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Animal Body 2 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

When can inflammation start to cause a problem?

A

When the reaction is very strong, it is prolonged and it is inappropriate

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2
Q

What part of the immune system is inflammation a part of

A

Innate immune system

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3
Q

What is characteristic of acute inflammation

A

Fluid and plasma protein exudation, and neutrophilic leukocyte accumulation

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4
Q

What is characteristic of chronic inflammation

A

Influx of lymphocytes and macrophages, and associated vascular proliferation and fibrosis

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5
Q

Outline the 4 steps of initiating an inflammatory response

A
  1. Inflammatory stimuli
  2. PAMPs/DAMPs recognized by PRRs
  3. Activation of surveillance cells
  4. Release of mediators
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6
Q

Define exudation

A

Increased vascular dilation and permeability

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7
Q

Where does exudation happen in the vasculature

A

In capillaries and venules (NOT arterioles)

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8
Q

Define exudate

A

Extracellular fluid collection rich in proteins and/or cells

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9
Q

What are the events that lead to oedema in tissues

A

There is an altered balance in hydrostatic and osmotic pressure which causes an increase of fluid and plasma proteins in tissues - causing oedema

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10
Q

List 5 general features of inflammatory mediators

A
  1. Can be found inactive or active
  2. Some are newly synthesized
  3. Can act directly or indirectly
  4. Many give positive feedback
  5. Most have short half lives
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11
Q

What is a principle source of newly synthesized inflammation mediators

A

Leukocytes

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12
Q

Name 5 mediators of acute inflammation and if they’re preformed or not

A

Histamine (P)
Serotonin (P)
Cytokines (NS)
Leukotrienes (NS)
Prostaglandins (NS)

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13
Q

What are the two phases of changes in vascular dilation and what cells/molecules are responsible for both

A

Immediate - histamine, serotonin, complement and blood clotting factors
Delayed - kinins, prostaglandins and leukotrienes

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14
Q

Name the cytokine:
Key role in triggering inflammation, induces cardinal signs of inflammation, prolongs and amplifies inflammation

A

TNF-alpha

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15
Q

Name the cytokine:
Responsible (with TNF-alpha) for sickness behavior, causes fever, lethargy and lack of appetite

A

Interleukin-1

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16
Q

Name the cytokine:
Produced by innate immune cells after stimulation (e.g. by PAMPs), affects both inflammation and acquired immunity, and is major mediator of the acute-phase reaction of septic shock

A

Interleukin-6

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17
Q

Serous exudate

A

Watery, clear, cloudy and relatively low in protein

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18
Q

Fibrinous exudate

A

Abundant in fibrinogen, observed in more severe reactions of the lungs and connective tissues

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19
Q

Catarrhal exudate

A

Cloudy, thin mucinous, associated with inflammation of mucous membranes

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20
Q

Suppurative/purulent exudate

A

Associated with bacterial infection by pyogenic organisms, characterized by large amounts of pus, usually causes an abscess but sometime diffuses and causes cellulitis

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21
Q

Hemorrhagic exudate

A

Usually in organs with a rich vascular supply

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22
Q

Necrotizing exudate

A

May be the result of ischemia, thrombosis of vasculature or acute venous congestion, often caused by the presence of necrotizing toxins produced by bacteria

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23
Q

What are 4 functions of exudate

A
  1. Dilute toxins
  2. Distribute mediators/clotting factors
  3. Neutralize toxins
  4. Drainage to lymphatics
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24
Q

What is the term used to describe inflammation of the lymphatic vessels

A

Lymphangitis

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25
Q

What is the term used to describe inflammation of the lymph nodes

A

Lymphadenitis

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26
Q

Which cell type has a major population in blood leukocytes

A

PMNs (neutrophils)

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27
Q

Where do leukocytes exit the vasculature during extravasation

A

Through veins (not arteries)

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28
Q

What receptor is involved in the immediate pathway of neutrophil migration and what stimulates this pathway

A

P selectin
Stimulated by histamine, C5a and PAF at the site of injury

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29
Q

What receptor is involved in the delayed pathway of neutrophil migration and what stimulates this pathway

A

E selectin
Stimulated by IL-1, TNF-alpha and other chemo attractants at the site of injury

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30
Q

Name 3 functions of neutrophils during inflammation

A

Phagocytosis
Liquefaction by lysosomal enzymes
Amplification of inflammation by making PGs, LTs, and PAF

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31
Q

Why is monocyte migration slower than neutrophils

A

Because MCP-1 production is relatively slow and there are way more neutrophils than monocytes

32
Q

List 4 roles of macrophages in acute inflammation

A
  1. Phagocytosis
  2. Secrete toxic factors
  3. Secrete cytokines and chemokines to alert effector cells
  4. Secrete colony stimulating factors to promote differentiation of immature immune cells
33
Q

List the 5 systemic effects of acute inflammation

A

Leukocytosis
Acute phase response
Induction of fever
Anemia
Septic shock

34
Q

Describe the “shift to the left” of neutrophils during acute inflammation

A

Since the body is trying to compensate and replace neutrophils during infection, it releases them from the bone marrow before they are matured resulting in more immature neutrophils in circulation

35
Q

What is the acute phase response

A

Increased production of several plasma proteins by the liver

36
Q

Name 2 plasma proteins released during acute phase response and their function

A

C-reactive - bacterial clearance
Serum amyloid A - leukocyte migration

37
Q

What are 3 characteristics of septic shock

A

Fever
Increased vascular permeability
Disseminated intravascular coagulation (DIC)

38
Q

What is the difference between resolution and repair

A

Resolution - return to normal
Repair - formation of scar tissue

39
Q

What are the 3 broad groups of resolution mediators

A

Lipoxins, resolvins and protectins

40
Q

What are the precursors to resolvins and protectins

A

Fatty acids eicosapentanoic acid (only resolvins) and docosahexanoic acid

41
Q

What is the precursor of lipoxins and what is an example

A

Arachidonic acid
ex. LXA4

42
Q

When is LXA4 produced and by what

A

When neutrophils recognize PGE2 without an antigen present, it will product LXA4 which will stop further neutrophil recruitment and reduce vascular permeability

43
Q

How are resolvins and protectins anti-inflammatory

A

They induce PMNs to expose their PS apoptosis markers so their removed by macrophages

44
Q

Define macrophage switch

A

After a macrophage ingests an apoptotic PMN it will start releasing anti-inflammatory and reparative cytokines

45
Q

What mediates regeneration and what produces them

A

Wound cytokines (TGF-beta, VEGF) - produced by macrophages

46
Q

What produces a fibrous scar

A

Granulation tissue

47
Q

What is granulation tissue

A

Small, red granular foci that bleed easy
Newly formed blood vessels that proliferate
Fibroblast proliferation
New connective tissue production

48
Q

What is suppuration

A

It is pus formation from intense and prolonged neutrophil emigration that happens when pyogenic bacteria resist uptake

49
Q

What are two events leading to chronic inflammation

A

Persistent suppuration and a foreign body response

50
Q

What characterizes chronic inflammation

A

A progressive change of cell types present at the site of inflammation and simultaneous destruction and repair of the tissues

51
Q

Name 3 common denominators of chronic inflammation

A

Persistent infection, autoimmune reactions and prolonged foreign body responses

52
Q

Name 4 cellular mediators of chronic inflammation

A

T cells, B cells, Monocytes/macrophages and NK cells (mononuclear cells)

53
Q

Which receptors mediate lymphocyte migration in chronic inflammation

A

VLA-4 (lymphocyte) and VCAM-1 (vasculature)

54
Q

How do T helper cells help propagate the immune response and how are they activated

A

Macrophages and dendritic cells present antigens to Th cells which then become active and secrete cytokines that stimulate other cell populations (B cells, CD8 cells and macrophages)

55
Q

Which chemical effector promotes lymphocyte/monocyte migration through the endothelia during chronic inflammation

A

IFN-gamma

56
Q

What mediates a foreign body reaction

A

Macrophages

57
Q

Define amyloidosis

A

A build up of abnormal protein (amyloid fibrils) in tissues

58
Q

Define amyloidosis in the context of chronic inflammation

A

Secondary/reactive amyloidosis happens as a complication of existing chronic inflammatory disease, and involves the deposition of serum amyloid A fragments (misfolded proteins that aggregate to insoluble fibrils)

59
Q

Which phase of the immune response is responsible for hypersensitivity reactions

A

The effector phase - late primary, chronic, or recall of the adaptive immune response

60
Q

Which hypersensitivity reaction is mediated by IgE antibodies

A

Type I

61
Q

Which hypersensitivity reaction is mediated by IgG or IgM

A

Type II

62
Q

Which hypersensitivity reaction is mediated by Ag/Ab complexes, IgG or IgM

A

Type III

63
Q

Which hypersensitivity reaction is mediated by antigen-specific T cells and macrophages

A

Type IV

64
Q

What response coordinates IgE mediated hypersensitivity reactions

A

Th2 response (associated with alternatively activated macrophages)

65
Q

Name 3 granulocytes involved in type I hypersensitivity

A

Eosinophils, mast cells and basophils

66
Q

What specific event happens to cause immediate hypersensitivity in type I reactions

A

Binding of the antigen to IgE and cross-linking of FceRI receptor on mast cells

67
Q

Define atopy

A

A predisposition to suffer IgE mediated allergic reactions

68
Q

Define anaphylaxis

A

Generally describes instances where the allergen is distributed systemically through blood circulation, rapid onset, mild to severe, systemic histamine release

69
Q

What is hypotonic shock

A

Reduced blood pressure - vascular consequence of anaphylaxis

70
Q

List 3 events that can happen during a type II hypersensitivity reaction

A
  1. opsonization via IgG abs
  2. opsonization/lysis via complement (MAC)
  3. Antibody-dependent (IgG) cell-mediated cytotoxicity
71
Q

List 2 examples of a type II hypersensitivity reaction

A
  1. Autoimmune hyperthyroidism
  2. Immune mediated thrombocytopenia
72
Q

What happens to cause Ag/Ab complexes to persist in circulation

A

There is no/little cross linking of Ag/Abs so the complexes are very small and therefore not cleared by the body (complement & phagocytosis)

73
Q

List 3 examples of type III hypersensitivity reactions

A
  1. Serum sickness
  2. Chronic obstructive pulmonary disease (COPD)
  3. Arthus reaction (vaccine reaction)
74
Q

When does the inflammatory response typically occur in type IV hypersensitivity reactions

A

24-48 hours after contact (in sensitized individuals)

75
Q

Which T cell response is seen in type IV hypersensitivity reactions

A

Th1 cell response

76
Q

What do macrophages differentiate into in granulomatous inflammation

A

Epithelioid cells and giant cells

77
Q

List 3 examples of type IV hypersensitivity reactions

A
  1. tuberculin reaction
  2. contact sensitivity
  3. granulomatous inflammation

Animal Body 2 (6 decks)

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