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Unit 11: Movement and trauma > Pharmacology of inflammation > Flashcards

Pharmacology of inflammation Flashcards

1
Q

What type of drug is aspirin?
What is it derived from?
What are the clinical effects of aspirin ?

A 
NSAID - Non steroidal anti inflammatory drug 
Derived from salicylic acid 
- Anti inflammatory
- Anti pyretic
- Analgesic
- Anti thrombotic : Only aspirin
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2
Q

What are ecosanoids?

What are some examples of molecules with are ecosanoids?

A 
Type of lipid 
Inflammatory mediators 
- Prostaglandins
- Leukotrienes 
- Thromboxanes
- Lipoxins
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3
Q

Describe the structure of a phospholipid

A

Phosphate group
Glycerol
2 fatty acids
1 fatty acid may be arachidonic acid

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4
Q

Describe arachidonic acid metabolism

Which enzymes are responsible

A

2 stages
Arachidonic acid -> Prostaglandin G2 = COX
Prostaglandin G2-> prostaglandin H2 = COX

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5
Q

What is another name for COX1/COX2?

A

PGH2 synthase

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6
Q

What do NSAIDS do? ( activity)

A

Competitive reversible inhibitors at COX enzymes

Inhibit the formation of Prostaglandin G2 + prostaglandin H2

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7
Q

What activity does aspirin have?

A

Irreversible inhibitors at COX enzymes

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8
Q

Why is blocking prostaglandin G2 + prostaglandin H2 bad?

A

Many prostaglandins are derived from Prostaglandin H2

E.g PGD2, PGE2, PGI2, thromboxane

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9
Q

What type class are prostanoid receptors?

A

GPCRS

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10
Q

What type of drugs are

  • OST
  • Iprant
A

Agonists

Anatagonists

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11
Q

What are the desired effects of NSAIDS and why do these occur?

A

Anti inflammatory : Blockage of PGE2,PGD2 + PGI2
Anti pyretic: Blockage of PGE2
Analgesic : Blockage of PGE2
Anti thrombotic: Blocks synthesis of TxA2 which activates platelets

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12
Q

What are the roles of PGE2?

What converts PGH2 -> PGE2?

A
  • Vasodilation + inflammation
  • Sensitise nerve endings
  • Fever
  • Protects gastric mucosa

PGE2 synthase

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13
Q

What are the undesired effects of NSAIDS?

A

GI bleeding + ulceration: PGE2 contribues to defense layer of the gastric mucosa by decreasing gastric acid/ increases bicarb

Altered renal blood flow: PGE2 + PGI2 regulate renal blood flow

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14
Q

Where are exogenous steroids derived from?

A

Cholesterol

Precursor to vitamin D, contributes to bile acids and steroid hormones

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15
Q

What are the main corticosteroids and where are they produced?

A

Glucocorticoids - zona fasiculata
mineralocorticoids - zona glomerulosa
sex steroids - zona reticularis

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16
Q

How do steroids pass into the nucleus?

A

Steroids are lipid soluble so can pass into any cell
They enter cell and bind to cytoplasmic receptors (GR/MR/Sex steroid receptors)
Receptors coupled with heat shock proteins which dissociate upon binding
Steroid receptor complex dimerises
Translocates to the nucleus
Binds to response elements of DNA
Transactivation or transrepression

17
Q

Why does cortisol have a higher affinity for MR but does not activate them?

What is the inactive form of cortisol?

A

Pre receptor metabolism
Cortisone = inactive at GR + MR
Cortisol = active at both

Enzymes:
11 beta HSD type 1 : Converts cortisone -> cortisol

11 beta HSD type 2: Converts cortisol -> cortisone

18
Q

Where is 11 beta HSD type 1 normally found?

Where is 11 beta HSD type 2 normally found?

A

Abundant + with gluco-corticoid receptors so cortisone -> cortisol and receptor activation

Restricted distribution e.g in renal tubules. + with mineralocorticoid receptors. So cortisol -> cortisone to prevent MR activation

19
Q

What do steroids upregulate ( transactivation)?

A
  • Annexin A1 which inhibits PLA2 so decreases eicosanoids, prostaglandins and leukotrienes
  • Upregulate anti inflammatory cytokines e.g IL-10
20
Q

What is Annexin 1?

A

Lipocortin
Inhibits PLA2
Decreases eicosanoids, prostaglandins + leukotrienes

21
Q

What do steroids down regulate ( transrepression)?

A

Pro inflammatory

  • COX-2
  • PLA2
  • NOS
  • Pro inflammatory cytokines
22
Q

Compare NSAIDS vs Steroids

A

NSAIDS: Real adverse affects, targeted action COX
Steroids: Severe and predictable adverse effects, potent, non selective action

23
Q

What is the final end product of purine metabolism in humans ?

A

Uric acid
Purines -> xanthine
Xanthine -> uric acid by xanthine oxidase

24
Q

What does increased uric acid lead to?

A

Urate crystal production -> inflammation

25
Q

Describe the mechanism of action of prednisone

A

Class = corticosteroid
Small molecule
synthetic glucocorticoid
metabolise to active prednisolone

Activity : Higher affinity for GR>MR

  • Agonist at GR
  • Agonist at GR

Physiology:
Transactivation: Annexin 1 to inhibit PLA2, anti inflammatory cytokines e.g IL-10
Transrepression: COX, LOX, PLA2, pro inflammatory cytokines

MR activation

  • Increase expression of eNACS
  • Increase expression + activity of Na+/K+ ATPases
  • Increases Na+ reabsorption

Unit 11: Movement and trauma (11 decks)

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