inflammation Flashcards

(48 cards)

1
Q

Define inflammation.

A

A local physiological response to tissue injury.

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2
Q

how is inflammation classed x2

A

acute
chronic

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3
Q

summary of acute inflammation

A

1- initial reaction of tissue to injury
2- vascular component- dilation of vessels
3- exudative component, leakage of protein rich fluid
4- neutrophil is the first cell at the scene
5- outcome may be resolution, suppuration, organisation or progression to chronci

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4
Q

what cells are involved in inflammation 5

A

neutrophil polymorphs
* Macrophages
* Lymphocytes
* Endothelial cells
* Fibroblasts

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5
Q

what is chronic inflammation

A

Slow onset or sequel to acute
– Long duration
– May never resolve

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6
Q

Causes of acute inflammation

A

Microbial infections
Hypersensitivity reactions
Physical agents
Bacterial toxins

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7
Q

Characteristics of neutrophil polymorphs

A

Short lived cells
* First on the scene of acute inflammation
* Cytoplasmic granules full of enzymes that
kill bacteria
* Usually die at the scene of inflammation
* Release chemicals that attract other
inflammatory cells such as macrophages

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8
Q

characteristics of macrophages

A

Long lived cells (weeks to months)
* Phagocytic properties
* Ingest bacteria and debris
* May carry debris away
* May present antigen to lymphocytes

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9
Q

characteristics of lymphocytes

A

Long lived cells (years)
* Produce chemicals which attract in other
inflammatory cells
*produces memory cells from past infections

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10
Q

what to endothelial cells produce that stops things from sticking

A

nitrous oxide

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11
Q

why does an inflamed area look red and swollen

A

capillaries are open
swollen as it has more blood and fluid

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12
Q

what does sepsis look like

A

all blood vessels are open,
not enough blood to fill them

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13
Q

characteristics of fibroblasts

A

-Long lived cells
-Form collagen in areas of chronic
inflammation and repair
-spindle shaped

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14
Q

what is a granuloma

A

An aggregate of epitheloid histocytes

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15
Q

best known chemical mediator in acute inflammation

A

histamine

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16
Q

what does histamine do

A
  • causes vascular dilation
    -increases vascular permeability
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17
Q

what is the role of mast cells

A
  • On stimulation by c3a/c5a complement components they release preformed inflammatory mediators
    -metabolise arachidonic acid into newly synthesised inflammatory mediators
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18
Q

what is a prostaglandin

A

chemical mediator of inflammation

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19
Q

5 cardinal signs of inflammation

A
  1. Redness (rubor).
  2. Swelling (tumor).
  3. Pain (dolor).
  4. Heat (calor).
  5. Loss of function.
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20
Q

define exudate

A

fluid that leaks out of vessel walls due to increased vascular permeability

21
Q

what are the benefits of exudate formation

A

-dilution of toxins
-entry of antibodies
-transport of drugs
-fibrin formation

22
Q

what are the 4 systemic effects of acute inflammation

A
  1. Fever.
  2. Feeling unwell.
  3. Weight loss.
  4. Reactive hyperplasia of the reticuloendothelial system
23
Q

What are the 4 outcomes of acute inflammation

A
  1. Resolution.
  2. Suppuration- formation of pus
  3. Organisation (scar tissue formation).
  4. Progression onto chronic inflammation.
24
Q

what is resolution

A

initiating factor removed
tissue undamaged or able to regenerate

25
what is repair
-initiating factor still present tissue damaged and unable to regenerate
26
what is suppuration
formation of pus, a mixture of living, dying and dead neutrophils and bacteria
27
what is organisation
the replacement by granulation tissue as part of the process of repair
28
Give 4 causes of chronic inflammation.
1. Primary chronic inflammation. 2. Transplant rejection. 3. Recurrent acute inflammation. 4. Progression from acute inflammation.
29
sequence of chronic inflammation
either progression from acute inflammation or starts as ‘chronic’ inflammation such as infectious mononucleosis * no or very few neutrophils * macrophages and lymphocytes, then usually fibroblasts * can resolve if no tissue damage (e.g. viral infection like glandular fever) but often ends up with repair and formation of scar tissue
30
what is healing by 2nd intention
when you cant get the edges of skin together so the wound will be left open to heal naturally may be due to excess trauma
31
why does repair occur
when tissue damage occurs where tissue can't regenerate
32
what cells do not regenerate
* myocardial cells * neurones
33
Names of the 4 stages of neutrophilic action
/Margination Adhesion Emigration Diapedesis
34
Describe the 4 stages of neutrophilic action
Migration - increase in plasma viscosity , neutrophils line up along plasmatic zone Adhesion to neutrophils - adhesion to vascular endothelium occurs and attach Emigration - neutrophils pass through endothelial cells onto vessel wall Diapedesis- rbcs may also escape from vessels , indicates severe vascular injury
35
What conditions might you see a granuloma
TB, LEPROSY chrons Sarcoodosis
36
What are some macroscopic features of chronic inflammation
Chronic ulcer Chronic abscess activity Granulomatous inflammation Fibrosis
37
The activity of what enzyme in the blood can act as a marker for granulomatous disease
ACE
38
You suspect a patient has sarcoidosis which blood marker do you investigate
ACE - released by granulomas
39
What is resolution
The complete restoration of tissues to normal Minimal cell death
40
What is suppuration
Formation of pus Becomes surrounded by pyogenic membrane
41
What is organisation
Replacement by granulation tissue New capillaries grow into the inflammatory exudate
42
What is progression
Causative agent is not removed so there is progression to chronic inflammation
43
what is the name of the cell that produces collagen in fibrous scarring
fibroblasts
44
appendicitis is an example of ?
acute inflammation
45
crohns disease is an example of ?
granulomatous inflammation
46
Benefits on inflammation
Destruction of invading microbes
47
Harmful effects of inflammation
Digestion of normal tissues Swelling Inappropriate inflammatory response
48
what is the role of mast cells
- On stimulation by c3a/c5a complement components they release preformed inflammatory mediators -metabolise arachidonic acid into newly synthesised inflammatory mediators