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pharmacology > Pain Relief > Flashcards

Pain Relief Flashcards

1
Q

How is arachadonic acid synthesised? What is it a precursor to?

A

It is made from cell membrane phospholipids via phospholipase A

It is a precursor to prostaglandin G via COX 1 / COX 2

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2
Q

What does prostaglandin G go on to make?

A

Prostaglandin H, DEF and I via PG enzymes.

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3
Q

What is the role of COX 1?

A

It is expressed in a wide range of tissue types and has a cytoprotective role as it ensures optimal local perfusion.

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4
Q

Why do prostagandins need to be constantly synthesised?

A

They have a short half life of only 10 minutes.

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5
Q

What is the role of COX 2?

A

It is induced by injurious stimuli and inflammatory mediators eg bradykinin. It also is constitutively expressed in parts of the brain and kidney.

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6
Q

Which prostaglandin is most important in mediating the inflammatory response?

A

Prostanglandin E

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7
Q

What are the effects of PG E?

A

Vasodilation
Hyperalgesia
Fever
Immunomodulation

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8
Q

How does prostaglandin E cause pyrexia?

A

Via EP 3 receptors:
In infection/ inflammation endotoxins stimulate macrophages to release IL 1. This stimulates PGE 2 synthesis in hypothalamus via induction of COX 2.
PGE 2 binds to EP3 receptor which is a Gi type GPCR. This results in increased heat production and decreased heat loss.

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9
Q

How does PGE cause increased vasodilation?

A

Increased sustained nociceptive signalling in peripheries results in increased cytokine levels in dorsal horn cell body. This causes increased COX 2 synthesis and increased PGE 2 synthesis. This acts via an EP2 receptor which is a Gs, which causes vasodilation in peripheries.

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10
Q

What is central sensitisation?

A

Increased sensitivity and discharge rate of secondary interneurones via removal of glycinergic inhibition

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11
Q

How does PGE cause hyperalgesia?

A

Increased Na+ channel sensitivity
Increased C fibre activity- Gq activation leads to increased intracellular Ca2+ so increased neurotransmitter release
Inhibition of K+ channels.
Increased neuronal sensitivity to bradykinin.

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12
Q

What is allodynia?

A

The point in hyperalgesia where c fibre discharge rate rises above the pain threshold.

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13
Q

What is the main therapeutic effect of NSAIDs?

A

COX 2 inhibition

COX 1 is narrow mouthed so only fits small drugs like aspirin, COX 2 is wide mouthed so fits big blunt drugs.

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14
Q

What are the 3 main therapeutic actions of NSAIDs?

A

Analgesia
Anti inflammatory
Antipyretics

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15
Q

What are the pharmacokinetics of NSAIDs?

A

Heavily protein bound
Linear pharmacokinetics within therapeutic range
Wide variation in affinity, efficacy, and COX 1/2 selectivity

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16
Q

What are the major ADRs of NSAIDs in the GI tract?

A

Most are due to disruption to PG synthesis which has a constitutive expression.
Eg GI tract- COX 1 stimulates cytoprotective mucus secretion throughout Gi tract, reduces acid secretion and promotes mucosal blood flow. ADRs include stomach pain, nausea, heartburn, gastric bleeding and ulceration

17
Q

What is the effect of NSAIDs in the renal/ renovascular system?

A

PGE I2 and PGI 2 maintain renal blood flow. Therefore NSAIDs cause decrease in GFR.

18
Q

What other ADRs do NSAIDs cause?

A

Bronchial asthma
Hypersensitivity of skin- sometimes stevens johnson syndrome which is a very serious hypersensitivity reaction
Increased bleeding time
Reyes syndrome (paeds)- serious brain/liver injury, usually in viral infections treated with aspirin.

19
Q

How does aspirin cause anticoagulation?

A

Aspirin inhibits platelet aggregation via inhibition of platelet thromboxane synthesis. Therefore reduces thrombus formation on surface of damaged arterial wall.

20
Q

What are the pharmacokinetics of aspirin?

A

Irreversibly inhibits COX enzymes by acetylation
Half life less than 30 mins as rapidly hydrolysed to salicylate
Lower doses has first order kinetics
Higher doses zero order kinetics.

21
Q

What are the drug interactions of NSAIDs?

A

With opiates- extended range of pain relief
When given with aspirin may interfere with cardioprotective function

Majority of their DDIs come from protein binding:
Sulfonylurea—> hypoglycaemia
Warfarin—> increased bleeding time
Methotrexate—> wide ranging serious ADRs

22
Q

What is the therapeutic effect of paracetemol?

A

Analgesia
Antipyretic
No antiinflammatory action

23
Q

What is the mechanism of action of paracetemol?

A

Unknown- is a weak COX 1/ COX 2 inhibitor

24
Q

What is the pharmacokinetics of paracetemol?

Why is it dangerous in overdose?

A

At normal doses has linear order kinetics and is mainly metabolised via phase II conjugation into glucoronide and sulphate. If these enzymes become saturated then phase I oxidation takes over producing NAPQI. At normal doses this is detoxified by glutathione, but when this runs out NAPQI is toxic to liver cells as binds to macromolecules and mitochondria.

25
Q

What is the treatment for paracetemol overdose?

A

If seen within 0-4 hours give activated charcoal orally to reduce uptake of drug

If seen within 36 hours start N acetylcysteine IV, methionine by mouth if NAC cannot be given promptly.

26
Q

What is the pain pathway from peripheral stimulus to the brain?

A

Nociceptor—> either type C (non myelinated) or type A(myelinated) pain fibres—-> dorsal root of spinal cord. Produces substance P as neurotransmitter.—> spinothalamic pathway—> thalamus—> produces negative feedback on dorsal root of spinal cord/ feeds information to primary sensory cortex.

27
Q

What is the gate theory of how opioids work?

A

Opioids inhibit release of substance P from nerve terminals in the dorsal horn of the spinal cord.

28
Q

What are the central psychoactive effects of opioids?

A

Stimulation of inhibitory descending pathways from higher centres in brain

29
Q

What endogenous opioid peptides does the body produce itself?

A

Dysnorphins
Endorphins
Enkephalins

30
Q

What are the 3 receptors which opioids can bind to? What do they each do?

A

Mu- produces supraspinal alagesia

Delta- enkephalin mediated pain relief

Kappa- analgesia at spinal cord

31
Q

How does opioid binding to its receptor cause pain relief?

A

Opioid binding causes outward flux of K+.= decreased excitability.= decreased influx of Ca2+= decreased cAMP synthesis so decreased release of neurotransmitters.

32
Q

What are the adverse drug reactions of opioids?

A 
Nausea
Vomiting
Constipation
Drowsiness
Miosis
Respiratory depression
Hypotension
Dependence+withdrawal symptoms.
33
Q

What are the pharmacodynamics and pharmacokinetics of opioids?

A

Can either be agonists (morphine), partial agonists (buprenorphine) or mixed agonist/antagonist (nalbuphine), full antagonist- naloxone

Half life varies widely- morphine has a half life of 1.3- 6.7 hours.

In most cases oral bioavailability is 90% but with morphine is 25% so is IV.

pharmacology (22 decks)

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