Acute v Chronic inflammation Flashcards

1
Q

What is Acute inflammation

A

Response to infection/damage​

Rapid onset, yet short-term​

Involves only the innate immune system (e.g., neutrophils)​

Response is localized​

Complete restoration of tissues

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2
Q

What can cause acute inflammation

A

Microbial infection​

Physical agents​

Irritants e.g., corrosive chemicals​

Tissue necrosis

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3
Q

What causes chronic inflammation

A

Persistent exposure to
-microbial infection
-physical agents
-irrantants e.g. corrosive chemicals
-tissue necrosis

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4
Q

What makes it chronic inflammation

A

Long-term, can last up to years​

Involves both the innate and adaptive immune system​

Associated with tissue damage (e.g., fibrosis- formation of scar tissue) – no restoration​

Symptoms may be less pronounced, but more persistent​

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5
Q

What are the signs of 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 of tissues and due to release of chemical mediators​

Loss of function

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6
Q

What causes redness (rubor) and heat (calor)

A

Small blood vessels adjacent to site of damage become dilated - excessive bloodflow​

Endothelial cells swell and retract​

Exudation – the vessels become ‘leaky’ and allow passage of fluids​

Endothelial cells activated to promote immune cells passage to damaged/infected tissues

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7
Q

What isswelling

A

Defined as an excess of watery fluid collecting in tissues of the body​

Increased blood and lymph flow

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8
Q

What does inflammatory exudate (watery fluid) consist of

A

Fluids and salts – dilute the microorganisms​

Glucose and oxygen – support response and immun cells​

Soluble mediators​

Fibrin

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9
Q

What causes pain with inflammation

A

Stretching of tissues and due to release of soluble mediators​

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10
Q

What are the main types of soluble mediatorss

A

Histamine​

Prostaglandins​

Leukotrienes​

Serotonin​

Bradykinin

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11
Q

What are the main roles of prostaglandins in inflammation

A

Causes vascular dilation​

Acts of nerve fibres – itching​

Role in tissue remodelling

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12
Q

What produces prostaglandins

A

Produced by macrophages and neutrophils (with leukotrienes)​

Product of fatty acid metabolism​ (arachidonic acid - (red meat, fish)

Most abundant is Prostaglandin E2

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13
Q

What is coagulation factor 7

A

Hageman factor
-A serine protease found circulating inactive in blood

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14
Q

What are the main plasma factor systems activated by the hageman factor

A

Kinin system
Fibrinolytic system
Coagulation system
Complement system

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15
Q

What is the kinin system

A

Kinin System​

Involves plasma proteins​

Kallikrein (plasma protein) is generated by Hageman factor​

Neutrophils also engage in the kinin-kallikrein system.​

Kallikrein converts kininogens to kinins (e.g., bradykinin – widespread effect, can stimulate the changes in the vascular (inflammation))​

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16
Q

What does the coagulation system consist of

A

Intrinsic (internal trauma)​
Initiated by contact with collagen​

Extrinsic (external trauma)​

Each pathway converges into:
Common pathway – formation of stable blood clot (fibrin) through action of thrombin​

17
Q

What is the purpose of the fibrinolytic system

A

Results in activation of plasmin​

Kallikrein and Hageman factor play a role in its conversion ​

Involved in breakdown of fibrin​

Prevents excess clotting​

Activates complement (plasmin cleaves C3 complement protein)

18
Q

How is plasminogen converted to plasmin

A

Kallikrein
Urokinase (thrombolytic drug)
Hageman factor
Tissue plasminogen activator (tPA found in endothelial cells)

19
Q

What is haemostasis

A

To stop the flow of blood

20
Q

What is the balance between the coagulation and fibrinolytic system called

A

Haemostasis

21
Q

What are the two balancing factors in haemostasis

A

Bleeding to death - Trauma, major surgery,hemophilia
Clotting to death - thrombosis, MI, stroke

22
Q

What are the disordered of the plasma factor systems

A

Von Willebrand disease​

Haemophilia A​

Haemophilia B​

Warfarin ​

Heparin

23
Q

What drugs are used to combat excessive bleeding

A

Warfarin
Heparin
-promote antithrombin acitivity preventing excessive clot formation

24
Q

What are examples of acute inflammation

A

Gingivitis​

Abscess formation ​

Pericoronitis​

Cellulitis​

Angular Cheilitis​

Ludwig’s Angina

25
Q

What is abscess formation

A

Pus forms in a pyogenic membrane

26
Q

What are the different types of dental abscesses

A

Gingival - gum tissue
Periodontal - Infection deeper in the gum
Periapical - infection of the pulp

27
Q

What are the two classes of chronic inflammation

A

Non-specific​
Persistent acute inflammation​
Excessive suppuration​

Specific​
Arises de novo​
Persistent exposure to agent​
Can be granulomatous​

28
Q

What is non-specific chronic inflammation

A

Infiltrate dominated by tissue macrophages, T cells and B cells (more adaptive immune cells)​

Characterized by tissue destruction vs repair

29
Q

Whar is the most relevant non-specific chronic inflammation

A

Periodontitis

30
Q

What is specific chronic inflammation

A

Induced by non-immunological or immunological agents ​

Autoimmune diseases​

Can be granulomatous (involving the formation of granulomas)​

Characterized by excessively activated tissue macrophages

31
Q

What are the most prevelant dental related autoimmune diseases

A

Rheumatoid arthritis - loss of tolerance to citrullinated proteins in synovial fluid

Sjogren’s syndrome - host T and B cells attack the cells of the salivary and lacrimal

32
Q

What is OFG (orofacial granulomatosis)

A

Characterized by excessively activated tissue macrophages​

Epithelioid macrophages​

Giant cells consist of these macrophages fused together ​

B and T cells also present​

Granulomas form in the soft tissue

33
Q

What does the kinin system lead to the production of

A

bradykinins

34
Q

How does the fibrinolytic system prevent excessive clotting

A

Involves plasmin which degrades fibrin