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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
How can systemic infection spread?
Through lymph or blood
26
What factors control the spread of infection?
``` Virulence of the organisms Host condition (i.e.immunosuprresion) Low protein levels Poor vascular supply Treatment given ```
27
What are the four key clinical features of a systemic inflammatory response?
Increased respiratory rate Increased heart rate High or low temperature High or low white cell count
28
In what cases will there by resolution of acute inflammation?
If there is minimal tissue damage Occurs in tissue with regenerative capacity Cause is rapidly removed or destroyed Good vascular drainage
29
In what cases will there be healing by fibrosis following acute inflammation?
After substantial tissue damage If tissue is incapable of regeneration If there is abundant fibrin exudate
30
In what cases will acute inflammation persist to chronic inflammation?
Persistence of stimulus | Tissue destruction leading to ongoing inflammation
31
What is an exudate?
An extracellular fluid with a high protein and cellular content
32
What is a transudate?
An extracellular fluid with a low protein and cellular content
33
What is the role of an exudate in inflammation?
Allows delivery of nutrients Dilution of toxins Entry of antibodies Stimulates immune response
34
Describe a serous exudate
Usually transudate, found in pleural, pericardial, peritoneal spaces
35
Describe a fibrinous exudate
fluid rich in fibrin, often on serial surface/meninges
36
Describe a suppurative exudate
Pus forming, an exudate ruch in neutrophil polymorphs
37
Describe a haemorrhagic exudate
severe vascular injury or depletion of coagulator factors
38
Describe a membranous exudate
epithelium becomes coated in membrane formed by fibrin, epithelial cells and inflammatory cells
39
Describe a pseudomembranous (ulceration) exudate
surface exudate on mucosal/exudate sites e.g. c diff colitis
40
Describe a necrotising exudate
high tissue pressure leading to vascular occlusion and thrombosis
41
When is inflammation defined as chronic?
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
Chronic inflammation will always lead to scarring. T/F?
True - there will always be a degree of scarring
43
What cells are involved in chronic inflammation?
Macrophages, plasma cells, lymphocytes
44
What factors determine whether or not chronic inflammation will take place?
``` Site affected Type of wound Presence of infection Type of organism involved Presence of indigestible material Treatment given Background disease ```
45
What is granulomatous inflammation?
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
Giant cells are formed from fused epithelioid macrophages. T/F?
True
47
What type of inflammation is classically seen in tuberculosis?
Caseous necrosis
48
Give examples of infectious agents which can cause granulomatous inflammation?
Tuberculosis Leprosy Toxoplasmosis
49
Give examples of substances/conditions, other than infectious agents which can cause granulomatous inflammation?
Talc or other foreign materials Sarcoidosis Chron's disease Hodgkin's lymphoma
50
What are epithelioid macrophages?
Modified macrophages arranged in small nodules or clusters which have a mainly secretory role
51
The formation of granulomas is an example of what type of hypersensitivity?
Type 4
52
What tissues are affected by rheumatoid arthritis?
``` Skin Blood vessels Heart Lungs Joints Muscle ```
53
In rheumatoid arthritis, what WBCs are present in the synovial fluid?
Neutrophils
54
Which type of WBC are particularly involved in the pathogenesis of atherosclerosis?
Macrophages - these become foam cells in atherosclerosis
55
In choleric granulomatous disease there is a defect in which enzyme system?
NADPH oxidase system
56
In which condition is there a defect in the NADPH oxidase system which results in an inability to kill intracellular organisms by respiratory burst?
Chronic granulomatous disease
57
What type of wound heals by primary intention?
Incised wound
58
Healing by primary intension is more likely to leave a scar than healing by secondary intention. T/F?
False- the opposite is true
59
In fracture healing, how long does it take the soft callus to ossify?
4-6 weeks
60
in fracture healing, for how long does remodelling occur?
Months to years
61
What are the steps in fracture healing?
Formation of a haematoma Recruitment of leucocytes to the site and formation of granulation tissue soft callus formation remodelling
62
What are the steps in cutaneous wound healing?
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
Give examples of local factors which can affect wound healing.
``` Type, size and location of wound Movement within wound Infection Presence of foreign/necrotic material Irradiation Poor blood supply ```
64
Give examples of systemic factors which can affect wound healing.
``` age nutrition systemic disease drugs smoking ```

Pathological Mechanisms (10 decks)

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