Inflammation Flashcards

1
Q

What is the purpose of inflammation?

A

To destroy or control the harmful stimulus, initiate repair and restore function

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2
Q

Give examples of situations in which inflammation occurs pathologically?

A

Autoimmune disease
Atheroma
Cancer

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3
Q

During inflammation what factors mediate vasodilation?

A

Histamine from mast cells

Prostaglandins and NO

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4
Q

During inflammation, what factors result in neutrophil activation?

A

C5
Leukotrienes
B4
Bacterial products

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5
Q

During inflammation, what factors result in endothelial activation?

A
5-HT 
Histamine
C3
C5
Bradykinin
Leukotrienes
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6
Q

What is the result of activation of the endothelium in inflammation?

A

Increased cell adhesion molecules
Increased leakiness of endothelium
Movement of plasma proteins (immunoglobulins, complement, fibrinogen) into tissues

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7
Q

What cytokines do macrophages produce in an inflammatory reaction?

A

TNF
IL-1
IL-6

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8
Q

The binding of which type of antibody stimulates degranulation of mast cells?

A

IgE

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9
Q

Other than the binding of IgE, what can stimulate mast cells to degranulate?

A

Injury

Complement

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10
Q

What is the role of plasma cells in inflammation?

A

Antibody production

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11
Q

Rolling adhesion of white cells in the blood is regulated by selecting. What factors up regulate selections?

A

IL-1
TNF
(FROM MACROPHAGES)

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12
Q

What factors mediate the adhesion of white blood cells to the endothelial walls prior to diapedesis?

A

Integrins

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13
Q

GPCRs recognise products of short bacterial peptide, complement and prostaglandins in order to induce chemotaxis and production of the respiratory burst. Which leucocytes utilise this type of receptor?

A

Plasma cells

Macrophages

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14
Q

Receptors for opsonins exist on the surface of WBCs, What is the purpose fo these?

A

These coat a particle to target for ingestion

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15
Q

What cytokine can activate macrophages?

A

INF-gamma

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16
Q

What is the purpose of C5a in the complement pathway?

A

Chemotactic for neutrophils
Increases vascular permeability
Releases histamine from mast cells

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17
Q

What factors in the complement pathway have cytolytic activity?

A
C5
C6
C7
C8
C9
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18
Q

What factors in the complement pathway opsonise bacteria?

A

C4b
C2a
C3b

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19
Q

What are the steps involved in phagocytosis?

A
Opsonisation
Engulfment using pseudopodia
Formation of phagosomes
Fusion with lysosomes containing enzymes to form phagolysosomes
Destruction of material
Removal from the cell by pinocytosis
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20
Q

What are the clinical signs of inflammation and how are these caused?

A

Redness, heat and swelling caused by hyperaemia
Pain caused by release of bradykinin and PGE2
Loss of function caused by combination of above signs

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21
Q

How is acute inflammation terminated?

A
Removal of stimulus
Short half life of neutrophils
Variation in cytokine stimuli
Neural impulses
Macrophages activated to perform different functions
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22
Q

How can infection by spread?

A

Natural barriers
Air borne
Blood borne
Immune factors

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23
Q

What are the benefits of acute inflammation?

A
Dilutes toxins through oedema
Increases entry of antibodies
Increases drug transport
Fibrin traps micro-organisms
Delivers nutrients
Stimulates immune response
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24
Q

What are the detrimental effects of acute inflammation?

A

Digestion of normal tissues
Swelling e.g. epiglottitis
Inappropriate responses e.g. hypersensitivity

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25
Q

How can systemic infection spread?

A

Through lymph or blood

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26
Q

What factors control the spread of infection?

A
Virulence of the organisms
Host condition (i.e.immunosuprresion)
Low protein levels
Poor vascular supply
Treatment given
27
Q

What are the four key clinical features of a systemic inflammatory response?

A

Increased respiratory rate
Increased heart rate
High or low temperature
High or low white cell count

28
Q

In what cases will there by resolution of acute inflammation?

A

If there is minimal tissue damage
Occurs in tissue with regenerative capacity
Cause is rapidly removed or destroyed
Good vascular drainage

29
Q

In what cases will there be healing by fibrosis following acute inflammation?

A

After substantial tissue damage
If tissue is incapable of regeneration
If there is abundant fibrin exudate

30
Q

In what cases will acute inflammation persist to chronic inflammation?

A

Persistence of stimulus

Tissue destruction leading to ongoing inflammation

31
Q

What is an exudate?

A

An extracellular fluid with a high protein and cellular content

32
Q

What is a transudate?

A

An extracellular fluid with a low protein and cellular content

33
Q

What is the role of an exudate in inflammation?

A

Allows delivery of nutrients
Dilution of toxins
Entry of antibodies
Stimulates immune response

34
Q

Describe a serous exudate

A

Usually transudate, found in pleural, pericardial, peritoneal spaces

35
Q

Describe a fibrinous exudate

A

fluid rich in fibrin, often on serial surface/meninges

36
Q

Describe a suppurative exudate

A

Pus forming, an exudate ruch in neutrophil polymorphs

37
Q

Describe a haemorrhagic exudate

A

severe vascular injury or depletion of coagulator factors

38
Q

Describe a membranous exudate

A

epithelium becomes coated in membrane formed by fibrin, epithelial cells and inflammatory cells

39
Q

Describe a pseudomembranous (ulceration) exudate

A

surface exudate on mucosal/exudate sites e.g. c diff colitis

40
Q

Describe a necrotising exudate

A

high tissue pressure leading to vascular occlusion and thrombosis

41
Q

When is inflammation defined as chronic?

A

Persistent and lacks resolution when the inflamed tissue is unable to overcome the effects of the injurious agent
Persists for weeks, months or years
Characterised by infiltrates of lymphocytes, plasma cells and macrophages

42
Q

Chronic inflammation will always lead to scarring. T/F?

A

True - there will always be a degree of scarring

43
Q

What cells are involved in chronic inflammation?

A

Macrophages, plasma cells, lymphocytes

44
Q

What factors determine whether or not chronic inflammation will take place?

A
Site affected
Type of wound
Presence of infection
Type of organism involved
Presence of indigestible material
Treatment given
Background disease
45
Q

What is granulomatous inflammation?

A

A distinctive pattern of chronic inflammation where the predominant cell types involved are activated macrophages with a modified appearance (epithelioid macrophages) and giant cells

46
Q

Giant cells are formed from fused epithelioid macrophages. T/F?

47
Q

What type of inflammation is classically seen in tuberculosis?

A

Caseous necrosis

48
Q

Give examples of infectious agents which can cause granulomatous inflammation?

A

Tuberculosis
Leprosy
Toxoplasmosis

49
Q

Give examples of substances/conditions, other than infectious agents which can cause granulomatous inflammation?

A

Talc or other foreign materials
Sarcoidosis
Chron’s disease
Hodgkin’s lymphoma

50
Q

What are epithelioid macrophages?

A

Modified macrophages arranged in small nodules or clusters which have a mainly secretory role

51
Q

The formation of granulomas is an example of what type of hypersensitivity?

52
Q

What tissues are affected by rheumatoid arthritis?

A
Skin
Blood vessels
Heart
Lungs
Joints
Muscle
53
Q

In rheumatoid arthritis, what WBCs are present in the synovial fluid?

A

Neutrophils

54
Q

Which type of WBC are particularly involved in the pathogenesis of atherosclerosis?

A

Macrophages - these become foam cells in atherosclerosis

55
Q

In choleric granulomatous disease there is a defect in which enzyme system?

A

NADPH oxidase system

56
Q

In which condition is there a defect in the NADPH oxidase system which results in an inability to kill intracellular organisms by respiratory burst?

A

Chronic granulomatous disease

57
Q

What type of wound heals by primary intention?

A

Incised wound

58
Q

Healing by primary intension is more likely to leave a scar than healing by secondary intention. T/F?

A

False- the opposite is true

59
Q

In fracture healing, how long does it take the soft callus to ossify?

60
Q

in fracture healing, for how long does remodelling occur?

A

Months to years

61
Q

What are the steps in fracture healing?

A

Formation of a haematoma
Recruitment of leucocytes to the site and formation of granulation tissue
soft callus formation
remodelling

62
Q

What are the steps in cutaneous wound healing?

A

Formation of blood clot, formation of granulation tissue, cell proliferation and collagen deposition, scar formation, wound contraction, connective tissue remodelling, recovery of tensile strength

63
Q

Give examples of local factors which can affect wound healing.

A
Type, size and location of wound
Movement within wound
Infection
Presence of foreign/necrotic material
Irradiation
Poor blood supply
64
Q

Give examples of systemic factors which can affect wound healing.

A
age
nutrition
systemic disease
drugs 
smoking