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2. General Pathological Mechanisms > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

Briefly outline the process of the acute inflammatory response, including the 2 categories.

Include the mediators/proteins which are involved in each stage.

A

VASCULAR CHANGES:

  1. Vasoconstriction
  2. Vasodilation (histamine, NO)
  3. Increased vascular permeability (histamine, bradykinin, substance P)
  4. Vascular congestion
  5. Endothelial activation

CELLULAR CHANGES:

  1. Margination
  2. Rolling (selectins, L-selectin)
  3. Adhesion (IL1, TNF, chemokines)
  4. Migration/diapedesis/extravasation (chemokines)
  5. Chemotaxis (bacterial products, IL8, complement factors, leukotriene B)
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2
Q

What are the 5 cardinal signs of inflammation?

A 
Redness
Heat
Swelling
Pain
Loss of function
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3
Q

Which processes cause the 5 cardinal signs of inflammation?

A

Redness - vasodilation

Heat - increased blood flow; fever

Swelling - accumulation of fluid in ECM

Pain - tissue stretching; activation of nociceptors

Loss of function - pain; severe swelling

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4
Q

What are the 4 main causes of inflammation?

A

Infection
Tissue necrosis
Foreign material
Immune reactions

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5
Q

List the 4 types of receptor involved in leukocyte activation and recognition of microbes.

Include which cell they are found on.

A

Toll-like receptors (leukocytes)

G-protein coupled receptors (PMNs, macrophages)

Opsonin receptors (leukocytes)

Cytokine receptors (leukocytes)

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6
Q

What is stimulated by activation of toll-like receptors?

A

Microbe killing

Cytokine production

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7
Q

What is stimulated by activation of G-protein coupled receptors on PMNs and macrophages?

A

Migration of cells

Production of respiratory burst

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8
Q

What is stimulated by activation of opsonin receptors?

A

Antibody formation
Complement activation
Phagocytosis

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9
Q

Briefly outline the process of phagocytosis.

A
  1. Opsonisation
  2. Engulfment using pseudopodia
  3. Formation of phagosomes
  4. Phagosomes fuse with lysosomes (forms phagolysosomes)
  5. Microbes are destroyed; removed from cell via pinocytosis
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10
Q

Give 4 examples of cellular derived inflammatory mediators.

A
  1. Vasoactive amines (e.g. histamine)
  2. Arachidonic acid metabolites (e.g. leukotrienes)
  3. Nitric oxide
  4. Cytokines (e.g. TNF, IL1/6)
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11
Q

Give 3 examples of plasma protein derived inflammatory mediators.

A
  1. Complement factors
  2. Coagulation system
  3. Kinin system (e.g. bradykinin)
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12
Q

List the 7 types of exudate.

A
  1. Serous
  2. Fibrinous
  3. Membranous
  4. Pseudomembranous (ulcerative)
  5. Haemorrhagic
  6. Suppurative
  7. Necrotising (gangrenous)
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13
Q

List 4 factors which might influence the development of chronic inflammation.

A

Site affected
Presence of infection/type of organism
Presence of indigestible material
Background disease

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14
Q

List the 5 things present in chronic inflammation.

A 
Lymphocytes
Plasma cells
Macrophages
Fibrosis
Granulomas
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15
Q

What is a granuloma?

A

Clusters of epithelioid macrophages, giant cells (fused macrophages) and lymphocytes

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16
Q

What are the 3 causes of chronic inflammation?

Give examples of each.

A
  1. Progression from acute inflammation
    (e. g. undrained abscess; foreign materials)
  2. Repeated bouts of acute inflammation
    (e. g. chronic cholecystitis)
  3. De novo
    (e. g. infections with delayed type hypersensitivity - TB; insoluble foreign materials - asbestos; autoimmune reactions - RA; unknown causes - Crohn’s disease)
17
Q

List the 5 cell types involved in chronic inflammation.

What are the functions of each?

A

Macrophages
Function: tissue destruction; fibrosis

Lymphocytes
Function: cytokine synthesis (to attract/activate macrophages and fibroblasts); inflammatory mediators

Plasma cells
Function: produce antibodies

Neutrophils

Eosinophils

18
Q

What are the 2 types of macrophage associated with chronic inflammation?

A

M1 - inflammatory macrophage (causes tissue destruction via TNF alpha, IL12 etc.)

M2 - fibrosis macrophage (causes wound repair/fibrosis via TGF beta, IL10 etc.)

19
Q

List the 6 macrophage products which cause tissue destruction in chronic inflammation.

A 
Toxic oxygen metabolites
Proteases
Neutrophil chemotactic factors
Coagulation factors
Arachidonic acid metabolites
NO
20
Q

List the 4 macrophage products which cause fibrosis in chronic inflammation.

A 
Growth factors (PDGF, FGF)
Fibrogenic cytokines (TGF beta)
Angiogenesis factors
Remodelling collagenases
21
Q

How do you differentiate between acute and chronic inflammation?

A

ACUTE:
Exudative
Neutrophils most common
Terminates in resolution

CHRONIC:
Productive (i.e. cellular and fibrous tissue formed)
Macrophages, lymphocytes, plasma cells most common
Results in tissue destruction and necrosis

22
Q

What is granulomatous inflammation?

A

A type of chronic inflammation caused by the presence of granulomas, i.e. clusters of epithelioid macrophages and giant cells

23
Q

Give 2 examples of granulomatous inflammation.

A

TB

Crohn’s disease

24
Q

List the 3 main cell types involved in granulomatous inflammation.

What are their functions?

A

Epithelioid macrophages
Function: secretory

Giant cells (fused macrophages)
Function: dealing with material that is difficult to digest

Lymphocytes
Function: produce IFN gamma to activate macrophages

25
Q

What are the 2 types of granulomatous inflammation? Give an example.

A

Necrotising - e.g. TB

Non-necrotising

26
Q

List 5 causes of granulomatous inflammation.

A 
Infection (e.g. TB, leprosy)
Foreign materials (e.g. talc)
Sarcoidosis
Crohn's disease
Response to tumours (e.g. Hodgkin lymphoma)
27
Q

Give 4 examples of diseases which involve chronic inflammation.

A

Atherosclerosis
Cancer
Chronic granulomatous disease
Neurodegenerative diseases (e.g. Alzheimer’s)

28
Q

Summarise how you would differentiate between acute, subacute, chronic and granulomatous inflammation.

A

Acute - loads of neutrophils

Subacute - loads of eosinophils

Chronic - presence of macrophages, lymphocytes, plasma cells

Granulomatous - presence of granulomas

2. General Pathological Mechanisms (4 decks)

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