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IOD - Cell Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A

The bodies response to any form of cellular injury e.g. infection, heat, trauma, hypoxia, radiation etc.

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2
Q

What is the aim of inflammation?

A
  1. To remove injurious agents
  2. To clear away dead tissue
  3. To trigger healing of damaged tissue.
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3
Q

What are the 2 types of inflammation?

A
  1. Acute - usually a rapid, transient process involving vascular changes and neutrophil accumulation.
  2. Chronic - A more persistent form of inflammation in which there is on going tissue destruction and attempt to repair.
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4
Q

What is malaise?

A

A general feeling of discomfort, illness, or unease whose is exact cause is difficult to identify.

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5
Q

What is neutrophil leukocytosis?

A

An abnormally high number of neutrophils in the blood.

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6
Q

What is an acute phase response?

A

Part of the early defence or innate immune system, which is triggered by different stimuli including trauma, stress, neoplasia and inflammation.

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7
Q

Acute phase proteins

A

Are blood proteins primarily synthesised by hepatocytes as part of the APR.

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8
Q

What orchestrates acute inflammation?

A

Cytokines released by injured cells e.g histamine, serotonin, prostaglandins, leukotrienes and platelet-activating factor.

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9
Q

Acute inflammation =

A

Cell injury + Vascular changes + Neutrophil leukocytosis

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10
Q

What are the 2 major events of acute inflammation?

A
  1. Vascular changes

2. Neutrophil leukocytosis and accumulation in area of damage

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11
Q

What happens during the vascular changes of acute inflammation?

A

There is dilatation of blood vessels resulting in increased blood flow to the area of injury. in addition, endothelial cell activation causes increased permeability of capillaries which result in leaking of fluids and small proteins (e.g. fibrinogen) into the area of damage.

Activation of the coagulation cascade results in the production of thrombin which converts fibrinogen into insoluble fibrin in the area of damage.

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12
Q

What causes neutrophil leukocytosis?

A

Increased neutrophil production in the bone marrow.

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13
Q

What causes the accumulation of neutrophils in the area of damage?

A

Endothelial activation leads to up regulation of adhesion molecules on endothelial cells (e.f. ICAM-1, VCAM-1) and also neutrophils migrate into the area of damage.

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14
Q

What are the local effects of acute inflammation?

A
  1. Warmth (calor)
  2. Redness (rubor)
  3. Swelling (tumor)
  4. Pain (dolor)
  5. Loss of function (functio laesa)
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15
Q

When would you see the 5 signs of inflammation?

A

Loss of function

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16
Q

What causes systemic affects during inflammation?

A

Inflammatory mediators e.g. IL-1, IL-6 and TNF-a

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17
Q

What are the effects of inflammatory mediators?

A
  • Fever
  • Secretion of acute phase proteins from the liver (e.g. CRP)
  • Hormone production e.g. ADH, cortisol, adrenaline -> malaise, weakness, appetite loss.
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18
Q

What is acute inflammatory exudate?

A

Made up of fluid, fibrin, neutrophils. the fibrin acts as a scaffold which neutrophils can use to move around the area of inflammation. Neutrophils phagocytose and kill microorganisms and release enzymes to breakdown the damaged tissue

19
Q

CRP

A

Acute phase protein produced by the liver in response to IL-6 secreted by macrophages.

  • Opsonin
  • facilitates phagocytosis of bacteria (opsonin mediated phagocytosis)
  • Raised CRP may indicate bacterial infection but not reliable as not specific
20
Q

What are the outcomes of inflammation?

A
  1. Regeneration (resolution)
  2. Repair with scarring
  3. Progression to chronic inflammation
21
Q

When can CRP be raised?

A
  • Bacterial infection
  • Burns
  • Trauma
  • Polymyalgia rheumatica,
  • Giant cell arteritis.
22
Q

Raised CRP is a risk factor for atherosclerosis - T/F?

A

T - independent risk factor. However no role in screening etc.

23
Q

What is resolution (regeneration) in acute inflammation?

A

This is complete restoration of the normal structure and function. It is the best outcome.

Example - split thickness skin graft.

24
Q

What is repair in acute inflammation?

A

Repair results in fibrous scar formation.

More likely when there is substantial tissue destruction leading damage to the connective tissue framework. The damaged cells are unable to regenerate.

25
Q

What are the 2 main steps of repair in acute inflammation?

A
  1. Organisation

2. Scar formation

26
Q

What is organisation during repair of acute inflammation?

A

Replacement of inflammatory exudate by granulation tissue. Granulation tissue is a fragile complex of proliferating capillaries, macrophages and fibroblasts. Macrophages phagocytose the debris. The capillaries give granulation tissue its distinctive red colour.

27
Q

What happens in scar formation?

A

Granulation tissue is replaced by a scar. The scar is laid down by fibroblasts. A scar is composed mainly of fibrosis tissue. Collagen fibres are the main component of fibrous tissue.

The scar is mechanically strong but lacks the specialised function of the original tissue leading to a loss of specialised function.

Examples: myocardium following an MI.

28
Q

What is an abscess?

A

An abscess is a localised collection of pus within a newly formed cavity in a tissue.

29
Q

What causes an abscess to form?

A

Abscess formation is usually initiated by certain bacterial infections (so-called “pyogenic” organisms such as staphyloccocus aureus). The bacteria cause damage to the tissues and so the body mounts an inflammatory response. The inflammatory response is characterised by massive emigration of neutrophils which die after phagocytosis of the organisms and release large amounts of lysosomal enzymes. This, together with bacteria-derived substances (exotoxins) that also damage tissues, results in the formation of a cavity. The cavity contains pus - a thick, opaque yellow-green fluid.

30
Q

What are the zones of an abscess?

A
  • A cavity which contains pus. Pus contains liquefied dead (necrotic) tissues with dead and dying neutrophils, fibrin and oedema fluid.
  • At the periphery of the pus there is a layer of living neutrophils and fibrin (remember the main components of acute inflammatory exudate).
  • A wall (sometimes called a “membrane”) composed of two distinct zones:
    ○ An inner layer of granulation tissue containing new capillaries
    ○ An outer layer of fibroblastic tissue laying down scar tissue.
    The two layers of the wall represent the body’s attempt to repair the area of damage. (see above)
31
Q

Is abscess formation protective?

A

Yes, The abscess wall also acts as a barrier to prevent further spread of the infection and so, from the point of view of localising the infection, abscess formation is protective. However, the abscess wall prevents the release of the abscess contents without which healing cannot occur. Therefore, abscess usually require “incision and drainage” to enable healing to occur

32
Q

How do you treat an abscess?

A

Incision and drainage

33
Q

What are the most common sites of abscess formation?

A

The most common sites of abscess formation are in the skin and in association with a tooth (“dental abscess”). However, in theory an abscess can form within any solid tissue.

34
Q

What is the difference between empyema and abscess?

A

Empyemas are accumulations of pus in pre-existing rather than a newly formed anatomical cavity.

35
Q

What is chronic inflammation?

A

Chronic inflammation is said to occur when inflammation persists for weeks, months or longer. It may arise from unresolved acute inflammation or occur from the outset. It is important as it is much more likely to cause tissue destruction and heal with irreversible scarring rather than regeneration.
• Due to persistent injury
• Cells: lymphocytes, macrophages and plasma cells.

36
Q

Give examples of chronic inflammation?

A
  • Persistent infection e.g. H. pylori, M. tuberculosis, Hepatitis C.
  • Autoimmune diseases
  • Non-living material e.g. asbestos –> asbestosis; coal dust –> pneumoconiosis.
37
Q

What 3 processes occur simultaneously in chronic inflammation?

A

• Persistent tissue injury and destruction
• An on-going inflammatory response to limit the damage.
○ The main inflammatory cells are macrophages, lymphocytes and plasma cells.
• Attempts to organise and heal by fibrous (scarring).

38
Q

Using a chronic gastric ulcer as an example, describe chronic inflammation?

A

A good example of chronic inflammation: Chronic gastric ulcer - example of chronic inflammation.
- On going tissue damage, the acid is killing cells.
3 things that happen:
1. Stale mate - acid repair vs acid
2. Can put someone on a PPI - therefore you can lever the amount of acid and healing can occur.
3. Perforate - fatal

39
Q

What are the consequences of chronic inflammation?

A

• Scarring (=fibrosis)
- Healing by scarring may lead to problems e.g. chronic gastric ulcer causing gastric outlet obstruction.
• Tissue destruction
- E.g. gastric ulcer causing perforation or haemorrhage
• Development of cancer
- E.g. H. pyori gastritis predisposes to gastric carcinoma
• Diversion of nutrients
- There is huge demand to maintain inflammatory/ immune response and regeneration. In time this leads to weight loss, anaemia of chronic disease, deceased host resistance.
• Amyloidosis
- Reactive systemic amyloid (AA amyloid)

40
Q

What is granulomatous inflammation?

A

Granulomatous inflammation is a specific type of chronic inflammation.
A granuloma is an aggregate of activated (epithelioid) macrophages.
[‘-oid’ = resembles; ‘epitheloid’= resemble epithelial cells]

* Type of chronic inflammation, has macrophages 
* E.g. TB (get the walling off of the TB, therefore it is protective), chron's, sarcoidosis  and leprosy

A granuloma: aggregation of activated macrophages.(epithelioid - as they look like epithelial cells)

41
Q

Examples of granulomatous inflammation

A
  • Infections e.g. mycobacteria
  • Sarcoidosis
  • Crohn’s disease
42
Q

Cells involved in granulomas

A

Causes caseous necrosis (looks like cream cheese) - seen in TB.
Lots of tiny granulomas outside of the structure in the middle.
IFN-y helps the fusing of the giant macrophages.
Collagen can form to make an abscess as forms on the outside then you get pus in the middle.
Langhans cells - horse shoe shaped nucleus.

43
Q

Atherosclerosis?

A

• Normally only occurs in arteries as it needs the high blood pressure - that injures the endothelial lining leading to an acute inflammatory response.
• It affects the tunica intima
• Smoking, HBP, dyslipidaemia and diabetes. - they either damage the lining or contribute to depositing things in the lining.
LDL cholesterol - more responsible.
When macrophage is activated it looks foamy, therefore called foam cell.
Foam cell: Are a type of macrophage that localize to fatty deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance.

Fatty streak - low level inflammation in the intima.

IOD - Cell Pathology (18 decks)

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