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PP > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Inflammation

A

response of living tissue to injury

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2
Q

Two phases of inflammation

A

Vascular phase
Cellular phase

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3
Q

Describe the the vascular phase

A

Changes in blood flow
Accumulation of exudate

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4
Q

Cellular phase

A
  1. Removal of pathogens, necrotic tissue
    (e.g. delivery of neutrophils)
  2. Release inflammatory mediators
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5
Q

What causes inflammation

A

Trauma
Hypersensitivity
Micro-organisms
Necrosis

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6
Q

What happens in the vascular phase

A
  1. Vasoconstriction (sec)
  2. Vasodilation (min)
  3. Increased permeability
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7
Q

Hydrostatic pressure

A

Pressure exerted on a vessel wall by fluid
(Pushed fluid away)

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8
Q

Oncotic pressure

A

Pressure exerted by proteins
(Draws fluid towards)

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9
Q

Signs of acute inflammation

A

Rubor, tumour, calor, dolor, loss of function

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10
Q

Explain the tissue changes that occur in acute inflammation

A
  1. ⬆️ capillary hydrostatic pressure
  2. Plasma proteins move into interstitium,
    　⬆️ Interstitial oncotic pressure
  3. Fluid moves OUT of vessel INTO interstitium
    　➡️OEDEMA
  4. Movement of fluid OUT of vessel
  5. Reduced flow through vessel
    ➡️ STASIS
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11
Q

Types of interstitial fluid

A

Exudate
Transudate

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12
Q

Difference between exudate and transudate

A

Exudate is protein rich, ⬆️vascular permeability, occurs in inflammation

Transudate is due to ⬆️capillary hydrostatic pressure/⬇️capillary oncotic pressure, vascular permeability unchanged, occurs in heart, hepatic, renal failure

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13
Q

How is the vascular phase in acute inflammation effective

A

-Interstitial fluid dilutes toxins
-Exudate delivers proteins such as immunoglobulins
-Carry antigens to lymph nodes

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14
Q

Features of neutrophil

A

-Primary WBC involved in acute inflammation
-Trilobed nucleus

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15
Q

List the key chemical mediators involved in acute inflammation

A
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16
Q

How do neutrophils escape vessels

A

Margination
Rolling
Adhesion
Emigration (Diapedesis)

17
Q

Typical features of inflammation

A

Immediate
Short duration
Innate
Stereotyped
Limits damage

18
Q

What is the ‘Starling’s Law’

A

Movement of fluid is controlled by the balance of hydrostatic pressure and oncotic pressure

19
Q

How is the vascular phase effective

A

-Interstitial fluid dilutes toxins
-Exudate deliver proteins
(e.g. Fibrin- mesh limits spread of toxin,
Immunoglobulins- from adaptive immune response)
Carry antigens to lymph nodes)

20
Q

What are the adhesion molecules involved in the cellular phase of acute inflammation

A

Selectins
Integrins

21
Q

Which processes are the adhesion molecules responsible for

A

Selectins- rolling
Integrins- adhesion

22
Q

How is selectin involved in the cellular phase of acute inflammation

A

-Expressed on activated endothelial cells
-Cells activated by chemical mediators

23
Q

How is integrin involved in the cellular phase of acute inflammation

A

-Found on neutrophil surface
-Change from low to high affinity state

24
Q

How do neutrophils move through the interstitium

A

Chemotaxis:
Movement along an increasing chemical gradient of chemoattractants

25
Q

What process is neutrophil involved in

A

Phagocytosis
1.Phagosome fuses with lysosome
2. Produce secondary phagolysosomes
3. Release inflammatory mediators

26
Q

How do neutrophils recognise what to phagocyte

A

Via Opsonisation (labelling pathogen)

-Toxin covered in C3b (compliment capsule) & Fc (opsonins)
-Corresponding receptors for C3b and Fc on neutrophil surface

27
Q

What are inflammatory mediators

A

Chemical messengers

-control and co-ordinate the inflammatory response
-varying chemical structures, overlapping functions

28
Q

Where do inflammatory mediators originate from

A

Activated inflammatory cells
Platelets
Endothelial cells
Toxins

29
Q

Which inflammatory mediators are involved in ‘VASODILATION’

A

Vasodilation:
Histamine
Serotonin
Prostaglandins
Nitric oxide

30
Q

Which inflammatory mediators are involved in ‘VASCULAR PERMEABILITY’

A

Vascular permeability:
Histamine
Bradykinin
Leukotrienes
C3a & C5a

31
Q

Which inflammatory mediators are involved in ‘CHEMOTAXIS’

A

C5a, LTB4
TNF-a (tumour necrosis factor)
IL-1(interleukin 1)
Bacterial peptides

32
Q

Which inflammatory mediators are involved in ‘PYROGEN’

A

IL-1
IL-6
TNF-a

33
Q

Which inflammatory mediators are involved in ‘PAIN’

A

Bradykinin
Substance P
Prostaglandins

34
Q

What happens after acute inflammation

A
  1. Complete resolution
  2. Repair with connective tissue (FIBROSIS)
  3. Progression to chronic inflammation
35
Q

What happens after acute inflammation

A
  1. Complete resolution
  2. Repair with connective tissue (FIBROSIS)
  3. Progression to chronic inflammation
36
Q

What is opsonin

A

Coats foreign material and make them easy to phagocyte

37
Q

Examples of opsonins

A

C3b
Fc

38
Q

Diapedesis

A

Emigration of leucocytes out of venues

PP (15 decks)

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