Inflammation Flashcards

1
Q

What is Inflammation

A

Damage to the tissue that initiates vascular and cellular events that are designed to clean out cellular debris and pathogens to initiate repair

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2
Q

What do mast cells do?

A

Mast Cells secrete Histamines, Leukotrienes and Prostaglandins

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3
Q

What is the function of the chemicals released by mast cells

A

These chemicals bind to receptors on the surface of epithelial cells and can cause the formation of selectins.
They can also cause the cells to contract creating space between the endothelial cells which causes plasma cells to leak out through the intercellular clefts and as it accumulates in the intracellular space it causes swelling

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4
Q

What does PLA 2 do?

A

PhosphoLipase A2 breaks down phospholipids in a damaged cell membrane during the inflammation process into Arachidonic Acids. These Acids are worked on by 2 enzymes, Lipo oxygenase which converts it into specific leukotrienes and cyclooxygenase which converts it into prostaglandins.

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5
Q

What is the function of Bradykinins?

A

Bradykinins activate pain receptors during inflammation which causes pain along with the pressure from the plasma leaking through intercellular space in the endothelial cells

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6
Q

How is Vasodilation caused in inflammation and what are its effects?

A

Vasodilation is caused when the smooth muscle cells are acted on by the chemicals released by MAST cells which causes it to relax, leading to vasodilation. This causes more blood to flow leading to heat and redness in the area.

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7
Q

What is the function of selectin proteins?

A

Selectins Hook onto Macrophages and Neutrophils flowing in the blood to stop them and bring them to the site of inflammation via a process known as margination. When the white blood cells reach the intracellular space, they react with PCAMS that allow it to squeeze through the space, in a process called diapedesis.

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8
Q

Explain the function of IL-1 and TNF-alpha

A

Interleukin 1 and TNF-alpha are secreted by macrophages once they reach the pathogen, and they bind to receptors on endothelial cells to stimulate the formation of E selectins which attract more monocytes and neutrophils.

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9
Q

What does IL-8 do?

A

Interleukin 8 binds to a receptor on the surface of the endothelial cells which stimulates synthesis of ICAM and VCAM proteins. They also activate proteins on the WBCs which interact with ICAM and VCAM, facilitating diepedises

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10
Q

Explain the phagocytic process

A

In the phagocytic process, the macrophages and neutrophils engulf the pathogen by forming pseudopods which pull it into itself forming a vesicle called a PHAGOCOL containing the pathogen.
Other vesicles called lysozyme which fuses with the phagosome forming a phagolysosome and the hydrolytic enzymes which break down the cell wall of the pathogen. All that’s left over now is the antigens.

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11
Q

What happens to antigens which remain after the phagocytic process in inflammation?

A

The Neutrophil phagolysosome binds to the cell membrane and releases the antigens by exocytosis to go to the lymph nodes.

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12
Q

Briefly define oxidative burst

A

In the case of extremely strong pathogen like bacteria, the neutrophil can bring in free radicals to destroy the pathogen but in the process it will also be destroyed. This is known as Oxidative Burst.

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13
Q

What are the differences between chronic and acute inflammation?

A

ACUTE inflammation is rapid, can take place within minutes or hours
The cells involved are neutrophils and tissue injury is mild
In CHRONIC , the response is slow and can take several days, the cells involved are lymphocytes, monocytes and macrophages. The tissue damage is usually severe and progressive. The local and systemic signs are more prominent in acute inflammation

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14
Q

List the 5 Rs of inflammatory response

A
There are 5 steps to inflammation known as the 5 Rs and these are
Recognition on the injurious agent
Recruitment of leukocytes
Removal of the injurious agent
Regulation of inflammatory response
Repair of the damaged cells
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15
Q

Describe vascular changes and cellular events of acute inflammation

A

The vascular changes which take place in inflammatory response is the dilation of blood vessels and increased blood flow to recruit more cells and proteins to the site of injury

The cellular change is the recruitment and activation of leukocytes to destroy the invaders and activation of mediators. The invaders are usually destroyed by phagocytosis.

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16
Q

List 5 stimuli for acute inflammation

A
The stimuli for acute inflammation are:
Infection
Tissue necrosis
Trauma from physical or chemical injuries
Immune reactions
Foreign bodies
17
Q

How are the stimuli for acute inflammation recognized?

A

These signs are recognized by TOLL LIKE RECEPTORS and INFLAMMASOMES
Toll-like receptors are microbial sensors present in the plasma membrane and endosomes . They recognize bacteria and other pathogens and result in the release of mediators of inflammation.
Inflammasomes are a multiprotein cytoplasmic complex which recognize products of cell death and activate caspase 1 which leads to activation of IL-1, a mediator of leukocyte recruitment to phagocytose the dead cells.

18
Q

What are 3 mechanisms of vascular permeability

A

Contraction of the endothelial cells caused by histamine, bradykinins and leukotrienes. It is short lived but is the most common.
Direct damage to the endothelial cells due to burns microbes or toxins
Endothelial injury due to leukocytes by neutrophils adhering to it