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Cell Pathology > 2. Inflammation > Flashcards

2. Inflammation Flashcards

1
Q

Inflammation

A

Reaction of living vascularised tissue to sub-lethal injury

A protective response geared towards removing cause and consequences of injury

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2
Q

What 5 cell types are involved in inflammation?

A 
Neutrophils
Macrophages
Lymphocytes
Eosinophils
Mast cells
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3
Q

What 4 soluble factors are involved in inflammation?

A

Antibodies
Cytokines
Complement system
Coagulation system

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4
Q

Acute inflammation

A

rapid non-specific response to cellular injury
Orchestrated by mediators released from injured cells
Leukocyte and vascular response

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5
Q

Chronic inflammation

A

Persistent inflammatory response
Ongoing inflammation and repair over weeks- years
May arise from acute inflammation

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6
Q

Name a specific subtype of chronic inflammation

A

Granulomatous

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7
Q

Which disease states are underlied by inflammatory processes?

A

Excessive / inappropriate inflammatory response e.g. Allergic reaction
Autoimmune diseases
Infection
Inadequate inflammatory response- immunocompromised
Trauma
Granulomatous diseases e.g. Crohns

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8
Q

Which disease states that are not primarily inflammatory does inflammation contribute to?

A

Atherosclerosis
Type II Diabetes
Cancer

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9
Q

How is acute inflammation recognised?

A

On examination by cardinal signs

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10
Q

What are the Cardinal signs?

A

Rubor (redness)
Calor (heat)
Tumor (swelling)
Dolor (pain)

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11
Q

3 main components of acute inflammation

A

Vasodilation
Increased vascular permeability
Emigration, accumulation and activation of leukocytes at the focus of injury

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12
Q

What causes heat and redness in acute inflammation?

A

Vasodilation

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13
Q

What induces vasodilation in inflammation?

A

Several mediators including histamine and nitric oxide

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14
Q

What has the richest source of histamine?

A

Mast cells

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15
Q

What triggers histamine release?

A

Triggered by binding of surface IgE to Fc receptors on mast cells
Antigens bind to the IgE and cause cross-linking and mast cell degranulation
Also: trauma, heat, cold, complement C3a/C5a, cytokines IL-1 / IL-8

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16
Q

Effects of histamine

A

Vasodilation and increased vascular permeability

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17
Q

Histamine dsyregulation can be seen in allergic reactions

A

Type 1 hypersensitivity

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18
Q

How is increased vascular permeability mainly achieved?

A

Endothelial cells contract, increasing inter-endothelial spacing
Also:
Histamine
Nitric Oxide

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19
Q

What can also cause increased vascular permeability?

A 
Endothelial cell injury (burns, toxins)
Leukocyte-mediated vascular injury (late stage inflammation)
Increased transcytosis (VEGF)
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20
Q

What does increased vascular permeability create?

A

Exudate

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21
Q

What is an exudate?

A

Fluid with high protein content and cellular debris, which leaves vessels and deposits in tissues or on tissue surfaces

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22
Q

What is transudate created by?

A

Increased hydrostatic pressure

Decreased osmotic pressure

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23
Q

What does transudate contain?

A

Ultrafiltrate of blood plasma
Low protein content
Low specific gravity
Low cell content

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24
Q

What does exudate serve to do?

A

Dilute pathogens
“Wall off” pathogens
Permit spread of soluble inflammatory mediators
Provide substrate for inflammatory cell migration

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25
Q

Which are the most important leukocytes in the initial phase of typical acute inflammation?

A

Those capable of phagocytosis

Neutrophils and Macrophages

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26
Q

Why are neutrophils and macrophages the most important leukocytes in the initial phase of typical acute inflammation?

A

Kill bacteria and eliminate foreign and necrotic material

Produce multiple factors and mediators that interact with other cells

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27
Q

Where are neutrophils produced?

A

Bone marrow

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28
Q

Which cells are usually 1st to a damaged area?

A

Neutrophils

29
Q

How are the main roles of a neutrophil (kill bacteria and recruit additional cells) achieved?

A

Phagocytosis

Degranulation- enzymes, free radicals, soluble mediators

30
Q

How do leukocytes exit a vessel lumen to reach site of injury? (Extravasation)

A

Margination- move away from middle of lumen, come to edge
Rolling
Adhesion to activated endothelium
Transmigration (diapedesis) across endothelium through vessel wall
Migration through tissues towards chemotactic stimulus

31
Q

What do leukocytes do once at site of injury?

A

Recognise microbes and necrotic tissue

Activate to ingest and destroy microbes and necrotic tissue whilst amplifying inflammatory response

32
Q

Which receptors in leukocytes may be activated once at site of injury?

A 
Toll-like receptors for certain microbial products e.g. endotoxin
G-protein coupled receptors for certain bacterial peptides (N-formylmethionyl residues)
Opsonin receptors (IgG and C3b especially)
Cytokine receptors (macrophages: interferon-𝛾)
33
Q

What are the 3 stages of phagocytosis?

A

Attachment
Engulfment & formation of phagocytic vacuole
Degradation by various substances

34
Q

What are the mechanisms of action for degradation in phagocytosis?

A

Reactive oxygen species; myeloperoxidase (neutrophils)
Lysozyme (antibacterial)
Lactoferrin (iron binding; prevents bacterial reproduction)
Major Basic Protein (produced by eosinophils; antiparasitic)

35
Q

What contributes to termination of the Acute Inflammatory response?

A

Inflammatory mediators and neutrophils have short half life
Macrophages release anti-inflammatory products
Mast cells and lymphocytes produce anti-inflammatory products e.g. Lipoxins
Cause of injury (e.g. bacteria) is removed

36
Q

Neutrophil appearance

A

Multi-lobed

37
Q

Eosinophil appearance

A

Stain pink as pick up Eosin stain well

38
Q

Mast cell appearance

A

lilac cytoplasm

39
Q

What coexists in chronic inflammation?

A

Inflammation
Tissue injury
Attempts at tissue repair

40
Q

How might chronic inflammation arise?

A

From acute inflammation

From insidious, low-grade, smouldering infection

41
Q

What insidious, low-grade, smouldering infections may lead to chronic inflammation?

A

Persistent infection e.g. TB
Prolonged exposure to toxins (endogenous, exogenous)
Autoimmunity e.g. rheumatoid arthritis
Foreign body (silica)

42
Q

What is chronic inflammation characterised by?

A

Mononuclear cell infiltrate (macrophages, lymphocytes, plasma cells)
Tissue destruction, induced by persistent inflammatory agent/ inflammatory cells themselves
Attempts at healing by replacement of damaged tissue with connective tissue
Accomplished by fibrosis & accompanied by angiogenesis
“Granulation tissue”

43
Q

Where do macrophages originate?

A

Bone marrow

44
Q

What do macrophages circulate as in blood?

A

Monocytes

45
Q

What roles may a macrophage have? (depending on their activation pathway)

A

Phagocytosis (outlive neutrophils)
Amplification of inflammation (cytokine release)
Wound repair and fibrosis
Anti-inflammatory effects

46
Q

In acute phase of inflammation macrophages destroy offending agent either directly or by stimulating other pathways that do so

A

When offending agent is cleared, the macrophages fade away

47
Q

In chronic inflammation macrophages persist & cause significant tissue destruction

A

Ongoing tissue destruction can trigger inflammatory cascade in of itself
Thus Acute and Chronic inflammation may co-exist

48
Q

What other cell types are involved in chronic inflammation?

A

T-Lymphocytes (can be stimulated by macrophages; regulate immune reaction and can be cytotoxic)
Plasma cells (develop from activated B-lymphocytes and produce antibodies)
Eosinophils (in response to parasites or IgE mediated inflammation)
Mast cells
Neutrophils if co-existing acute inflammation

49
Q

Vascular endothelial growth factor (VEGF) is released from macrophages and endothelial cells in chronic inflammation, so

A

there is prominent angiogenesis

50
Q

Macrophage appearance

A

Large cell

Large “kidney bean” nucleus

51
Q

Lymphocyte appearance

A

Small

Stain dark purple

52
Q

Plasma cell appearance

A

“clock face nucleus”

Many markings and small pink area

53
Q

Granulomatous inflammation

A

Distinctive pattern of chronic inflammation showing granuloma formation

54
Q

Granuloma

A

an aggregate of activated macrophages
an attempt to eliminate a resistant offending agent
triggered by strong and specific T-lymphocyte reaction

55
Q

Causes of granulomatous inflammation

A

Infections (TB, leprosy)
Foreign material e.g. suture (foreign body granuloma)
Tumour reaction
Granulomatous diseases (Crohn’s disease)

56
Q

Granulomatous inflammation appearance

A

Swirl of cells in centre

Giant cells surrounding

57
Q

Undesirable outcomes of inflammation

A

Excessive tissue damage and scarring, possibly with detrimental effect on adjacent tissue
Systemic involvement with multi-organ failure: Septic shock, amyloid

58
Q

Positive outcomes of inflammation

A

Removal of offending agent
Cessation of inflammatory response
Healing of tissue damage with preservation of integrity and function (resolution)

59
Q

Wound healing

A

Heal either by resolution or scarring

60
Q

Resolution (healing)

A

involves regeneration of parenchymal cells with restoration of function
Only occurs if tissue can regenerate and there is little structural damage

61
Q

Repair by scarring

A

involves angiogenesis, migration and repair of fibroblasts, scar formation and connective tissue remodelling
Occurs when there is significant tissue loss and tissue is unable to regenerate; results in loss of function

62
Q

Example of something that can heal with resolution

A

Bronchopneumonia

63
Q

Example of resolution with some scarring

A

Ulcer

64
Q

Example of scarring

A

Cirrhosis of liver

65
Q

What may impair wound healing?

A

Poor nutrition
Vitamin deficiency (Vitamin C, Vitamin A)
Mineral deficiency (Zinc)
Suppressed inflammation (Steroids, Old Age)
Poor local blood supply (Peripheral vascular disease)
Persistent foreign body
Movement

66
Q

Hypertrophic scar

A

More exuberant response

Build up of collagen

67
Q

Scar tissue can contract

A

Leading to loss of function of a limb

68
Q

What may occur around scarring?

A

Alterations of surrounding area to assume function of damaged/scarred tissue

Cell Pathology (6 decks)

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