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Phase 2a - ICS > Acute & Chronic inflammation > Flashcards

Acute & Chronic inflammation Flashcards

1
Q

What is inflammation?

A

The local physiological response to injury/infection involving cells such as neutrophils and macrophages.

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2
Q

Example of beneficial effects of inflammation?

A

Destruction of pathogens during infections. During injury it can start of the healing process as well.
Walling off an abscess cavity, thus preventing the spread of infection.

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3
Q

Example of harmful effects of inflammation?

A

Autoimmune disease when body mounts an anti-inflammatory response to a tissue.
Abscess in brain is a space occupying lesion - compressing on vital surrounding structures.
Fibrosis as a result of chronic inflammation distort the tissue and alters its function.

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4
Q

What are the classifications of inflammation?

A

Acute: the initial and often transient series of tissue reactions to injury.

Chronic: the subsequent and often prolonged tissue reactions following the initial reactions.

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5
Q

What are the characteristics of acute and chronic inflammation?

A

Acute: Sudden onset, short duration, and usually resolves. Neutrophils are the predominant cell types.

Chronic: Slower onset or sequel to acute inflammation. Long duration and may never resolve. Macrophages and lymphocytes are the predominant cell types.

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6
Q

Summarise acute inflammation:

A
  • Initial reaction of tissue to injury
  • Vascular component: dilation of vessels
  • Exudate: protein-rich fluid
  • Neutrophils are the most abundant
  • Outcome may be resolution, suppuration (abscess), organisation, or progression to chronic inflammation.
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7
Q

What are the four outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration
  3. Organisation
  4. Progression to chronic inflammation.
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8
Q

True or false?
The acute inflammatory response is similar whatever the causative agent is.

A

True.

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9
Q

What are the principal causes of inflammation?

A
  1. Microbial infections (pyogenic bacteria, viruses)
  2. Hypersensitivity reactions (parasites, tuberculi bacili)
  3. Physical agents (trauma, heat, cold, ionising radiation)
  4. Chemicals (corrosives, acids, alkalis, bacterial toxins)
  5. Tissue necrosis (ischeamic infarction)
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10
Q

Microbial infections.

A

Commonest

Viruses - intracellular multiplication=death

Bacteria - exotoxins, endotoxins.

Organisms - immunologically mediated inflammation through hypersensitivity reactions (parasitic infections and tuberculous)

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11
Q

Hypersensitivity reactions.

A

Inappropriate or excessive immune reaction that leads to tissue damage.

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12
Q

What are the essential macroscopic signs of acute inflammation?

A
  1. Redness (Rubor)= dilation of small blood vessels.
  2. Heat (Calor)= increased blood flow to the peripheral parts. In systemic response, fever from chemical mediators.
  3. Swelling (Tumor)= from oedema. Fluid accumulates in extravascular space - exudate.
  4. Pain (Dolor)= Partly from stretching and distortion of tissues due to oedema or pus in an abscess cavity. Chemical mediators: bradykinin, PGs and 5HT also induce pain.
  5. Loss of function= movement of an inflamed ares is consciously and reflexly inhibited by pain. Severe swelling may immobilise the tissue.
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13
Q

What is essential for the histological diagnosis of acute inflammation?

A

The presence of neutrophil polymorph.

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14
Q

What are the three processes involved in the acute inflammatory response:

A
  1. Change in vessel calibre.
  2. Increased vascular permeability and formation of fluid exudate.
  3. Formation of cellular exudate - neutrophils move into extravascular space.
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15
Q

Describe the changes in vessel calibre:

A

Arterioles: thick muscular wall
Capillaries: no smooth muscle, so narrow that RBC pass in single file
Venules: thin walled

The smooth muscle of arterioles= precapillary sphincters which regulate blood flow.

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16
Q

Describe laminar blood flow:

A

Blood cells flow in the centre (axial flow) and area near the vessel carries plasma.

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17
Q

Describe increased vascular permeability:

A

High hydrostatic pressure at the arterial end= fluid into extravascular space.
Low hydrostatic pressure at the venous end= fluid returns.
In acute inflammation: increased capillary hydrostatic pressure and escape of plasma proteins into extravascular space - raises osmotic pressure there leading to a fluid exudate.

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18
Q

What are the features of fluid exudate?

A

Proteins escape from vessels = concentration up to 50g/L.
Igs, coag. factors (fibrinogen).
Fibrinogen transformed into fibrin when in contact with tissues: fibrinous exudate.

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19
Q

What is the ultrastructural basis of increased vascular permeability?

A

Histamine injection - gap in small veins and venules (0.1-0.4 micrometers) in endothelial cells. This is NOT damage; contractile proteins i.e. actin. THIS IS ONLY CONFINED IN VENULES AND SMALL VEINS.

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20
Q

Summary of causes of increased vascular permeability:

A

Immediate transient: chemical mediators.
Immediate sustained: severe direct vascular injury.
Delayed prolonged: endothelial cell injury by bacterial toxins.

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21
Q

Do tissues have varying sensitivity to chemical mediators?

True or false

A

True - brain is barely sensitive, while tissues in skin, bronchial mucosa are highly sensitive.

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22
Q

What are the steps in leucocytes reaching the tissues? MAED

A

Margination
Adhesion
Emigration
Diapedesis

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23
Q

Describe the migration of neutrophils:

A

Due to loss of intravascular fluid and increase in viscosity slows the flow which allows neutrophils to now flow in the plasmatic zone (around the edge of the vessels).

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24
Q

Describe the adhesion of neutrophils:

A

At the site of inflammation called pavementing. Only seen in venules.
Interaction between adhesion molecules on leucocytes and endothelium.

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25
Q

Describe the emigration of neutrophils:

A

Amoeboid movement through walls of small veins and venules.
Insertion of pseudopodia between endothelial cells then through basal lamina. SELF-HEALING.

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26
Q

Describe diapedesis:

A

RBCs can escape via a passive process (depends on hydrostatic pressure). If there is large number of RBC= severe vascular injury i.e. tear in vessel wall.

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27
Q

What two molecules are released by the original inflammatory stimulus:

A

Histamine and thrombin.

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28
Q

What are the results of endogenous chemical mediators?

A

Vasodilation
Emigration of neutrophils
Chemotaxis
Increased vascular permeability
Itching and pain

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29
Q

Histamine is realised by…

A

Mast cells. Also present in basophil and eosinophil leucocytes, and platelets.

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30
Q

Histamine release is stimulated by…

A

Complement proteins (C3a and C5a) and lysosomal proteins released from neutrophils.

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31
Q

What other chemical mediators are released by cells?

A

Lysosomal compounds, eicosanoids, 5HT, chemokines.

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32
Q

What are the four enzymatic cascade systems in plasma?

A

Complement system
Kinins
Coagulation factors
Fibrinolytic system

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33
Q

What are the characteristics of the four systems in plasma?

A

Inactive precursors
Each step is an amplification
Large number of possible regulators
Each step-> end products with possibly different activities.

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34
Q

How is the complement system activated in tissue necrosis?

A

By enzymes released from dying cells.

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35
Q

How is the complement system activated during infection?

A

AG-AB complex via classical p.w.
Endotoxin via alternative p.w.

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36
Q

What is the role of TISSUE macrophages during acute inflammation?

A

Secrete cytokines (IL-1; TNF-alpha) this happens after stimulation by histamine and thrombin.

Later products: E-selectin, chemokines (IL-8 epithelium derived neutrophil attractant 78).

IL-1 and TNF-alpha cause endothelial cells, fibroblasts and epithelial cells to secrete MCP-1 (=monocyte chemoattractant protein-1) to attract neutrophil polymorphs.

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37
Q

What is a unique feature of lymphatic vessels?

A

The basal lamina of lymphatic vessels is incomplete - the junctions between cells are simpler and less robust than in capillary endothelial cells. Gaps tend to open up passively allowing large protein molecules to enter.

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38
Q

What are the role of neutrophil polymorphs?

A

Movement
Adhesion to microorganisms
Phagocytosis
Intracellular killing of microorganisms
Release of lysosomal products

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39
Q

Neutrophil polymorph movement:

A

Contraction of microtubules + gel/sol changes in cytoplasmic fluidity = amoeboid
Depends on Ca2+ and cyclic nucleotides intracellularly.
Directional movement!

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40
Q

Neutrophil polymorph adhesion to microorganisms:

A

Opsonisation by immunoglobulins or complement proteins (C3b).

Bacterial LPS - alternative p.w.
AG-AB - classical p.w.

IGs bind to microorganisms by Fab portion - leaving Fc free and neutrophils have receptors for these.

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41
Q

Describe how neutrophil polymorphs phagocytose…

A

Ingestion of solid particles.
1. Adhesion of particle to cell surface (facilitated by opsonisation).
2. Ingestion by wrapping pseudopodia around particle.
3. Becomes phagosome.
4. Lysosomes fuse with phagosome= phagolysosome (where killing takes place).

42
Q

Neutrophil polymorphs intracellular killing…

A

Highly specialised cells containing microbicidal agents.

43
Q

How can microbicidal agents be grouped?

A

Oxygen-dependent and oxygen-independent.

44
Q

How do oxygen-dependent microbicidal agents work?

A

Neutrophils produce hydrogen peroxide. This reacts with myeloperoxidase in the cytoplasmic granules in the presence of halides such as Cl-.
Agents by oxygen reduction: peroxide anions, hydroxyl radicals and singlet oxygen.

45
Q

How do oxygen-independent microbicidal agents work?

A

Lysosome (muramidase), lactoferrin= chelates iron required for bacterial growth), cationic proteins and low pH inside vacuoles.

46
Q

Release of lysosomal products…

A

Cell damage - proteolysis (elastase and collagenase) activates factors XII and attracts more leucocytes.
Other compounds can increase vascular permeability, others are pyrogens.

47
Q

The role of mast cells…

A

Activated by C3a/C5a - release preformed inflammatory mediators.
Metabolise arachidonic acid into leucotrienes, PGs and thromboxanes.

48
Q

What are the macroscopic appearances of acute inflammation?

A

Signs are modified according to the tissues involved:
- serous inflammation
- suppurative (purulent)
- membranous
- pseudomembranous
- necrotising (gangrenous)

49
Q

What are the beneficial effects of fluid and cellular exudates?

A
  • Dilution of toxins
  • Entry of ABs
  • Transport of drugs
  • Fibrin formation (impede movement of microorganisms and serves as matrix for the formation of granulation tissue)
  • Delivery of nutrients and O2 (neutrophils have high EN demand)
  • Stimulation of immune response (via lymph nodes)
50
Q

Describe macrophages:

A

One big round nucleus, filled with enzymes. They live longer (months, weeks) do not die at the site. May be APCs. Responsible for clearing away debris and damaged cells.

51
Q

What is the effect of macrophages and neutrophils discharging their lysosomal enzymes?

A

Either by exocytosis or when cells die - assist in digestion of the inflammatory exudate.

52
Q

What are the harmful effects of inflammation?

A
  • Digestion of normal tissue (Vascular damage in type III hypersensitivity reactions, in glumerulonephritis, and in abscess cavities
  • Swelling: in children the epiglottis can swell due to Haemophilus influenzae= obstruction in the airway. Serious in enclosed spaces such as cranial cavity -> pressure coning.
  • Inappropriate inflammatory response: type I hypersensitivity reactions (hay fever) may be life-threatening.
53
Q

What are the possible outcomes of acute inflammation?

A

Resolution
Suppuration
Repair and Organisation
Fibrosis
Chronic Inflammation

54
Q

Resolution

A

Complete restoration of tissue to normal after an episode of acute inflammation.

55
Q

What are the conditions that favour resolution?

A
  • Minimal cell death and tissue damage.
  • Occurs in an organ that has regenerative capacity
  • Rapid destruction of casual agent (phagocytosis of bacteria)
  • Rapid removal of fluid and debris by good local vascular drainage.
56
Q

Give an example of an inflammatory condition that completely resolves?

A

Acute lobar pneumonia.
Alveoli become filled with exudate containing fibrin, bacteria and neutrophil polymorphs.
Does not destroy alveolar wall.

57
Q

Suppuration

A

Formation of pus. A mixture of living, dying and dead neutrophils and bacteria, cellular debris and sometimes globules of lipids.

58
Q

What are the common causative agents of suppuration?

A

Pyogenic bacteria (Staphylococcus aureus, Streptococcus pyogenes, Neisseria species.

59
Q

Pus accumulation leads to…

A

Pus accumulations leads to pyogenic membrane formation (sprouting capillaries, neutrophils, fibroblasts).

Manifestation of healing, resulting in granulation tissue and scarring.

60
Q

Why is it hard to treat bacteria in an abscess cavity?

A

Relatively inaccessible to Abx - osteomyelitis is VERY difficult to treat.

61
Q

Abscess

A

Points, bursts then cavity collapses then obliterated by organisation and fibrosis leaving a small scar.

62
Q

What happens if pus accumulates inside hollow organs?

A

The mucosal layers of the outflow tract become fused together by fibrin resulting in an empyema.

63
Q

What is a fistula?

A

An abnormal passage connecting two mucosal surfaces or one mucosal surface to the skin surface.

64
Q

What is a complication of long standing abscesses?

A

The fibrous walls may become complicated by dystrophic calcification.

65
Q

Organisation

A

Tissue replacement by granulation tissue as part of the repair process.

66
Q

What are the circumstances favouring organisation?

A
  • large amounts of fibrin formed which cannot be removed by fibrinolytic enzymes.
  • substantial volume of tissue becomes necrotic.
  • exudate and debris cannot be removed or discharged.
67
Q

What happens during organisation?

A

New capillaries grow into the inflammatory exudate, macrophages migrate into the zone and fibroblasts proliferate (TGF-beta) resulting in fibrosis.
Example: pleural space following lobar pneumonia. Resolution only occurs in the lung parenchyma - extensive fibrous exudate fills the pleural space.

68
Q

What happens if the causative agent is not removed?

A

Might lead to chronic inflammation.

69
Q

What are the characteristic of cellular exudate in chronic inflammation?

A

Lymphocytes, plasma cells, macrophages (including sometimes multi-nucleated giant cells).

70
Q

True or false?

Chronic inflammation never occurs as a primary event.

A

False - there are cases when there is no preceding period of acute inflammation.

71
Q

What are the systemic effects of inflammation?

A

Pyrexia - endogenous pyrogens produced by polymorphs and macrophages. IL-2.
Constitutional symptoms - malaise, anorexia and nausea.
Weight loss - due to negative nitrogen balance.
Reactive hyperplasia of the reticuloendothelial system - lymph node enlargement (splenomegaly in malaria, infectious mononucleosis)
Heamatological changes - Increased ESR (due to alterations in plasma proteins resulting in increased rouleaux formation of RBCs).

72
Q

Why is there leucocytosis in inflammation?

A

Neutrophilia occurs in pyogenic infections.
Eosinophilia in allergic disorders and parasitic infection.
Lymphocytosis in chronic infections.

73
Q

What is the cause of anaemia in inflammation?

A

Either form blood loss, haemolysis or anaemia of chronic disorders due to the depression of the bone marrow.

74
Q

Amyloidosis

A

Long-standing chronic disorders lead to increased serum amyloid A protein (SAA) causes amyloid-deposition in various tissues resulting in secondary (reactive) amyloidosis.

75
Q

Chronic inflammation

A

Lymphocytes, plasma cells and macrophages predominantly.
- Usually primary (ab initio) but can be after acute
- Granulomatous inflammation is a specific type of inflammation
- Granuloma is an aggregate of epithelioid hystiocytes
- May be complicated by secondary (reactive) amyloidosis.

76
Q

Examples of chronic inflammation:

A
  • Resistance of infective agent to phagocytosis and intracellular killing: TB, viral infections.
  • Endogenous material: necrotic adipose tissue, uric acid crystals
  • Exogenous material: silica, asbestos fibres
  • Some autoimmune diseases: Hashimoto’s (organ specific)
    RA (non-organ specific)
    Contact hypersensitivity reactions (self AGs altered by nickel)
  • Specific disease of unknown aetiology: UC
  • Primary granulomatous diseases: Chron’s, sarcoidosis
77
Q

What type of acute inflammation progresses into chronic?

A

Supparative

78
Q

What does foreign material cause?

A

Chronic inflammation - chronic suppuration.

79
Q

Foreign bodies have a common tendency to cause what?

A

Granulomatous inflammation and cause macrophages to form multi-nucleate giant cells= foreign body giant cells.

80
Q

Example of recurrent episodes of acute inflammation:

A

Chronic cholecystitis due to the presence of gall stones. Leads to the replacement of wall muscle by fibrous tissue and predominant cell type becomes lymphocytes.

81
Q

Macroscopic appearances of chronic inflammation:

A

Chronic ulcer - peptic ulcer (breach of the mucosa, based lined with granulation tissue and fibrous tissue extending through the muscle layers of the wall.

Chronic abscess cavity - osteomyelitis.

Thickening of the wall of a hollow viscus: Crohn’s disease

Granulomatous inflammation: TB

Fibrosis: most of the chronic cell filtrate has subsided.

82
Q

Microscopic features of chronic inflammation:

A

Lymphocytes + plasma cells + macrophages.

83
Q

Paracrine stimulation of CT proliferation.

A

In healing: regeneration and migration of specialised cells.

In repair: angiogenesis followed by fibroblast proliferation and collagen synthesis resulting in granulation tissue.

These processes are regulated by growth factors.

84
Q

Describe cellular cooperation in chronic inflammation:

A

B lymphocytes in contact with AG and turn into plasma cells - production of ABs.

T lymphocytes cell-mediated immunity.

85
Q

Macrophages:

A
  • Relatively large cells.
  • Move by amoeboid motion through tissues.
  • Phagocytic capabilities (microorganisms and debris)
  • Long-lived.
  • Can harbour viable organisms if they are unable to kill them.
86
Q

What organisms can survive inside macrophages?

A

Mycobacterium tuberculosis and Mycobacterium leprae
Histoplasma capsulatum

87
Q

What does the mononuclear phagocyte system include?

A

Macrophages
Fixed tissue histiocytes
Osteoclasts

All derived from monocytes which come from heamatopoietic stem cells.

88
Q

Activation of macrophages

A

Increase in size
Protein synthesis
Mobility
Phagocytic activity
Content of lysosomal enzymes

89
Q

What are the important cytokines produced by macrophages?

A

INF-alpha
INF-beta
IL-1
IL-6
IL-8
TNF-alpha

90
Q

What is a granuloma?

A

Aggregate of epithelioid histiocytes. I.e. TB

91
Q

Epithelioid histiocytes

A

Vague histological resemblance to epithelial cells but have large vesicular nuclei, plentiful eosinophilic cytoplasm and often elongated.

Arranged in clusters.

Little phagocytic activity but secretory function. (ACE)

92
Q

What is a common feature of the many stimuli that induce granulomatous inflammation?

A

The indigestibility of particular matter by macrophages.

93
Q

Causes of granulomatous diseases

A

Specific infection: TB

Materials that resist digestion: keratin (endogenous), talc, silica (exogenous)

Specific chemicals: beryllium

Drugs: allopurinol (hepatic granulomas)

Unknown: Crohn’s disease, Sarcoidosis, Wegener’s granulomatosis.

94
Q

Histiocytic giant cells

A

Indigestible matter accumulates

Foreign particles are too big

Thought to develop accidentally when two or more macrophages attempt to phagocytes the same particle simultaneously.
The fused cell has little phagocytic activity and no known function.

95
Q

Langhans giant cells

A

Horseshoe arrangement of peripheral nuclei at one pole of the cell. Seen in TB.

96
Q

Foreign body giant cells

A

Large cells with nuclei randomly scattered around the cytoplasm.

97
Q

What is the role of inflammation in atheroma development?

A

Macrophages adhere to endothelium.

Migrate into the intima.

With T-cells express adhesion molecules for other cells.

Macrophages are involved in processing lipids that accumulate in the atheroma.

98
Q

Exudate vs transudate

A

Exudate: high protein content as a result of increased vascular permeability.

Transudate: low protein content as the vessels have normal permeability characteristics.

99
Q

Granuloma vs granulation tissue

A

Granuloma: aggregate of epithelioid histiocytes (seen in some chronic inflammatory disorders)

Granulation tissue: important component of healing and comprises of small blood vessels in the CT matrix with myofibroblasts.

100
Q

Monocytes vs macrophages vs histiocytes

A

Monocyte: newly formed cells of the mononuclear phagocyte system.

After a few hours they enter the tissue and undergo differentiation into macrophages.

Some macrophages have specific names (Kupffer cells) others are referred to as histiocytes.

101
Q

Fibrin vs fibrous

A

Fibrin: deposited in blood vessels and tissues or on surfaces as a results of the action of thrombin on fibrinogen.

Fibrous: describes texture of a non-mineralised tissue mainly composed of collagen (scar tissue).

Phase 2a - ICS (43 decks)

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