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Sem 5 > Pharmacology 7: NSAIDs and Narcotic Analgesics > Flashcards

Pharmacology 7: NSAIDs and Narcotic Analgesics Flashcards

1
Q

What are most established NSAIDs derived from?

A

carboxylic acid

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2
Q

main therapeutic effects of NSAIDs?

A

analgesia
anti-inflammation
anti-pyresis

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3
Q

primary mode of action of NSAIDs?

A

competitive inhibition of COX which converts arachidonic acid= produced through cleavage of membrane phospholipids, to eicosanoids e.g. prostanoids- PGs, prostacyclins and thromboxanes.
inhibition occurs as sit within COX-1 and 2, so compete with arachidonic acid for binding

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4
Q

blocking which enzyme seems responsible for most NSAID ADRs?

A

COX-1

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5
Q

which enzyme is considered the site for NSAIDs exerting their therapeutic anti-inflammatory/analgesic effect?

A

COX-2= induced in inflammatory cells following activation by cytokines.

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6
Q

how does aspirin differ from the other NSAIDs in terms of its action on COX?

A

aspirin irreversibly inhibits COX enzymes by acetylation= covalent, which allows it to inhibit platelet aggregation through inhibition of COX-1 which inhibits thromboxane A2 production.
other NSAIDs reversibly inhibit COX

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7
Q

describe how NSAIDs exert an ANALGESIC effect

A

inhibit COX-2, reducing PG synthesis hence reducing the senstitisation of nociceptors to inflammtory mediators- both peripherally and centrrally.
reduces headache pain as inhibits cerebral vasodilation mediated by PGs
May also have secondary effect on PG facilitation of afferent pain signal in SC dorsal horn neurones- central sensitisation-inhinit PGE2 acting on secondary nociceptive neurones in dorsal horn which would increase perception of pain.

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8
Q

what do NSAIDs primarily reduce with respect to their anti-inflammtory action?

A

erythema, swelling and pain response assoc. with swelling through inhibition of COX-2 and hence PG prod.

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9
Q

how do NSAIDs exert their antipyresis function?

A

inhibition of PG-E2 production, which is produced by the hypothalamus following the release of endogenous pyrogen IL-1 from macrophages when triggered by bacterial endotoxins, (IL-1 possibly induces COX-2 to stimulate PGE2 production?). PG-E2 elevates set point on central ‘thermostat’ of hypothalamus via EP3 receptor - Gi type GPCR, so decrease cAMP and increase Ca2+ in neurones regulating temperature causing increased heat production and reduced heat loss

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10
Q

what type of elimination kinetics does aspirin exhibit?

A

dose-dependent, so low doses= 1st order, t1/2 4hrs, whereas high dose= 0 order kinetics

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11
Q

ADRs of NSAIDs due to COX-1 inhibition?

A

gastric ulcers- haemorrhage, perforation, as inhibition of PGE2 production via COX-1 which protects gastric mucosa by increasing mucosal blood flow and stimulating alkali and mucus production which protects the mucosa from gastric acid production by parietal cells. Also stimulates cytoprotective mucus secretion throughout GI tract.
nausea, diarrhoea, GI discomfort- dyspepsia
Renal ADRs in susceptible patients- reversible reduction in GFR as PGE2 and PGI2 inhibition
hypersensitivity reactions- rashes, asthmatic bronchospasm and allergic response
prolonged bleeding time

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12
Q

which patients are at particular risk of GI and renal ADRs of NSAIDs?

A

neonates, elderly and patients with compromised Renal, Hepatic- increased risk of GI bleeding and fluid retention, and Cardiac function- NSAIDs may impair renal function- inhibit PG production which dilates renal afferent arteriole, or reduced blood volume

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13
Q

ADRs of selective COX-2 inhibitors?

A

Diclofenac and the selective inhibitors of cyclo-oxygenase-2 (celecoxib, etoricoxib, and parecoxib) are contra-indicated in ischaemic heart disease, cerebrovascular disease, peripheral arterial disease, and mild to severe heart failure.
COX-2 selective inhibitors, diclofenac (150 mg daily) and ibuprofen (2.4 g daily) are associated with an increased risk of thrombotic events.
Selective inhibitors of COX-2 are associated with a lower risk of serious upper gastro-intestinal side-effects than non-selective NSAIDs
selective COX-2 assoc with increased risk of hypertension, cardiac and renal failure

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14
Q

important DDIs of NSAIDs and aspirin with non-NSAID drugs

A

with corticosteroids: corticosteroids may increase incidence and/or severity of ulceration assoc. with NSAIDs, increasing possibility of GI bleeding
aspirin and warfarin- aspirin displaces warfarin for plasma protein binding sites as aspirin=class II drug, so warfarin= higher free plasma concentration, more at risk of toxic SEs= higher bleeding risk, AND both affect platelet aggregation= PDs
NSAIDs and ACEIs- NSAIDs can attenuate their action by blocking prod. of vasodilating PGs, so may massively reduced GFR
with sulfonylureas- increase risk of hypoglycameia
with methotrexate- increase risk of MTX ADRs

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15
Q

what monitoring is required for patients on chronic NSAID therapy?

A

regular review of GI symptoms

monitor renal function

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16
Q

why might aspirin be useful in GI cancer prophylaxis?

A

inhibits PGE2 production which is synthesised by cancers in colon, rectum and possibly upper GI, and this PGE2 promotes tumour growth
may also be prophylactic in breast cancer and other cancers.

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17
Q

1st agent of choice for mild to moderate cases of pain or fever?

A

paracetemol

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18
Q

how does paracetemol appear to have an analgesic and antipyretic property?

A

Currently unknown mechanism – weak COX-1 / COX-
2 inhibitor.Considered to primarily act in CNS possibly on a COX-3 isoform and one of its metabolites in CNS can combine with arachidonic acid to form a substrate that inhibits COX-1 and -2 activity.

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19
Q

within what time period should a paracetemol OD be ideally treated and with what?

A

within 8 hours
IV N-acetylcysteine- but this can protect the liver if infused up, and possibly beyond, 24 hrs of paracetemol ingestion
oral methionine= both increase hepatic glutathione levels

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20
Q

after what time period is a patient likely to die of liver failure following paracetemol OD?

A

after 48 hours

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21
Q

what damaging conditions may occur secondarily to paracetemol OD?

A

renal tubular necrosis

hypoglycaemic coma

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22
Q

what may be monitored in patients on LT paracetemol?

A

hepatic and renal function

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23
Q

where are endogenous opioids found in body?

A

specific parts of CNS and PNS: limbic system, thalamus, SC, primary afferent peripheral terminals

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24
Q

3 major groups of endogenous opioids?

A

enkephalins
endorphins e.g. beta-endorphin from POMC
dynorphins e.g. dynorphin

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25
Q

how is the period of effective analgesia extended with morphine?

A

one of its metabolic products= morphine-6-glucuronide is at least pharmacologically equivalent to morphine with t1/2=4-5hrs
slow release oral morphine preps used in chronic pain control

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26
Q

what effect do opiates have that is responsible for resp depression?

A

mu receptor mediated action on CO2 sensitivity

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27
Q

opioid ADRs?

A

resp depression- action on mu receptors in brainstem
euphoria
confusion
miosis- constricted pupil
psychosis
dependance
tolerance
drowsiness- due to central effect on brain (sedatory effect?)
coma
nausea- mu receptors in brainstem
vomiting-direct stimulatory effect on vomiting centre in brain so may need to also prescribe an anti-emetic
constipation- espec. codeine- given orally
hypotension

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28
Q

what enzyme allows conversion of membrane phospholipids to arachidonic acid?

A

phospholipase A2

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29
Q

why are most NSAID ADRs mediated by inhibiton of COX-1?

A

constitutive expression of COX-1, found in wide range of tissue types
PG synthesis via this enzyme has major cytoprotective role= gastric mucosa, myocardium and renal parenchyma as ensures optimised local perfusion-reduces ischaemia

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30
Q

how do PGs contribute to increased vascular permeability?

A

don’t do so directly, but synergise actions of bradykinin and histamine

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31
Q

typical dosing route for NSAIDs?

A

oral

but many topical applications for soft tissue injury

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32
Q

key factor in pharmacokinetics of NSAIDs in terms of drug distribution?

A

mainy heavily bound to plasma proteins- 90-99%
*importance with DDIs, if displace drugs from their protein binding sites then increase free plasma conc and so can increase risk of drug toxicity

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33
Q

what can be given to patients to offset GI ADRs in the LT with NSAID therapy?

A

PPIs e.g. lansoprazole, omeprazole

misoprostol- synthetic PGE1 analogue

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34
Q

why do ADRs commonly occur with combination NSAIDs?

A

patients self-medicating with NSAIDs e.g. ibuprofen, and then receiving prescribed NSAIDs, PD DDI

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35
Q

examples of highly protein bound drugs affected by NSAIDs?

A

sulphonylureas e.g. gliclazide
warfarin
methotrexate

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36
Q

what is aspirin rapidly hydrolysed to in plasma?

A

salicylate

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37
Q

therapeutic doses of paracetemol?

A

up to 8 500mg tablets/day

38
Q

how do opioids act via gate theory to inhibit pain?

A

inhibit substance P release from nerve terminals in dorsal horn of SC required for activation of 2nd order afferents for pain transmission*

39
Q

when is liver damage maximal after paracetamol OD?

A

3-4 days after OD
nausea and vomiting= only early features, and usually settle within 24 hrs
persistence beyond this and onset of right subcostal pain and tenderness usually indicates hepatic necrosis development
signs of hepatic necrosis= jaundice, right subcostal pain/tenderness

40
Q

when should oral activated charcoal be considered following acute paracetemol OD?

A

if paracetamol in excess of 150mg/kg thought to have been ingested within previous hr
but can give if within 4 hrs, reduce uptake by 50-90%.

41
Q

how can patients at risk of liver damage and hence requiring N-acetylcysteine following paracetemol OD be identified?

A

Single measurement of plasma paracetemol conc related to time from ingestion if at least 4 hrs from time of ingestion, plotted on a paracetemol treatment graph.
N-acetylcysteine given immediately in those whose plasma-paracetamol concentration falls on or above the treatment line on the paracetamol treatment graph.

And in those who present 8–24 hours after taking an acute overdose of more than 150 mg/kg of paracetamol, even if the plasma-paracetamol concentration is not yet available; acetylcysteine can be discontinued if the plasma-paracetamol concentration is later reported to be below the treatment line on the paracetamol treatment graph, provided that the patient is asymptomatic and liver function tests, serum creatinine and INR are normal.

The prognostic accuracy of a plasma-paracetamol concentration taken after 15 hours is uncertain, but a concentration on or above the treatment line on the paracetamol treatment graph should be regarded as carrying a serious risk of liver damage.

0-36hrs can start N-acetylcysteine, oral methionine if can’t give NAC IV and OD within 10-12 hrs and patient not vomiting.

42
Q

why might prescribing a NSAID to a known asthmatic worsen their airway narrowing?

A

inhibtion of COX means increase in arachidonic acid so more metabolised via lipo-oxygenase pathway which results in increased leukotriene production which contributes to airway inflammation in asthma.

43
Q

why is COX-1 constitutively expressed?

A

constant synthesis is required of PGs as very short t1/2= 10 mins

44
Q

what characteristic of COX-2 selective inhibitor’s structure was designed in order to cause COX-2 selectivity?

A

large molecular structure so unable to sit in relatively narrow AS of COX-1
only approved for use in US and EU in short term treatment.

45
Q

via which bonds are NSAIDs bound to plasma proteins?

A

ionic bonds
so drug once bound to plasma protein can be displaced from protein by other drugs
*important for DDIs- NSAIDs may displace sulphonylureas, warfarin and methotrexate from plasma proteins, increasing their risk of ADRs

46
Q

what may influence your decision as to which NSAID to prescribe?

A

how severe is the pain? some more potent than others e.g. naproxen= highly potent BUT increased risk of ADRS e.g. skin rash, so may also want to ascertain other RFs in pateint for ADRs e.g. elderly- may be compromised renal function, so would want to prescribe an NSAID with less risk of ADRs.
Cost?
chronic pain= would use NSAID with a longer t1/2, do taking drug once daily, t1/2>10hrs
dosing regimen to fit in with everyday activities e.g. naproxen= longer t1/2 so given less frequently.
dominant disease state and individual patient response?
elderly, previous GI ulcers, also on anti-platelet or corticosteroid therapy?- increased risk of GI ADRs to may prescribe selective COX-2 inhibitor.

47
Q

aspirin dose given daily for cardioprotective purpose?

A

75mg

48
Q

describe how peripheral sensitisation is mediated by PGs

A

PGE2 in particular following tissue injury binds to EP1 GPCR on C pain fibres.
=GqGPCR= PLC- PIP2 to IP3 and DAG= increase Ca2+ sp increase NT release.
Also increase neurona sensitivity to bradykinin, increase Na+ channel sensitivity and inhibit K+ channels. So increase C fibre activity.
Increased sensitivity responsible for hyperalgesia= increased pain at normal threshold, and allodyniaNS- activation of surrounding fibres? upregulation of NMDA receptors- increased excitation?

49
Q

how do PGs mediate central sensitisation causing pain?

A

increased cytokines in dorsal horn as increased nociceptive signalling peripherally.
PGE2 binds to GPCR=Gs in dorsal horn- activates adenylyl cyclase, increase cAMP, activate PKA-phosphorylation of glycine receptor- reduce binding affinity so glycine can’t bind to inhibit pain= increases sensitivity and discharge rate of secondary interneurones.

50
Q

therapuetic pharmacodynamic interactions of NSAIDs?

A

low-dose opiates= extends therapeutic range for treating pain so more pain can be treated, and reduces ADRs seen with opiates alone.

51
Q

DDIs with NSAIDs in combination?

A
  • increase risk of ADRs, often occurs due to self medication with NSAIDs- PDs and PKs altered, PKs-disaplacement from plasma protein binding sites.
  • NSAIDs and low dose aspirin- compete for COX-1 so may interfere with cardiprotective function of aspirin.
52
Q

T1/2 of aspirin?

A

<30 mins, rapidly hydrolysed in plasma to salicylate

53
Q

T1/2 of salicylate at low doses of aspirin?

A

4hrs

54
Q

t1/2 of paracetemol given at therapeutic dose?

A

2-4hrs

55
Q

how is paracetemol normally metabolised at therapeutic doses?

A

1st order Pks
mainly undergoes phase II metabolism with glucuronide (60%), 30% with sulphate
10% undergoes phase I oxidation producing toxic metabolite NAPQI= very reactive, free radical. This then detoxified with glutathione in phase II conjugation=linear, but limited by glutathione availability.

56
Q

ADR associated with IV paracetemol, and dose of paracetemol given by IV infusion?

A

hypotension
>50kg= 1000 mg every 4-6hrs, max= 4000mg daily
if 10-50kg= 15mg/kg every 4-6hrs, max= 60mg/kg daily.

57
Q

how does toxicity occur with paracetemol OD?

A

single doses >10g (>20 tablets) potentially fatal.
PKs become zero order as phase II metabolism becomes saturated.
So rather than 10% undergoing phase I oxidation, now most is undergoing this pathway, so increased toxic NAPQI produced.
As phase II pathways saturated, glutathione conjugation pathway also saturated as rate limited, glutathione rapidly consumed and unavailable to remove NAPQI so more around to exert toxic effect, binding to sulfydryl groups on heaptocytes and mitochondria and promoting heaptocyte necrosis.
Glutathione consumption also makes hepatocytes susceptible to damage from other free radicals which would glutathione would normally protect cells against.
Can also cause renal failure.

58
Q

precursors of endogenous opioid peptides?

A

pro-enkephalin
POMC
pro-dynorphin

59
Q

why might giving opioids LT result in immunosuppression?

A

mu-opioid receptors expressed on lymphocytes so function inhibited

60
Q

which opioid receptor is involved most with giving pain relief (analgesia)?

A

mu
receptor has important effects in brain (supraspinal)
found pre and post synaptically

61
Q

where are kappa and delta opioid receptors found in the body?

A 
kappa= SC- analgesia
delta= widely distributed, acted on by enkephalins
62
Q

what happens when mu receptors activated?

A

increased permeability to K+, so hyperpolarisation and hence reduced neuronal excitability

63
Q

what happens when kappa receptors activated?

A

reduce Ca2+ influx via channels

64
Q

what happens when delta receptors activated?

A

reduce cAMP synthesis

65
Q

what can all subtypes of opioid receptor when activated definitely achieve in terms of activating a GPCR?

A

decrease cAMP

66
Q

In the pre-synaptic neurone (e.g. interneurone of substantia gelatinosa?) how can activation of the different subtypes of opioid receptor cause inhibition of pain?

A

ALL cause decrease in Ca2+ so vesicle containing substance P neurotransmitter is inhibited from fusing with the pre-synaptic membrane which is necessary for NT release and subsequent activation of 2nd order afferent to allow pain transmission.
mu receptor activated- increase K+ efflux which will decrease IC Ca2+
kappa activated- inhibit Ca2+ channels so decrease Ca2+
delta activated- inhibition of adenylate cyclase, so decrease cAMP which decreases Ca2+

67
Q

via which receptor do most ADRs of opioids come about?

A

mu-opioid

68
Q

why is ADR of dependence with opioid drugs so problematic in terms of health risk to patient?

A

have to take the drug or will suffer severe withdrawal symptoms, but opioids also cause tolerance, so the dose of the drug will need to be increased to achieve the same desired therapeutic effect, and this will increase the risk of fatal respiratory depression, which often causes death.

69
Q

ADRs associated with kapa receptora?

A

dysphoria- low mood, distress e.g. with pentazocine

70
Q

how do agonist/antagonist properties of opioid drugs differ?

A

pure agonist= morphine
partial agonsit= buprenorphine- unable to achieve maximal response even when all available receptors bound, but if more receptors were available, it may be able to achieve max effect and so become a full agonist. With a higher affinity but lower efficacy, it is more likely to bind to receptors than herorin, but less able to activate them so reduce rosk of ADRs?
agonist/antagonist- action different depending on which opioid receptor it acts on, e.g. nalbuphine- antagonsit at mu, partial agonist at kappa, and weak agonist at delta.
anatagonist= naloxone, important if patient overdoses on morphine and goes into resp depression, can reverse this.

71
Q

why does morphine have a LOW oral bioavailability?

A

poorly lipid-soluble= passive factor affecting absorption- poor, so not much of the drug reaches the systemic circulation in an unchanged form to exert its desired therapeutic effect.

72
Q

t1/2 of morphine?

A

1.3-6.7 hours

73
Q

t1/2 of methadone?

A

15-30 hours
can be given as an oral syrup
can maintain people dependent on opioids with this
90% oral bioavailability

74
Q

oral bioavailability of codeine?

A

90%

75
Q

t1/2 of herorin (diamorphine)?

A

5 mins

76
Q

why diamorphine such short t1/2?

A

ester bonds- rapidly broken down by esterases in blood and tissues, producing mono-acetyl morphine then MORPHINE= active drug.

77
Q

what is benefit of IV diamorphine?

A

acetyl groups make it very lipid soluble so IV allows easy access to brain by crossing BB barrier where then converted to morphine and so has an immediate euphoric effect.
Morphine alone wouldn’t pass as easily across BB barrier as not very lipid soluble due to presence of OH groups.

78
Q

codeine is a prod-drug. How is it activated?

A

via CYP450 system in liver- CYP2D6- degree of polymorphism so codeine may be ineffective in some people as lack this enzyme system, espec. in chinese patients. Converted to morphine.

79
Q

examples of opioids being used as anaesthetics?

A

Fentanyl- 100X more potent than morphine
Alfentanil
Remifentanil- short t1/2- hydrolysed very quickly.
BUT can cause quite severe itching as cause cross linking of mast cells which cause histamine release.

80
Q

what might the opioid pethidine be used for?

A

analgesic in labour IM
BUT prolongs labour and crosses placenta so naloxone has to be given to baby once born.
Also musn’t give frequent repeat doses as metabolite norpethidine can accumulate and cause convulsions.

81
Q

naloxone t1/2?

A

1-1.5hrs
*morphine t1/2=4hrs, so effects of nalxone will wear off more quickly than morphine, so may need to give repeated doses, so must monitor patient.
reverse resp depression with opioid toxicity. can also treat dependence- but causes withdrawal so very severe, done under very controlled conditions.
can also give naltrexone=oral=t1/2 4hrs

82
Q

examples of schedule 2 controlled drugs-opioids?

A

morphine
diamorphine
pethidine
remifentanil

83
Q

example of schedule 5 controlled drug-opioids?

A

codeine- can be sold OTC but pharmacists should keep invoices for any codeine sold as abuse potential.

84
Q

new endogenous opioid peptides and receptor?

A

ORL-1= opioid receptor like 1
nociceptin= peptide for this receptor. Then nocistatin- blocks nociceptin.
also endomorphins 1 and 2= high affinity and specificity for mu receptor= possible future target to mimic these endomorphins.

85
Q

potential problems for patient when using opioids for day-surgery cases e.g. for optimal control of perioperative and postoperative pain?

A

nausea and sedation

86
Q

why would a patient on morphine for pain who is being switched to codeine be tapered off the morphine gradually?

A

prevent opioid withdrawal symptoms e.g. irritability, sweats, nausea, vomiting, diarrhoea, abdominal cramping, muscle pains, low energy, insomnia.

87
Q

why is aspirin not given to children?

A

fear of Reye’s syndrome= hepatic encephalopathy and liver steatosis in young children.

88
Q

how is visceral pain normally treated?

A

with opioid analgesics

89
Q

why can fentanyl be useful for pain relief in a patient that suffers with intractable nausea or vomiting when taking opioids?

A

fentanyl can be given transdermally in those with chronic stabilised pain, and so ADRs of oral opioids avoided

90
Q

what is the main way in which tramadol has an analgesic action?

A

enhanced serotoninergic neurotransmission
*serotoninergic neurones travel from the brainstem to the substantia gelatinosa, stimulating the inhibitory interneurones which release enkephalins which act on opioid receptors, inhibiting the ascending pain pathway.

91
Q

typical agent used in treating trigeminal neuralgia e.g. due to nerve compression or MS?

A

carbamazepine *CYP450 inducer
gabapentin
=anti-epileptics

92
Q

how do PGs cause local vasodilation/erythema?

A

PGE2 acts on Gs GPCRs- activates adenylate cyclase, increases cAMP, activates PKA= inhibits MLCK which normally phosphorylates myosin light chains, so light chain affinity for Ca2+ is reduced in arteriolar smooth muscle, causing relaxation hence vasodilation.

Sem 5 (35 decks)

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