steroids and non steroidal antiinflammatory drugs Flashcards Preview

Yr 2 - Pharmacology > steroids and non steroidal antiinflammatory drugs > Flashcards

Flashcards in steroids and non steroidal antiinflammatory drugs Deck (96)
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1

What are Eicosanoids?

A precursor generated from phospholipids in the CNS

2

What are the 3 key groups of Eicosanoids?

- prostaglandins (PGs)

- thromboxanes (TXA)

- Leukotrienes

3

Which enzyme produces Eicosanoids from the phospholipids in the plasma membrane?

Phospholipase A2

4

What activates phospholipase A2 to produce Eicosanoids (5)?

- bradykinin

- antigen-antibody binding on mast cells

- thrombin

- complement C5a

- cell damage

5

What is the precursor of Eicosanoids?

Arachidonic acid

6

What other chemical mediator is produced from plasma membrane?

Platelet activating factor

7

Which two Eicosanoids can also be called prostanoids?

Prostaglandins

Thromboxanes

8

What is the nomenclature of prostaglandins?

PG = prostaglandin

Letter = basic structure it comes from

Number = the no of C=C

9

Most often (arachidonic acid is the precursor)

- how many C=C does PG have?

2

10

Which cells release prostaglandins?

ANY injured cell

11

Which process is Prostaglandin a key mediator in?

Inflammation

12

What are the effects of prostaglandin in blood vessels?

Vasodilation (PGE1&2, PGI1)

13

What are the effects of prostaglandin in healing?

Inhibit platelet aggregation (PGI2 & PGE)

n.b. TXA2 = increased platelet aggregation

14

What are the effects of prostaglandin in the respiratory system?

N.b. varies with prostaglandin

Bronchodilation = PGI2 & PGE2

Bronchoconstriction = PGF2 & TXA2

15

How do prostaglandins affect pain?

Sensitise nociceptive neurones to the action of mediators (bradykinin & serotonin) = activate pain fibres

16

How do prostaglandins affect fever?

Act on the hypothalamus = increase body temperatureInflammation = macrophages release IL-1 = AA-> PGE2 = acts on neurones in pre optic area (sets our internal core temp) = increase thermostatic set point = heat generation (shivering, skin vasoconstriction = destroy infection)

When PG production stops (immediately broken down) = decrease set point = heat dissipating (sweating and vasodilation)

17

Which enzyme converts arachidonic acid (AA) to PG H2 = prostanoid precursor?

Cyclo-oxygenases (COX)

18

How many active sites does COX have?

2

19

What are the actions of the two COX active sites?

- Cycloxegynase site = AA -> PGG2

- Heme with peroxidase activity = reduces PGG2 to PGH2

20

How many COX isoenzymes exist?

3

COX-1

COX-2

COX-3 (not really understood = splice variant of COX-1)

n.b. different tissues express varying levels of COX-1 & 2= SELECTIVE INHIBITION POSSIBLE

21

Where is COX-1 found?

Consitutive (always there) in most cells

22

What does COX-1 do?

Maintains tissue homeostasis

Housekeeping: gastric protection, blood clotting, renal blood regulation

n.b. inflammation is NOT the main role

23

What is the key difference between COX-1 & COX-2?

COX-1 binding pocket is NARROW

COX-2 binding picket is WIDE

24

What induces COX-2?

Inflammation (abundant in activated macrophages)

25

When is COX-2 unregulated?

In various carcinomas

26

What does COX-2 produce?

Prostanoids = mediate inflammation

27

What are the two main types of anti-inflammatory agents?

- non steroidal anti-inflammatory drugs (NSAIDs)

- Glucocorticoids

28

Which 3 other drugs act as anti- inflammatory agents?

- H1 receptor antagonists

- chondroprotective drugs

- immunosupressants

29

What does NSAIDs stand for?

Non steroidal anti-inflammatory drugs

30

How do NSAIDS target inflammation?

inhibit cyclo-oxygenase (COX) = reduced prostaglandin & thromboxane synthesis