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acute inflammation Flashcards

1
Q

define inflammation

A

the local physiological response to tissue injury (a reaction to injury involving cells such as neutrophils and macrophages - from lec)

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2
Q

give examples of cells involved in inflammation

A

neutrophils, macrophages, lymphocytes, endothelial cells, fibroblasts

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3
Q

give features of neutrophils

A

short-lived
first inflammatory cells in acute inflammation
cytoplasmic granules with enzymes that kill bacteria
dise at the scene of inflammation
release chemokine (that attract other inflammatory cells e.g. macrophages)

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4
Q

give features of acute inflammation

A 
sudden onset
short duration 
usually resolves
neutrophils 
dilation of vessels
exudate- vascular leakage of protein rich fluid
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5
Q

give features of chronic inflammation

A

slow onset/sequel to acute
long duration
may never resolve/slow resolution
lymphocytes, plasma cells and macrophages

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6
Q

neutrophils do not carry out phagocytosis? T or F

A

False

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7
Q

what do endothelial cells do in inflammation?

A

become sticky to allow inflammatory cells to adhere to them
become porous to allow inflammatory cells to pass into tissues
grow into areas of damage to form new capillaries

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8
Q

what happens to capillaries in inflammation and why

A

they fill with blood as there is vasodilation of arterioles and opening of pre-capillary sphincters

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9
Q

why is there oedema?

A

as the endothelial lining becomes more porous, plasma protein leaves the vessels and fluid leaves the vessels by osmosis, as the oncotic pressure is greater outside the vessels

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10
Q

What are the steps of migration of neutrophils?

A
  1. margination of neutrophils
  2. pavemetation of neutrophils
  3. pass between endothelial cells
  4. pass through basal lamina and migrate into adventitia
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11
Q

What systems are interlinked in inflammation?

A

Four plasma enzymatic cascade systems:

coagulation, fibrinolytic, kinin and complement

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12
Q

give an example of acute inflammation and info about it

A 
acute appendicitis 
unknown cause
neutrophils
dilation of blood vessels
inflammation of serial surfaces
pain
result:
1. appendix surgically removed  2. inflammation resolves
3. appendix bursts giving generalised peritonitis and possible death
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13
Q

give examples of the stages of acute peritonitis

A
  1. oedema and swelling with dilated blood vessels
  2. pus
  3. rupture of contents
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14
Q

what is the difference between exudate and transudate?

A

exudate has a high protein content because they result from increased vascular permeability
transudates have a low protein content as the vessels have normal permeability characteristics

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15
Q

give an example of a drug use for inflammation

A

ibuprofen (NSAIDs)

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16
Q

what are the beneficial effects of inflammation?

A

destruction of invading microorganisms

walling off of an abscess cavity, preventing spread of infection

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17
Q

What are the harmful effects of inflammation?

A
  1. may produce disease
    e. g. an abscess in the brain may act as a space-occupying lesion, compressing vital surrounding structures
  2. fibrosis from chronic inflammation may distort the tissues and permanently alter their function
  3. digestion of normal tissues
  4. swelling
  5. inappropriate inflammatory response
18
Q

define acute inflammation

A

initial and often transient series of tissue reactions to injury

19
Q

chronic inflammation

A

subsequent and prolonged tissue reactions following the initial response (beware though not always following acute inflammation)

20
Q

causes of acute inflammation

A

microbial infections -pyogenic bacteria and viruses
hypersensitivity reactions - parasites, tubercle bacilli
physical agents - trauma, ionising radiation, heat, cold
chemicals - corrosives, acids, alkalis, reducing agents
tissue necrosis - ischaemic infarction (due to peptides released from dead tissue)
bacterial toxins that lead directly to inflammation

21
Q

define hypersensitivity reaction

A

occurs when an altered state of immune responsiveness causes an inappropriate or excessive immune reaction that damages tissues

22
Q

what are the essential macroscopic appearances of acute inflammation?

A 
Rubor
Calor
Tumor
Dolor
loss of function
23
Q

explain rubor

A

dilation of small blood vessels within the damaged area

24
Q

explain calor

A

hyperaemia in periphery due to vasodilation

systemic fever due to chemical mediators of inflammation

25
Q

explain tumor

A

this is selling of the area due to oedema - the accumulation of fluid in the extravascular space due to fluid exudate
also from the physical mss of inflammatory cells migrating to the area
formation of connective tissue contributes to swelling in later stages

26
Q

explain dolor

A

pain

  1. from stretching and situation of tissues due to oedema and pus under pressure in an abscess cavity
  2. chemical mediators e.g. bradykinin, prostaglandins and serotonin cause pain
27
Q

explain loss of function

A
  1. movement inhibited by pain

2. severe swelling may physically immobilise the tissues

28
Q

what three processes are important in acute inflammation?

A
  1. change in vessel calibre and flow
  2. increased vascular permeability and formation of the fluid exudate
  3. formation of the cellular exudate - neutrophils
29
Q

what are the three causes of increased vascular permeability?

A
  1. immediate transient chemical mediators e.g. histamine, bradykinin, NO, C5a, leukotriene, PAF
  2. immediate sustained severe direct vascular injury e.g. trauma
  3. delayed prolonged endothelial cell injury - x-rays, bacterial toxins
30
Q

What causes neutrophil adhesion to the endothelial surface?

A

histamine and thrombin, interleukins, C5a, leukotriene and PAF
cause up-regulation of adhesion molecules on the surface of endothelial cells

31
Q

What do endogenous chemical mediators cause?

A 
vasodilation
emigration of neutrophils
chemotaxis
increased vascular permeability
itching and pain
32
Q

Name some endogenous chemical mediators that cause vasodilation

A 
histamine
VIP
NO
PAF
prostaglandins
33
Q

Name some endogenous chemical mediators that cause increased vascular permeability

A 
histamine
bradykinin
NO
C5a
leukotriene B4
PAF
34
Q

name some endogenous chemical mediators that cause neutrophil chemotaxis

A

leukotriene B4

Il-8

35
Q

name special macroscopic appearances of acute inflammation

A 
serous
suppurative 
membranous
pseudomembranous
necrotising (gangrenous)
So Special Macroscopic Parts Now
36
Q

what are the outcomes of acute inflammation?

A

resolution
suppuration
organisation
progression to chronic inflammation

37
Q

what are the systemic effects of acute inflammation?

A 
pyrexia
constitutional symptoms
weight loss
reactive hyperplasia of the RES
haematological changes
amyloidosis
38
Q

what is resolution?

A

complete restoration of tissue to normal

39
Q

what is suppuration?

A

formation of pus - living and dead neutrophils, bacteria, cell debris, e.g. abscess

40
Q

What is organisation?

A

replacement of tissue by granulation tissue as part of repair (granulation tissue consists of small blood vessels in a connective tissue matrix with myofibroblasts)

41
Q

why does acute inflammation sometimes progress to chronic?

A

causative agent not removed

Pathology (11 decks)

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