Acute Inflammation Flashcards

(38 cards)

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
What process is neutrophil involved in
Phagocytosis 1.Phagosome fuses with lysosome 2. Produce secondary phagolysosomes 3. Release inflammatory mediators
26
How do neutrophils recognise what to phagocyte
Via Opsonisation (labelling pathogen) -Toxin covered in C3b (compliment capsule) & Fc (opsonins) -Corresponding receptors for C3b and Fc on neutrophil surface
27
What are inflammatory mediators
Chemical messengers -control and co-ordinate the inflammatory response -varying chemical structures, overlapping functions
28
Where do inflammatory mediators originate from
Activated inflammatory cells Platelets Endothelial cells Toxins
29
Which inflammatory mediators are involved in ‘VASODILATION’
Vasodilation: Histamine Serotonin Prostaglandins Nitric oxide
30
Which inflammatory mediators are involved in ‘VASCULAR PERMEABILITY’
Vascular permeability: Histamine Bradykinin Leukotrienes C3a & C5a
31
Which inflammatory mediators are involved in ‘CHEMOTAXIS’
C5a, LTB4 TNF-a (tumour necrosis factor) IL-1(interleukin 1) Bacterial peptides
32
Which inflammatory mediators are involved in ‘PYROGEN’
IL-1 IL-6 TNF-a
33
Which inflammatory mediators are involved in ‘PAIN’
Bradykinin Substance P Prostaglandins
34
What happens after acute inflammation
1. Complete resolution 2. Repair with connective tissue (FIBROSIS) 3. Progression to chronic inflammation
35
What happens after acute inflammation
1. Complete resolution 2. Repair with connective tissue (FIBROSIS) 3. Progression to chronic inflammation
36
What is opsonin
Coats foreign material and make them easy to phagocyte
37
Examples of opsonins
C3b Fc
38
Diapedesis
Emigration of leucocytes out of venues