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MOD (Semester 2) > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

What are the five clinical signs of acute inflammation?

A

Redness, swelling, heat, pain and loss of function.

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2
Q

What can cause acute inflammation?

A

Foreign bodies, tissue necrosis, physical or chemical agents, trauma, infections and immune reactions.

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3
Q

What happens to blood vessels in acute inflammation?

A

Initially they constrict, but then they dilate so that there is increased perfusion to the tissue.

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4
Q

What vascular changes occur in acute inflammation?

A

The blood vessels increase in permeability, and so there is exudate on of fluid.

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5
Q

What are the consequences of swelling and exudate on of fluid?

A

Leads to slowing of the circulation, increased RBC concentration and increased blood viscosity.

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6
Q

What chemical is a key player at the beginning of acute inflammation? What does it cause?

A

Histamine. It causes pain, arteriolar dilation and venular leakage.

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7
Q

In what cells is histamine found?

A

Mast cells, basophils and platelets

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8
Q

What stimuli can lead to histamine release?

A

Physical damage, immune reactions and complement components.

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9
Q

What is the difference between serotonin and histamine?

A

They have similar properties but serotonin also stimulates fibroblasts.

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10
Q

What are prostaglandins? What drug can block their production?

A

These are produced by membrane phospholipids and cause vasodilation. Aspirin blocks their production, reducing pain and swelling.

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11
Q

In normal conditions, what molecules leave capillaries?

A

Water and electrolytes

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12
Q

What is the main driving force of fluid back into the blood?

A

Colloidal osmotic pressure of plasma proteins.

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13
Q

What three factors cause the main flow of fluid to be out of vessels in acute inflammation?

A

The semi-permeable membranes have become leaky, the capillary pressure driving fluid out increases and the force driving fluid back into capillaries is reduced as proteins escape through tissue spaces.

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14
Q

State the three consequences of increased fluid moving out of blood vessels

A

Oedema, increased lymphatic drainage (presents antigens to immune system), delivery of plasma proteins such as fibrin

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15
Q

What is the difference between transudate and exudate?

A

Transudate has a low protein content whilst exudate has a high protein content.

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16
Q

What can cause to transudate oedema?

A

Heart failure.

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17
Q

What do bradykinin and complement components induce?

A

Vascular leakage.

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18
Q

What defensive proteins are found in exudate?

A

Opsonins, complement and antibodies

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19
Q

What is inflammation?

A

It is the response of living, vascularised tissue to injury.

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20
Q

What is the primary cell type associated with acute inflammation?

A

Neutrophils

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21
Q

What is chemotaxis?

A

It is directional movement towards a chemical attractant.

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22
Q

What can be a chemotaxin?

A

Leucocytes, clotted blood, bacterial products, injured cells.

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23
Q

What happens to a neutrophil when a chemotaxin binds?

A

Na and Ca flow into the cell, it swells and points towards stimulus. It switches to a higher metabolic rate and is activated.

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24
Q

What is a Pseudopodia?

A

A projection of a neutrophil which occurs in a acute inflammation.

25
Q

In acute inflammation, once a neutrophil has been activated - what happens next?

A

Margination - move to the edges of blood vessels
Rolling - roll along the wall and bind to selections
Adhesion - bind to integrins

26
Q

What do neutrophils bind to when rolling?

A

Selectins

27
Q

What increases selectin/ integrins activation?

A

Inflammatory mediators and chemotaxins

28
Q

What is diapedesis?

A

This is the movement of leucocytes which move by pulling along collagen fibres of other tissue structures.

29
Q

Name two opsonins which can be recognised by neutrophils.

A

IgG antibody - if not the first encounter

C3b fragment of complement which is released on activation.

30
Q

What is degranulation?

A

This is the process of cell granules combining with the phagosome and injecting bactericidal substances into it.

31
Q

When in acute inflammation can local tissue injury occur?

A

Early degranulation before the particle is completely enclosed within the phagosome.

32
Q

Name the two mechanisms by which phagocytose do articles are killed.

A

Oxygen dependant - free radicals (oxygen/respiratory burst)

Oxygen independent - enzymes e.g. Proteases

33
Q

Name a vasoactive peptide.

A

Histamine and seratonin.

34
Q

What is the inhibitor of bradykinin?

A

It is cleaved by kallikrein in the blood.

35
Q

What is the function of complement?

A

These form tubes in membranes and so lead to death of bacteria. In the blood this circulates as diassembled proteins.

36
Q

Name some biproducts of complement components.

A

Inflammatory mediators C3a/c5a and opsonins c3b

37
Q

What is the precursor for prostaglandins?

A

Arachadonic acid

38
Q

What is the difference between a cytokine and a chemokine?

A

Cytokines are chemical messengers between cells whilst chemokines are involved in chemotaxis.

39
Q

Give an example of an endogenous mediator

A

endotoxins which causes inflammation in tissue.

40
Q

What are four common complications of acute inflammation?

A

Fluid loss, obstruction of tubes/ compression, normal tissue damage and pain and loss of function.

41
Q

Why does acute inflammation cause fever?

A

Exogenous pyrogens (endotoxins) stimulate macrophages to produce pyrogenic cytokines. These increase prostaglandin production in anterior hypothalamus and therefore increase the body thermostat.

42
Q

Why is fever advantageous in acute inflammation?

A

Inflammatory response is more effective at higher temperatures.

43
Q

What substance produces an increase in neutrophils in acute inflammation?

A

Colony stimulating factor from macrophages and endothelial cells. This stimulates the bone marrow to produce more neutrophils.

44
Q

What is acute phase response?

A

This is a response produced by cytokines where there is a change in plasma proteins as a result of altered synthesis by liver

45
Q

What is shock?

A

This is when inflammatory mediators/ bacterial products enter the blood stream and leads to whole body inflammation. Vasodilation and massive exudate of fluid leads to a drop in blood pressure.

46
Q

What stops the acute inflammation response?

A

Mediators only have short half lives and so they are degraded. Also inflammation triggers are reduced and so there is no emigration of neutrophils.

47
Q

What happens in the tissues after acute inflammation?

A

Neutrophils are phagocytose do, fluid is reabsorbed and fibrin is degraded. If the tissue has parenchymal cells then it regenerates. Otherwise an extensive fibrous scar will remain.

48
Q

What is pus?

A

It is an exudate that is creamy white due to its high neutrophil content.

49
Q

When do haemorrhagic exudates occur?

A

This is seen I don’t extractive infection or when there is extensive vascular damage. Exudate contains RBC and so appears bloody.

50
Q

Where might you see a serous exudate?

A

Blisters - no colour and no neutrophils.

51
Q

What is a seroma?

A

This is a fluid filled pocket with sterile fluid. This usually occurs post op.

52
Q

When can we clinically identify a fibrinous exudate?

A

If there is deposition of fibrin in the pericardium or pleural sacs then the surfaces cannot move over each other smoothly and so a rubbing sound is heard.

53
Q

What causes hereditary angio-oedema?

A

C1 esterase inhibitor deficiency. Sufferers have attacks of angio-oedema and abdominal pain.

54
Q

What problems are associated with a1- anti trypsin deficiency?

A

Neutrophils act unchecked and so this can lead to damage to the lungs - emphysema.
Also causes liver problems as ER secretes an incorrectly folded protein which cannot leave ER.

55
Q

What is chronic granulomatous disease?

A

This is where phagocytes are unable to produce superoxide and so no oxygen burst is created.

56
Q

Name the microorganism which causes lobar pneumona.

A

Streptococcus pneumoniae

57
Q

Name a microorganism which can cause Appendicitis

A

Escherichia coli

58
Q

What condition can Neisseria meningitidis cause?

A

Bacterial meningitis

59
Q

What can cause liver abscess?

A

Escherichia coli

MOD (Semester 2) (12 decks)

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