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Semester 1 flashcards > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

Aidan

1
Q

What are the causes of acute inflammation?

A
  • Microbial infections.
  • Hypersensitivity reactions.
  • Physical agents.
  • Chemical agents.
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2
Q

What are hypersensitivity reactions?

A

Allergies.

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3
Q

How to recognise (acute) inflammation?

A
  • Redness.
  • Heat.
  • Swollen.
  • Painful/Tender.
  • Loss of function.
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4
Q

What causes the characteristic redness of Acute inflammation?

A

Dilation of blood vessels.

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5
Q

What causes the characteristic heat of Acute inflammation?

A
  • Peripheral inc. in temperature.

- Due to increased blood flow (hyperaemia).

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6
Q

What causes the characteristic swelling of Acute inflammation?

A
  • Due mainly to oedema.

- Some contribution from inflammatory cells.

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7
Q

What causes the characteristic pain/tenderness of Acute inflammation?

A

-Stimulation of nerve endings by pressure and chemical mediators.

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8
Q

What is oedema?

A

Influx of fluid into a tissue that doesn’t normally have as much fluid in it.

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9
Q

What are the phases of acute inflammation?

A

-Vascular and Exudative phases.

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10
Q

What is the characteristic cell of Acute inflammation?

A

Neutrophil polymorphs.

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11
Q

What happens in the vascular phase?

A

Dilation and increased permeability.

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12
Q

What happens in the exudative phase?

A

Fluid and cells escape from permeable venules.

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13
Q

What is the net flow in a normal blood vessel compared to a blood vessel affected by acute inflammation.

A

In a normal vessel there is no net flow as fluid leaks in or out.

in acute inflammation there is net flow out as the vessel has increased permeability

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14
Q

What are the features of exudate?

A
  • High protein content.
  • Proteins may include immunoglobulins.
  • Fibrinogen turns into fibrin.
  • High turnover.
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15
Q

Why are immunoglobulins important?

A

They may be important for the destruction of invading organisms.

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16
Q

When does fibrinogen turn into fibrin and what does this cause?

A

It changes on extravascular contact and acutely inflamed organ surfaces are commonly covered by fibrin.

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17
Q

What causes the high turnover of exudate?

A

It is continuously removed by lymphatics.

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18
Q

Differences between exudate and transudate?

A
  • Exudate; net flow out, inc. vascular permeability and high protein content.
  • Transudate; Net flow out, normal vasc permeability and low protein content.
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19
Q

What happens with increased vascular permeability?

A

Stimulation of endothelial cell cytoskeletons causes them to change shape and transient intracellular gaps appear.

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20
Q

What happens to endothelial cells after inflammation has been dealt with?

A

They return to normal shape after and are not damaged by the process.

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21
Q

How is increased vascular permeability caused?

A

caused by chemical mediators including; histamine and bradykinin.

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22
Q

What happens to the lymphatic system in inflammation?

A
  • Lymphatics dilated
  • Drain fluid from exudate
  • Antigens carried to lymph notes + recognised by lymphocytes.
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23
Q

What is the number of lymph nodes in the body?

A

Varies from person to person but average is 250-300.

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24
Q

What is Lymphangitis?

A

Inflammation of the lymphatic vessels.

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25
Q

What is Lymphadentis?

A

Inflammation of the lymph nodes.

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26
Q

What do neutrophils have to do with diagnosing acute inflammation?

A

Neutrophil accumulation in the extracellular space is the diagnostic feature of acute inflammation.

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27
Q

What do neutrophils do?

A
  • Kill organisms.
  • Degrade necrotic tissue.
  • Ingest offending agents.
  • Produce chemical mediators, toxic oxygen radicals and tissue damaging enzymes.
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28
Q

What are the stages of neutrophils leaving vessels?

A

1-Magination (beginning to stick).
2-Pavementing (flattening out).
3-Pass between endothelial cells.

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29
Q

What are some chemotactic compounds?

A
  • bacterial products.
  • Some complement components.
  • Products of neutrophil activity.
30
Q

How do neutrophils locate/track down antigens?

A

Chemotaxis; follows the gradient of particle concentration to where it is strongest which is where the antigen is.

31
Q

What is chemotaxis?

A

Where neutrophils track down antigens by following the gradient of particle concentration to where it is strongest which is where the antigen is.

32
Q

What do chemical mediators cause during acute inflammation?

A

Vasodilation, emigration of neutrophils, chemotaxis, inc. vascular permeability, itching and pain.

33
Q

What are the four enzymatic cascade systems in plasma?

A

1) Complement system.
2) The kinins.
3) The coagulation factors.
4) Fibrinolytic system.

34
Q

What do neutrophils do?

A

Kill organisms, Degrade necrotic tissue. Ingest offending agents and produce chemical mediators, toxic oxygen radicals and enzymes.

35
Q

How do neutrophils work?

A

Movement (chemotaxis), recognition of and adhesion to micro-organisms, Phagocytosis and intra-cellular killing of micro-organisms.

36
Q

Which has a higher turnover RBC’s or neutrophils?

A

RBC lifespan = 3 months.

Neutrophil lifespan = 24/48 hours.

37
Q

When are most micro-organisms not recognised by neutrophils?

A

When they are not coated in opsonins.

38
Q

What do opsonins do?

A

They bind to specific receptors on leucocytes and greatly enhance phagocytosis.

39
Q

Name a major opsonin.

A

Collectins (plasma proteins that bind to micorbial cell walls.

(Another example would be the Fc fragment of IgG)

40
Q

What would you notice in a patient on drugs which affect bone marrow? (stop cell production)

A

Neutrophils would drop off a lot quicker than RBC’s.

41
Q

What is phagocytosis?

A

The process where cells such as neutrophils and macrophages ingest solid particles.

42
Q

What does acute serous inflammation look like?

A

Protein rich exudate.

43
Q

What does acute catarrhal inflammation look like?

A

Mucus hypersecretion.

44
Q

What does acute fibrinous inflammation look like?

A

Exudate contains plentiful fibrin.

45
Q

What does acute haemorrhagic inflammation look like?

A

Severe vascular injury.

46
Q

What does acute suppurative inflammation look like?

A

Production of pus.

47
Q

What does acute membranous inflammation look like?

A

Epithelium coated by fibrin.

48
Q

What does acute psuedomembranous inflammation look like?

A

Superficial mucosal slough.

49
Q

What is suppuration?

A

Formation of pus- neutrophils, bacteria, cellular debris.

50
Q

What is the causative stimulus of suppuration?

A

Virtually always infective agent.

51
Q

What is an abcess?

A

A colection of pus surrounded by a membrane of sprouting capillaries, neutrophils and occasional fibroblasts is called an abcess.

52
Q

Where might deep-seated abcesses drain?

A

Along a sinus tract or fistula.

53
Q

What is a fistula?

A

Technically and abnormal joining of two places in the body that wouldn’t normally be joined.

54
Q

What is an ulcer?

A

An ulcer is a local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing of inflammatory necrotic tissue.

55
Q

Where are ulcers most commonly encountered?

A
  • Inflammatory necrosis of the mucosa; mouth, stomach, intestine.
  • Chronic leg ulcers in those with circulatory disturbance.
56
Q

What are the beneficial effects of the acute inflammation?

A

Dilution of toxins, entry of antibodies, fibrin formation, transport of drugs, delivery of nutrients and oxygen and stimulation of the immune response.

57
Q

What are the harmful effects of acute inflammation?

A

Digestion of normal tissues, swelling (eg. laryngeal odema, brain swelling), inappropriate inflammatory response (eg. type 1 hypersensitivity).

58
Q

What are the systemic effects of acute inflammation?

A
  • Pyrexia (increased body heat).
  • Malaise, anorexia and nausea.
  • Weight loss due to -ve nitrogen balance.
  • Haematological changes; inc. erythrocyte sedimentation rate, anaemia and leukocytosis.
59
Q

What does acute inflammation usually lead to?

A

Resolution.

60
Q

What does acute inflammation usually lead to in cases with excessive exudate?

A

Suppuration, which then leads either to discharge of pus or repair and organisation then to fibrosis.

61
Q

What does acute inflammation usually lead to in cases with excessive necrosis?

A

Repair and organisation then fibrosis.

62
Q

What does acute inflammation usually lead to in cases with a persistent causal agent?

A

Chronic inflammation then fibrosis.

63
Q

What are the factors favouring resolution?

A
  • Minimal cell death and tissue damage.
  • Occurrence in an organ or tissue with regenerative capacity e.g. liver.
  • Rapid destruction of the causal agent.
  • Rapid removal of fluid and debris by good local vascular drainage.
64
Q

What is organisation?

A

Replacement of destroyed tissue by granulation tissue.

65
Q

What are the factors favouring granulation?

A
  • Large amounts of fibrin.
  • Substantial necrosis.
  • Exudate and debris cannot be removed or discharged.
66
Q

What happens in organisation?

A

Ingrowth of new capillaries into the damaged area + influx of immune cells and proliferation of fibroblasts.

67
Q

What happens to the tissue in granulation?

A

Much of the skin is destroyed and the underlying tissue is undergoing repair, the damaged area is being replaced by vascular granulation tissue.

68
Q

What replaces exudate in granulation tissue?

A

Capillaries, macrophages, fibroblasts and collagen.

69
Q

What is granulation tissue regulated by?

A

Growth factors, i.e; TNF, EGF, FGF.

70
Q

There is a fair amount of overlap between acute and chronic inflammation, true or false?

A

True.

Semester 1 flashcards (33 decks)

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