Acute and Chronic inflammation Flashcards

1
Q

What is acute inflammation?

A

Response of living tissue to infection/damage
Develops quickly
Initiation for innate immunity

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2
Q

What are the three processes involved in acute inflammation?

A

Vascular dilation
Increased vascular permeability
Neutrophil activation and migration

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3
Q

What are the four main causes of acute inflammation?

A

Microbial infection
Resulting from microbial recognition Physical agents, Physical trauma
Ultraviolet or other ionizing radiation, Heat (burns), Cold
Irritant and corrosive chemicals
Acids, alkali, oxidizing agents
Microbial virulence factors
Tissue necrosis
Lack of oxygen or nutrients
Inadequate blood flow (infarction)

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4
Q

What are the consequences of acute inflammation?

A

Redness (rubor)
Dilation of small blood vessels
Heat (calor)
Increased blood flow (hyperaemia)
Swelling (tumor)
Accumulation of fluid in extra vascular space (oedema)
Pain (dolor)
Stretching/distortion of tissues due to oedema.
Chemical mediators induce pain
Loss of function

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5
Q

what is an example of acute inflamation?

A

gingivitis

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6
Q

What is meant by amplification?

A

recruitment and activation of innate immune cells via chemokine/cytokine activity and vascular dilation

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7
Q

what is the vascular response to acute inflammation?

A

Small blood vessels adjacent to site of damage become dilated
Endothelial cells swell and retract
Exudation – the vessels become ‘leaky’ and allow passage of water, salts and some proteins
Endothelial cells activated to promote immune cells passage to damaged tissues

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8
Q

What is oedema?

A

defined as excess of watery fluid collecting in the cavities or tissues of the body.
increased blood and lymph flow.

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9
Q

in tissues what allows for the diffusuion of mediators?

A

salt and fluids

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10
Q

Give 3 examples of mediators involved in inflammation

A

chemical- Histamine
Bradykinin
Leukotrienes
Serotonin
Prostaglandins
Protein- cytokines, chemokines

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11
Q

Describe and explain histamines role here?

A

Product of breakdown of amino acid histidine
Stored in granules of immune cells such as mast cells
Degranulation releases histamine
Role as a neurotransmitter – itching
Causes vascular dilation
Many immune cells express histamine receptors

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12
Q

Describe prostaglandins and explain their role.

A

Produced by macrophages and neutrophils (with leukotrienes)
Product of fatty acid metabolism
Most abundant is Prostaglandin E2 (PGE2)
Causes vascular dilation
other roles- Regulate cytokine production
Regulate cell recruitment
Act on nerve fibres – pain
Involved in tissue remodeling

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13
Q

What are the 4 enzymatic cascades?

A

Complement (covered in innate immunity II)
The kinin system
Coagulation
Fibrinolytic system

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14
Q

describe a complement cascade?

A

3 pathways
Classical pathway – antibody attached to microbe
(2) Alternative pathway – microbial cell wall
(3) Mannose binding lectin pathway (MBL) – carbohydrates on pathogen surface

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15
Q

what is generated by Hageman factor?

A

Kallikrein

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16
Q

In the kinin system what does Kallikrein convert?

A

Kallikrein converts kininogens to kinins (e.g., bradykinin)

17
Q

what do all three pathways of the coagulation system result in?

A

Production of thrombin which in turn produces fibrin (clot formation)
intrinsic and extrinsic

18
Q

What does the fibrinolytic system result in?

A

activation of plasmin

19
Q

What is involved in the fibrinolytic system?

A

invokved in blood clots

20
Q

The balance between which two systems is essential for homeostasis?

A

Coagulation and fibrinolytic

21
Q

Acute inflammation leads to what that chronic doesn’t?

A

resolution

22
Q

Absess formation (suppuration) is an outcome of what?

A

acute inflammation

23
Q

3 types of gingival absesses?

A

Gingival abscess
Periodontal abscess
Periapical abscess

24
Q

What is the difference between acute and chronic inflammation?

A

accute- rapid (days)
chronic inflammation persistent can occur over months, years

25
Q

What are three types of chronic inflammation?

A

Non-specific chronic inflammation
specific (primary inflammation)
Chronic Granulomatous inflammation

26
Q

Describe non-specific chronic inflammation

A

Failure to resolve acute inflammation
Persistent bouts of acute inflammation
Excessive suppuration

27
Q

describe primary/ specific chronic inflammation

A

persistent exposure to agent
Can be non-granulomatous or granulomatous (type 3)
Characterized by excessively activated macrophages
Induced by: Non-immunological agents
Foreign body reactions
Inert noxious material (e.g. silica and asbestos)

28
Q

What can induce specific chronic inflammation?

A

Induced by: Immunological agents
Infective organisms that grow in cells
Hypersensitivity reactions (Lecture 10)
Autoimmune reactions
Infection by fungi, protozoa or parasites

29
Q

How does Rheumatoid arthritis develop?

A

PAD enzymes (Peptidyl arginine deiminase) – naturally produced by host cells such as neutrophils but also produced by Pgingivalis
This enzyme citrullinates proteins – arginine conversion to citrulline which is not a normal naturally occurring amino acid
The host see this amino acid as a a foreign body – attack it (loss of tolerance)

30
Q

describe chronic granulomatous inflammation

A

Differs from normal chronic inflammation as the predominant cell types are modified activated macrophages;
Known as epithelioid macrophages
Giant cells (multi-nucleated: formed from fused epithelioid macrophages)
Also B and T cells present in tissue.

31
Q

describe chronic granulomatous inflammation

A

Differs from normal chronic inflammation as the predominant cell types are modified activated macrophages;
Known as epithelioid macrophages
Giant cells (multi-nucleated: formed from fused epithelioid macrophages)
Also B and T cells present in tissue.

32
Q

What causes chronic granulomatous inflammation?

A

Causes;
Immunological (delayed hypersensitivity type reaction or invading pathogens)
Non-immunological (Foreign body in tissue e.g. asbestos particles)

33
Q

What is orofacial Granulomatosis (OFG) an example of?

A

chronic granulomatous inflammation

34
Q

What macrophages are essential in repair?

A

M1 V M2