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Year 3 Drugs > Pain / MSK Drugs > Flashcards

Pain / MSK Drugs Flashcards

1
Q

NSAIDs examples

A

Naproxen, Ibuprofen, Diclofenac, Etoricoxib, Diclofenac

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2
Q

NSAIDs indications

A
  1. PRN treatment of mild - moderate pain

2. Regular treatment of pain related to inflammation, particularly MSK

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3
Q

NSAIDs MOA

A

Inhibits COX-enzymes

  • COX-1: Stimulates prostaglandin synthesis essential to preserve gastric mucosa, maintain renal perfusion and inhibit thrombus formation at vascular endothelium. COX-1 inhibition produces adverse effects.
  • COX-2: expressed in response to inflammatory stimuli, producing prostaglandins that cause inflammation and pain. COX-2 inhibition produces therapeutic benefit.
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4
Q

NSAIDs administration

A

Oral
Topical
Suppositories
Injectable

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5
Q

NSAIDs contraindications

A

Absolute Contraindications:

  • sever renal impairment
  • heart failure
  • liver failure

Caution in:

  • peptic ulcer disease
  • GI bleed
  • CV disease
  • renal impairment
  • asthma
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6
Q

NSAIDs side effects

A
  • GI toxicity
  • Renal impairment
  • Cardiovascular events: MI and stroke
  • Hypersensitivity reactions: bronchospasm and angioedma
  • Fluid retention
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7
Q

NSAIDs interactions

A
  1. GI ulceration: aspirin, corticosteroids
  2. GI bleed: anti-coagulants, SSRIs, venflaxine
  3. Renal impairment: ACEi, diuretics
  4. Bleeding: Warfarin
  5. Reduce therapeutic effects of anti-hypertensives and diuretics
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8
Q

NSAIDs patient info

A

Take with food to minimise GI upset

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9
Q

Strong opioids examples

A

Morphine, oxycodone

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10
Q

Strong opioids indications

A
  1. Rapid relief of acute severe pain inc. post-op and MI pain
  2. Relief of chronic pain, when paracetamol / NSAIDs / weak opiates are insufficient
  3. Relief of breathlessness in end-of-life care
  4. Relief of breathlessness and anxiety in acute pulmonary oedema
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11
Q

Strong opioids MOA

A
  • opioids = naturally occurring opiates + synthetic analogues
  • activate opioid mu-receptors in CNS
  • activation reduces neuronal excitability and pain transmission
  • in medulla, blunt the respiratory response to hypoxia / hypercapnoea - reduces respiratory drive and breathlessness
  • reduce sympathetic nervous system activity
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12
Q

Strong opioids administration

A

Acute: IV
Chronic: oral

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13
Q

Strong opioids contraindiations

A
  • caution in hepatic / renal impairment / elderly as eliminated by liver and kidneys
  • avoid in biliary colic as can cause spasm of the sphincter of oddi
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14
Q

Strong opioids side effects

A
  1. Respiratory depression by reducing respiratory drive
  2. Euphoria and detachment, neurological depression in high doses
  3. Nausea and vomiting as can activate chemoreceptor trigger zone
  4. Pupillary constriction due to activation on Edinger-Westphal nucleus
  5. Activation of mu-receptors in large intestine increases smooth muscle tone + decreases motility = constipation
  6. Histamine in skin = itching, urticarial vasodilation and sweating
  7. Tolerance in continued use
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15
Q

Strong opioids interactions

A

Interact with other sedating drugs e.g. antipsychotics, benzodiazepines, tricyclic antidepressants

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16
Q

Strong opioids patient information

A
  • Advise may feel drowsy

- Good hydration to avoid constipation

17
Q

Weak opioids examples

A

Tramadol, codeine, dihydrocodeine

18
Q

Weak opioids indications

A

PRN for mild / moderate pain when simple analgesics are insufficient

19
Q

Weak opioids MOA

A
  • Metabolised in liver to form small amounts of morphine / dihydromorphine
  • Metabolites are mu-receptor agonists
20
Q

Weak opioids administration

A

Oral

IM during operations

21
Q

Weak opioids contraindications

A
  • Caution in renal / hepatic impairment / elderly as eliminated by liver and kidneys
  • Tramadol lowers seizure threshold - avoid in epilepsy and contraindicated if severe epilepsy
22
Q

Weak opioids side effects

A
  • Nausea
  • Constipation
  • Dizziness and drowsiness
  • Can cause neurological and respiratory depression when taken in overdose
  • Codeine / dihydrocodeine must never be given IV as can cause anaphylactic - type reactions
23
Q

Weak opioids interactions

A
  • Other sedating drugs: antipsychotics, benzodiazepines, tricyclics
  • Tramadol should not be used with other drugs that lower the seizure threshold e.g. SSRuIs, tricyclics
24
Q

Weak opioids patient info

A
  • Most effective if taken at regular intervals

- Advise may feel drowsy

25
Q

Paracetamol indications

A
  1. First-line analgesic for acute and chronic pain

2. Anti-pyretic to reduce fever and associated symptoms

26
Q

Paracetamol MOA

A

Weak inhibitor of COX:

  • increases pain threshold
  • reduces prostaglandin concentrations in thermoregulatory region of hypothalamus, controlling fever
  • specific to COX-2 however weak anti-inflammatory as actions are inhibited by presence of peroxides
27
Q

Paracetamol administration

A

Oral

IV or rectal if NBM

28
Q

Paracetamol contraindications

A

Dose reduction in people at increased risk of liver toxicity:

  • Increased NAPQI production e.g. chronic alcohol use
  • Reduced glutathione stores e.g. malnutrition, low body weight, severe hepatic impairment
29
Q

Paracetamol side effects

A
  • None at treatment doses
  • At overdose: liver failure. Metabolised by p450 enzymes to toxic metabolite NAPQI, which is conjugated with glutathione before elimination. After overdose, this pathway is saturated, and NAPQI accumulation causes hepatocellular necrosis.
  • OD treatment: glutathione precursor, acetlycysteine
30
Q

Paracetamol interactions

A

-Cytochrome P450 inducers increase rate of NAPQI production and risk liver toxicity after overdose

31
Q

Xanthine Oxidase Inhibitors example

A

Allopurinol

32
Q

Xanthine Oxidase Inhibitors indications

A
  1. Acute gout attacks
  2. Prevent uric acid and calcium oxalate renal stones
  3. Prevent hyperuricaemia and tumour lysis syndrome associated with chemotherapy
33
Q

Xanthine Oxidase Inhibitors MOA

A
  • Xanthine oxidase metabolises xanthine (produced from purine) into uric acid
  • Inhibition lowers plasma uric acid concentrations and reduces precipitation of uric acid in joints and kidneys
34
Q

Xanthine Oxidase Inhibitors administartion

A

oral

35
Q

Xanthine Oxidase Inhibitors contraindications

A
  1. During acute gout attack as causes sudden fluctuations in uric acid levels
  2. If hypersensitivity / severe recurrent skin rash occurs
  3. Metabolised in liver / kidney, dose reduction needed in impairment
36
Q

Xanthine Oxidase Inhibitors side effects

A
  1. Most common is skin rash - an also indicate serious hypersensitivity e.g. Stevens Johnson syndrome or toxic epidermal necrolysis
  2. Drug hypersensitivity syndrome: life-threatening reaction to allopurinol which includes fever, eosinophilia, lymphadenopathy and multi-organ involvement
  3. Starting allopurinol can trigger / worsen acute gout attack
37
Q

Xanthine Oxidase Inhibitors interactions

A
  1. Mercaptopurine and azathioprine (mercaptopurine pro-drug): require xanthine oxidase for metabolism, may lead to toxicity
  2. Amoxicillin: increased risk of skin rash
  3. ACEi / thiazides: increased risk of hypersensitivity
38
Q

Xanthine Oxidase Inhibitors patient info

A

Take after meals

Good hydration: 2-3 litres water per day

Year 3 Drugs (9 decks)

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