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3154 haem & MSK - nat > ic13.1 analgesics > Flashcards

ic13.1 analgesics Flashcards

1
Q

What are eicosanoids (3 points)

A

Lipoxins, Prostaglandins, Leukotrienes

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2
Q

What is the pathway that produces eicosanoids

A

1) Phospholipase A2 produces Arachidonic Acid
2) Arachidonic acid produces Eicosanoids via several enzymes

15-Lipoxygenase → Lipoxins

Cyclooxygenase (COX) → Prostaglandins
Prostaglandins cause acute inflammation
Examples of Prostaglandins: PGI2, PGE2, TXA2

5-Lipoxygenase → Leukotrienes
Leukotrienes produce chronic inflammatory response and immune response

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3
Q

What are the 3 types of prostaglandins and function

A

PGI2 = Prostacyclin
Causes vasodilation, inhibit platelet aggregation
PGE2 = Classical Prostaglandins
Causes vasodilation, vascular permeability, pain
TXA2 = Thromboxanes
Cause vasoconstriction, platelet aggregation

How to rmb
TXA2 (A for Aggregation)
TXA2 is released in open wounds, bleeding → hence will try to limit bleeding by causing vasoconstriction and platelet aggregation
PGI2 (I for inhibit aggregation)
PGI2 is released in closed wound or infection, where we want more blood to flow so inhibit platelet aggregation and vasodilation

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4
Q

4 functions of NSAIDS

A

Antiinflammatory
Analgesic
Antipyretic
Antiplatelet

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5
Q

How does antiinflammation occur

A

Block PGE2 and PGI2
This reduces vasodilation, reduce vascular permeability, and pain associated with inflammation

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6
Q

How does analgesia occur

A

Block PGE2
PGE2 sensitises the nociceptive fibres (multiplies the effect of pain)
Hence there is an analgesic ceiling → pain is only reduced, not completely removed
Pain is caused by Bradykinin and Leukotriene instead

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7
Q

How does antipyretic occur

A

During a fever, neutrophils release cytokines eg. IL-1
IL1 increases expression of COX in hypothalamus
COX releases PGE2, which causes fever
NSAID blocks COX and hence PGE2, reducing fever

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8
Q

How does antiplatelet occur

A

Platelets contains COX-1 which produces TXA2
TXA2 promote platelet aggregation and vasoconstriction
Inhibit TXA2 → inhibit platelet aggregation for 1-2 weeks
Platelets dont have a nucleus, so cannot produce new COX enzyme

Endothelial cells contains COX-2 which produces PGI2
PGI2 inhibit platelet aggregation and cause vasodilation
Inhibit PGI2 → promote platelet aggregation, but this effect is short-lived as new COX enzyme is produced by endothelial cell after a few hours

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9
Q

Adverse effects of NSAIDs (4 points)

A

1) GI side effects
2) Renal side effects
3) Pseudoallergy reaction, Asthma
4) Bleeding

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10
Q

How does GI side effects occur

A

Prostaglandins help to protect GI
Reduce gastric acid secretions
Increase mucosal blood flow
Increase mucus secretion
Increase secretion of bicarbonate
Side effects eg. dyspepsia, N/V, ulcer formation, GI bleeding
Peptic ulcer risk increases > 5 days of use

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11
Q

How does renal side effects occur

A

Causes Na+ and water reabsorption (Effect of inhibition of PGE2 > PGI2)

Inhibition of PGE2
Sodium and water retention
Peripheral oedema
Hypertension

Inhibition of PGI2
Suppress renin and aldosterone secretion
Hyperkalaemia
Acute renal failure

What happens:
1) At the thick ascending limb, PGE2 inhibited, causing 25% Na+ absorption
2) At the Collecting duct, normally aldosterone secretion will cause 1-2% of Na+ reabsorption. Since PGI2 is inhibited, aldosterone is not secreted, 1-2% of Na+ is not reabsorbed. However, the 25% of Na+ is still reabsorbed earlier, so overall net Na+ absorption
3) Aldosterone normally secretes K+ in urine, but now since PGI2 is inhibited, secretion of Aldosterone is inhibited, so K+ remains in the blood

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12
Q

How do ACE/ARB affect GFR

A

Prevent efferent arteriole vasoconstriction

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13
Q

How does pseudoallergy and asthma occur

A

Since COX is inhibited, arachidonic acid travels down 5-Lipoxygenase pathway to produce more Leukotrienes
Leukotrienes can trigger mast cell degranulation, lead to bronchospasm in asthmatics and allergic reaction symptoms

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14
Q

Why is aspirin CI in children

A

Cause Reye’s syndrome
swelling of brain and liver
Symptoms: vomiting, personality changes, listlessness, delirium, convulsions, loss of consciousness

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15
Q

Traits of Naproxen, Indomethacin, DIclofenac

A

Naproxen
Long half life (12-14hrs)
Hence fewer doses needed eg. BD
Higher free fraction in women → more effective
Used for dysmenorrhea

Indomethacin
MOA similar to steroids, block Phospholipase A2
CNS adverse effects eg. confusion, depression, psychosis, hallucinations

Diclofenac
Short half life (<2hrs), hence low GI side effects
Longer half life in synovial fluid
Topical preparations available

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16
Q

acronym for NSAIDs COX 1 -> COX 2

A

KANID CE

17
Q

Adverse effects unique to COX-2

A

Reproductive chance
Increased risk of stroke

18
Q

How do Coxibs reduce chance of pregnancy

A

Delay follicular rupture
Reduces chances of pregnancy but not completely contraindicated

19
Q

Why are NSAIDs CI in third trimester of pregnancy

A

Causes fetal lung bypass

20
Q

How do coxib increase risk of stroke

A

Since COX-2 is blocked, more arachidonic acid goes down COX-1 pathway
More TXA2 produced, promote more platelet aggregation, increase risk of thrombosis

21
Q

Contraindications of NSAIDs (9 points)

A

Severe renal impairment (eGFR < 30ml/min)

Severe heart failure

Active GI ulcer or bleeding

Bleeding disorders eg. haemophilia

Use of systemic corticosteroids, antiplatelets

Risk factors for NSAID toxicity eg. elderly with history of GI bleeding

3rd trimester of pregnancy

Children (for Aspirin only)

Active asthma (COX-1 cannot, COX-2 use with caution)
Based on IC16 OA slides

22
Q

Which NSAID has lowest risk of cardiovascular toxicity?

A

Technically non selective have the lowest cardio risk (due to COX-2 stroke risk)
Use Celecoxib, Ibuprofen, Naproxen for max 5 days
Avoid Diclofenac and Etoricoxib

23
Q

How does paracetamol cause liver toxicity?

A

Paracetamol convert to toxic metabolite by CYP2E1 via minor pathway
Toxic metabolite is metabolised by glutathione to nontoxic metabolite
Alcohol can 1) induce CYP2E1, 2) deplete glutathione → increased toxic metabolites
Glutathione is replenished by N-acetyl-cysteine

24
Q

How to take paracetamol and ibuprofen for pain and fever?

A

Combine for pain
Alternate every 3hrs for fever

25
Q

What are weak opioids

A

Tramadol
Codeine

26
Q

What are strong opioids

A

Morphine
Oxycodone
Fentanyl

27
Q

Acronym for opioids

A

TCMOF

28
Q

Why is there variable response to codeine

A

Codeine converted to Morphine via CYP2D6
Response to Codeine depends on polymorphism of 2D6 to more potent Morphine

29
Q

What is orphenadrine

A

central muscle relaxant

30
Q

5 MOA of Orphenadrine

A

1) Muscarinic receptor antagonist (in basal ganglia)
2) H1 antihistamine
3) NMDA receptor antagonism
Inhibit Glutamate from binding to NMDA receptor
4) NE and DA reuptake inhibitor
Similar to Bupropion
5) Sodium channel blocker

31
Q

Adverse effect of orphenadrine

A

Anticholinergic SE eg. N/V, constipation, dry mouth, flushing, dilated pupils

3154 haem & MSK - nat (12 decks)

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