Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MCD > Cell pathology 2 - Inflammation > Flashcards

Cell pathology 2 - 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 cause 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What cells are involved in inflammation?

A
  • Neutrophils
  • Macrophages
  • Lymphocytes
  • Eosinophils
  • Mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What soluble factors are involved in inflammation?

A
  • Antibodies
  • Cytokines
  • Complement system
  • Coagulation system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is acute inflammation?

A
  • Acute inflammation is a rapid non-specific response to cellular injury
  • It is orchestrated by mediators released from injured cells
  • Leukocyte and vascular response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is chronic inflammation?

A
  • Chronic inflammation is a persistent inflammatory response
  • Ongoing inflammation and repair over weeks to years
  • May arise form acute inflammation (Granulomatous inflammation is a specific subtype of chronic inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is acute inflammation recognised?

A
  • Rubor (Redness)
  • Calor (Heat)
  • Tumor (Swelling)
  • Dolor (Pain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the purpose of the acute inflammatory response?

A

Rapid delivery of leukocytes and plasma proteins to the site of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the three main components of acute inflammation?

A
  • Alteration in the calibre of blood vessels to increase flow
  • Structural changes to the microvasculature to allow proteins and leukocytes to leave the circulation
  • Emigration, accumulation and activation of leukocytes at the focus of injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is vasodilation?

A
  • Increased diameter and loss of fluid slow down flow and lead to stasis
  • May be preceded by brief arteriolar constriction
  • Causes the heat and redness of acute inflammation
  • Quickly followed by increased permeability of microvasculature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes vasodilation?

A
  • Induced by several mediators including histamine and nitric oxide
  • Histamine is a major vasoactive amine, which comes from mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is increased vascular permeability?

A

Endothelial cells contract, resulting in increased interendothelial spacing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causes of increased vascular permeability?

A
  • Histamine and Nitric Oxide
  • Endothelial cell injury (burns, toxins)
  • Leukocyte-mediated vascular injury (late stage inflammation)
  • Increased transcytosis (VEGF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is exudate?

A

A fluid secreted from the cells, as a result of increased vascular permeability.

  • High protein content (fibrin and antibodies)
  • High specific gravity
  • May be purulent (leukocyte-rich)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is transudate?

A
  • Ultrafiltrate of blood plasma caused by increased hydrostatic pressure or decreased osmotic pressure
  • Low protein content (albumin)
  • Low specific gravity
  • Low cell content
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the purpose of exudate?

A
  • Dilute pathogens
  • ‘Wall off’ pathogens
  • Permit spread of soluble inflammatory mediators
  • Provide substrate for inflammatory cell migration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the first leukocytes in the intial phase of typical acute inflammation and what do they do?

A
  • Nautrophils & Monocytes (capable of phagocytosis)
  • Kill bacteria and eliminate foreign and necrotic material
  • Produce multiple factors and mediators that interact with other cells
  • Overactivation may prove harmful in the long term
17
Q

Describe the process of leukocytes exiting the vessel lumen.

A
  • Margination (leukocytes are close to the surface)
  • Rolling (on the vessel surface)
  • Adhesion to activated endothelium
  • Transmigration across the vessel wall
  • Migration up the chemotactic gradient.
18
Q

What receptors may be activated at the site of injury?

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)
19
Q

Describe the basic stages of phagocytosis.

A
  • Attachment
  • Engulfment and formation of phagocytic vacuole
  • Degradation by various substances (reactive oxygen species, lysozyme, major basic protein)
20
Q

What are the stages in histology of the acute inflammatory response?

A

Normal lung -> vascular congestion and stasis -> leukocytes infiltrate

21
Q

How/when is the acute inflammatory response terminated

A
  • Inflammatory mediators and neutrophils have a short half life
  • Macrophages, mast cells and lumphocytes release a number of anti-inflammatory products
  • Lipoxins
  • The cause of the injury (e.g. bacteria) is removed
  • Under normal conditions, process comes to a stop
22
Q

What is chronic inflammation?

A

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

23
Q

When does chronic inflammation occur?

A
  • Can follow from acute inflammation, or rise from a low grade smouldering inflammation
  • May include persistant infection, prolonged exposure to toxins, autoimmunity or a foreign body.
24
Q

How is chronic inflammation characterised?

A
  • Mononuclear cell infiltrate (macrophages, lymphocytes, plasma cells)
  • Tissue destruction, induced by persistent inflammatory agent or by the inflammatory cells themselves
  • Attempts at healing by replacement of damaged tissue with connective tissue
  • Accomplished by fibrosis and accompanied by angiogenesis
25
Q

What is the role of macrophages in the chronic inflammatory response?

A

They persist and cause significant tissue destruction

26
Q

What cell types¬ other than macrophages¬ are involved in chronic inflammation?

A
  • T-Lymphocytes (can be stimulated by macrophages; regulated 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
27
Q

What cases prominent angiogensis in chronic inflammation?

A

Vascular endothelial growth factor (VEGF) from macrophages and endothelial cells

28
Q

What is granulomatous inflammation?

A
  • Chronic inflammation where granulomas form (aggregates of activated macropages), which attempt to eliminate a resistant offending agent.
  • Triggered by a strong and specific T lymphocyte reaction
29
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)
30
Q

Compare acute and chronic inflammation?

A
  • Acute onset is faster and lasts a few days, chronic inflammation takes longer and lasts a long time.
  • Acute is mainly neutrophils, chronic is mainly monocytes or macrophages
  • Acute involves necrosis (cell death), chronic involves scarring as repair occurs
31
Q

What are the long term sequelae of inflammation (outcomes)?

A
  • Removal of offending agent
  • Cessation of the inflammatory response
  • Healing of tissue damage with preservation of integrity and function (resolution)
  • Excessive tissue damage and scarring (may affect adjacent tissue)
  • Multiorgan failure (septic shock)
32
Q

List the possible ways wounds may heal.

A
  • Resolution (involves regeneration of parenchymal cells with restoration of function)
  • Scarring (involves angiogenesis, migration and repair of fibroblasts, scar formation and connective tissue remodelling)
33
Q

When does resolution/scarring in wound repair occur?

A

Resolution - tissue can regenerate, with little structural damage

Scarring - significant tissue loss, tissue is unable to regenerate so there is loss of function

34
Q

What factors can impair wound healing?

A
  • Poor nutrition (protein, energy)
  • 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

MCD (56 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions