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Principles of Disease > Inflammation, Hypersensitivity, and Autoimmunity > Flashcards

Inflammation, Hypersensitivity, and Autoimmunity Flashcards

1
Q

What are the signs of inflammation?

A 
Rubour - redness
Calor - heat
Tumour - swelling
Dolor - pain
Loss of function
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2
Q

What are the possible causes of acute inflammation? (6)

A

Microorganisms (infection)
Mechanical (injury)
Chemical (upset pH, bile and urine in the wrong place causing irritation)
Physical (extreme heat, cold, radiation)
Dead Tissue (necrotic tissue irritating adjacent tissue)
Hypersensitivity

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3
Q

What makes up the microcirculation?

A 
Capillary beds (arterioles, venules)
Extracellular compartment and contents`
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4
Q

Where does the process of inflammation occur?

A

In the microcirculation

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5
Q

Describe the process of inflammation

A

Change in vessel radius alters blood flow
Change in vessel wall permeability causes exudation
Neutrophils move from the vessel into the extravascular space

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6
Q

Contrast normal laminar flow and blood flow in inflammation

A

Normal: Heaviest components (neutrophils) in centre of vessel, intermediate components farther from centre (erythrocytes), lightest components nearest edges of vessel (plasma)

In inflammation:
Neutrophils migrate to edge of vessel, erythrocytes collect in centre.

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7
Q

What is neutrophil margination?

A

Neutrophils migrate toward vessel wall

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8
Q

What is neutrophil pavementing?

A

Neutrophils adhere to endothelium

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9
Q

What is neutrophil emigration?

A

Neutrophils actively squeeze between endothelial cells into the extravascular tissues

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10
Q

What term would be used to describe inflammation of the peritoneal cavity?

A

Peritonitis

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11
Q

What term would be used to describe inflammation of the meninges?

A

Meningitis

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12
Q

What term would be used to describe inflammation of the appendix?

A

Appendicitis

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13
Q

What term would be used to describe inflammation of the lung?

A

Pneumonia

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14
Q

What term would be used to describe inflammation of the pleural cavity?

A

Pleurisy

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15
Q

What is the function of neutrophils and how do they act?

A

Mobile phagocytes

Neutrophils release granule contents and phagocytose and destroy foreign antigens. .

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16
Q

What do neutrophil granules contain?

A

Granules possess oxidants (eg hydrogen peroxide) and enzymes (eg proteases)

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17
Q

What are the consequences of neutrophil action?

A

Neutrophils die when granule contents are released (as they digest self in addition to pathogen)
Pus production
May extend into other tissues to progress the inflammation

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18
Q

What is pus?

A

Fluid
Cell remnants
Endogenous protein

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19
Q

What are the three general types of mediators of acute inflammation?

A

Molecules on endothelial cell surface membrane
Molecules released from cells
Molecules in the plasma

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20
Q

What are the general effects of mediators of acute inflammation?

A 
Vasodilation/Vasocontriction
Altered permeability
Neutrophil adhesion
Chemotaxis
Itch 
Pain
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21
Q

Why do mediators of acute inflammation result in a dynamic balance?

A

They have both positive and negative effects which can favour and inhibit inflammation and they are relative to need.

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22
Q

What are some of the immediate systemic effects of acute inflammation?

A

Pyrexia
Feeling unwell (malaise, anorexia, naurea, and also abdominal pain and vomiting in children)
Neutrophilia

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23
Q

What are some of the longer term system effects of inflammation?

A

Lymphadenopathy
Weight loss
Anaemia

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24
Q

What is an abscess?

A

A collection of pus (suppuration) under pressure

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25
Q

What is pus formed from? (7)

A 
Dead Tissue
Organisms
Exudate
Neutrophils
Fibrin
Red Cells
Debris
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26
Q

What surrounds the pus in an abscess?

A

A pyogenic membrane

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27
Q

What is a multiloculated abscess?

A

Occurs when pus bursts through the pyogenic membrane and forms new cavities.

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28
Q

What occurs in organisation in the context of acute inflammation?

A

Granulation tissue formation
Healing and repair
Leads to fibrosis and scarring

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29
Q

What is granulation tissue formed by/from?

A

New capillaries
Fibroblasts and collagen
Macrophages

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30
Q

What is dissemination in the context of acute inflammation?

A

Spread of inflammation (infection) to blood stream - sepsis

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31
Q

Contrast the terms:
Bacteraemia
Septicaemia
Toxaemia

A

Bacteria: bacteria in blood
Septicaemia: GROWTH of bacteria in blood
Toxaemia: toxic products in the blood

32
Q

What is shock?

A

An inability to perfuse the tissues

33
Q

What are the symptoms of septic shock?

A 
Peripheral vasodilation
Tachycardia
Hypotension
Pyrexia
Haemorrhagic rash (sometimes)
34
Q

Describe the pathogenesis of sepsis

A

Systemic release of mediators in the plasma

  • Cause vasodilation
  • Results in catecholamine (adrenaline and noradrenaline) release
  • Tachycardia results as heart attempts to compensate for above

Bacterial endotoxin released
-Interlukin-1 released which acts on hypothalamus causing pyrexia

35
Q

What are the predominant cell types in chronic inflammation?

A

Lymphocytes
Plasma Cells
Macrophages

36
Q

What are the features of chronic inflammation?

A

Tissue/organ necrosis

Loss of function

37
Q

Describe the clinical presentation of chronic inflammation

A

Often no specific localised pain
Malaise and weight loss
Loss of function

38
Q

Describe the formation of granulation tissue

A

Capillaries grow into inflammatory mass
Presence of plasma proteins and macrophages
Fibroblasts lay down collagen to repair damaged tissue
Collagen replaces exudate

39
Q

What is the function of granulation tissue?

A

Patches tissue defects
Replaces necrotic tissue
Contracts and pulls together wound

40
Q

What are the products of organisation (granulation tissue formation)

A

Scar (fibrous tissue)
Fibrosis (can be problematic)
-this can progress to chronic inflammation

41
Q

What are the possible causes of primary chronic inflammation? (4) Give an example for each cause

A

Autoimmune disease
-Thyroiditis

Material resistant to digestion

  • Mycobacteria, brucella, viruses
  • Cell wall resistant to enzymes

Exogenous substances

  • Sutures, Metal/plastic (eg joint replacement), glass
  • Do not provoke immune response

Endogenous substances

  • Necrotic tissue, keratin, hair
  • Cannot be easily phagocytosed
42
Q

What are the functions of B-lymphocytes in chronic inflammation?

A 
Differentiate to form plasma cells
Facilitate the immune response
Act with macrophages (presenting the antigen)
Act with T-lymphocytes
Have immune memory
43
Q

What are the functions of T-lymphocytes in chronic inflammation?

A

Produce cytokines

  • Attract and hold macrophages
  • Activate macrophages
  • Affect permeability

Produce interferon

  • Antiviral effects
  • Attract and stimulate other cells

Damage and lyse other cells and destroy antigen
-Using granule proteins

44
Q

What are the functions of natural killer cells in chronic inflammation?

A

Destroy antigens and cells

-Using granule proteins

45
Q

What are the functions of macrophages in chronic inflammation?

A

Remove debris

Antigen present

46
Q

Describe the mechanism of action of macrophages in chronic inflammation.

A

Motile phagocytes that move from the blood
Take over from neutrophils (macrophages are longer lived)
Contain enzymes and produce interferon and other chemicals

47
Q

What are the functions of fibroblasts in chronic inflammation

A

Make and assemble structural proteins (collagen)

48
Q

What is a granuloma?

A

An aggregate of epithelioid macrophages

49
Q

What is an epithelioid macrophage?

A

A macrophage that looks like an epithelial cell.

50
Q

What is a giant cell?

A

Multinucleate cells with a large cytoplasm

Possible result from the fusion of macrophages to form larger cells.

51
Q

What are the different cell types that may be associated with granulomas?

A 
!Epithelioid macrophages
Giant cells
Lymphocytes
Neutrophils
Eosinophils
52
Q

State factors favouring wound healing (6)

A 
Cleanliness
Good nutrition
Metabolic stability
Normal coagulation
Local mediators
Apposition of edges
-No haematoma
53
Q

State factors impairing wound healing. (7)

A 
Dirty, gaping wound
Haematoma
Poor nutrition
-Lack of vitamins A and C
Abnormal carbohydrate metabolism
Diabetes
Corticosteroid therapy
Inhibition of angiogenesis
54
Q

Summarise the process of wound healing

A
  1. Injury
  2. Blood clot
  3. Acute inflammation
  4. Fibrin
  5. Granulation tissue growth
    - Angiogenesis
  6. Phagocytosis of fibrin
  7. Myofibroblasts lay down collagen
  8. Contraction of scar
  9. Re-epithelialisation
55
Q

What cells types are present in fracture healing in addition to those found in normal wound healing?

A

Osteoblasts in addition to fibroblasts in granulation phase

56
Q

What is type I hypersensitivity?

A

Inappropriate synthesis of IgE by the immune system (allergy)

57
Q

What is IgE production which is associated with symptoms known as?

A

Allergy

58
Q

What is IgE production which is not associated with symptoms known as?

A

Atopy (subclinical sensitisation)

59
Q

Describe the pathogenesis of type I hypersensitivity

A

Allergen Exposure
Mast cell + allergen specific IgE
Release of inflammatory mediators (eg histamine and prostaglandins)
Signs and Symptoms (muscosal oedema, capillary leakage, secretions, smooth muscle contraction, vasodilatation)

60
Q

What is type II hypersensitivity?

A

IgG and IgM mediated hypersensitivity directed against antigens (either exogenous or self) on the surface of cells or fixed within tissues

61
Q

Describe the mechanism of type II hypersensitivity

A

Antibody binds to relevant antigen
Complement activated
Fc binding of immunoglobulin and stimulation of phagocytes
Antibody dependent cellular cytotoxicity (ADCC)

62
Q

What is type III hypersensitivity?

A

The abnormal deposition of formed immune complexes (antigen/antibody complexes)

63
Q

What is the normal fate of immune complexes?

A

Enter blood stream and travel to liver and spleen to be taken up and destroyed by fixed phagocytes

64
Q

What occurs to immune complexes in type III hypersensitivity and what are the consequences of this?

A

Precipitate out into tissues.
Causes inflammation
-Serum sickness (systemic illness with complexes deposited in many tissues)
-Arthus reaction (complexes localised to a particular tissue)

65
Q

What is type IV hypersensitivity?

A

Delayed-type hypersensitivity

Hypersensitivity mediated by Th1 and cytokines in response to inert environmental substances and certain infections

66
Q

Why does type IV hypersensitivity occur?

A

The body struggles to destroy the agents

67
Q

What is a Hapten?

A

A non-infectious agent of low molecular weight which elicits a type IV hypersensitive response

68
Q

What is a carrier protein? (in the context of type IV hypersensitivity)

A

A protein to which a hapten is bound

69
Q

How long does type IV hypersensitivity take to produce a clinical effect?

A

48-72 hours

70
Q

Describe the pathogenesis of type IV hypersensitivity to a non-infectious agent

A

Exogenous low molecular weight antigen (hapten) + endogenous protein (carrier)
Antigen uptake and presentation (MHC II)
Th1 antigen recognition/cytokine production
Inflammation

71
Q

Describe the pathogenesis of type IV hypersensitivity to an infectious agent

A

Microorganism (eg mycobacterium)
Antigen uptake and presentation (MHC II)
Th1 antigen recognition/cytokine production
Inflammation

72
Q

What is autoimmunity?

A

An immune response against autoantigens

73
Q

What is tolerance?

A

The process by which the immune system avoids damaging reactions against autoantigens

74
Q

How is tolerance accomplished?

A

(Central tolerance) Deletion of autoreactive lymphocytes during maturation
(Peripheral tolerance) inhibition of autoreactive cells which escape central tolerance

75
Q

What are the effector mechanisms involved in autoimmunity?

A

Identical to normal immune response, hence:

T-cell and antibody activity
Antibody activation of complement mediated inflammation
Immune complex formation
Recruitment of innate immune cells

76
Q

What two factors are the most important contributors to the manifestation of autoimmunity?

A

Environmental and genetic

Principles of Disease (6 decks)

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