

Physical damage, immunologic reactions
C3a, C5a, IL-1
Factors from neutrophils and platelets

Question 9

What is starling’s law?

Answer 9

Fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure

Question 10

Why is fluid lost from vessels?

Answer 10

Increased hydrostatic pressure increases fluid flow out of vessels (arteriolar dilatation leads to more blood in capillaries)
Increased permeability of vessel walls leads to loss of protein into interstitium increasing colloid osmotic pressure of interstitium

Question 11

Consequence of vascular leakage?

Answer 11

Oedema - excess of fluid in interstitium

Can be transudate (due to hydrostatic pressure) or exudate (protein rich - fluid loss in inflammation)

Question 12

Mechanisms of vascular leakage?

Answer 12

Endothelial contraction -> gaps (histamine, leukotrienes, bradykinin)
Cytoskeletal reorganisation -> gaps (cytokines: IL-1 and TNF)
Leukocyte dependent injury (toxic ROS from leucocytes)
Increased transcytosis - more channels (VEGF)

Question 13

What does fibrin do?

Answer 13

Prevents movement into and out of site of injury

Question 14

What cells are involved in acute inflammation?

Answer 14

Neutrophils