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Cell Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is meant by inflammation

A

Complex reaction in viable vascularised tissues to sublethal cellular injury

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2
Q

What is the function of inflammation

A

A protective response geared towards removing the cause and consequences of the injury
Sets stage for potential healing

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3
Q

What is involved in the process of inflammation

A

Tightly regulated process consisting mainly of leukocyte and vascular responses
Triggered by various cell types and soluble mediators

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4
Q

Which cells are involved in inflammation

A 
Neutrophils
Macrophages
Lymphocytes
Eosinophils
Mast cells
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5
Q

Which soluble mediators are involved in inflammation

A

Antibodies
Cytokines
Complement system
Coagulation system

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6
Q

Describe acute inflammation

A

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

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7
Q

Describe 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
Often damage coexists with attempts to heal.

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8
Q

Describe the inflammatory processes that underlie many disease states

A

Excessive / inappropriate inflammatory response- allergies
Inadequate inflammatory response- impaired healing in the immunocompromised
Chronic inflammation- fibrosis in occupational lung diseases
Granulomatous inflammation- Chron’s disease

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9
Q

What does an understanding of inflammation allow us to do

A

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

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10
Q

List the disease states that involve inflammation

A 
Infections
Autoimmune diseases
Hypersensitivity reactions
Trauma
Chronic granulomatous diseases
Chronic fibrosing diseases
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11
Q

How may inflammation contribute to disease states that are not inflammatory in nature

A

Atherosclerosis
Type II Diabetes- microvascular complications due to vascular inflammation
Cancer

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12
Q

What are the cardinal signs of acute inflammation

A

Recognised on examination by the cardinal signs:
Rubor (Redness)- increased blood flow
Calor (Heat)- increased blood flow
Tumor (Swelling)- loss of definition due to leaky vessels
Dolor (Pain)- white cells

These features appear quickly

Loss of function is sometimes considered to be the 5th cardinal sign.

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13
Q

What is the key aim of acute inflammation and which 3 components help to achieve this

A

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

Three main components:
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

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14
Q

Describe the role of vasodilation in acute inflammation

A

Vasodilation is one of the earliest manifestations
May be preceded by brief arteriolar constriction
Causes the heat and redness of acute inflammation

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15
Q

What is responsible for this vasodilation

A

Induced by several mediators including histamine and nitric oxide
Affect vascular smooth muscle- causes it to relax.

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16
Q

Describe the roles of histamine, including what it is, where it is found and what triggers its release

A

Histamine is a major vasoactive amine
Richest source is mast cells
Preformed and released as the cell degranulates
Triggered by binding of surface IgE, trauma, heat, cold, complement C3a/C5a, cytokines IL-1 / IL-8
Leads to vasodilation and also increased vascular permeability

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17
Q

Describe some of the problems associated with histamine

A

Dysregulation can be seen in allergic reactions

Type 1 Hypersensitivity

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18
Q

What is vasodilation often followed by in acute inflammation

A

Quickly followed by increased permeability of microvasculature
Increased diameter and loss of fluid slow down flow and lead to stasis over site of injury- increased bioavailability of substances.

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19
Q

How can we increase vascular permeability

A

Endothelial cells contract; increased interendothelial spacing
Immediate Transient Response
Histamine and Nitric Oxide

Can also be caused by:
Endothelial cell injury (burns, toxins)
Leukocyte-mediated vascular injury (late stage inflammation)
Increased transcytosis (VEGF)

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20
Q

What are the key properties of exudate

A

Result of increased vascular permeability
High protein content (fibrin, antibodies)
High specific gravity
Contains cells and cell debris
May be purulent (leukocyte-rich)

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21
Q

What are the key properties of transudate

A

Ultrafiltrate of blood plasma caused by increased hydrostatic pressure or decreased osmotic pressure
Low protein content
Low specific gravity
Low cell content

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22
Q

Why may exudate appear pink

A

Fibrous exudate- lots of fibrin.

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23
Q

What is the purpose of exudate

A

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

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24
Q

What is a key problem with exudate

A

Intravascular fluid losses can be very high

Life threatening in severe burns

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25
Q

When does transudate occur compare this to exudate

A

Transudate- high hydrostatic pressure, low colloid oncotic pressure- normal
Exudate- vasodilation, increased permeability and stasis- inflammation.

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26
Q

Which immune cells are important in the initial phase of acute inflammation and what do they do

A

The most important leukocytes in the initial phase of typical acute inflammation are those capable of phagocytosis
Neutrophils
Macrophages
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

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27
Q

Describe neutrophils

A

Neutrophils are produced in bone marrow
Circulate in blood and migrate towards damaged tissues
Often the first cell into a damaged area
Rapid response
Main roles are to kill bacteria and recruit additional cells
Phagocytosis
Degranulation – enzymes, free radicals, soluble mediators

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28
Q

Describe the leukocyte response in acute inflammation

A

Leukocytes first need to be recruited to the site of injury
The process of exiting the vessel lumen (extravasation) has the following steps:
Margination
Rolling
Adhesion to activated endothelium
Transmigration (diapedesis) across endothelium through vessel wall
Migration through tissues towards chemotactic stimulus

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29
Q

What do the leukocytes need to do at the site of the injury

A

Once at the site of injury, leukocytes need to:
Recognise microbes and necrotic tissue
Activate to ingest and destroy the microbes and necrotic tissue whilst amplifying the inflammatory response

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30
Q

Which receptors may be activated

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)
Different receptors= vast array of responses.
31
Q

What needs to be done once the bacteria and necrotic tissue have been recognised and what does this require

A

Once recognised, microbes and necrotic tissues need to be destroyed
Phagocytosis requires:
Attachment
Engulfment and formation of phagocytic vacuole
Degradation by various substances
Reactive oxygen species; myeloperoxidase (neutrophils)
Lysozyme (antibacterial)
Lactoferrin (iron binding; prevents bacterial reproduction)
Major Basic Protein (produced by eosinophils; antiparasitic)

32
Q

Describe myeloperoxidases

A

Contain peroxidases- that break down the bacterial cell wall.

33
Q

Summarise the role of histamines including its source

A

Mast cells, basophils, platelets

Vasodilation, increased vascular permeability, endothelial activation

34
Q

Summarise the role of prostaglandins including its source

A

Mast cells, leukocytes

Vasodilation, pain, fever

35
Q

Summarise the role of cytokines, including their source

A 
Macrophages, endothelial cells, mast cells
Endothelial activation (adhesion molecules), fever, malaise, pain, anorexia, shock
36
Q

Summarise the role of chemokines, including their source

A

Leukocytes, activated macrophages

Chemotaxis, leukocyte activation

37
Q

Summarise the role of complement including its source

A

Plasma (produced in the liver)

Leukocyte chemotaxis and activation, vasodilation (mast cell stimulation), opsonisation

38
Q

Describe the importance of terminating the acute inflammatory response

A

Negative feedback when the causative agent is removed, to prevent further damage from chronic inflammation.

39
Q

Describe the process of terminating acute inflammation

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
Lipoxins
The cause of the injury (e.g. bacteria) is removed
Once stimulus is lost- neutrophils stop arriving and quickly fade away.

40
Q

Describe the histology of eosinophils

A

Pink granular cytoplasm

41
Q

Describe the histology of mast cells

A

Lilac cytoplasm; histamine granules

42
Q

What is meant by chronic inflammation

A

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

43
Q

What may chronic inflammation arise from

A

May follow from acute inflammation
May arise as insidious, low-grade smouldering inflammation
Persistent infection (mycobacteria, fungi, parasites, viral)
Prolonged exposure to toxins (endogenous, exogenous)
Autoimmunity (rheumatoid arthritis)- constant state of inflammation.
Foreign body (silica)- difficult to get rid of

44
Q

What is chronic inflammation characterised by

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
“Granulation tissue”

45
Q

Describe macrophages

A

Macrophages originate in bone marrow
Circulate as small numbers as monocytes in blood
Once in tissue become macrophages (several types)
Complex role depending on activation pathway
Phagocytosis (outlive neutrophils)
Amplification of inflammation (cytokine release)
Wound repair and fibrosis
Anti-inflammatory effects
Dominant player in chronic inflammation

46
Q

Describe the specialised macrophages found in distinct tissues

A

Microglia (CNS)
Alveolar macrophages
Kuppfer cells (Liver)
osteoclasts (bone)

47
Q

Describe the importance of the chemical environment in the development of phagocytes

A

M1 Phagocytes- Acute inflammation, phagocytic

M2- Anti-inflammatory, involved in repair.

48
Q

Describe the typical role of macrophages in acute inflammation

A

In the acute phase of inflammation macrophages destroy the offending agent either directly or by stimulating other pathways that do so
When the offending agent is cleared, the macrophages fade away

49
Q

Describe the situation with macrophages in chronic inflammation

A

In chronic inflammation macrophages persist and cause significant tissue destruction
Ongoing tissue destruction can trigger the inflammatory cascade in of itself
Acute and Chronic inflammation may co-exist

50
Q

Describe the issue of the endless cascade

A

Damage caused by macrophages can trigger acute inflammation

Cells newly injured- acute inflammation

51
Q

Which other cells are involved in acute 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

52
Q

Describe the role of angiogenesis in acute inflammation

A

There is prominent angiogenesis
VEGF from macrophages and endothelial cells
Due to chronic nature- enough time for it to occur- to deliver substances involved in repairing the damage- granuloma formation.

53
Q

Describe the histology of macrophages

A

very large and appear foamy as have fatty material

54
Q

Describe the histology of leukocytes

A

black/dark blue sites; will be dense in chronic; small and dark nuclei

55
Q

Describe the histology of plasma cells

A

clock face nucleus with pink area next to it called a perinuclear hof

56
Q

Describe the histology of granulation tissue

A

Lots of loose connective tissue- pink
New blood vessels
Lots of fibroblasts, lymphocytes, plasma cells

57
Q

Describe granulation tissue

A

Distinctive pattern of chronic inflammation showing granuloma formation
A granuloma is an aggregate of activated macrophages; an attempt to eliminate a resistant offending agent
Triggered by strong and specific T-lymphocyte reaction

58
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)
Suture material- suture granulomas common.

59
Q

Describe the histology of granulomatous inflammation

A

swirl in centre and giant cells formed by macrophage aggregates trying to clear something

60
Q

List the key characteristics of acute inflammation

A 
Immediate onset; lasts a few days
Vasodilation, increased vascular permeability, leukocyte response
Neutrophils predominate
Histamine release
Prominent necrosis
Outcomes include:
Complete resolution
Progression to Chronic Inflammation
61
Q

List the key features of chronic inflammation

A 
Delayed onset; may last weeks, months or years
Persistent inflammation, ongoing tissue injury, attempts at healing
Ongoing cytokine release
Monocytes / Macrophages predominate
Prominent scarring
Outcomes include:
Scarring
Loss of function
62
Q

What are the positive outcomes of inflammation

A

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

63
Q

What are the undesirable outcomes of inflammation

A

Excessive tissue damage and scarring
Possibly with detrimental effect on adjacent tissue
Systemic involvement with multiorgan failure
Septic shock (loss of fluid in one part of the body), amyloid (binding of compounds to form abnormal proteins that can decrease organ function).

64
Q

What are the two outcomes for wound healing

A

Wounds may heal either by resolution or scarring

65
Q

Describe resolution

A

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

66
Q

Describe repair by scarring

A

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

67
Q

Describe the signs of inflammation in bronchopneumonia

A 
Congestion
Red hepatisation (exudate with neutrophils, erythrocytes, fibrin)
Grey hepatisation (fibrinosuppurative exudate)
68
Q

Describe resolution of bronchopneumonia

A

Resolution (digestion and resorption of consolidated exudate)

69
Q

What 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

70
Q

What are some of the complications of wound healing

A

Keloid scarring - collagen build-up to form hypertrophic scarring
Scar tissue can contract and remodel to pull on skin/limbs
Alterations of surrounding area to assume function of damaged/scarred tissue

71
Q

When may scars form in response to acute injury

A

Deep wounds
MI
Parenchymal cell death

72
Q

Describe amyloidosis

A

In response to chronic inflammation anywhere in body, liver produces and releases increased amounts of serum amyloid A protein into the blood.
In some cases this is deposited in tissue as dense protein (amyloid)

73
Q

How can scarring result in impaired mobility

A

Fibrous scar tissue contracts as it matures. If scarring occurs across a joint it can cause poor joint mobility.
Impaired function
e.g. fibrous scars in the myocardium after a hear attack

74
Q

What are vitamin A and C required for

A

Vitamin C – needed by fibroblasts to make collagen

Vitamin A- required for epithelial regeneration

Cell Pathology (6 decks)

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