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Physiology and Pharmacology > L11 - Anti-inflammatories - NSAIDs > Flashcards

L11 - Anti-inflammatories - NSAIDs Flashcards

1
Q

Aspirin discovery - 1828

A

White powder called salicin isolated and converted to salicylic acid

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2
Q

Aspirin discovery - 1897

A

Felix Hoffmann derivatized hydroxyl groups in salicylic acid with an acetyl group

  • Reduced the negative effect of salicylic acid
  • First patented on March 6, 1899
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3
Q

NSAIDs are prescribed for

A

Rheumatic musculoskeletal pains
Aches
Pains
Swelling

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4
Q

Arachidonic acid is produced by?

A

Produced from membrane phospholipids by Phospholipase A2

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5
Q

Arachidonic acid role

A

Acts as a second messenger and substrate for lipoxygenases and cyclooxygenase

  • Leads to generation of lipid-soluble mediators
  • Lipoxygenase and cyclooxygenase pathway
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6
Q

Lipoxygenase pathway

A

Production of leukotrienes

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7
Q

Cyclooxygenase pathway

A

Production of prostaglandins and thromboxanes

- E.g. prostaglandin E2

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8
Q

Prostaglandins

A

Unlike most hormones, they are created by cells and then act only in the surrounding area

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9
Q

Prostaglandins control

A

Constriction of muscle cells around blood vessels
Aggregation of platelets
Constriction of the uterus
Delivering and strengthening pain signals
Inducing inflammation

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10
Q

Properties of NSAIDs

A

Anti-inflammatory
Analgesic
Antipyretic
Effectiveness against headaches

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11
Q

Properties of NSAIDs - anti-inflammatory

A

Modify inflammatory reaction decreasing vasodilation and oedema
Ineffective against mediators that contribute to tissue damage associated with chronic inflammatory conditions

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12
Q

Properties of NSAIDs - analgesic

A

Decrease production of prostaglandins in damaged and inflamed tissue
Sensitises nociceptors to inflammatory mediators

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13
Q

Properties of NSAIDs - antipyretic

A

Lower raised temperature

Thermostat in hypothalamus activated via IL-1 induced COX2 production of prostaglandin

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14
Q

Properties of NSAIDs - headaches

A

Reduce vasodilator effect of prostaglandins on cerebral vasculature

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15
Q

COX1/COX2 selective NSAIDS

A

COX2-selective NSAIDs/inhibitors reduce effect of gastrointestinal toxicity (antiarthritic and analgesic)
- Concerns regarding cardiovascular safety

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16
Q

Most NSAIDs show little selectivity

A

Main differences are in toxicity, duration of action, and patient tolerance

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17
Q

NSAID effects from COX1 inhibition

A

Undesirable – gastrotoxicity

Desirable – antithrombotic

18
Q

NSAID effects from COX2 inhibition

A

Undesirable – increased blood pressure, salt retention, prothrombotic
Desirable – anti-inflammatory, analgesic

19
Q

COX1 and COX2 inhibitors inhibit

A

Cyclooxygenation reaction of Arachidonic Acid to prevent production of PGE2

20
Q

COX2 structure

A

Wider at the bend because it has a smaller amino acid (valine)
Cox1 has an isoleucine
- This gives rise to a gap which can act as a filter for drug

21
Q

Side effects of NSAIDs - gut

A

Prostaglandins normally inhibit acid secretion and protect mucosa
Leads to dyspepsia, diarrhoea, nausea, vomiting, gastric bleeding, ulceration
Co-administration of prostaglandin analogue may be protective

22
Q

Side effects of NSAIDs - liver

A

Leads to liver damage

Paracetamol creates toxic, reactive intermediate

23
Q

Side effects of NSAIDs - renal

A

Prostaglandins normally maintain renal blood flow

Leads to renal failure

24
Q

Side effects of NSAIDs - lung

A

Bronchospasm asthma attacks

More common with aspirin

25
Q

Side effects of NSAIDs - bleeding disorders

A

Thromboxane is involved in platelet aggregation

Too many drugs can reduce thromboxane

26
Q

Side effects of NSAIDs - GI complications

A

34-45% users will sustain some form of GI damage

Small percentage lead to serious effects and hospitalisation

27
Q

Aspirin binds to?

A

Aspirin binds covalently to a ser residue in COX

Prevents arachidonic acid from reaching the cyclooxygenase site

28
Q

What is a suicide inhibitor?

A

Useful cardiovascular drug due to inhibition of platelet aggregation
Acts on both cox1 and cox2
Aspirin and warfarin increase risk of bleeding

29
Q

Aspirin blocks?

A

The cyclooxygenase active site
Aspirin has two parts - an acetyl group attached to salicylic acid
When it attacks cyclooxygenase, it connects its acetyl group to a serine amino acid, permanently inactivating the enzyme

30
Q

Aspiring overview

A

Anti-platelet action

Reduced risk of colonic and rectal cancer

Reduces risk of Alzheimer’s

Weak acid, rapid and efficient absorption in the ileum

Suicide inhibitor

31
Q

Paracetamol overview

A

Analgesic-antipyretic due to CNS effects

Weak anti-inflammatory

Well absorbed and metabolised in the liver

Less side effects than aspirin with long term use

Large doses may increase kidney damage

Competitive inhibitor

32
Q

Ibuprofen overview

A

Like aspirin except it is a competitive inhibitor

33
Q

Clinical uses of NSAIDs

A

Antithrombotic
Analgesia
Anti-inflammatory
Antipyretic

34
Q

Clinical uses of NSAIDs - antithrombotic

A

Aspirin for patients at high risk of arterial thrombosis

35
Q

Clinical uses of NSAIDs - analgesia

A

Short term - aspirin, paracetamol, ibuprofen

Chronic pain - longer lasting more potent drug

36
Q

Clinical uses of NSAIDs - anti-inflammatory

A

Ibuprofen

Naproxen

37
Q

Clinical uses of NSAIDs- antipyretic

A

Paracetamol

38
Q

COX subunits

A

Two identical subunits, each with two catalytic sides
A cyclooxygenase site that binds to the endoplasmic reticulum
A endoperorixase site

39
Q

COX1

A

Found in most cells and is constitutively active, so a NSAID binding to COX1 may have many adverse side effects

40
Q

COX2

A

Found in most cells and is active only when induced, so a NSAID binding to COX2 will have few, selective side effects

41
Q

COX3

A

Found mostly on cells within the CNS and paracetamol binds to it

Physiology and Pharmacology (13 decks)

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