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Locomotor > Drugs to Treat Inflammation > Flashcards

Drugs to Treat Inflammation Flashcards

1
Q

What is the mechanism of action of glucocorticosteroids?

A

inhibit arachidonic acid metabolism and release

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2
Q

What is the mechanism of action of NSAIDs?

A

inhibit cyclooxygenases

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3
Q

What is the mechanism of action of CysLT1 receptor antagonists?

A

block LTC4 and LTD4 actions

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4
Q

Where is COX-1 located?

A

constituitively in most cells - makes prostacyclins

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5
Q

Where is COX-2 located?

A

inducible in inflammatory cells, fibroblasts, smooth muscle and endothelium - makes prostaglandins

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6
Q

What is the relationship between endogenous canabinoids and inflammation?

A

endogenous canabinois are anti inflammatory

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7
Q

Why aren’t prostaglandins used very much as a drug?

A

because they are relatively unstable and are difficult to synthesise

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8
Q

What is epoprostenol and what is it used for?

A

a PGI2 analogue - used in pulmonary hypertension

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9
Q

What is misoprostol and what is it used for?

A

a PGE1 analogue - used in abortion

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10
Q

What are the effects of NSAIDs?

A

anti-inflammatory, analgesic, anti-pyretic, anti-aggregatory

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11
Q

Why is aspirin contra indicated in gout?

A

because it competes with uric acid for excretion in the kidney

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12
Q

What are the gastrointestinal side effects of NSAIDs and why do they occur?

A

peptic ulcers - occurs because of the lack of protective effects from PGE2 (increase in mucous secretion, decrease in acid secretion, increase in blood flow and promotion of angiogenesis)

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13
Q

Why do NSAIDs cause increased bleeding time?

A

because they decrease TXA2 synthesis which impairs platelet aggregation

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14
Q

How do NSAIDs compromise renal blood flow?

A

because of decreased prostacyclin dilation

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15
Q

How do NSAIDs increase blood pressure?

A

decreased PGE2 natureisis

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16
Q

What patients are at risk of renal failure when given NSAIDs?

A

elderly patients with hypovolaemia, underlying renal disease and heart failure

17
Q

Which patients have a hypersensitivity to NSAIDs?

A

10% of asthmatics who over produce leukotrienes (for unknown reasons) when COX is inhibited causing bronchoconstriction

18
Q

Why is aspirin special?

A

because it binds irreversibly to COX so new enzymes need to be synthesised - this is not possible in platelets but is possible in the endothelium so will result in an altered ratio of PGI2/TXA2 - also because of the synthesis of aspirin triggered lipoxins which are implicated in inflammation resolution

19
Q

What are the side effects of aspirin which are not side effects of other NSAIDs?

A

Reye’s syndrome, tinnitis, uric acid retention

20
Q

What is the mechanism of action of paracetamol?

A

unclear

21
Q

What is paracetamol used for?

A

analgesic, anti pyretic - but not anti inflammatory

22
Q

What are the different side effects for COX-1 and COX-2 selective NSAIDs?

A

COX-1 selective have gastrointestinal side effects but COX-2 selective have cardiovascular side effects

23
Q

What percentage of the genome is affected by glucocorticosteroids?

A

10-20%

24
Q

What are the 3 mechanisms of action of glucocorticosteroids?

A

direct transactivation (stimulates gene expression), direct transrepression (inhibits gene expression) and tethered transpression (as a result of interaction with another protein target)

25
Q

What are the anti-inflammatory effects caused by transactivation?

A

MKP-1, GILZ, neutral endopeptidase

26
Q

What are the anti-inflammatory effects caused by transrepression?

A

cytokines, inducible PLA2/COX-2, adhesion molecules

27
Q

What are the adverse effects caused by transactivation?

A

cortisol supression, impaired gluconeogenesis, osteoporosis, muscle wasting

28
Q

What are the adverse effects caused by transrepression?

A

impaired wound healing, immunosupression, gastric ulcer, anti-leukocyte

Locomotor (16 decks)

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