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Flashcards in Inflammation 1 Deck (19):
1

OVERVIEW

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.

2

WHAT DOES INFLAMMATION DO TO MICROBES/NEOPLASTIC CELLS?

Kills or sequesters them.

3

WHAT ARE THE CARDINAL SIGNS OF INFLAMMATION?

Redness (erythema)
Heat
Swelling
Pain
Loss of function

4

WHAT ARE THE STEPS OF THE INFLAMMATORY RESPONSE?

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

5

WHAT ARE THE CELLULAR COMPONENTS OF THE INFLAMMATORY RESPONSE?

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.

6

OTHER COMPONENTS OF THE INFLAMMATORY RESPONSE

Plasma proteins
Vascular endothelial cells
Extracellular matrix

7

ACUTE INFLAMMATORY REACTION

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.

8

VASCULAR CHANGES IN INFLAMMATION

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.

9

INCREASED VASCULAR PERMEABILITY IN INFLAMMATION

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.

10

INCREASED VASCULAR PERMEABILITY CAUSES WHAT?

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.

11

TRANSUDATE

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)

12

MODIFIED TRANSUDATE

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

13

EXUDATE

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

14

INFLAMMATORY EXUDATES

-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.

15

CONSEQUENCES OF ACUTE INFLAMMATION

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.

16

OUTCOMES OF ACUTE INFLAMMATION

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).

17

RESOLUTION OF INFLAMMATION

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.

18

UNDESIREABLE CONSEQUENCES OF INFLAMMATION

-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.

19

FIBROSIS

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