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Cell Pathology > 4 - Inflammation > Flashcards

4 - Inflammation Flashcards

1
Q

What is inflammation?

A

Reaction of living vascularised tissue to sub-lethal cellular injury

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2
Q

What is the function of inflammation?

A

Remove cause of injury and initiate repair.

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3
Q

Types of inflammation

A

acute (hours/days)
chronic (weeks/months)
Different cell types and mechanisms

BUT NOTE – inflammation can also have harmful effects – Can cause tissue destruction

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4
Q

Causes of inflammation

A

Infection… BUT inflammation is NOT JUST caused by infectious organisms…

Foreign body

Tissue destruction – mechanical trauma, chemical injury, radiation injury, endogenous (autoimmune reaction, crystal deposition)

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5
Q

What are the inflammatory cells?

A

Neutrophils
Macrophages
Lymphocytes

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6
Q

What are the vascular changes involved with inflammation?

A

Immediate supply of cells and soluble factors

Extracellular matrix and resolution or repair

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7
Q

What are neutrophils and what is their role?

A

Produced in bone marrow
Circulate in blood
Contain cytoplasmic granules

ROLE
Phagocytosis (gobble up) of organisms, debris.
Degranulation (release contents of granules)
Enzymes
Free radicals
Soluble mediators

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8
Q

What are monocytes/macrophages and what do they do?

A

Monocytes in blood
Once in tissue give rise to macrophages

ROLE
Phagocytosis
Control many other inflammatory cells
Release cytokines

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9
Q

What do Eosinophils do?

A

Seen in allergic and parasitic causes of inflammation

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10
Q

What do mast cells do?

A

Also seen in allergic diseases

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11
Q

What are the vascular changes involved in inflammation? Explained…

A

Vascular calibre and flow increased REDNESS & HEAT

Dilatation and increased blood flow to injured area enables rapid delivery of inflammatory cells and mediators

Adhesion molecules expressed on endothelium

Inflammatory cells stick to vessel wall

Vascular permeability -> SWELLING

Leaky capillaries allow cells and mediators to enter tissue – EXUDATE

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12
Q

What is exudate?

A

What comes out of leaky vessels – fluids, cells, proteins (fibrin, antibodies, small molecules involved in cell signaling)

  • Purulent
  • Serous
  • Haemorrhagic
  • Fibrinous
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13
Q

How do white cells change during inflammation?

A

Leave blood and enter tissue
Migrate through tissue to injured site (chemotaxis)
Become activated
Ingest organisms/cell debris (phagocytosis)
Secrete soluble mediators that aid inflammatory process

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14
Q

How do cells get to the sight of injury?

A

Chemotaxis…
Move towards injured area
Exogenous and endogenous compounds attract cells.

Activation…
Phagocytosis

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15
Q

What is inside the phagosome?

A 
Oxygen Independent cell killing
Bactericidal permeability increasing protein – “does what is says on the tin”
Lysozyme
Lactoferrin
Major basic protein
Defensins
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16
Q

What soluble factors are in exudate?

A

-Factors produced locally by cells
-Vasoactive amines
Released from mast cells, basophils and platelets
Histamine
Causes increased vascular permeability
e.g. Acute asthmatic reactions
Other Factors
Platelet Activating Factor
Clotting factors
Nitric oxide
CYTOKINES – proteins produced by many cell types (lymphocytes, macrophages, endothelial cells, etc) that modulate function of other cells – IL1 and Tumour necrosis factor (TNF).
-Circulating plasma proteins
-Antibodies

17
Q

Clinical features of acute inflammation.

LOCAL

A

RUBOR – redness
TUMOUR – swelling (oedema)
CALOR – heat
DOLOR – pain

Loss of function

18
Q

Clinical features of acute inflammation.

SYSTEMIC

A

Fever

shock

19
Q

Summary of acute inflammation

A

Acute co-ordinated response: vessels, cells and soluble mediators

Neutrophil is main cell

Exudate formed

Variety of outcomes

20
Q

Outcome of acute inflammation

RESOLUTION

A

Tissue returns to normal
Only occurs if :-
Tissue contains cells that can regenerate to replace lost cells
Little structural damage done – cells need a framework to build on.
Classic example – Pneumococcal pneumonia

21
Q

Outcome of acute inflammation

REPAIR

A

Tissue loss too great, and cells unable to regenerate
Replace normal tissue with fibrous scar tissue
Fibroblasts – produce collagen
Collagen – strong “scar” type collagen
Remodelling – reorientation of collagen fibres for maximal tensile strength
Abscess

22
Q

What hinders repair?

GENERAL

A

Poor nutrition…
Protein needed for collagen production and energy needed for cell function.
Vitamin deficiency
Vitamin C – needed by fibroblasts to make collagen
Vitamin A- required for epithelial regeneration
Mineral deficiency
e.g. Zinc

Suppressed inflammation…
e.g. By steroids
Old age
Diabetes

23
Q

What hinders repair?

LOCAL

A

Poor blood supply
Persistent foreign body
Movement e.g across a fracture site, hence the need for a cast.

24
Q

What hinders repair?

COMPLICATIONS

A

Keloid (area of irregular fibrous tissue formed at the site of a scar or injury) formation

Excess collagen deposition

Contractures (shortening and hardening of muscles, tendons, or other tissue, often leading to deformity and rigidity of joints)

Fibrous scar tissue contracts as it matures. If scarring occurs across a joint it can cause poor joint mobility.
Impaired function
e.g. fibrous scars in the myocardium after a heart attack

25
Q

Chronic inflammation.

CAUSES?

A 
Persistent damage
Persistent infection
Prolonged exposure to toxic agent
Autoimmunity
Foreign body e.g. splinter
26
Q

Cells of chronic inflammation?

note – some differences to acute inflammation

A

Macrophages

Lymphocytes

Neutrophil exudate

27
Q

What is a granuloma?

A

A mass of granulation tissue, typically produced in response to infection, inflammation, or the presence of a foreign substance

28
Q

What is GRANULOMATOUS?

A

a special type of chronic inflammation

Macrophage is key cell - Clusters of macrophages involved in a specific immune reaction to T cells

29
Q

What causes granulomatous?

A

Infection – TB
Foreign material
Reaction to tumours
Immune diseases (sarcoid)

30
Q

What is Amyloidosis?

A

In response to chronic inflammation anywhere in body, liver produces and releases increased amounts of serum amyloid A protein into the blood.

In some cases this is deposited in tissue as dense protein (amyloid).
A harmful effects of chronic inflammation

31
Q

Summary of chronic inflammation

A

Usually follows acute, but occasionally develops straight off
Main cells are lymphocytes and macrophages
Causes include viruses, autoimmune disease, chemicals,
Special type = granulomatous
Variety of causes – TB good example.

Cell Pathology (5 decks)

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