Infalmmation Flashcards

1
Q

Inflammation

A

This is the stereotype response of living vascularized cell to a sub lethal injury

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2
Q

Exudation

A

Is an inflammatory response at site of injury due to increase permeability of small blood vessels.
•movement of fluid, proteins, and blood cells from the vascular system into the interstitium or body cavities.
•Are extravascular fluid having high protein concentration, contains cellular debris, and has a high specific gravity >1.020

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3
Q

Transudate

A

An extra vascular fluid with low specific gravity <1.012, low protein, low cellular component.

It does not have to do with increased membrane permea

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4
Q

Edema

A

Accumulation of fluid in the interstitial or serous cavities, either exudate or transudate

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5
Q

Purulent exudate

A

inflammatory exudate rich in leukocytes, the debris of dead cells debris and microbes

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6
Q

Hallmark of acute inflammation

A

The production of protein rich exudate- edema

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7
Q

Factors for vascular leakage

A

increased formation of interendothelial spaces in venules elicited by many chemical mediators: histamine, bradykinin, leukotrienes, the neuropeptide substance P.
•2.Direct endothelial injury by apoptosis
delayed prolonged leakage, and affecting ve Ike’s and arterioles
3. Leukocyte mediated endothelial injury
4. Increased transcytosis: vesiculovacuolar organelles are located around the intercellular junctions and cause leakage from the vessel via vegf
5. Newly formed blood vessel have immature intercellular junctions and therefore they are prone to vascular leakage

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8
Q

Cellular components of acute inflammation

A
  • neutrophils
  • macrophages
    -chemical mediators
  • chemical substances that drive the inflammation
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9
Q

How do leukocytes leave the vascular system

A

They secrete collagenases

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10
Q

Chemotaxis

A

Unilateral movement of leucocytes toward a chemical attractant.

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11
Q

Components of acute inflammation

A

A. Changes in vascular calibre that lead to increased blood flow.
•B. Increased vascular permeability allowing plasma protein and leucocyte to leave circulation through structural changes in microvasculature
•C. Leukocyte emigration (extravasations),accumulation at site of injury, activation to eliminate offending agent (phagocytosis)

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12
Q

Causes of acute inflammation

A

Infections: bacterial, viral, fungal, parasitic and microbial toxins
•Tissue necrosis : ischemia (myocardial infarct), trauma, hypoxia and physical and chemical injury (thermal injury, burns,frostbite, irradiation,environmental chemicals).
•Foreign bodies: splinters, dirts, sutures.
•Immune reactions: hypersensitivity reactions or autoimmune diseases.

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13
Q

Chemotactic factors

A

Bacteria products.
•Complement component - C5a
•Arachidonic acid metabolites esp. leukotiene B4(LBT4), HETE-hydroxyeicosatetraenoic acid and kallikrein.
•Cytokines -IL8.

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14
Q

Phagocytosis

A

Ingestion of particulate material by phagocytic cells(neutrophils & monocyte-macrophages).

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15
Q

Opsonisation

A

the coating of a particulate material by substances called opsonin to facilitate phagocytosis.

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