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Pathology. Inflammation. > 1. > Flashcards

1. Flashcards

1
Q

What is inflammation?

A

The response of living tissue to injury.

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2
Q

What do we need to determine about injuries during a post-mortem exam?

A

Whether the injuries occurred before or after death.

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3
Q

Can inflammation occur after death?

A

No.

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4
Q

What is the goal of treating inflammation?

A

We want to get rid of what is causes the inflammation and return the body to homeostasis.

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5
Q

What 4 things cause inflammation?

A

Pathogenic organisms.

Poisons and toxins.

Mechanical and thermal injuries.

Immune reactions.

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6
Q

What are the 5 cardinal signs of inflammation?

A

Rubor (redness).

Calor (heat).

Tumor (swelling).

Dolar (pain).

Functio laesa (loss of function).

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7
Q

What causes the redness and heat associated with inflammation?

A

The dilation of the blood vessels.

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8
Q

What causes the swelling associated with inflammation?

A

An accumulation of fluid from leaky blood vessels.

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9
Q

What 2 factors lead to the pain associated with inflammation?

A

Bradykinin.

Prostaglandin.

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10
Q

What causes the loss of function associated with inflamamtion?

A

The pain and swelling.

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11
Q

What are the 5 main steps in the vascular response following inflammation?

A

Vasodilation.

Increased vascular permeability.

Change in blood flow.

Leukocyte margination, rolling and adhesion.

Leukocyte emigration.

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12
Q

What are the 2 major factors that lead to vasodilation?

A

Histamine.

Bradykinin.

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13
Q

What is hyperemia?

A

Excess blood in the blood vessels.

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14
Q

Why is vasodilation beneficial to the inflammatory response?

A

It allows more blood into the injured area.

This means more cells and nutrients are delivered to that area.

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15
Q

Can food and environmental hypersensitivities result in vasodilation?

A

Yes.

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16
Q

What cardinal signs are caused by vasodilation?

A

Redness and heat.

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17
Q

Is vasodilation ever responsible for swelling?

A

No.

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18
Q

What are the 4 ways in which increased vascular permeability can occur?

A

Increased hydraulic pressure.

Physical mediators.

Direct injury.

Damage cause by white blood cells.

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19
Q

When does increased hydraulic pressure occur?

A

When there is increased blood within a vessel.

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20
Q

How does increased hydraulic pressure lead to increased vascular permeability?

A

It forces some fluid out of the vessel and into the extra cellular environment.

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21
Q

Is the fluid lost lost following increased hydraulic pressure ever reabsorbed?

A

Yes, it is reabsorbed in the venules.

22
Q

When will more fluid be forced out of the blood than can be reabsorbed?

A

When there is inflammation.

23
Q

How can physical mediators lead to increased vascular permeability?

A

They bind to the endothelial cells and cause them to retract.

This enlarges the gap junction between cells and allows for fluid to leave the blood.

24
Q

The blood vessels in what area of the body are most likely to be damaged?

A

The vessels in the lung.

The glomerular blood vessels.

25
Q

How can white blood cells lead to increased vascular permeability?

A

They can release enzymes that damage the walls of blood vessels and this causes fluid to leak out.

26
Q

What is diapedesis?

A

The leakage of red blood cells through widened gap junctions in the blood vessel wall.

27
Q

What is true haemorrhage?

A

Blood cells that leak out when the blood vessel wall is ruptured.

28
Q

What is a condition in horses that can be caused by increased vascular permeability?

A

Hives.

29
Q

What cardinal sign is caused by increased vascular permeability?

A

Tumor (swelling).

30
Q

What determines the location of vascular permeability?

A

The severity of the injury.

Mild injuries affect the post capillary venules.

Moderate injuries affect the post-capillary venules and the capillaries.

Severe injuries affect the post-capillary venules, the capillaries and the arterioles.

31
Q

What causes leakage in the post-capillary venules?

A

Mild injuries e.g. when histamine and serotonin bind to the blood vessel walls and cause slight damage.

32
Q

How long does the leakage associated with mild injuries last for?

A

Around 1/2 an hour.

33
Q

Why is mild vascular permeability said to be monophonic?

A

Because it only affects one area.

34
Q

Why are moderate injuries that lead to vascular permeability said to be biphasic?

A

As they affects 2 areas.

35
Q

How long does the leakage associated with moderate injuries last for?

A

Minutes to days. .

36
Q

What are the 3 mediators for the leakage associated with moderate injuries?

A

Kinin.

Prostaglandins.

Leukotrienes.

37
Q

Why is the increased vascular permeability caused by severe injuries said to be biphasic?

A

As the venules are affected first and then the capillaries and the arterioles are affected at the same time.

38
Q

How long does the increased vascular permeability caused by severe injuries usually last for?

A

Weeks or months.

39
Q

What are the 5 mediators for vascular permeability caused by severe injuries?

A

Kinin.

Prostaglandins.

Leukotrienes.

Histamine.

Serotonin.

40
Q

What happens to blood flow as it reaches a site of injury?

A

It slows down.

41
Q

What 2 things cause blood flow to slow down at the site of injury?

A

The loss of plasma and other fluids increases the viscosity of blood.

Histamine causes swelling of endothelial cells.

42
Q

Why is it important that blood flow slows at the site of injury?

A

So more nutrients can accumulate at the injury site.

43
Q

Where are blood cells found when blood is flowing normally?

A

In the centre of the blood vessel as this is where there is the least resistance.

44
Q

Where are blood cells found when blood is flowing slowly?

A

At the edges of the blood vessel.

45
Q

What is the marginating pool of blood vessels?

A

The blood cells at the edge of a blood vessel.

There are 2 marginating pools, one for each wall.

46
Q

Where is the circulating pool of blood vessels found?

A

In the middle of the blood vessel.

47
Q

How white blood cells exit the blood vessel after enterinf the marginating pool?

A

They bounce off blood vessel walls.

As they hit the walls they give off adhesion molecules that stick to the wall and this stops the WBCs.

It then crawls along the undamaged endothelium to a gap junction and exits the blood vessel.

48
Q

What is transmigration?

A

When WBCs that are stuck to the blood vessel wall exit the vessel via gap junctions.

49
Q

What is the emigration of white blood cells?

A

After the WBCs have left the blood vessel they follow a chemical gradient to the injury site.

50
Q

What are the 5 steps of the vascular response to inflammation?

A

Vasodilation.

Increased vascular permeability.

Stasis of blood flow.

Leukocyte margination.

Leukocyte emigration.

51
Q

Does the stasis of blood flow contribute towards increased vascular permeability and swelling?

A

No.

The stasis of blood flow is a result of the increased vascular permeability.

Pathology. Inflammation. (7 decks)

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