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PP A > Session 2 Lecture 1 > Flashcards

Session 2 Lecture 1 Flashcards

1
Q

Define acute inflammation

A
  • Response of living tissue to injury
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2
Q

Describe some features of acute inflammation

A

Innate, immediate, early, stereotypes (always the same) and has a short duration (minutes/hours/few days).

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3
Q

What is the purpose of acute inflammation?

A
  • Protect the body against infection
  • Clear tissue damage
  • Initiate tissue repair
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4
Q

What controls acute inflammation?

A

Chemical mediators

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5
Q

What are the causes of acute inflammation?

A
  • Foreign bodies
  • Immune reaction
  • Infection
  • Tissue necrosis
  • Trauma
  • Physical and chemical agents
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6
Q

What are the clinical signs of acute inflammation in Latin?

A

Rubor, tumor, calor, dolor and loss of function

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7
Q

Rubor

A

Redness

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8
Q

Tumor

A

Swelling

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9
Q

Calor

A

Heat

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10
Q

Dolor

A

Pain

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11
Q

What are the phases of acute inflammation

A
  1. Vascular phase

2. Cellular phase

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12
Q

What are the tissue level changes that occur in acute inflammation?

A
  1. Changes in blood flow
  2. Exudation of fluid into tissues
  3. Infiltration of inflammatory cells
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13
Q

What is the first part of vascular phase of inflammation?

A

Changes in blood flow

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14
Q

What is the second part of the vascular phase of inflammation?

A

Exudation of fluid into tissues

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15
Q

Give an overview of what happens in acute inflammation

A
  1. Transient vasoconstriction of arterioles
  2. Vasodilation of arterioles and then capillaries
  3. Increased permeability of blood vessels
  4. Conc of RBC in the small vessels increases
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16
Q

What is a chemical mediator that is important in acute inflammation?

A

Histamine - responsible for the immediate early response

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17
Q

Where is histamine released from?

A

Mast cells, basophils and platelets

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18
Q

When is histamine released?

A

IN response to many stimuli: physical damage; immunological reactions; C3a, C5a, IL-1; factors from neutrophils and platelets.

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19
Q

What does histamine cause?

A
  • Vascular dilatation
  • Transient increases in vascular permeability
  • Pain
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20
Q

What is Starling’s law?

A

Fluid flow across vessel walls is determines by the balance of hydrostatic and colloid osmotic pressure comparing plasma ad interstitial fluid.

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21
Q

What happens with increased hydrostatic pressure?

A

Increase fluid out of the vessel

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22
Q

What happens with increased colloid osmotic pressure on interstitium?

A

Increased fluid flow out of vessel

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23
Q

Explain/ describe how you can get oedema in acute inflammation?

A
  • Arteriolar dilatation leads to inc hydrostatic pressure
  • Inc permeability of vessel walls leads to loss of protein into interstitium
  • Net flow of fluid out of the vessel leads to oedema
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24
Q

Define oedema

A

Excess fluid in interstitium

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25
Q

What are the two different types of oedema?

A
  • Transudate

- Exudate

26
Q

Transudate oedema

A

Oedema has a lower protein content than the plasma.

- Caused when the fluid loss is due to hydrostatic pressure imbalance only

27
Q

Exudate oedema

A

Oedema has a higher protein content than plasma

- caused when you have fluid loss due to inflammation

28
Q

What causes endothelial contraction?

A

Histamine and leukotrienes

29
Q

What causes cytoskeleton reoganisation?

A

Cytokines, IL-1 and TNF

30
Q

What causes increased transcytosis?

A

VEGF

31
Q

What are the different mechanisms of vascular leakage?

A
  • Endothelial contraction
  • Cytoskeletal reorganisation
  • Direct injury
  • Leukocyte dependent injury
  • Increased transcytosis
32
Q

What delivers plasma proteins to the site of injury?

A

Fibrin

33
Q

What is fibrin?

A
  • Part of the haemostatic cascade

- Crucial to blood clotting because it causes a sticky meshwork to form. Good way to localise inflammation.

34
Q

What is the primary type of white blood cell that is involved in inflammation?

A

Neutrophils

35
Q

What are neutrophils?

A

Type of granulocyte

36
Q

What part of inflammation are neutrophils involved in?

A

Cellular phase

37
Q

What are the different steps to the infiltration of neutrophils?

A

Margination, Rolling, Adhesion and Emigration

38
Q

How do neutrophils escape from vessels?

A
  • Relaxation of inter-endothelial cells junctions
  • Digestion of vascular basement membrane
  • Movement
39
Q

How do neutrophils move?

A

Chemotaxis

40
Q

What is chemotaxis?

A

The movements along concentration gradients of chemoattractants.

41
Q

What do neutrophils do?

A

Phagocytosis

42
Q

What are the different stages of phagocytosis?

A

Contact, recognition and internalisation

43
Q

What facilitates the process of recognition?

A

Opsonisation

44
Q

What are the two main killing mechanisms?

A
  • Oxygen dependent

- Oxygen independent

45
Q

What are the main groups of chemical mediators involved in acute inflammation?

A
  • Proteases
  • Protaglandins/leukotrienes
  • Cytokines/chemokines
46
Q

What are the different types of proteases?

A
  • Kinins
  • Complement system C3a, C5a
  • Coagulation/fibrinolytic system
47
Q

Which chemical mediators increase blood flow?

A

Histamine and prostaglandins

48
Q

Which chemical mediators cause vascular permeability?

A

Histamine and leukotrienes

49
Q

Which chemical mediators cause neutrophil chemotaxis?

A

C5a, LTB4, bacterial peptides

50
Q

Which chemical mediators cause phagocytosis?

A

C3b

51
Q

What is the hallmark of acute inflammation?

A
  1. Exudate of oedema fluid

- Infiltrate of inflammatory cells

52
Q

How does exudation of fluid combat injury?

A
  • Delivers plasma proteins to area of injury
  • Dilutes toxins
  • Increases lymphatic drainage
53
Q

How does infiltration of cells combat injury?

A

Removes pathogenic organisms, necrotic debris

54
Q

How does vasodilation help combat injury?

A

Increases delivery and increases temperature

55
Q

How does pain and loss of function help combat injury?

A

Enforces rest, reduces chance of further traumatic damage

56
Q

What are the local complications of acute inflammation?

A
  • Swelling - blockage of tubes eg bile duct
  • Exudate - compression
  • Loss of fluid - burns
57
Q

What are the systemic effects of acute inflammation?

A
  • Fever

- Leukocytosis

58
Q

Define shock

A

A clinical syndrome of circulatory failure

59
Q

What might happen after the development of acute inflammation?

A
  • Complete resolution
  • Continued acute inflammation
  • Chronic inflammation and fibrous repair
  • Death
60
Q

What are the mechanisms of resolution?

A
  • All mediators of acute inflammation have short half lives
  • May be inactivated by degredation
  • Inhibitors may bind

PP A (13 decks)

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