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Pathology > inflammation > Flashcards

inflammation Flashcards

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
Q

what is repair

A

-initiating factor still present
tissue damaged and unable to regenerate

26
Q

what is suppuration

A

formation of pus, a mixture of living, dying and dead neutrophils and bacteria

27
Q

what is organisation

A

the replacement by granulation tissue as part of the process of repair

28
Q

Give 4 causes of chronic inflammation.

A
  1. Primary chronic inflammation.
  2. Transplant rejection.
  3. Recurrent acute inflammation.
  4. Progression from acute inflammation.
29
Q

sequence of chronic inflammation

A

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
Q

what is healing by 2nd intention

A

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
Q

why does repair occur

A

when tissue damage occurs where tissue can’t regenerate

32
Q

what cells do not regenerate

A
  • myocardial cells
  • neurones
33
Q

Names of the 4 stages of neutrophilic action

A

/Margination
Adhesion
Emigration
Diapedesis

34
Q

Describe the 4 stages of neutrophilic action

A

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
Q

What conditions might you see a granuloma

A

TB, LEPROSY
chrons
Sarcoodosis

36
Q

What are some macroscopic features of chronic inflammation

A

Chronic ulcer
Chronic abscess activity
Granulomatous inflammation
Fibrosis

37
Q

The activity of what enzyme in the blood can act as a marker for granulomatous disease

A

ACE

38
Q

You suspect a patient has sarcoidosis which blood marker do you investigate

A

ACE - released by granulomas

39
Q

What is resolution

A

The complete restoration of tissues to normal
Minimal cell death

40
Q

What is suppuration

A

Formation of pus
Becomes surrounded by pyogenic membrane

41
Q

What is organisation

A

Replacement by granulation tissue
New capillaries grow into the inflammatory exudate

42
Q

What is progression

A

Causative agent is not removed so there is progression to chronic inflammation

43
Q

what is the name of the cell that produces collagen in fibrous scarring

A

fibroblasts

44
Q

appendicitis is an example of ?

A

acute inflammation

45
Q

crohns disease is an example of ?

A

granulomatous inflammation

46
Q

Benefits on inflammation

A

Destruction of invading microbes

47
Q

Harmful effects of inflammation

A

Digestion of normal tissues
Swelling
Inappropriate inflammatory response

48
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

Pathology (6 decks)

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