Acute Inflammation Flashcards

1
Q

What is acute inflammation a response to

A

The response of living tissue to injury

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2
Q

How do you know if a condition is related to inflammation

A

The condition will end in “itis”

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3
Q

Name some exogenous causes of inflammation

A
  • Trauma
  • Infection
  • Chemicals
  • Temperature
  • Radiation
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4
Q

What are the endogenous causes of inflammation

A
  • Anoxia
  • Antigen/antibody complexes
  • Body chemicals
  • Metabolic products (urate crystals)
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5
Q

What are the macroscopic/cardinal signs of inflammation

A
  • Redness (rubor)
  • Swelling (tumor)
  • Heat (calor)
  • Pain (dolor)
  • Loss of function (functio laesa)
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6
Q

What microscopic changes occur due to inflammation

A
  • Initial constriction then dilation of vessels
  • Increased blood flow
  • Increased permeability
  • Formation of exudate
  • Migration of leukocytes through wall
  • Oedema
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7
Q

What does increased permeability of blood vessels contribute to inflammation

A
  • Enhances migration of cells
  • Dilution of toxins
  • Stimulate lymphatics/immune response
  • Deposition of proteins e.g. fibrin to form mechanical barrier
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8
Q

What does the movement of WBCs from blood flow to focus of injury allow to happen

A

– margination
– pavementing
– transmigration/diapedesis

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9
Q

What is chemotaxis

A

movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance.

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10
Q

What are the features and roles of neutrophil polymorphs in inflammation

A
  • First cell to arrive
  • Predominant cell for 6-24h
  • Mobile, phagocytic and responds to chemotaxis
  • Segmented nucleus, granular cytoplasm full of granules containing enzymes
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11
Q

What is the most common polymorph

A

neutrophils

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12
Q

Describe the features and roles of eosinophils

A
  • Used especially in allergy and helminth infections

* bilobed, red granules

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13
Q

What are the features and roles of basophils/mast cells

A
  • Acts very early
  • Blue/pruple cytoplasm
  • Degranulates with release of vasoactive amines
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14
Q

Where are monocytes/macrophages found

A

Circulating/tissue

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15
Q

Describe the features and morphology of monocytes/macrophages

A
  • second main cell of acute inflammation
  • predominate after 24h
  • mobile, phagocytic, responds to chemotaxis
  • attacks and clears up
  • bean shaped nucleus, copious cytoplasm
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16
Q

Name some substances that can cause polymorphs to react by chemotaxis

A
  • Bacteria
  • fungi
  • immune complexes
  • toxins
  • complement components
  • lipoxygenase products
  • white cell breakdown products
17
Q

What are the 3 main stages of phagocytosis

A
  • Recognition and attachment
  • Engulfment
  • Killing and Degradation
18
Q

What processes happen in the recognition and attachment stage of phagocytosis

A

– mechanical contact

– opsonisation

19
Q

What structures are formed in the engulfment stage of phagocytosis

A

– pseudopods

– phagosome

20
Q

What is used to kill the contents of a phagosome

A

Lysosomal contents/enzymes

21
Q

What processes are increased in the engulfment stage of phagocytosis

A

Glycolysis

RNA, protein and membrane synthesis

22
Q

What is opsonisation

A

This is when an antibody that has attached to an antigen binds to a receptor on a polymorph/macrophage and elicits a response

23
Q

Where do local mediators come from

A

Circulation

Intracellular - some are preformed and some are synthesised and released upon damage

24
Q

Name some mediators that affect inflammation

A
Histamine
Serotonin
Lysosomal enzymes
Prostaglandins
Leukotrienes
Cytokines
25
Q

What is the role of mediators in inflammation

A

They regulate the generation, maintenance and resolution of the inflammatory response

26
Q

Clinical features of acute inflammation?

A
  • Pyrexia
  • drowsiness
  • lethargy
  • leukocytosis
  • decreased appetite
  • acute phase proteins
27
Q

What outcome is there from the resolution of acute inflammation

A

– clearance of injury
– clearance of inflammatory cells and mediators
– replacement of any injured cells
– normal function resumed

28
Q

What outcome is there from the repair of acute inflammation

A
  • some tissue lost may not be able to regenerate therefore replacement with granulation tissue and fibrosis
  • likely less than ideal function
29
Q

Describe suppurative inflammation resulting from acute inflammation

A
  • pus is more exaggerated form of acute inflammation
  • neutrophils, dead cells, bacteria and debris
  • if walled-off and surrounded by a fibrous rim it becomes an abscess
30
Q

Describe septicaemia resulting from acute inflammation

A
  • organism gains access to lymphatics then blood or blood direct
  • response heightened
  • mortality high
31
Q

What are the 5 potential outcomes of acute inflammation

A
Resolution
Repair
Chronic inflammation - repeated episodes
Suppurative inflammation
Septicaemia