Week 2 - Acute inflammation Flashcards

1
Q

What is inflammation? What is its function?

A

response to injury of vascularised living tissue to deliver defensive material- leucocytes and plasma proteins to the site of injury protecting the body against infection and to clear damaged tissue initiating repairesponse to injury of vascularised living tissue to deliver defensive material- leucocytes and plasma proteins to the site of injury protecting the body against infection and to clear damaged tissue initiating repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give three properties of acute inflammation

A

Innate, stereotyped and rapid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When is acute inflammation needed?

A

When local defenses are no longer adequate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do most defensive agents circulate?

A

In the blood in inactive form and are delivered/ activated when needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What must defensive agents be able to do?

A

leave blood vessel at the site without interrupting blood flow as this is needed at further sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give 6 causes of acute inflammation

A
Foreign bodies
Immune reactions
Infections and microbial toxins
Tissue necrosis
Trauma ( blunt and penetrating)
Physical and chemical agents( thermal injury, environmental chemicals)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give the 5 signs of acute inflammation and explain why

A

Rubor – redness caused by dilation of blood vessels
Color- heat caused by dilation of blood vessels
Tumour – swelling caused by fluid and leucocytes in tissue
Dolor – pain caused by specialised nerve endings stimulated by mediators - bradykinin
Loss of function which enforces rest and decreases chance of further damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give the first stage of formation of exudate

A

Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give the second step in the formation of exudate and what brings this about?

A
  1. Vasodilation of arterioles- brought about by vasoactive mediators histamine from mast cells and platelets, nitric oxide from macrophages and endothelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What changes about the venule walls during exudate formation? What does this allow?

A

They become leaky allowing plasma to escape through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Loss of fluid from the venules leads to what?

A

Increased haemocrit within the venules and increased resistance to blood flow reducing it to further along venules and increased pressure upstream. This causes their lumens to dilate and reducing the blood flow speed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The increased pressure in the venules leads to what?

A

Increased fluid into the tissues and therefore increased proteins to the site of injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is generally the first mediator in acute inflammation?

A

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is histamine found usually?

A

Cells in the tissue and platelets. It is also stored in the granules of Mast cells and basophils.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is histamine used as in the brain?

A

Neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What effects does histamine induce in acute inflammation?

A

Produces pain.
Causes arteriolar dilation
Venular leaking by causing endothelial cells to contract and pull apart allowing proteins to pass

17
Q

What other mediator is similar to histamine in terms of the effects exerted? What other effect does it cause ?

A

Serotonin

Stimulates fibroblasts

18
Q

What chemical mediator is made from cell membrane phospholipids?

A

Prostaglandins

19
Q

What effects do prostaglandins have?

A

Vasodilation
Makes skin increase sensitive
Cause fever

20
Q

What drugs block the production of prostaglandins? How?

A

Steriods - inhibit the phopholipases therefore cannot go from phospholipids to arachondonic acid
Aspirin and NSAIDs inhibit cyclo-oxygenases therefore cannot go from arachadonic acid to prostaglandin

21
Q

What defensive proteins are found in the exudate? What are their functions?

A

Opsonins – coat foreign material and make them easy to phagocytose
Complement – group of proteins assembled locally to produce bacteria perforating structure
Antibodies – bind to surface of microorganisms – act as opsonins

22
Q

Explain how lymphadenitis occurs

A

 Excessive fluid drains from tissue in lymphatic taking with it microorganisms and antigens therefore presenting them to the immune system within lymph nodes – can become inflamed, swollen and painful – LYMPHADENITIS

23
Q

Explain the difference between exudate and transudate

A

Rich in proteins - exudate

Low in proteins - transudate

24
Q

When does transudate occur?

A

secondary to osmotic or hydrostatic imbalance across a vessel wall without increase in permeability

25
Q

What chemical mediators induce vascular leakage

A

histamine, serotonin, bradykinin and complement components c3a, c4a and c5a

26
Q

Under normal conditions where are neutrophils found

A

blood and bone marrow

27
Q

What is the lifespan of a neutrophil

A

12-20hrs

28
Q

What must neutrophils be able to do to be effective in inflammation

A
  1. Chemotaxis
  2. Activation
  3. Margination
  4. Diapedisis
  5. Recognition attachment
  6. Phagocytosis
  7. Kill
29
Q

Explain chemotaxis for a neutrophil

A

Summoned to the place of injury. Movement towards chemotaxins.

30
Q

How do neutrophils move?

A

By producing filopodia that pull back of cell in direction of extension

31
Q

Give some example of chemotaxins for neutrophils

A

Bacterial products
Leukotrienes (B4)
C3a/4a/5a
Clotted blood - fibrin

32
Q

Explain what activation means in terms of neutrophils

A

Switching a to a higher metabolism level and increased stickiness

33
Q

How is the change in activation of a neutrophil brought about?

A

Binding of chemotaxin which leads to influx of sodium and calcuim ions. Electrolytes moving causes water to also move.

34
Q

Explain margination of a neutrophil.

A

Sticking to the endothelium surface. Leucocytes assume marginal position in vessel ,sticking to the walls of venules and roll along before becoming trapped and crawl out of the vessel.

35
Q

What mediators are invovled during margination of a neutrophil? What happens to the number of these during acute inflammation?

A

Selectins and integrins

Increase

36
Q

What is diapedisis of a neutrophil?

A

Crawling through the endothelim by production of collagenase whihc digests the basement membrane

37
Q

Once outside the venule how do neutrophils move?

A

Pulling on collagen fibres