pharmacology Flashcards
clinical uses of antidepressants
moderate to severe depression dysthymia generalised anxiety disorder panic disorder, OCD, PTSD premenstrual dysphoric disorder bulimia nervosa neuropathic pain
classes of antidepressants
monoamine oxidase inhibitors tricylics non-selective reuptake inhibitors selective serotonin repute inhibitors noradrenaline reuptake inhibitors atypical drugs
which neurotransmitters are targeted by antidepressants
noradrenaline
serotonin
dopamine
describe the monoamine hypothesis
depression results from a functional deficit of monoamine transmitters, in particular serotonin and noradrenaline, therefore most drugs that treat depression act to increase monoaminergic transmission
examples of monoamine oxidase inhibitors
phenelzine
moclobemide
how do MAO-Is work
inhibit the action of MOA
serotonin/noradrenaline is not broken down
more serotonin/noradrenaline available for transport
side effects of MOA-Is
hypertensive crisis potentiates actions of some other drugs insomnia postural hypotension peripheral oedema
what causes hypertensive crisis in MAO-Is and how can it be avoided
caused by inhibition of MAO-A in the gut by irreversible inhibitors preventing breakdown of dietary tyramine
avoid food like cheese, red wine, cured meats
examples of TCAs
imipramine
dosulepin
amitriptyline
lofepramine
mode of action of TCAs
block the reuptake of monoamines into presynaptic terminals
side effects of TCAs
anti-cholinergic S/Es sedation weight gain postural hypotension tachycardia arrhythmias cardiotoxic in OD
what are anti-cholinergic S/Es
blurred vision
dry mouth
constipation
urinary retention
examples of SSRIs
fluoxetine
citalopram/escitalopram
sertraline
paroxetine
mode of action of SSRIs
selectively inhibit reuptake of serotonin from the synaptic cleft
S/Es of SSRIs
nausea headache sweating vivd dreams worsened anxiety sexual dysfunction transient increase in self-harm/suicidal ideation in <25 years
mode of action of SNRIs
block reuptake of monoamines (noradrenaline and serotonin) into presynaptic terminals
examples of SNRIs
venlafaxine
duloxetine
SE of SNRIs
similar to SSRIs
more limited SEs than TCAs
examples of atypical antidepressant
mirtazapine
bupropion
mode of action of atypical antidepressant
mixed receptor effects
why can it be beneficial to give mirtazapine alongside an SSRI
can block serotenergic side effects
acute aims of bipolar treatment
reduce mood in episodes of mania
raise mood in episodes of depression
long term aims of bipolar treatment
stabilise mood and prevent recurrence of both mania and depression
SEs of lithium
dry mouth/strange taste polydipsia/polyuria tremor hypothyroidism reduced renal function nephrogenic DI weight gain
symptoms of lithium toxicity
vomiting diarrhoea ataxia/coarse tremor drowsiness convulsions coma
which anticonvulsants can be used as mood stabilisers
valproic acid
lamotrigine
carbamazepine
which antipsychotics can be used as mood stabilisers
quetiapine
aripiprazole
olanzapine
lurasidone
what is the usual first line treatment of depression
SSRIs
what factors should be considered when choosing an anti-depressant
previous response comorbidities and risk factors patient preference safety in pregnancy/breastfeeding treatment of specific symptoms risk of overdose patient's willingness to adhere to monitoring
how long do antidepressants typically take to work
2-6 weeks
what combination of drugs can be used to treat psychotic depression
antidepressant and antipsychotic
define nonresponse to an antidepressant
no response or inadequate response after 6 weeks at the maximum BNF dose or highest tolerated dose
how long should antidepressants be continued for after full resolution of symptoms
6-12 months after a first episode
12-24 months for a recurrence
indefinitely if after a third episode
what is the mainstay of treatment of bipolar disorder
mood stabilisers
eg lithium, anticonvulsants and antipsychotics
lamotrigine is good for which bipolar symptoms
bipolar depression
valproate is good for which bipolar symptoms
mania/hypomania
which class of drugs should be avoided in bipolar
antidepressants, unless short term in severe depressive episode and always with a mood stabiliser
why are antidepressant less effective in treating bipolar depression
they can cause switching to mania/hypomania or mood instability
why should SSRIs be taken in the morning
to reduce insomnia
which SSRI is safest to use in cardiac conditions
sertraline
which SSRI is safest in epilepsy
citalopram
which SSRI is associated with long QTc
citalopram
why should TCAs be taken at night
due to sedation
why should TCAs be avoided in patients with suicidal intent
cardiac toxicity in OD
what other uses are there for TCAs
neuropathic pain OCD anxiety disorders migraine prophylaxis nocturnal enuresis (bedwetting) cataplexy
what class of drug is mirtazapine
noradrenergic and specific serotenrgic antidepressant
when might mirtazapine be prescribed
insomnia
poor appetite
poor response to SSRI
which drugs can be used in combination with mirtazapine
SSRIs
venlafaxine
why should mirtazapine be taken at night
sedative effect
why should mirtazapine not be mixed with alcohol
causes GI upset
when should SNRIs be taken
in the morning to avoid insomnia
examples of irreversible MAOIs
phenelzine
isocarboxazid
examples of reversible MAOIs
moclobemide
what is the difference between reversible and irreversible MAOIs
irreversible ones permanently block the action of MAO to prevent break down of monoamines
therefore cause more side effects
reversible MAOIs cause less side effects but are less effective
why might there be difficulty with adherence in treatment with MOAIs
three times daily dosing
why can MAOIs cause hypertensive crisis
tyramine is a potent releaser of noradrenaline leading to elevated BP
if MAO-A is inhibited and a high-tyramine meal is taken, noradrenaline can accumulate and cause hypertensive crisis
symptoms of MAOI hypertensive crisis
headache
SOB
nosebleed
anxiety
examples of high tyramine foods
cheese red wine dried/smoked/fermented meats stock cubes pate black pudding caffeine soy/tofu
how is hypertensive crisis treated
phentolamine infusion
what is the most effective treatment for bipolar disorder
litium carbonate
when should lithium be taken
at night due to sedation
which drugs does lithium interact with
NSAIDs
ACEIs/ARBs
diuretics
which tests must be done before initiating lithium treatment
U+Es
TFTs
ECG
which tests should be done when stabilising lithium levels
lithium level (12 hours last dose) U+E every 5 days until lithium level stable within therapeutic range
how often should lithium levels and U+Es be monitored during treatment
every 3 months
how often should TFTs be monitored during treatment
every 6 months
should lithium be stopped if there is evidence of hypothyroidism
hypothyroidism is usually treated with levothyroxine rather than stopping lithium
warning signs of lithium toxicity
GI upset blurred vision coarse tremor ataxia drowsiness
signs of severe lithium toxicity
confusion LOC seizures coma death
causes of lithium toxicity
increased dose
dehydration (physical illness, lack of fluid intake, hot weather, alcohol, exercise)
drug interactions
reduction in salt intake
treatment of lithium toxicity
stop lithium
IV fluids
monitor renal function
may need dialysis in severe cases
when is semisodium valproate used
bipolar mania/hypomania
what type of drug is semisodium valproate
anticonvulsant
what is the mechanism of action of semisoidum valproate
blocks voltage sensitive sodium channels to increase levels of GABA
why should valproate be avoided in women of childbearing age
highly teratogenic (neural tube defects)
which tests should be done prior to starting valproate treatment
platelet count
LFTs
what type of drug is lamotrigine
anticonvulsant
when is lamotrigine used
treatment and prophylaxis of bipolar depression
antimanic ??
which serious side effect is associated with lamotrigine
stevens johnson syndrome
which atypical antipsychotics are available as depot IM preparations
risperidone
olanzapine
which tests should be done prior to starting atypical antipsychotics
BP weight lipids blood glucose ECG FBC, U+Es, LFTs
how often should monitoring be done on patients being treated with atypical antipsychotics
at one month
yearly thereafter
more often depending on results and risk factors
