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Clinical Pharmacology, Therapeutics & Principles of Prescribing > Session 13 > Flashcards

Session 13 Flashcards

1
Q
  • Describe the major classes of drugs used in the treatment of depression, psychoses and anxiety disorders
  • Understand the underlying patho- physiological basis of these disorders and relate them to pharmacological targets
  • Describe the mechanism of action of these major classes in altering mood and reducing symptoms
  • Describe the major toxicities of these drugs
  • Recognise the potential for misuse of and attempted suicide using many of these medications
  • Appreciate the evidence base that supports the choice of drugs in these conditions
A
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2
Q

Key transmission and modulatory pathways in CNS

A
  • Noradrenergic pathways
  • Dopaminergic pathways
  • Serotonergic (5HT pathways)
  • GABA-nergic pathways
  • Cholinergic pathways
  • Glutamate pathways

​

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3
Q

What may cause this individual to have a psychiatric disorder?/Formulation of Psychiatric Disorders

A
  • Genetic vulnerability to the expression of the disease
  • Life events (divorce, bereavement)
  • Individuals personality, coping skills, social support
  • Other environmental influences e.g. viruses, toxins, recreational drugs, other diseases – physical health
  • BIOPSYCHOSOCIAL MODEL
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4
Q

Biopsychosocial Approach – Assessment and Management of psychiatric disorders

A
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5
Q

What are the core & secondary symptoms for depression?

A
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6
Q

What are the pathophysiological theories for depression

A
  1. The Monoamine Hypothesis
  2. Neurotransmitter Receptor Hypothesis

3.

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7
Q

Explain the The Monoamine Hypothesis

A
  • Depression due to a deficiency of monoamine neurotransmitters- noradrenaline and serotonin- therefore certain drugs that depleted these could induce depression- e.g. Reserpine – mixed evidence
  • E.g. Monoamine oxidase inhibitors (MAOIs) block the enzyme monoamine oxidase from destroying neurotransmitters
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8
Q

Explain the Neurotransmitter Receptor Hypothesis

A
  • An abnormality in the receptors for monoamine transmission leads to depression
  • Depletion of neurotransmitter causes compensatory up regulation of post synaptic receptors- some post mortem evidence​
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9
Q

Explain the Monoamine Hypothesis of Gene Expression

A
  • Deficiency in molecular functioning
  • Hypothesised problem within the molecular events distal to the receptor
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10
Q

Describe the major classes of drugs used in the treatment of depression, psychoses and anxiety disorders LO

Which drugs can we give for depression?

A
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11
Q

Selective Serotonin reuptake Inhibitors- SSRIs

  1. Used for?
  2. Give examples
  3. Mechanism of action?
A
  1. Treatment of moderate to severe depression (with CBT) – first line medication
  2. Fluoxetine, citalopram, paroxetine, sertraline

Citalopram most selective, paroxetine most potent reuptake inhibitor

    • The serotonin transporter (SERT) is a monoamine transporter protein.

This is a membrane protein that transports serotonin from synaptic spaces into presynaptic neurons.

  • Selective serotonin reuptake inhibitors and other antidepressants block the SERT transporter. The result is an increased availability of serotonin in the synaptic space.
  • Implications in terms of regulation of 5HT1A receptors - > downregulated
  • there are less 5HT1A receptors expressed in the somatodendritic region, the neuron is now disinhibited.

As a consequence, firing rate is increased. This in turn increases serotonin release to the synaptic space, which stimulates postsynaptic serotonin receptors.

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12
Q

• Describe the major toxicities of these drugs LO

SSRI

  1. Pharmacokinetics - frequency, metabolised, dosage?
  2. State the common and rare side effects
A
  1. • Almost completely absorbed from gut
  • Long elimination half lives (once daily dosage)
  • Metabolised in liver
  1. • Common- anorexia, nausea, diarrhoea
  • Rare- precipitation of mania, Possible increased suicidal ideation and neurological side effects such as tremor, extrapyramidal syndromes
  • NB – reasonably safe in overdose if taken on own.
  • Recent Update – Citalopram prolongs QTc
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13
Q
  • Describe the mechanism of action of these major classes in altering mood and reducing symptoms LO
  • Describe the major toxicities of these drugs LO
  • Recognise the potential for misuse of and attempted suicide using many of these medications LO

Tricyclic Antidepressants (TCAs)

  1. First generation antidepressants, still used – but less often and not first line. Give examples.
  2. Mechanism of action (in lecture wa put under other effects) LO
  3. Pharmacokinetics
  4. Side effects and toxicity (5)
A
  1. Amitriptyline, Imipramine, Clomipramine, Lofepramine
    • Inhibition of noradrenalin uptake, resulting in enhanced nor-adrenergic neurotransmission (sympathomimetic effect)
      - Muscarinic cholinoceptor blockade- reduced cholinergic neurotransmission (anticholinergic effect)
      - Alpha 1-adrenoceptor blockade- suppression of noradrenergic neurotransmission (sympatholytic effect)
  3. • Lipid soluble
  • Absorbed from gut
  • Long half lives
  • Metabolised in liver
  1. • CNS- sedation and impairment of psychomotor performance, lowering of seizure threshold
  • Autonomic nervous system, reduction in glandular secretions, eye accommodation block
  • CVS- tachycardia, postural hypotension, impair myocardial contractility
  • GI-constipation
  • What would be the consequences of overdose?
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14
Q
  • Describe the mechanism of action of these major classes in altering mood and reducing symptoms LO
  • Describe the major toxicities of these drugs LO

‘Pure’ non-selective monoamine uptake inhibitors ( SNRIs)

  1. Developed as SSRIs with property of noradrenaline uptake inhibition grafted on. E.g. ?
  2. What line drugs are they?
  3. What do we mean by SNRIs are dose dependent?
  4. Side effects & toxicity
A
  1. Venlafaxine and Duloxetine
  2. Second/third line drugs
  3. Lower doses serotonin action, higher doses noradrenaline
  4. • As with SSRIs – but more because of additional actions
  • Also sleep disturbance, increased BP, dry mouth, hyponatraemia
  • Relatively short half- life therefore may be a withdrawal syndrome on discontinuation.

(SSRIs side effects:

Common- anorexia, nausea, diarrhoea

• Rare- precipitation of mania, Possible increased suicidal ideation and neurological side effects such as tremor, extrapyramidal syndromes)

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15
Q

Schizophrenia- Psychosis

  1. Schizophrenia is an example of a mental illness with Psychotic symptoms. Other examples of illnesses where there may be psychosis are ?
  2. Psychosis means a ?
  3. What are the symptoms of Paranoid Schizophrenia ?
A
  1. mania, severe depression with psychosis, organic syndromes, delusional disorder,
    delirium, dementia
  2. lack of contact with reality
  3. • Disturbances of thinking
  • Hallucinations
  • Delusions
  • Unusual speech- thought disorder
  • Behavioural changes
  • Lack of insight
  • Negative symptoms

​

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16
Q
  1. Hallucination-
  2. Delusion-
A
  1. Hallucination- a perception in the absence of an external stimulus-auditory, olfactory, visual, gustatory, tactile.
  2. Delusion- a fixed false belief that it out of keeping with someone’s culture or religious beliefs
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17
Q

• Understand the underlying patho- physiological basis of these disorders and relate them to pharmacological targets LO

  1. State some factors that increase the risk of schizophrenia
  2. Explain the dopamine theory of schizophrenia
A
  1. Image
  2. • Amphetamine causes symptoms very similar to positive symptoms of schizophrenia
  • Dopamine antagonists are the best treatment for schizophrenia (antipsychotics)
  • Some evidence of increased dopamine function in schizophrenics
  • But
  • Amphetamine does not cause negative symptoms
  • Dopamine antagonists do not treat negative symptoms
  • Changes in dopamine function may be a response to long term drug treatment
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18
Q

Main dopamine pathways (4)

A
  • Mesolimbic- emotional response and behaviour
  • Meso-cortical- important in arousal and mood
  • Nigrostriatal- key pathway damaged in Parkinson’s disease
  • Tuberoinfundibular - in hypothalamus and pituitary gland
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19
Q

What are the positives on blocking D2 receptors and the negatives?

A
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20
Q

Is schizophrenia associated with increased 5HT function?

A
  • 5HT has been implicated in a number of behaviours which are disturbed in schizophrenia (e.g. perception, attention, mood, aggression, sexual drive, appetite, motor behaviour, sleep)
  • Many of the most effective antipsychotic drugs are antagonists at 5HT-2A receptors. (Clozapine)
  • Precursors of 5HT (e.g. tryptophan) exacerbate schizophrenia
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21
Q

Is schizophrenia associated with decreased cortical glutamate function ?

A
  • Glutamate is the predominant excitatory neurotransmitter in the brain
  • Phencyclidine (PCP: angel dust: non-competitive antagonist at NMDA-type glutamate receptors) induces symptoms very similar to schizophrenia
  • Post-mortem studies have shown
  • increased cortical glutamate receptors
  • increased binding of glutamate receptor ligands in cortex, basal ganglia and hippocampal formation.
  • Glutamate systems ARE important, but mechanism unclear – and we have not been able to develop a treatment that has a direct action on the glutamate system
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22
Q
  • Describe the major classes of drugs used in the treatment of depression, psychoses and anxiety disorders
  • Describe the mechanism of action of these major classes in altering mood and reducing symptoms
  1. Drugs used in Schizophrenia? Give examples. (2)
  2. Action of all antipsychotics
A
  1. • First generation or typical antipsychotics - haloperidol, chlorpromazine (1950s)
  • Atypical antipsychotics - olanzapine, risperidone, quetiapine (1990s)
  • Clozapine
  • Oral vs Depot preparations
  1. • Sedation- within hours
  • Tranquilisation- within hours
  • Antipsychotic - several days or weeks
  • Activating effect within weeks- negative symptoms (probably not the typicals)
  • Production of extrapyramidal side effects- hours or days. – Much less with the atypical antipsychotics
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23
Q

• Describe the major toxicities of these drugs LO

  1. Atypical antipsychotics advantages
  2. Side Effects of Atypical antipsychotics
A
  1. • Less EPSE side effects therefore more acceptable to patient
  • Different preparations e.g. dissolvable
  • Some once daily dosage
  • Differing side effect profiles can be matched to patient characteristics
  • First line treatment in schizophrenia now as recommended by NICE
  1. • Vary between drugs
  • Can have extrapyramidal side effects at high doses
  • Weight gain- e.g. Olanzapine
  • Increased prolactin e.g. Risperidone
  • Sedation

​

24
Q

• Describe the major toxicities of these drugs LO

Clozapine

  1. Typical or atypical?
  2. Meta-analysis – ?
  3. ? line agent
  4. Monitoring – ?
  5. Side effects –
A
  1. Atypical antipsychotic
  2. efficacy
  3. 3rd
  4. FBC (weekly initially)
  5. severe constipation, sedation, hypersalivation, weight gain ++++

• Neutropenia/Agranulocytosis

25
Q

• Describe the mechanism of action of these major classes in altering mood and reducing symptoms LO

Typical antipsychotics

  1. ? safe in emergencies
  2. More ?
  3. Well known side effects
  4. Wide range of pharmacological action…?
A
  1. Haloperidol
  2. sedating

3.

  1. Dopamine receptor blockade, anticholinergic effects, alpha-adrenergic blockade, antihistamine effect
26
Q

• Describe the major toxicities of these drugs LO

  1. Side effects of typical antipsychotics (6)
  2. Toxicities

• Appreciate the evidence base that supports the choice of drugs in these conditions LO

  1. Evidence
A
  • Extrapyramidal side-effects- parkinsonism, acute dystonia, akathisia, tardive dyskinesia
  • Neuroleptic malignant syndrome - severe rigidity, hyperthermia, increased CPK, autonomic lability
  • Postural hypotension
  • Weight gain
  • Endocrine changes (e.g. hyperprolactinaemia)
  • Pigmentation
  1. • Central nervous system depression
  • Cardiac toxicity
  • Risk of sudden death with high dose
  1. Evidence
    • The Northwick Park study of first episodes of schizophrenia. A RCT of prophylactic neuroleptic treatment. Br J Psychiatry 1986 148 120-7

• Clozapine for the treatment resistant schizophrenic. A double- blind comparison with chlorpromazine. Arch Gen psychiatry 1988;45:789-96 Kane J

27
Q

• Understand the underlying patho- physiological basis of these disorders and relate them to pharmacological targets LO

Anxiety disorders

  1. What is anxiety?
  2. Behavioural symptoms - ?
  3. Psychological symptoms - ?
  4. Physical symptoms – ?
  5. What is the pathophysiology of anxiety?
A
  1. Fear out of proportion to situation
  2. Avoidance
  3. Fear of dying, going crazy
  4. light headedness, shortness of breath, hot & cold flushes, nausea, palpitations, numbness, pins & needles
28
Q

Treatment of anxiety (3)

A
  • Non pharmacological approaches first line - CBT
  • Treat any coexistent disorder
  • Drugs- antidepressants, anxiolytics, occasionally antipsychotics.
29
Q

Principle Neurotransmitter systems (3)

A
30
Q

Benzodiazepines

  1. E.g.
  2. Mechanism of action:
  3. Aministration? When is conc maximum?
  4. Hydrophilic or hydrophobic?
  5. Excreted by?
  6. ? half life
A
  1. Diazepam, lorazepam
  2. • Exerts effects through structure known as GABA- BDZ receptor complex
  • Benzodiazepines only bind to BDZ receptor of which there are 2 main groups- high and low affinity
  • High affinity group- important in anxiolytic, hypnotic and anticonvulsant effects of BDZs
  • Inhibitory effects in brain
  • Act as full agonists at these receptor sites
  • Lead to enhancement of GABA
  1. Bioavailability following oral admin. Almost complete- maximum concentrations 30-90 minutes
  2. Highly lipid soluble- CNS diffusion rapid (hydrophobic)
  3. Renal excretion
  4. Long
31
Q

What is an important factor to consider when administering benzodiazipines

A

Tolerance and Dependence

  • Tolerance can occur i.e. need to increase the dose to achieve the same effect.
  • Dependence-on discontinuation of treatment can get withdrawal effects e.g. insomnia, agitation, anxiety
  • What other drugs have a dependency syndrome?
32
Q

Side Effects of anxiolytics i.e. benzodiazepines

  1. Common
  2. Occasional
  3. Rare
A
  1. Common - drowsiness, dizziness, psychomotor impairment
  2. Occasional - dry mouth, blurred vision, gastrointestinal upset, ataxia,
    headache, reduced blood pressure
  3. Rare - amnesia, restlessness, rash
33
Q

• Describe the major toxicities of these drugs LO

Toxicity for anxiolytics e.g. benzodiazepines

A
  • ?Cleft lip and palate if used in pregnancy
  • If taken late in pregnancy may cause respiratory depression and feeding difficulties in baby
34
Q

• Recognise the potential for misuse of and attempted suicide using many of these medications LO

Treatment of Overdose?

A
  1. • Deaths are rare – respiratory depression
  2. • Support
  3. • Flumazenil an antagonist/partial inverse agonist at BDZ receptors may be useful in reversing effects
35
Q

• Appreciate the evidence base that supports the choice of drugs in these conditions LO

Evidence for anxiolytics

A
  • Mental Health foundation 1992. Guidelines for the prevention & treatment of benzodiazepine dependence.
  • New insights into the role of the GABA(A) benzodiazepine receptor in psychiatric disorder . Br J psych 2001 179 390-6. Nutt DJ
36
Q

Bipolar Disorder Mania, Hypomania, Depression

What is Bipolar Disorder?

Pathophysiology?

A

Episodes of Depression and hypomania/mania

37
Q

What is mania

A

Mania

– Feeling unusually excited, happy, optimistic or feeling irritable

– Overactive

– Poor concentration and short attention span

– Poor sleep

– Rapid speech, jump from one idea to another

– Poor judgement (overspending)

– Increased interest in sex

– Psychotic symptoms- hallucinations, grandiose delusion

38
Q

Give some examples of Bipolar disorder mood stabilisers

A
  • Lithium
  • Sodium valproate
  • Carbamazepine
  • Lamotrigine
  • Antipsychotics
39
Q

• Describe the mechanism of action of these major classes in altering mood and reducing symptoms LO

Lithium- Theories for mechanism of action

A
  1. Electrolytes and channels- may compete with magnesium and calcium ions
  2. Neurotransmitters - Li increases 5HT, chronic Li may reduce 5-HT receptor sites
  3. Second messenger systems- lithium attenuates the effects of certain neurotransmitters on their receptors without altering receptor density
40
Q

Clinical pharmacology of Lithium

  1. Excretion?
  2. Frequency of administration?
  3. Monitoring?
A
  1. Renal excretion
  2. Slow release preparations can be given once daily
  3. • Lithium levels need to be monitored (at least 3 monthly) and taken 12 hours after last oral dose – narrow therapeutic window

• Need check renal function, and thyroid function before starting and every 6 months

41
Q

Uses of Lithium (4)

A
  • Prophylaxis of Mania & Depression in bipolar disorder
  • Augmentation of antidepressants in unipolar depression
  • Good evidence for reducing suicidality
  • Of all mood stabilisers Lithium has the best evidence
42
Q

Side effects of lithium

A
  • Memory problems- 52%
  • Thirst- 42%
  • Polyuria-38%
  • Tremor- 34%
  • Drowsiness-24%
  • Weight gain- 18%

Other effects

• Effect on kidneys • Endocrine changes- hypothyroidism • Hair loss • Rashes

​

43
Q

• Describe the major toxicities of these drugs LO

  1. Toxic effects of Lithium
  2. Treatment of Toxicity
A
  1. • Need to monitor blood levels closely
  • Vomiting
  • Diarrhoea
  • Coarse tremor
  • Dysarthria
  • Cognitive impairment
  • Restlessness
  • Agitation
  1. • Supportive measures
  • Anticonvulsants
  • Increase fluid intake / IV Fluids etc
  • Haemodialysis may be necessary

​

44
Q
  1. Give examples of Antiepileptics as Mood Stabilisers
  2. Evidence
A
  1. • Sodium Valproate
  • Lamotrigine
  • Carbamazepine
  • Consider issues in women of child bearing age – What might we use in these patients?
  1. • A 12 week , double- blind comparison ofmolanzapine v haloperidol in the treatment of acute mania. Arch Gen Psych 2003 60 1218-26 Tohen A

• Doses of carbamazepine and valproate in bipolar disorder. Psych Bull 1997 21 221-3 Taylor D

45
Q

Dementia Medication

A

Acetyl Cholinesterase Inhibitors
- Donepezil - Galantamine - Rivastigmine

NMDA antagonist
- Memantine

46
Q

Dementia Medication

  1. Give examples of Acetyl Cholinesterase Inhibitors
  2. Acetyl-choline plays a role in ?
  3. NICE guidance advices the medication to be available for ?
  4. Important side effects include:
A
    • Donepezil - Galantamine - Rivastigmine
  2. arousal, memory, attention and mood
  3. mild and moderate dementia (was only moderately severe before)
  4. Slows down progression of Alzheimer’s Disease
    • Nausea, vomiting, anorexia, diarrhoea
      - Fatigue, insomnia, headache
      - Bradycardia
      - Worsening of COPD
      - Gastric/duodenal ulcers
47
Q

Dementia Medication NMDA antagonist - Memantine

  1. Licensed for ?
  2. Usually well tolerated
  3. Common side effects include: ?
A
  1. moderate to severe dementia

2.

  1. hypertension, dyspnoea, headache, dizziness, drowsiness
48
Q

Depression

  1. Cause:
  2. Presentation:
  3. Diagnosis/Severity
  4. Management
A
  1. Theory of low serotonin production in brain
    + environmental triggers e.g. death, divorce, trauma + genetic susceptibility
  2. Mental - Low mood, anhedonia, fatigue, sleep disturbance, alcohol excess, suicidal thoughts.
    Physical (somatic) – pain, irritable bowel, loss of appetite, low libido, weight loss/gain
    • Becks depression Scale: mild/moderate/severe? Are activities of daily living affected?
    • Assess suicide risk? May need mental health act assessment/sectioning
      - Psychological therapy .g. Counselling/Cognitive behavioural therapy = first line
      - Antidepressants – first line = SSRI’s
49
Q

Antidepressants

  1. Indications
  2. Examples
A
  1. depression, anxiety, neuropathic pain
    • FIRST LINE = SSRI’s (serotonin selective reuptake inhibitor)
      - TCAs = Tricyclic Antidepressants
      - SNRI’s (serotonin/noradrenergic reuptake inhibitor)
      - MAOI’s (monoamine oxidase inhibitor)
      - Try one antidepressant for at least 6 weeks before switching to another
      - Even if feeling better it is recommended to continue for at least a year to reduce relapse risk
50
Q

SSRI’s – Serotonin Selective Reuptake Inhibitors

  1. Examples:
  2. Mechanism:
  3. Side effects:
  4. Serotonin Syndrome:
A
  1. Citalopram, fluoxetine
  2. Limiting reabsorption (reuptake) of serotonin into the presynaptic cell (neurone), increasing the level of serotonin in the synaptic cleft available to bind to the postsynaptic receptor and carry on action potential.
  3. Common - nausea, sexual dysfunction, insomnia
  4. life threatening presentation which occurs within a few weeks of initiating SSRI or when 2 used at once. Causes - tachycardia, sweating, dilated pupils, myoclonic, hyperreflexia, hyperthermia. Can lead to seizures, muscle breakdown and complications of hyperthermia.
51
Q

Tricyclic Antidepressants

  1. Examples:
  2. Uses:
  3. Mechanism:
  4. ADR:
  5. CAUTION:
A
  1. Amitriptyline
    • Depression - Neuropathic pain
  3. Act largely as SNRIs (serotonin noradrenaline reuptake inhibitors)
  4. All the following are quite common and due to anti muscarinic action: Dry mouth, dry nose, blurry vision, constipation (lowered gastrointestinal motility), urinary retention, cognitive and/or memory impairment, and increased body temperature.
    - CARDIOTOXIC: can result in life threatening inhibitors
    - NEUROTOXIC: seizures, hallucinations, delirium and coma
  5. Do not prescribe if suicidal ideation as tricyclics are lethal in overdose as wide range of toxic effects as described above.
52
Q

Antipsychotics can be separated into? Give examples for each.

A
53
Q

Side effects of Antipsychotics

A

NOTE: Clozapine can cause agranulocytosis resulting in neutropenia so requires FBC monitoring

54
Q

Extra-pyramidal side effects

Caused by? State the effects

A

All dopamine antagonists, however more prominent in the typical antipsychotics as these largely act on D2 receptors resulting in the below effects.

  1. Dystonia = sustained muscle contraction resulting in abnormal fixed posture
  2. Akathisia = internal feeling of restlessness
  3. Tardive dyskinesia = abnormal, involuntary, repetitive movements e.g. grimacing,
    sticking out the tongue or smacking of the lips
  4. Pseudo-parkinsonism = rigidity, tremor and increased tone
55
Q

Extra-pyramidal side effects

What is Neuroleptic Malignant Syndrome – ​

A

life threatening reaction within 2 weeks of initiating antipsychotics

characterised by: fever, altered mental status, muscle rigidity, and autonomic dysfunction (tachycardia, labile BP, flushing)

56
Q

Anxiolytics – Benzodiazepines

  1. Examples?
  2. Uses -
  3. Mechanism - Potentiate (increase) the action of GABA (main inhibitory neurone) - Increase opening of chloride channels – hyperpolarized membrane Nobody knows why this reduces anxiety ?overall increased depression of cortical transmission as it’s increasing the inhibitory neurotransmitter.
A
  1. Lorazepam, diazepam, midazolam
  2. Anxiolytic in the short term to treat anxiety (orally)
    - Anticonvulsant in acute seizure (IM, IV, buccal)
    - Sedative

NOTE: should only be used in short term as people become dependent (get withdrawal symptoms if stopped) and develop tolerance (need higher doses to have same effect.

Clinical Pharmacology, Therapeutics & Principles of Prescribing (19 decks)

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