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Inflammation Flashcards

1
Q

List the 3 phases of acute inflammation

A
  1. Vascular phase
  2. Exudative cellular phase
  3. Outcome
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2
Q

What is included in the vascular phase of acute inflammation

A
  • Change in vessel calibre
  • Increased vascular permeability
  • Formation of fluid exudates
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3
Q

What occurs in the exudative cellular phase of acute inflammtion

A
  • Adhesion of neutrophils
  • Neutrophil migration
  • Diapedesis
  • Neutrophil chemotaxis
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4
Q

List the causes of acute inflammation

A
  • Microbial infection
  • Hypersensitivity reactions
  • Chemical agents
  • Physical agents e.g. trauma
  • Tissue necrosis
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5
Q

List the macroscopic signs and symptoms of acute inflammation

A
  • Redness (rubor)
  • Heat (calor)
  • Swelling (tumour)
  • Pain (dolor)
  • Loss of function
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6
Q

Outline the triple response to injury in vessels

A
  1. Flush - dull red line due to capillary dilatation
  2. Flare - red irregular zone due to arteriolar dilatation
  3. Weal - zone of oedema due to fluid exudate in the intravascular space
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7
Q

Why does fluid leave the vessels in acute inflammation

A
  • Capillary hydrostatic pressure is increased
  • More fluid leaves vessels than returns
  • An exudate is formed
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8
Q

List the stages of cellular exudate formation in acute inflammation

A
  1. Margination of neutrophils
  2. Neutrophil adhesion to leucocytes and endothelial surfaces
  3. Neutrophil migration
  4. Diapedesis (escape of red cells from capillaries)
  5. Neutrophil chemotaxis
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9
Q

What increases leucocyte surface adhesion molecule expression

A
  • Complement C5a
  • Leucotriene B4
  • TNF
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10
Q

What increases endothelial expression of adhesion molecules

A
  • IL-1
  • Endotoxins
  • TNF
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11
Q

What stimulates neutrophil chemotaxis

A
  • Leukotriene B4

- IL-8

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12
Q

What is the action of histamine in inflammation

A
  • Vasodilation

- Transiently increases vascular permeability

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13
Q

What is the action of prostaglandins in inflammation

A
  • Potentiate increased vascular permeability
  • Platelet aggregation
  • Platelet disaggregation
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14
Q

What is the role of C5a and C3a

A
  • Chemotactic for neutrophils
  • Increase vascular permeability
  • Trigger release of histamine from mast cells
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15
Q

Describe the kinin system

A
  • Activated by coag factor 7
  • Converts prekallikrein to kallikrein
  • Kallikrein cleaves kininogen to release bradykinin
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16
Q

What is the role of bradykinin

A

Controls vascular permeability and is a chemical mediator of pain

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17
Q

How are macrophages stimulated

A

Local infection (endotoxins) or injury

18
Q

What do macrophages produce and why

A
  • IL-1
  • TNF

Both stimulate endothelial cells to produce adhesion molecules which bind and activate neutrophils

19
Q

What is the characteristic cell of acute inflammatory exudates

A

Neutrophil polymorphs

20
Q

What cells dominate in acute inflammation

A

Neutrophils

21
Q

What cells dominate in chronic inflammation

A
  • Lymphocyte
  • Macrophages
  • Plasma cells
22
Q

Describe suppurative inflammation

A
  • Production of pus (dying and degenerate neutrophils)
  • May become walled off by fibrin to become and abscess
  • May form empyema
23
Q

Give an example of membranous inflammation

A

Grey membrane seen in pharyngitis due to diphtheria

24
Q

Give an example of pseudomembranous inflammation

A

C.diff colitis (superficial mucosal inflammation and ulceration with sloughing of mucosa, fibrin, mucus, inflammatory cells)

25
Benefits of exudate production
- Dilution of toxins - Arrival of antibodies - Transport of drugs - Fibrin formation - Delivery of oxygen/nutrients - Stimulation of the immune response
26
How is resolution of acute inflammation achieved
1. Phagocytosis of bacteria 2. Fibrinolysis 3. Phagocytosis of debris by macrophages 4. Resolution of vascular dilatation
27
Describe the process of organisation with respect to inflammation
Replacement of tissue by granulation tissue
28
What circumstances favour granulation
- Excess fibrin formation - Substantial necrotic tissue - Exudate and debris cannot be removed or discharged
29
How does acute inflammation progress to chronic inflammation
- If the causative agent is not removed | - Tissues become organised with the cellular exudate changing to lymphocytes, plasma cells, macrophages, and giant cells
30
What are the causes of chronic inflammation
- Primary chronic inflammation - Progress from acute inflammation - Recurrent episodes of acute inflammation - Transplant rejection
31
List the causes of primary chronic inflammation
- Resistance of infective agents to phagocytosis and killing e.g. TB - Foreign body reactions - Autoimmune diseases e.g. RA - Specific diseases of unknown aetiology e.g. UC - Primary granulomatous disease e.g. CD
32
What type of acute inflammation is most likely to progress to chronic inflammation
Suppurative - inadequate drainage of pus which is deep seated
33
Outline the pathology of non-specific chronic inflammation
1. Tissue macrophages recruited by bloodstream monocytes 2. T-helper cells activate B lymphocytes to produce plasma cells via IL-4 3. Plasma cells produce antibodies against the persistent antigen 4. Plasma cells divide under the influence of IL-1 from macrophages 5. A degree of scarring occurs 6. Fibrosis is stimulated by TGF-beta
34
What are some of the possible macroscopic appearances of chronic inflammation
- Chronic ulceration - Chronic abscess - Caseating granulomatous inflammation - Thickening of hollow viscus - Fibrosis
35
What type of collagen is laid down in scarring
Type 1
36
What is a granuloma
Aggregate of epitheloid histiocytes
37
List the features of epitheloid histiocytes
- Arranged in clusters - Little phagocytic activity - Produce ACE - Caseous necrosis may occur - Can be converted to Giant cells
38
Where is TNF primarily secreted from
Macrophages
39
What type of giant cell is characteristically seen in TB
Langhans cells - horseshoe arrangement of peripheral nuclei at one pole of the cell
40
What infections cause granulomatous disease
- Mycobacteria e.g. TB - Atypical fungi - Parasites
41
What drugs cause granulomatous inflammation
- Allopurinol - Phenylbutazone - Sulphonamides

Pathology (7 decks)

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