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Week 1 Flashcards

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1
Q

What is pharmacokinetics?

A

What your body does to a drug

Absorption, distribution, metabolism, elimination

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2
Q

What is pharmacodynamics?

A

What a drug does to your body

Biochemistry and physiology

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3
Q

What is bioavailability?

A

Fraction of the administered dose of drug that reaches the systemic circulation

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4
Q

What letter represents bioavailability?

A

F

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5
Q

How is volume of distribution calculated?

A

Volume of distribution = total drug in body/blood plasma concentration

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6
Q

What is the volume of distribution if the total drug in body is 100mg and the plasma concentration is 1 mg/L?

A

100L

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7
Q

What is clearance?

A

Volume of plasma/blood cleared of drug per unit time

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8
Q

What is half-life?

A

Time required for plasma concentration of a drug to decrease by half

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9
Q

What is half-life determined by?

A

Clearance and volume of distribution

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10
Q

How many half lives does it take for a drug to reach steady state?

A

4-5

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11
Q

What are loading doses used for?

A

When the drug being administered has a long-half life but its effects are required quickly

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12
Q

What medications require loading doses?

A

Antibiotics (e.g. gentamicin)

Digoxin

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13
Q

What is elimination half-life?

A

Time taken for the concentration to fall to half

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14
Q

What is linear pharmacokinetics?

A

Concentration that results from a dose is proportional to the dose - double the dose, double the concentration
Rate of elimination is proportional to the concentration - 50% of drug will be eliminated in a given time frame

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15
Q

What is non-linear pharmacokinetics?

A

Concentration that results is not proportional to dose; small increase in dose = large increase in concentration
Rate of elimination is constant regardless of amount of drug present
Dosage increases can saturate binding sites and result in non- proportional increase in drug levels; or opposite in dose decrease

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16
Q

Why might changing administration of morphine from oral to subcutaneous cause opioid toxicity?

A

Morphine oral bioavailability is lower than subcutaneous - dose needs to be 1/3 of original

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17
Q

Will the loading dose be the same in a large man and a frail woman? Why?

A

No

Depends on volume of distribution

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18
Q

Will the loading dose be the same in a man with kidney failure and a woman with normal kidney funtion of comparable weights? Why?

A

Yes

Volume of distribution unaffected by kidney function

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19
Q

How is a loading dose calculated?

A

Loading dose (mg) = target concentration (mg/L) x volume (L/kg)

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20
Q

What are the 4 main receptor classes?

A

Enzyme-linked
Ion channel linked
G-protein linked
Nuclear/gene linked

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21
Q

What is affinity?

A

Measure of propensity of a drug to bind receptor; the attractiveness of drug and receptor

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22
Q

What is efficacy?

A

Ability of a bound drug to change the receptor in a way that produces an effect

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23
Q

What is potency?

A

Relative position of the dose-effect curve along the dose axis

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24
Q

Is a low potency drug considered disadvantageous?

A

Only if the dose is so large that it is awkward to administer

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25
Q

Do agonists have affinity and efficacy?

A

Yes

Yes

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26
Q

Do antagonists have affinity and efficacy?

A

Yes

No

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27
Q

Do partial agonists have affinity and efficacy?

A

Yes

Yes, but less than full

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28
Q

What are agonists?

A

Drugs that interact with and activate

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29
Q

What is a full agonist?

A

An agonist with maximal efficacy

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30
Q

What is a partial agonist?

A

An agonist with less than maximal efficacy

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31
Q

What are the 2 types of agonist?

A

Full

Partial

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32
Q

What are the 2 types of antagonist?

A

Competitive

Non-competitive

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33
Q

What is an antagonist?

A

Interacts with the receptor but does not change the receptor

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34
Q

What is a competitive antagonist?

A

Competes with agonist for receptor
Surmountable with increasing agonist concentrations
Shifts dose response curve to the right
Reduces the apparent affinity of the agonist

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35
Q

Is a higher or lower therapeutic index more advantageous?

A

Higher

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36
Q

How is the therapeutic index calculated?

A

Therapeutic index = toxic/lethal dose 50/effective dose 50

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37
Q

How does renal disease affect pharmacology and what changes need to be made?

A

Increased half-life/prolonged elimination

Dosing interval needs to be increased

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38
Q

What is VD?

A

Volume in which the amount of drug would need to be uniformly distributed to produce observed blood concentration

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39
Q

How does hepatic disease affect pharmacology and what changes need to be made?

A

Increased half-life/slower rate of enzyme metabolism

Decrease dosage and increase dosing interval

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40
Q

How does cystic fibrosis affect pharmacology and what changes need to be made?

A

Increased metabolism and elimination

Increase dosage and decrease dosing interval

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41
Q

How does ageing affect elimination of drugs?

A

Variable decrease in GFR

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42
Q

How are pharmacodynamic effects increased and decreased in the elderly?

A

Increased - alcohol, opiates

Decreased - isoproterenol and β-blockers

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43
Q

Why are the elderly at high risk of adverse drug reactions?

A

The more medications a person is on, the higher the risk of drug-drug interactions/adverse drug reactions and non-adherence

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44
Q

Give some examples of drug-drug interactions

A

Statins and erythromycin/other antibiotics
Verapamil and β-blockers
Warfarin and aspirin/multiple drugs
ACE inhibitors and sulfonylureas

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45
Q

What conditions can be worsened by NSAIDs, decongestants and calcium channel blockers?

A

NSAIDs - chronic HF
Decongestants - BPH urinary retention
Calcium - constipation

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46
Q

What drugs should be avoided in renal disease?

A

Metformin

NSAIDs

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47
Q

What drugs should be used with caution in renal disease?

A

ACE inhibitors

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48
Q

What drugs should be given in a reduced dose in renal disease

A

Antibiotics
Heparin
Digoxin
Phenytoin

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49
Q

What is TD50?

A

Dose at which there is a toxic effect in 50% of cases

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50
Q

What is LD50?

A

Dose at which there is death in 50% of cases

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51
Q

What is ED50?

A

Dose at which a drug is effective in 50% of cases

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52
Q

What is the ratio of males:females affected by hyperkinetic disorders?

A

3-4:1

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53
Q

What could be the reason for differences in prevalence reporting rates of hyperkinetic disorders?

A

Under-reporting
Lack of recognition in females
Differences in diagnostic practice
Differences in cultural expectations of behaviour

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54
Q

What are the 3 core features of ADHD?

A

Inattentiveness
Hyperactivity
Impulsiveness

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55
Q

What does ADHD stand for?

A

Attention deficit hyperactivity disorder

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56
Q

What are some common signs/symptoms of ADHD?

A

Tendency to move from one task to another without completion
Disorganisation
Fidgeting
Accident prone
Social disinhibition
Poor maintenance of personal relationships

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57
Q

What are the specifications for symptoms to fall under in order to diagnose ADHD?

A

Symptoms apparent before age 7/12
Symptoms excessive for child’s age
Pervasive (symptoms occur in more than 1 environment)

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58
Q

Give some examples of genes which are thought to contribute to susceptibility to ADHD

A

DRD4 receptor 7-repeat alleles
Dopamine - SLC6A3/DAT1 and DRD5
Serotonin - SLC6A4/5HTT and HTR1B

59
Q

What is the mean heritability of ADHD in children and adults?

A

Children - 75%

Adults - 30%

60
Q

What networks/circuits are involved in inattention?

A

Anterior fronto-striatal networks

Posterior parieto-cerebellar circuits

61
Q

What parts of the brain are smaller in adolescents?

A

Frontal and parietal cortex
Basal ganglia
Right dorso-lateral prefrontal lobe
Cerebellar vermis

62
Q

What executive functions are controlled by the prefrontal cortex?

A

Regulation of attention
Planning
Impulse control
Processing

63
Q

Where do projections from the prefrontal cortex go?

A

Cerebellum and striatum

64
Q

What is the result of dysfunction of the prefrontal cortex?

A 
Forgetfulness
Distractibility
Impulsivity
Impairment in working memory
Impairment of mental flexibility
65
Q

What is the limbic system responsible for?

A

Regulation of emotion and memory

Connects higher and lower brain functions

66
Q

What is response inhibition?

A

Suppression of no-longer required or inappropriate actions, which supports flexible and goal-directed behaviour in ever-changing environments

67
Q

What is working memory?

A

Cognitive short-term memory buffer with a limited capacity that is responsible for the transient holding, processing, and manipulation of stored information
Important process for reasoning and the guidance of decision making and behaviour

68
Q

What co-morbidities are associated with ADHD?

A 
Sleep disorders
Behavioural difficulties 
Learning disabilities 
Social communication problems 
Anxiety and mood 
Tic disorders
69
Q

Prenatal exposure to what substances has been linked with development of ADHD?

A 
Lead
Alcohol
Sodium valproate 
Cocaine
Opiates
70
Q

How is ADHD assessed?

A 
Direct observations in >1 setting
Psychoeducational assessment
Questionnaires/interviews
Identification of co-morbidities 
Developmental history
71
Q

What information should be obtained from an ADHD history?

A 
Current behaviours
Activity levels
Impulsivity
Emotional reactivity
Ability to sustain interest/attention (with/without adult involvement)
Eating and sleep habits; impact
Responses to and interactions with others
Parental management strategies  
Developmental and prenatal/perinatal
72
Q

What are the early signs of ADHD?

A 
Increased foetal movements in pregnancy
Difficult feeder
Irregular sleeper
Unusually active/distractible toddler
Language delay
Increasingly challenging behaviour
Socially disinhibited with adults
Learning difficulties
73
Q

What aspects of family history are important in ADHD?

A

Medical/social history
Learning difficulties in the family (specific and global)
Current parental use of alcohol and/or illicit drug use
Current stressors on the family
Structure of extended family
Child’s care history

74
Q

What aspects of the child’s school life are important to explore in ADHD?

A

Kind of school
Presentation during structured/less structured activities Inattentive/‘daydream’ behaviours in class
Concentration and speed of work
Impulsivity
Quality of relationships with peers/adults
Levels of attainment

75
Q

What additional assessments can be done for a child with suspected ADHD?

A

Hearing and vision screening checks
Previous health problem investigation
Screening for neurological signs and physical anomalies
Baseline height and weight (record on growth chart)
Baseline blood pressure and heart sounds

76
Q

Why must there be regular communication between health and education staff when a child has ADHD?

A

Promotes understanding of the difficulties of ADHD
Ensures a consistent approach to patient across settings
Monitors effectiveness of interventions

77
Q

How would ADHD in pre-school children be managed?

A

Behavioural

78
Q

How would mild ADHD in a school aged child be treated?

A

Behavioural

79
Q

How would moderate/severe ADHD in a school age child be treated if there are no co-morbidities?

A

Medication

80
Q

How would moderate/severe ADHD in a school age child be treated if there is aggressive behaviour/ODD?

A

Behavioural and medication

81
Q

How would moderate/severe ADHD in a school age child be treated if there is GAD?

A

Behavioural and medication

82
Q

What behaviour training strategies can be used for children with ADHD?

A

Encourage consistency
Positively reinforce appropriate behaviour
Be firm and in control without being coercive
Set clear rules with consequences
Use routine, count-downs and reminders
Use quiet time, planned ignoring and timeout (age appropriate)
Do not give instructions without first gaining the child’s attention
Ask the child to repeat the instructions back to ensure they have heard and understood them

83
Q

What type of drug is given as a 1st line treatment for ADHD? Give 2 examples

A

Psychostimulants

Methylphenidate (MPH) and dexamphetamine (DEX)

84
Q

How does the psychostimulant methylphenidate work?

A

Blocks dopamine and noradrenaline re-uptake via their transporters

85
Q

How does the psychostimulant dexamphetamine work?

A

Released dopamine stored in pre-synaptic vesicles

86
Q

What 2nd line drug is used to treat ADHD? How does it work?

A

Atomoxetine
Inhibits re-uptake of noradrenaline, blocks noradrenaline transporter and increases noradrenaline and dopamine in prefrontal cortex

87
Q

What 3rd line drugs are used to treat ADHD? How do they work?

A

Clonidine and guanfacine

α2-receptor agonists

88
Q

What is the difference between clonidine and guanfacine?

A

Clonidine stimulates all subtypes of α-adrenoceptor; more potent at presynaptic
Guanfacine is more selective for α2-adrenoceptor; more potent at postsynaptic

89
Q

What are the common side-effects of psychostimulants?

A 
Insomnia 
Decreased appetite
Abdominal discomfort
Headaches
Emotional lability 
Depression and psychosis
Tolerance
90
Q

What are the common side-effects of clonidine?

A

Sedation
Constipation
Headaches
Hypotension

91
Q

What ADHD drugs can be taken in liquid and tablet form?

A

Methylphenidate

Clonidine

92
Q

What ADHD drugs are the quickest to act?

A

Psychostimulants

93
Q

Which ADHD drugs take longer to act?

A

Guanfacine - 3 weeks

Clonidine and atomoxetine - 6 weeks

94
Q

What is lisdexamfetamine?

A

Elvanse
Pro-drug which is metabolised to dexampthetamine by RBCs
Increases dopamine and noradrenaline
Rapid onset, long (13 hours) duration

95
Q

How can anorexia/weight loss/growth concerns while taking psychostimulants be addressed?

A

Administer with food
Reduce dose
Monitor height and weight
Provide dietary advice

96
Q

How can sleep difficulties while taking psychostimulants be addressed?

A

Sleep hygiene advice
Reduce evening dose/administer earlier
Consider atomoxetine

97
Q

How can dizzziness/headaches while taking psychostimulants be addressed?

A

Monitor, may be temporary

Reduce or discontinue

98
Q

How can involuntary movements/tics while taking psychostimulants be addressed?

A

Monitor, may be temporary

Change to non-psychostimulant

99
Q

How is medication monitored for ADHD?

A

Regular review (<6 monthly) but more frequent when titrating meds
Monitor response to medication
Monitor side-effects
Monitor height, weight, pulse and BP
Safe prescribing – compliance, misuse, medical history, access to regular monitoring

100
Q

What factors are associated with persistence of ADHD into adulthood?

A 
Progressive reduction in cerebellar and hippocampal volumes
Maternal depression
Marital discord
Negative parent-child interaction
Family socio-economic disadvantage
Familial ADHD
101
Q

How can family circumstances influence ADHD prognosis?

A

Those living in adverse social-economic conditions have more impairment and increased co-morbid problems and poorer long-term outcomes

102
Q

What is the prognosis for adults with ADHD?

A

~50% will improve with less hyperactivity but they may still have problems organising and planning, not attain academically as well as expected, find relationships and jobs harder to sustain

103
Q

What co-morbidities are associated with ADHD in adulthood?

A

Mood disorders
Substance abuse
Antisocial/borderline personality disorders

104
Q

What neurotransmitter is involved in alertness, concentration and energy?

A

Noradrenaline

105
Q

What neurotransmitter is involved in pleasure, reward, motivation and drive?

A

Dopamine

106
Q

What neurotransmitter is involved in obsession, compulsion and memory?

A

Serotonin

107
Q

What neurotransmitters are involved in anxiety, impulse and irritability?

A

Noradrenaline and serotonin

108
Q

What neurotransmitters are involved in attention and arousal?

A

Noradrenaline and dopamine

109
Q

What neurotransmitters are involved in appetite, sex and aggression?

A

Serotonin and dopamine

110
Q

What neurotransmitters are involved in mood and cognitive function?

A

Noradrenaline, serotonin and dopamine

111
Q

What are the 3 components of ADHD?

A

Attention deficit
Motor hyperactivity
Impulsivity

112
Q

How are the functions of dopamine related to ADHD?

A

Enhances signal

Improves attention - behaviour and cognition

113
Q

How are the functions of noradrenaline related to ADHD?

A

Dampens noise
Executive operations
Increases inhibition

114
Q

How is the prefrontal cortex involved in ADHD/arousal systems?

A

Defective inhibitory response - insufficient information processing (inattention, hyperactivity, impulsivity)
Unable to distinguish between important signals and background noise - easily distracted/can’t focus

115
Q

What is hypo-arousal?

A

Low tonic firing of dopamine/noradrenaline neurons

116
Q

How can improving the signal to noise ratio relieve ADHD symptoms and what is used to do this?

A

Increases the drive of the arousal network to improve efficiency of information processing
Stimulants - amplify tonic firing rates

117
Q

What is hyper-arousal?

A

Excess stimulation of receptors by dopamine and noradrenaline which causes signal to noise detection to deteriorate (poor attention and impulsivity)
Increased phasic firing of dopamine and noradrenaline

118
Q

What drugs are used to treat ADHD?

A

1st - psychostimulants (methylphenidate, dexamphetamine)
2nd - atomoxetine
3rd - adrenergic drugs (clonidine, guanfacine); antidepressants (venlafaxine, TCAs, MAOIs); dopaminergic drugs (modafinal); all used to augment therapy

119
Q

How does dexamfetamine work?

A

Facilitates release of dopamine from presynaptic cytoplasmic storage vesicles and blocks dopamine transporter protein (inhibits reuptake) - net increase in dopamine

120
Q

How does methylphenidate work?

A

Acts on dopamine transporter - increase in dopamine

121
Q

How effective are psychostimulants?

A

75%

122
Q

How is methylphenidate given?

A

5mg tablets 3-4 times a day

Preparation cannot be manipulated for easier administration

123
Q

What brand names of methylphenidate are available?

A

Ritalin
Equasym
Medikinet
Concerta

124
Q

How is dexamfetamine given?

A

5mg tablets/trans-dermal patch

Can be dissolved in water

125
Q

What is the onset and duration of methylphenidate?

A

Rapid onset

Duration 8-12 hours

126
Q

What is the onset and duration of dexamfetamine?

A

Rapid onset

Duration 13 hours

127
Q

What brand names of dexamfetamine are available?

A

Elvanse (pro-drug)

Daytrana (patch)

128
Q

What are the side-effects of psychostimulants?

A 
Growth retardation
Anorexia 
BP/HR irregularities 
Insomnia 
Sadness, irritability, abdominal pain, headaches
129
Q

What are the components of physical health monitoring for psychostimulants?

A

HR and BP
Height and weight
History of medicines, disorders, family sudden cardiac/unexplained death

130
Q

What is the legal status of psychostimulants?

A

Schedule 2 controlled drugs - prescription required with a 28 day validity and signed on collection as proof of identity
Private prescription must have prescriber’s ID number; standardised forms
30 days supply

131
Q

What information is required for a controlled drugs prescription to be dispensed?

A

Form and strength of preparation
Total quantity to be supplied in words and figures
Dose to be administered
Signature and date from prescriber

132
Q

How does atomoxetine work?

A

Enhances noradrenaline transmission in prefrontal cortex by inhibiting its reuptake from the synaptic cleft

133
Q

Which ADHD drug is effective for co-morbid anxiety and depression?

A

Atomoxetine

134
Q

What are the side effects of atomoxetine?

A

Nausea/vomiting, excessive tiredness, insomnia, abdominal pain, appetite suppression, weight loss, constipation, headaches, mood swings, hepatic impairment, increased HR/BP, suicidal ideation

135
Q

What adrenergic drugs are used to treat ADHD?

A

Clonidine

Guanfacine

136
Q

How do adrenergic agonists act on the brain to treat ADHD?

A

Increased action of adrenoreceptors

137
Q

What are the side effects of clonidine and guanfacine?

A

Sedation, dizziness, hypotension

138
Q

What is the onset of adrenergic agonists used for ADHD?

A

4-6 weeks

139
Q

Why are antidepressants used to treat ADHD?

A

Enhance the amount of monoamines at the synapse

140
Q

What antidepressants are used to treat ADHD and what are their side-effects?

A

Nortriptyline and imipramine

Anticholinergic effects, seizures, heart effects

141
Q

What ADHD drugs are not used in CAMHS?

A

Antidepressants

Modafinil

142
Q

What is modafinil?

A

Weak psychostimulant
Decreases GABA and increases glutamate
Effects on hypothalamic arousal

143
Q

How is modafinil taken and what are its side effects?

A

100-300mg in divided doses

GI problems, appetite, abdominal pain, dry mouth, tachycardia

144
Q

What is the role of vitamins/minerals/diet in ADHD?

A

Omega 3/6, Fe, B vitamins and zinc have all been linked or are marketed to improve concentration etc/ but evidence is lacking

People and Illness (4 decks)

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