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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

Psychiatry (63 decks)

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