MoD Session 2- Acute Inflammation Flashcards Preview

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

Define acute inflammation.

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

1

What is the purpose of acute inflammation? (3)

Deliver blood cells and fluid to:
- protect against infection
- clear damaged tissue
- initiate tissue repair

2

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

Chemical mediators

3

What are the 5 causes of acute inflammation?

-microbial infection
-tissue necrosis
-physical and chemical agents
-hypersensitivity reactions
-foreign bodies

4

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

Redness, swelling, heat, pain, loss of function
(Rubor, Tumor, calor, dolor)

5

What changes occur to blood flow in acute inflammation?

-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

Why is fluid exudated in acute inflammation?

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

7

What is exudate oedema?

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

8

What are the primary leukocytes involved in acute inflammation?

Neutrophils

9

What does the presence of neutrophils in tissue indicate?

Injury

10

Where are neutrophils produced?

Bone marrow

11

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

-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

What are chemical mediators?

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

13

What does histamine do?

It causes vasodilation and increased vascular permeability.

14

What does bradykinin do?

It causes increased vasodilation and permeability of vasculature.

15

What does the complement system do?

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

What do prostaglandins do?

They cause vasodilation and therefore increased blood flow.

17

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

-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

What are five local complications of acute inflammation?

-normal tissue damage
-compression of structures
-obstruction of tubes
-loss of fluid
-pain and loss of function

19

What are the four systemic effects of acute inflammation?

-fever
-leukocytosis
-acute phase response
-shock

20

How is acute inflammation resolved? (4)

-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

What is the sequelae of acute inflammation? (4)

- 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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