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Module 204 MSK & Immune system > T1 L14 Pharmacology of immunology > Flashcards

T1 L14 Pharmacology of immunology Flashcards

1
Q

Describe the discovery of aspirin

A 
Rev Edmund Stone (1763)
 - White willow (Salix alba)
 - Used bark to treat fever and joint pain 
Felix Hoffman (Bayer)(1899)
 - Acetylsalicylic acid ‘aspirin’
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2
Q

Give examples of NSAIDs

A 
Aspirin
Paracetamol
Propionic acid derivatives
Arylalkanoic acids
Oxicams
Fenamic acids
Butazones
Coxibs
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3
Q

How are phospholipids converted to arachidonic acid?

A

Phospholipases

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4
Q

How is arachidonic acid converted to leukotrienes?

A

Lioxygenases

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5
Q

How is arachidonic acid converted to prostaglandin H2?

A

Cyclo-oxygenases

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6
Q

What can prostaglandin H2 be converted to?

A

Thromboxanes
Prostaglandins
Prostacyclins

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7
Q

What is arachidonic acid?

A

Polyunsaturated 20 carbon lipid which is either metabolised into leukotrienes of prostaglandin H2 depending on tissue and inflammatory stimuli.

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8
Q

What are thromboxanes involved in?

A

Platelet aggregation and small vessel tone

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9
Q

What are prostacyclines involved in?

A

Vasodilator properties

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10
Q

What are prostaglandins involved in?

A

Bronchial tone
Vascular tone
Sensitivity of nerve fibres

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11
Q

What is the NSAID mechanism?

A

Inhibits cyclo-oxygenase

Prevents conversion of arachidonic acid to prostaglandin H2

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12
Q

What are the 3 isoforms for cyclo-oyxygenase?

A

COX-1
COX-2
COX-3

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13
Q

What is COX-1 involved in?

A

Constitutes expression for all tissues
Stomach, kidney, platelets, vascular endothelium
inhibiting has an anti-platelet activity

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14
Q

What is COX-2 involved in?

A

Induced in inflammation
Injury, infection, neoplasia
Inhibition leads to analgesia and anti-inflammatory actions

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15
Q

What is COX-3 involved in?

A

CNS

Inhibited specifically by paracetamol leading to antipyretic and analgesic effects

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16
Q

What are the indications for NSAID therapy?

A 
As mild analgesics 
 - mechanical pain
 - minor trauma
 - headaches, dental pain, dysmenorrhoea
Potent analgesics
 - peri-operative pain
 - ureteric colic
Anti-inflammatories 
 - gout
 - inflammatory arthritis
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17
Q

Why is aspirin use for pain and inflammation limited?

A

GI toxicity
Tinnitus
Reye’s syndrome

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18
Q

What is Reye’s syndrome?

A

Severe, sudden hepatic failure in children

19
Q

Describe the metabolism of paracetamol

A

Phase II conjugation reaction in liver to paracetamol sulphate and glucuronide which is then excreted.
Excess paracetamol is shunted to phase I oxidation reaction to produce NAPQI which causes hepatic necrosis

20
Q

What does the treatment for paracetamol toxicity rely on?

A

Provision of substrates which body can use to synthesis glutathione

21
Q

What do prostaglandins E2 and I2 do in the GI tract?

A

Decrease acid production
Increase mucus production
Increase blood supply

22
Q

What is the effect of the inhibition of prostaglandins in the gut?

A

Irritation
Ulcers
Bleeding

23
Q

What are the risk factors for an upper GI bleed?

A

Previous GI bleed
Age
Chronic disease e.g. rheumatoid disease
Steroids

24
Q

Describe the changes in glomerular blood flow caused by NSAIDs

A

Decrease in glomerular filtration rate
Sodium retention
Hyperkalaemia
Papillary necrosis

25
Q

Why do 10% of asthmatics experience bronchoconstriction following NSAID?

A

Arachidonic acid is shunted down 5-lipoxygenase pathway as COX pathway is inhibited by aspirin

26
Q

Give examples of non-selective NSAIDs

A

Ibuprofen
Naproxen
Diclofenac
Indometacin

27
Q

What is diclofenac widely prescribed for?

A

Severe, short-term analgesia

28
Q

How is GI toxicity prevented when using NSAIDs?

A

Treat with gastroprotective drugs
- misoprostol
Avoid in renal failure and adjust dose if necessary

29
Q

What are COX-2 inhibitors?

A

Selective inhibition of COX-2

Anti-inflammatory and analgesic

30
Q

What are some examples of coxibs?

A

Celecoxib
Etoricoxib
Foecoxib
Valdecoxib

31
Q

When are COX-2 inhibitors indicated instead of non-selective NSAIDs?

A

Patients at high risk of developing gastroduodenal ulceration, perforation or bleeding
After an assessment of cardiovascular risk

32
Q

What functions does cortisol influence?

A 
Carbohydrate and protein metabolism
Fluid and electrolyte balance 
Lipid metabolism
Psychological effects
Bone metabolism
Profound modulator of immune response
33
Q

How do steroids reduce immune activation?

A

Alter gene expression in numerous cell types
Steroid receptors found in cytoplasm complexed with heat-shock protein Hsp90. Steroids cross cell membrane and bind to complex releasing Hsp90.
Steroid receptor complex crosses nuclear membrane.
In nucleus, steroid receptor binds to specific gene regulatory sequences and activates transcription

34
Q

Describe immunomodulation by steroids

A

Cell trafficking
- lymphopenia, monocytopeniaa
- neutrophilic and impaired phagocyte migration
Cell function
- T-cell hyporesponsiveness
- inhibited B-cell maturation
- decreased IL-1, IL-6 and TNF alpha production
- widespread inhibition of Th1 and Th2 cytokines
- inhibition of COX
- impaired phagocyte killing
- decrease collagenases, elastases

35
Q

What is the clinical use of steroids?

A

Suppress inflammation - asthma, Crohn’s, Eczema, MS, sarcoid, allergy, rheumatoid arthritis, SLE
Suppress specific immunity - graft rejection

36
Q

Describe the potency, lipid solubility, systemic and topical use of hydrocortisone

A

Low potency
Good lipid solubility
Systemic use as replacement
Topical use for skin and joints

37
Q

Describe potency, lipid solubility, systemic and topical use of prednisolone

A

Medium potency
Good lipid solubility
Systemic use as anti-inflammatory
Topical use for enema

38
Q

Describe potency, lipid solubility, systemic and topical use of beclomethasone

A

Medium potency
Poor lipid solubility
No systemic use
Topical use for asthma, Crohn’s

39
Q

Describe potency, lipid solubility, systemic and topical use of dexamethasone

A

High potency
Good solubility
Systemic use for cerebral oedema
No topical use

40
Q

Describe potency, lipid solubility, systemic and topical use of triaminiclone

A

High potency
Poor lipid solubility
No systemic use
Topical use in skin and joints

41
Q

What are the early side effects of steroid therapy?

A

Weight gain
Glucose intolerance
Mood change
Suppression of ACTH release

42
Q

What are the later effects of chronic steroid use?

A 
Proximal muscle weakness
Osteoporosis
Skin changes
Body shape changes
Hypertension
Cataracts
Adrenal suppression
43
Q

Describe the increased risk of infection with steroids

A

Early risk of phagocytic defects
- bacterial infection e.g. S.aureus, enteric bacteria
- fungal infection e.g. candida, aspergillus
Later risks of cell-mediated defects
- intracellular pathogens e.g. TB, varicella, listeria, pneumocystis

Module 204 MSK & Immune system (44 decks)

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