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PR3154 > Pharmacology - Analgesics > Flashcards

Pharmacology - Analgesics Flashcards

1
Q

What are the eicosanoids, precursor and their respective-related enzymes?

A

Phospholipase A2 -> production of Arachidonic Acid;

Arachidonic acid is used to form:
15-Lipoxygenase -> Lipoxins;
Cyclooxygenase (COX) -> Prostaglandins;
5-Lipoxygenase -> Leukotrienes.

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2
Q

What is the physiological response towards an increase in Leukotriene B4 secretion?

A

Mast cell degranulation
Bronchospasm
May cause a pseudo-allergic reaction / asthma attack.

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3
Q

What do Steroids target in the Arachidonic acid pathway?

A

Phospholipase A2 -> inhibit arachidonic acid formation.

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4
Q

What do NSAIDs target in the Arachidonic acid pathway?

A

Cyclooxygenase enzymes -> inhibit formation of TXA2, PGI2, and PGE2.

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5
Q

What is the function of TXA2, PGI2 and PGE2 in relation to pain and platelet activity?

A

TXA2 is involved in vasoContriction and platelet aggregation.
PGI2 is involved in vasoDilation and inhibition of platelet aggregation.

PGE2 (classical prostaglandins) is involved in vasoDilation, increasing vascular permeability and pain. This occurs during acute inflammation.

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6
Q

What are the physiological effects of NSAIDs?

A
  • Inhibits vasodilation -> less heat, redness and swelling;
  • Inhibits an increase in vascular permeability -> less swelling;
  • Less sensitization of the nociceptive fibres -> less stimulation by other inflammatory mediators -> “Analgesic ceiling”

Acts on peripheral and central nervous system.
Leads to 3 outcomes:
1. Anti-inflammation
2. Analgesia
3. Antipyretic

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7
Q

Explain how NSAIDs lead to the following:
1. Anti-inflammation
2. Analgesia
3. Antipyretic
4. Antiplatelet

A
  1. Anti-inflammation -> Less PGI2 and PGE2 -> less vasodilation, less vascular permeability effects
  2. Analgesia -> reduced sensitization of nociceptive fibres
  3. Antipyretic -> reduced PGE2 formation in hypothalamus -> reduced temperature raise
  4. Antiplatelet
    - COX-1 : less TXA2 production, less platelet aggregation.
    - COX-2 : less PGI2 production, less inhibition of platelet aggregation (but COX-2 is replaced within hours).
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8
Q

What are the S&S of Reye’s Syndrome? And which population has an increased risk?

A

[What] Swelling of brain and liver

Vomiting
Personality changes
Listlessness
Delirium
Convulsions
Loss of consciousness

Increased risk -> children w/ viral infections

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9
Q

What are the unique features of Naproxen?

A

t1/2 12-14 hrs -> BD dosing
More effective in women due to higher free fraction.
Used for Dysmenorrhoea.

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10
Q

What are the unique features of Indometacin?

A

Phospholipase A inhibition -> Strong anti-inflammatory activity
CNS Adverse effects (confusion, depression, psychosis, hallucinations)

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11
Q

What are the unique features of Diclofenac?

A

Short t1/2 (<2hr) -> low GI risk
Long t1/2 in synovial fluid -> useful in inflammatory joint disease.
Topical application available.

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12
Q

What are the effects of reduced Prostaglandins (PGE2) concentration on the GI system?

A
  • Increased gastric acid secretions
  • Decreased mucosal blood flow
  • Decreased secretion of mucus
  • Decreased secretion of bicarbonate
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13
Q

What are the effects of reduced Prostaglandins (PGE2) concentration on the Kidneys?

A
  • Sodium and Water retention
  • Peripheral oedema
  • Hypertension
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14
Q

What are the effects of reduced Prostacyclins (PGI2) concentration on the Kidneys?

A
  • Suppression of renin and aldosterone secretion
  • Hyperkalaemia
  • Acute renal failure
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15
Q

What are the Side Effects of typical NSAIDs?

A

1) Dyspepsia, N/V
2) Ulcer formation (risk greatly increased if used > 5 days)
3) Potential haemorrhage risk in chronic users

4) Acute kidney injury
5) Peripheral oedema
6) Hypertension
7) Hyperkalaemia, Hypernatremia

8) Bleeding risk (greater risk for non-selective NSAIDs)

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16
Q

What is the Triple Whammy?

A

1) Diuretics -> reduced renal blood flow
2) NSAIDs -> inhibition of COX-1/COX-2 -> less PGE2 -> vasoconstriction of afferent arteriole
3) ACEi -> less Angiotensin II formation -> Less vasoconstriction of efferent arteriole

17
Q

List the NSAIDs from most GI side effect

A

Ketoprofen
Piroxicam
Indometacin
Aspirin
Naproxen
Ibuprofen

Diclofenac
Mefenamic acid
Meloxicam
Celecoxib
Parecoxib
Etoricoxib

18
Q

Where can Constitutive COX-2 be found? And what are the effects?

A

1) CNS -> Nausea?
2) Kidneys -> Na and H2O retention, oedema, hypertension
3) Female reproductive tract -> delayed follicular rupture
4) Synovium -> inhibit to reduce inflammation

19
Q

List the NSAIDs from most anti-platelet activity to most pro-thrombotic.

A

Aspirin

Ketoprofen
Piroxicam
Indometacin

Naproxen
Ibuprofen
Diclofenac (COX-2 ~ COX-1)

Mefenamic acid
Meloxicam
Celecoxib
Parecoxib
Etoricoxib

20
Q

What are side effects which are still present in COX-2 selective inhibitors?

A
  • Renal toxicity
  • Delayed follicular rupture
  • Premature closure of ductus arteriosus in late pregnancy
  • Impairment of wound healing

(!) Increased risk of thrombosis due to more TXA2.

21
Q

Contraindications and Cautions for NSAIDs

A

Contraindications:
- Kidney (eGFR < 30ml/min)
- Heart Failure (severe)
- Ulcer / bleeding (active, GIT)
- Bleeding disorders (eg. haemophilia)
- Drugs: systemic corticosteroids / antiplatelet agents / anticoagulants
- Multiple risk factors for NSAID toxicity
- Pregnancy (3rd trimester)

Caution:
- Elderly
- Hx of Cerebrovascular or Cardiovascular disease

22
Q

Management strategies for NSAID toxicity risks

A

1) Renal -> discuss with managing doctor

2) CVS
- avoid Diclofenac and COX-2 selective (other than Celecoxib).
- Limit use to <= 5d.
- Consider Paracetamol.

3) GI
- avoid Non-selective, caution for COX-2 selective.
- Co-prescribe a GI protectant.

4) NSAID-related bronchospasm +/- pseudoallergic rxn
- avoid Non-selective, caution for COX-2 selective.

23
Q

Contraindications for COX-2 selective

A

Cardiovascular toxicity eg. Cerebrovascular event.
Recent / impending CABG.

24
Q

Counseling Points for NSADs

A

1) Side effects:
- stomach discomfort
- mild bleeding
- Rare: swollen facial features, difficulty breathing, itchy skin rashes
- Serious bleeding (urine, stools, cough up, sudden severe headache w/ nausea or loss of consciousness)
2) To use for shortest duration possible. If more than 5 days, seek medical advice.
3) Not to take w/ food (absorption rate reduced)

25
Q

What are the disadvantages of using paracetamol?

A
  • Good anti-pyretic but Weak anti-inflammation
  • Toxic doses -> liver damage, N/V (max dose 4g per 24 hrs)
  • Allergic skin reactions

Go to A&E if >= 10g per 24 hrs.

26
Q

What is the MoA of Tramadol?

A

Binds to opioid receptors -> inhibit pain transmission.
Is a SNRI -> potentiates pain inhibition pathway.

27
Q

How is codeine metabolised to morphine?

A

CYP2D6

28
Q

[Side Effects] Opioids

A
  • GI effect (N/V/C)
  • Hormonal effects
  • Depression
  • Sedation / drowsiness
  • Respiratory effects
  • Overdose and death
  • Falls and Fractures
  • Tolerance, physical dependence, addiction, withdrawal
  • Opioid-induced hyperalgesia
29
Q

What are the Risk Factors for Opioid analgesics?

A
  • Combine w/ other CNS depressants
  • Other comorbidities (eg. mental health)
  • Renal or hepatic insufficiency, age > 65 yo
  • Pregnancy
  • Personal or Family hx of substance use disorder
  • High dose, long duration of use
  • Risk of diversion
  • Risk of opioid use disorder
30
Q

What is the MoA of Ophenadrine?

A

Central muscle relexant
Muscarinic receptor antagonist -> basal ganglia

Also: h1 antihistamine, nmda receptor antagonism, NDRI, sodium channel blockers

31
Q

[Side Effects] Orphenadrine

A

Common:
N/V
Flushing
Dilated pupils
Dry mouth

At higher doses:
Tachycardia
Ataxia
Nystagmus
Drowsiness
Delirium
Agitation
Visual hallucinations

32
Q

Contraindications or Cautions for Orphenadrine

A

Contraindications:
- Glaucoma
- BPH
- Myasthenia gravis

Caution in concomitant use of:
- CNS sedatives, depressants
- 1st gen antihistamines
- Anticholinergics
- Antiparkinsonian drugs (eg. Amantadine, Ropinirole)

33
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34
Q
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PR3154 (10 decks)

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