Inflammatory Response Acute & Chronic Flashcards

1
Q

Inflammation

A

Local response of tissue to injury/trauma/insult

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2
Q

Stimulus of inflammation

A

Microbial
Immunological
Physical
Chemical agents

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3
Q

Acute inflammation

A

Quick response.
Short duration.
Non specific.
Mainly neutrophils and macrophages.
Cardinal signs likely to be present

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4
Q

Causes of acute inflammation

A

Tissue necrosis
Foreign bodies
Immune
Trauma
Infections

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5
Q

Cardinal signs of inflammation

A

Rubor - redness
Calor - heat
Tumor - swelling
Dolor - pain
Loss of function

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6
Q

Patterns of inflammation

A

Serous - blister/fluid
Fibrinous - big leakage/body cavities
Suppurative - pus/necrotic tissue
Ulcerative - break in surface of epithelial tissue.

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7
Q

Chemical mediators what do they do?

A

Chemical messengers that act to cause inflammatory response.
Need a trigger- usually a blood vessel.

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8
Q

Endogenous chemical mediators

A

Come form body host response, send out chemical mediators to call upon more cells.
- plasma
- leukocytes
- endothelial cells
- fibroblasts

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9
Q

Exogenous chemical mediators

A

Come from microbial insult.

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10
Q

What produces cytokines

A

Macrophages
B lymphocytes
Epithelial cells
Gingival fibroblasts
Osteoblasts

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11
Q

Cytokines

A

Chemical proteins produced by many PMNs.
Mediate and regulate immune and inflammatory reactions.
Make a certain set of events happen to call upon more cells.
Can be pro or anti inflammatory.

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12
Q

Prostaglandins

A

Produced by mast cells, macrophages, endothelial cells.
Fat based cytokine.
Vascular and systemic reactions.
Vasodilation, fever and pain
Pro inflammatory

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13
Q

Leukotrienes

A

Produced by leukocytes and mast cells through lipoxygenase.
After as chemotatic for neutrophils.
Releases lysosomal enzymes.
Usually accompanied by histamine.
Vasoconstriction- anti inflammatory

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14
Q

Chemokines

A

Small proteins.
Act as chemo attractants for specific leukocytes.
Enhance chemotaxis - attracting leukocytes.

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15
Q

Chemotaxsis

A

Leukocyte recruitment to site

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16
Q

Examples of chemical mediators

A

Cytokines
Prostaglandins
Leukotrienes
Chemokines

17
Q

Vasoactive amine

A

Histamine - comes from mast cells.
Acts in blood cells to cause dilation of arterioles and increase permeability.

18
Q

2 types of phagocytic cells

A

PMNs - early inflammatory response
Monocytes and macrophages

19
Q

Opsonisation

A

Coating of antigen - marking it to become engulfed

20
Q

First events of acute inflammation

A

Vascular event- Vasodilation.
Redness occurs when blood vessels get bigger to try and recruit more white blood cells to injury.

21
Q

What causes an increase in vascular permeability

A

Endothelial cell contraction.
Endothelial injury - trauma or leukocytes trying to break through.
Increase in transcytosis fluid.

22
Q

Cellular events of acute inflammation

A

Chemotaxsis
Phagocytosis

23
Q

What cells release proteolytic enzymes at inflamed tissue site

A

Neutrophils and macrophages

24
Q

What are proteolytic enzymes

A

Protease
Collagenase
Elastase
Lipase
The neutophils and macrophage release proteolytic enzymes that break down the collegen and leads to tissue destruction.

25
Chronic inflammation
Occurs after delay. Longer duration. Specific. Lymphocytes, plasma cells, macrophages, fibroblasts. Less obvious - can sit there for long periods of time and go unnoticed.
26
Chronic inflammation conditions examples
Periodontitis Rheumatoid arthritis Cancer Autoimmune disease Cardiovascular disease Chronic fatigue syndrome Osteoporosis
27
Chronic inflammation considerations
Process is longer - likely to have more tissue damage. More fibrotic appearance Granulomas may be present Patient may have no symptoms or be unaware of.
28
Granuloma
Extension of tissue with own blood supply which allows it to keep alive and nutrient supply. Usually seen in chronic inflammation.
29
Angiogenesis
Formation of new extended blood vessels.