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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
What is pus formed from? (7)
``` Dead Tissue Organisms Exudate Neutrophils Fibrin Red Cells Debris ```
26
What surrounds the pus in an abscess?
A pyogenic membrane
27
What is a multiloculated abscess?
Occurs when pus bursts through the pyogenic membrane and forms new cavities.
28
What occurs in organisation in the context of acute inflammation?
Granulation tissue formation Healing and repair Leads to fibrosis and scarring
29
What is granulation tissue formed by/from?
New capillaries Fibroblasts and collagen Macrophages
30
What is dissemination in the context of acute inflammation?
Spread of inflammation (infection) to blood stream - sepsis
31
Contrast the terms: Bacteraemia Septicaemia Toxaemia
Bacteria: bacteria in blood Septicaemia: GROWTH of bacteria in blood Toxaemia: toxic products in the blood
32
What is shock?
An inability to perfuse the tissues
33
What are the symptoms of septic shock?
``` Peripheral vasodilation Tachycardia Hypotension Pyrexia Haemorrhagic rash (sometimes) ```
34
Describe the pathogenesis of sepsis
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
What are the predominant cell types in chronic inflammation?
Lymphocytes Plasma Cells Macrophages
36
What are the features of chronic inflammation?
Tissue/organ necrosis | Loss of function
37
Describe the clinical presentation of chronic inflammation
Often no specific localised pain Malaise and weight loss Loss of function
38
Describe the formation of granulation tissue
Capillaries grow into inflammatory mass Presence of plasma proteins and macrophages Fibroblasts lay down collagen to repair damaged tissue Collagen replaces exudate
39
What is the function of granulation tissue?
Patches tissue defects Replaces necrotic tissue Contracts and pulls together wound
40
What are the products of organisation (granulation tissue formation)
Scar (fibrous tissue) Fibrosis (can be problematic) -this can progress to chronic inflammation
41
What are the possible causes of primary chronic inflammation? (4) Give an example for each cause
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
What are the functions of B-lymphocytes in chronic inflammation?
``` Differentiate to form plasma cells Facilitate the immune response Act with macrophages (presenting the antigen) Act with T-lymphocytes Have immune memory ```
43
What are the functions of T-lymphocytes in chronic inflammation?
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
What are the functions of natural killer cells in chronic inflammation?
Destroy antigens and cells | -Using granule proteins
45
What are the functions of macrophages in chronic inflammation?
Remove debris | Antigen present
46
Describe the mechanism of action of macrophages in chronic inflammation.
Motile phagocytes that move from the blood Take over from neutrophils (macrophages are longer lived) Contain enzymes and produce interferon and other chemicals
47
What are the functions of fibroblasts in chronic inflammation
Make and assemble structural proteins (collagen)
48
What is a granuloma?
An aggregate of epithelioid macrophages
49
What is an epithelioid macrophage?
A macrophage that looks like an epithelial cell.
50
What is a giant cell?
Multinucleate cells with a large cytoplasm | Possible result from the fusion of macrophages to form larger cells.
51
What are the different cell types that may be associated with granulomas?
``` !Epithelioid macrophages Giant cells Lymphocytes Neutrophils Eosinophils ```
52
State factors favouring wound healing (6)
``` Cleanliness Good nutrition Metabolic stability Normal coagulation Local mediators Apposition of edges -No haematoma ```
53
State factors impairing wound healing. (7)
``` Dirty, gaping wound Haematoma Poor nutrition -Lack of vitamins A and C Abnormal carbohydrate metabolism Diabetes Corticosteroid therapy Inhibition of angiogenesis ```
54
Summarise the process of wound healing
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
What cells types are present in fracture healing in addition to those found in normal wound healing?
Osteoblasts in addition to fibroblasts in granulation phase
56
What is type I hypersensitivity?
Inappropriate synthesis of IgE by the immune system (allergy)
57
What is IgE production which is associated with symptoms known as?
Allergy
58
What is IgE production which is not associated with symptoms known as?
Atopy (subclinical sensitisation)
59
Describe the pathogenesis of type I hypersensitivity
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
What is type II hypersensitivity?
IgG and IgM mediated hypersensitivity directed against antigens (either exogenous or self) on the surface of cells or fixed within tissues
61
Describe the mechanism of type II hypersensitivity
Antibody binds to relevant antigen Complement activated Fc binding of immunoglobulin and stimulation of phagocytes Antibody dependent cellular cytotoxicity (ADCC)
62
What is type III hypersensitivity?
The abnormal deposition of formed immune complexes (antigen/antibody complexes)
63
What is the normal fate of immune complexes?
Enter blood stream and travel to liver and spleen to be taken up and destroyed by fixed phagocytes
64
What occurs to immune complexes in type III hypersensitivity and what are the consequences of this?
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
What is type IV hypersensitivity?
Delayed-type hypersensitivity | Hypersensitivity mediated by Th1 and cytokines in response to inert environmental substances and certain infections
66
Why does type IV hypersensitivity occur?
The body struggles to destroy the agents
67
What is a Hapten?
A non-infectious agent of low molecular weight which elicits a type IV hypersensitive response
68
What is a carrier protein? (in the context of type IV hypersensitivity)
A protein to which a hapten is bound
69
How long does type IV hypersensitivity take to produce a clinical effect?
48-72 hours
70
Describe the pathogenesis of type IV hypersensitivity to a non-infectious agent
Exogenous low molecular weight antigen (hapten) + endogenous protein (carrier) Antigen uptake and presentation (MHC II) Th1 antigen recognition/cytokine production Inflammation
71
Describe the pathogenesis of type IV hypersensitivity to an infectious agent
Microorganism (eg mycobacterium) Antigen uptake and presentation (MHC II) Th1 antigen recognition/cytokine production Inflammation
72
What is autoimmunity?
An immune response against autoantigens
73
What is tolerance?
The process by which the immune system avoids damaging reactions against autoantigens
74
How is tolerance accomplished?
(Central tolerance) Deletion of autoreactive lymphocytes during maturation (Peripheral tolerance) inhibition of autoreactive cells which escape central tolerance
75
What are the effector mechanisms involved in autoimmunity?
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
What two factors are the most important contributors to the manifestation of autoimmunity?
Environmental and genetic

Principles of Disease (6 decks)

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