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EMS - MoD > 4. Acute inflammation > Flashcards

4. Acute inflammation Flashcards

1
Q

What are the causes of acute inflammation?

A
  • tissue death (ischaemia, trauma, toxins, chemical insults, thermal injury, radiation)
  • infection (especially bacterial, pyogenic)
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2
Q

Define pyogenic

A

Pus forming

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3
Q

Define suppuration

A

The formation of pus

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4
Q

What is pus?

A

An accumulation of acute inflammatory cells, dead cells, bacteria etc.

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5
Q

What comes after acute inflammation?

A

Either

  • healing by regeneration
  • healing by repair
    or
  • chronic inflammation
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6
Q

When does healing by regeneration occur?

A

After acute inflammation, when the cells can regrow

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7
Q

When does healing by repair occur?

A

After acute inflammation, when the cells canon regrow

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8
Q

When does chronic inflammation occur following acute inflammation?

A

After acute inflammation, when the damaging agent persists

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9
Q

What are the purposes of acute inflammation?

A
  • clear away dead tissues
  • locally protect from infection
  • allow access of immune system components
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10
Q

What are the 4 cardinal signs of inflammation?

A
  • calor (=heat)
  • rubor (=redness)
  • dolor (=pain)
  • tumor (=swelling)
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11
Q

In addition to the main 4 cardinal signs of inflammation, what is the extra one?

A

Disturbance of function

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12
Q

Why does rubor (redness) and calor (heat) occur in inflammation?

A

Due to vascular dilation

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13
Q

Why does swelling occur in inflammation?

A

Due to inflammatory exudate into surrounding tissues

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14
Q

Acute inflammation will look different in different organs. Name 4 different types of acute inflammation.

A
  • serous
  • fibrinous
  • purulent
  • pseudomembranous
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15
Q

What occurs in serous inflammation?

A

Fluid accumulates in cavity

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16
Q

What occurs in fibrinous inflammation?

A

Precipitation of fibrin

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17
Q

What occurs in purulent inflammation?

A

Formation of pus

This is very common

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18
Q

What are 3 components of the acute inflammatory reaction?

A
  1. vascular reaction
  2. exudative reaction
  3. cellular reaction
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19
Q

What is the vascular reaction? (a stage of acute inflammatory response)

A

Dilatation of blood vessels (=rubor), changes in flow

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20
Q

What is the exudative reaction? (a stage of acute inflammatory response)

A

Vessels become leaky, formation of inflammatory exudate (=tumor)

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21
Q

What is the cellular reaction? (a stage of acute inflammatory response)

A

Migration of inflammatory cells out of vessels

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22
Q

Define pyrexia

A

High temperature due to inflammation

23
Q

How can the severity of acute inflammatory response in a patient be quantified?

A
  • pyrexia

- acute phase reaction

24
Q

Give an example of a protein that is measured in acute phase reaction?

A

C-reactive protein

ESR (erythrocyte sedimentation rate)

25
Q

What is the acute phase reaction?

A

Systemic and metabolic changes that occur within hours of an inflammatory stimulus. - acute phase proteins.

26
Q

Describe the vascular reaction?

A

Microvascular dilation causes an increase in flow and then flow eventually deceases as the vessels become leaky

27
Q

What causes increased permeability of vessels?

A

Mediated =

histamine 
bradykinin 
NO
leukotriene B4 
complement components

Non-mediated =

direct damage to endothelium eg. toxins, physical agents

28
Q

How can we interfere with increased vascular permeability?

A

Drugs can affect the mediators which cause mediated increased permeability

29
Q

What happens in a capillary if there is a greater hydrostatic pressure?

A

Fluid is pushed out of the capillaries

30
Q

What happens in a capillary if there is a greater oncotic pressure?

A

Fluid will enter the capillaries

31
Q

At the arterial end of a capillary, is hydrostatic or oncotic pressure higher?

A

Hydrostatic pressure > oncotic pressure at the ARTERIAL end

32
Q

What does acute inflammatory exudate consist of?

A

Protein rich (50g/l)

  • immunoglobins
  • fibrinogen
33
Q

What are the benefits of acute inflammatory exudate?

A

constantly turning over

  • dilution of noxious agents
  • transport to lymph nodes
  • supply of nutrients, O2
  • spread of drugs
  • spread of antibodies
  • spread of inflammatory mediators
34
Q

What is pericarditis?

A

Inflammation of the pericardium of the heart

35
Q

What do you see in pericarditis?

A

A friable shaggy covering of the heart rather than being smooth and shiny.

This is due to fibrinous inflammation (the shaggy material is precipitated fibrin from the inflammatory exudate)

36
Q

What happens during the cellular reaction?

A
  • accumulation of neutrophils in the extracellular space (neutrophils are normally present in the blood but migrate into the extracellular space in infection)
  • in severe cases, accumulation of neutrophils, cellular debris and bacteria forms pus
37
Q

What do you see in acute meningitis caused by a pyogenic bacterial infection?

A

Rather than being clear and shiny, the arachnoid covering over the cerebellum is cloudy because of the cell rich exudate in the subarachnoid space (pus)

38
Q

What type of cells are in the subarachnoid space in acute bacterial meningitis?

A

Neutrophil polymorphs, these are characteristic of acute inflammation

39
Q

How would the alveoli feel in the case of bronchopneumonia?

A

It would feel solid compared to the surrounding lung as the alveoli are filled with the acute inflammatory exudate rather than air

40
Q

What are the main characteristics of neutrophils?

A
  • produced in the bone marrow
  • commonest white cell in the blood
  • increase in acute inflammation
  • motile, amoeboid, can move into tissues
  • directional chemotaxis
  • short lifespan (hours in tissues)
  • phagocytic, microbiocidal
41
Q

Where are neutrophils produced?

A

In the bone marrow

42
Q

What is the most common white cell in the blood?

A

Neutrophils

43
Q

Do neutrophils have a long or short lifespan?

A

Short.

hours in tissues

44
Q

What are the stages as neutrophils flow in the blood during inflammatory response?

A
  1. margination
  2. rolling - adhesion (pavementing - can see this microscopically)
  3. migration (RBC diapedesis)
  4. chemotaxis
45
Q

Where are the mediators of acute inflammation derived?

A

Cell derived or plasma derived

46
Q

List the plasma derived mediators of acute inflammation

A
  • kinin system
  • clotting pathway
  • thrombolytic pathway
  • complement pathway
47
Q

What are the cell derived mediators of acute inflammation?

A 
Stored = histamine 
Synthesised =
prostaglandins
leukotrienes
PAF
cytokines (IL1, IL8, TNFa)
NO 
chemokines
48
Q

Why are the mediators of acute inflammation important to know about?

A

We can interfere with them with drugs

49
Q

What contributes to laboratory assessment of inflammation?

A
  • full blood count
  • erythrocyte sedimentation rate
  • acute phase reaction eg. C-reactive protein
50
Q

What diseases are caused by the inflammatory pathway going wrong?

A
  • systemic inflammatory response syndrome
  • acute (adult) respiratory distress syndrome
  • chronic granulomatous disease of childhood
  • hereditary angio-oedema
  • amyloidosis
51
Q

What is resolution?

A

After acute inflammation when there is minimal tissue damage

52
Q

What is fibrosis?

A

After acute inflammation when these is some tissue damage

53
Q

What happens after acute inflammation when there is marked neutrophil reaction with tissue damage?

A

Suppuration - abscess

54
Q

What may happen following acute inflammation?

A
  • resolution
  • fibrosis
  • suppuration - abscess
  • chronic inflammation

EMS - MoD (17 decks)

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