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ESA2 - Pathological Processes > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What are some features of acute inflammation?

A

Innate, immediate and early, stereotyped, short-duration

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2
Q

Why is acute inflammation initiated?

A

Initiated to limit the tissue damage (preserve itself)

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3
Q

What accumulates in tissues in acute inflammation?

A

Fluid exudate and neutrophils

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4
Q

What is acute inflammation controlled by?

A

A variety of chemical mediators derived from plasma or cells

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5
Q

What are some causes of acute inflammation?

A

Microbial infections, hypersensitivity reactions, physical agents, chemicals, tissue necrosis

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6
Q

What are the main clinical signs of acute inflammation?

A 
Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)
Loss of function
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7
Q

What changes occur in tissues in acute inflammation?

A

1) Changes in blood flow
2) Exudation of fluid into tissues
3) Infiltration of inflammatory cells

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8
Q

What changes in blood flow occur in acute inflammation?

A

1) Transient vasoconstriction of arteriole
2) Vasodilation of arterioles and then capillaries
3) Increased permeability of blood vessels
4) Increased viscosity of blood

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9
Q

What effect does the vasodilation of arterioles and capillaries have?

A

Increase in blood flow - heat and redness

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10
Q

What effect does the increased permeability of blood vessels have?

A

Exudation of protein-rich fluid into tissues and slowing of cirulation - swelling

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11
Q

What effect does the increased viscosity of blood have on the flow?

A

Flow slows

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12
Q

What is an example of a chemical mediator?

A

Histamine

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13
Q

What is histamine released from?

A

Mast cells, basophils and platelets

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14
Q

What is histamine released in response to?

A

Many stimuli eg physical damage, immunologic reactions, C3a, C5a, IL-1, factors from neutrophils and platelets

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15
Q

What does histamine cause?

A

Vascular dilation, transient increase in vascular permeability, pain

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16
Q

What is fluid flow across vessel walls determined by?

A

Balance of hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid

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17
Q

What does increased hydrostatic pressure result in?

A

Increased fluid flow out of the vessel

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18
Q

What does increased colloid osmotic pressure of interstitium result in?

A

Increased fluid flow out of the vessel

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19
Q

What is oedema?

A

Increased fluid in tissue spaces

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20
Q

Does oedema lead to increased or decreased lymphatic drainage?

A

Increased lymphatic drainage

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21
Q

How does exudate and transudate differ?

A

Exudate = fluid loss in inflammation = high protein content

Transudate = fluid loss due to hydrostatic pressure imbalance = low protein content (usually caused by cardiac failure)

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22
Q

What are some mechanisms of vascular leakage?

A

Endothelial contraction, cytoskeletal reorganisation, direct injurt, leukocyte dependent injury and increased transcytosis

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23
Q

What contributes to endothelial contraction?

A

Histamine, leukotrienes

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24
Q

What contributes to cytoskeletal reorganisation

A

Cytokines, IL-1 and TNF

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25
Q

What sorts of things can cause direct injury that leads to vascular leakage?

A

Toxic burns, chemicals - damage vessel walls

Eg sunburn

26
Q

What is VEGF?

A

Vascular endothelial growth factor - leads to increased transcytosis

27
Q

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

A

Neutrophil leucocyte

28
Q

What are neutrophils a type of?

A

Type of granulocyte (also known as polymorph)

29
Q

What are the four stages of the infiltration of neutrophils?

A

1) Margination
2) Rolling
3) Adhesion
4) Emigration

30
Q

What happens during the margination phase of neutrophil infiltration?

A

Stasis causes neutrophils to line up at the edge of blood vessels along the endothelium

31
Q

What happens during the rolling phase of neutrophil infiltration?

A

Neutrophils rolls along endothelium, sticking to it intermittendtly

32
Q

What happens during the adhesion phase of neutrophil infiltration?

A

Neutrophils stick to endothelium more avidly

33
Q

What happens during the emigration phase of neutrophil infiltration?

A

Neutrophils emigrate through blood vessel wall into tissue

34
Q

How do neutrophils escape from vessels?

A

Relaxation of inter-endothelial cell junctions and digestion of vascular basement membrane

35
Q

What is chemotaxis?

A

Movement along concentration gradients of chemoattractants

36
Q

Give some examples of chemotaxins

A

C5a, LTB4, bacterial peptides

37
Q

In the oxygen-dependent mechanism of killing, what is produced?

A

Superoxide and hydrogen peroxide

38
Q

What does the H2O2-Myeloperoxidase-halide system produce?

A

HOCl

39
Q

What are involved in the oxygen-independent killing mechanism

A

Lysozyme and hydrolass, BPI, cationic proteins

40
Q

Where are proteases produced?

A

Liver

41
Q

What are the 3 main families of proteases involved in acute inflammation?

A

Kinins, complement system and coagulation/fibrinolytic system

42
Q

What are prostaglandins/leukotrienes metabolites of?

A

Arachidonic acid

43
Q

What are cytokines/chemokines produced by?

A

White blood cells

44
Q

What are 2 important cytokines?

A

Interleukin-1 and TNF alpha

45
Q

What chemical mediators are important in the increase of blood flow?

A

Histamine and prostaglandins

46
Q

What chemical mediators are important in vascular permeability?

A

Histamine and leukotrienes

47
Q

What chemical mediators are important in neutrophil chemotaxis?

A

C5a, LTB4, bacterial peptides

48
Q

What chemical mediator is important in phagocytosis?

A

C3b

49
Q

How does exudation of fluid combat injury?

A

Delivers plasma proteins (fibrogen, inflammatory mediators, immunoglobulins) to area of injury

Dilutes toxins

Increases lymphatic drainage - delivers microbes to phagocytes and antigens to immune system

50
Q

How does infiltration of cells (polymorphs and macrophages) combat injury?

A

Removes pathogenic organisms and necrotic debris

51
Q

How does vasodilation combat injury?

A

Increases delivery and increases temperature

52
Q

How does pain/loss of function combat injury?

A

Enforces rest and reduces change of further traumatic damage

53
Q

What are some local complications of acute inflammation?

A

Swelling - can lead to blockage eg of bile duct
Exudate - compression eg cadiac tamponade and serositis
Loss of fluid - eg burns, easy to dehydrate
Pain and loss of function

54
Q

What are some systemic effects of acute inflammation?

A

Fever (production of endogenous pyrogens)
Leukocytosis
Acute phase response (decreased appetite, raised pulse etc)

55
Q

What are some acute phase proteins?

A 
C-reactive protein
a1-antitrypsin
Haptoglobin
Fibrinogen
Serum amyloid A protein
56
Q

What is shock?

A

A clinical syndrome of circulatory failure (can’t maintain BP and HR increases)

57
Q

What could happen after the development of acute inflammation?

A

1) Complete resolution
2) Continued acute inflammation with chrone inflammation (eg abscess)
3) Chronic inflammation and fibrous repair
4) Death

58
Q

If acute inflammation is resolved, what happens to the exudate and fibrin?

A

Exudate drains to lymphatics, fibrin degraded by plasmin

59
Q

What is ascites?

A

Oedema in peritoneum

60
Q

What are some examples of disorders of acute inflammation?

A

Hereditary angio-oedema
Alpha1 antitrypsin deficiency
Inherited complement deficiencies
Defects in neutrophil function/numbers

ESA2 - Pathological Processes (9 decks)

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