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pharmacology pain Flashcards

1
Q

signs of inflammation

A

heating, redness, swelling, pain

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2
Q

how pain occurs

A

pain transmission through spinothalamic tract

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3
Q

how inflammation symptoms occur

A

cell damage -> cell phospholipid broken down by phospholipase A2 into arachidonic acid

1) Acute inflammation

  • arachidonic acid broken down into prostaglandin H2 -> broken down by isomerase into prostanoids:

** prostacyclin (PGI2): cause vasodilation, inhibit platelet aggregation
** classical prostaglandin (PGE2): vasodilation (redness, heating), vascular permeability (oedema, swelling), pain
** thromboxane (TXA2): vasoconstriction, platelet aggregation

  • types of injury results in different amounts of prostanoids produced

2) chronic inflammatory immune response

  • arachidonic acid broken down by 5-lipoxygenase into leukotrienes -> prolonged inflammation
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4
Q

how does fever occur?

A

inflammation -> neutrophils respond and release cytokines -> increase COX expression -> produce PGE2 in hypothalamus -> change in body thermostat -> fever

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5
Q

COX 1 vs COX 2

A

COX-1 constitutive

  • present all the time in GI, kidney

COX-2 inducible

  • only produced by cells involved in inflammatory and tissue repair
  • so COX-2 selective enzymes have lesser GI and renal AE
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6
Q

types of NSAID to remember

A

1) non-selective COX inhibitor

  • irreversible: aspirin (COX 1&raquo_space;> COX 2)
  • reversible: naproxen (COX 1&raquo_space; COX 2), ibuprofen (COX 1 > COX2), diclofenac, mefenamic acid (COX 2 > COX 1)

2) reversible COX-2 inhibitor

  • celecoxib
  • parecoxib -> valdecoxib
  • etoricoxib
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7
Q

types of non NSAIDs involved

A

1) CNS-selective COX inhibitor

  • paracetamol

2) opioids/narcotic analgesics

  • tramadol, codeine, morphine, oxycodone, fentanyl
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8
Q

aspirin MOA

A

1) anti-inflammatory

  • block COX -> block PGI2, PGE2
    ** block vasodilation -> reduce warmth, redness, swelling
    ** block increased vascular permeability -> reduce swelling
    ** block pain associated with inflammation

2) analgesic

  • block production of prostaglandins -> sensitise nociceptive fibres to stimulation by other inflammatory mediators
    ** reduce pain signals so pain not that intense
    ** result in analgesic ceiling (NSAID not so effective for severe pain)

3) antipyretic

  • NSAIDs block COX -> reduce PGE2 -> reset body thermostat back to normal
  • X alter normal body temperature

4) antiplatelet

  • block COX-1 -> inhibit TXA2 production -> inhibit platelet activation and aggregation -> need to be restored by formation of new platelet
  • block COX-2 -> inhibit PGI2 production -> inhibit platelet aggregation -> restored by synthesis of new COX enzyme
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9
Q

aspirin dose-dependent AE

A
  • mostly caused by salicylate chemical structure

** high dose > 50mg/dL -> salicylate toxicity -> renal/respi failure

  • gastric intolerance: bleeding
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10
Q

aspirin CI

A

X use in children cuz of Reye’s syndrome

  • increased risk if aspirin + child w viral infection
  • encephalitis (swelling of brain) and hepatomegaly (swelling of liver)
  • vomiting, personality change, listlessness, delirium, convulsions, loss of consciousness
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11
Q

naproxen, indomethacin, diclofenac - MOA

A

1) anti-inflammatory

  • block COX -> block PGI2, PGE2
    ** block vasodilation -> reduce warmth, redness, swelling
    ** block increased vascular permeability -> reduce swelling
    ** block pain associated with inflammation

2) analgesic

  • block release of prostaglandin -> sensitise nociceptive fibres to stimulation by other inflammatory mediators
    ** reduce pain signals so pain not so intense
    ** analgesic ceiling so not effective for severe pain

3) antipyretic

  • NSAID block COX -> reduce PGE2 -> reset body thermostat back to normal
  • X alter body normal temperature
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12
Q

naproxen specifics

A
  • long t1/2 so BD dose
  • more effective in women
  • often used in dysmenorrhea
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13
Q

indomethacin specific

A
  • strongly anti-inflammatory due to additional steroid-like phospholipase A inhibition
  • CNS AE: confusion, depression, psychosis, hallucination
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14
Q

diclofenac specific

A
  • can be applied topically
  • short t1/2, lesser GI risk
  • longer t1/2 in synovial fluid
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15
Q

AE for all non-selective tldr

A

1) GI related
2) renal related
3) pseudo-allergic reactions
4) haematological effects: bleeding risk
5) increase BP and HTN
6) CVS problems

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16
Q

non-selective NSAID AE - GI related - role of prostaglandin

A
  • reduce gastric acid secretion
  • increase mucosal blood flow, mucous secretion, bicarbonate secretion
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17
Q

non-selective NSAID AE - GI related - AE caused

A
  • dyspepsia, N/V
  • ulcer formation and potential haemorrhage risk in chronic users (> 5 day use)
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18
Q

non-selective NSAID AE - GI related - risk factors

A

1) > 65 yo
2) history of ulcer
3) use of high dose/chronic NSAIDs
4) concurrent glucocorticoid, antiplatelet, anticoagulants

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19
Q

non-selective NSAID AE - GI related - when to refer?

A

fatigue, severe dyspepsia, signs of GI bleed, unexplained blood loss, anemia, iron deficiency

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20
Q

non-selective NSAID AE - renal related - how does it happen?

A

1) alter renal blood flow
2) inhibit PGE2 production

  • Na & water retention in thick ascending limb -> peripheral oedema -> HTN

3) inhibition of PGI2 production

  • suppression of renin and aldosterone secretion in distal convoluted tubule, not enough to counteract Na action
  • hyperkalaemia -> acute renal failure

4) triple whammy

  • NSAIDs, diuretics, ACEi can all cause renal failure
    ** ACEi/ARB prevent afferent arteriole vasoconstriction required to maintain GFR
    ** diuretics cause volume depletion
  • need to check renal failure if using any 2
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21
Q

non-selective NSAID AE - renal related - risks for AKI

A

1) increase age, chronic HTN, atherosclerosis

  • narrowing of renal afferent arterioles -> reduce capacity for renal afferent dilation

2) pre-existing glomerular disease/renal insufficiency

  • renal afferent dilation required to maintain GFR
  • volume depletion
  • true volume/effective volume
    ** lower afferent glomerular arteriolar pressure -> stimulate secretion of angiotensin II
  • triple whammy
  • aminoglycosides, amphotericin B, radiocontrast material
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22
Q

non-selective NSAID AE - pseudo-allergic reaction - how it happens?

A

inhibit COX -> more arachidonic acid converted to lipoxin/leukotriene -> excess leukotriene cause bronchospasm and allergic like reactions

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23
Q

non-selective NSAID AE - pseudo-allergic reaction - possible symptoms

A
  • skin rash, swelling, itching, nasal congestion, anaphylactic shock
  • trigger bronchospasm in susceptible asthmatics
  • caution in pt w asthma, chronic urticaria (hives), nasal polyps
  • stronger effect for aspirin cuz irreversible
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24
Q

non-selective NSAID AE - haematological problems

A
  • inhibition of COX-1 -> inhibition of TXA2 production -> prevent clot formation
  • greater risk for COX-1 than COX-2 inhibition
  • mild bleeding (gums, nose bleed, small cuts) and serious bleeding (blood in pee/shit, cough blood, unexplained large bruises)
  • stop 3 days before surgery
25
non-selective NSAID AE - increase BP and HTN
monitor BP, discontinue/lower dose if BP increase
26
non-selective NSAID AE - CVS problems
MI, stroke, vascular death
27
non-selective NSAID CI
1) 3rd trimester of pregnancy 2) children, elderly 3) asthma, chronic urticaria, nasal polyps 4) severe renal impairment (eGFR < 15 or CrCl < 30) 5) severe HF, active GI ulcer/bleed, bleeding disorders 6) use of systemic corticosteroids (too immunosuppressive) 7) use of antiplatelet/anticoagulant (high bleeding risk) 8) multiple risk factors for NSAID toxicity 9) cross-sensitivity, hypersensitivity
28
reversible COX-2 selective inhibitors - MOA
1) anti-inflammatory - block COX -> block PGI2, PGE2 ** block vasodilation -> reduce warmth, redness, swelling ** block increased vascular permeability -> reduce swelling ** block pain associated w inflammation 2) analgesic - block production of prostaglandin -> sensitise nociceptive fibre to stimulation by other inflammatory mediators ** reduce pain signals so pain not so intense ** analgesic ceiling: not effective for severe pain 3) antipyretics - NSAIDs block COX -> reduce PGE2 -> reset body thermostat back to normal - X alter normal body temperature
29
reversible COX-2 selective inhibitors - dosing instruction
- take for shortest duration possible - avoid taking > 5 days
30
reversible COX-2 selective inhibitors - AE - tldr
1) renal problems 2) ovulation effects 3) pregnancy problems 4) impairment of wound healing 5) increased risk of thrombosis 6) risk of heart attack and stroke
31
reversible COX-2 selective inhibitors - AE - why not free from COX-1 AE?
- constitutive COX-2 still found in CNS, kidneys, female reproductive tract, synovium - COX-2 not helpful if patient already have pre-existing GI ulcer - still have some renal toxicity
32
reversible COX-2 selective inhibitors - AE - renal toxciity - how it happens?
(basically same as non selective, j recapping) 1) alter renal blood flow 2) inhibit PGE2 production - Na and water retention in thick ascending limb - peripheral oedema -> HTN 3) inhibition of PGI2 production - suppression of renin and aldosterone secretion in distal convoluted tubule, not enough to counteract Na retention 4) triple whammy - NSAIDs, diuretics, ACEi can cause renal failure **ACEi/ARB prevent afferent arteriole vasoconstriction required to maintain GFR ** diuretics cause volume depletion - need to check renal failure if using any 2
33
reversible COX-2 selective inhibitors - AE - renal toxicity - risks for AKI
(same as non selective, j revising) 1) increased age, chronic HTN, atherosclerosis - narrowing of renal afferent arterioles - reduce capacity for renal afferent dilation 2) pre-existing glomerular disease/renal insufficiency - renal afferent dilation required to maintain GFR - volume deficiency - true volume/effective volume ** lower afferent glomerular arteriolar pressure -> stimulate secretion of angiotensin II - triple whammy
34
reversible COX-2 selective inhibitors - AE - ovulation effects
delayed follicular rupture
35
reversible COX-2 selective inhibitors - AE - pregnancy effects
premature closure of ductus ateriosus in late pregnancy -> baby problems
36
reversible COX-2 selective inhibitors - AE - impairment of wound healing
- can worsen ulcer - caution for ** existing ulcer/other ulcer risk ** post-surgical analgesia ** concern over non-union of fractures and bone repairs
37
reversible COX-2 selective inhibitors - AE - increased risk of thrombosis
lesser COX-2 to break down arachidonic acid to PGI2 and PGE2 -> more COX-1 to break down arachidonic acid to TXA2 -> increased platelet aggregation -> increased risk of thrombosis
38
reversible COX-2 selective inhibitors - AE - risk of heart attack and stroke
- renal effect (HTN) + risk of prothrombotic effect - greater caution in elderly, history of cerebrovascular/cardiovascular disease - risk extends to non-selective NSAIDs
39
reversible COX-2 selective inhibitors - CI
(same as non selective j recap) 1) 3rd trimester of pregnancy 2) children, elderly 3) asthma, chronic urticaria, nasal polyps 4) severe renal impairment (eGFR < 15 or CrCl < 30) 5) severe HF, active GI bleed/ulcer, bleeding disorders 6) use of systemic corticosteroids (too immunosuppressive) 7) use of antiplatelet/anticoagulant (high bleeding risk)
40
types of topical NSAIDs
1) ketoprofen fastum gel PRN 2) ketoprofen patch PRN 3) voltaren diclofenac gel PRN
41
topical NSAIDs AE
- generally safe - mild irritation and redness - pseudoallergy or allergy - X use in open wound or rashes (eczema/psoriasis) - can induce photosensitivity so X go under sun - a lot of dermatological caution
42
how to choose the right NSAIDs
1) risk of CV toxicity -use celecoxib or ibuprofen max 5 days - avoid diclofenac and etoricoxib - if X use celecoxib/ibuprofen/naproxen then consider paracetamol alone 2) risk of renal toxicity - consult doctor, look out for triple whammy 3) risk of GI toxicity - use COX-2 selective - avoid non-selective NSAIDs - consider adjunctive GI protectant (PPi) 4) risk of bronchospasm - use COX-2 selective - avoid non-selective NSAIDs
43
MOA of paracetamol
selectively inhibit COX in CNS -> modulate CNS interpretation of pain -> reduced sensation of pain
44
advantages of paracetamol
1) analgesic for mild - moderate pain 2) antipyretic 3) spare GI tract 4) few and uncommon SE 5) few DDI 6) safe for paediatric use
45
disadvantages of paracetamol
1) weakly anti-inflammatory 2) toxic doses cause N/V, liver damage 3) possible allergic reaction
46
how does paracetamol cause liver damage?
hepatoxicity if overdose/chronic alcohol use/abuse - minor metabolism pathway of paracetamol induced by alcohol to form toxic metabolite - toxic metabolite metabolised by glutathione but glutathione also depleted by alcohol - result in accumulation of toxic metabolites -> hepatotoxicity - can replenish glutathione with N-acetyl-cysteine (NAC) so it can be used for paracetamol toxicity/overdose
47
dosing for paracetamol
- max dose 500mg per day due to analgesic ceiling - reduce dose for: liver impairment, underweight, frail - overdose ** if ≥ 4g in 24 hrs then caution cuz increase risk of liver damage ** if ≥ 10g in 24 hrs then refer to A&E
48
combination therapy for NSAIDs and paracetamol
- reduce pain: combine dose for synergistic effect - reduce fever: alternate dose for sustained effect
49
general opioids
- not first line for pain - NSAID (+/- paracetamol) more effective than opioid combination for pain associated with acute inflammation - not anti-inflammatory
50
opioids MOA
inhibit transmission of nociceptive signals to brain
51
dosing for opioids
- lowest effect dose of weakest opioid for shortest duration - X prescribe extra to prevent abuse
52
types of opioids
weak opioid: tramadol, codeine strong opioid: morphine, oxycodone, fentanyl
53
opioid dose conversion
based on morphine milligram equivalent (mg/day) - codeine 0.15 - tramadol 0.2 - oxycodone 1.5 - methadone 4.7 - fentanyl (transdermal in mcg/hr) 2.4
54
opioids AE
1) GI effects: C, N/V 2) imbalance of hormonal systems 3) depression 4) respiratory depression if overdose 5) overdose and death 6) sedation, drowsiness 7) falls and fractures (cuz sedation) 8) tolerance, physical dependence, addiction +/- withdrawal 9) opioid-induced hyperalgesia
55
CI for opioids
1) combination w other CNS depressants 2) other comorbidities (mental health condition) 3) renal, hepatic insufficiency 4) age > 65 yo 5) pregnancy (risk to both mother and fetus) 6) personal or family history of substance abuse 7) already prescribed an opioid - increases risk with increase dose and duration of use - risk of diversion - risk of opioid use disorder
56
orphenadrine indication
for muscular pain esp lower back and neck pain
57
orphenadrine MOA
- muscarinic receptor antagonist at basal ganglia - tertiary amine that passes BBB - H1 antihistamine, NMDA receptor antagonism, norepinephrine and dopamine reuptake inhibitor, Na channel blocker
58
orphenadrine SE
1) common - N/V, flushing, dilated pupils, dry mouth 2) higher dose - tachycardia, ataxia, nystagmus, drowsiness, delirium, agitation, visual hallucination - hepatotoxicity, allergic reaction
59
orphenadrine DDI
additive effective with 1st gen antihistamines, anticholinergics, anti PD

end of y3 (8 decks)

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