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Y1S2Pharmacology > Analgesia: mechanisms of pain management > Flashcards

Analgesia: mechanisms of pain management Flashcards

1
Q

What is an analgesic?

A

Analgesics/painkillers, is any member of the group of drugs that are used to achieve analgesia (the relief from pain)

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2
Q

What are the analgesic drugs?

A

1) Narcotics
2) Non-steroidal anti-inflammatory drugs (NSAIDs)
3) Acetaminophen

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3
Q

What is a narcotic analgesic/opioid?

A

Opioids are natural, semisynthetic, or synthetic compounds that produce morphine-like effects

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4
Q

What are the examples of natural opioids?

A

1) Morphine ((stronger than codeine)

2) Codeine

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5
Q

What are some examples of semisynthetic opioids?

A
  • In semisynthetic opioids, we add H2 or O2

1) Hydromorphone

2) Hydrocodone

3) Oxycodone

4) Oxymorphone

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6
Q

What are some examples of synthetic opioids?

A

1) Fentanyl

2) Meperidine

3) Methadone

4) Tapentadol

5) Tramadol

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7
Q

How do narcotic analgesics relieve pain?

A

By binding to opioid receptors that are present in the central and peripheral nervous system causing a state of unconsciousness

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8
Q

What are the types of opioid receptors?

A

1) mu receptor
2) Kappa receptor (K)
3) Delta receptors
4) Sigma receptor

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9
Q

What is the mechanism of action of opioids?

A
  • All opioid receptors are G-proteins couples receptors that inhibit adenylate cyclase

They also inhibit neural activity by:

1) In the presynaptic neuron the reduce the influx of calcium, inhibiting the release of neurotransmitters (like glutamate & substance P), thus no pain signals

2) They increase the efflux of calcium in the postsynaptic neuron reducing its charge, furthermore increasing the threshold (causes hyperpolarization) making it difficult to excite the cell

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10
Q

What is the role of mu receptors in opioids?

A
  • They are thought to be responsible for most of the analgesic effects of opioids and some major unwanted effects (euphoria)
  • Most of the analgesic opioids are mu-receptors agonist
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11
Q

What is the role of kappa K-receptors in opioid analgesics?

A
  • They contribute to analgesia at the spinal level, which might elicit sedation and dysphoria
  • They relatively produce few unwanted effects and do not contribute to dependance
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12
Q

What is the role of delta receptors in opioid analgesics?

A
  • They are more important in the periphery and might contribute to analgesia
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13
Q

What is the role of sigma receptors in opioid analgesics?

A
  • Their true role is unclear but they regulate the activity of mu-receptors
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14
Q

What are the different classifications of opiates?

A
  • Based on their receptor specificity and their efficacy

1) Pure agonist (Heroin)
2) Partial agonist (Buprenorphine)
3) Antagonist (Naloxone)

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15
Q

What are some examples of pure agonist narcotic analgesics?

A

1) Morphine

2) Heroin

3) Methadone

4) Fentanyl

5) Codeine (used for dry cough)

  • They all have a high affinity for the mu receptors and they generally have a low affinity for kappa and delta receptors
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16
Q

Describe the morphine drug

A
  • It is given either by injection or by mouth (as slow-release tablets)
  • It acts as an:
    1) Analgesic
    2) Euphoria & sedation
    3) Suppression of cough
    4) Respiratory depression
    5) Nausea and vomiting
    6) Reduces GI motility which might cause constipation
    7) Releases histamine (causing bronchoconstriction)
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17
Q

What are the side effects of morphine?

A

1) Addiction (due to the euphoric effects)

2) Dryness of mouth

3) Mental clouding

4) Vomiting

5) Headache

6) Fatigue

7) Constipation

8) Overdosing can cause poisoning (coma, respiratory depression & miosis)

18
Q

Describe fentanyl (an opioid agonist)

A

1) Highly potent opioid
2) Used mainly in anesthesia
3) Used in patient-controlled infusion system
4) Applied as a transdermal patch for chronic pain

19
Q

Describe the partial agonist opioids

A
  • Pentazocine (has a degree of agonist and antagonist activity on different receptors)
  • It is a partial agonist depending on the dosage at mu receptors but a full agonists on delta and kappa receptors
  • Most of the drugs in this group tend to cause dysphoria by acting on kappa receptors (most probably that is the reason)
20
Q

Describe opioids antagonists

A
  • Naloxone (treats resp depression caused by opiate overdose)
  • They produce little effects when given on their own but block the effects of opiates
  • Saves someone with respiratory distress
  • Causes withdrawal symptoms in addicts
21
Q

Describe NSAIDs?

A

1) They are drugs with analgesic, antipyretic, and inflammatory effects

2) Non-narcotic

3) The do not produce sedation or respiratory depression nor do they have an addiction rate

4) The most prominent drugs of this group are Aspirin and ibuprofen

22
Q

List some common examples of NSAIDs

A

1) Ibuprofen

2) Aspirin (acetylsalicylic acid)

3) Ketoprofen

4) Naproxen (moderate effectiveness)

5) Diclofenac (voltaren and cataflam “absorbed fater diclofenac potassium”)

6) Indomethacin (greater anti-inflammatory effects)

7) Piroxicam

8) Ketorolac (great analgesic effects)

23
Q

What is the mechanism of action of NSAIDs?

A
  • Inhibits cyclo-oxygenase enzyme (COX), inhibiting the formation of inflammatory mediators (prostaglandins, prostacyclin, and thromboxanes)
24
Q

What are the different isoforms of cyclooxygenase?

A

1) COX-1 constitutive good cox produces:
- Thromboxane A2
- Prostacyclin PGI2
- Prostaglandin E2

2) COX-2 “inducible” (bad cox)
- It is upregulated at sites of inflammation

25
What distinguishes Aspirin from other NSAIDs?
Aspirin irreversibly inactivates COX-1 & 2 by the acetylation of specific serine residues, while other NSAID reversibly inhibits these enzymes
26
What is the pharmacokinetics (ADME) of NSAIDs?
1) Absorption: it is absorbed well from the stomach and intestinal mucosa 2) Well distributed as it has high plasma protein-binding affinity (>95%) 3) Metabolized in the liver mainly 4) Excreted by the urine and some of them are partially excreted in bile
27
What is the order of kinetics of aspirin?
Zero-order kinetics (loses a certain amount over time)
28
What are some of the clinical applications of NSAIDs?
1) Rheumatoid arthritis 2) Osteoarthritis 3) Acute gout 4) Dysmenorrhoea 5) Metastatic bone pain 6) Headache
28
What are some of the drug interactions of NSAIDs?
1) Enhances the action of anticoagulants like (warfarin) - Because aspirin displaces it from the binding sites on the serum albumin in addition to the anti-platelet effects of aspirin 2) Aspiring also displaces tolbutamide (anti-diabetic), phenytoin (anti-convulsant) and other drugs from the plasma protein-binding site 3) Aspirin decreases the renal excretion of sodium urate (contraindicated in patients with gout taking uricosuric agents) 4) Aspirin competes for tubular secretion with penicillin G increasing its half-life 5) NSAIDs reduce the blood flow to the kidneys, reducing the action of diuretics decreasing the elimination of some drugs
29
What are the adverse effects of NSAIDs?
1) GI adverse effects (Direct & indirect irritation of the GIT causing, nausea, dyspepsia, gastric ulceration/bleeding and diarrhea), this is because acidic drugs directly irritate the gastric mucosa and the inhibition of COZ-1 which reduces the levels of protective PGI2 2) Renal effects: - Causes salt & fluid retention - Hypertension - Renal impairment, due to the change of renal hemodynamics that prostaglandins E2 ordinarily mediates 3) CVS risks, as NSAIDs increase the risk of myocardial infarction (both new COX-2 inhibitors and high doses of traditional anti-inflammatory) with the exception of naproxen 4) Hypersensitivity (Rashes, bronchospasm, rhinitis, edema, or an anaphylactic reaction with shock)
30
What can you in order to reduce the risk related to the adverse effects of NSAIDs?
1) Use the lowest effective dose for the shortest period of time 2) Suppress acid production by the concomitant use of proton pump inhibitors like (omeprazole)
31
Which NSAIDs are exempted from causing risk on the CVS
Naproxen
32
Are NSAIDs safe during pregnancy?
No, as they might cause CVS and renal impairment in addition to their link with premature birth, paracetamol/acetaminophen is regarded as safe during pregnancy
33
What are the contraindications of NSAIDs?
1) Peptic ulcer and renal impairment 2) Hemophilia and bleeding tendency 3) Aspirin can reduce the incidence of patent ductus arteriosus in preterm infants and increase their responsiveness to postnatal treatment of PDA 4) Aspirin can cause Reye's syndrome in children and adolescence with viral infections like influenza or chicken pox
34
What is Reyes syndrome?
- Progressive encephalopathy (behavioral changes, and unconsciousness) with hepatic dysfunction
35
How does aspirin develop Reyes syndrome in children and adolescents?
Due to the mitochondrial damage caused by salicylates that might be intensified during viral illness and by the endotoxins and cytokines - Other risk factors might include inborn error of metabolism - Give panadol instead
36
What are the adverse effects of COX-2 inhibitors?
1) Celecoxib is associated with acute CVS events 2) Rofecoxib and valdecoxib are withdrawn from the world 3) Increases the Blood Pressure (10-17%) 4) Some evidence of renal impairment
37
Describe paracetamol/acetaminophen
- Has a negligible anti-inflammatory activity - Weak inhibitor of COX-1 & COX-2 - In the CNS it inhibits the formation of prostaglandins causing fever and pain - It is a good antipyretic and analgesic - In the liver, it is metabolized to a toxic intermediate (N-acetyl-p-benzoquinone imine), which can cause hepatotoxicity if not removed by glutathione
38
What are some examples of COX-2 selective inhibitors?
1) Celecoxib 2) Etoricoxib (3-10 times more selective) - They selectively inhibit COX-2 (associated with pain and inflammation) while leaving COX-1
39
What are the advantages in the use of selective COX-2 inhibitors?
1) Reduces GI irritation and ulcer rate, with similar efficacy to non-selective NSAIDs 2) Useful for long-term in treatment of chronic conditions

Y1S2Pharmacology (5 decks)

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