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Locomotor > Drugs to treat Inflammation > Flashcards

Drugs to treat Inflammation Flashcards

1
Q

What is the main function of glucocorticoids?

A

Inhibit Arachidonic Acid Release and metabolism

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2
Q

What is the main function of NSAIDs?

A

Blocking of COX1 and COX2

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3
Q

What is the main function of CysLT1 receptor antagonists?

A

block the effects of leukotrienes (bronchosopasm and vasodilation) LTC4 & LTD4

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4
Q

Leukotrienes are formed by the action of —–1—- on —–2—

A

5-lipoxygenease

Arachidonic Acid

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5
Q

Which of the 2 COX is ubiquitous and which is inducible?

A

COX1 in most cells

COX2 inflammatory cells and endothelium

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6
Q

what is the main reason phospholipid mediators do not have systemic functions?

A

metabolised in the lungs

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7
Q

Canabinoid receptors have anti-inflammatory functions. The one not expressed in neuronal tissues but in the periphery is

A

CB2

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8
Q

What are some of the effects mediated by CB1 and CB2

A 
appetite stimulation/anti-nauseant 
analgesia
sedation
psychoactivity
anti-inflammatory
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9
Q

what are some of the functions for NSAIDs

A

Anti-inflammatory
Analgesia
Antipyretic (paracetamol preferred tho)

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10
Q

how do NSAIDs achieve analgesia?

A

by blocking COX1 and COX2 there is an inhibition on their production of prostaglandins (to some extent prostacylcin too) that sensitise nerve endings to algesic agents

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11
Q

why is aspirin contraindicated in gout?

A

because it uses the same weak ion transporter that uric acid uses for excretion

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12
Q

why do NSAIDs cause gastrointestinal side-effects?

A

because it inhibits the production of PGE2 that is gastroprotective

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13
Q

what are the gastroprotective functions of PGE2

A

increased mucus secretion
reduces gastric acid secretion
promotes blood flow
promotes angiogenesis (revascularisation after injury)

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14
Q

why do NSAIDs increase bleeding time?

A

by blocking COX1 and COX2 there is an inhibition on their product thromboxane [TXA2] that induces platelet aggregation

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15
Q

What is the function of Prostaglandins (PGE2) in the kidney and how is it affected in NSAIDs use?

A

it causes relaxation of the mesangial cells of the kidney allowing for an increase in GFR
if COX1 is blocked tone is increased and there will be less GFR AND an increase in BP

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16
Q

What is the function of Prostacyclins (PGI2) in the kidney and how is it affected in NSAIDs use?

A

they cause vasodilation of the arterioles of the kidney if perfusion is too low

17
Q

why do some asthmatics present respiratory distress when using NSAIDs?

A

they overproduce leukotrienes to start with therefore when no prostaglandins are produced, bronchospasm ensues

18
Q

Aspirin is…

A

Irreversible COX inhibitor by acetylation in portal circulation

19
Q

if aspirin blocks COX how is it that it is cardioprotective?

A

blocks the ability of platelets to produce thromboxane BUT the peripheral ability of the endothelium to produce prostacyclin remains unaffected
[PGI2]/TxA2–> ratio increased

20
Q

how does aspirin decreases inflammation?

A

by producing lipoxins-like substances that are implicated in the resolution of inflammation
This occurs because there is a modification in the functionality of COX (changes the type of oxygenation that occurs)

21
Q

What is Reye’s Syndrome and why is it caused?

A

Hepatotoxic response resulting in the bile like molecules raising in the plasma and they can have CNS consequences.
Reason why aspirin is contraindicated in people younger than adolescents

22
Q

What cells are able to produced lipoxins?

A

Inflammatory cells with COX2 that have been acetylated

OR physiologically by inflammatory cells with lipoxygenases

23
Q

to what receptor do lipoxins bind to?

A

Annexin A1 receptors (FPR2)

24
Q

What is annexin A1?

A

pro-resolution mediator, product of the stimulation by glucocorticoids that tend to turn off the infiltration of neutrophils

25
Q

Paracetamol is

A

Analgesic
Antipyretic
NOT anti-inflammatory

26
Q

What are the 3 main mechanisms of action of glucocorticoids?

A

Direct Transactivation
Direct Transrepression
Tethered Transrepression

27
Q

Direct Transactivation is

A

binding to a GRE (Glucocorticoid response elements within the promoter sequence of a gene) and causing the activation of transcription

28
Q

Direct Transrepression is

A

binding to the receptor induces it to bind to negative GRE within the promoter region of target genes recruiting co-repressors, silencing gene transcription

29
Q

Tethered Transrepression is

A

GR interacting [blocking] with another protein target such as NFKb (significant transcription factor for cytokines, their receptors and adhesion molecules —> All proinflamatory)

30
Q

some of the adverse effects of glucocorticoids thanks to their Direct Transactivation
Direct Transrepression activity is

A 
cortisol supression
osteoporosis 
muscle wasting
immunosupression
gastric ulcers
impaired healing

Locomotor (20 decks)

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