4- Inflammation Flashcards

1
Q

Compare acute and chronic inflammation

A
Acute Inflammation
Neutrophils
Histamine
Prominent necrosis
Immediate onset
Lasts a few days
Outcomes include:
Complete resolution
Progression to chronic inflammation
Chronic Inflammation
Monocytes/Macrophages
Cytokines
Prominent scar tissue
Delayed onset
Lasts weeks/months/years
Outcomes include
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2
Q

Define inflammation

A

Reaction of living vascularised tissue to sub-lethal cellular injury.

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3
Q

What are the local clinical features of acute inflammation

A
RUBOR – redness
	TUMOUR – swelling (oedema)
	CALOR – heat
	DOLOR – pain
Loss of function
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4
Q

Gives examples of targeting inflammatory regulators

A
Histamine
–Antihistamine
•Prostaglandins
–Aspirin
•IL-1 and TNF
–Anti-TNF antibodies
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5
Q

What are exudates?

A
“What comes out of leaky vessels due to inflammation – fluids, cells, proteins (fibrin, antibodies, small molecules involved in cell signaling)
Purulent
Serous
Haemorrhagic
Fibrinous
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6
Q

What is the cause of chronic inflammation?

A

Usually due to persistence of injury causing agents
(Persistent damage
•Persistent infection (HCV, TB)
•Prolonged exposure to toxic agent (uric acid)
•Autoimmunity (RA, SLE)
•Foreign body (splinter, silica))

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7
Q

What are the components ofinflammation?

A

Cells, vessels, ecm, soluable factors

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8
Q

What is histamine?

A
A vasoactive amine
•Produced by mast cells
•Preformed and released cell degranulates
–Degranulation triggered by cell surface IgE antibody interaction with antigen
•Leads to..
–Vasodilation
–Increased vascular permeability
•Dysregulation
–allergy (Type 1 hypersensitivity)
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9
Q

What are some inflammatory mediators?

A

Histamines, prostaglandins, chemokines, cytokines, complements

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10
Q

What is transudate?

A
TRANSUDATE - caused by disturbances in hydrostatic and colloid osmotic
pressure, NOT CAUSED BY INFLAMMATION
Low protein
Cell poor
Low Specific Gravity
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11
Q

How does wbc move from vessel to tissue?

A

Margination, Rolling, Adhesion, Transmigration, Chemotaxis, Phagocytosis

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12
Q

Define chronic inflammation

A

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

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13
Q

What is granulomatous inflammation ?

A

Particular form of chronic inflammation showing granuloma formation
–Cluster of macrophages
–Involves specific immune reaction T cells

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14
Q

What causes granulomatous inflammation?

A

FORM OF CHRONIC INFLAMMATION - shows granuloma formation
• Clusters of macrophages
• Involves specific immune reaction T cells

Infection – TB, fungi
–Foreign material
–Reaction to tumours
–Immune diseases (sarcoid, Crohn’s)

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15
Q

What are the long term sequelae of inflammation?

A
Good: Removal of causative agent
 Cessation of the inflammatory reaction
 Healing of tissue damage to preserve integrity and function (resolution)
Bad:
LOCAL
•Can cause excess local tissue damage and scarring
•Secondary effects on nearby tissue
–E.g. Bronchoconstriction in asthma

SYSTEMIC
•Can evolve into systemic inflammatory reaction and secondary multi-organ failure
–E.g. Septic shock
–Amyloid

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16
Q

What are “the sequential changes in wound healing?

A

Parenchymal cell regeneration and RESOLUTION

•REPAIR by connective tissue and SCAR TISSUE FORMATION

17
Q

What are the components of fibrous scar tissue?

A

Fibroblasts – produce collagen
•Collagen – strong “scar” type collagen
•Remodelling – reorientation of collagen fibres for maximal tensile strength

18
Q

What can hinder repair?

A

General
–POOR NUTRITION - Require protein for collagen production, and energy for cell function.
–VITAMIN DEFICIENCY
Vitamin C – needed by fibroblasts to make collagen
Vitamin A - required for epithelial regeneration
–MINERAL DEFICIENCY eg. Zinc
–SUPPRESSED INFLAMMATION by steroids, old age, diabetes
•Local
–POOR BLOOD SUPPLY eg. ischaemic leg ulcers
–PERSISTENT FOREIGN BODY eg. splinter
–MOVEMENT e.g across a fracture site -> need for a cast.

19
Q

What are complications of repair?

A

Keloid Formation
• Excess collagen deposition
• You can get 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
• This affects organ function

20
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). ”

21
Q

What are the cells of chronic inflammation?

A

Macrophages and lymphocytes

22
Q

What is the function of exudate

A

Exudate consist of: fluid, cells, proteins including fibrin, 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

23
Q

What are the types of exudate

A
Serous = fluid filled
EXAMPLE: Blister
Lower protein content of all the exudates
• Fibrinous = High fibrin content
More due to traumatic injury
EXAMPLE: Viral Pericarditis
• Purulent = pus filled
Combination of fibrin, inflammatory cells, debris and fluid EXAMPLE: peritonitis following bowel perforation
24
Q

What is suppuration

A

The formation of pus, neutrophils, bacteria and cellular debris Suppuration is an example of exudate formation that commonly occurs as part of the body’s immune response.