Inflammation Flashcards

1
Q

what is inflammation/the inflammatory response?

A

the physiological response to tissue damage/injury and is accompanied by a characteristic series of local changes

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2
Q

what is the purpose of inflammation?

A

to be protective

  • isolate
  • inactivate
  • remove

both the causative agent and damaged tissue, so that healing can take place

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3
Q

primary signs/symptoms of inflammation?

A
  • redness
  • heat
  • swelling
  • pain
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4
Q

how are inflammatory conditions labelled/described?

A

by their latin suffix ‘itis’

  • appendicitis; inflammation of the appendix
  • laryngitis; inflammation of the larynx
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5
Q

general cause of inflammation?

A

any form of tissue damage will stimulate the inflammatory response, even in the absence of infection

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6
Q

does infection have to be present for inflammation to occur?

A

no, tissue damage alone can stimulate the inflammatory response

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7
Q

examples of causes of inflammation?

A
  • extremes of temperature
  • trauma
  • corrosive chemicals including extremes of pH
  • abrasion
  • infection by pathogen(s)
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8
Q

what is acute inflammation?

A
  • typically short in duration, e.g., days-weeks
  • may range from mild to severe, depending on extent of tissue damage
  • e.g., inflammatory response following cutting your hand
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9
Q

what is chronic inflammation?

A
  • slow, long-term inflammation lasting prolonged periods of time
  • several months- years
  • inflammation which ‘sticks around’ long after injury/infection
  • processes involved are similair to those in acute inflammation, but as process is longer, more tissue damage is likely
  • causes; untreated acute inflammation and autoimmune disorders (chronix exposure to an irritant), etc.
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10
Q

difference between acute and chronic inflammation?

A
  • acute; body’s response to sudden tissue damage
  • chronic; body continues to send inflammatory cells despite no cause/need
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11
Q

list of changes that occur during an inflammatory response

A
  • increased blood flow
  • accumulation of tissue fluid
  • migration of leukocytes
  • pain and suppuration (pus production)
  • increased core temperature

These changes in the body will significantly overlap one another and develop together during an inflammatory response

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12
Q

increased blood flow

A
  • arterioles and local capillaries supplying damaged area dilate, increasing blood flow to the site of injury
  • this is mainly caused by chemical mediators released from damaged cells, e.g., serotonin and histamine
  • increased blood flow to the site of injury provides more O2 and nutrients
  • increased blood flow causes the increased temperature and erythema of an inflamed area, and contributes to the swelling (oedema)
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13
Q

increased tissue fluid formation

A

*common sign of inflammation is swelling of involved tissues, caused by fluid leaving local blood vessels and entering interstitial spaces

  • this is partly due to increased capillary permeability caused by inflammatory mediators; serotonin, histamine, and prostoglandins
  • also partly due to elevated pressure within vessels due to increased blood flow
  • most excess tissue fluid drains away in the lymphatic vessels, taking damaged tissue, dead/dying cells, and toxins with it
  • plasma proteins (normally retained within the blood) also escape into tissues through leaky capillary walls and this increases osmotic pressure, draining more fluid out of the blood
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14
Q

how is increased tissue fluid/oedema harmful and helpful?

A

helpful; swelling around a painful, inflammed joint cushions it and limits movement, encouraging healing

harmful; swelling around respiratory passages can obstruct breathing, whilst significant swelling can cause pain

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15
Q

increased temperature

A
  • the increased temperature of inflamed tissues has twin beenfits of both inhibitng growth & division of microbes, whilst promoting activity of phagocytes
  • inflammatory response may be accomadated by a rise in core body temperature (pyrexia/fever) especially if bacteria infection is present
  • pyrexia increases the metabolic rate of cells in the inflamed area, causing an increased need for O2 and nutrients
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16
Q

pain

A
  • occurs when local swelling compresses sensory nerve endings
  • pain is exacerbated by chemical mediators of the inflammatory process, e.g., bradykinin and postaglandins which increase the sensitivity of sensory nerve endings to painful stimuli
  • although unpleasant, pain may indirectly promote healing as it encourages protection of the damaged site
17
Q

suppuration (pus formation)

A
  • pus consists of dead phagocytes, dead cells, fibrin, inflammatory exudate and living/dead microbes
  • a localised collection of pus within the tissues is called an abscess
18
Q

outcomes of acute inflammation

A

resolution; occurs when the cause has been successfully overcome. new, healthy tissue is formed in replacement, repair is complete, with or without scar formation

development of chronic inflammation; can occur if resolution is not complete, e.g., if live microbes remain at site of injury, in deep seated abscesses, wound infections, bone infections

19
Q

migration of leukocytes

A
  • loss of fluid from the blood thickens it, slowing blood flow and allowing normally fast-flowing WBCs to make contact & ahdere to the damaged vessel wall
  • on acute inflammation, the most important luekocyte is the neutrophil conducts phagoctyosis of antigens once within the tissues
  • phagocyte activity is promoted by the increased temperature (local & systemic) associated with inflammation
  • after 24hrs, macrophages become most dominant WBC at inflammed site, and persist if situation is not resolved, resulting in chronic inflammation
  • chemotaxis; the chemical attraction of leukocytes, including neutrophils and macrophages, to an area of inflammation
20
Q

what are inflammatory mediators?

A

substances which act on blood vessels and/or cells to promote an inflammatory response. they are released by tissues, blood, and primarily relevant cells, e.g., types of WBCs

21
Q

types of inflammatory mediators

A
  • histamine
  • serototonin
  • prostaglandins
  • heparin
  • bradykinin
22
Q

histamine

A

made by; mast cells (tissues) & basophils (blood)

trigger for release; binding of an antibody to mast cells and basophils

main pro-inflammatory actions; vasodilation, increased vascular pearmeability, degranultion, smooth muscle contraction (such as bronchocinstriction)

23
Q

serotonin

A

made by; platelets (tissues), basophils (blood)

tirgger for release; when platelets are activated and when mast cells/basophils degranulate

main pro-inflammatory actions; vasoconstriction, increased vascualr permeability

24
Q

prostaglandins

A

made by; nearly all cells, not stored but made from cell membranes as requiered

trigger for release; various stimuli, e.g., drugs, toxins, other inflammatory mediators, hormones, trauma, etc.

main pro-inflammatory actions; diverse, sometimes opposing e.g., pyrexia, pain, vasodilation or vasoconstriction, increased vascular permeability

25
Q

heparin

A

made by; liver, mast cells, basophils

trigger for release; when cells degranulate

main pro-inflammatory actions; anticoagulant (prevents blood clotting), which also maintains blood supply (nutrients & O2) to injured tissue and washes away microbes and wastes

26
Q

bradykinin

A

made by; tissues & blood

trigger for release; when blood clots, in trauma and inflammation

main pro-inflammatory actions; pain & vasodilation