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Cell pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A

Reactions of living vascularised tissue to sub-lethal cellular injury. Evolutionary development to protect against infection and trauma. Can be local/systemic, tightly regulated and involves many cell types/mediators.

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2
Q

What is acute inflammation?

A

Short and early response to injury

  • Hours/few days
  • Involves release of chemical mediators
  • Vascular and leukocyte response
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3
Q

What is chronic inflammation?

A

Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair occur simultaneously.

  • Weeks/months/years
  • Usually due to persistent injury causing agent
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4
Q

What are the main components of the inflammatory response and healing?

A
  • Cells
  • ECM
  • Soluble factors
  • Vessels
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5
Q

Which cells are involved in inflammation and healing?

A

Neutrophils, macrophages, lymphocytes, eosinophils, mast cells

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6
Q

Which components of the ECM are involved in inflammation and healing?

A
  • collagen
  • proteoglycans
  • fibroblasts
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7
Q

What is the role of vessels in inflammation and healing?

A
  • immediate supply of cells and soluble factors
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8
Q

Which soluble factors are involved in inflammation and healing?

A
  • Antibodies
  • Cytokines
  • Complement system
  • Coagulation system
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9
Q

What are the cardinal signs of inflammation?

A
  • RUBOR: redness (slowed blood flow and vasodilation by histamine)
  • CALOR: heat (vasodilation by histamine)
  • DOLOR: pain
  • TUMOUR: swelling (oedema due to increase in permeability by histamine)
  • FUNCTIO LAESA: loss of function (due to swelling and pain)
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10
Q

What is histamine?

A
  • Vasoactive amine
  • Produced by mast cells
  • Packaged into granules inside mast cells - when antigen binds to IgE on the surface of mast cells - causes cross-linking and degranulation
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11
Q

What are the two main effects of histamine?

A

Vasodilation

Increased Vascular Permeability

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12
Q

What does dysregulation of histamine result in?

A

Allergy (Type 1 Hypersensitivity)

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13
Q

What are some other important mediators in inflammation and what do they do?

A

Prostaglandins: PGE2 causes vasodilation, pain and fever
PGI2 causes vasodilation

Chemokines: activate neutrophil chemotaxis

Complement: variety of proteins and actions including stimulating mast cell degranulation, neutrophil chemotaxis and osponisation

Cytokines (Interleukins and TNF): actions include pro and anti inflammatory signalling, inducing fever, weight loss and malaise

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14
Q

How are histamines, prostaglandins and IL-1 and TNF targeted?

A

prostaglandins- aspirin
histamine - anti-histamine
IL-1, TNF - anti TNF antibodies

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15
Q

What is exudate?

A

A fluid with a high content of protein and cellular debris which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces, usually as a result of inflammation. FLUID LEAKS

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16
Q

What is transudate?

A

Caused by disturbances in hydrostatic and colloid osmotic pressure, not caused by inflammation.
FLUID FORCED OUT

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17
Q

What is the composition of transudate?

A
  • low protein
  • few cells
  • low specific gravity: ratio of density of substance to reference substance
18
Q

What is the function of exudate?

A

It contains cells, fluid, proteins and antibodies etc.

Fluid - dilutes pathogen and allows soluble mediators to spread

Fibrin - walls off pathogen to stop it spreading. Gives inflammatory cells substrate to hold on to/migrate through

19
Q

What are the types of exudate?

A

Serous = fluid filled
Lowest protein content of all the exudates. E.g. blister

Fibrinous = High fibrin content
More due to traumatic injury
E.g. Viral Pericarditis

Purulent = pus filled
Combination of fibrin, inflammatory cells, debris and fluid
E.g peritonitis following bowel perforation

20
Q

What are the cellular events that occur during acute inflammation and what is the main cell involved?

A

NEUTROPHILS

1) Enters into tissues
2) Migrate via chemotaxis
3) They become activated
4) They carry out phagocytosis
5) They release mediators and interact with other cells

21
Q

What is the main role of neutrophils?

A
  • Kill bacteria and recruit more cells
  • Phagocytosis
  • Degranulation

FIRST CELLS TO SITE

22
Q

How do phagocytes kill the engulfed material?

A

By free radicals, lysozyme, lactoferrin (binds iron and stops bacteria reproducing), major basic protein (produced by eosinophils - cytotoxic to helminth parasites)

23
Q

How is the inflammation reaction controlled?

A
  • Mediators and neutrophils have short half life
  • Stimulus (e.g. bacteria) removed
  • Mast cells and lymphocytes release anti-inflammatory products (lipoxins)
  • Macrophages release anti-inflammatory products
24
Q

Can tissue damage occur during acute inflammation?

A

Yes, the body responding tot the agent causing inflammation can lead to necrosis.

25
Q

What are the histological features of acute inflammation?

A
  • Lots of neutrophils
  • Mast cells
  • Eosinophils
26
Q

How does acute inflammation differ to chronic?

A
  • fewer neutrophils in chronic
  • other cell types involved in chronic e.g. macrophages, lymphocytes and plasma cells
  • time period
  • no exudate in chronic inflammation
  • necrosis isn’t as prominent in chronic
  • formation of granulation tissue while repairing in chronic
27
Q

What are the causes of chronic inflammation?

A
  • Persistent infection
  • Prolonged exposure to toxic agent
  • Autoimmunity
  • Foreign body
28
Q

What are the histological features of chronic inflammation?

A

Macrophages, lymphocytes and plasma cells will be abundant

29
Q

What is granulomatous inflammation, its features and what are its causes?

A

Form of chronic inflammation characterised by granuloma formation

  • Clusters of macrophages
  • Involves specific immune reaction T cells

Causes:

  • Infection
  • Foreign Material
  • Reaction to tumours
  • Immune Diseases (e.g. Crohn’s)
30
Q

What are the histological features of granulomatous inflammation?

A
  • macrophages in the middle and lymphocytes around the outside
  • horse-shoe shaped nuclei - fused macrophages seen during later stages
31
Q

What are the differences between acute and chronic inflammation?

A

Acute:

  • neutrophils
  • histamine
  • necrosis
  • exudate
  • immediate onset
  • lasts a few days
  • complete resolution
  • may progress to chronic

Chronic:

  • macrophages
  • cytokines
  • scar tissue
  • delayed onset
  • lasts weeks/months/years
  • scar tissue
  • disability
32
Q

What are the good long term outcomes of inflammation?

A
  • removed causative agent
  • inflammation stops
  • resolution
33
Q

What are the bad outcomes of inflammation?

A

Local:

  • excess damage and scarring
  • secondary effects on nearby tissue

Systemic:

  • systemic inflammation
  • secondary multi-organ failure e.g. septic shock
34
Q

What is resolution and when can it occur?

A

regeneration of normal functional parenchymal cells

  • tissue is capable of regeneration e.g. liver cells
  • little structural damage is done as a framework is needed e.g. BM
35
Q

What is repair?

A

connective tissue and scar tissue formation

happens when tissue loss is too great and cannot be regenerated

36
Q

Example of resolution

A

Pneuomococcal lobar pneumonia:

  • initially you get exudation
  • red hepatisation (erythrocytes move into alveolar cells and it become like liver)
  • erthrocytes break down causing grey hepatisation
  • as long as BM is intact the body can resolve the problem
37
Q

What is the process of repair?

A
  • fibroblasts make collagen
  • collagen is a string scar type
  • then remodelling of collagen fibres for maximal tensile strength
38
Q

Which factors hinder repair?

A

General:

  • Poor nutrition (protein needed for collagen production)
  • Vitamin Deficiency (C needed by fibroblasts to make collagen, A needed for epithelial regeneration)
  • Mineral Deficiency
  • Suppressed Inflammation

Local:

  • Poor blood supply
  • Persistent foreign body
  • Movement (e.g. broken bones)
39
Q

What are some of the complications of repair?

A

Keloid Formation:
Excess collagen deposition ( can result in scar tissue formation other than at the site of original injury).

Contractures:
Fibrous scar tissue contracts as part of its maturing process. If this happens across a joint, you can get reduced joint mobility.

Impaired Organ Function:
Fibrous scars forming in organs will cause loss of functional tissue which can affect organ function.

40
Q

Stages of wound healing

A

1) hemostasis (stop bleeding)
2) inflammation (vessel growth and remove pathogens)
3) proliferation (wound closed)
4) remodelling

Cell pathology (6 decks)

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