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Part 3 – PM3A > (PM3A) Inflammation > Flashcards

(PM3A) Inflammation Flashcards

1
Q

What is inflammation?

A

Response to stimuli that can cause body damage

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2
Q

What is the function of inflammation?

A

Protection from danger/ damage

Promote healing

CAN lead to tissue damage

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3
Q

What are the cardinal signs for inflammation?

A

(1) Heat – calor
(2) Redness – rubor
(3) Swelling – tumor
(4) Pain –dolor
(5) Loss of function

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4
Q

What is the timescale of an inflammatory response?

A

(1) Irritant/ vaccine injection/ injury
- Production of inflammatory mediators
- Elimination of pathogen

(2) Resolution
- Removal of inflammatory stimuli

(3) Post-resolution
- Influx of adaptive immune cells

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5
Q

What is the innate immune response?

A

Largely inflammation

Non-adaptive

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6
Q

How is the innate immune response triggered?

A

Pattern recognition receptors

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7
Q

What is the adaptive immune response?

A

Triggered or recruited by innate immune response

Immunological memory

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8
Q

What is the summary of inflammatory events of a physical injury, e.g. a splinter?

A

(1) Pathogens recognised by macrophages
(2) Stimulates sentinel cells (mast cells)

(3) Signals to blood vessels to recruit other components
- Leukocytes
- Increase blood vessel dilatation

(4) Movement of fluid into affected area from blood vessel
(5) Phagocytosis of pathogen

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9
Q

What is pattern recognition?

A

The trigger of inflammatory responses

Pattern recognition receptors (PRRs) triggered by pattern-associated molecular patterns (PAMPs)

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10
Q

What are some examples of pattern recognition receptors?

A

Toll-like receptors

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11
Q

How can different stimuli cause a different inflammatory response?

A

Different pattern recognition receptors

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12
Q

What are sentinel cells?

A

Mast cells/ dendritic cells/ macrophages

Release cytokines + inflammatory mediators

Trigger inflammatory responses

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13
Q

What are mast cells?

A

Reside in most tissues

Activated by IgE + C3a + C5a proteins

Release pro-inflammatory mediators
- e.g. histamine/ prostaglandins/ platelet activating factor

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14
Q

What is the role of endothelial cells in the inflammatory response?

A

(1) Respond to pro-inflammatory mediators

(2) Release mediators that cause vasodilatation
- e.g. prostaglandins + nitric oxide

(3) Express adhesion molecules for leukocytes
- e.g. selectins

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15
Q

What are some inflammatory-mediating cells that reside in the tissue?

A

(1) Mast cells
(2) Endothelial cells (of blood vessels)
(3) Macrophages
(4) Leukocytes
(5) Platelets

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16
Q

What are the vascular events of the inflammatory response?

A

Account for rubor/ tumor/ calor

Triggered by cytokines + mediators

Causes:

(1) Vasodilatation
(2) Vascular permeability to fluid
(3) Expression of adhesion molecules on endothelial cells

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17
Q

What are proteolytic cascades?

A

Convert factor XIIa from plasma into pro-inflammatory products

These products activate the complement cascade
ø C1-C9

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18
Q

What are leukocytes?

A

Form the pus

Roll + extrude endothelial cell layer to enter inflammation site

Attracted to pathogens by chemotaxis

Engulf + kill + digest pathogens

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19
Q

What is leukocyte extrusion?

A

(1) Rolling of leukocytes down endothelial cells of blood vessel (veins ONLY) by inflammatory site
(2) Binding to selectins on endothelial membrane
(3) Extrusion of leukocytes through endothelial cells into tissue

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20
Q

What are some later cellular events in inflammation?

A

Caused by monocytes + macrophages

Secondary arrival hours after neutrophils

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21
Q

What is chemotaxis?

A

Movement of leukocytes to site of pathogen

Following chemical signals

Process in inflammatory response

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22
Q

How does failure of healing affect inflammation?

A

Causes chronic inflammation

Leads to loss of function

Can be:

(1) Hypersensitivity – e.g. asthma
(2) Infectious disease – e.g. tuberculosis
(3) Auto-immune diseases

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23
Q

What are some molecular hallmarks of non-resolving inflammation?

A

(1) TNF increasing
(2) IFNs increasing
(3) IL-6 increasing

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24
Q

What are some examples of acute inflammatory responses?

A

(1) Hayfever
(2) Contact dermatitis
(3) Acute asthma attack
(4) Uritcaria

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25
What are some examples of chronic inflammatory responses?
(1) Asthma (2) Rheumatoid arthritis (3) Atherosclerosis
26
What is the role of chemokines and cytokines?
Mediation of inflammatory signals
27
What are cytokines?
Protein/ peptide signalling molecules Modulate function of other cells in inflammation + immunity C3a/ TNF-alpha/ IL-1 are some major pro-inflammatory cytokines
28
What are chemokines?
Type of cytokine Control leukocyte migration e.g. C3a/ C5a/ LTB4
29
What happens following intradermal injection of inflammation?
(1) Flush - arterial vasodilatation (2) Oedema/ swelling (wheal) (3) Flare – sensory nerve induced dilatation
30
What occurs following stimulation of H1 receptors by histamine?
(1) GIT constriction (2) Bronchial smooth muscle constriction (3) Dilatation of blood vessels – stimulates endothelial cells (4) Itch – associated with wound healing
31
How is histamine released?
Mast cell degranulation Caused by C3a, C5a + IgE
32
What are eicosanoids?
Lipid-derived mediators
33
What is the major component for forming lipid-derived inflammatory mediators?
Arachidonic acid
34
What are prostanoids?
Type of eicosanoids Formed by the action of cyclooxygenases (COXs) Most are termed 'prostaglandins'
35
How many types of prostanoid receptor are there?
5 classes DP/ FP/ IP/ EP/ TP EP have 4 subtypes
36
What is the key prostanoid that influences the inflammatory response?
Prostaglandin E2 – PGE2 PGI2 also important
37
How many PGE2 cause fever?
Can alter thermoregulation of hypothalamus
38
What are some types of eicosanoids?
(1) Prostanoids/ prostaglandins (2) Leukotrienes (3) Lipoxins
39
What is 5-lipoxygenase?
Leukotrienes
40
What is the role of leukotrienes?
Constrict bronchial smooth muscle Increase vascular permeability Evoke wheal + flare Antagonists of leukotriene receptors used in treated of asthma - e.g. montelukast
41
What properties do lipoxins have?
Pro resolving properties Help to resolve inflammation
42
What is platelet activating factor (PAF)?
Stimulates the signs + symptoms of inflammation Induces pain Formation is inhibited by glucocorticoids
43
What is the significance of nitric oxide as an inflammatory mediator?
Bioactive gas Evokes vasodilatation High concentrations are cytotoxic + can kill pathogens
44
What is TNF-alpha?
Type of inflammatory mediator
45
What is the significance of bradykinin as an inflammatory mediator?
Peptide mediator that can modulate inflammatory response
46
What is the use of histamine antagonists?
Treatment of hypersensitivity reactions Oral/ topical creams
47
Why is histamine antagonist use limited?
A lot of redundancy Lots of other pro-inflammatory pathways
48
When are histamine antagonists often used?
(1) Hayfever (2) Urticaria (3) Can be used as anti-emetics
49
What is loratadine indicated for?
Symptomatic relief of allergy Such as hayfever or chronic idiopathic urticaria
50
What is the mechanism of action of aspirin?
Non-selective inhibition of COX1 + COX 2 COX1 irreversibly inhibited
51
What is the mechanism of action of naproxen?
Non-selective inhibition of COX1 + COX2
52
What is the mechanism of action of ibuprofen?
Non-selective inhibition of COX1 + COX2
53
What is the mechanism of action of diclofenac?
Non-selective inhibition of COX1 + COX2
54
Which type of COX has 'housekeeping' properties?
GIT/ renal/ platelets COX1
55
What is the purpose of NSAID treatment for inflammation?
Reduce the formation of (1) Prostaglandins (2) Thromoxane
56
Which enzyme(s) do most NSAIDs inhibit?
COX1 and COX2
57
What does the suffice -coxib mean?
COX2 selective inhibitors
58
What are some examples of COX2 selective inhibitors?
(1) Celecoxib | (2) Etoricoxib
59
What is 'COX'?
Cyclooxygenase enzymes
60
What is a risk of COX2 selective inhibitors?
Cardiovascular events
61
How do NSAIDs exhibit an antipyretic effect?
Prostaglandin-2 formation in hypothalamus is triggered by fever causing pathogens – e.g. bacterial endotoxin/ IL-1 (1) NSAIDs prevent prostaglandin production so reduce fever Do NOT affect normal maintenance body temperature
62
What is the role of prostaglandins in pain?
Sensitise nociceptors (pain receptors)
63
How do NSAIDs reduce inflammation?
(1) Reduce inflammation caused by prostaglandins (2) Reduces vasodilatation caused by prostaglandin-2 (3) Reduce oedema by reducing vascular permeability ONLY reduce inflammatory response dependent on prostaglandin formation
64
What are some unwanted side effects of NSAIDs?
(1) Gastric COX1 produces prostaglandins which decrease acid secretion + promote mucosa formation – Can cause mild/ severe symptoms – Mild: Discomfort, dyspepsia, diarrhoea – Severe: Bleeding, ulceration (2) Skin reactions (3) Pregnancy – especially in 1st and 2nd trimesters – ibuprofen may be used in 3rd trimester (4) Renal effects – caused by reduction in renal blood flow – Contraindicated in patients with renal failure – Analgesic nephropathy associated with overuse/ abuse of OTC NSAIDs
65
What is a benefit of COX2 selective inhibitors, regarding the GIT?
Fewer GI side effects
66
What are some cardiovascular complications of NSAIDs?
Mainly related to thrombotic events
67
Why may COX2 selective inhibitors cause more cardiovascular side effects?
Reduced PGI2 production
68
Why did diclofenac become a POM from P med?
Increases thrombotic event risk
69
Why is paracetamol not considered an NSAID?
Has no effect on COX1 and COX2 No anti-inflammatory effect DESPITE a strong analgesic and antipyretic effect
70
What is a glucocorticoid?
Corticosteroid
71
Which hormones control the production of corticosteroids within the body?
(1) Corticotrophin-releasing hormone (CRH) | 2) Adrenocorticotrophin hormone (ACTH
72
What factors up-regulate corticosteroid production?
(1) Stress | (2) Pro-inflammatory mediators
73
What type of feedback does cortisol (hydrocortisone) provide for itself?
Negative feedback loop Inhibits its own release
74
Where is cortisol produced?
In the adrenal glands
75
Where is corticotrophin-releasing hormone (CRH) produced?
In the hypothalamus
76
Where is adrenocorticotrophin (ACTH) produced?
In the pituitary gland
77
What is the mechanism of action of glucocorticoids (corticosteroids)?
(1) Pass from blood vessel via lipid biller into target cell (2) Binds to cytosolic glucocorticoid receptor (3) Once bound it translocates into the nucleus (4) Binds to response elements on the chromosome (5) Alters genetic transcription
78
What effect does low circulating concentrations of glucocorticoid have on the normal inflammatory response?
Reduces response
79
How do glucocorticoids reduce the inflammatory response?
(1) Reduce synthesis of inflammatory mediators (2) Affect function of inflammatory cells (3) Reduce cardinal signs of inflammation (4) Provides immunosuppressant actions (5) Reduce almost all stimuli + actions of the inflammatory response
80
Name two examples of molecules inhibited by glucocorticoids.
(1) Phospholipase A | (2) COX2
81
What are the anti-inflammatory properties of glucocorticoids?
(1) Reduce prostaglandin synthesis (2) Reduce cytokine generation (3) Reduce complement proteins in blood plasma (4) Reduce production of nitric oxide (5) Increase anti-inflammatory factors – IL-1 – IL-10 – Annexin-1
82
What effect do glucocorticoids have on anti-inflammatory cells?
(1) Decreased movement of neutrophils (2) Decreased action of leukocytes/ immune cells (3) Decreased fibroblast function
83
What are some common uses of glucocorticoids?
(1) Asthma (2) Topically in inflammatory conditions of the skin (3) Hypersensitivity reactions (4) Auto-immune + inflammatory disorders – Arthritis – IBS
84
What are some unwanted effects of glucocorticoids?
Can be severe (1) Reduced wound healing (2) Susceptibility to injury/ infection (3) Changes in electrolytes – e.g. hypoglycaemia (4) Osteoporosis (5) Mental health problems (6) Cushing's syndrome – can be caused by prolonged exposure to corticosteroids
85
Why does glucocorticoid use have to be tapered down gradually?
Glucocorticoid use impairs natural glucocorticoid production in the body Could produce a dramatic increase in inflammatory response following cessation of treatment

Part 3 – PM3A (28 decks)

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