MoD Session 2- Acute Inflammation Flashcards Preview

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Flashcards in MoD Session 2- Acute Inflammation Deck (22)
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0
Q

What is the purpose of acute inflammation? (3)

A

Deliver blood cells and fluid to:

  • protect against infection
  • clear damaged tissue
  • initiate tissue repair
1
Q

Define acute inflammation.

A

It is the response of living tissue to injury that is innate, immediate, short lived and stereotyped.

2
Q

What controls the movement of leukocytes and fluid to the injury site?

A

Chemical mediators

3
Q

What are the 5 causes of acute inflammation?

A
  • microbial infection
  • tissue necrosis
  • physical and chemical agents
  • hypersensitivity reactions
  • foreign bodies
4
Q

What are the five clinical signs of acute inflammation? (And their equivalent Latin names)

A

Redness, swelling, heat, pain, loss of function

Rubor, Tumor, calor, dolor

5
Q

What changes occur to blood flow in acute inflammation?

A
  • arterioles initially constrict.
  • arterioles and capillaries then dilate, therefore increasing blood flow. Rubor and calor.
  • vessels are increasingly permeable, therefore fluid moves into tissues. Tumor.
6
Q

Why is fluid exudated in acute inflammation?

A

Because hydrostatic pressure increases and forces fluid out of vessels into surrounding tissues.

7
Q

What is exudate oedema?

A

Fluid loss into tissues shown in inflammation; it has a high protein content.

8
Q

What are the primary leukocytes involved in acute inflammation?

A

Neutrophils

9
Q

What does the presence of neutrophils in tissue indicate?

A

Injury

10
Q

Where are neutrophils produced?

A

Bone marrow

11
Q

What are the 8 steps of neutrophil emigration in acute inflammation?

A
  • chemo taxis- chemotaxins summon neutrophils to damaged area.
  • activation- chemotaxins bind to receptors and cause swelling by ion entry. Cells are more sticky.
  • margination- leukocytes marginate in vessels
  • rolling- stick to walls and roll along endothelium
  • adhesion- stick
  • diapedesis- dig themselves out of vessel.
  • recognition and phagocytosis- attach to opsonins and phagocytose
  • kill- oxygen dependent using free radicals, or oxygen independent using enzymes
12
Q

What are chemical mediators?

A

They are molecules that are produced during inflammation and modulate the inflammatory response somehow.

13
Q

What does histamine do?

A

It causes vasodilation and increased vascular permeability.

14
Q

What does bradykinin do?

A

It causes increased vasodilation and permeability of vasculature.

15
Q

What does the complement system do?

A

C3a and C5a come together to form a tube which punch holes in bacteria and cause them to die. They also generate C3b which aids phagocytosis.

16
Q

What do prostaglandins do?

A

They cause vasodilation and therefore increased blood flow.

17
Q

How do changes due to acute inflammation combat the injury? (4)

A
  • vasodilation- increases temperature and blood flow
  • fluid exudation- dilutes toxins and delivers nutrients, oxygen, plasma proteins etc to the site of injury
  • loss of function and pain- enforces rest and therefore minimises the likelihood of further damage
  • cell infiltration- removes dead and foreign material by phagocytosis.
18
Q

What are five local complications of acute inflammation?

A
  • normal tissue damage
  • compression of structures
  • obstruction of tubes
  • loss of fluid
  • pain and loss of function
19
Q

What are the four systemic effects of acute inflammation?

A
  • fever
  • leukocytosis
  • acute phase response
  • shock
20
Q

How is acute inflammation resolved? (4)

A
  • because mediators have short half lives they are degraded soon after their release.
  • normal vascular tone and permeability returns.
  • neutrophil emigration stops.
  • exudate is taken back up into venules or drained via lymphatics.
21
Q

What is the sequelae of acute inflammation? (4)

A
  • if damaged tissue tissue can regenerate, there will be complete resolution.
  • if acute inflammation continues and some chronic occurs, an abscess forms.
  • if damage is too extensive and chronic inflammation occurs, a fibrous scar will form.
  • death

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