Pathology - Inflammation Flashcards

1
Q

What is inflammation?

A

A local physiological response to tissue injury (not a disease)

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2
Q

What are the benefits of inflammation?

A

Destroy invading micro organisms = prevent spread of infection

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3
Q

What is the negative of inflammation?

A

May produce disease

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4
Q

What are 2 causes of chronic inflammation and the cells involved?

A

Autoimmunity eg. Graves’ disease, MS
Recurrent infection
Macrophages and lymphocytes

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5
Q

What are the 6 causes of acute inflammation?
Examples

A

Microbial infections (pyogenic bacteria & viruses)
Hypersensitivity (parasites)
Physical agents (trauma, ionizing radiation, heat, cold)
Chemicals (corrosives, acids, alkalis)
Bacterial toxins
Tissue necrosis (death of tissue due to lack of O2 or nutrient filled blood)

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6
Q

5 physical signs of acute inflammation?
What they mean?

A

Rubor (redness)
Calor (heat)
Tumor (swelling)
Dolor (pain)
Loss of function

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7
Q

Why would you have rubor?

A

Redness due to dilation of small blood vessels in damaged area (vasodilation)

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8
Q

Why would u have calor?

A

Heat due to hyperaemia = increased vasodilation = increased warm blood to area

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9
Q

What causes tumor?

A

Swelling from oedema - accumulation of fluid in ECF

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10
Q

Why would you have dolor?

A

Pain from stretching/distortion of tissue due to inflammatory oedema
Chemical mediators (bradykinin, prostaglandins and serotonin induce pain)

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11
Q

What are the 3 stages of inflammation in detail?

A
  1. Increased vessel calibre - inflammatory cytokines (bradykinin, prostacyclin, NO) mediate vasodilation
  2. Fluid exudate - vessels become leaky, protein rich fluid forced out of vessel

3.cellular exudate - neutrophil polymorphs into extra vascular space

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12
Q

What is the main cell involved in acute inflammation?

A

Neutrophils

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13
Q

What is a diagnostic histological feature of acute inflammation?

A

Neutrophil polymorphs into extra vascular space

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14
Q

What are the 4 stages in neutrophil action of acute inflammation?

A

Margination (migrate to edge of BV)

Adhesion (selections bind to neutrophil, cause ‘rolling along BV margins)

Emigration + diapedesis (movement out of BV, thru or in between endothelium & other inflammatory cells follow)

Chemotaxis (site of inflammation)

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15
Q

What are the 3 things happening at the site of inflammation?

A
  1. Phagocytosis
  2. Phagolysosome and bacterial killing
  3. Macrophages clear debris
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16
Q

What are the 5 outcomes of acute inflammation?

A

Resolution- normal

Supporation - pus formation

Organization - granulation tissue + fibrosis (scar tissue)
Note - cardiac tissue + neurons never resolve, most become this fibrotic tissue

Progression - excessive recurrent inflammation becomes chronic + fibrotic tissue

17
Q

What is a granuloma?

A

Aggregates of an epitheloid histocytes (essentially macrophages)

18
Q

What shape do granulomas form and what disease?

A

Form a granulomatous ‘horse shoe’ shape
Granulomatous disease

19
Q

What are some examples or granulomatous diseases?

A

TB, leprosy, crohns, sarcoidosis (granulomas in organs, especially skin and lungs)

20
Q

What is the most common cause of granuloma?

A

TB

21
Q

What is a feature seen in a granulomatous disease and give an example of which disease?

A

Central (caseous) necrosis ‘cheese like’
In TB

22
Q

Is there central necrosis in sarcoidosis, leprosy, vasculitis or crohns?

A

No central necrosis

23
Q

The presence of 2 things indicates a parasitic infection?

A

Granuloma and eosinophil
(Worms)

24
Q

What do granulomas secrete?
What can this be used as?

A

ACE
Blood marker