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BMS > Inflammatory Response Acute & Chronic > Flashcards

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
Mainly neutrophils
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
Q

Chronic inflammation

A

Occurs after delay
Longer duration
Less obvious - can sit there for long periods of time and go unnoticed.

26
Q

Chronic inflammation conditions examples

A

Periodontitis
Rheumatoid arthritis
Cancer
Autoimmune disease
Cardiovascular disease
Chronic fatigue syndrome
Osteoporosis

27
Q

Chronic inflammation considerations

A

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
Q

Granuloma

A

Extension of tissue with own blood supply which allows it to keep alive and nutrient supply.
Usually seen in chronic inflammation.

29
Q

Angiogenesis

A

Formation of new extended blood vessels.

BMS (37 decks)

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