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Year 3 > Psycho-Pharmacology > Flashcards

Psycho-Pharmacology Flashcards

1
Q

list the indications for antidepressants

A
  • Unipolar and bipolar depression
  • Organic mood disorders
  • Schizoaffective disorder
  • Anxiety disorders including OCD
  • Panic
  • Social phobia
  • PTSD
  • Premenstrual dysphoric disorder
  • Impulsivity associated with personality disorders
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2
Q

on the 1st, 2nd and 3rd episode of depression how long would you continue antidepressants?

A

1st - 6months - year
2nd - 2 years
3rd - lifelong

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3
Q

what side effects may TCAs have?

A

antihistiminic
anticholinergic
antiadrenergic

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4
Q

why are TCAs only dispensed in small amounts?

A

lethal in OD of even just 1 week supply

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5
Q

what ECG change can TCAs cause?

A

QT lengthening

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6
Q

what are tertiary TCAs, why may they have more side effects?

A

tertiary amine side chains

cross react with other types of receptors

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7
Q

give 4 examples of tertiary TCAs

A

imipramine, amitriptyline, doxepin and clomipramine

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8
Q

name two active metabolites of tertiary TCAs

A

desipramine and nortriptyline

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9
Q

what are secondary TCAs?

A

often metabolites of tertiary amines that primarily block noradrenaline

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10
Q

name two secondary TCAs

A

desipramine and nortriptyline

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11
Q

compared with tertiary TCAs what are the SEs of secondary TCAs like?

A

same but generally less severe

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12
Q

describe the MoA of MAOIs

A

MAOIs bind irreversible to monoamine oxidase thereby preventing the inactivation of amines such as
norepinephrine, dopamine and serotonin leading to increased synaptic levels.

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13
Q

what are MAOIs useful for treating?

A

resistant depression

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14
Q

list the side effects of MAOIs

A

orthostatic hypotension, weight gain, dry mouth,

sedation, sexual dysfunction and sleep disturbance.

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15
Q

what is the Cheese Reaction?

A

Hypertensive crisis can develop when MAOIs are

taken with tyramine-rich foods or sympathomimetics

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16
Q

how may serotonin syndrome develop?

A

if an MAOI is taken alongside medications that increase serotonin or have sympathomimetic actions

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17
Q

symptoms of serotonin syndrome

A

abdo pain, diarrhoea,

sweats, tachycardia, HTN, myoclonus, irritability, delirium

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18
Q

what can serotonin syndrome lead to?

A

hyperpyrexia, cardiovascular

shock and death

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19
Q

how long must you wait when switching from an SSRI to an MAOI (excluding fluoxetine)?

A

2 weeks

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20
Q

how long must you wait when switching from fluoxetine to an MAOI and why?

A

5 weeks - long half life

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21
Q

what do SSRIs do?

A

block presynaptic serotonin reuptake

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22
Q

what are SSRIs used for?

A

anxiety and depression

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23
Q

what are the most common SEs of SSRIs?

A

GI upset, sexual dysfunction (30% +), anxiety,

restlessness, nervousness, insomnia, fatigue or sedation, dizziness.

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24
Q

what may stopping SSRIs cause? what is this?

A

Discontinuation syndrome results in agitation, nausea, disequilibrium and dysphoria.

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25
Q

when starting SSRI patients may experience symptoms. what are these and how long does it normally last?

A

Activation syndrome results from an increased serotonin that can be depressing for the patient.
Nausea, increased anxiety, panic and agitation are common symptoms. These typically last 2-10 days
so always warn the patient.

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26
Q

activation and discontinuation syndrome are both more common with what kind of SSRIs? what may you give instead?

A

short half life drugs

fluoxetine

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27
Q

give examples of SSRIs

A 
paroxetine
sertaline
fluoxetine (prozac)
citalopram
escitalopram
fluvaxamine
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28
Q

discuss paraxetine

A

This drug has a short half-life with no active metabolites. This means there is no build-up which is good
if hypomania develops. It has sedating properties (dose taken at night) and offers good initial relief
from anxiety and insomnia. likely to cause discontinuation syndrome

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29
Q

what side effects are associated with paroxetine?

A

sedation
weight gain
anticholinergic

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30
Q

discuss sertraline

A

Sertraline has very weak interactions with P450 enzymes, only slightly with CYP2D6. It has a short halflife
with lower build-up of metabolites. It is less sedating when compared to paroxetine. For max
absorption it is necessary to take on a full stomach which may be problematic in some patients. There
is also an increased number of GI adverse drug reactions.

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31
Q

discuss fluoxetine

A

Fluoxetine has a long half-life and as a result there is decreased incidence of discontinuation
syndromes. It is good for patients with medication noncompliance issues. Initially activating so may
provide increased energy. Secondary to its long half-life, you can give one 20mg tablet to taper
someone off an SSRI to try and prevent SSRI discontinuation syndrome.
Its long half-life and active metabolites may result in build up, so it is not a good choice in patients
with hepatic illness. It has significant interaction with P450, so it may not be a good choice in patients
already on a number of different medication. Initial activation may cause an increase in anxiety and
insomnia. It is more likely to induce mania than some of the other SSRIs.

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32
Q

compared to other SSRIs fluoxetine is more likely to induce what?

A

mania

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33
Q

discuss citalopram

A

Citalopram has a low inhibition of P450 enzymes and as such there are fewer drug-drug interactions.
Its half-life is intermediate. Doses >40mg/day are not recommended as there is dose-dependent QT
prolongation with doses between 10 and 30 mg. it can be sedating as it has mild antagonism at H1
receptors. It has some GI SEs, but these are less than sertraline.

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34
Q

discuss escitalopram

A

This is the s-enantiomer of the racemic derivative citalopram. Escitalopram has a low overall inhibition
of P450s and as such there are fewer drug-drug interactions. Its half-life is intermediate. Due to acute
response and remission it is more effective than citalopram. There is dose dependent QT interval
prolongation with doses of 10-30mg daily. Nausea and headache is associated.

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35
Q

discuss fluvoxamine

A

This has the shortest half-life and has been found to possess some analgesic properties.

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36
Q

what side effects are associated with fluvoxamine?

A

GI distress
headaches
sedation
weakness

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37
Q

fluvoxamine is a strong inhibitor of what enzymes?

A

CYP1A2

CYP2C19

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38
Q

discuss SNRIs

A

These drugs inhibit both serotonin and noradrenergic reuptake like the TCAs but without the
antihistamine, antiadrenergic and anticholinergic SEs.

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39
Q

what are SNRIs used for?

A

depression
anxiety
neuropathic pain

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40
Q

give 2 examples of SNRIs

A

venlafaxine

duloxetine

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41
Q

discuss venlafaxine

A

There is minimal drug interactions and almost no P450 activity. It has a short half-life and fast renal
clearance avoids build up. Therefore, this is a good drug for geriatric populations. However, it can
cause a 10-15 mmHg dose dependent increase in diastolic BP

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42
Q

what SE are associated with venlafaxine

A

significant nausea
bad discontinuation syndrome
QT prolongation
sexual

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43
Q

discuss duloxetine

A

There is some data to suggest that there is efficacy for the physical symptoms of depression. Thus far
there is less BP increase when compared to venlafaxine, however this may change with time. It is a
CYP2D6 and CYP1A2 inhibitor. You cannot break the tablet as the active ingredient is not stable within
the stomach. In a pooled analysis there was a high dropout rate with people taking duloxetine.

44
Q

name two novel antidepressants

A

mirtazapine

bupropion

45
Q

mirtazapine is useful for augmenting what other drug?

A

SSRIs

46
Q

MoA of mirtazapine

A

5HT2 and 5HT3 receptor antagonist

47
Q

SE of mirtazapine

A

very sedating at low dose
activating at high
increased serum cholesterol
increased triglycerides

48
Q

MoA of bupropion

A

reuptake inhibition of dopamine and NE

49
Q

what is bupropion NOT associated with?

A

weight gain
sexual SE
sedation
cardiac interactions

50
Q

bupropion may induce what?

A

mania

51
Q

bupropion is a 2nd line therapy in what?

A

ADHD

52
Q

in high doses bupropion may cause what?

A

increased seizure risk

53
Q

bupropion should be avoided in patients with what?

A

TBI
bulimia
anorexia

54
Q

why should bupropion not be used to treat anxiety?

A

causes anxiety, agitation and insomnia

55
Q

why does bupropion have a potential for abuse?

A

psychotic symptoms in high doses

56
Q

list the indications for mood stabilisers

A

bipolar
cyclothymia
schizoaffective disorders

57
Q

name 3 classes of mood stabilisers

A

lithium
anticonvulsants
antipsychotics

58
Q

lithium is the only medication to reduce what?

A

suicide rate

59
Q

list the factors predicting a positive response to lithium

A
  • Prior long-term response or family member with good response
  • Classic pure mania
  • Mania is followed by depression
60
Q

before starting lithium treatment what investigations must be done?

A

U+E
TSH
Pregnancy test

61
Q

taking lithium during the first trimester is associated with what?

A

Ebstein’s anomaly

62
Q

describe the monitoring of lithium

A

steady state should be achieved
after 5 days so check 12 hrs after last dose. Once stable check level 3 months and TSH and creatinine
after 6. Goal should be a blood level between 0.6-1.2.

63
Q

list the SE of lithium

A

• Most common are GI distress including reduced appetite, nausea/vomiting, diarrhoea
• Thyroid abnormalities
• Non-significant leucocytosis
• Polyuria/dysdyspia secondary to ADH antagonism. In a smaller number of patients can cause
interstitial renal fibrosis
• Hair loss, acne
• Reduces seizure threshold, cognitive slowing, intention tremor

64
Q

discuss lithium toxicity (mild, moderate, severe)

A

• Mild – levels 1.5-2.0
o Vomiting, diarrhoea, ataxia, dizziness, slurred speech, nystagmus
• Moderate – 2.0-2.5
o Nausea, vomiting, anorexia, blurred vision, clonic limb movements, convulsions,
delirium, syncope
• Severe – >2.5
o Generalised convulsions, oliguria, and renal failure

65
Q

give examples of anticonvulsants

A

valproic acid (depakote)
carbamazepine (tegretol)
lamotrigine (lamictal)

66
Q

factors predicting a positive response to valproic acid

A
  • Rapid cycling patient (F>M)
  • Comorbid substance issues
  • Mixed patients
  • Patients with comorbid anxiety disorders
67
Q

valproic acid is often more tolerated than?

A

lithium

68
Q

before valproic acid is started what investigations must be done?

A

baseline LFTs, pregnancy, FBC

69
Q

discuss valproic acid monitoring

A

A steady state achieved after 4-5 days check 12 hours

after the last dose and repeat CBC and LFTs. Goal is a target level between 50-125.

70
Q

side effects of valproic acid

A

• Thrombocytopenia and platelet dysfunction
• Nausea, vomiting, weight gain
• Sedation, tremor
• Increased risk of neural tube defect 1-2% vs 0.14-0.2% in general population secondary to
reduction in folic acid
• Hair loss

71
Q

carbamazepine is the first line treatment for?

A

acute mania and mania prophylaxis

72
Q

carbamazepine is indicated for what kind of patients?

A

rapid cyclers and mixed patients

73
Q

before carbamazepine is started what investigations must be done?

A

LFTs
FBC
ECG

74
Q

discuss carbamazepine monitoring

A

A steady state
is achieved after 5 days so check 12 hours after last does and repeat CBC and LFTs. Goal is target levels
of 4-12mcg/ml. need to check level and adjust dosing after around a month because it induces its own
metabolism.

75
Q

SE of carbamazepine

A
  • Rash – most common SE seen
  • Nausea, vomiting, diarrhoea
  • Sedation, dizziness, ataxia, confusion
  • AV conduction delays
  • Aplastic anaemia and granulocytosis (<0.002%)
  • Water retention due to vasopressin like effect which can result in hyponatremia
  • Drug-drug interactions – don’t need to know but check BNF
76
Q

what can lamotrigine also be used for?

A

neuropathic/chronic pain

77
Q

before lamotrigine what tests must be done?

A

LFTs

78
Q

discuss lamotrigine dosing

A

Indication/titration: start with 25mg daily x2 weeks then
increase to 50mg x2 weeks then increase to 100mg – faster titration has a higher incidence of serious
rash. If the patient stops the medication for 5 days or more then you have to start again at 25mg.

79
Q

SE of lamotrigine

A

• Nausea and vomiting
• Sedation, dizziness, ataxia, confusion
• The most severe
o Toxic epidermal necrolysis and Stevens Johnson’s syndrome
§ The character/severity of the rash is not a good predictor of severity of
reaction. Therefore, if any rash develops, discontinue use immediately
• Blood dyscrasias have been seen in rare cases
• Drugs that increase lamotrigine levels
o VPA – doubles concentration so use slower dose titration
o Sertraline

80
Q

what are the indications for antipsychotics?

A

• Schizophrenia
• Schizoaffective disorder
• Bipolar disorder – mood stabilisation and/or when psychotic features are present
• Psychotic depression
Augmenting agent in treatment resistant anxiety disorders

81
Q

name the key dopamine pathways

A

mesocortical
mesolimbic
nigrostriatal
tuberoinfundibular

82
Q

discuss the mesocortical pathway

A

Projects from the ventral tegmentum (brain stem) to the cerebral cortex. This pathway is felt to be
where the negative symptoms and cognitive disorders (lack of executive function) arise. Problem here
for psychotic patient is too little dopamine. Reduced IQ, reduced socialisation.

83
Q

discuss the mesolimbic pathway

A

Projects from the dopaminergic cell bodies in the ventral tegmentum to the limbic system. This
pathway is where the positive symptoms come from (hallucinations, delusions, and though disorders).
Problem here in a psychotic patient is there is too much dopamine.

84
Q

discuss the nigrostriatal pathway

A

Projects from the dopaminergic cell bodies in the substantia nigra to the basal ganglia. This pathway
is involved in movement regulation. Remember that dopamine suppresses acetylcholine activity.
Dopamine hypoactivity can cause Parkinsonian movements (i.e. rigidity, bradykinesia, tremors),
akathisia and dystonia.

85
Q

discuss the tubuloinfundibular pathway

A 
Projects from the hypothalamus to the anterior pituitary. Remember that dopamine release
inhibits/regulates prolactin release. Blocking dopamine in this pathway will predispose your patient
to hyperprolactinaemia (gynaecomastia/galactorrhoea/decreased libido/menstrual dysfunction).
86
Q

give examples of high potency typical antipsychotics

A

fluphenazine
haloperidol
pimozide

87
Q

MoA of typical antipsychotics

A

D2 recepto antagonists

88
Q

typical antipsychotics that bind to D2 receptor with high affinity, this results in?

A

higher risk of extrapyramidal and sexual side effects

89
Q

typical antipsychotics that bind to D2 receptor with low affinity, this results in?

A

tend to interact with
nondopaminergic receptors resulting in more cardiotoxic and anticholinergic adverse effects including
sedation, hypotension.

90
Q

give examples of low potency typical antipsychotics

A

chlorpromazine

thioridazine

91
Q

MoA of atypical antipsychotics

A

serotonin dopamine 2 antagonists

92
Q

why are atypical antipsychotics considered atypical?

A

in the way
they affect dopamine and serotonin neurotransmission in the four key dopamine pathways in the
brain

93
Q

atypicals tend not to cause what?

A

extrapyramidal SE
weight gain
increased cholesteral
T2DM

94
Q

give examples of atypicals

A 
risperidone
olazapine
quetiapine
aripiprazole
clozapine
95
Q

discuss risperidone

A

Available in regular tablets, IM depot forms and rapidly dissolving tablet. It functions more like a
typical antipsychotic at doses greater than 6mg. Increased extrapyramidal side effects are dose
dependent. Most likely atypical to induce hyperprolactinemia. Weight gain and sedation is dosage
dependent.

96
Q

discuss olanzapine

A

Available in regular tablets, immediate release IM, rapidly dissolving tablet, depo form. Weight gain
which can be as much as 30-50lbs with even short-term use. May cause hypertriglyceridemia,
hypercholesterolemia, hyperglycaemia even without weight gain. May cause hyperprolactinaemia (<
risperidone). In 2% of all patients it will cause abnormal LFTs.

97
Q

discuss quetipine

A

Available in regular tablet form only. In 6% of patients it will cause abnormal LFTs. May be associated
with weight gain though less than with olanzapine. May cause hypertriglyceridemia,
hypercholesterolemia, hyperglycaemia (even without weight gain), however less than olanzapine.
Most likely to cause orthostatic hypotension.

98
Q

discuss aripiprazole

A

Available in regular tablets, immediate release IM formulation and depo form. It is unique in
mechanism of action as a D2 partial agonist. Low EPS, no QT prolongation, low sedation. CYP2D6
(fluoxetine and paroxetine), 3A4 (carbamazepine and ketoconazole) interactions that the
manufacturer recommends adjusted dosing. Could cause potential intolerability due to
akathisia/activation. Not associated with weight gain.

99
Q

discuss clozapine

A

Available in 1 form a regular tablet. Is reserved for treatment resistant patients because of the side
effects but it does work. Associated with agranulocytosis (0.5-2%) and therefore requires weekly
blood draws x6 months, then Q 2 weeks x 6 months. Increased risk of seizures (especially if lithium is
also on board). Associated with the most sedation, weight gain and abnormal LFTs. Increased risk of
hypertriglyceridemia, hypercholesterolemia, hyperglycaemia, including nonketotic hyperosmolar
coma and death with and/or without weight gain.

100
Q

what are the antipsychotic adverse effects?

A

Tardive dyskinesia (TD) is involuntary muscle movements that may not resolve with drug
discontinuation. The risk of this is approximately 5% per year.
Neuroleptic malignant syndrome (NMS) characterised by severe muscle rigidity, fever, altered mental
status, autonomic instability, elevated WBC, CPK and LFTs. It is potentially fatal.
Extrapyramidal side effects (EPS) include acute dystonia, Parkinson syndrome and akathisia.

101
Q

how may you treat extrapyramidal side effects?

A 
• Anticholinergics
o Benztropine, trihexyphenidyl, diphenhydramine
• Dopamine facilitators
o Amantadine
• Beta-blockers
o Propranolol
• Need to watch for anticholinergic SE particularly if taken with other medicines with
anticholinergic activity i.e. TCAs
102
Q

what can anxiolytics be used for?

A

panic disorder, generalised anxiety disorder,

substance related disorders and their withdrawal, insomnias, and parasomnias.

103
Q

in anxiety disorders anxiolytics are often used in combination with?

A

SSRIs or SNRIs

104
Q

discuss buspirone

A

This is a good drug for augmenting therapy. It is a 5HT1A agonist. It works independent of endogenous
release of serotonin. It is not associated with sedation.
However, it takes around 2 weeks before patients will notice any difference. It will not reduce anxiety
in patients that are used to taking benzodiazepines as there is no sedation to “take the edge off”.

105
Q

what are benzos used for?

A

insomnia
parasomnia
anxiety disorder

106
Q

SE of benzos

A
  • Somnolence
  • Cognitive deficits
  • Amnesia
  • Disinhibition
  • Tolerance
  • Dependence

Year 3 (164 decks)

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