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Y3 - psychiatry > psychopharmacology > Flashcards

psychopharmacology Flashcards

1
Q

general pharmacology strategies - indication

A

establish a diagnosis and identify the target symptoms that will be used to monitor therapy response

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2
Q

general pharmacology strategies - choice of agent and dosage

A

select an agent w/ an acceptable side effect profile and use the lowest effective dose

remember the delayed response for many psych meds and drug-drug interactions

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3
Q

general pharmacology strategies - management

A

adjust dosage for optumum benefit, safety and compliance

use adjunctive and combination therapies if needed however always strive for the simplest regime

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4
Q

indications for antidepressants

A

unipolar and bipolar depression

organic mood disorders

schizoaffective disorder

anxiety disorders incl OCD, panic, social phobia

PTSD

premenstrual dysphoric disorder and impulsively associated with personality disorders

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5
Q

how do antidepressants work

A

not fully understood

antidepressants increase levels of neurotransmitters (serotonin, noradrenalin) in the brain

increasing these neurotransmitters changes receptors in the brain

response rate of ~60-70% and NNT 3

takes a little while for response to occur

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6
Q

general guidelines for antidepressant use

A

antidepressant efficacy is similar (there isn’t any one that is much better than the others) so selection is based on past hx of a response, side effect profile and coexisting medical conditions

delay of ~2-4wks after a therapeutic dose is achieved before symptoms improve

if no improvement is seen after a trial of adequate length (at least 2mths) and adequate dose, either switch to another antidepressant or augment with another agent

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7
Q

antidepressant classifications

A

TCAs - tricyclics
MAOIs - monoamine oxidase inhibitors
SSRIs - selective serotonin reuptake inhibitors
SNRIs - serotonin/noradrenaline reuptake inhibitors
novel antidepressants

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8
Q

TCAs - how effective

A

very effective but potentially unacceptable side effect profile

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9
Q

side effect profile of TCAs and other problems

A

side effects: antihisatminic (weight gain, sleepy), anticholinergic (blurred vision)

lethal in overdose - even a one week supply

can cause QT lengthening, even at a therapeutic serum

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10
Q

how do TCAs work

A

increase both serotonin, dopamine and noradrenaline

hit a lot of different receptors

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11
Q

what are tertiary TCAs

A

have tertiary amine side chains

side chains are prone to cross react with other types of receptors –> more side effects

e.g. imipramine, amitriptyline, doxepin, clomipramine

have active metabolites incl desipramine and nortriptyline

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12
Q

what are secondary TCAs

A

often metabolites of 3y amines

primarily block noradrenaline

side effects are the same as 3y TCAs but generally are less severe

e.g. desipramine, nortriptyline

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13
Q

how to MAOIs work

A

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

very effective for resistant depression

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14
Q

side effects of MAOIs

A

orthostatic hypotension

weight gain

dry mouth

sedation

sexual dysfunction

sleep disturbance

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15
Q

MAOIs cheese reaction

A

hypertensive crisis can develop when MAOIs are taken with tyramine rich foods or sympathomimetics

can be fatal

  • restrict diet: cheese, red wine, some processed meats
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16
Q

MAOIs and serotonin syndrome

A

serotonin syndrome can develop if take MAOI w/ meds that increase serotonin or have sympathomimetic actions

also if using combination of antidepressants

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17
Q

symptoms of serotonin syndrome

A 
abdo pain 
diarrhoea 
sweats 
tachycardia 
HT
myoclonus 
irritability 
delirium

can lead to hyperpyrexia, CV shock and death

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18
Q

how do SSRIs work

A

block the presynaptic serotonin reuptake

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19
Q

what are SSRIs used for

A

treatment of anxiety and depressive sx

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20
Q

most common side effects of SSRIs

A 
GI upset
sexual dysfunction (30%)
anxiety
restlessness
nervousness
insomnia 
fatigue or sedation 
dizziness
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21
Q

other risks from SSRIs

A

very little risk of cardiotoxicity in overdose

can develop a discontinuation syndrome with agitation, nausea, disequilibrium and dysphoria - occurs when people stop them quickly

more common with shorter half life drugs, consider switching to fluoxetine - slowly reducing concentration and reduces problems

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22
Q

SSRIs and activation syndrome

A

caused by increased serotonin

can be distressing for patient

sx: increased anxiety, panic, agitation, nausea

typically lasts 2-10 days - warn patient

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23
Q

pros of sertraline

A

very weak P450 interactions, only slight CYP2D6 - less drug interactions

short half life with lower build up of metabolites - quick activating

less sedating when compared to paroxetine

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24
Q

cons of sertraline

A

max absorption requires a full stomach

increased number of GI adverse drug reactions

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25
Q

pros of fluoxetine (prozac)

A

long half life - decreased incidence of discontinuation syndromes, good for pts w/ medication noncompliance issues

initially activating - may provide increased energy

2y to long half life, can give one 20mg tab to taper someone off SSRI when trying to prevent discontinuation syndrome

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26
Q

cons of fluoxetine

A

long half life and active metabolite may build up - not good w/ hepatic illness

significant P450 interactions - not a good choice on pts already on a number of meds

initial activation may increase anxiety and insomnia

more likely to induce mania than some of the other SSRIs

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27
Q

what are SNRIs
how do they work
what are they used for

A

serotonin/noradrenaline reuptake inhibitors

inhibit both serotonin and noradrenergic reuptake like TCAs BUT w/o antihistamine/antiadrenergic/anticholinergic side effects

used for depression, anxiety and possibly neuropathic pain

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28
Q

pros of venlafaxine

A

minimal drug interactions and almost no P450 activity

short half life and fast renal clearance avoids build up - good for geriatrics

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29
Q

cons of venlafaxine

A

can cause a 10-15mmHg dose dependent increase in diastolic BP

may cause significant nausea, primarily w/ immediate release tabs

can cause a bad discontinuation syndrome, taper recommended after 2wks of use

QT prolongation

sexual side effects in >30%

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30
Q

duloxetine pros

A

some data to suggest efficacy for the physical symptoms of depression

far less BP increase as compared to venlafaxine - may change in time

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31
Q

duloxetine cons

A

CYP2D6 and CYP1A2 inhibitor

cannot break capsule as active ingredient not stable within stomach

higher drop out rate

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32
Q

what type of antidepressant is mirtazapine

A

novel

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33
Q

pros of mirtazapine

A

different mechanism of action may provide a good augmentation strategy to SSRIs

can be used as a hypnotic at lower doses 2y to antihitaminic effects

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34
Q

how does mirtazapine work

A

5HT2 and 5HT3 receptor antagonist

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35
Q

cons of mirtazapine

A

increases serum cholesterol by 20% in 15% of pts and triglycerides in 6% of pts

very sedating at lower doses
- at doses 30mg and above it can become activating and require change of administration time to the morning

associated w/ weight gain - esp at doses <45mg

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36
Q

how do we manage treatment resistant depression

A

combination of antidepressants e.g. SSRI/SNRI + mirtazepine

adjunctive treatment w/ lithium

adjunctive treatment w/ atypical antipsychotic e.g. quetiapine, olanzapine, aripiprazole

ECT

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37
Q

prophylaxis following treatment w/ antidepressants

A

1st episode - continue for 6-12mths
2nd episode - continue for 2yrs
3rd episode - discuss life long

american studies suggest:

  • stop before 6mths - 80% relapse
  • phrophylaxis >6mths - 20% relapse
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38
Q

management of anxiety

A

serotonergic anti-depressants e.g. SSRI/SNRI

tricyclic chlomipramine

adjunctive treatment: mainly antipsychotics e.g. risperidone, quetiapine

try and avoid symptomatic relief e.g. diazepam

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39
Q

indications for mood stabilisers

A

bipolar
cyclothymia
schizoaffective

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40
Q

classes of mood stabilisers

A

lithium
anticonvulsants
antipsychotics

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41
Q

how to choose which mood stabiliser

A

depends on what you are treating and the side effect profile

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42
Q

what is the only medication to reduce suicide rate

A

lithium

has been shown to reduce the rate of completed suicide in BAD by ~15%

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43
Q

when is lithium used as prophylaxis

A

effective in long term prophylaxis of both mania and depressive episodes in >70% of BAD pts

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44
Q

factors predicting positive response to lithium

A

prior long term response or family member with good response

classic pure mania

mania is follower by depression

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45
Q

what to do before starting lithium

A

baseline U+E and TSH

in women check a pregnancy test

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46
Q

risk of lithium use during pregnancy

A

during the first trimester is associated w/ Ebstein’s anomaly 1/1000
20x greater risk than in the general pop

47
Q

monitoring with lithium use

A

steady state acheived after 5 days

check 12 hrs after last dose

once stable check level 3mths
TSH and creatinine 6mths

goal: blood level 0.6-1.2

48
Q

lithium side effects

A

most common are GI distress incl reduced appetite, N+V, diarrhoea

thyroid abnormalities

nonsignificant leukocytosis

polyuria/polydipsia 2y to ADH antagonism

small number of pts - interstitial renal fibrosis

hair loss, acne

reduces seizure threshold, cognitive slowing, intention tremor

49
Q

lithium toxicity

A

mild (1.5-2) - vomiting, diarrhoea, ataxia, dizziness, slurred speech, nystagmus

moderate (2-2.5) - N+V, anorexia, blurred vision, clonic limb movements, convulsions, delirium, syncope

severe (>2.5) - generalised convulsions, oliguria, renal failure

50
Q

examples of anticonvulsants

A

valproic acid (Depakote)
carbamazepine (Tegretol)
lamotrigine (lamictal)

51
Q

effectiveness of valproic acid

A

as effective as lithium in mania prophylaxis

not as effective in depression prophylaxis

52
Q

factors predicting a +ve response to valproic acid

A

rapid cycling pts (F>M)

comorbid substance issues

mixed pts

pts w/ comorbid anxiety disorders

53
Q

how well tolerated is valproic acid

A

better tolerated than lithium

54
Q

what to do before starting valproic acid

A

baseline LFTs

pregnancy test

FBC

55
Q

why can valproic acid not be used in women of childbearing age

A

neural tube defects

increased risk 1-2% vs 0.14-0.2% in general population

2y to reduction in folic acid

56
Q

monitoring during valproic acid use

A

steady state achieved after 4-5days

check 12hrs after last dose and repeat CBC and LFTs

goal - target level 50-125

57
Q

valproic acid side effects

A

thrombocytopaenia and platelet dysfunction

N+V, weight gain

sedation, tremor

hair loss

58
Q

when is carbamazepine (Tegretol) indicated

A

1st line for acute mania and mania prophylaxis

indicated for rapid cyclers and mixed pts

59
Q

what to do before starting carbamazepine

A

baseline LFT, FBC, ECG

60
Q

monitoring during carbamazepine use

A

steady state acheived after 5 days

check 12hrs after last dose

repeat CBC and LFTs

goal - target levels 4-12mcg/ml

need to check level and adjust dosing ~1mth - induces own metabolism

61
Q

carbamazepine side effects

A

rash - most common SE

N+V, diarrhoea

sedation, dizziness, ataxia, confusion

AV conduction delays

aplastic anaemia and agranulocytosis (<0.002%)

water retention - vasopressin like effect –> hyponatraemia

drug-drug interactions

62
Q

indications for lamotrigine (lamictal)

A

indications similar to other anticonvulsants

also used for neuropathic/chronic pain

used more commonly as it doesn’t cause as many problems in women of childbearing age

SJS not as serious an issue

63
Q

what to do before starting lamotrigine

A

baseline LFTs

64
Q

initiation/titration of lamotrigine

A

start w/ 25mg daily for 2wks
then increase to 50mg for 2wks
then increase to 100mg

faster titration has a higher incidence of SJS

if the patient stops the med for ≥5 days, have to start at 25mg again

65
Q

lamotrigine side effects

A

N+V

sedation, dizziness, ataxia, confusion

stevens Johnson’s syndrome and toxic epidemal necrolysis

blood dyscrasias - rare

66
Q

severity of rash and severity of reaction w/ lamotrigine

A

severity/character of rash isn’t a good predictor of reaction severity

if any rash develops, immediately stop use

67
Q

what drugs increase lamotrigine levels and what do we do in these cases

A

VPA - doubles concentration, use slower dose titration

sertraline

68
Q

approved indications in bipolar disorder

A

aripiprazole (abilify) - manic, mixed, maintenance

risperidone (risperdal) - manic, mixed

quetiapine (seroquel) - manic, mainenance*
quetiapine modified release (XR) (seroquel XR) - manic, maintenance*, depressed
olanzapine (zyprexa) - manic, mixed, maintenance

69
Q

when are antipsychotics useful

A

acutely unwell pts when they are manic

also have a sedative effect

not as good for maintenance

70
Q

prophylaxis for bipolar disorder

A

generally lifelong

relapse is almost inevitable but impossible to predict when (could be mths or yrs)

71
Q

indications for antipsychotic use

A

schizophrenia
schizoaffective disorder
bipolar disorder for mood stabilisation and/or when psychotic features are present
psychotic depression
augmenting agent in treatment resistant depressive and anxiety disorders

72
Q

what is the mesocortical pathway

A

projects from the ventral tegmentum (brain stem) to the cerebral cortex

is felt to be where the -ve symptoms and cognitive disorders arise

problem in psychotic patients is too little dopamine

73
Q

what is the mesolimbic pathway

A

projects from the dopaminergic cell bodies in the ventral tegmentum to the limbic system

this is where the +ve symptoms come from (hallucinations, delusions, thought disorders)

problem in psychotic patients is there is too much dopamine

74
Q

what is the nigrostriatal pathway

A

projects from the dopaminergic cell bodies in the substantia nigra to the basal ganglia

involved in movement regulation

75
Q

effect of dopamine on acetylcholine activity

A

dopamine suppresses acetylcholine activity

76
Q

what is the result of dopamine hypoactivity in the nigrostriatal pathway

A

parkinsonian movements e.g. rigidity, bradykinesia, tremors

akathisia

dystonia

77
Q

what is the tuberoinfundibular pathway

what does blocking dopamine lead to

A

projects from the hypothalamus to the anterior pituitary

blocking dopamine in this pathway will predispose your patient to hyperprolactinaemia

78
Q

effect of dopamine on prolactin

A

dopamine release inhibits/regulates prolactin release

79
Q

result of hyperprolactinaemia

A

gynaecomastia

galactorrhea

decreased libido

menstrual dysfunction

80
Q

how do typical antipsychotics work

examples

A

D2 dopamine receptor antagonists

high potency typical antipsychotics bind to the D2 receptor w/ high affinity
- higher risk of extrapyramidal side effects

fluphenazine, haloperidol, pimozide

81
Q

low potency typical antipsychotics

example

A

less affinity for D2 receptors but tend to interact with nondopaminergic receptors resulting in more cardiotoxic and anticholinergic adverse effects e.g. sedation, hypotension

chlorpromazine

82
Q

how do atypical antipsychotics work

A

serotonin-dopamine 2 antagonists (SDAs)

considered atypical in the way they affect dopamine and serotonin neurotransmission in the 4 key dopamine pathways in the brain

83
Q

examples of atypical antipsychotics

A

risperidone (risperdal)
olanzaprine (zyprexa)
quetiapine (seroquel)
aripiprazole (abilify)

84
Q

risperidone

formation
effects

A

available in regular tablets, IM depot forms and rapidly dissolving tablet

functions more like a typical antipsychotic at doses >6mg

85
Q

side effects of risperidone

A

increased extrapyramidal side effects (dose dependent)

most likely atypical to induce hyperprolactinaemia

weight gain and sedation (dose dependent)

86
Q

olanzapine formation

A

regular tablets

immediate release IM

rapidly dissolving tablet

depot form

87
Q

olanzapine side effects

A

weight gain (up to 30-50lbs even with short term use)

may cause: hypertriglyceridaemia, hypercholesterolaemia, hyperglycaemia (even w/o weight gain)

may cause hyperprolactinaemia (< risperidone)

may cause abnormal LFTs (2%)

88
Q

quetiapine formation

A

regular tablet only

89
Q

quetiapine side effects

A

abnormal LFTs (6%)

weight gain (less than olanzapine)

hypertriglyceridaemia, hypercholesterolaemia, hyperglycaemia (even w/o weight gain) - less than olanzapine

most likely to cause orthostatic hypotension

90
Q

aripiprazole formation

A

regular tablets
immediate release IM
depot formation

91
Q

how does aripiprazole work

A

unique mechanism of action as a D2 partial agonist

92
Q

apiprazole side effects

A

low extrapyramidal side effects, no QT prolongation, low sedation

not associated w/ weight gain

could cause potential intolerability due to akathisia/activation

93
Q

aripiprazole interactions

A

CYP2D6 (fluoxetine and paroxetine) and 3A4 (carbamazepine and ketoconazole) interactions
- adjust dosing

94
Q

antipsychotic efficacy

A

no evidence to suggest difference between 1st line agents

choice based on side effect or preparation

general rule of 1/3 good response, 1/3 some response, 1/3 poor response

95
Q

what antipsychotic is used for treatment resistant patients

A

clozapine (clozaril)

96
Q

what classifies someone as treatment resistant on antipsychotics

A

they have tried one antipsychotic for at least 8 weeks and then a 2nd for the same period of time of treatment and neither have worked

97
Q

what formation is clozapine available in

A

regular tablet only

98
Q

why is clozapine reserved for treatment resistant patients

A

due to its side effect profile

but it is very effective

99
Q

clozapine side effects

A

associated w/ agranulocytosis (0.5-2%) - wkly bloods for 6mths then 2wkly tests for 6mths then monthly

increased risk of seizures (esp if also using lithium)

associated w/ the most sedation, weight gain and abnormal LFTs

increased risk of hypertriglyceridaemia, hypercholesterolaemia, hyperglycaemia, including nonketoic hyperosmolar coma and death, w/ or w/o weight gain

100
Q

efficacy of clozapine

A

general rule of 1/3s

101
Q

antipsychotic adverse effects

A

tardive dyskinesia

neuroleptic malignant syndrome

extrapyramidal side effects

102
Q

what is tardive dyskinesia

A

involuntary muscle movements that may not resolve w/ drug discontinuation e.g. tongue protruding, lip smacking, neck movements

risk ~5% per yr

esp w/ typical antipsychotics

103
Q

what is neuroleptic malignant syndrome

A

severe muscle rigidity

fever

altered mental status

autonomic instability

elevated WBC, CPK and LFTs

  • potentially fatal
104
Q

what are extrapyramidal side effects

A

acute dystonia

parkinson syndrome

akathisia

105
Q

agents for extrapyramidal side effects

A

anticholinergics e.g. benztropine, trihexyphenidyl, diphenhydramine
- need to watch for anticholinergic SE esp if taken w/ other meds w/ anticholinergic activity i.e. TCAs

dopamine facilitators e.g. amantadine

beta blockers e.g. propranalol

106
Q

anti-psychotic prophylaxis

A

life long relapse inevitable

commonest psychotic symptoms is lack of insight

people w/ psychotic illnesses relapse most commonly due to non-compliance

only 30% of pts take medication as prescribed

107
Q

level of functioning after schizophrenic episode

A

after 3rd episode of sz - clear link to reduced functioning, lower IQ and -ve symptoms

consider long acting IM

108
Q

what are anxiolytics used for

A

used to treat many diagnoses including panic disorder, GAD, substance related disorders and their withdrawal, insomnias and parasomnias

in anxiety disorders often use anxiolytics in combination w/ SSRIs or SNRIs for treatment

109
Q

what are benzodiazpines used for

A

used to treat insomnia, parasomnias and anxiety disorders

often used for CNS depressant withdrawal protocols e.g. alcohol withdrawal

110
Q

side effects of benzodiazepines

A 
somnolence
cognitive deficits
amnesia
disinhibition
tolerance
dependence
111
Q

examples of benzodiazepines and dosage

A

diazepam

chlordiazepoxide

doses of ~20mg, 4x/day OR 10mg PRN up to 8x/day

112
Q

different types of benzodiazepines

A
113
Q

important points about benzodiazapines

A

remember dependence develops

increased tolerance - people need more and more; also becomes less effective

try and reserve for short term use only e.g. emergency sedation and withdrawal states

for psychiatric disorder use meds which treat the underlying cause

Y3 - psychiatry (27 decks)

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