Response to Injury II Flashcards

1
Q

What is inflammation?

A

A response of vascularized tissues to infections and tissue damage that brings cells and molecules of host defence from the circulation to the sites where they are needed, to eliminate the offending agents.

The complex biological response of tissues to harmful stimuli and is a protective response involving blood vessels, immune cells and molecular mediators.

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2
Q

Why study inflammation?

A
  • Caries
  • Periodontal disease
  • Majority mucosal disorder
  • Majority of dental cysts

Are all the result of inflammation.
Also, when taken tooth out or scalpel against someone gingiva you will cause inflammation.

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3
Q

How is inflammation classified?

A

Inflammation is classified as acute or chronic.

Acute inflammation develops in minutes. Chronic inflammation had a protracted course. Sometimes the two occur together.

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4
Q

What is the purpose of acute inflammation?

A

Destroy/contain noxious stimulus this is brought about by dilution of toxins and the entry of phagocytic leukocytes to the site of entry.

Ultimately the goal of acute inflammation is to repair and return the tissue/organ to function. This is bought about by fibrin formation to acts a scaffold to initiate repair and transport of nutrients and drugs to the site of damage.

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5
Q

What is Overview Sequence of Events that happen during inflammation?

A

Recognition of local cells to a stimulus. The stimulus maybe for an ex example necrosis, presence of microbes or antigen presenting cells.

Following recognition starts of a sequence of event. This can be classed at vascular events followed by cellular events leading to the outcome of healing.

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6
Q

What are the vascular events that happen during inflammation?

A

The earliest event in acute inflammation is the increase in the capillary vasculature size or vasodilation.

This result from the direct action on the capillary smooth muscle cells and endothelial cells by certain chemical inflammation mediators that are released due to tissue damage. These include:
* Histamine
* Prostaglandins
* Platelet activating factor
* Kinins

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7
Q

During acute inflammation what does vasodilation lead to?

A

Vasodilation leads to a decrease in the flow rate of blood in the vessel and vascular congestion leads to heat and redness at site of injury.

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8
Q

During acute inflammation what happens after vasodilation?

A

Soon after there is increase in vascular permeability this is due to the gaps between the endothelial cell opening up resulting in leakage of fluid and plasma proteins into the extravascular space. Increase in gaps is due to the direct action of chemical inflammation mediators these include:
* Histamine
* Leukotriene
* Platelet activating factor
* Kinins

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9
Q

What is exudation?

A

The process of which there is net flow of fluid and plasma proteins from within the vessels into the extravascular space is called exudation. Therefore, the fluid that collects in the space is called the fluid exudate.

Normally there is no gain of fluid into the extravascular space due to the hydrostatic forces at the venous end. However, there is in acute inflammation due to increased vascular permeability and increased osmotic pressure in the extravascular space at the venous end.

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10
Q

What are the cellular events that take place during acute inflammation?

A

Cellular events of acute inflammation centre around neutrophil/polymorphonuclear leukocytes. They are recognised by their multi-lobed nucleus.

As neutrophils marginate, they are able to, via various receptors, detect ligands expressed on endothelial cell.

One particular group are the selectins. The selectins are upregulated due to various cytokines included IL-1 and TNF (these are expressed because of a result of tissue damage).

The bond between the neutrophils and endothelial via selectin is weak. As a result, they roll along the endothelial surface through attachment and detachment in a process called rolling. This process come to end once the neutrophil finally attaches firmly, this is brough about by integrins on the neutrophil the receptor for these ligands are ICAM-1 found on the surface of the endothelial cells.

The neutrophil exit through the gaps between the endothelial cells and becomes part of the extravascular fluid. The neutrophil migrates to the site where it’s most needed. It does so from the attraction of chemotaxis factors these include:
* Bacterial products
* Chemokines
* Complement especially C5a
* Leukotriene B4

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11
Q

What are the types of exudate?

A

Serous
Fibrinous
Purulent

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12
Q

What is serous exudate?

A

Least common it is characterised by a cell poor fluid this is formed in mucosal and skin blister and can be features if certain viruses like herpes.

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13
Q

What is fibrinous exudate?

A

Characterised where the is significant vascular damage for example extract a tooth. This is the most common type.

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14
Q

What is purulent exudate?

A

Also known as the suppurative characterised by cell rich envenomed usually neutrophils. Examples are abscess and occurs mostly commonly in bacterial infections.

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15
Q

What do Neutrophils do at the site of inflammation?

A

Neutrophils at site of inflammation remove bacteria and necrotic debris via phagocytosis.

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16
Q

Explain the process of phagocytosis.

A
  1. Adherence & ingestion
  2. Phagosome formation -bacterium is contained in a membrane bound cytosolic vesicle
  3. Phagolysosome – formation of lysosomes with phagosome
  4. Digestion – lysosomes has enzymes that causes digestion without cause damage to surroundings
  5. Residual body
  6. Discharge
17
Q

What is ROS?

A

ROS are bought about by the reduction of NADPH to NADP+ on the phagolysosome membrane. ROS is then converted to hydrogen peroxide is not potent, it is much more efficient when hydrogen peroxide reacts with myeloperoxidase which is found in the granules on the neutrophils.

Myeloperoxidase in the presence of chloride produces hydrochloride which has very potent killing activity.

18
Q

What are the Cardinal signs of inflammation?

A
  • Heat is due to vasodilation and increased blood flow
  • Redness is due to vasodilation and increased blood flow
  • Swelling is due to exudate
  • Pain due to the release of mediators, exudate and Inflammatory cell influx
  • Loss of function
19
Q

What are the benefits of acute inflammation?

A

Dilution of toxins
Entry of antibodies
Transport of drugs
Fibrin formation
Transport of nutrients

20
Q

What are the adverse effects of acute inflammation?

A

Tissue damage
Swelling
Pyrexia - fever

21
Q

What are the outcomes of acute inflammation?

A

Acute inflammation is highly potent tool if left unchecked can be seriously damaging hence is highly regulated.

It come to an end once the stimulus has been removed. Once the acute inflammation is terminated cells and tissues undergo resolution.

If there is significant damage the tissues will heal through scar formation through the generation of fibrous tissue also known as repair. Sometimes acute inflammation can lead to chronic inflammation.