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Year 3 > Block 33 PPT > Flashcards

Block 33 PPT Flashcards

1
Q

anxiety/ panic management - step 1?

A

STEP 1:All known and suspected presentations of GAD

Identification and assessment; education about GAD and treatment options; active monitoring

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2
Q

step 2 in anxiety/ panic management?

A

STEP 2:Diagnosed GAD that has not improved after education and active monitoring in primary care

Low-intensity psychological interventions: individual non-facilitated self-help, individual guided self-help and psychoeducational groups

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3
Q

step 3 in anxiety management?

A

STEP 3:GAD with an inadequate response to step 2 interventions or marked functional impairment

Choice of a high-intensity psychological intervention (cognitive behavioural therapy [CBT]/applied relaxation) or a drug treatment

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4
Q

step 4 in anx management is needed when ?

A

Complex treatment-refractory generalised anxiety disorder (GAD) and very marked functional impairment, such as self-neglect or a high risk of self-harm

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5
Q

what does step 4 in anx management need?

A

Highly specialist treatment, such as complex drug and/or psychological treatment regimens; input from multi-agency teams, crisis services, day hospitals or inpatient care

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6
Q

first line when a pharmacological approach is needed for anxiety?

A
  • SSRI - sertraline first line
  • if ineffective, offer alt SSRI or SNRI
  • If the person cannot tolerate SSRIs or SNRIs, consider offering pregabalin.
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7
Q

how should benzos be used in GAD?

A
  • Don’t offer a benzo for the treatment of GAD except as a short term measure during crises
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8
Q

SSRI may need to be prescribed w?

A
  • inc risk of bleeding associated w SSRIs espec for older people or ppl taking other drugs which can damage the GI mucosa or interfere w clotting (NSAIDs, aspirin) - use omeprazole
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9
Q

for ppl aged under 30 who are offered a SSRI or SNRI:

A
  • warn them that these drugs are associated w an increased risk of suicidal thinking and self harm
  • see them within 1 week of first prescribing
  • monitor the risk of suicidal thinking and self-harm weekly for the first month
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10
Q

what should be used for rapid tranquilisation?

A
  • IM lorazepam for rapid tranquilisation
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11
Q

Tx of acute behavioural disturbance?

A
  • de-escalation: calming techniques and distraction
  • offer them the opportunity to move away from the situation in which the violence is occuring
  • only use restrictive techniques if all attempts to defuse the situation have failed
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12
Q

which other drugs can be used for rapid tranquilisation?

A
  • NICE suggests lorazepam, olanzapine or haloperidol (if using haloperidol, consider an anticholinergic drug).
  • oral medications preferred
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13
Q

first line in a non-psychotic behavioural disturbance?

A
  • Lorazepam should be considered first for non-psychotic behavioural disturbance - oral if possible but intramuscular if necessary.
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14
Q

behavioural disturbance in the context of psychosis?

A
  • Behavioural disturbance in the context of psychosis should be treated with lorazepam combined with an antipsychotic.
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15
Q

what should be avoided in patients w dementia?

A
  • Olanzapine (and risperidone) should be avoided in patients withdementia, due to an increased risk of stroke and death.
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16
Q

what should be used for maintenance treatment in opiod dependence?

A
  • methadone and buprenorphine for maintenance treatment
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17
Q

buprenorphine is associated w ?

A
  • Buprenorphine is associated with reduced risk of fatal overdose in the first weeks of treatment initiation.
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18
Q

opiod withdrawal?

A
  • Withdrawal - increasing the dose by small increments until the signs of withdrawal have disappeared
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19
Q

For people who wish to stop using heroin completely or want to continue to use some heroin?

A
  • Stop using heroin completely— high-dose methadone or buprenorphine may be more suitable as the blockade effects of both interfere with the subjective effects of additional heroin use.
  • Continue to use some heroin— low-dose methadone treatment may be preferred.
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20
Q

emergency Tx of opiod overdose?

A
  • IV or IM naloxone: has a rapid onset and relatively short duration of action
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21
Q

methadone mechanism?

A
  • methadone is a full agonist of the mu-opioid receptor- binds to these receptors in the brain and fully activates them.
  • This action can relieve withdrawal symptoms and cravings.
  • Has a long half-life
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22
Q

buprenorphine mechanism?

A
  • buprenorphine is a partial agonist of the mu-opioid receptor and an antagonist of the kappa-opioid.
  • It binds to the mu-opioid receptors in the brain but only partially activates them.
  • This partial activation is enough to alleviate cravings and withdrawal symptoms in individuals with opioid dependence
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23
Q

adult patient who wishes to undertake a programme of smoking cessation?

A
  • referral to local NHS stop smoking services
  • advised to stop abruptly
  • Offered drug treatment to reduce withdrawal symptoms.
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24
Q

drug treatment for smoking cessation?

A
  • NRT
  • varenicline or bupropion.
  • Varenicline or combination NRT (a patch plus a short-acting preparation) have been shown to be the most effective treatments.
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25
Q

adult patient who wishes to undertake a programme of alcohol withdrawal?

A
  • Long acting benzodiazepine like chlordiazepoxide hydrochlorideordiazepam should be used to attenuate alcohol withdrawal symptpms
    *
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26
Q

Fixed dose regimen in alcohol withdrawal?

A
  • This involves using a standard, initial dose (determined by the severity of alcohol dependence or level of alcohol consumption), followed by dose reduction to zero, usually over 7–10days
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27
Q

what can be used instead or chlorodiazepoxide in alc withdrawal?

A
  • carbamazepine can be used as an alt treatment in alcohol withdrawal
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28
Q

management of withdrawal seizures?

A
  • if withdrawal seizures occur, a fast acting benzo like lorazepam should be used to reduce likelihood of further seizures
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29
Q

delirium tremens?

A
  • medical emergency
  • characterised by agitation, confusion, paranoia, and visual and auditory hallucinations
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30
Q

first line for DT?

A

oral lorazepam

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31
Q

What be given w lorazapam for DT?

A
  • haloperidol can be given as an adjunctive therapy if symptoms persist
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32
Q

In harmful drinkers or patients with mild alcohol dependence what should be offered?

A
  • a psychological intervention (such as cognitive behavioural therapy) should be offered.
  • drug therapy can be added
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33
Q

drugs that can be used for alcohol dependence?

A
  • In those who have not responded to psychological interventions alone:,acamprosate or oralnaltrexonecan be used in combination with a psychological intervention.
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34
Q

Relapse prevention for alcohol dependence?

A
  • acamprosate or naltrexone in comb w CBT are recommended for relapse prevention in moderate- severe alcohol dependence
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35
Q

alt to camprosate or naltrexone?

A

disulfiram

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36
Q

How does heroin work - mu?

A
  • acts on CNS opiod receptors mu, kappa, and delta
  • Mu receptor effects account for both the analgesic effects (Mu1) and the respiratory depression and euphoria (Mu2)
  • Activation of Mu2 receptors also causes miosis, reduced gastrointestinal (GI) motility, and physiologic dependence.
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37
Q

heroin - kappa receptor?

A
  • Kappa receptor activation causesanalgesiaas well.
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38
Q

heroin - delta receptor?

A
  • Delta receptors are more involved in spinal analgesia phenomena.
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39
Q

heroin metabolizes to?

A
  • heroin metabolizes to monoacetylmorphine in the CNS - more potent mu-receptor agonist than morphine
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40
Q

risks associated with heroin use?

A
  • collapsed veins and skin abscesses
  • blood borne viruses - HIV and hepatitis
  • increased risk of pneumonia
  • loss of relationships
  • risks of overdose
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41
Q

interactions of heroin - benzos?

A
  • benzodiazepine - potentially fatal respiratory depression
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42
Q

heroin + ? interaction causes inc risk of opiate withdrawal?

A
  • buprenorphine - inc risk of opiate withdrawal
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43
Q

other heroin interactions?

A
  • naltrexone
  • avoid alcohol - inc risk of overdose
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44
Q

side effects of heroin?

A
  • arrhythmias
  • hallucination
  • miosis
  • resp depression w high doses
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45
Q

morphine mechansim?

A
  • mu receptor agonist -> analgesia
  • acts on the descending inhibitory pathway of the CNS
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46
Q

opiods with benzos can increase risk of?

A

increase risk of resp depression, coma and death

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47
Q

side effects of morphine?

A
  • arrythmias
  • dry mouth
  • resp depression
  • vomiting on initiation
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48
Q

? causes rapid release of morphine?

A

alcohol

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49
Q

inc risk of withdrawal w ? when using morpine

A
  • Buprenorphine - inc risk of withdrawal when given w morphine
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50
Q

morphine interacts w ? to increase risk of CNs excitation/ depression

A

phenelzine

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51
Q

Signs of opiod overdose?

A
  • Opioids (narcotic analgesics) cause coma, respiratory depression, and pinpoint pupils.
  • antidote: naloxone
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52
Q

Mechanism of cannabis?

A
  • acts on cannabinoid receptors of the endocannabinoid system which are found in the PNS, CNS
  • Binding to different parts of the CNS mediates the different properties, paticularly of THC
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53
Q

cannabis on the hippocampus?

A

impairment of STM

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54
Q

cannabis on the basal ganglia?

A

altered reaction time and movement

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55
Q

cannabis on the hypothalamus?

A

inc appetite

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56
Q

cannabis on the NA?

A

euphoria

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57
Q

cannabis on the amygdala?

A

panic and paranoia

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58
Q

Cannabis interactions?

A
  • ciclosporin - cannabidiol increases concerntration
  • tacrolimus
  • valproate - inc risk of ALT concs
  • carbamazepine
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59
Q

side effecs of cannabis

A
  • aggression
  • suicidal behaviour
  • cough
  • increased risk of infection
  • seizure
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60
Q

risks w cannabis?

A
  • risks of suicidal thoughts
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61
Q

amfetamine mechanism?

A
  • CNS stimulant
  • increases amounts of dopamine, NE, serotonin in the synaptic cleft
  • inhibits MAO
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62
Q

indications of amfetamine /

A
  • ADHD
  • narcolepsy
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63
Q

interactions of amfetamine?

A
  • bupropion - inc risk of serotonin syndrome
  • fluoxetine
  • moclobemide
  • phenelzine - inc risk of hypertensive crisis
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64
Q

side effects of amfetamine?

A
  • arrythmias
  • arthralgia
  • depression
  • palpitations
  • decreased weight
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65
Q

amfetamine overdose?

A
  • Amfetamines cause wakefulness, excessive activity, paranoia, hallucinations, and hypertension
  • followed by exhaustion, convulsions, hyperthermia, and coma
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66
Q

MDMA mechanism?

A
  • releaser and reuptake inhibitor of serotonin, dopamine and NE
  • -> happiness, inc energy, extroversion, feeling close to others, changed perception of colours and sounds
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67
Q

MDMA acute toxicity episodes?

A
  • The serotonin syndrome (increased muscle rigidity, hyperreflexia, and hyperthermia), is characteristic of acute toxicity episodes.
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68
Q

Short-term physical side effects of MDMA ?

A
  • dilated pupils
  • a tingling feeling
  • tightening of the jaw muscles
  • raised body temperature
  • increased heart rate
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69
Q

interactions of MDMA - serotonin syndrome?

A
  • serotonergic drugs -> serotonin syndrome
  • MAOI like phenelzine
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70
Q

MDMA interactions - cns depression?

A
  • benzodiazepine - risk of CNS depression
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71
Q

cocaine mechanism?

A
  • blocks dopamine transporter preventing dopamine reuptake from the synaptic cleft -> euphoria ans arousal
  • blocks reuptake of serotonin and NE
  • stimulates reward pathway in the brain
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72
Q

mental effects of cocaine?

A
  • Mental effects may include anintense feeling of happiness,sexual arousal,loss of contact with reality, oragitation.
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73
Q

physical effects of cocaine?

A
  • Physical effects may include afast heart rate, sweating, anddilated pupils.
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74
Q

CV side effects of cocaine?

A
  • coronary artery spasm→ myocardial ischaemia/infarction
  • both tachycardia and bradycardia may occur
  • hypertension
  • QRS widening and QT prolongation
  • aortic dissection
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75
Q

Neurological side effects of cocaine?

A
  • seizures
  • mydriasis
  • hypertonia and hyperreflexia
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76
Q

psychiatric side effects of cocaine?

A
  • agitation
  • psychosis
  • hallucinations
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77
Q

GI side effect of cocaine?

A
  • ischaemic colitis - should be considered if patients complain of abdominal pain or rectal bleeding
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78
Q

muscle, temp, electrolyte

other side effects of cocaine?

A
  • hyperthermia
  • rhabdomyalysis
  • metabolic acidosis
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79
Q

management of cocaine toxicity?

A
  • first line: benzodiazepines
  • chest pain: benzodiazepines+ glyceryl trinitrate
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80
Q

Heroin + cocaine?

A

overdose

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81
Q

cocaine + MDMA - >

A

an increase the risk of heart attack, heart strain, and psychosis.

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82
Q

cocaine and methamphetamine ->

A

cardiac

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83
Q

mild-moderate depression Tx?

A
  • Psychological therapies - low intensity psychosocial intervention and group CBT
  • AD
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84
Q

when should antidepressants be used for depression?

A
  • consider in those with a history of moderate-severe depression, persistent subthreshold symptoms or subthreshold/mild depression that does not respond to non-pharmacological interventions.
  • Also consider in those in whom mild depression is complicating the management of other conditions.
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85
Q

what else needs to be done for depression?

A
  • sleep hygiene advice
  • early follow up (within 1-2 weeks)
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86
Q

Management of moderate-severe depression?

A
  • high intensity psychosocial intervention
  • AD therapy
  • sleep hygiene
  • follow up
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87
Q

SSRIs/ SNRIs - increased risk of suicide?

A
  • SSRIs and SNRIs have been implicated in an increased risk of suicide, suicidal ideation and self-harm, particularly below the age of 30.
  • All patients commenced in this age group should have review within one week of starting therapy with weekly reviews for at least one month.
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88
Q

acute mania management?

A
  • AP - haloperidol, olanzapine, quetiapine, risperidone
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89
Q

what can be added to the tx response?

A
  • lithium and valproate can be added if inadequate tx response
  • AP can be used with lithium or valproate in the initital treatment of severe acute episodes
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90
Q

asenapine?

A
  • 2nd gen AP
  • moderate to severe manic episodes w bipolar
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91
Q

olanzapine in bipolar?

A
  • LTM management of bipolar
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92
Q

benzos in mania?

A
  • benzos: e.g. lorazepam
  • may be helpful in the initial stages of treatment for behavioural disturbance or agitation.
  • Benzodiazepines should not be used for long periods because of the risk of dependence.
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93
Q

lithium?

A
  • mania or hypomania
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94
Q

carbamazepine?

A
  • LTM management of bipolar
  • to prevent recurrence of acute episodes in patients unresponsive to lithium therapy
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95
Q

AP in bipolar?

A
  • Antipsychotics: used as a therapeutic trial to treat mania.
  • May be switched to mood stabiliser once the acute episode resolved. Options can include haloperidol, olanzapine or quetiapine
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96
Q

lithium?

A

Lithium: used for many years, still unclear mechanism. Often referred to as the ‘gold-standard’. Used in acute mania, recurrent depressive episodes or long-term maintenance.

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97
Q

antiepileptics in bipolar ?

A
  • Antiepileptics: also used as mood stabilisers in bipolar.
  • Options include sodium valproate, lamotrigine or carbamazepine.
  • May be used alone or in combination.
  • It can help prevent depression relapses.
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98
Q

Antidepressants in bipolar?

A
  • Antidepressants: may be restricted due to the risk of inducing mania or rapid-cycling (frequent, distinct episodes).
  • The selective-serotonin reuptake inhibitor fluoxetine is commonly used.
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99
Q

Psych therapies - individual psychoeducation?

A

trained to identify and cope with early warning signs of mania and/or depression.

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100
Q

Psych therapies - CBT?

A

talking therapy. Focuses on the emotional response to thinking and behaviour.

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101
Q

bipolar - interpersonal and social rhythm therapy?

A

focuses on the role of interpersonal factors (i.e. interpersonal relationships, role conflicts) and circadian rhythm stability (i.e. sleep-wake cycle, work-life balance) in the context of bipolar.

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102
Q

bipolar - group psychoeducation?

A
  • high frequency and intensity sessions to help patients become experts in their own condition.
  • Aims to improve mood stability, medication adherence and self-management.
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103
Q

mania - family focused therapy?

A
  • psychoeducation for families with one individual suffering from bipolar.
  • Looks at risks, communication and problem-solving within the family to prevent relapses.
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104
Q

Prior to starting an antipsychotic NICE recommend the following are recorded:

A
  • Weight
  • Height
  • Waist circumference
  • Pulse and blood pressure
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105
Q

what should be recorded before AP are commenced?

A
  • Assessment of any movement disorders
  • Assessment of nutritional status, diet and level of physical activity
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106
Q

Monitoring on AP?

A
  • Weight:every week for 6 weeks, then every 12 weeks, then at 1 year, then annually (plot on graph).
  • Waist circumference:measure yearly (plot on graph).
  • Pulse and blood pressure:measure at twelve weeks, then at 1 year, then annually.
  • Fasting glucose, HbA1c, blood lipids: at 12 weeks, then at 1 year, then annually.
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107
Q

Clozapine?

A
  • if the patient has failed to respond to 2 different AP - one of which is an atypical that is not clozapine
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108
Q

clozapine monitoring?

A
  • The risk of neutropenia and agranulocytosis is high and close monitoring (and regular FBCs) is required.
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109
Q

Stopping APs?

A
  • associated w increased risk of relapse
  • high risk of relapse if treatment is stopped in the first 1-2 years.
  • Patients need to be followed up for signs of relapse for at least 2 years after stopping medication.
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110
Q

psychological therapies for schiz?

A
  • individual CBT
  • family therapy
  • advised to use psychological therapies + an AP
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111
Q

compliance =

A

the extent to which a person takes his or her medicine

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112
Q

adherence =

A

the extent to which a patients follow medical advice

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113
Q

concordance =

A

healthcare professional and patient create an agreed plan for treatment (medications) which takes into account the patient wishes

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114
Q

reasons for poor aherence ?

A
  • poor knowledge of illness and medication
  • independent pausing, stopping or controlling of the medication
  • lack of competence in self management
  • fear towards drug
  • diseases where poor control doesn’t yet present symptoms
  • challenges with lifestyle changes
  • Replacing prescription drugs with self-administered drugs
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115
Q

doctor oriented approaches to improving adherence?

A
  • clear communication
  • setting achievable goals
  • Continuity of care and permanent doctor–patient relationships
  • Equal relationships with patients, with a coaching attitude
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116
Q

medication oriented approaches to improving adherence?

A
  • Medication reconciliation (nurse or pharmacist)
  • Medicines optimisation (pharmacist)
  • Medication review (pharmacist)
  • Combination of products to minimise the number of medicines
  • prepacked dispensing boxes
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117
Q

patient oriented approaches to improving adherence?

A
  • Focus on health outcomes of self-management and drug therapies
  • Support for patients to better understand their disease and its management
  • Pharmacists as coaches for drug therapies
  • Medication counselling for caregivers
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118
Q

how is poor health literacy identified?

A
  • REALM-R is a way of identifying patients w poor health literacy
  • patient is asked to read 11 words
  • score of 6 or less out of 9 indicates poor health literacy - only score if pronounced correctly
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119
Q

implications of being a CYP2D6 ultra-rapid metaboliser?

A
  • Codeine is a prodrug and its analgesic properties are not manifest until it is metabolized by CYP2D6, primarily to morphine and and codeine-6-glucuronide
  • ppl who are ultra-rapid metabolizers based upon CYP2D6 genotype have higher than expected morphine levels (an initial “overdose”), with more side effects and a shorter than expected duration of pain control
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120
Q

which drugs are affected by being a CYP2D6 ultra-rapid metaboliser?

A
  • hydrocodone, oxycodone, tramadol
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121
Q

tramadol mechanism?

A
  • Tramadol & its active metabolite (M1) bind to μ-opiate receptors → inhibition of ascending pain pathways & inhibits reuptake of norepinephrine and serotonin
  • metabolised to O-desmethyltramadol which has a 200 fold greater affinity for u-opiod receptors compared to tramadol
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122
Q

ultra-rapid metaboliser (CYP2D6) of tramadol?

A
  • ↑ peak plasma concentrations of O-desmethyltramadol after a dose of tramadol
  • Greater analgesia
  • Stronger miosis
  • ↑ nausea
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123
Q

TPMT deficiency?

A
  • TMPT metabolises thiopurine drugs such as azathioprine, mercaptopurine, & tioguanine
  • TMPT gene located on chromosome 6
  • Mutations of the gene encoding TPMT → varying functional activity → TMPT deficiency
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124
Q

Azathioprine and TMPT?

A
  • risk of myelosuppression increased in patients with reduced activity of the TPMT enzyme
  • If TPMT activity is:
  • Absent: should not receive thiopurine drugs
  • Reduced: treated under specialist supervision
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125
Q

Pharmacogenetics =

A

single drug-gene interactions

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126
Q

pharmacogenomics =

A

genome-wide association approach, incorporating genomics and epigenetics while dealing with the effects of multiple genes on drug response

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127
Q

inter-individual differences in drug action?

A
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128
Q

medicines act 1968?

A
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129
Q

definition of a medicinal product?

A

“a manufactured article, intended to be taken by or administered to a person or animal, which contains a compound or compounds with proven biological effects, plus excipients, or excipients only, and may also contain contaminants.”

any substance or article administered for a medicinal purpose.

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130
Q

Product licence is from

A

Marketing Authorisation

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131
Q

unlicensed =

A

no licensing, wholly responsibility of prescriber

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132
Q

off label =

A

licensed drugs not used for a licensed indication or by unlicensed route

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133
Q

General sales list products?

A
  • Can be sold anywhere e.g. including supermarket
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134
Q

other types of medicinal products?

A
  • Pharmacy Only Medicines (P)
  • Prescription Only Medicines (POM)
  • Controlled Drugs (CD)
135
Q

prescriptions in the community?

A
  • FP10 – GPs (SS – computer, NC – hand-written)
  • FP10HNC (hospital hand-written)
136
Q

POM legal requirements?

A
  • signature
  • dispensed within 6 months
  • date
  • in ink or otherwose indelible
  • address and role of practioner
  • name and adress of patient
  • age if under 12
  • dose
137
Q

Scale and consequences of non-adherence?

A
  • studies show that patients with chronic illnesses take only ~50% of medications prescribed
  • consequences: waste of medication, disease progression, lower QOL, increased hospital admissisions and visits
138
Q

To be able to describe the influence of patients’ beliefs on adherence?

A
  • beliefs about illness, treatment or self efficacy to adhere
  • higher perceived barrier to treatment -> lower compliance
  • negative beliefs -> lower adherence
  • cultural beliefs - herbal remedies
139
Q

the barriers to achieving shared decision making with patients?

A
  • perceived time constraints
  • perceptions that shared DM cannot be applied bc of patient’s characteristics
  • nature of the clinical situation
  • difficulties in communication
  • complexity of info
  • patient not ready to participate in SDM
  • patient reluctant to decide
140
Q

what is variability?

A
  • Variability in the response to drugs is due to three principal components—the disease, the responsiveness of tissues, and the concentration of the drug at its site of action (as reflected by its plasma concentration).
  • variability arises bc of inter-individal differences in rates of drug abs. drug distribution and elimination
141
Q

factors influencing variability in drug response?

A
  • age
  • drug interactions
  • impaired metabolism and excretion
  • degree of plasma protein binding -> influences distribution, action, metabolism and renal excretion of drugs
142
Q

Other factors producing variation in response?

A
  • diet, co-morbidities, age, weight, drug–drug interactions, sex, and genetics.
  • ethnicity
  • pregnancy
143
Q

how altered pharmacokinetic handling of drugs produces variation in response - GI?

A
  • arises bc of variable delivery of a dose of a drug to target sites - variability in the relationship between drug dose and plasma and tissue drug concentrations.
  • Gastrointestinal absorption may be slowed by atropine or opiates, or accelerated by metoclopramide, which hastens gastric emptying.
144
Q

To be able to explain how altered pharmacokinetic handling of drugs produces variation in response - muscle mass?

A
  • Muscle mass is greater and adipose tissue mass smaller in men than in women.
  • Thus, water-soluble drugs have larger distribution volumes in men and lipid-soluble drugs (e.g. diazepam, propranolol) have larger distribution volumes in women.
145
Q

how altered pharmacokinetic handling of drugs produces variation in response?

A
  • Highly extracted drugs (e.g. propofol, propranolol) with clearance close to hepatic blood flow are sensitive to changes in hepatic blood flow
146
Q

how can pharmacogenetic variation influence resp to drugs?

A
  • genetic polymorphisms which can result in altered responsivenes in drug targets e.g. receptor function or altered drug handling (enzyme activity)
  • if patients metabolize certain drugs rapidly, they may require higher more frequent doses to achieve therapeutic concerntrations
147
Q

How can pharmacodynamic factors impact drug responses?

A
  • Pharmacodynamic variability arises because of variability in the relationship between drug concentration and effect.
  • differences in receptor number and structure
  • receptor coupling mechanism s
  • physiological changes in target organs resulting from differences in genetics, age and health
148
Q

Genetic variation’s impact on the handling and response to drugs?

A
  • differences in inherited makeup among individuals affects what the body does to the drug and vv
  • in some cases the level of enzyme can be measured before staring the therapy - should be considered before prescirbing
  • some ppl metabolise drugs slowly - drug can accumulate -> toxicity
  • drug can be metabolised so fast that the drug levels never become high enough for the drug to be effective
149
Q

where pharmacogenetic variation influences prescribing - primaquine?

A
  • primaquine induced haemolysis in individuals with glucose 6-phosphate dehydrogenase deficiency whose red blood cells are thereby more susceptible to the effect of oxidative stress
150
Q

where pharmacogenetic variation influences prescribing - methyldopa?

A
  • and immune-mediated haemolytic anaemia caused by methyldopa – a drug that commonly causes antidrug antibodies – whereas only a few individuals expressing such antibodies develop haemolysis
151
Q

where pharmacogenetic variation influences prescribing - HLA?

A
  • polymorphisms in HLA
  • Structural mutations in HLA can lead to different clinical responses in patients
    some variations are responsible for hypersensitivity reactions
152
Q

explain how increasing knowledge of pharmacogenetic variation will influence future prescribing practice?

A
  • as understanding of the human genome improbes, together with the introduction of simoler methods to identify genetic differences between individuals, it will become possible to use genetic information spec to an indiv patient to preselect a drug that will be effective and not cause toxicity - personalised medicine
  • several human leukocyte antigen (HLA) variants that predict toxicity of abacavir, carbamazepine andclozapine
153
Q

Pharmacokinetic changes w age?

A

Pharmacokinetic changes include a reduction in renal and hepatic clearance and an increase in volume of distribution of lipid soluble drugs (hence prolongation of elimination half-life)

154
Q

pharmacodynamic changes?

A

pharmacodynamic changes involve altered (usually increased) sensitivity to several classes of drugs such as anticoagulants, cardiovascular and psychotropic drugs.

155
Q

special care w dosing needed?

A
  • Children, and particularly neonates, differ from adults in their response to drugs.
  • Special care is needed in the neonatal period (first 28 days of life) and doses should always be calculated with care.
156
Q

neonates have a higher?

A
  • NB neonates have a higher relative amount of water so for water soluble drugs the dose must be increased to compensate for the high Vd.
157
Q

when is TDM undertaken?

A

narrow therapeutic index

158
Q

measuring plasma drug concs?

A

optimize drug dosing and ensure therapeutic efficacy while minimizing the risk of toxicity.

159
Q

measuring clinical outcomes?

A
  • evaluating patients symptoms and signs and disease status to monitor effects of drug therapy on teir health outcomes
  • This may include subjective assessments (e.g., pain scales, symptom questionnaires) and objective measurements (e.g., vital signs, physical examination findings
160
Q

measuring pharmacodynamic responses?

A
  • by measuring the physiological indices of therapeutic responses such as lipid conc, blood glucose, blood pressure and clotting
161
Q

advantages of measuring plasma drug concentrations?

A
  • precision
  • individualisation of therapy
  • minimises risk of toxicity using TDM
  • early detection of problems - Changes in plasma drug concentrations may indicate issues such as poor adherence, drug interactions, altered drug metabolism, or impaired renal or hepatic function
162
Q

disadvantages of measuring plasma drug concs?

A
  • cost - equipment, trained personnel for sample collection, processing and analysis
  • time consuming - espec w long half lives
  • invasiveness - venepuncture, can impact adherence to monitoring protocols
163
Q
  • of measuring plasma drug conc - endpoints?
A
  • surrogate endpoint - Plasma drug concentrations are often used as surrogate endpoints in clinical practice, assuming that achieving target concentrations will result in improved clinical outcomes.
  • limited predictive value - Plasma drug concentrations provide information about drug exposure but may not always correlate directly with therapeutic efficacy or clinical outcome
164
Q

prerequisites for plasma drug conc?

A
  • established therapeutic range
  • reliable assays
  • clinical justification - drugs with narrow therapeutic indices, significant interpatient variability in pharmacokinetics, complex dosing regimens, risk of drug interactions, potential for toxicity,
  • access to monitoring services
  • patient co-operation and adherence - willingness to undergo blood sampling procedures, provide accurate medication histories, adhere to prescribed dosing regimens, and follow-up with healthcare providers
165
Q

prerequisites of using clinical outcomes?

A
  • established clinical endpoints - Clearly defined clinical endpoints relevant to the therapeutic goals of drug therapy must be identified.
  • E.g. mortality, morbidity, symptom relief, disease progression, quality of life, and functional status.
  • clinical justification
  • outcome emasures - valid reliable and responsive to changes in clinical status
166
Q

using clinical outcomes - baseline?

A
  • baseline assessment - Baseline assessment of clinical outcomes before initiating drug therapy provides a reference point for monitoring treatment effects over time.
  • Baseline characteristics may include demographic factors, disease severity, comorbidities, functional status, and previous treatment history.
  • regular follow up assessments to monitor changes in clinical outcomes
167
Q

advantages of using clinical outcomes to monitor drugs?

A
  • Direct Assessment of Treatment Effects: Clinical outcomes provide direct information about the impact of drug therapy on patients’ health status, symptoms, and overall well-being
  • Holistic Approach: Clinical outcomes capture the multidimensional effects of drug therapy on patients’ lives, including improvements in symptoms, functional status, quality of life, and long-term prognosis
  • Patient-Centered Care: Focusing on clinical outcomes promotes patient-centered care by aligning treatment goals with patients’ preferences, values, and priorities.
  • Allows for LT monitoring of treatment effects and disease progression ovetime
168
Q

disadvantages of using clinical outcomes?

A
  • subjectivity - Clinical outcomes may be subjective and influenced by patients’ perceptions, expectations, and reporting biases
  • time and resource intensive
  • Heterogeneity of Endpoints: Clinical outcomes encompass a wide range of endpoints, each with its own measurement properties, interpretation criteria, and clinical significance
  • delayed detection of effects - outcomes may take time to mainfest and may not be immediately apparent
169
Q

prequisites of measuring pharmacodynamic response?

A
  • clear understanding of pharmacodynamics - mechanism, receptors and pathways
  • established pharmacodynamic markers - should be measurable, sensitive to changes induced by the drug and clinically meaningful
  • Baseline assessment of pharmacodynamic markers before initiating drug therapy provides a reference point for monitoring treatment effects over time.
  • Baseline characteristics may include pre-existing disease status, baseline levels of pharmacodynamic markers, and other relevant patient factors
170
Q

advantages of measuring pharmacodynamic resp?

A
  • direct measurement of treatment effects
  • relevence to therapeutic goals - Pharmacodynamic responses are closely linked to the therapeutic goals of drug therapy, such as symptom relief, disease control, or physiological normalization.
  • quantitative assessment - using objective endpoints, biomarkers, or physiological parameters.
171
Q

pharmacodynamic + - individualization?

A
  • individualization of therapy - personalized approach helps optimize treatment regimens, tailor dosing strategies, and maximize therapeutic benefits while minimizing the risk of adverse effects.
  • early detection of treatment effects
172
Q

disadvantages of measuring pharmacodynamic effects?

A
  • complexity of assessment
  • subjectivity and variability
  • Interpretation Challenges: Interpreting pharmacodynamic responses requires careful consideration of confounding factors, baseline variability, and changes over time
  • limited PV: Pharmacodynamic responses may not always correlate directly with clinical outcomes or long-term treatment effects.
173
Q

examples where measuring drug conc are imp?

A
  • individualised dosing - Some patients may require dosage adjustments based on their individual pharmacokinetic profiles, which can be influenced by factors such as age, weight, renal function, hepatic function, genetic polymorphisms, and concomitant medication
  • drug-drug interactions
  • treatment of spec conditions e.g. epilepsy, organ transplantation, cancer chemo - precise control of drug concentrations is critical for maximizing therapeutic efficacy and minimizing the development of drug resistance or adverse effects.
  • special populations - neonates, elderly, pregnant women, renal/ hepatic impairment
174
Q

ways in which drug effects can be measured?

A
  1. clinical assessment - observations, examination findings, signs and symptoms
  2. lab tests - e.g. blood glucose levels, serum drug levels
  3. imaging - visualising changes in response to drug therapy
  4. physiological monitoring - ECG, O2 sats, resp rate
  5. functional assessments - ability to perform spec tasks
  6. measurement of biomarkers - can provide surrogate endpoints for assessing treatment effects
175
Q

why is the impact of drugs on clinical outcomes is difficult to measure?

A
  • multiple factors influencing clinical outcomes
  • varianbility in patient response - variability in patient response can make it difficult to predict and measure the overall impact of a drug on clinical outcomes across diverse patient populations.
  • delayed onset of action - can require long term follow up
  • heterogeneity of clinical endpoints
176
Q

difficulty of measuring clinical outcomes - longitudinal?

A
  • longitudinal nature of disease processes - Many diseases have a chronic or progressive course, and the impact of drug therapy on clinical outcomes may evolve over time.
  • unforseen adverse effects
177
Q

surrogate outcome =

A

prediction of clinical benefit. Method of getting drugs to the market faster.

178
Q

surrogate markers are used when…

A

Surrogate markers are used when the primary endpoint is undesired (e.g., death), or when the number of events is very small, thus making it impractical to conduct a clinical trial to gather astatistically significantnumber of endpoints

179
Q

what is a hard outcome?

A

Hard ouctome: Objective or “hard” outcomes are those which are unambiguous and can be consistently measured by different assessor

180
Q

features of a good surrogate outcome - predictive value?

A
  • predictive value - should reliably predict the outcome of interest
181
Q

features of a good surrogate outcome - biological plausibility?

A
  • biological plausibility - There should be a clear biological rationale for why changes in the surrogate marker would be associated with changes in the clinical endpoint
  • easily measurable and quantifiable
182
Q

features of a good surrogate outcome - sensitivity and specificity?

A
  • Sensitivity: It should be sensitive to changes induced by the intervention being studied, allowing for meaningful detection of treatment effects.
  • Specificity: Changes in the surrogate outcome should be specifically attributable to the mechanism of action of the intervention rather than confounding factors.
183
Q

surrogate outcome - clinical relevance?

A
  • Clinical Relevance: The surrogate outcome should be meaningful in the context of the disease being treated and should reflect improvements in patient outcomes.
184
Q

surrogate outcome - validation and feasibility?

A
  • Validation: Ideally, the surrogate outcome should be validated through empirical evidence demonstrating its association with the clinical endpoint in relevant populations and settings.
  • Feasibility: It should be feasible to measure the surrogate outcome in the context of clinical trials, considering factors such as cost, time, and resources required for assessment.
185
Q

variable relation between dose and plasma conc?

A
  • when there is variable relation between drug dose and plasma drug conc, it means that the conc of the drug in the BS does not change proportionally w changes in dose
186
Q

non-linear pharmacokinetics?

A
  • non-linear pharmacokinetics - doubling the dose may not result in a doubling of the plasma concentration.
  • Nonlinear pharmacokinetics can occur due to saturation of drug-metabolizing enzymes or transporters,
187
Q

variation in drug dose and plasma conc - FPM & binding?

A
  • FPM - Drugs that undergo extensive first-pass metabolism in the liver may exhibit variable plasma concentrations
  • binding to plasma proteins - because changes in dose can saturate protein binding sites, leading to nonlinear changes in free drug concentrations.
188
Q

variable relation between dose and plasma drug concentration - metabolism?

A
  • Induction or Inhibition of Metabolism: Co-administration of drugs that induce or inhibit drug-metabolizing enzymes can lead to variable plasma concentrations by altering the rate of drug metabolism and clearance.
189
Q

genetic variability?

A
  • Genetic Variability: Genetic factors can contribute to variability in drug metabolism, distribution, and elimination, leading to variable plasma concentrations in response to changes in dose among different individuals.
190
Q

variability between drug conc anc effect - pharmacodynamic variability?

A
  • Pharmacodynamic Variability: Differences in individual patients’ pharmacodynamic responses to a drug can result in variable effects at similar drug concentrations.
  • Factors such as genetic variability, disease state, age, and concomitant medications can influence pharmacodynamic responses.
191
Q

other factors impacting variability between drug conc and effect?

A
  • receptor sensitivity
  • tolerance
  • downstream signalling pathways
  • drug interactions
  • disease state
192
Q

downstream signalling pathways?

A
  • Downstream Signaling Pathways: The downstream signaling pathways activated by a drug-receptor interaction can vary among individuals, leading to variable effects at similar drug concentrations.
193
Q

tolerance =

A
  • Tolerance: Long-term exposure to a drug can lead to the development of tolerance, where higher doses are required to achieve the same therapeutic effect. This can result in a variable relation between drug concentration and effect over time.
194
Q

disease state?

A
  • disease state - conditions with altered receptor expression or function like cancer or HF can lead to an unpredictable response
195
Q

characteristics that make a drug suitable for monitoring by measurement of concentration?

A
  • narrow therapeutic index - closely to ensure therapeutic efficacy while avoiding adverse effects.
  • variable pharmacokinetics
  • complex dosing regimes
  • risk of toxicity
  • clinical resp variability
  • patient characteristics
196
Q

clinical resp variability?

A
  • clinical response variability - where clinical response does not correlate well with dose or where there’s sig interpatient variability in response
197
Q

patient characteristics?

A
  • patient characteristics - Patient-specific factors such as age, renal function, hepatic function, and concomitant medications can influence drug concentrations
198
Q

List common medicines whose use is facilitated by measurement of drug concentration?

A
  • Antibiotics - vancomycin, gentamicin
  • cardiac - digoxin, procainamide, lidocaine
  • phenytoin
  • immunosuppressants - cyclosporine and tacrolimus
  • bipolar drugs - lithium, valproic acid
199
Q

Describe the practicalities of measuring plasma drug concentrations.

A
  1. sample collection
  2. timing of sampling - Samples may be collected at specific time points relative to drug administration (e.g., peak concentration, trough concentration) or as part of a pharmacokinetic profile to assess ADME over time
  3. sampling and processing
  4. analytical methods
200
Q

Explain how to interpret drug concentration measurements appropriately?

A
  • establishing therapeutic range
  • compare measured conc to therapeutic range
  • If the measured concentration is below the therapeutic range, it may indicate suboptimal drug exposure and insufficient therapeutic effect.
  • If the measured concentration is above the therapeutic range, it may suggest excessive drug exposure and an increased risk of adverse effects or toxicity.
  • consider clinical factors - monitor for signs and symptoms of therapeutic failure or toxicity
  • adjust dosage
  • follow up monitoring
201
Q

drug conc below the therapeutic range?

A
  • If drug concentrations are below the therapeutic range and clinical response is inadequate, consider increasing the dosage or frequency of administration.
202
Q

drug conc above the therapeutic range?

A
  • If drug concentrations are above the therapeutic range and/or adverse effects are present, consider decreasing the dosage or extending the dosing interval.
203
Q

adjusting dose in light of drug concentration measurements?

A
  • Take into account patient-specific factors such as age, weight, renal function, hepatic function, genetic polymorphisms, and concomitant medications when adjusting dosage.
204
Q

ADR =

A

An unwanted or harmful reaction experienced following the administration of a drug or combination of drugs under normal conditions of use and suspected to be related to the drug

e.g. anaphylaxis

205
Q

adverse drug event =

A

Untoward occurrence after exposure to a drug that is not necessarily caused by the drug

206
Q

frew of adverse drug reactions?

A
  • 10-20% of hospital inpatients
207
Q

impacts of ADR?

A
  • healrhcare burden
  • ADRs can cause significant morbidity and mortality, leading to prolonged hospitalizations, disability, and even death
  • reduced QOL - pain, discomfort, impaired functioning
  • drug safety concerns - public mistrust
208
Q

explain why all drugs have both beneficial and adverse effects?

A
  • drugs targets often shared by other biological processes leading to unintended effects
  • indiv variability
  • off target effects - These effects may be beneficial, such as when a drug used to treat one condition also improves symptoms of another condition, or adverse, resulting in unwanted side effects.
209
Q

ABCDE classification of ADR?

A
  • A - augmented
  • B - bizzare
  • C - continuing/ chronic
  • D - delayed
  • E - end of use
210
Q

which type of drug reaction is the most common?

A

type A - 80% of all reactions

211
Q

what happens in type A reactions?

A
  • primary effects - augmentation of therapeutic action
  • e.g. beta blocker and bradycardia
  • secondary effects - can rationalise from pharmacology
  • e.g. BB and bronchospasm
212
Q

other examples of type A reactions?

A
  • constipation w opiods
  • sedation w antihistamines
  • dopamine antagonism: galactorrhaea, amenorrhoea, EPS
213
Q

type a reactions tend to be?

A
  • dose dependent and predictable
  • They often result from the desired pharmacological action of the drug but are exaggerated or intensified beyond the therapeutic range.
214
Q

type b reactions?

A
  • bizzare
  • Not associated with known pharmacology of the drug e.g. allergic responses
  • e.g. steven-johnson syndrome
215
Q

Type c reactions?

A
  • continuing
  • Occur with long-term drug use e.g. adrenal suppression from steroids
  • drug induced nephrotoxicity or hepatotoxicity
216
Q

type d reactions?

A
  • delayed
  • Delayed from onset of the drug use e.g. secondary cancers from alkylating agents or tardive dyskinesia from AP
  • These effects may occur days, weeks, or even months after starting treatment and can be challenging to attribute directly to the drug.
217
Q

type E reactions?

A
  • end of use
  • occur when drug course is completed e.g. benzo withdrawal
218
Q

DOTS classification of drug reactions?

A
  • d - definitie
  • O - probable
  • T - possible
  • S - suspected
219
Q

Definite drug reactions?

A
  • where a clear cause-and-effect relationship between the drug and the adverse event has been established through documented evidence, such as rechallenge or specific diagnostic tests.
220
Q

O - probable drug reactions?

A
  • where there is a reasonable likelihood that the drug caused the adverse event, based on temporal relationship, known pharmacological properties of the drug, and absence of alternative explanations.
221
Q

T - possible drug reactions?

A

ADRs classified as “Possible” are those where a causal relationship with the drug cannot be ruled out, but there is insufficient evidence to establish a definitive or probable association

222
Q

S - suspected drug reactions?

A

ADRs categorized as “Suspected” are those where there is a clinical suspicion of a drug-related adverse event, but no further evidence or investigation has been conducted to confirm or refute the association. This classification is typically used when there is anecdotal or preliminary evidence suggesting a potential link between the drug and the adverse event

223
Q

risk factors for drug allergy/ anaphylaxis?

A
  • A history of other allergies, such as food allergy or hay fever
  • A personal or family history of drug allergy
  • Increased exposure to a drug, because of high doses, repeated use or prolonged use
  • Certain illnesses commonly associated with allergic drug reactions, such asHIVinfection or the Epstein-Barr virus
224
Q

other factors inc anaphylaxis risk?

A

*History of atopic allergy (hay fever, asthma, eczema) - higher risk
*Hx of anaphylaxis, urticaria or rash immediately after penicillin
*DO NOT treat with a penicillin, cephalosporin or beta-lactam based antibiotic

225
Q

Common symptoms of a drug allergy include?

A
  • Hives
  • Itching of the skin or eyes (common)
  • Skin rash (common)
  • Swelling of the lips, tongue, or face
  • Wheezing
  • Bleeding
226
Q

anaphylaxis symptoms?

A
  • Abdominal pain or cramping
  • Confusion
  • Diarrhea
  • Difficulty breathing with wheezing or hoarse voice
  • Dizziness
  • Fainting, lightheadedness
  • Hives over different parts of the body
  • Nausea, vomiting
  • Rapid pulse
  • Sensation of feeling the heart beat (palpitations)
227
Q

characterisisation of an allergic drug reaction?

A
  • Timing - immedate or delayed (days to weeks after initiation of treatment)
  • Symptoms - urticaria, pruritus, angioedema, resp symptoms, GI symptoms, CV symptoms
  • severity: Allergic drug reactions can range from mild, localized symptoms to severe, life-threatening reactions such as anaphylaxis.
  • reproducibility: allergic drug reactions are often reproducible upon re-exposure
  • mechanism - IgE mediated or T cell mediated delayed hypersensitivity
228
Q

explain the importance of accurate diagnosis and recording of allergic reactions to drugs?

A
  • patient safety - avoid using the same drugs
  • treatment planning
  • prevention of adverse events
  • avoidance of diagnostic delays - Mislabeling non-allergic adverse drug reactions as allergies can lead to unnecessary avoidance of potentially beneficial medications,
229
Q

explain the precautions that should be taken to prevent allergic reactions?

A
  • thorough history
  • medication reconcillation and verify allergy info
  • drug allergy assessment
  • avoidance of known allergens
  • allergy testing e.g. skin prick
  • adverse drug reporting to MHRA
230
Q

describe the principles of assessing drugs as a possible cause of new symptoms and signs?

A
  • Temporal relationship
  • drug history - look for interactions
  • symptom profile - is presentation consistent with known adverse effects of the implicated drug or suggests an alternative diagnosis.
  • are the symptoms consistent w the expected pharmacological effects of the drug
  • dose - response relationship between exposure and symptom severity
231
Q

explain how to respond if an adverse drug reaction is suspected.

A
  • Report to MHRA via yellow card scheme
  • assessment and evaluation of clinical significance and contributing factors
232
Q

how to manage a suspected adverse drug reaction?

A
  • Discontinuation or dose adjustment of the offending drug.
  • Symptomatic treatment to alleviate ADR-related symptoms.
  • Substitution with an alternative medication that is less likely to cause a similar reaction
  • Monitoring for resolution of symptoms and assessing for any long-term consequences of the ADR.
233
Q

imp RF that predict susceptibility to adverse drug reactions - age?

A
  • Age - changes in pharmacokinetics and pharmacodynamics, comorbidities, polypharmacy
234
Q

important risk factors that predict susceptibility to adverse drug reactions - polypharmacu?

A
  • polypharmacy - interactions, cumulative toxicity
  • underlying health conditions - altered drug metabolism and clearance
235
Q

important risk factors that predict susceptibility to adverse drug reactions - drug characteristics?

A
  • drug characteritics - high potency, narrow therapeutic index
236
Q

important risk factors that predict susceptibility to adverse drug reactions - chronic drug use?

A
  • chronic use of drugs - especially w drugs associated w cumulative toxicity, delayed onset reactions, drug induced organ damage
237
Q

important risk factors that predict susceptibility to adverse drug reactions - patient factors?

A
  • patient factors - sex, body weight, genetic predisposition, lifestyle factors (e.g., smoking, alcohol consumption), and adherence to medication regimens
238
Q

how can identification of risk factors for adverse drug reactions can influence prescribing decisions?

A
  • drug selection - using drugs with lower risk of ADRs e.g. enteric coated formulation to minimise risk
  • dosing adjustments based on renal/hepatic function, age, body weight, genetic variability
  • monitoring and surveillence
  • medication reviews
239
Q

sources of information about adverse drug reactions?

A
  • BNF
  • MHRA safety alerts under the important safety information section
  • MHRA interactive drug analysis profiles - iDAPs - display data from the Yellow Card Scheme and provide information on the number of “yellow card” reports of suspected adverse drug reactions (ADRs) received for a medicine.
240
Q

explain the importance of warnings in preventing adverse reactions.?

A
  • risk communication
  • Warnings, including boxed warnings, contraindications, precautions, and adverse reaction information in drug labels and prescribing information, communicate important safety information to healthcare providers and patients.
  • Informed DM - allows patients to make informed decisions about medication therapy by balancing the benefits of treatment with the potential risks of ADRs.
  • warnings prompt healthcare professionals to take preventative measures to reduce risk of ADRs
241
Q

Imp of monitoring in preventing ADR?

A
  • risk mitigation
  • helps identify emerging risks, trends and patterns of ADRs
  • This information informs regulatory decisions, labeling updates, risk management strategies, and public health interventions to mitigate the risk of ADRs and enhance medication safety.
  • early detection
242
Q

monitoring of ADR and QI?

A
  • QI - Monitoring ADRs contributes to quality improvement initiatives aimed at enhancing medication safety practices, reducing medication errors, and optimizing patient outcomes.
243
Q

explain why the adverse drug reaction profile of individual drugs is unclear at their launch onto the market.?

A
  • limited clincial trial data - small patient group -> rare ADR missed
  • short term follow up -> long term outcomes missed
  • underreporting of ADR - voluntary reporting of ADRs can lead to undereporting due to lack of awareness, uncertainty abt causality, reporting fatigue
  • limited post marketing data
  • patient variability - age, sex genetics, concomitant medications The diversity of patient populations encountered in real-world clinical practice may reveal ADRs that were not observed or anticipated during pre-market clinical trials.
  • off label use
244
Q

What is pharmacovigilance?

A
  • = activites related to the detection, assessment, prevention of adverse effects associated w drugs
  • encompasses the collection, monitoring, analysis, and dissemination of information on the safety and efficacy of medications throughout their lifecycle
245
Q

pharmacovigilance plays a role in?

A
  • Pharmacovigilance plays a critical role in ensuring the safe and effective use of medications by identifying, evaluating, and preventing adverse drug reactions (ADRs)
246
Q

what are the roles of pharmacovigilance?

A
  • patient safety - by preventing ADRs
  • public health protection by monitoring the safety profiles of meds
  • regulatory compliance - Regulatory authorities require pharmaceutical companies to conduct pharmacovigilance activities as part of their ongoing regulatory compliance obligations.
  • required in drug development and approval
  • facilitates risk communication
247
Q

prescriber’s resp in pharmacovigilance?

A
  • recognising and reporting ADRs
  • reporting to MHRA - yellow card scheme
  • educating patients on risks and benefits of medications including the importance of reporting ADRs
248
Q

yellow card scheme?

A
  • Report adverse reactions to drugs - self medication and prescribed, blood products, vaccines, radiographic contrast media, complementary, homeopathic and herbal products
  • The Yellow Card scheme can also be used to report medical device adverse incidents, defective medicines, suspected falsified (fake) medicines, as well as safety concerns associated with e-cigarettes and their refill containers (e-liquids).
  • reporting of reactions that are serious, medically sig or result in harm
249
Q

Interaction of ramipril and naproxen?

A

*ACEi/ARBs - > haemodynamic reduction in glomerular filtration rate due to efferent arteriolar vasodilation
*NSAIDs -> inhibition of prostacyclin synthesis -> renal afferent arteriolar vasoconstriction
*Combinations such as this increase the risk of AKI due to both impacting renal function, and do so through different mechanisms

250
Q

Drug related acute kidney injury is commonly associated with:

A

*antiretroviral drugs
*aminoglycoside antibiotics
*non-steroidal anti-inflammatory drugs (NSAIDs)

251
Q

CYP450 induces?

A
  • carbamazepine
  • rifampicin
  • rifabutin
  • St Johns wort
252
Q

CYP450 inhibitors?

A
  • Fluconazole
  • clarithromycin
  • erythromycin
  • grapefruit juice
  • ritonavir
253
Q

enzyme induction ->

A

Enzyme induction → increased metabolism and excretion

→ tolerance or decreased effectiveness
→ increased doses
→ slow development = days to weeks

254
Q

Enzyme inhibition →

A

Enzyme inhibition → decreased metabolism
→ sensitivity
→ decreased doses
→ drug accumulation
→ rapid development = days

255
Q

warfarin and carbamazepine interaction?

A

*Carbamazepine is an enzyme inducer, so will therefore induce metabolism of warfarin
*This results in decreased effectiveness of the current warfarin dose & a lower INR
*Develops over days-weeks

256
Q

drug development process?

A
  • drug discovery and phase 0 trials
  • phase 1
  • phase 2
  • phase 3
  • regulatory approval
  • phase 4
257
Q

phase 1 of drug development?

A

*Safety & efficacy testing
- computerised models
- cells
- animals

*Clinical Trial Approval
- safety & pharmacology in healthy volunteers (20 to 100)

258
Q

phase 2?

A

*Efficacy of compound in volunteers with disease
*Determine effective dose
*Further monitoring of safety

259
Q

phase 3?

A

*Testing in larger population (1000 - 5000)
*Overall risk-benefit
*Licensing application based on safety & efficacy data

260
Q

regulatory approval?

A
  • Committee on Safety of Medicines – legal framework for control of medicines (now CHM)
  • Submission for marketing authorisation (UK – MHRA) manufacturing process, pharmacology and toxicity of the compound, human pharmacokinetics, results of the clinical trials, and proposed labelling.
261
Q

phase 4?

A
  • post marketing studies/ surveillence
  • Monitoring of long term effectiveness & safety - e.g. rofecoxib
  • Cost effectiveness
  • Yellow Card Scheme
262
Q

potential for interacting drugs to cause beneficial effects?

A
  • Some drug interactions result in synergistic pharmacological effects, where the combined action of two or more drugs produces a greater therapeutic effect than the sum of their individual effects.
  • For example, combining an opioid analgesic with a nonsteroidal anti-inflammatory drug (NSAID) may provide more effective pain relief than either drug alone.
263
Q

interacting drugs causing beneficial effects - therapeutic effect?

A
  • potentiatuon of therapeutic efficacy - Interacting drugs may potentiate the therapeutic efficacy of one another by enhancing their pharmacological actions or targeting complementary pathways involved in disease pathogenesis.
  • combination therapy - Drug interactions can be intentionally utilized to achieve therapeutic goals through combination therapy.
264
Q

harmful effects of interacting drugs?

A

nteracting drugs can increase risk of ADRs by altering drug pharmacokinetics or pharmacodynamics -> unpredictable or exaggerated responses
* Drug interactions may result in drug accumulation, overdose, or toxicity due to alterations in drug metabolism, clearance, or distribution
* therapeutic failure - Interacting drugs can interfere with one another’s therapeutic efficacy by reducing drug bioavailability, antagonizing pharmacological effects, or inducing drug resistance.

265
Q

ways in which interactions occur pharmacokinetic - Abs?

A
  • absorption - Interactions that affect the absorption of drugs from the gastrointestinal tract, such as alterations in gastric pH, chelation, or binding interactions that decrease bioavailability.
266
Q

ways in which interactions occur pharmacokinetic - dist?

A
  • distribution - Interactions that influence the distribution of drugs within the body, such as displacement from protein binding sites, which can increase the concentration of unbound drug in plasma and potentially enhance pharmacological effects or toxicity.
267
Q

ways in which interactions occur pharmacokinetic - metabolism?

A
  • Metabolism (Biotransformation): Interactions that affect the metabolism of drugs in the liver or other tissues, particularly through inhibition or induction of drug-metabolizing enzymes, such as cytochrome P450 (CYP) enzymes.
  • Inhibition of metabolism can lead to increased plasma concentrations and prolonged half-life of drugs, while induction can result in decreased drug levels and reduced efficacy.
268
Q

ways in which interactions occur pharmacokinetic - excretion?

A
  • excretion - Interactions that affect the renal or hepatic elimination of drugs, such as competition for renal tubular secretion or inhibition of renal or hepatic transporters, leading to altered drug clearance and systemic exposure.
269
Q

ways in which drugs interact - altered pharmacokinetics?

A
  • Altered Pharmacokinetics: Interactions that occur indirectly through changes in physiological processes or disease states that affect drug absorption, distribution, metabolism, or excretion.
  • For example, alterations in gastrointestinal motility, renal function, hepatic blood flow, or plasma protein binding can influence drug pharmacokinetics and the likelihood of interactions.
270
Q

ways in which drugs interact - pharmacodynamic?

A
  • receptor interactions
  • enzyme inhibition/ induction
  • pharm antagonism
271
Q

receptor interactions?

A
  • receptor interactions - interactions that affect the renal or hepatic elimination of drugs, such as competition for renal tubular secretion or inhibition of renal or hepatic transporters, leading to altered drug clearance and systemic exposure.
272
Q

pharm antagonism?

A
  • Pharmacological Antagonism: Interactions where one drug counteracts the effects of another drug by blocking its action at the receptor level or by interfering with the physiological processes involved in drug response
273
Q

explain why the potential for drug interactions in increasing?

A
  • polypharmacy
  • expanding treatment options
  • self medications and OTC drugs
  • electronic prescribing systems - interactions might be missed
274
Q

dentify sources of information about drug interactions to inform prescribing.?

A
  • BNF
  • electronic medicines compenidum (EMC)
  • MHRA
275
Q

predicting drug interactions?

A
  • comprehensive medication review - Identify potential interactions based on known pharmacokinetic and pharmacodynamic properties of the drugs involved.
  • assess patient factors - Consider individual patient factors that may influence the risk of drug interactions, such as age, sex, weight, renal function, hepatic function, genetic polymorphisms, comorbidities, and concurrent use of medications with narrow therapeutic indices.
  • Evaluate the pharmacokinetic properties of the drugs involved in the interaction, including their metabolism, protein binding, bioavailability, half-life, and route of elimination.
  • Drugs with similar metabolic pathways or competing for the same drug transporters are more likely to interact.
276
Q

preventing drug interactions?

A
  • minimize polypharmacy - Limit the number of medications prescribed whenever possible to reduce the risk of drug interactions.
  • Use the lowest effective doses and avoid unnecessary drug combinations, particularly in elderly patients or those with multiple comorbidities.
  • Educate patients about the importance of medication adherence, potential drug interactions, and strategies for avoiding or minimizing interactions.
  • Encourage patients to inform healthcare providers about all medications, supplements, and herbal products they are taking to facilitate accurate assessment and monitoring.
277
Q

explain how to adjust drug dosage in anticipation of a drug interaction that cannot be avoided.?

A
  • assess clinical significance - evaluate the clinical impact of the drug interaction based on factors such as severity of the interaction, the therapeutic index of the affected drug, the patient’s medical condition, and the availability of alternative treatment options.
  • review drug interactions - guidelines and pharmacovigilance
  • Understand how the interaction affects drug pharmacokinetics, including absorption, distribution, metabolism, and elimination.
  • Adjust drug dosages based on changes in drug clearance, bioavailability, half-life, and plasma concentrations to maintain therapeutic drug levels and minimize the risk of adverse outcomes.
278
Q

imp of liver cytochromes as a point of drug clearance?

A
  • liver cytochromes especially CYP family are resp for the biotransformation of a wide range of drugs, toxins and pollutants
  • These enzymes catalyze Phase I reactions, such as oxidation, reduction, and hydrolysis, to convert lipophilic drugs into more polar metabolites that are readily excreted from the body.
  • drug clearance
279
Q

what do liver cytochromes acc do?

A
  • Liver cytochromes are essential for the elimination of drugs from the body by facilitating their metabolism and conversion into water-soluble metabolites that can be excreted via urine or bile.
  • The rate of drug clearance by hepatic metabolism influences the duration of drug action, the need for dosage adjustment, and the risk of drug accumulation or toxicity with repeated dosing.
280
Q

Drugs that extensively metabolised by hepatic enzymes?

A
  • Drugs that are extensively metabolized by hepatic enzymes are susceptible to interactions with other drugs that affect enzyme activity or expression.
  • liver metabolism is a critical point of interaction between drugs, influencing drug pharmacokinetics, efficacy, and safety
281
Q

COPS - CYP450 inducers?

A
  • carbamazepine
  • Oxcarbazepine
  • phenytoin/ phenobarbital
  • smoking
282
Q

what do CYP450 inducers acc do?

A
  • faster metabolism amd excretion of the drug
  • drug may not reach a threshold value of benefit if cleared more rapidly by the body
  • can cause failure of the oral contraceptive
    *
283
Q

What do CYP450 inhibitors do?

A
  • causes other drugs to accumulate to toxic levels where overdoses and side effects may occur.
284
Q
A
285
Q

mneumonic for CYP450 inhibitors?

A

SICK FACES. COM

  • Sodium valproate
  • Isoniazid
  • Cimetidine
  • Ketoconazole
  • Fluconazole
  • Alcohol &Grapefruit juice
  • Chloramphenicol
  • Erythromycin
  • Sulfonamides
  • Ciprofloxacin
  • Omeprazole
286
Q

how are drugs discovered?

A
  • 1) identification of biological targets implicated in disease
  • 2) target validation - suitability as therapeutic targets
  • 3) lead discovery - identification of chemical compounds or molecules that have the potential to modulate the activity of the target and exert therapeutic effects.
  • 4) lead optimisation
  • 5) preclinical evaluation - Lead candidates that demonstrate favorable pharmacological and pharmacokinetic properties in vitro undergo preclinical evaluation in animal models to assess their safety, efficacy, and toxicological profiles in vivo
  • 6) Clinical Development: Promising lead compounds that pass preclinical testing progress to clinical development, where they undergo rigorous evaluation in human clinical trials to assess their safety, efficacy, and tolerability in patients - phase 1-4 trials
  • 7) regulatory approval
  • 8) post marketing surveillence
287
Q

Phase 1 involves?

A
  • small studies (e.g. 100) on healthy volunteers
  • used to assess pharmacodynamics and pharmacokinetics
288
Q

phase 2 involves?

A
  • small studies (e.g. 100-300) on actual patients
  • examines efficacy, adverse effects
289
Q

phase 3 involves?

A
  • larger studies (e.g. 500-5,000 patients)
  • examines efficacy, adverse effects
  • may compare drug with existing treatments
  • studies of special groups e.g. renal, elderly
290
Q

phase 4 involves?

A
  • post-marketing surveillence
291
Q

risks assoc w drug development?

A
  • Research and discovery costs - includes expenses related to laboratory equipment, personnel, materials, and infrastructure.
  • lead optimisation and preclinical testing
  • clinical trials - most costly and time consuming phase of drug development
  • regulatory compliance costs
  • manufacturing and scaling up of drug production
  • intellectual property protection e.g. patents, trademarks and copyrights
292
Q

risks assoc w developing drugs?

A
  • Drug development is inherently risky, with high rates of attrition at each stage of development.
  • Many drug candidates fail to progress beyond preclinical or clinical testing due to safety concerns, lack of efficacy, or commercial viability.
  • The costs associated with failed drug development efforts, including sunk costs and opportunity costs, represent significant financial losses for pharmaceutical companies and investors.
293
Q

types of clinica trial?

A

interventional and obs

294
Q

interventional clinical trials?

A
  • objective - looks at specific interventions
  • study design - random assigment - RCTs are the gold standard
  • data collection - prospective
295
Q

+ of intv clinical trials

A
  • controlled conditions - control of key variables e.g. randomisation to minimise bias and confounding
  • causality - Interventional trials provide strong evidence for establishing causality and making causal inferences about the effects of the intervention on health outcomes
  • can assess efficacy and safety
  • standardised data collection
296
Q
  • of intv clinical trials?
A
  • resource intensive
  • ethical considerations
  • external validity and generalisability - controlled conditions
  • placebo issues
297
Q

What happens during obs clinical trials?

A
  • Observational trials aim to observe and analyze real-world data on patient characteristics, exposures, treatments, and outcomes in observational studies.
  • These trials investigate associations, risk factors, prognostic factors, treatment patterns, and natural history of diseases or conditions without intervening or manipulating exposures or treatments
298
Q

obs clinical trials use?

A
  • non randomised designs and no use of control groups
  • Observational trials collect retrospective or prospective data on patient demographics, medical history, treatments, clinical outcomes,
  • e.g. cohort, case control, cross sectional, database analyses
299
Q

+ of obs trials?

A
  • real world data - inc generalisability and EV
  • large sample sizes and long follow up periods
  • ethical considerations - These studies do not involve experimental interventions or randomization of participants, minimizing risks, burdens, and ethical concerns related to randomization
  • cost effective and less resource intensive than inteventional trials
300
Q
  • of obst trials?
A
  • confounding and bias - non random allocation
  • limited IV - bias
  • missing data - reliance on existing data sources and medical records
  • reverse causality
  • Observational studies may lack external validity or generalizability due to selection bias, population heterogeneity, or differences in study populations, settings, or healthcare systems.
301
Q

consent and ethics in a trial?

A
  • informed consent process
  • ethical review and approval needed
  • participant autonomy
  • respect for participant dignity, privacy, confidentiality and personal intergrity
  • beneficence and non-maleficence
302
Q

selection bias?

A

*Selection bias occurs when there are systematic differences between the characteristics of participants in different treatment groups or between participants and non-participants, leading to an imbalance in baseline characteristics that may influence study outcomes.

303
Q

mitigating selection bias?

A

randomization, allocation concealment, and blinding/masking to ensure unbiased assignment of participants to treatment groups and minimize differences in baseline characteristics.

304
Q

what is allocation bias?

A

also known as assignment bias or treatment allocation bias, occurs when the process of assigning participants to treatment groups is influenced by factors other than randomization, such as clinician preference, patient characteristics, or knowledge of treatment assignments.

305
Q

How is allocation bias reduced?

A
  • Randomization, allocation concealment, and blinding/masking help prevent allocation bias by ensuring that treatment assignment is independent of investigator or participant preferences and expectations.
306
Q

what is performance bias?

A
  • Performance Bias: Performance bias occurs when there are systematic differences in the delivery or administration of interventions between treatment groups, leading to differential exposure or adherence to treatment protocols.
306
Q

how is performance bias reduced?

A
  • Blinding/masking of participants, investigators, and outcome assessors helps minimize performance bias by reducing the influence of awareness or expectations regarding treatment assignment on study conduct and outcomes.
306
Q

what is detection/ ascertainment bias?

A
  • systematic differences in the ascertainment, measurement, or interpretation of study outcomes between treatment groups, leading to differential detection or reporting of outcomes.
306
Q

how can ascertainment bias be reduced?

A

Blinding/masking of outcome assessors and objective, standardized outcome measures help minimize detection bias by ensuring unbiased assessment and reporting of study outcomes.

306
Q

What is attrition bias?

A
  • attrition bias - differences in the completion or retention of participants between treatment groups, leading to biased estimation of treatment effects.
306
Q

how can attrition bias be reduced?

A
  • Strategies to minimize attrition bias include maximizing participant retention, implementing intention-to-treat analysis, and conducting sensitivity analyses to assess the impact of missing data on study conclusions.
306
Q

what is reporting bias?

A
  • reporting bias - difference in reporting/ publication based on the direction/ magnitude of the findings
306
Q

how is reporting bias dealt w?

A
  • To mitigate reporting bias, clinical trials should adhere to transparent reporting guidelines (e.g., CONSORT statement) and register study protocols and outcomes a priori to promote accountability, transparency, and completeness in reporting study findings.
306
Q

PUBLICATION BIAS =

A
  • publication bias - Publication bias occurs when studies with positive or statistically significant results are more likely to be published or reported than studies with negative or non-significant results, leading to an overestimation of treatment effects and an incomplete representation of the evidence base.
306
Q

how can publication bias be reduced?

A
  • To address publication bias, efforts should be made to disseminate study findings through peer-reviewed publications, conference presentations, clinical trial registries, and systematic reviews, regardless of the direction or significance of the results.
307
Q

good clinical trial - statistics- sample size determinaion? ?

A
  • sample size determination - ensuring that the study is adequately powered to detect clinically meaningful differences or effects with sufficient precision and confidence.
307
Q

statistical methods used in good clinical trials?

A
  • randomisation and allocation concealment
  • statistical analysis plan - outlines the methods and procedures for analyzing the study data, including primary and secondary endpoints, statistical tests, adjustment for confounding factors, handling of missing data, and sensitivity analyses. T
  • confidence intervals
  • meta analyses and evidence synthesis to generate summary estimates of treatment effects and assess consistency
307
Q

explain why drugs need to be regulated

A
  • safety
  • efficacy
  • quality
  • clinical use - Drug regulation promotes appropriate and evidence-based use of medications
  • enhances public confidence
307
Q

MHRA?

A
  • The MHRA is the regulatory agency responsible for regulating medicines, medical devices, and blood components for transfusion in the UK.
  • The MHRA assesses applications for marketing authorization, conducts inspections of manufacturing facilities, monitors the safety of medicines through pharmacovigilance activities, and enforces regulatory compliance with applicable laws and standards
307
Q

European Medicines Agency (EMA) - European Union (EU):

A
  • responsible for coordinating the evaluation, approval, and supervision of medicines for human and veterinary use within the European Union (EU) a
  • The EMA assesses marketing authorization applications, provides scientific advice to applicants, conducts pharmacovigilance activities, and facilitates regulatory harmonization and cooperation among EU member states.
307
Q

the european commission - EU

A
  • key role in the regulatory framework for medicines in the EU, overseeing the implementation and enforcement of EU legislation, regulations, and directives related to pharmaceuticals
307
Q

approval process for new drugs?

A
  • preclinical testing - assesing safety, efficacy, pharmacodynamics and pharmacokinetics
  • clinical trials
  • marketing authorization application to the MHRA
  • MHA reviews the MAA to assess the safety, efficacy, and quality of the drug and determine whether it meets regulatory standards for approval.
307
Q

if a drug meets requirements then…

A
  • if the drug meets requirements the MHRA grants marketing authorization allowing the drug to be marketed and sold in the UK
  • post marketing suveillence - The MHRA continues to evaluate the safety and effectiveness of the drug through pharmacovigilance activities, post-market studies, and periodic safety updates.
308
Q

imp of market exclusitivity and patents?

A
  • Market exclusivity and patents provide pharmaceutical companies with a period of exclusivity during which they can recoup their R&D investment and earn a return on investment - incentivises them
  • fosters competition
309
Q

imp of patents?

A
  • protecting intellectual property - Patents grant inventors exclusive rights to their inventions for a limited period, typically 20 years from the date of filing.
  • Patents protect pharmaceutical companies’ intellectual property rights and prevent competitors from manufacturing, selling, or distributing the patented drug without authorization.
  • This protection encourages companies to disclose their innovations and inventions, fostering knowledge sharing and technological advancement.
310
Q

explain how drug sales can be protected when patents expire.

A
  • developing new formulations, strengths, delivery mechanisms
  • brand loyalty
  • authorised genertics marketed and distrubuted by the original manufacturer
  • price adjustments
311
Q

explain the basics of how drugs are marketed by the pharmaceutical industry?

A
  • product positioning and targeting
  • medical education and scientific communication to educate HCPs e.g. conferences
  • promotional materials
  • direct to consumer adveritising campaigns to stimulate demand
312
Q

explain the legal constraints on the marketing process for drugs.

A
  • regulatory oversight - compliance w rules
  • labelling and packaging inserts need to be accurate and comprehensive
  • prohibition from promoting off label uses - illegal
  • false or misleading claims
  • fair balance in promotional materials by presenting benefits and risks
313
Q

recognize the role of the ABPI code of conduct

A
  • sets ethical standards and guidelines for pharmaceutical companies operating in the UK.
  • The Code governs the promotion of prescription medicines to healthcare professionals, the provision of information to patients and the public, and interactions with healthcare organizations and patient groups
314
Q

what does the ABPI code of conduct ensure?

A
  • ensures ethical marketing practices
  • protects patient welfare - means no misleading or deception
  • promotes transparency and accountability
  • addresses complaints and disputes related to breaches of the code
315
Q

describe the potential for the marketing process to change attitudes.

A
  • information disseminating - creating awareness of medical conditions, treatment options, and available therapies
  • perception of need and demand - Marketing efforts can shape perceptions of need and demand for prescription drugs by highlighting the prevalence, severity, and impact of medical conditions, as well as the availability of effective treatments.
  • Marketing efforts targeted at healthcare professionals, such as detailing visits, promotional materials, sponsored educational events, and peer-to-peer interactions, can influence prescribing behavior and treatment choices
  • patient empowerment through DTC advertising
316
Q

uses of the drug promotion process?

A
  • education and information
  • disease awareness
  • access to treatment by promoting availability, affordability and benefits
317
Q

abuses of the drug promotion process?

A
  • misleading/ inaccurate claims
  • off label promotion - illegal
  • undue influence on prescribing
  • conflict of interest
318
Q
A

Year 3 (45 decks)

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