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Y2 MECHANISMS OF DISEASE > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is inflammation and what is its aim?

A

it is protective response to injury

it aims to rid the body of the initial cause of injury and the consequences of such injury

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2
Q

What suffix indicates that inflammation is present?

A

itis

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3
Q

What is acute inflammation and how long does it last for?

A

it is the initial tissue reaction to injury

it is short-lived - mins, hrs, days

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4
Q

What is the characteristic cell of acute inflammation?

A

the neutrophil polymorph

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5
Q

What will acute inflammation deliver to the injured site?

A

White cells and plasma proteins (e.g. antibodies)

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6
Q

What are the 5 physical characteristics of acute inflammation?

A
  1. redness (rubor)
  2. heat (calor)
  3. swelling (tumor)
  4. pain (dolor)
  5. loss of function (functio laesa)
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7
Q

What are the 5 main causes of acute inflammation?

A
  1. physical agents
  2. infection
  3. hypersensitivity reactions
  4. chemicals
  5. tissue necrosis
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8
Q

What are examples of physical agents that can cause acute inflammation?

A

thermal injuries e.g. burns, frostbite

physical trauma

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9
Q

How can a hypersensitivity reaction cause acute inflammation?

A

the immune system damages the individual’s own tissues

this is persistent and difficult to cure as the stimulus cannot be removed

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10
Q

What is involved in the fibrinous reaction of the inflammatory response?

A

Fibrinogen leaks out of the blood vessels and comes into contact with extracellular tissues where it forms fibrin strands

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11
Q

What is the consequence of serous inflammation?

A

thin fluid from plasma or mesothelial cell secretions

accumulation of fluid results in effusion

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12
Q

What are the 3 major components of acute inflammation?

A
  1. changes in vessel calibre
  2. increased vascular permeability and fluid exudate formation
  3. cellular exudate formation
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13
Q

Why do vessels undergo changes in acute inflammation?

A

to maximise the movement of plasma proteins and cells into the site of injury

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14
Q

What causes most of the swelling in acute inflammation?

A

the fluid exudate

the cellular exudate only contributes slightly to the swelling

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15
Q

What is the definition of exudate?

A

extravascular fluid with high protein concentration, containing cellular debris

it implies inflammation

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16
Q

What is the definition of transudate?

A

extravascular fluid with low protein concentration and little or no cellular component

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17
Q

What is the definition of oedema?

A

excess fluid in the interstitial tissue/serous cavities

this can be exudate or transudate

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18
Q

What is the definition of pus?

A

inflammatory exudate rich in neutrophils, dead cell debris and microbes

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19
Q

What is the initial change in vessel calibre at the onset of acute inflammation?

A

There is a very short initial transient vasoconstriction

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20
Q

What happens after the initial transient vasoconstriction?

A

Vasodilation that lasts from 15 mins to several hours

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21
Q

What is the result of vasodilation in acute inflammation?

A

it increases blood flow to the injured area by up to 10 times

this produces heat and redness

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22
Q

How is vasodilation in acute inflammation mediated?

A

by histamine and nitrous oxide on vascular smooth muscle

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23
Q

What causes formation of the fluid exudate?

A

increased permeability of microvasculature results in the escape of protein rich fluid into the tissue

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24
Q

What are the 3 main causes of fluid exudate formation?

A
  1. chemical mediators - histamine, NO and leukotriene
  2. direct vascular injury
  3. endothelial injury
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25
Q

Normally, how does hydrostatic pressure vary in the capillary beds?

A

High hydrostatic pressure at the arteriole end due to plasma proteins forces fluid out

The fluid returns to the vessel at the venous end, where hydrostatic pressure is low

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26
Q

In acute inflammation, how does hydrostatic pressure in the capillary beds change?

A

There is increased hydrostatic pressure, meaning fluid cannot return at the venous end

Plasma proteins escape into the extravascular space, increasing osmotic pressure

This leads to exudation - more fluid leaving the vessel

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27
Q

How does the fluid exudate help with treatment of acute inflammation?

A

It allows for transport of drugs to the injured area

Increased blood flow allows drugs to rapidly reach the injured area

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28
Q

What are the other effects of the fluid exudate?

A
  1. it dilutes toxins
  2. it allows entry of antibodies
  3. it helps in fibrin formation
  4. it allows delivery of nutrients and oxygen to the injured tissue
  5. it stimulates the immune response
29
Q

What is the role of fibrin in acute inflammation?

A

it provides a scaffold for the formation of granulation tissue

this is the start of the healing process

30
Q

What is the turnover of the fluid exudate like?

A

It has a high turnover

31
Q

How does the viscosity of the blood change in acute inflammation?

A

The loss of fluid into the tissues increases the cell:fluid ratio

The blood becomes more viscous and the flow of blood slows down

32
Q

How do neutrophils usually travel along a blood vessel?

A

They travel in the axial stream

This is in the central part of blood vessels

33
Q

What are the 4 stages in formation of the cellular exudate?

A
  1. margination of neutrophils
  2. pavementing of neutrophils
  3. neutrophils pass between endothelial cells
  4. neutrophils pass through the basal lamina and into adventitia
34
Q

What is margination of neutrophils and when does it start?

A

it begins when the blood becomes more viscous

This is where neutrophils come to lie closer to the endothelial cells

35
Q

What is pavementing of neutrophils?

A

The neutrophils roll along the endothelium and eventually stick to the endothelial cells

36
Q

How are gaps in the endothelial cells created?

A

they are either chemically mediated or there is direct trauma to the blood vessel

37
Q

What chemicals are involved in rolling and pavementing of neutrophils?

A

selectins are involved in rolling

integrins are involved in pavementing

38
Q

What is meant by neutrophils moving by chemotaxis?

A

they respond to chemicals and move in a certain way depending on the chemical they are attracted to

39
Q

Where are neutrophils produced and how does their presence vary in acute inflammation?

A

they are produced in the bone marrow

they are increased in acute inflammation

40
Q

What is the lifespan of a neutrophil?

A

the lifespan is short

they live for hours in tissues

41
Q

What is the term used to describe movement of neutrophils?

A

they move by an amoeboid process

42
Q

Why may a full blood count be performed in acute inflammation?

A

an increase in the number of white cells (neutrophils) is indicative of acute inflammation

43
Q

What are the 4 roles of chemical mediators in acute inflammation?

A
  1. vasodilatation
  2. migration of neutrophils
  3. chemotaxis
  4. increased vascular permeability
44
Q

What are the 5 cell derived mediators of acute inflammation?

A
  1. histamine
  2. prostaglandins
  3. lysosomal components
  4. leukotrienes
  5. cytokines
45
Q

What are the 4 plasma derived mediators of acute inflammation?

A
  1. complement system
  2. kinin system
  3. coagulation system
  4. fibrinolytic system
46
Q

What is the role of histamine in acute inflammation?

A

it is released by mast cells and increases vascular dilation and permeability

47
Q

What are prostaglandins?

A

long chain fatty acids from arachidonic acid

48
Q

What are leukotrienes and what is their role in acute inflammation?

A

derived from arachidonic acid

they have vasoactive properties

49
Q

What is the role of aspirin in treating acute inflammation?

A

It inhibits cyclooxygenase

This prevents production of prostaglandins that cause vasodilation

50
Q

What is the role of glucocorticoid steroids in treating inflammation?

A

they move into cells and suppress the proteins that go on to promote inflammation

51
Q

What is the difference between COX-1 and COX-2?

A

COX-1 protects the stomach lining

COX-2 plays a role in inflammation

52
Q

How do NSAIDs prevent acute inflammation?

A

They inhibit COX-1 and COX-2 to relieve pain and inflammation

53
Q

What is the function of leukotriene receptor antagonists?

A

They inhibit 5-lipooxygenase inhibitors

54
Q

What is the role of 5-lipooxygenase?

A

It is involved in producing leukotrienes

These cause vasoconstriction, bronchospasm and increased permeability

55
Q

What are the 4 general effects of acute inflammation?

A
  1. pyrexia
  2. lymph node enlargement
  3. nausea, malaise, anorexia
  4. leukocytosis
56
Q

What is pyrexia?

A

high temperature

57
Q

What is leukocytosis?

A

a raised white cell count

58
Q

What is an erythrocyte sedimentation rate used to measure?

A

how quickly erythrocytes settle at the bottom of a test tube

59
Q

What can an erythrocyte sedimentation rate be used to measure in acute inflammation?

A

Normally red blood cells settle relatively slowly

A faster-than-normal rate that may indicate inflammation in the body

60
Q

What are acute phase proteins?

A

Plasma proteins which change in circulating concentrations in response to inflammation

61
Q

How can C-reactive protein be used to detect inflammation?

A

A high level of CRP in the blood is a marker of inflammation

62
Q

What are the 3 harmful effects of acute inflammation?

A
  1. digestion of normal tissues
  2. swelling
  3. inappropriate inflammatory response
63
Q

What is systemic inflammatory response syndrome (SIRS)?

A

Clinical criteria for sepsis/septic shock

64
Q

What are the SIRS criteria?

A

Two of the following must be present:

  1. temperature > 38.5 or < 36
  2. tachycardia
  3. tachypnea
  4. abnormal leukocyte count or >10% immature cells
65
Q

What is acute respiratory distress syndrome?

A

ARDS is a type of respiratory failure characterised by rapid onset of widespread inflammation in the lungs

66
Q

What are the common symptoms of ARDS?

A
  1. shortness of breath
  2. rapid breathing
  3. bluish skin coloration
67
Q

What happens in chronic granulomatous disease?

A

cells of the immune system have difficulty forming reactive oxygen compounds used to kill certain ingested pathogens

this leads to the formation of granulatomata in organs

68
Q

What is hereditary angioedema?

A

a disease characterised by recurrent episodes of severe swelling

69
Q

What is amyloidosis?

A

a group of rare, serious conditions caused by a build-up of abnormal amyloid protein in organs and tissues

Y2 MECHANISMS OF DISEASE (36 decks)

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