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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
Which are the most important leukocytes in the initial phase of typical acute inflammation?
Those capable of phagocytosis | Neutrophils and Macrophages
26
Why are neutrophils and macrophages the most important leukocytes in the initial phase of typical acute inflammation?
Kill bacteria and eliminate foreign and necrotic material | Produce multiple factors and mediators that interact with other cells
27
Where are neutrophils produced?
Bone marrow
28
Which cells are usually 1st to a damaged area?
Neutrophils
29
How are the main roles of a neutrophil (kill bacteria and recruit additional cells) achieved?
Phagocytosis | Degranulation- enzymes, free radicals, soluble mediators
30
How do leukocytes exit a vessel lumen to reach site of injury? (Extravasation)
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
What do leukocytes do once at site of injury?
Recognise microbes and necrotic tissue | Activate to ingest and destroy microbes and necrotic tissue whilst amplifying inflammatory response
32
Which receptors in leukocytes may be activated once at site of injury?
``` 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
What are the 3 stages of phagocytosis?
Attachment Engulfment & formation of phagocytic vacuole Degradation by various substances
34
What are the mechanisms of action for degradation in phagocytosis?
Reactive oxygen species; myeloperoxidase (neutrophils) Lysozyme (antibacterial) Lactoferrin (iron binding; prevents bacterial reproduction) Major Basic Protein (produced by eosinophils; antiparasitic)
35
What contributes to termination of the Acute Inflammatory response?
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
Neutrophil appearance
Multi-lobed
37
Eosinophil appearance
Stain pink as pick up Eosin stain well
38
Mast cell appearance
lilac cytoplasm
39
What coexists in chronic inflammation?
Inflammation Tissue injury Attempts at tissue repair
40
How might chronic inflammation arise?
From acute inflammation | From insidious, low-grade, smouldering infection
41
What insidious, low-grade, smouldering infections may lead to chronic inflammation?
Persistent infection e.g. TB Prolonged exposure to toxins (endogenous, exogenous) Autoimmunity e.g. rheumatoid arthritis Foreign body (silica)
42
What is chronic inflammation characterised by?
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
Where do macrophages originate?
Bone marrow
44
What do macrophages circulate as in blood?
Monocytes
45
What roles may a macrophage have? (depending on their activation pathway)
Phagocytosis (outlive neutrophils) Amplification of inflammation (cytokine release) Wound repair and fibrosis Anti-inflammatory effects
46
In acute phase of inflammation macrophages destroy offending agent either directly or by stimulating other pathways that do so
When offending agent is cleared, the macrophages fade away
47
In chronic inflammation macrophages persist & cause significant tissue destruction
Ongoing tissue destruction can trigger inflammatory cascade in of itself Thus Acute and Chronic inflammation may co-exist
48
What other cell types are involved in chronic inflammation?
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
Vascular endothelial growth factor (VEGF) is released from macrophages and endothelial cells in chronic inflammation, so
there is prominent angiogenesis
50
Macrophage appearance
Large cell | Large "kidney bean" nucleus
51
Lymphocyte appearance
Small | Stain dark purple
52
Plasma cell appearance
"clock face nucleus" | Many markings and small pink area
53
Granulomatous inflammation
Distinctive pattern of chronic inflammation showing granuloma formation
54
Granuloma
an aggregate of activated macrophages an attempt to eliminate a resistant offending agent triggered by strong and specific T-lymphocyte reaction
55
Causes of granulomatous inflammation
Infections (TB, leprosy) Foreign material e.g. suture (foreign body granuloma) Tumour reaction Granulomatous diseases (Crohn’s disease)
56
Granulomatous inflammation appearance
Swirl of cells in centre | Giant cells surrounding
57
Undesirable outcomes of inflammation
Excessive tissue damage and scarring, possibly with detrimental effect on adjacent tissue Systemic involvement with multi-organ failure: Septic shock, amyloid
58
Positive outcomes of inflammation
Removal of offending agent Cessation of inflammatory response Healing of tissue damage with preservation of integrity and function (resolution)
59
Wound healing
Heal either by resolution or scarring
60
Resolution (healing)
involves regeneration of parenchymal cells with restoration of function Only occurs if tissue can regenerate and there is little structural damage
61
Repair by scarring
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
Example of something that can heal with resolution
Bronchopneumonia
63
Example of resolution with some scarring
Ulcer
64
Example of scarring
Cirrhosis of liver
65
What may impair wound healing?
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
Hypertrophic scar
More exuberant response | Build up of collagen
67
Scar tissue can contract
Leading to loss of function of a limb
68
What may occur around scarring?
Alterations of surrounding area to assume function of damaged/scarred tissue

Cell Pathology (6 decks)

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