Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Year 1 > Analgesic Drugs > Flashcards

Analgesic Drugs Flashcards

1
Q

Define analgesic drugs:

A

Drugs that relieve pain by modifying transmission pathways without blocking nerve impulse conduction, reducing consciousness or markedly altering sensory function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 2 major classes of analgesic drugs

A

simple analgesics and opioid analgesics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 2 differences between efferent and afferent neurones?

A

Afferent neurons cary sensory information from receptors to CNS whereas efferent neurons carry motor info from the brain to the Peripheral NS

Afferent cell bodies are located outside of the spinal cord whereas efferent cell bodies are located in the ventral horn of the spinal cord.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the name for paracetamol in america?

A

Acetaminophen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of analgesic is paracetamol?

A

An aniline analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mechanism of action of paracetamol

A

It is a weak cox-inhibitor with its analgesic effects mediated in the CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pharmacokinetics of paracetamol? (4)

A
  1. Is rapidly absorbed through the GI tract, peak plasma conc reached after 1-2 hours.
  2. It extensively undergoes phase 2 metabolism in the liver to form sulphate and glucuronide conjugates which are secreted in the urine.
  3. A minor fraction of the drug is converted to highly reactive alkylating metabolite which is inactivated by reduced glutathione and excreted as cysteine and mercapturic acid conjugates.
  4. Plasma half life in healthy subjects around 2 hours.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the clinical effects, indications, contraindications and cautions for paracetamol?

A

Clinical effects: pain relief and fever reduction

Clinical indications: mild to moderate pain and pyrexia

Contraindications: None

Cautions: low body mass, liver disease and those at risk of liver disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the common formulations of paracetamol? (4)

A
  • 500mg tablets or capsules
  • 24mg/mL oral suspension.
  • IV
  • Suppositories
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the dose of paracetamol and in what circumstances should you reduce this dose?

A
  • 500mg-1g PO ever 4-6/24
  • Max daily dose= 4g/day
  • dose reductions for <50kg, liver disease, children
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What compound formulations does paracetamol come in? (2)

A
  • Co-codamol 30/500 tablets (w/ 30mg codeine)
  • Co-dydramol 30/500 tablets (w/ 30g dihydrocodeine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What adverse drugs reactions can paracetamol have?

A
  • relatively few
  • Rare hypersensitivity reactions like thrombocytopenia, leukopenia and skin reactions
  • Hepatotoxicity from overdose.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What important drug interactions does paracetamol have? (2)

A
  • warfarin - increases anticoagulation effect
  • enzyme-inducing anti-epileptic drugs like carbamazepine increases hepatotoxicity risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Step by step metabolism of paracetamol at therapeutic dose: (2 steps)

A
  1. Predominantly metabolised by phase 2 reactions in liver to sulphate or glucuronide conjugates that are excreted in urine.
  2. Small amount metabolised by phase 1 reaction in cytochrome P450 system to a toxic intermediate NAPQI oxidising radical which is detoxified by reduction with glutathione
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Step by step metabolism of overdose of paracetamol:

A
  1. capacity of phase 2 conjugating enzyme pathway is overwhelmed
  2. Large proportion undergoes phase 1 cytochrome P450 metabolism
  3. Toxic NAPQI radical accumulates as liver stores of glutathione depleted causing rapid hepatocellular necrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What circumstances may increase rate of NAPQI radial production making hepatotoxicity more likely?

A
  • Co-administration of enzyme inducing drugs
  • Circumstances that also deplete glutathione e.g. malnutrition, alcohol dependancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the treatment for paracetamol overdose?

A

If recognised at early stage it can be prevented by administering supplementary reducing equivalents in the form of N-acetylcysteine (NAC)

18
Q

What is the difference between opiates and opioids?

A

Opiates refer to the natural opioids whereas opioids refers to all natural and synthetic opioids

19
Q

What are opioids?

A

Molecules capable of being agonists at endogenous opioid receptors.

20
Q

What are the 3 main subtypes of opioid receptor?

A

G-protein coupled receptors Mu, kappa and delta.

21
Q

3 examples of endogenous opioid peptides:

A

B-endorphin, enkephalin, dynorphins.

22
Q

7 examples of strong opiates:

A

Morphine, diamorphine, oxycodone, fentanyl, pethidine, methadone, tramadol

POMMDFT

23
Q

2 examples of weak opioids:

A

Codeine and dihydrocodeine.

24
Q

How do opioids work on Mu-opioid receptors? (4 steps)

A
  1. Mu-opioid receptors are coupled to adenylate cyclase, opioid binding to receptor causes inhibition.
  2. Reduced availability of cAMP
  3. Less cAMP causes inhibition of Ca2+ entry, in turn inhibiting release of nociceptive neurotransmitters like substance P, GABA, dopamine, Ach, and NA.
  4. Reduced cAMP facilitates entry of K+ through inwardly rectifying channels, hyperpolarize cell membranes.
25
Q

What are the pre and post synaptic actions of opiods?

A

Pre-synaptic:
Inhibit Ca2+ channels on nociceptive afferents to inhibit release of neurotransmitters like substance P and Glutamate.

Post-synaptic:
Open inward k+ channels to hyperpolarize cell membranes increasing required action potential to generate nociceptive transmission.

26
Q

How do opioid actions at pre and postsynaptic neurons influence the ascending pain pathway?

A
  • Signals glutamate and substance P requires at synapse between 1st and 2nd order neurons in the dorsal horn.

Spinal cord contains opioid neurons that release endogenous opioid neurotransmitters targeted at pre and postsynaptic opioid receptors

  • Activation of presynaptic opioid receptors inhibits the release of excitatory neurotransmitters
  • Activation of postsynaptic opioid receptors inhibits impulse formation in second order neurons.
27
Q

How do actions of opioids at pre and postsynaptic neurons influence inhibitory descending pain pathway?

A
  • Descending pathway is under inhibitory control by GABAergic neurons that release GABA
  • Endogenous opioid neurons in the CNS reduce inhibition of descending inhibitory pathway by activating presynaptic opioid receptors preventing the release of GABA enhancing inhibitory descending pathways.
28
Q

What is the pharmacokinetics of morphine?

A
  • rapidly absorbed from the GI tract
  • Extensive first pass metabolism in the lIver PHASE 2
  • Peak plasma conc reached after 1-2 hrs
  • Plasma half life 2-3 hours
29
Q

What does GABA stand for?

A

Gamma aminobutyric acid

30
Q

Explain how morphine is metabolised?

A
  1. Extensive phase 2 metabolism in the liver
  2. Forms 3- and 6- glucuronide conjugates which are excreted in the urine.
  3. <10% excreted as unchanged parent drug.
31
Q

How are most other opioids (other than morphine) metabolised and what is the exception?

A
  • Most others undergo phase 1 metabolism inn cytochrome P450 system prior to renal excretion
  • exception is remifentanil which is metabolised by non-specific tissue and plasma enterase.
32
Q

What is significant about codeine metabolism?

A

Around 10% of a codeine dose is metabolised by phase 1 metabolism to morphine which accounts for its analgesic effects.

Minority of population who are poor metabolizers therefore derived little analgesic effect from codeine.

33
Q

What are the clinical effects, indications, contraindications and cautions of opioid analgesics?

A

Clinical effects: Pain relief

Clinical indications: acute pain, chronic (cancer) pain, pulmonary oedema, suppressing intractable cough

Contra-indications: respiratory depression and reduced conscious state as can mask pupillary response.

Cautions: Elderly and those with pre-existing respiratory disease.

34
Q

What are the common formulation options for opioid analgesics?

A
  • By mouth: immediate or modified release tablets or oral solutions such as oramorph
  • Injection: intravenous, intramuscular, subcutaneous in palliative care.
  • Transdermal: fentanyl and buprenorphine.
35
Q

What are some common doses of opioid analgesics?

A
  • Immediate release: 5-10mg PO 4/24 or 1/6 of normal dose for breakthrough pain.
  • Modified release every 12-24 hours
  • parenteral 5-10mg IV slowly
36
Q

When should opioid doses be reduced?

A

Elderly, hepatic and renal impairments

37
Q

What are the adverse effects of opioids on CNS, Respiratory, GI and urinary systems and any other effects?

A

CNS: confusion, drowsiness, euphoria, hallucination, miosis, withdrawal syndrome.

Respiratory: respiratory depression with high doses, cough suppression

GI system: constipation, dry mouth, nausea and vomiting (common on initiation)

urinary system: Urinary retention

Other: flushing, hypotension with high doses.

38
Q

Pharmacodynamic interactions of opioid analgesics?

A

Drugs that also inhibit the CNS activity

39
Q

Pharmacokinetic interactions of opioid analgesics?

A

drugs that enhance or inhibit the phase 1 metabolism of opioids - those metabolised through phase 2 less likely to have drug interactions.

40
Q

What advice should you give to patients when prescribing opioid analgesics?

A
  • How to take meds
  • take as prescribed
  • Clarify review point
  • Driving and other skilled tasks (lessened reaction time and coordination).
41
Q

What monitoring arrangements should be put into place when prescribing opioid analgesics?

A
  • For acute parenteral administration monitor cardiorespiratory depression
  • For chronal oral prescription monitor analgesic efficiency, adverse effects, features of dependance.

Pharmacology Year 1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions