BPAD maudsley

Lithium is the second element of the periodic table, in the same column as hydrogen and sodium.

Lithium can increase intracellular concentrations of sodium and calcium in people with bipolar illness.

Glycogen synthase kinase 3 (GSK3) is not a potential mechanism of action of lithium.

Lithium has been shown to inhibit the creation of new neurons in the hippocampus.

Lithium has no neuroprotective effects.

Lithium is only present in high levels in the environment.

The BAP guidelines suggest that in the event of relapse, a non-urgent plasma lithium level should be obtained to indicate the level of compliance with lithium therapy.

Lithium is only effective in treating manic episodes but not depressive episodes in bipolar disorder.

The aim of maintenance treatment of bipolar disorder is to achieve partial remission of both manic and depressive episodes.

Lithium augmentation of selective serotonin reuptake inhibitors (SSRIs) is most effective at a lithium plasma level of 0.4-0.6 mmol/L.

Lithium has been shown to be ineffective in preventing relapses that require hospitalization in unipolar depression.

A head-to-head trial of lithium versus quetiapine augmentation in treatment-resistant depression is not underway and will not report in 2021.

Lithium has been proposed to treat patients with unipolar depression who have suffered at least three depressive episodes in 5 years.

The optimal plasma level range for lithium prophylaxis is 0.4-0.6mmol/L.

Lithium can cause an increase in the white blood cell (WBC) count in patients not receiving clozapine.

The target plasma level range for prophylaxis in patients who have unipolar depression is 0.6-0.8mmol/L.

Blood samples for plasma lithium level estimations should be taken 10-14 hours post dose in patients who are prescribed a twice daily dose of a prolonged release preparation.

Lithium citrate liquid is available in three strengths.

Lithium levels of >1.2 mmol/L are associated with a higher risk of renal toxicity.

Renal effects of lithium treatment can be irreversible after long-term treatment (>10 years).

Lithium toxicity reliably occurs at levels >2.5 mmol/L.

Thyroid function tests (TFTs) should be checked every 3 months in patients on lithium treatment.

Lithium treatment can increase the risk of hypoparathyroidism.

Lithium is contraindicated in women of child-bearing age.

The use of automated reminder systems has been shown to worsen monitoring rates.

Discontinuing lithium treatment abruptly may worsen the natural course of bipolar illness.

The risk of relapse can be reduced by increasing the dose rapidly over a period of at least a month.

Patients who had been in remission for at least 2 years and had discontinued lithium very slowly had a lower recurrence rate than those who continued lithium.

A quarter of patients prescribed lithium took almost all of their prescribed doses.

One in five patients prescribed long-term lithium treatment had a plasma level below the therapeutic range.

ACE inhibitors can increase renal sodium reabsorption by the kidney, resulting in a decrease in lithium plasma levels.

The risk of lithium toxicity is decreased in patients with heart failure, dehydration, and renal impairment.

Angiotensin II receptor antagonists do not require frequent monitoring of eGFR and plasma lithium when co-prescribed with lithium.

The full effect of ACE inhibitors on lithium plasma levels can be seen immediately after co-prescription.

ACE inhibitors can precipitate renal failure when co-prescribed with lithium.

Elderly patients have a decreased risk of hospitalization due to lithium toxicity when taking ACE inhibitors.

Trandolapril is not an ACE inhibitor.

The combination of lithium and loop diuretics is generally well-tolerated without any significant interactions.

All NSAIDs can be purchased over-the-counter without a prescription.

The risk of an interaction between lithium and loop diuretics is greatest after a year of co-prescription.

Valproate's mechanism of action is fully understood and involves only one or two pathways.

Thiazide diuretics can reduce the renal clearance of lithium, but the effect is always less than 25%.

Carbamazepine does not cause hyponatraemia, which can lead to lithium retention and toxicity.

The combination of lithium and COX-2 inhibitors has no potential for interaction and does not require increased plasma lithium monitoring.

Valproic acid is responsible for the pharmacological activity of sodium valproate and semi-sodium valproate.

A dose of sodium valproate is equivalent to a dose of semi-sodium valproate.

Valproate has been shown to be more effective than olanzapine in the treatment of acute mania.

A 2020 meta-analysis placed divalproex as the most effective treatment for bipolar depression.

RCT data have shown that valproate is effective in the prophylaxis of bipolar affective disorder.

Patients with rapid cycling illness had a better response to olanzapine than to valproate in a post hoc analysis.

Valproate has been shown to inhibit histone deacetylase, which may confer some effects on neuroplasticity.

Valproate is recommended as a first-line option for the treatment of acute episodes of depression in women of child-bearing potential.

The BALANCE study found valproate to be numerically superior to lithium in treating bipolar disorder.

Aripiprazole alone is superior to valproate alone in treating bipolar disorder.

The Cochrane review found strong evidence to support the use of valproate as prophylaxis.

Valproate is commonly used to treat anxiety disorders.

The use of valproate has decreased in recent years due to the increased use of lithium.

Risperidone augmented with valproate is superior to risperidone alone in reducing hostility in patients with schizophrenia.

Valproate is sometimes used to treat aggressive behaviors of variable etiology.

The NICE recommends valproate as a first-line option for the treatment of acute episodes of mania.

Valproate serum levels of $50mg/L are associated with the most robust response in acute mania.

Plasma level monitoring is of more limited use with valproate than with lithium or carbamazepine.

Starting doses of valproate above $500mg/day can occasionally cause lethargy and confusion.

Optimal serum levels during the maintenance phase of valproate treatment are known to be at least $75mg/L.

Valproate can cause both gastric irritation and hyperkalemia, leading to nausea.

Valproate is associated with an increased risk of suicidal behavior in all patients.

The once daily Chrono form of sodium valproate produces higher peak plasma levels than the conventional formulation.

Valproate is eliminated mainly through the liver.

NICE recommends valproate as a first-line option for the treatment of acute episodes of depression in women of child-bearing potential.

The risk of unplanned pregnancy is likely to be below population norms in women with mania who are taking valproate.

The therapeutic range of carbamazepine when used as an antiseizure medication is generally considered to be 4-6mg/L

Carbamazepine is not considered to be a hepatic enzyme inducer

The initial plasma half-life of carbamazepine is around 12 hours

Carbamazepine has been shown to be effective in the management of alcohol withdrawal symptoms, and the evidence is strong enough to support its use for this indication

Around 10% of patients treated with carbamazepine develop a generalised erythematous rash

Carbamazepine has been implicated in an increased risk of suicidal behaviour in patients with bipolar illness.

NICE recommends repeating urea and electrolytes, full blood count, and liver function tests after 3 months of carbamazepine treatment.

Valproate can decrease the plasma levels of some drugs by inhibition of glucuronidation.

The anticonvulsant activity of carbamazepine is increased by drugs that lower the seizure threshold.

Carbamazepine is licensed for the treatment of bipolar illness in patients who respond to lithium.

Carbamazepine is a potent inhibitor of hepatic cytochrome enzymes and is metabolised by CYP3A4.

Valproate is highly protein bound and can be displaced by other protein bound drugs such as warfarin.

A dose of at least 100mg aspirin is required to inhibit the metabolism of valproate.

The risk of unplanned pregnancy is below population norms in women with mania who are sexually disinhibited.

Oxcarbazepine, a structural derivative of carbamazepine, only blocks voltage-dependent sodium channels.

Olanzapine/fluoxetine in combination is licensed for maintenance treatment in the European Union.

Risperidone has been shown to be superior to lithium in mania treatment according to network meta-analyses.

The combination of antipsychotics with mood stabilizers is associated with fewer side effects than monotherapy with either medication.

First-generation antipsychotics are less likely to cause depression than haloperidol in bipolar disorder.

The use of first-generation antipsychotic depots is well-supported by robust evidence in bipolar disorder.

Aripiprazole is not effective in acute treatment of mania as an add-on agent.

Quetiapine is not effective in the acute treatment of bipolar depression.

Asenapine is not associated with weight gain and metabolic disturbance.

Aripiprazole LAI is not effective for prophylaxis in bipolar 1 disorder.

Olanzapine is not effective in the acute treatment of bipolar depression when combined with fluoxetine.

Paliperidone LAI is effective in the maintenance treatment of bipolar disorder.

Lurasidone is not effective in the acute treatment of bipolar depression.

Cariprazine is not effective in the acute treatment of bipolar depression.

Aripiprazole is effective in the acute treatment of depression in bipolar disorder.

Risperidone LAI is not effective in the maintenance treatment of bipolar disorder.

Cariprazine has a high propensity for weight gain.

Lurasidone is licensed by the FDA as monotherapy for acute treatment of bipolar depression.

Olanzapine is not effective in mania.

Quetiapine has a high propensity for EPSEs.

Risperidone LAI is not effective as prophylaxis against mania in the longer term.

Aripiprazole LAI does not protect against manic relapse.

Paliperidone LAI has a different effect than risperidone LAI.

Clozapine has not been studied in people with treatment-resistant BD.

Lurasidone is associated with significant metabolic effects, including weight gain.

Iloperidone is not effective in mixed episodes.

The largest study conducted with flupentixol LAI showed a significant effect in reducing the risk of depressive episodes.

Risperidone LAI has been shown to increase the risk of depressive relapse in bipolar patients.

FGA LAIs have been shown to be effective in preventing recurrence of depression in bipolar patients.

The use of LAIs offers the advantage of transparency with respect to compliance in bipolar maintenance.

A Taiwanese retrospective cohort study found that patients prescribed FGA LAIs had a lower risk of depressive episode recurrence compared to those prescribed risperidone LAI.

Haloperidol LAI has been shown to increase the risk of manic relapse in bipolar patients.

Flupentixol decanoate (20mg every 2–3 weeks) has been shown to increase the risk of depressive episodes in bipolar patients.

The evidence suggests that FGA LAIs are more effective than SGA LAIs in reducing the risk of recurrence of mania/hypomania in bipolar patients.

The largest study conducted with flupentixol LAI showed no effect and no superiority over lithium.

The use of FGA LAIs is strongly supported by the evidence in bipolar maintenance.

The initial dose reduction of lithium or mood stabilizers should be 50% of the current dose

Lithium levels of 1.2 mmol/L are considered safe

Valproate can increase the plasma levels of some drugs by inhibition of glucuronidation

A gradual reduction of lithium or mood stabilizers is not necessary to avoid withdrawal symptoms

Ongoing monitoring is not necessary after complete cessation of lithium or mood stabilizers

Tablet cutters are not required to achieve small doses of valproate

Difficulty reducing medication precludes a further attempt at reduction

Other modalities such as family therapy and cognitive behavioural therapy are not effective in treating bipolar disorder

Each reduction of lithium or mood stabilizers should be calculated as a fixed amount of the previous dose

The final dose of lithium or mood stabilizers before completely stopping may not be very small