Inflammation 1

Question 1

OVERVIEW

Answer 1

Inflammation evolved as a protective response of the body to injury.
Kills/sequesters microbes and neoplastic cells.
Helps remove damaged tissues.
May cause undesirable damage to cells if prolonged/excessive.
Provides wound healing factors to traumatised tissue.

Question 2

WHAT DOES INFLAMMATION DO TO MICROBES/NEOPLASTIC CELLS?

Answer 2

Kills or sequesters them.

Question 3

WHAT ARE THE CARDINAL SIGNS OF INFLAMMATION?

Answer 3

Redness (erythema)
Heat
Swelling
Pain 
Loss of function

Question 4

WHAT ARE THE STEPS OF THE INFLAMMATORY RESPONSE?

Answer 4

Recognition of injurious agent
Recruitment of white blood cells
Removal of injurious agent
Regulation (control) of response
Resolution/repair.

Question 5

WHAT ARE THE CELLULAR COMPONENTS OF THE INFLAMMATORY RESPONSE?

Answer 5

BLOOD LEUKOCYTES.
POLYMORPHONUCLEAR LEUKOCYTES- Neutrophils, eosinophils, basophils
MONONUCLEAR LEUKOCYTES- Monocytes (macrophages), lymphocytes, plasma cells, Mast cells.

These cells come from pluripotent stem cells.
MYELOID LINE- Polymorphonuclear leukocytes, macrophages, platelets, erythrocytes.
LYMPHOID LINE- Lymphocytes, plasma cells, NK cells, T cells.

Question 6

OTHER COMPONENTS OF THE INFLAMMATORY RESPONSE

Answer 6

Plasma proteins
Vascular endothelial cells
Extracellular matrix

Question 7

ACUTE INFLAMMATORY REACTION

Answer 7

Occurs almost immediately after injury (12-24 hours). See diagram.
Involves recruitment of cellular component of inflammatory response, (-> phagocytosis)
Release of chemical mediators,
Exudation of fluids and proteins from blood vessels.

Question 8

VASCULAR CHANGES IN INFLAMMATION

Answer 8

Follow acute response.
1. Initial transient vasoconstriction
2. Vasodilation of arterioles.
Local increase in blood flow (local hyperaemia)
Engorgement of capillary beds
Erythema (redness)
3. Increased intravascular pressure.
Fluid forced out of vessels by increased intravascular hydrostatic pressure.
Fluid is TRANSUDATE, an ultrafiltrate containing water and electrolytes (low protein).
This causes OEDEMA.

Question 9

INCREASED VASCULAR PERMEABILITY IN INFLAMMATION

Answer 9

Allows movement of protein-rich exudate in to interstitium. Caused by various things.

1. Endothelial cell CONTRACTION. Reversible.
2. Endothelial cell RETRACTION. Longer lasting.
3. Direct endothelial cell injury.
4. Leukocyte mediated endothelial cell injury.
5. Increased transocytosis- movement of proteins via intracellular vesicular pathway.
6. New vessels made during angiogenesis are highly permeable.

Question 10

INCREASED VASCULAR PERMEABILITY CAUSES WHAT?

Answer 10

Increased gaps between endothelial cells.
This allows plasma proteins and leukocytes to infiltrate the site of infection.
Fluid (transudate/exudate) leakage in to interstitium causes OEDEMA.

Question 11

TRANSUDATE

Answer 11

Early, low protein/cell fluid containing water and electrolytes.
Seen with increased hydrostatic pressure (eg. right sided congestive heart failure) or decreased colloid osmotic pressure (eg. low albumin, increased protein loss/decreased protein synthesis. Liver disease/kidney disease)

Question 12

MODIFIED TRANSUDATE

Answer 12

Intermediate between transudate and exudate.
Contains water, electrolytes, high protein levels but few cells.
Clinical pathology.

Question 13

EXUDATE

Answer 13

Contains water, electrolytes, HIGH protein/cells (leukocytes).
Leaks out between large gaps in cells, caused by inflammation (vasodilation and stasis)
eg. Kidney disease.

Question 14

INFLAMMATORY EXUDATES

Answer 14

• SUPPURATIVE EXUDATE- aka. PURULENT. Many neutrophils.
• MUCOPURULENT EXUDATE- Contains mucous and abundant neutrophils.
• FIBRINOUS EXUDATE-High protein fluid with abundant deposits of fibrin. Caused by more severe injuries, which cause greater vascular permeability.
• FIBRINONECROTIC EXUDATE- Necrotic cellular debris with abundant fibrin and degenerate neutrophils. Diphtheritic membrane.

Question 15

CONSEQUENCES OF ACUTE INFLAMMATION

Answer 15

Acute inflammation is modified by the nature and intensity of the injury, the site and tissue affected, and the ability of the host to mount a response.

Question 16

OUTCOMES OF ACUTE INFLAMMATION

Answer 16

RESOLUTION- Neutralisation, decay, degradation of chemical mediators.

• Normalisation of vascular permeability
• Cessation of leukocyte emigration.

PROGRESSION TO CHRONIC INFLAMMATION- If the offending/injurious agent is not removed. May be seen at onset of injury in some cases. (eg. Johne’s)
Return to normalcy depends on initial and continued injury and ability of tissue to regenerate.

SCARRING AND FIBROSIS- Results from substantial tissue destruction, or where tissues cannot regenerate (eg. brain).

Question 17

RESOLUTION OF INFLAMMATION

Answer 17

Macrophages play a central role.

1. Return of normal vascular permeability.
2. Drainage of oedema fluid in to lymphatic system, or in to macrophages by pinocytosis.
3. Phagocytosis of apoptotic neutrophils by macrophages.
4. Phagocytosis of necrotic cellular debris by macrophages.
5. Disposal of macrophages.

Question 18

UNDESIREABLE CONSEQUENCES OF INFLAMMATION

Answer 18

• Uncontrolled severe inflammation. eg. severe thermal burns
• Prolonged persistent inflammation- injurious agent cannot be removed. eg. Johne’s.
• Inappropriate inflammatory response.
  eg. Autoimmune disease- inflammatory response directed against self antigens
  eg. Allergic disease- excessive response to harmless environmental antigens eg. pollen.

Question 19

FIBROSIS

Answer 19

Scar tissue formation following injury (acute inflammation with abscess formation or chronic inflammation). LOSS OF FUNCTION.