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MCD - cell pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A
  • Complex reaction in viable vascularised tissues to sublethal cellular injury
  • A protective response geared towards removing the causes and consequences of the injury
  • Sets stage for potential healing
  • Tightly regulated process consisting mainly of leukocyte and vascular responses
  • Triggered by various cell types and soluble mediators
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2
Q

Name the cell types involved in inflammation

A
  • Neutrophils
  • Macrophages
  • Lymphocytes
  • Eosinophils
  • Mast cells
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3
Q

Name soluble factors involved in inflammation

A
  • Antibodies
  • Cytokines
  • Complement system
  • Coagulation system
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4
Q

What is acute inflammation?

A

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

What is chronic inflammation?

A

Inflammation of prolonged duration in which inflammation, tissue injury and attempts at tissue repair coexist.

  • May arise from acute inflammation
  • May arise as insidious, low-grade smouldering inflammation
    • Persistent infection (mycobacteria, fungi, parasites, viral)
    • Prolonged exposure to toxins
    • Autoimmunity
    • Foreign body (silica)
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6
Q

TRUE OR FALSE:

Granulomatous inflammation is a specific subtype of acute inflammation

A

FALSE

It is a specific subtype of CHRONIC inflammation

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7
Q

Why is an understanding of inflammation important?

A

Allows:

  • Prediction of sequelae and complications of inflammatory reactions
  • Intervention to prevent or reduce adverse effects
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8
Q

Name disease states that involve inflammation

A
  • Infections
  • Autoimmune diseases
  • Hypersensitivity reactions
  • Trauma
  • Chronic granulomatous diseases
  • Chronic fibrosing diseases
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9
Q

TRUE OR FALSE:

Inflammation may contribute to disease states that are not primarily inflammatory

A

TRUE

E.g. atherosclerosis, type II diabetes, cancer

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10
Q

How is acute inflammation recognised on examination?

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

NOTE: these features appear quickly

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11
Q

What are the 3 main components of acute inflammation?

A
  1. Alteration in the calibre of blood vessels to increase flow (vasodilation)
  2. Structural changes to the microvasculature to allow proteins and leukocytes to leave the circulation (swelling)
  3. Emigration, accumulation and activation of leukocytes at the focus of injury
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12
Q

What is vasodilation induced by in acute inflammation?

A

Several mediators including histamine and nitric oxide (affect vascular smooth muscle)

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13
Q

Vasodilation is one of the earliest manifestations. What is it quickly followed by?

A

An increased permeability of microvasculature

Increased diameter and loss of fluid slow down flow and lead to stasis

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14
Q

Where is the richest source of histamine?

A

In mast cells

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15
Q

What are the causes of increased vascular permeability?

A
  • Histamine and nitric oxide
    • Endothelial cells contract –> increased interendothelial spacing
  • Endothelial cell injury (burns, toxins)
  • Leukocyte-mediated vascular injury (late stage inflammation)
  • Increased transcytosis
    • Vascular endothelial growth factor (VEGF) increases transfer of material across cells
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16
Q

What is the difference between exudate and transudate?

A

EXUDATE:

  • Fluid that leaks around the cells of the capillaries caused by inflammation
  • Result of increased vascular permeability
  • High protein content
  • Contains cells and cell debris

TRANSUDATE:

  • Ultrafiltrate of blood plasma caused by increased hydrostatic pressure or decreased osmotic pressure
  • Low protein content
  • Low cell content
17
Q

What is the role of exudate?

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

NOTE: intravascular fluid losses can be very high –> life threatening in severe burns

18
Q

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

A

Those capable of phagocytosis (neutrophils and macrophages)

WHY?

  • Kill bacteria and eliminate foreign and necrotic material
  • Produce multiple factors and mediators that interact with other cells

NOTE: overactivation may prove harmful in the long term

19
Q

During a leukocyte response, a number of receptors may be activated. Name 2 of these receptors.

A
  • Toll-like receptors for certain microbial products such as endotoxin
  • G-protein coupled receptors for certain bacterial peptides (N-formylmethionyl residues)
  • Opsonin receptors (IgG and C3b especially)
  • Cytokine receptors (macrophages: interferon-γ)
20
Q

How is the acute inflammatory response terminated?

A
  • Inflammatory mediators and neutrophils have a short half life
  • Macrophages release a number of anti-inflammatory products
  • Mast cells and lymphocytes produce anti-inflammatory products (e.g. lipoxins)
  • Cause of injury (e.g. bacteria) removed
21
Q

TRUE OR FALSE:

This image shows what happens during a chronic inflammatory response

A

FALSE

This shows an acute inflammatory response

22
Q

What are the 3 main features of chronic inflammation?

A
  1. Mononuclear cell infiltrate (macrophages, lymphocytes, plasma cells)
  2. Tissue destruction, induced by persistent inflammatory agent or by the inflammatory cells themselves
  3. Attempts at healing by replacement of damaged tissue with connective tissue
    • Accomplished by fibrosis and accompanied by angiogenesis
    • “Granulation tissue”
23
Q

TRUE OR FALSE:

Neutrophils are the most dominant player in chronic inflammation

A

FALSE

Macrophages are, not neutrophils

24
Q

What is the difference between the role of macrophages in the acute phase of inflammation and in the chronic phase?

A

ACUTE: macrophages destroy offending agent either directly or by stimulating other pathways that do so

CHRONIC: macrophages persist and causes significant tissue destruction (can trigger inflammatory cascade)

25
Q

Name cell types involved in chronic inflammation, other than macrophages

A
  • T-lymphocytes
  • Plasma cells
  • Eosinophils
  • Mast cells
  • Neutrophils (if co-existing acute-inflammation)
26
Q

What is granulomatous inflammation?

A

Distinctive pattern of chronic inflammation showing granuloma formation

Triggered by strong and specific T-lymphocyte reaction

27
Q

What is a granuloma?

A

An aggregate of activated macrophages; an attempt to eliminate a resistant offending agent

28
Q

What are the causes of granulomatous inflammation?

A
  • Infections (TB, leprosy, syphilis, fungi)
  • Foreign material (foreign body granuloma)
  • Tumour reaction
  • Granulomatous diseases (Sarcoidosis, Crohn’s disease)
29
Q

Compare the outcomes of acute and chronic inflammation

A

ACUTE:

  • Complete resolution
  • Progression to chronic inflammation

CHRONIC:

  • Scarring
  • Loss of function
30
Q

What are the long term sequelae of inflammation?

A

POSITIVE:

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

UNDESIRABLE:

  • Excessive tissue damage and scarring
    • Possibly with detrimental effect on adjacent tissue
  • Systemic involvement with multiorgan failure
    • Septic shock, amyloid
31
Q

Wounds may heal either by…?

A

Resolution or scarring

32
Q

What does repair by resolution involve?

A

Regeneration of parenchymal cells with restoration of function

Only occurs if tissue can regenerate and there is little structural damage

33
Q

What does repair by scarring involve?

A

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)

34
Q

What might wound healing be impaired by?

A
  • Poor nutrition (protein, energy)
  • Vitamin deficiency (vit C, vit A)
  • Mineral deficiency (zinc)
  • Suppressed inflammation (steroids, old age)
  • Poor local blood supply (peripheral vascular disease)
  • Persistent foreign body
  • Movement
35
Q

What are some complications of wound healing?

A
  • Build-up of collagen –> hypertrophic scar/keloid
  • Scar tissue contracts and pulls
  • Adjacent muscle alters behaviour due to scar tissue nearby

MCD - cell pathology (6 decks)

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