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Year 3 - Psychiatry > Psychopharmacology 1 + 2 > Flashcards

Psychopharmacology 1 + 2 Flashcards

1
Q

• Discuss the use and adverse effects of psychiatric drugs

Identify general pharmacologic strategies

Discuss antidepressants including indications for use and side effects

Describe mood stabilizers including indications for use and side effects

Review antipsychotics including how to choose an antipsychotic and side effects (none is better than the other; chosen based on side effect profile)

Identify anxiolytic classes and indications for use

A

.

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2
Q

What conditions are indicated for antidepressant use (5)

A

Unipolar and bipolar depression

Organic mood disorders

Schizoaffective disorder

Anxiety disorders including OCD, panic, social phobia

PTSD

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3
Q

No antidepressant Is better than another. The choice is based on past history of the response to the drug, side effects experienced and co-existing conditions

How much time delay is there before symptoms improve with antidepressants?

A

3-6 weeks of continuous medication

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4
Q

Classes of antidepressants (5)

A

Tricyclic antidepressants (TCAs)

Monoamine Oxidase Inhibitors (MAOIs)

Selective Serotonin Reuptake Inhibitors (SSRIs)

Serotonin/Noradrenaline Reuptake Inhibitors (SNRIs) or dual reuptake inhibitors

Novel antidepressants

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5
Q

Mode of action of TCAs

A

Inhibit reuptake of amines, mostly noradrenaline or serotonin

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6
Q

Give examples of side effects of TCAs

  • antihistaminic
  • anticholinergic
  • antiadrenergic
A

Sedation, weight gain

Dry mouth, dry eyes, constipation, memory deficits

Orthostatic hypotension, sedation, sexual dysfunction

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7
Q

TCAs are effective but what are the disadvantages (3)

A

Bad side effects - ‘dirty’ drugs
Lethal if overdosed
Lengthens QT interval

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8
Q

Tertiary TCAs have amine side chains which make them prone to what

A

Read with other types of receptors –> MORE SIDE EFFECTS

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9
Q

Examples of

  • tertiary TCAs (primarily block serotonin receptors)
  • secondary TCAs (primary block NA receptors)
A

Amitriptyline
Imipramine
Doxepin
Clomipramine

Desipramine
Nortriptyline

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10
Q

Mode of action of monoamine oxidase inhibitors (MAOIs)

A

Bind irreversibly to monoamine oxidase which inhibits its activity, thus preventing the breakdown of monoamine neurotransmitters (such as norepinephrine, dopamine, serotonin) and thereby increasing their availability (increased synaptic levels of it)

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11
Q

Side effects of MAOIs

A 
Orthostatic hypotension, 
Weight gain, 
Dry mouth, 
Sedation, 
Sexual dysfunction
Sleep disturbance
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12
Q

Drug interactions of MAOIs

A

HYPERTENSIVE CRISIS if taken with tyramine rich foods, e.g. cheese, red wine, processed meats, beans

SEROTONIN SYNDROME (abdo pain, diarrhoea, sweating, tachycardia, hypertension, myoclonus) if taken with medications that increase serotonin

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13
Q

Examples of MAOIS

A 
Selegiline
Rasagiline
Isocarboxazid
Phenelzine
Tranylcypromine
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14
Q

Mode of action of SSRIs

A

Block presynaptic serotonin reuptake
(increasing the extracellular level of serotonin by limiting its reabsorption (reuptake) into the presynaptic cell, increasing the level of serotonin in the synaptic cleft available to bind to the postsynaptic receptor)

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15
Q

Side effects of SRRIs

A 
GI upset
Sexual dysfunction (+30%)
Anxiety
Restlessness
Nervousness
Insomnia
Fatigue or sedation
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16
Q

Advantage of SSRIs

A

Little risk of cardiotoxicity when overdosed

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17
Q

What can develop when SSRIs are stopped

A

Discontinuation syndrome (agitation, nausea, disequilibrium and dysphoria)

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18
Q

Examples of SSRIs

A 
Paroxetine
Sertraline
Fluoxetine
Citalopram
Escitalopram
Fluvoxamine
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19
Q

Pros and Cons of PAROXETINE

A

Pros

  • Short half life
  • No active metabolite so no build up of the drug
  • good sedating effect for initial relief from anxiety and insomnia

Cons

  • Antihistaminic (sedating, weight gain), anticholinergic (dry mouth/eyes etc) side effects
  • Likely to cause discontinuation syndrome
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20
Q

Pros and cons of SERTRALINE

A

Pros

  • weak cytochrome P450 interaction
  • short half life
  • less sedating than paroxetine

Cons

  • max absorption requires full stomach
  • increased GI side effects
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21
Q

Pros and cones of FLUOXETINE

A

Pros

  • long half life so lower incidence of discontinuation syndrome
  • good for those with non-compliance issues
  • initially activating (ACTIVATION SYNDROME) so may provide increased energy

Cons

  • long half life and active metabolite may build up
  • significant P450 interactions
  • initial activation can increase anxiety + insomnia
  • can induce mania
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22
Q

Mode of action of Serotonin/Norepinephrine reuptake inhibitors (SNRIs) [dual reuptake inhibitors]

A

Inhibit both serotonin and noradrenergic reuptake like the TCAS but without the antihistamine, antiadrenergic or anticholinergic side effects

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23
Q

What conditions are SNRIs used for

A

Depression
Anxiety
Maybe neuropathic pain

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24
Q

Examples of SNRIs

A

Venlafaxine

Duloxetine

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25
Q

Pros and cons of VENLAFAXINE

A

Pros

  • minimal drug interactions
  • short half life
  • fast renal clearance so avoids build up

Cons

  • can increase BP
  • nausea
  • bad discontinuation syndrome
  • prolongs QT interval
  • sexual dysfunction side effects
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26
Q

Pros and cons of DULOXETINE

A

Pros
-far less BP increase than velafaxine

Cons

  • CYP2D6 and CPY1A2 inhibitor
  • cannot break drug capsule as active ingredient unstable in stomach
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27
Q

Examples of novel antidepressants

A

Mirtazapine

Buproprion

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28
Q

For a patient presenting with depression associated with hypersomnolence, would be appropriate to give a less sedating SSRI

Name the less sedating ones (3)

A

Citalopram, Fluoxetine or Sertraline

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29
Q

If drug resistance occurs, what options are there?

A

Combine different antidepressants
Add lithium
Add atypical antipsychotic, e.g. quetiapine
ECT

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30
Q

What conditions are indicated for use of mood stabilisers

A

Bipolar affective disorder
Cyclothymia (alternating symptoms of depression and mania but not enough to be a major depressive episode or hypomania)
Schizoaffective disorders

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31
Q

Classes of mood stabilisers (3)

A

Lithium
Anticonvulsants
Antipsychotics

32
Q

Side effects of lithium*

*good mania and depression long term prophylaxis

A 
Fine tremor
Dry mouth
Altered taste
Increased thirst
Urinary frequency 
GI distress - reduced appetite, N/V, diarrhoea
Hypothyroidism
Leukocytosis
Hair loss, acne
Teratogenic - Ebstein's anomaly
Nephrotoxic so avoid other nephrotoxic drugs
33
Q

Blood therapeutic range of lithium should be between 0.6-1.2

Mild lithium toxicity = 1.5-2

What symptoms do you get?

A

vomiting, diarrhea, ataxia, dizziness, slurred speech, nystagmus

34
Q

Moderate lithium toxicity = 2-2.5

What symptoms do you get?

A

nausea, vomiting, anorexia, blurred vision, clonic limb movements, convulsions, delirium, syncope

35
Q

Moderate lithium toxicity = >2.5

What symptoms do you get?

A

generalized convulsions, oliguria and renal failure

36
Q

Name some anticonvulsants

A

Valproic acid
Carbamazepine
Lamotrigine

37
Q

Side effects of valproic acid

A

Thrombocytopenia and platelet dysfunction
Nausea, vomiting, weight gain
Sedation, tremor
Increased risk of neural tube defect (very little)
Hair loss

38
Q

Before starting any mood stabilisers, what baseline investigations should be done

A 
U+Es
LFTs - then 6 monthly
TFTs - then 6 monthly
FBC
Pregnancy test
39
Q

The anticonvulsant, carbamazepine, is the 1st line agent for treating (2)

A

Acute mania

Mania prophylaxis

40
Q

Side effects of carbamazepine

A

Rash - COMMONEST
Nausea, vomiting, diarrhea
Sedation, dizziness, ataxia, confusion
AV conduction delays

41
Q

Drugs that interact with carbamazepine and increase its level/toxicity

A

acetazolamide, cimetidine, clozapine, diltiazem, INH, fluvoxamine

erythromycin, clarithromycin, metronidazole

fluconazole, itraconazole, ketoconazole

42
Q

Side effects of lamotrigine

A

Nausea/vomiting
Sedation, dizziness, ataxia and confusion

If severe - TEN, SJS

43
Q

Drugs that interact with lamotrigine and increase its levels

A

Valproic acid

Setraline

44
Q

What does the term ‘rapid cycler’ mean

A

4 or more depressive or manic episodes/year

45
Q

What anticonvulsants are indicated for rapid cyclers (4 or more depressive or manic episodes/year)

A

Valproic acid

Carbamazepine

46
Q

Anticonvulsants often increase baseline LFTs but don’t need to change or stop drug unless

A

LFTs have tripled from baseline

47
Q

What conditions are indicated for antipsychotic use (5)

A 
Schizophrenia, 
Schizoaffective disorder, 
Bipolar disorder  
Psychotic depression, 
Augmenting agent in treatment resistant anxiety disorders
48
Q

Key pathways affected by dopamine in the brain (4)

A

Mesocortical
Mesolimbic
Nigrostriatal
Tuberoinfundibular

49
Q

Describe the mesocortical pathway

  • anatomy
  • gives rise to what kind of symptoms
  • too much or too little dopamine in this pathway in psychotic patients
A

Projects from the ventral tegmentum (brain stem) to the cerebral cortex.

Felt to be where the negative symptoms and cognitive disorders (lack of executive function) arise

Problem - TOO LITTLE dopamine

50
Q

Describe the mesolimbic pathway

  • anatomy
  • gives rise to what kind of symptoms
  • too much or too little dopamine in this pathway in psychotic patients
A

Projects from the dopaminergic cell bodies in the ventral tegmentum to the limbic system.

Where the positive symptoms come from (hallucinations, delusions, and thought disorders).

Problem - TOO MUCH dopamine

51
Q

Describe the nigrostriatal pathway

  • anatomy
  • regulation of what
  • what happens when this pathway degenerates
A

Projects from the dopaminergic cell bodies in the substantia nigra to the basal ganglia.

Pathway is involved in movement regulation.

Degeneration of substantia nigra –> decreased dopamine production –> dopamine hypoactivity –> cause Parkinsonian movements i.e. rigidity, bradykinesia, tremors, akathisia and dystonia.

52
Q

Describe the tuberoinfundibular pathway

  • anatomy
  • dopamine release in this pathway regulates what
  • what happens if dopamine is blocked in this pathway
A

Projects from the hypothalamus to the AP

Inhibits/regulates prolactin release.

Blocking dopamine in this pathway will predispose to hyperprolactinemia (gynecomastia/galactorrhea/decreased libido/menstrual dysfunction).

53
Q

If wanting to start an antipsychotic, ideally would start with a typical or atypical

A

Atypical

54
Q

‘Typical’ antipsychotics are D2 dopamine receptor antagonists

What side effect profile do these have?

A

Extrapyramidal side effects (due to excessive DA blockade)

  • akathasia - restless
  • parkinsonism - tremor, slow movements, rigid, stiffness
  • tardive dyskinesia - uncontrollable facial movements
  • acute dystonias - muscles involuntarily contract
55
Q

Examples of typical antipsychotics

A

High potency:

  • Fluphenazine,
  • Haloperidol,
  • Pimozide

Low potency:

  • Chlorpromazine,
  • Thioridazine
56
Q

Atypical antipsychotics are serotonin-dopamine 2 antagonists (SDAs)

‘Atypical’ because they affect dopamine AND serotonin neurotransmission in the 4 key dopamine pathways in the brain

What side effect profile do these have?

A 
Sedation
Weight gain
Hyperprolactinaemia
Drowsy
Agitated
Dry mouth
Blurred vision
Menstrual abnormalities
Hypotension
Abnormal LFTs
Hypertriglyceridemia, hypercholesterolemia, hyperglycemia
57
Q

Examples of atypical antipsychotics

A

Risperidone - can still cause akathisia EPSE despite being an atypical, hyperprolactin
Olanzapine*
Quetiapine*
Apriprazole - no weight gain, low sedation!

Clozapine - for treatment resistant patients

*can cause hypercholesterolaemia so avoid in those with high cholesterol

58
Q

Antipsychotic drug given for treatment resistant patients

A

Clozapine

59
Q

What is the only psychiatric emergency condition

A

Neuroleptic Malignant Syndrome (NMS)

-characterised by severe muscle rigidity, fever, altered mental status, autonomic instability

60
Q

To overcome extrapyramidal side effects of, usually, typical antipsychotics, what type of drug is given

A

Anticholinergics
Dopamine facilitators
Beta blockers

61
Q

What baseline bloods to do before starting an antipsychotic

A

Fasting lipid profile
Fasting blood sugar
LFTs
FBC

62
Q

What conditions are indicated for anxiolytic* use (3)

*not great

A

Panic disorder,
Generalized Anxiety disorder - used alongside SSRI or other
Substance-related disorders and their withdrawal, insomnias and parasomnias

63
Q

Example of an anxiolytic

A

Buspirone

64
Q

What conditions are indicated for benzodiazepine use (4)

A

Insomnia,
Parasomnias,
Anxiety
Withdrawal syndromes

65
Q

Side effects of benzodiazepines

A 
Somnolence
Cognitive deficits
Amnesia
Disinhibition
Tolerance
Dependence
66
Q

Examples of benzodiazepines

A

Diazepam

Lorazepam

67
Q

TRUE OR FALSE
A) Typical antipsychotics are more effective in controlling the positive symptoms of schizophrenia than the atypicals

B) Atypicals have less side-effects than the typicals

C) Atypicals cause no EPSE (extra-pyramidal side effects)

D) Only Clozapine has been shown to cause no Tardive Dyskinesia

E) Atypical Antipsychotics are only indicated in the treatment of schizophrenia

A 
F
F
F
T
F
68
Q

Only antipsychotic to not cause tardive dyskinesia

A

Clozapine

69
Q

Side effects of clozapine

A 
Neutropenia	   	   	
Seizures	   	   	
Idiopathic hyperthermia	   	   	
Weight gain	   	   	
Hypersalivation
70
Q

Psychiatric drugs can directly cause physical disease.

3 main conditions to be aware of:

A

Weight Gain and Obesity (esp clozapine + olanzapine)

Diabetes

Metabolic Syndrome (syndrome of Obesity, Hypertension, Dyslipidaemia and Abnormal Glucose Metabolism)
3 or more of:
-BP >130/85
-Serum HDL Cholesterol >1.04 (male) or >1.29 (female)
-Serum Triglyceride >1.69
-Fasting Glucose >6.1
-Waist Circumference >102cm (male) or >88cm (female)

71
Q

Cardiac effects of antipsychotics

A

Prolong QTc interval –> torsade de pointes

72
Q

Baseline tests before starting antipsychotics

A

BMI

ECG

73
Q

What to monitor for on ECG with antipsychotic use

A

QTC prolongation

74
Q

Lithium levels should be monitored how often

A

Weekly after initiation and after each dose change until concentrations are stable, then every 3 months for the first year

75
Q

Symptoms of lithium toxicity

A 
Vomiting and diarrhoea 
Coarse tremor (larger movements, especially of hands) 
Muscle weakness 
Lack of coordination including ataxia 
Slurred speech 
Blurred vision 
Lethargy 
Confusion 
Seizures

Year 3 - Psychiatry (7 decks)

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