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MCD - Cell pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Define inflammation

A

Reactions of living vascularised tissue to sub- lethal injury

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2
Q

What are the three types of inflammation?

A

Acute
Chronic
Granulomatous (type of chronic inflammation)

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3
Q

What triggers histamine release and what effect do histamines have?

A

Binding of IgE to the Fc receptor on mast cells - Antigens bind to the IgE and cause cross-linking and mast cell degranulation Histamines cause: vasodilation + increased vascular permeability

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4
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, usually as a result of inflammation

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5
Q

What is a transudate?

A

Fluid escape from vessels due to disturbances in hydrostatic and colloid osmotic pressure – NOT CAUSED BY INFLAMMATION

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6
Q

What is the most important difference between exudates and transudates?

A

Exudates are associated with inflammation transudates are not

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7
Q

What are the three types of exudates and how do they differ?

A

Serous – fluid filled – lowest protein content of the three exudates

Fibrinous – high fibrin content – more due to traumatic injury

Purulent – pus filled – fibrin, inflammatory cells, debris and fluid

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8
Q

What is the main histological feature of acute inflammation?

A

Lots of neutrophils

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9
Q

What are the three main cell types involved in chronic inflammation?

A

Macrophages
Lymphocytes
Plasma Cells

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10
Q

What is an important difference between acute and chronic inflammation?

A

Acute inflammation produces an exudate whereas chronic inflammation doesn’t

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11
Q

What are the histological features of granulomatous inflammation?

A

Granuloma – collection of macrophages
You get a collection of macrophages in the middle and they may appear to have fused together
There will be lymphocytes and plasma cells around the outside

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12
Q

What is the good outcome of inflammation?

A

Resolution – healing of tissue damage to preserve integrity and function

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13
Q

What is ‘Repair’ in terms of wound healing?

A

Replacing normal tissue with scar tissue

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14
Q

Give an example of resolution and how it takes place.

A

Pneumococcul lobar pneumonia
Inititally you get exudation
Then you get red hepatisation (erythrocytes move into the alveolar cells)
Grey hepatisation – erythrocytes break down
Provided the basement membrane is still there – the body can remove the problem

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15
Q

What are three main complications of repair? Describe each of them

A

Keloids – excess collagen deposition
Contractures – scar tissue contracts after a while, if the scar tissue is over a joint it can affect joint mobility
Organ Function – if normal functional tissue is replaced with scar tissue

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16
Q

what are features of acute inflammation?

A
  • Transient and early response to injury
  • Hours/few days
  • Involves release of chemical mediators
  • Typical vascular and leucocyte response
  • NOT the same as infection
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17
Q

what are features of chronic inflammation?

A
  • Inflammation of prolonged duration
  • Weeks/months/years
  • Usually due to persistent injury causing agent
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18
Q

what is Granulomatous Inflammation?

A

Specialised form of chronic inflammation

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19
Q

what are the cells of the inflammatory response and healing?

A
  • neutrophils
  • macrophages
  • lymphocytes
  • eosinophils
  • mast cells
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20
Q

what are the soluble factors of inflammatory response and healing?

A
  • antibodies
  • cytokines
  • complement system
  • coagulation system
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21
Q

what are the cardinal signs of inflammation?

A
  • rubor - redness
  • calor - heat
  • tumour - swelling
  • dolor - pain
  • functio laesa - loss of function
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22
Q

what is calor caused by?

A

histamine mediated vasodilation

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23
Q

what is tumor caused by?

A
  • Oedema - increased fluid in interstitial fluid

- Caused by histamine mediated increase in permeability of vessels

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24
Q

what is rubor caused by?

A
  • blood flow isn’t as fast so you get redness
25
Q

what is loss of function caused by?

A
  • due to swelling and pain
26
Q

what is histamine?

A
  • vasoactive amine
  • produced by mast cells
  • packaged into granules inside mast cells
  • when an antigen binds to the IgE on the surface of mast cells it causes degranulation
  • leading to vasodilation and vascular permeability
27
Q

how to target

  • histamine
  • prostaglandins
  • IL- 1 and TNF
A
  • anti histamines
  • aspirin
  • anti TNF antibodies
28
Q

how do vessels become leaky?

A
  • consists of two factors
  • hydrostatic pressure and colloid osmotic pressure
  • hydrostatic pressure is the pressure exerted forcing water out of the vessels
  • colloid osmotic pressure is the osmotic pressure pulling water into the vessels
  • hydrostatic pressure > colloid osmotic pressure
29
Q

what does the exudate consist of?

what is the function of the exudate?

A
  • fluid, cells, proteins (fibrin)
  • fluid purpose
    dilutes pathogen and allows soluble mediators to spread
  • fibrin purpose
    stops the pathogen from spreading and gives the inflammatory cells substrate to hold onto
30
Q

what are the types of exudate ?

A 
serous - 
fluid filled (blisters)
fibrinous - 
high fibrin content due to trauma 
purulent- pus filled (Combination of fibrin, inflammatory cells, debris and fluid)
31
Q

what is the action of neutrophils in acute inflammation?

A
  1. Enter tissue
  2. Migrate to site of cell injury - chemotaxis
  3. Become activated
  4. Carry out their designated role - e.g. phagocytosis
  5. Interact with other cell types - release of soluble mediators
32
Q

what is the main role of neutrophils?

A

Main Role:
• Kill bacteria and recruit more cells
• Phagocytosis
• Degranulation

33
Q

what is cellular egress?

A

consists of :

margination
- cells are pushed to the edges of vessels

rolling and adhesion
- Once at the margin they can bind to endothelial cells through selectins on the neutrophil and endothelial cells
The selectin bonds are loose - the neutrophil rolls along the side of the blood vessel and is slowed down
As it slows down more permanent bonds are formed which fixes the
neutrophil to the vessel wall

transmigration
- Neutrophil dissolves basement
Enters interstitium

chemotaxis
- Follow chemical gradient to the site of inflammation

34
Q

what does phagocytosis consist of?

A
  • opsonisation
  • opsonins attach to the bacteria
  • ingestion
    pathogen is phagocytosed
  • killing
    destruction of phagocytosed material in vacuole
35
Q

what are eosinophils necessary for?

A

they are important in allergic and parasitic causes of inflammation

36
Q

what are mast cells important in?

A

allergic diseases

37
Q

how long does the inflammation last and what controls the length?

A

Mediators and neutrophils have short half life
• Stimulus (e.g. bacteria) removed
• Mast cells and lymphocytes release anti-inflammatory products (lipoxins)
• Macrophages release anti-inflammatory products

38
Q

what are the histological features of acute inflammation?

A

There are lots of Neutrophils

- There will also be mast cells and eosinophils

39
Q

what is the evolution of acute inflammation to chronic inflammation?

A
  • Breakdown of myofibres
  • Fewer neutrophils in chronic
    inflammation
  • Other cell types involved
40
Q

define prolonged inflammation?

A

Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at repair occur simultaneously.

41
Q

what is the cause of chronic inflammation?

A
  • Persistent infection
  • Prolonged exposure to toxic agent
  • Autoimmunity
  • Foreign body (e.g. splinter)
42
Q

what are the cells involved in chronic inflammation?

A

Macrophages
Lymphocytes
Plasma Cells

43
Q

what do monocytes and macrophages do?

A
  • Live longer than neutrophils
  • Phagocytosis
  • Control many other inflammatory cells - by releasing cytokines
  • Increase in viral and atypical bacterial infections
44
Q

what are the histological features of chronic inflammation?

A

Macrophages, lymphocytes and plasma cells present

45
Q

what is the histology of granulation tissue?

A

Lots of fibroblasts producing granulomatous tissue

46
Q

what is the basic pathology of Lots of fibroblasts producing granulomatous tissue?

A

FORM OF CHRONIC INFLAMMATION - shows granuloma formation
• Clusters of macrophages
• Involves specific immune reaction T cells

47
Q

what are the causes of granulomatous inflammation?

A

Infection
Foreign Material
Reaction to Tumours
Immune Diseases (e.g. Crohn’s)

48
Q

what are the histological features of granulomatous Inflammation?

A
  • Macrophages are in the middle and lymphocytes around the outside
  • Horseshoe shaped nuclei and fused macrophages are seen at latter stages of
    granulomatous inflammation
49
Q

what are the main differences between acute and chronic inflammation?

A

acute

  • neutrophils
  • histamine
  • necrosis
  • lasts a few days
  • complete resolution

chronic

  • monocytes
  • cytokines
  • prominent scar tissue
  • delayed onset
  • scar tissue
50
Q

what are the good outcomes of inflammation?

A
  • removes the causative agent
  • cessation of inflammatory reaction
  • heals the tissue damage to preserve integrity and function
51
Q

what are the bad effects of inflammation?

A

LOCAL:
• Excess local tissue damage/scarring
• Secondary effects on nearby tissue - e.g. bronchoconstriction in asthma

SYSTEMIC:
• Systemic inflammatory reaction
• Secondary multi-organ failure
eg. septic shock

52
Q

what is resolution ?

what is repair?

A

RESOLUTION = regeneration of normal functional parenchymal cells

REPAIR = connective tissue and SCAR TISSUE formation

53
Q

when does resolution happen?

A

Tissue contains cells that are capable of regeneration to replace lost cells:
• EXAMPLE: Liver cells
Little structural damage done

54
Q

when does repair happen?

A

tissue loss is too great and cells are unable to regenerate

55
Q

what happens when resolution happens? in Pneumococcal lobar pneumonia

A

Initially you get exudation

• Then you get red hepatisation - erythrocytes move into the alveolar cells

The erythrocytes break down causing grey hepatisation
• Provided that the underlying structure (BASEMENT MEMBRANE) is still there -
the body can remove the problem

56
Q

what happens when repair happens?

A
  • Fibroblasts - produce collagen
  • Collagen - strong scar type collagen
  • Remodelling - reorganisation of collagen fibres for maximal tensile strength
57
Q

what hinders repair?

generally?

A
  • Poor nutrition (protein needed for collagen production)
  • Vitamin Deficiency (C needed by fibroblasts to make collagen, A needed for epithelial regeneration)
  • Mineral Deficiency
  • Suppressed Inflammation
58
Q

what hinder repair locally?

A
  • Poor blood supply
  • Persistent foreign body (e.g. splinter)
  • Movement (e.g. broken bones need casts to hold the bones in place
59
Q

what are complications of repair?

A
  • Keloid Formation
    • Excess collagen deposition
  • Contractures
    • Fibrous scar tissue contracts as part of its maturing process

-Impaired Organ Function
• Fibrous scars forming in organs will cause loss of functional tissue

MCD - Cell pathology (6 decks)

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