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ICS > Topic 2 - Accute Inflamation > Flashcards

Topic 2 - Accute Inflamation Flashcards

1
Q

What is acute inflammation?

A
  • Acute inflammation is the initial and often transient (only lasts a short time) series of tissue reactions to injury or irritation (noted histologically by the presence of neutrophils).
  • Immflamuation is not a disease but instead a manifestation of disease
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2
Q

What are the benefits of inflammation?

A
  • Destroys invading organisms

- “Walling off” (isolation) of an abscess cavity - prevents the spread of infection

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3
Q

What are the limitations of inflammation?

A
  • Disease: eg an abscess in the brain will occupy limited space and compress the surrounding vital structures
  • Fibrosis - Resulting from chronic inflammation - distorts tissue and can permanently alter their function.
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4
Q

What are the steps of acute inflammation?

A

1) Initial reaction of the tissue to injury
2) Vascular - Dilation of vessels due to smooth muscle relaxation in arteriolar walls
3) Exudation - Protein rich fluid leaks out of the vessels due to a high hydrostatic pressure within the vessel
4) Neutrophil polymorph recruitment

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5
Q

What are the outcomes of inflammation?

A

1) Resolution - Goes away
2) Suppurations - Pus formation eg an abscess
3) Organisation - Healing by fibrosis
4) Progression to chronic inflammation

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6
Q

What in organisation as an outcome of inflammation?

A
  • Healing by fibrosis: occurs when there is substantial damage to connective tissue and the tissue lacks the ability to regenerate specialised cells
  • Dead tissues are removed by macrophages
  • The defect is then filled with granulation tissue
  • The granulation tissue then gradually produces collagen to form a fibrous scar.
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7
Q

What are the causes of inflammation?

A
  • Microbial infections: Bacteria, viruses
  • Hypersensitivity reactions: Parasites
  • Physical agents: Trauma, ionising radiation, heat and cold
  • Chemicals: Corrosives, acids and alkalis
  • Bacterial toxins: Toxins released by bacteria during infection
  • Tissue necrosis: ischaemic infarction
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8
Q

What is a hypersensitivity reaction?

A

A reaction that occurs when the immune system causes an inappropriate or excessive immune response that damages tissue.

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9
Q

What is the normal appearance of acute inflammation?

A
  • Redness (rubor)
  • Heat (calor)
  • Swelling (tumor)
  • Pain (Dolor)
  • Redness (rubor)
  • Loss of function
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10
Q

What causes Redness (rubor)?

A

The dilation of small blood vessels within the damaged tissue

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11
Q

What causes heat (calor)?

A

Increased blood flow (hyperaemia) through the tissue, resulting in vascular dilation

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12
Q

What causes swelling (tumor)?

A

The accumulation of fluid in the extravascular space as part of the fluid exudate (due to high hydrostatic pressure). And to a lesser extent from the physical mass of inflammatory cells migrating to the area.

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13
Q

What causes Pain (dolor)?

A

The stretching and distortion of tissues due to inflammatory oedema and from pressurised puss in an abscess cavity.

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14
Q

What causes loss of function?

A

Movement in an inflamed area is consciously and reflexly inhibited by pain, while severe swelling can physically immobilise tissue.

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15
Q

What are the early stages of acute inflammation?

A

Oedema fluid, fibrin and neutrophil polymorphism accumulate in the extracellular spaces of the damaged tissue.

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16
Q

What is essential for a histological diagnosis of acute inflammation?

A

The presence of neutrophil polymorphs.

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17
Q

Acute inflammatory response process:

A

1) The vessel gets bigger (change in vessel calibre) - consequently vessel flow increases
2) Increased vascular permeability
3) Formation of the cellular exudate

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18
Q

What are the vascular changes observed in acute inflammation?

A
  • The smooth muscle of arteriolar walls form precapillary sphincters which regulate blood flow through the capillaries (capillaries have no smooth muscle in their walls to control their calibre)
  • Acute inflammation causes these sphincters to relax thus increasing blood flow through the capillaries contributing to redness and heat.
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19
Q

How does acute inflammation affect fluid return to the vascular compartment?

A
  • Capillary hydrostatic pressure is increased as the precapillary sphincters relax
  • This causes the escape of plasma proteins into the extravascular space, increasing osmotic pressure outside the vessel
  • Vascular permeability increases causing swelling
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20
Q

Describe the movement of fluid in and out of a vessel under normal conditions.

A

High osmotic pressure inside the vessel, due to plasma proteins, favours fluid return into the vessel.

  • High hydrostatic pressure at the arteriolar end forces fluid out into the extravascular space
  • Lower hydrostatic pressure at the venous end allows for the return of fluid into the vascular compartment
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21
Q

What is Exudation?

A

The net escape of protein-rich fluid from the capillaries into the extravascular space.
- fluid is known as the fluid exudate.

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22
Q

What are the causes of increased vascular permeability and what is an example of each?

A
  • Immediate transient causes - chemical mediators such as histamine (these are immediate but not permanent)
  • Immediate sustained causes - Vascular injury - trauma
  • Delayed prolonged causes - Endothelial cell injury - X-rays & bacterial toxins
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23
Q

What are the stages of neutrophil polymorph emigration?

A

1) Margination of neutrophils
2) Adhesion of neutrophils
3) Neutrophil emigration

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24
Q

Describe the margination of neutrophils.

A
  • In normal circulation cells travel in the axial stream(centre of the vessel).
  • Inflammation causes loss of intravascular fluid and increased plasma viscosity which causes neutrophils to travel in the plasmatic zone (peripheral - near the vessel walls/ endothelium)
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25
Q

Describe the adhesion of neutrophils.

A
  • Neutrophils randomly come into contact with the endothelium in normal tissues but do not adhere
  • Adhesion occurs due to the interaction of paired adhesion molecules on leucocyte and endothelial surfaces
  • this only occurs in venules

The adhesion of neutrophils to the vascular endothelium is known as pavementing

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26
Q

Describe neutrophil emigration.

A
  • White blood cells migrate through the walls of venules and small veins but do not commonly exit from capillaries
  • Neutrophils insert pseudopodia between endothelial cells (which creates a small gap), they then migrate through the gap and then carry on through the basal lamina and into the vessel wall.
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27
Q

Describe Diapedesis.

A
  • Red blood cells escape from the vessels passively due to the high hydrostatic pressure in the vessels forcing cells out.
  • However the presence of a large number of RBC in the extracellular fluid implies vascular injury, such as a tear in a vessel wall
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28
Q

What is up-regulation?

A

An increase in the number of receptors on the surface of target cells, making the cells more sensitive to a hormone or another agent.

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29
Q

What stimulates up-regulation?

A

Histamine and thrombin released by the original inflammatory stimulus (occurs early in the response).

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30
Q

What is the overall effect of chemical mediators in acute inflammation?

A

Firm neutrophil adhesion to the endothelial surface

31
Q

What do endogenous chemical mediators cause?

A
  • Vasodilation
  • Emigration of neutrophils
  • Chemotaxis (attraction of neutrophil polymorphs)
  • Increased vascular permeability
  • Itching and pain
32
Q

What does Histamine cause to happen?

A
  • vascular dilation

- And the immediate transient phase of increased vascular permeability.

33
Q

What is the most important source of histamine?

A

Mast cells

34
Q

Why is the effect of histamine immediate?

A

It is storied in preformed granules and so is able to be instantly released in tissues

35
Q

What stimulates the release of histamine?

A

compliment components:

  • C3a
  • C5a
  • And lysosomal proteins released from neutrophils.
36
Q

What are 5 chemical mediators released from the cell in acute inflammation?

A
  • Histamine
  • Lysosomal compounds
  • Eicosanoids (a type of prostaglandin)
  • Serotonin
  • Chemokines
37
Q

What are the four enzymatic cascade systems present in the plasma?

A

1) the complement system
2) the kinins system
3) coagulation factors
4) fibrinolytic system

38
Q

What is the compliment system and what is its purpose?

A

It’s a series of interacting plasma proteins which form a major effector system for antibody-mediated immune reactions. The major purpose of the compliment system is to remove or destroy antigens by direct lysis or opsonisation

39
Q

Define opsonisation

A

The process by which bacteria are altered by opsonisation to become more readily and efficiently engulfed by phagocytosis

40
Q

What are the chemical mediators of vascular dilatation

A
  • Histamine
  • Prostaglandins
  • PGE2/12
  • VIP
  • Nitric oxide
  • PAF
41
Q

What are the chemical mediators of increased vascular permeability?

A

Transient phase - Histamine

Prolonged phase - Bradykinin, nitric oxide, C5a, Leucotriene B4 and PAF

42
Q

What are the chemical mediators involved in adhesion of leucocytes to the endothelium?

A
  • IL-8
  • C5a
  • Leucotriene
  • B4
  • PAF
  • IL-1
  • TNF-Alpha
43
Q

What are the chemical mediators of neutrophil polymorph chemotaxis?

A
  • Leucotriene B4

- IL-8

44
Q

What is the role of tissue macrophages in acute inflammation?

A

The are responsible for clearing away tissue debris and damaged cells

45
Q

What chemical mediators do tissue macrophages secrete when stimulated by local injury or infection?

A
  • Interleukin-1

- TNF-alpha (tumour necrosis factor alpha)

46
Q

When do macrophages become involved in acute inflammation?

A

Within a few hours, however they do not predominate until the later stages of infection when the neutrophil population has diminished.

47
Q

Why is lymph drainage important in the immune response?

A

Antigens are carried to regional lymph nodes for recognition by lymphocytes which then produce antibodies.

48
Q

What is the most common white blood cell?

A

Neutrophil polymorph - 60-70%

49
Q

What colours does a neutrophil polymorph stain under H&E?

A

Nucleus stains blue, the cytoplasm stains pink/purple

50
Q

What opsonises microorganisms?

A

Immunoglobulins or compliment proteins

51
Q

What is the alternative pathway?

A

Bacterial toxins (liopopolysaccharides) activate the compliment system generating component C3b which has opsonising properties

52
Q

What is the classical pathway?

A

When antibodies bind to bacterial antigens activating the compliment system generating C3b - which has opsonising properties

53
Q

How do neutrophils bind to immunoglobulins (antibodies)?

A

The microorganisms bind to the FAB components of the antibody (the arms) and the FC component is left available to be bound to by neutrophils.

54
Q

Which cells commonly implement phagocytosis?

A
  • Neutrophil polymorphs

- macrophages

55
Q

What are the stages of phagocytosis?

A

1) adhesion of the particle to be phagocytosed to the cell surface - facilitated by opsonisation
2) the phagocyte ingests the particle by sending a pseudopodia around it which meets and fuses so the particle is bound by a cell membrane in a phagosome.
3) lysosomes then fuse with the phagosome to form a phagolysosome - where the intracellular killing takes place

56
Q

What oxygen-dependent noxious microbial agents are used in the intracellular killing of microorganisms during phagocytosis

A
  • Hydrogen peroxide

Reacts with myeloperoxidase in the presence of a halide such as Cl- to produce a potent microbial agent

57
Q

What oxygen-independent noxious microbial agents are used in the intracellular killing of microorganisms during phagocytosis

A
  • Lysozymes (muramidase)

- Lactoferrin

58
Q

What are the effects of lysosomal products?

A
  • Damages local tissue by proteolysis (elastase and collagenase)
  • Activates coagulation factor XII (7)
  • Attracts other leucocytes to the area
  • Inc vascular permeability
  • Induce systemic fever by acting on hypothalamus (pyrogens)
59
Q

What is the role of mast cells in acute inflammation?

A
  • Release preformed inflammatory mediators (eg histamine)

- Metabolise arachidonic acid into inflammatory mediators such as leukotrienes, prostaglandins and thromboxanes.

60
Q

What is the macroscopic appearance of acute inflammation?

A
  • Serous inflammation - fluid release
  • Suppurative inflammation - pus
  • Membranous inflammation
  • Pseudomembranous inflammation - formation of a membrane of a mucosal surface
  • Necrotising inflammation - dead/ dying tissue
61
Q

What are the beneficial effects of the fluid exudate on acute inflammation?

A
  • dilution of toxins - carried away in lymphatics
  • entry of antibodies - inc vascular permeability
  • transport of drugs to site of infection
  • fibrin formation to impede the movement of microorganisms by trapping them
  • delivery of nutrients and O2 - essential for neutrophils which have high metabolic activity
  • Stimulation of immune response by antigens entering the lymphatic system
62
Q

What are the harmful effects of the fluid exudate on acute inflammation?

A
  • Digestion of normal tissues - particularly vascular damage in type 3 sensitivity reactions
  • Swelling - children - acute epiglottitis can obstruct the airway or in cranial cavity - raised intracranial pressure can impede bloodflow to brain - ischaemic damage
  • Inappropriate inflammatory response - type 1 HSR
63
Q

What are the four main outcomes of acute inflammation?

A

1) resolution
2) suppuration
3) organisation
4) progression to chronic inflammation

64
Q

What is resolution and what conditions favour this outcome?

A

The complete restoration of tissues to normal after an episode of acute inflammation

  • minimal cell death and damage
  • occurrence in an organ capable of regeneration such as the liver
  • rapid destruction of causal agent
  • rapid removal of fluid and debris by good local drainage

EG - acute lobar pneumonia

65
Q

What is suppuration and what conditions favour this outcome?

A

The formation of pus, a mixture of neutrophils, bacteria, cellular debris and sometimes globules of lipid

  • the causative stimulus must be fairly persistent - usually an infective agent - usually pyogenic bacteria (pus forming bacteria)
  • pus surrounded by pyogenic membrane - start of healing
  • collection of pus - an abscess - bacteria within the cavity are relatively inaccessible to antibodies and antibiotic drugs.
66
Q

What is empyema?

A

When pus accumulates inside a hollow organ, part of the organ may become fused together by fibrin resulting in an empyeme (pus filled pocket)

67
Q

What is organisation and what conditions favour this outcome?

A

Organisation is the replacement of tissue by granulation tissue.

  • large amounts of fibrin formed that cannot be removed completely by fibrinolytic enzymes from the plasma or neutrophil polymorphs
  • substantial volumes of tissue become necrotic or the dead tissue is not easily digested
  • exudate and debris cannot be removed or discharged

Eg - scaring in acute lobar pneumonia

68
Q

What is the progression to chronic inflammation and what conditions favour this outcome?

A

The progression to a slow, long term inflammation which can last for months or years

  • agent causing inflammation isn’t removed
  • chronic inflammation often occurs as a primary event with there being no preceding period of acute inflammation
69
Q

How does the nature of the fluid exudate change in chronic inflammation?

A

Instead of neutrophil polymorph:

  • lymphocytes
  • plasma cells (make antibodies)
  • macrophages (phagocytose)
  • multinucleate giant cells (comprising many macrophages that have combined all trying to engulf the same thing)
  • fibroblasts (lay down collagen)
70
Q

What are the systematic effects of inflammation?

A
  • Pyrexia (fever)
  • malaise (general feeling of unwellness)
  • Anorexia (loss of appetite)
  • Nausea
  • Weight loss - due to -VE nitrogen balance because of the energy required to produce inflammatory mediators
  • reactive hyperplasia
  • haematological changes
  • amyloidosis
71
Q

What are examples of reactive hyperplasia of the reticuloendothelial system (clear up system)

A
  • local or systematic lymph node enlargement

- Splenomegaly (spleen enlargement) - found in certain infections such as malaria and infectious mononucleosis

72
Q

What are examples of haematological changes due to acute inflammation?

A
  • increased levels of white blood cells
  • inc in neutrophils - in pyogenic infections and tissue destruction
  • inc in eosinophils - in allergic disorders and parasitic infections
  • inc lymphocytes in chronic infection (eg tuberculosis), many viral infections and whooping cough
  • increased amount of monocytes - in certain bacterial infections (eg tuberculosis and typhoid)
  • anaemia - blood loss into exudate or due to haemolysis
73
Q

What is amyloidosis and what cases it?

A

A build up of protein (amyloid plaque) - disrupting organ function
- long-standing chronic inflammation (eg TB)
- abnormal widening of the airways - inc mucus production
- elevation of serum amyloid A protein (SAA) can cause amyloid to be deposited in various tissues, resulting in secondary (reactive) amyloidosis.
(Secondary if it occurs due to another disease/ condition).

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