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Drugs > Pain > Flashcards

Pain Flashcards

1
Q

Name 3 NSAIDs

A

Naproxen, ibuprofen, diclofenac

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2
Q

What is the mechanism by which NSAIDs work?

A

COX inhibitor. Therefore, inhibit the synthesis prostaglandins from ARACHIDONIC ACID.

Benefits from blocking COX2, SEs from COX1

COX1: prostaglandins essential for:

  • Maintaining gastric mucosa
  • Maintaining renal perfusion
  • Preventing thrombus formation in vascular endothelium

COX2: prostaglandins:
- Release prostaglandins in response to inflammatory stimuli. Causes inflammation and pain.

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3
Q

What are the indications for NSAIDs?

A
  1. PRN for mild-to-moderate pain where paracetamol (1st line) is insufficient
  2. Tx of long term pain conditions caused by inflammation (especially MSK) - topical Tx preferred.
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4
Q

What are the CIs for NSAIDs

A

Severe renal Impairment
CV/liver failure
Hypersensitivity

Cautioned (use lowest dose for least amount of time) in:

  • Pts at risk of peptic ulceration/GI bleeds
  • CV disease
  • Renal impairment
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5
Q

What are the SEs of NSAIDs?

A
  • Peptic ulceration/GI bleeds
  • Hypersensitivity (bronchospasm)
  • Renal impairment (causing ^H2O/Na - ^BP)
  • Increases risk of CV events (increased BP)

Ibuprofen is safest NSAID

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6
Q

What are the potential drug interactions of NSAID

A

Increases risk of NSAID related adverse effects

  • GI ulceration - NSAIDs + corticosteroids
  • GI bleeds - NSAIDs + SSRIs + venafloxine
  • Renal impairment - NSAIDs + diuretics
  • Increases risk of bleeding with warfarin
  • Reduces therapeutics effects of diuretics and antihypertensives
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7
Q

How are NSAIDs excreted?

A

Renally

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8
Q

Name 2 strong opioids

A

Morphine (natural) oxycodon (synthetic)

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9
Q

What is the mechanism by which morphone/oxycodon works?

A

Activate CNS U (mu) receptors which reduce pain transmission and reduce excitability

Medulla - blunts response to hypoxia and hypercapnia, reducing respiratory drive and SOB

Reduced pain, SOB and anxiety reduces sympathetic drive. This, in context of MI and acute pulmonary oedema, reduces cardiac work and oxygen demand

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10
Q

What are the indications for morphine and oxycodon?

A
  1. Relief and Tx of acute severe pain (post operation, MI)
  2. Relief of chronic severe pain where paracetamol, NSAIDs and weak opioids have proved ineffective (3rd rung of analgesic ladder)
  3. Relief of breathlessness in context of palliative care
  4. Relief SOB and anxiety in pulmonary oedema (along with O2, furosemide and nitrates)
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11
Q

What are the contraindications for morphine and oxycodon?

A
  • Renal and hepatic impairment - reduce dose

- Elderly - reduce dose

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12
Q

What are the SEs of morphine/oxycodon?

A
  • Respiratory depression
  • Euphoria, detachment, neurological depression
  • Papillary constriction - reduced sympathetic drive and activation of Erdinger Westphal nucleus
  • Activates chemoreceptor trigger zone - nausea and vomiting
  • Histamine release - sweating, rashes, urticaria, vasodilation
  • Constipation - U receptor activation increases smooth muscle tone, reducing GI motility
  • Long term use can result in tolerance and dependence (cold turkey symptoms if withdrawn suddenly - opposite effects of morphine i.e. pain, dryness)
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13
Q

What are the potential drug interactions of morphine?

A

Avoid use with other sedating drugs e.g. antipsychotics, benzo’s, tricyclic antidepressants

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14
Q

Name 3 weak opioids

A

Codeine, dihydrocodeine, tramadol

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15
Q

What is the mechanism by which codeine and dihyrdocodeine work?

A
  • Both very weak opioids
  • Broken down to morphine (codeine) and dihydromorphine (dihydrocodeine) which are agonists of U receptors in CNS - reduce pain transmission
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16
Q

Why doesn’t codeine or dihydrocodeine work in everyone?

A

10% Caucasians have less active metabolising enzyme (Cytochrome P450 2D6) so are ineffective in such individuals

17
Q

What is the mechanism by which tramadol exerts its action?

A
  • Tramadol - synthetic codiene - moderate strength opoid
  • Tramadol and its active metabolite are agoinsts of the U receptor which reduces pain transmission
  • Also reduces the re-uptake of serotonin and noradrenaline
18
Q

What are the contraindications for tramadol, codeine and dihydrocodeine?

A

Caution in:

  • Hepatic and renal impairment
  • Severe respiratory disease (reduces respiratory drive)
  • Elderly (dose reduction)
  • Tramadol should be avoided in controlled/uncontrolled epilepsy (reduces seizure threshold)
19
Q

What are the SEs of tramadol, codiene and dihydrocodeine?

A
  • Nausea (activates chemoreceptor trigger zone?)
  • Dizziness
  • Constipation (U receptor activation increases smooth muscle tone and reduces motility)
  • Causes neurological and respiratory depression (in context of overdose)
  • Should NEVER give codeine or dihydrocodeine IV - can cause anaphylactic like reaction (but with no allergic basis)
20
Q

What are potential drug interactions of tramadol, codeine and dihydrocodeine?

A
  • Avoid in combination with sedating drugs e.g. benzos, tricyclic antidepressants, antipsychotics
  • Avoid tramadol in combo with drugs that reduce seizure threshold e.g. SSRI, tricyclic antidepressants
21
Q

What is the mechanism by which paracetamol works?

A
  • Weak, specific inhibitor of COX2
  • Reduces pain (increases pain threshold)
  • reduces prostaglandins in the thermoregulatory area of the hypothalamus, reducing temperature (reduces fever)
22
Q

What are the indications for paracetamol?

A
  1. First line for all types of pain - first step on analgesic ladder
  2. Antipyrexial - reduces fever and associated Sx (e.g. shivering)
23
Q

What are the CIs of paracetamol?

A

Risk of liver toxicity due to:

  • increased NAPQI production (chronic alcohol disease)
  • reduced glutathione (malnutrition, reduced body weight, excess alcohol intake)
24
Q

What are the SE of paracetamol?

A

Usually very well tolerated - COX2 specific inhibitor so has no effect on gastric mucosa, renal perfusion (CV events)

OVERDOSE - paracetamol metabolised by CYP450 –> NAPQI (toxic) — glutathione —> conjugated, excreted form

NAPQI causes hepatocellular necrosis. If overdose, pathway above is overwhelmed.

25
Q

What are the potential drug interactions of paracetamol

A

Very use and usually well tolerated

  • However, PCY450 inducers (e.g. carbamazepine, phenytoin, rifampicin, St Johns wort) increase paracetamol breakdown and increase NAPQI production, increasing risk of toxicity
26
Q

How is paracetamol excreted?

A

Hepatic (CYP450)

27
Q

Name 1 xanthine oxidase inhibitor

A

Allopurinol

28
Q

What is the mechanism by which allopurinol works?

A

Purines –> xanthine — xanthine oxidase –> uric acid

Reduces uric acid concentrations in the body and prevents its precipitation in joints and kidney

29
Q

What are the indications of allopurinol?

A
  1. PREVENTS acute attacks of gout
  2. Prevents formation of uric acid and calcium oxalate stones
  3. Tx of hyperuricaemia and tumour lysis syndrome associated with chemotherapy
30
Q

What are the CIs of allopurinol?

A

Should not be started during acute attack of gout (may precipitate or worsen attack)

Recurrent skin rashes

Hypersensitivity reactions (mild > serious e.g. Steven Johnson syndrome)

Renal and hepatic impairment (metabolised by liver and excreted by kidney)

31
Q

What are the SEs of allopurinol?

A

Most common = skin rash (mild to severe)

May precipitate or worsen an acute attack (continue if already on drug though)

Hypersensitivity reaction (rare but serious)

32
Q

What are the potential drug interactions of allopurinol?

A
  • Cytotoxic drugs e.g. mercaptoPURINE and azathiPURINE require xanthine oxidase for their metabolism. Allopurinol increases risk of drug toxicity

Co-prescription with amoxicillin increases risk of skin rash

Co-presciption with ACEi and thiazides increases risk of hypersensitivity

33
Q

How is allopurinol excreted?

A

Renal

34
Q

What should allopurinol be co-prescribed with for around about a month?

A

NSAIDs - prevents acute attack

Drugs (9 decks)

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