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Pathology > Inflammation > Flashcards

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
Q

Benefits of exudate production

A
  • Dilution of toxins
  • Arrival of antibodies
  • Transport of drugs
  • Fibrin formation
  • Delivery of oxygen/nutrients
  • Stimulation of the immune response
26
Q

How is resolution of acute inflammation achieved

A
  1. Phagocytosis of bacteria
  2. Fibrinolysis
  3. Phagocytosis of debris by macrophages
  4. Resolution of vascular dilatation
27
Q

Describe the process of organisation with respect to inflammation

A

Replacement of tissue by granulation tissue

28
Q

What circumstances favour granulation

A
  • Excess fibrin formation
  • Substantial necrotic tissue
  • Exudate and debris cannot be removed or discharged
29
Q

How does acute inflammation progress to chronic inflammation

A
  • If the causative agent is not removed

- Tissues become organised with the cellular exudate changing to lymphocytes, plasma cells, macrophages, and giant cells

30
Q

What are the causes of chronic inflammation

A
  • Primary chronic inflammation
  • Progress from acute inflammation
  • Recurrent episodes of acute inflammation
  • Transplant rejection
31
Q

List the causes of primary chronic inflammation

A
  • 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
Q

What type of acute inflammation is most likely to progress to chronic inflammation

A

Suppurative - inadequate drainage of pus which is deep seated

33
Q

Outline the pathology of non-specific chronic inflammation

A
  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
Q

What are some of the possible macroscopic appearances of chronic inflammation

A
  • Chronic ulceration
  • Chronic abscess
  • Caseating granulomatous inflammation
  • Thickening of hollow viscus
  • Fibrosis
35
Q

What type of collagen is laid down in scarring

A

Type 1

36
Q

What is a granuloma

A

Aggregate of epitheloid histiocytes

37
Q

List the features of epitheloid histiocytes

A
  • Arranged in clusters
  • Little phagocytic activity
  • Produce ACE
  • Caseous necrosis may occur
  • Can be converted to Giant cells
38
Q

Where is TNF primarily secreted from

A

Macrophages

39
Q

What type of giant cell is characteristically seen in TB

A

Langhans cells - horseshoe arrangement of peripheral nuclei at one pole of the cell

40
Q

What infections cause granulomatous disease

A
  • Mycobacteria e.g. TB
  • Atypical fungi
  • Parasites
41
Q

What drugs cause granulomatous inflammation

A
  • Allopurinol
  • Phenylbutazone
  • Sulphonamides

Pathology (7 decks)

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