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  • Question 1 - What is the most effective way to address sexual dysfunction in a male...

    Correct

    • What is the most effective way to address sexual dysfunction in a male patient who is taking sertraline and wishes to continue its use due to positive response to the medication?

      Your Answer: Sildenafil

      Explanation:

      The medication with the strongest evidence is sildenafil.

      Antidepressants can cause sexual dysfunction as a side-effect, although the rates vary. The impact on sexual desire, arousal, and orgasm can differ depending on the type of antidepressant. It is important to rule out other causes and consider non-pharmacological strategies such as reducing the dosage of taking drug holidays. If necessary, switching to a lower risk antidepressant of using pharmacological options such as phosphodiesterase inhibitors of mirtazapine augmentation can be considered. The Maudsley Guidelines 14th Edition provides a helpful table outlining the risk of sexual dysfunction for different antidepressants.

    • This question is part of the following fields:

      • Psychopharmacology
      10.1
      Seconds
  • Question 2 - Which of the following has the shortest half-life? ...

    Correct

    • Which of the following has the shortest half-life?

      Your Answer: Zopiclone

      Explanation:

      The ‘Z drugs’ (zopiclone, zolpidem, zaleplon) are beneficial for nighttime sedation due to their relatively brief half-lives.

      Benzodiazepines are a class of drugs commonly used to treat anxiety and sleep disorders. It is important to have a working knowledge of the more common benzodiazepines and their half-life. Half-life refers to the amount of time it takes for half of the drug to be eliminated from the body.

      Some of the more common benzodiazepines and their half-life include diazepam with a half-life of 20-100 hours, clonazepam with a half-life of 18-50 hours, chlordiazepoxide with a half-life of 5-30 hours, nitrazepam with a half-life of 15-38 hours, temazepam with a half-life of 8-22 hours, lorazepam with a half-life of 10-20 hours, alprazolam with a half-life of 10-15 hours, oxazepam with a half-life of 6-10 hours, zopiclone with a half-life of 5-6 hours, zolpidem with a half-life of 2 hours, and zaleplon with a half-life of 2 hours. Understanding the half-life of these drugs is important for determining dosages and timing of administration.

    • This question is part of the following fields:

      • Psychopharmacology
      4.2
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  • Question 3 - What molecule binds to the nicotinic acetylcholine receptor through allosteric regulation? ...

    Correct

    • What molecule binds to the nicotinic acetylcholine receptor through allosteric regulation?

      Your Answer: Galantamine

      Explanation:

      Mechanisms of Action of Different Drugs

      Understanding the mechanisms of action of different drugs is crucial for medical professionals. It is a common topic in exams and can earn easy marks if studied well. This article provides a list of drugs and their mechanisms of action in different categories such as antidepressants, anti dementia drugs, mood stabilizers, anxiolytic/hypnotic drugs, antipsychotics, drugs of abuse, and other drugs. For example, mirtazapine is a noradrenaline and serotonin specific antidepressant that works as a 5HT2 antagonist, 5HT3 antagonist, H1 antagonist, alpha 1 and alpha 2 antagonist, and moderate muscarinic antagonist. Similarly, donepezil is a reversible acetylcholinesterase inhibitor used as an anti dementia drug, while valproate is a GABA agonist and NMDA antagonist used as a mood stabilizer. The article also explains the mechanisms of action of drugs such as ketamine, phencyclidine, buprenorphine, naloxone, atomoxetine, varenicline, disulfiram, acamprosate, and sildenafil.

    • This question is part of the following fields:

      • Psychopharmacology
      3.5
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  • Question 4 - A female client at your clinic has mentioned that she is using various...

    Correct

    • A female client at your clinic has mentioned that she is using various herbal and dietary supplements to manage her depression. Which of these supplements is most likely to interact with her SSRI antidepressant medication?

      Your Answer: St John's wort

      Explanation:

      Omega 3 fatty acids, which are found in high amounts in oily fish, have been shown in some studies to improve depressive symptoms and can be safely combined with SSRIs. However, St John’s wort, which inhibits serotonin reuptake at nerve terminals, should not be taken with drugs that have a predominantly serotonergic action. Brewer’s yeast may cause a tyramine reaction with an MAOI, while evening primrose oil and ginkgo biloba have no interaction with SSRIs.

    • This question is part of the following fields:

      • Psychopharmacology
      10.1
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  • Question 5 - What factor increases the risk of developing neuroleptic malignant syndrome? ...

    Incorrect

    • What factor increases the risk of developing neuroleptic malignant syndrome?

      Your Answer: Being female

      Correct Answer: Having Parkinson's disease

      Explanation:

      The use of dopaminergic drugs in individuals with Parkinson’s disease increases their susceptibility to NMS. NMS is more likely to develop when there is a modification in the dosage of dopaminergic and antipsychotic medications. While it is possible, NMS does not typically arise without the administration of dopamine-affecting drugs.

      Serotonin Syndrome and Neuroleptic Malignant Syndrome are two conditions that can be difficult to differentiate. Serotonin Syndrome is caused by excess serotonergic activity in the CNS and is characterized by neuromuscular abnormalities, altered mental state, and autonomic dysfunction. On the other hand, Neuroleptic Malignant Syndrome is a rare acute disorder of thermoregulation and neuromotor control that is almost exclusively caused by antipsychotics. The symptoms of both syndromes can overlap, but there are some distinguishing clinical features. Hyper-reflexia, ocular clonus, and tremors are more prominent in Serotonin Syndrome, while Neuroleptic Malignant Syndrome is characterized by uniform ‘lead-pipe’ rigidity and hyporeflexia. Symptoms of Serotonin Syndrome usually resolve within a few days of stopping the medication, while Neuroleptic Malignant Syndrome can take up to 14 days to remit with appropriate treatment. The following table provides a useful guide to the main differentials of Serotonin Syndrome and Neuroleptic Malignant Syndrome.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 6 - An elevated risk of Ebstein's anomaly has previously been linked to which of...

    Correct

    • An elevated risk of Ebstein's anomaly has previously been linked to which of the following medications?

      Your Answer: Lithium

      Explanation:

      The previously assumed higher risk is now uncertain and may not actually exist. We include this question to ensure that you are aware of the past association, as it may still be present in exam materials that have not been revised.

      Lithium – Pharmacology

      Pharmacokinetics:
      Lithium salts are rapidly absorbed following oral administration and are almost exclusively excreted by the kidneys unchanged. Blood samples for lithium should be taken 12 hours post-dose.

      Ebstein’s:
      Ebstein’s anomaly is a congenital malformation consisting of a prolapse of the tricuspid valve into the right ventricle. It occurs in 1:20,000 of the general population. Initial data suggested it was more common in those using lithium but this had not held to be true.

      Contraindications:
      Addison’s disease, Brugada syndrome, cardiac disease associated with rhythm disorders, clinically significant renal impairment, untreated of untreatable hypothyroidism, low sodium levels.

      Side-effects:
      Common side effects include nausea, tremor, polyuria/polydipsia, rash/dermatitis, blurred vision, dizziness, decreased appetite, drowsiness, metallic taste, and diarrhea. Side-effects are often dose-related.

      Long-term use is associated with hypothyroidism, hyperthyroidism, hypercalcemia/hyperparathyroidism, irreversible nephrogenic diabetes insipidus, and reduced GFR.

      Lithium-induced diabetes insipidus:
      Treatment options include stopping lithium (if feasible), keeping levels within 0.4-0.8 mmol/L, once-daily dose of the drug taken at bedtime, amiloride, thiazide diuretics, indomethacin, and desmopressin.

      Toxicity:
      Lithium salts have a narrow therapeutic/toxic ratio. Risk factors for lithium toxicity include drugs altering renal function, decreased circulating volume, infections, fever, decreased oral intake of water, renal insufficiency, and nephrogenic diabetes insipidus. Features of lithium toxicity include GI symptoms and neuro symptoms.

      Pre-prescribing:
      Before prescribing lithium, renal function, cardiac function, thyroid function, FBC, and BMI should be checked. Women of childbearing age should be advised regarding contraception, and information about toxicity should be provided.

      Monitoring:
      Lithium blood levels should be checked weekly until stable, and then every 3-6 months once stable. Thyroid and renal function should be checked every 6 months. Patients should be issued with an information booklet, alert card, and record book.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 7 - Which of the following is not an inducer of the Cytochrome P450 system?...

    Correct

    • Which of the following is not an inducer of the Cytochrome P450 system?

      Your Answer: Fluoxetine

      Explanation:

      Cytochrome P450 is an important enzyme system involved in drug metabolism. Certain substances can either increase or decrease the activity of this system. Smoking, alcohol, barbiturates, carbamazepine, Phenytoin, and St John’s Wort are known to induce the activity of cytochrome P450. On the other hand, chlorpromazine, selective serotonin reuptake inhibitors (SSRIs), and grapefruit juice are known to inhibit the activity of cytochrome P450.

      The Cytochrome P450 system is a group of enzymes that metabolize drugs by altering their functional groups. The system is located in the liver and small intestine and is involved in drug interactions through enzyme induction of inhibition. Notable inducers include smoking, alcohol, and St John’s Wort, while notable inhibitors include grapefruit juice and some SSRIs. CYP2D6 is important due to genetic polymorphism, and CYP3A4 is the most abundant subfamily and is commonly involved in interactions. Grapefruit juice inhibits both CYP1A2 and CYP3A4, while tobacco smoking induces CYP1A2. The table summarizes the main substrates, inhibitors, and inducers for each CYP enzyme.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 8 - Which extrapyramidal side effect is the most difficult to treat? ...

    Incorrect

    • Which extrapyramidal side effect is the most difficult to treat?

      Your Answer: Opisthotonus

      Correct Answer: Akathisia

      Explanation:

      Treating akathisia is a challenging task, as there are limited options available. In many cases, the only viable solution is to decrease the use of antipsychotic medication.

      Extrapyramidal side-effects (EPSE’s) are a group of side effects that affect voluntary motor control, commonly seen in patients taking antipsychotic drugs. EPSE’s include dystonias, parkinsonism, akathisia, and tardive dyskinesia. They can be frightening and uncomfortable, leading to problems with non-compliance and can even be life-threatening in the case of laryngeal dystonia. EPSE’s are thought to be due to antagonism of dopaminergic D2 receptors in the basal ganglia. Symptoms generally occur within the first few days of treatment, with dystonias appearing quickly, within a few hours of administration of the first dose. Newer antipsychotics tend to produce less EPSE’s, with clozapine carrying the lowest risk and haloperidol carrying the highest risk. Akathisia is the most resistant EPSE to treat. EPSE’s can also occur when antipsychotics are discontinued (withdrawal dystonia).

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 9 - Which of the following is not a characteristic of lithium toxicity? ...

    Correct

    • Which of the following is not a characteristic of lithium toxicity?

      Your Answer: Hyporeflexia

      Explanation:

      Lithium – Pharmacology

      Pharmacokinetics:
      Lithium salts are rapidly absorbed following oral administration and are almost exclusively excreted by the kidneys unchanged. Blood samples for lithium should be taken 12 hours post-dose.

      Ebstein’s:
      Ebstein’s anomaly is a congenital malformation consisting of a prolapse of the tricuspid valve into the right ventricle. It occurs in 1:20,000 of the general population. Initial data suggested it was more common in those using lithium but this had not held to be true.

      Contraindications:
      Addison’s disease, Brugada syndrome, cardiac disease associated with rhythm disorders, clinically significant renal impairment, untreated of untreatable hypothyroidism, low sodium levels.

      Side-effects:
      Common side effects include nausea, tremor, polyuria/polydipsia, rash/dermatitis, blurred vision, dizziness, decreased appetite, drowsiness, metallic taste, and diarrhea. Side-effects are often dose-related.

      Long-term use is associated with hypothyroidism, hyperthyroidism, hypercalcemia/hyperparathyroidism, irreversible nephrogenic diabetes insipidus, and reduced GFR.

      Lithium-induced diabetes insipidus:
      Treatment options include stopping lithium (if feasible), keeping levels within 0.4-0.8 mmol/L, once-daily dose of the drug taken at bedtime, amiloride, thiazide diuretics, indomethacin, and desmopressin.

      Toxicity:
      Lithium salts have a narrow therapeutic/toxic ratio. Risk factors for lithium toxicity include drugs altering renal function, decreased circulating volume, infections, fever, decreased oral intake of water, renal insufficiency, and nephrogenic diabetes insipidus. Features of lithium toxicity include GI symptoms and neuro symptoms.

      Pre-prescribing:
      Before prescribing lithium, renal function, cardiac function, thyroid function, FBC, and BMI should be checked. Women of childbearing age should be advised regarding contraception, and information about toxicity should be provided.

      Monitoring:
      Lithium blood levels should be checked weekly until stable, and then every 3-6 months once stable. Thyroid and renal function should be checked every 6 months. Patients should be issued with an information booklet, alert card, and record book.

    • This question is part of the following fields:

      • Psychopharmacology
      4.1
      Seconds
  • Question 10 - You are asked to review a woman on a hospital ward with hemochromatosis...

    Incorrect

    • You are asked to review a woman on a hospital ward with hemochromatosis who has been observed to be low in mood. On review of her blood results you note significant hepatic impairment. Your history and examination confirms that she is depressed. Which of the following medications would be indicated to manage her depression?

      Your Answer: Duloxetine

      Correct Answer: Sertraline

      Explanation:

      Individuals with hepatic impairment should avoid taking agomelatine and duloxetine due to contraindications. It is recommended to avoid sedative TCAs, such as trimipramine, imipramine, dothiepin, and amitriptyline.

      Hepatic Impairment: Recommended Drugs

      Patients with hepatic impairment may experience reduced ability to metabolize drugs, toxicity, enhanced dose-related side effects, reduced ability to synthesize plasma proteins, and elevated levels of drugs subject to first-pass metabolism due to reduced hepatic blood flow. The Maudsley Guidelines 14th Ed recommends the following drugs for patients with hepatic impairment:

      Antipsychotics: Paliperidone (if depot required), Amisulpride, Sulpiride

      Antidepressants: Sertraline, Citalopram, Paroxetine, Vortioxetine (avoid TCA and MAOI)

      Mood stabilizers: Lithium

      Sedatives: Lorazepam, Oxazepam, Temazepam, Zopiclone 3.75mg (with care)

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 11 - What is the definition of priapism? ...

    Correct

    • What is the definition of priapism?

      Your Answer: A persistent and painful erection

      Explanation:

      Priapism: A Painful and Persistent Erection

      Priapism is a condition characterized by a prolonged and painful erection, which can occur in males and even in the clitoris. Although rare, certain medications such as antipsychotics and antidepressants have been known to cause priapism. The primary mechanism behind this condition is alpha blockade, although other mechanisms such as serotonin-mediated pathways have also been suggested. Some of the drugs most commonly associated with priapism include Trazodone, Chlorpromazine, and Thioridazine. Treatment involves the use of alpha-adrenergic agonists, which can be administered orally of injected directly into the penis. Priapism is a serious condition that can lead to complications such as penile amputation, although such cases are extremely rare.

    • This question is part of the following fields:

      • Psychopharmacology
      5.4
      Seconds
  • Question 12 - What factor is most likely to induce sedation and potentially impair a person's...

    Correct

    • What factor is most likely to induce sedation and potentially impair a person's driving ability?

      Your Answer: Chlorpheniramine

      Explanation:

      It is recommended to avoid using first generation H1 antihistamines such as chlorpheniramine in individuals who drive of operate heavy machinery due to their ability to easily penetrate the blood brain barrier and cause sedation.

      Antihistamines: Types and Uses

      Antihistamines are drugs that block the effects of histamine, a neurotransmitter that regulates physiological function in the gut and potentiates the inflammatory and immune responses of the body. There are two types of antihistamines: H1 receptor blockers and H2 receptor blockers. H1 blockers are mainly used for allergic conditions and sedation, while H2 blockers are used for excess stomach acid.

      There are also first and second generation antihistamines. First generation antihistamines, such as diphenhydramine and promethazine, have uses in psychiatry due to their ability to cross the blood brain barrier and their anticholinergic properties. They tend to be sedating and are useful for managing extrapyramidal side effects. Second generation antihistamines, such as loratadine and cetirizine, show limited penetration of the blood brain barrier and are less sedating.

      It is important to note that there are contraindications to first-generation antihistamines, including benign prostatic hyperplasia, angle-closure glaucoma, and pyloric stenosis in infants. These do not apply to second-generation antihistamines.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 13 - What is the most common cause of SIADH? ...

    Correct

    • What is the most common cause of SIADH?

      Your Answer: Stroke

      Explanation:

      It is crucial to recognize that SIADH can have various physical origins that could be the primary cause in a patient who has been given psychotropic medication and develops the condition. The hypothalamus can be affected by brain-related conditions such as stroke, leading to the development of SIADH. Additionally, it is important to remain vigilant for any underlying cancer.

      Hyponatremia in Psychiatric Patients

      Hyponatremia, of low serum sodium, can occur in psychiatric patients due to the disorder itself, its treatment, of other medical conditions. Symptoms include nausea, confusion, seizures, and muscular cramps. Drug-induced hyponatremia is known as the syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH), which results from excessive secretion of ADH and fluid overload. Diagnosis is based on clinically euvolaemic state with low serum sodium and osmolality, raised urine sodium and osmolality. SSRIs, SNRIs, and tricyclics are the most common drugs that can cause SIADH. Risk factors for SIADH include starting a new drug, and treatment usually involves fluid restriction and sometimes demeclocycline.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 14 - Which of the following is not a result of muscarinic blockade? ...

    Incorrect

    • Which of the following is not a result of muscarinic blockade?

      Your Answer: Ataxia

      Correct Answer: Miosis

      Explanation:

      Blurred vision occurs as a result of muscarinic blockade, which causes the pupils to dilate (mydriasis).

      Receptors and Side-Effects

      Histamine H1 Blockade:
      – Weight gain
      – Sedation

      Alpha 1 Blockade:
      – Orthostatic hypotension
      – Sedation
      – Sexual dysfunction
      – Priapism

      Muscarinic Central M1 Blockade:
      – Agitation
      – Delirium
      – Memory impairment
      – Confusion
      – Seizures

      Muscarinic Peripheral M1 Blockade:
      – Dry mouth
      – Ataxia
      – Blurred vision
      – Narrow angle glaucoma
      – Constipation
      – Urinary retention
      – Tachycardia

      Each receptor has specific effects on the body, but they can also have side-effects. Histamine H1 blockade can cause weight gain and sedation. Alpha 1 blockade can lead to orthostatic hypotension, sedation, sexual dysfunction, and priapism. Muscarinic central M1 blockade can cause agitation, delirium, memory impairment, confusion, and seizures. Muscarinic peripheral M1 blockade can result in dry mouth, ataxia, blurred vision, narrow angle glaucoma, constipation, urinary retention, and tachycardia. It is important to be aware of these potential side-effects when using medications that affect these receptors.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 15 - A woman taking quetiapine has an ECG and is found to have a...

    Incorrect

    • A woman taking quetiapine has an ECG and is found to have a QTc of 410 ms. What is the appropriate next step in her treatment plan?

      Your Answer: Continue quetiapine but take weekly ECG's

      Correct Answer: Continue quetiapine and just continue with routine monitoring

      Explanation:

      It is advisable to maintain the medication and regular monitoring as a QTC of 410 ms is within the normal range.

      Amantadine and QTc Prolongation

      Amantadine is a medication used to treat Parkinson’s disease and influenza. It has been associated with QTc prolongation, which can increase the risk of Torsades de points. Therefore, caution should be exercised when prescribing amantadine to patients with risk factors for QT prolongation. If a patient is already taking amantadine and develops a prolonged QTc interval, the medication should be discontinued and an alternative treatment considered. It is important to monitor the QTc interval in patients taking amantadine, especially those with risk factors for QT prolongation.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 16 - Which of the following is the least likely to cause discontinuation symptoms? ...

    Correct

    • Which of the following is the least likely to cause discontinuation symptoms?

      Your Answer: Fluoxetine

      Explanation:

      Antidepressants can cause discontinuation symptoms when patients stop taking them, regardless of the type of antidepressant. These symptoms usually occur within 5 days of stopping the medication and can last up to 3 weeks. Symptoms include flu-like symptoms, dizziness, insomnia, vivid dreams, irritability, crying spells, and sensory symptoms. SSRIs and related drugs with short half-lives, such as paroxetine and venlafaxine, are particularly associated with discontinuation symptoms. Tapering antidepressants at the end of treatment is recommended to prevent these symptoms. TCAs and MAOIs are also associated with discontinuation symptoms, with amitriptyline and imipramine being the most common TCAs and all MAOIs being associated with prominent discontinuation symptoms. Patients at highest risk for discontinuation symptoms include those on antidepressants with shorter half-lives, those who have been taking antidepressants for 8 weeks of longer, those using higher doses, younger people, and those who have experienced discontinuation symptoms before. Agomelatine is not associated with any discontinuation syndrome. If a discontinuation reaction occurs, restarting the antidepressant of switching to an alternative with a longer half-life and tapering more slowly may be necessary. Explanation and reassurance are often sufficient for mild symptoms. These guidelines are based on the Maudsley Guidelines 14th Edition and a study by Tint (2008).

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 17 - Which class of antidepressants share a molecular structure similar to carbamazepine? ...

    Incorrect

    • Which class of antidepressants share a molecular structure similar to carbamazepine?

      Your Answer: Tetracyclics

      Correct Answer: Tricyclics

      Explanation:

      Carbamazepine mechanism of action involves decreasing the metabolism of dopamine and noradrenaline, which is similar to tricyclic antidepressants due to their comparable molecular structure.

    • This question is part of the following fields:

      • Psychopharmacology
      11.5
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  • Question 18 - What is the least expected symptom in a patient who is taking sodium...

    Correct

    • What is the least expected symptom in a patient who is taking sodium valproate?

      Your Answer: Thrombocytosis

      Explanation:

      Thrombocytosis would not be an expected finding as valproate typically decreases platelet counts instead of increasing them.

      Valproate: Forms, Doses, and Adverse Effects

      Valproate comes in three forms: semi-sodium valproate, valproic acid, and sodium valproate. Semi-sodium valproate is a mix of sodium valproate and valproic acid and is licensed for acute mania associated with bipolar disorder. Valproic acid is also licensed for acute mania, but this is not consistent with the Maudsley Guidelines. Sodium valproate is licensed for epilepsy. It is important to note that doses of sodium valproate and semi-sodium valproate are not the same, with a slightly higher dose required for sodium valproate.

      Valproate is associated with many adverse effects, including nausea, tremor, liver injury, vomiting/diarrhea, gingival hyperplasia, memory impairment/confusional state, somnolence, weight gain, anaemia/thrombocytopenia, alopecia (with curly regrowth), severe liver damage, and pancreatitis. Increased liver enzymes are common, particularly at the beginning of therapy, and tend to be transient. Vomiting and diarrhea tend to occur at the start of treatment and remit after a few days. Severe liver damage is most likely to occur in the first six months of therapy, with the maximum risk being between two and twelve weeks. The risk also declines with advancing age.

      Valproate is a teratogen and should not be initiated in women of childbearing potential. Approximately 10% of children exposed to valproate monotherapy during pregnancy suffer from congenital malformations, with the risk being dose-dependent. The most common malformations are neural tube defects, facial dysmorphism, cleft lip and palate, craniostenosis, cardiac, renal and urogenital defects, and limb defects. There is also a dose-dependent relationship between valproate and developmental delay, with approximately 30-40% of children exposed in utero experiencing delay in their early development, such as talking and walking later, lower intellectual abilities, poor language skills, and memory problems. There is also a thought to be a 3-fold increase of autism in children exposed in utero.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 19 - Which of the following is classified as a phenothiazine? ...

    Correct

    • Which of the following is classified as a phenothiazine?

      Your Answer: Pipotiazine

      Explanation:

      Antipsychotics can be classified in different ways, with the most common being typical (first generation) and atypical (second generation) types. Typical antipsychotics block dopamine (D2) receptors and have varying degrees of M1, Alpha-1, and H1 receptor blockade. Atypical antipsychotics have a lower propensity for extrapyramidal side-effects and are attributed to the combination of relatively lower D2 antagonism with 5HT2A antagonism. They are also classified by structure, with examples including phenothiazines, butyrophenones, thioxanthenes, diphenylbutylpiperidine, dibenzodiazepines, benzoxazoles, thienobenzodiazepine, substituted benzamides, and arylpiperidylindole (quinolone). Studies have found little evidence to support the superiority of atypicals over typicals in terms of efficacy, discontinuation rates, of adherence, with the main difference being the side-effect profile. The Royal College also favors classification by structure.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 20 - Who is responsible for introducing chlorpromazine into clinical practice? ...

    Correct

    • Who is responsible for introducing chlorpromazine into clinical practice?

      Your Answer: Delay and Deniker

      Explanation:

      Chlorpromazine, also known as Thorazine, is a medication used to treat various mental health conditions such as schizophrenia, bipolar disorder, and severe anxiety. It was first synthesized by Paul Charpentier in 1950 and quickly became a popular antipsychotic medication due to its effectiveness in reducing symptoms such as hallucinations and delusions. Chlorpromazine works by blocking certain neurotransmitters in the brain, leading to a calming effect on the patient. Despite its success, chlorpromazine can cause side effects such as drowsiness, dry mouth, and blurred vision. It is important to consult with a healthcare professional before taking this medication.

      A Historical Note on the Development of Zimelidine, the First Selective Serotonin Reuptake Inhibitor

      In 1960s, evidence began to emerge suggesting a significant role of serotonin in depression. This led to the development of zimelidine, the first selective serotonin reuptake inhibitor (SSRI). Zimelidine was derived from pheniramine and was marketed in Europe in 1982. However, it was removed from the market in 1983 due to severe side effects such as hypersensitivity reactions and Guillain-Barre syndrome.

      Despite its short-lived availability, zimelidine paved the way for the development of other SSRIs such as fluoxetine, which was approved by the FDA in 1987 and launched in the US market in 1988 under the trade name Prozac. The development of SSRIs revolutionized the treatment of depression and other mood disorders, providing a safer and more effective alternative to earlier antidepressants such as the tricyclics and MAO inhibitors.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 21 - Which brain function is thought to be enhanced by lithium? ...

    Correct

    • Which brain function is thought to be enhanced by lithium?

      Your Answer: Serotonin

      Explanation:

      The college’s question is unjust as the precise workings of lithium are not fully comprehended. However, it is believed that lithium elevates serotonin levels and can lead to serotonin syndrome. Additionally, lithium has been associated with the norepinephrine system.

      Serotonin Syndrome and Neuroleptic Malignant Syndrome are two conditions that can be difficult to differentiate. Serotonin Syndrome is caused by excess serotonergic activity in the CNS and is characterized by neuromuscular abnormalities, altered mental state, and autonomic dysfunction. On the other hand, Neuroleptic Malignant Syndrome is a rare acute disorder of thermoregulation and neuromotor control that is almost exclusively caused by antipsychotics. The symptoms of both syndromes can overlap, but there are some distinguishing clinical features. Hyper-reflexia, ocular clonus, and tremors are more prominent in Serotonin Syndrome, while Neuroleptic Malignant Syndrome is characterized by uniform ‘lead-pipe’ rigidity and hyporeflexia. Symptoms of Serotonin Syndrome usually resolve within a few days of stopping the medication, while Neuroleptic Malignant Syndrome can take up to 14 days to remit with appropriate treatment. The following table provides a useful guide to the main differentials of Serotonin Syndrome and Neuroleptic Malignant Syndrome.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 22 - Which statement about neuroleptic malignant syndrome (NMS) is incorrect? ...

    Correct

    • Which statement about neuroleptic malignant syndrome (NMS) is incorrect?

      Your Answer: It is usually caused by benzodiazepine use

      Explanation:

      When apomorphine is withdrawn, it results in a decrease in dopamine activity in the brain, similar to the effect of starting an antipsychotic medication that blocks dopamine receptors.

      Serotonin Syndrome and Neuroleptic Malignant Syndrome are two conditions that can be difficult to differentiate. Serotonin Syndrome is caused by excess serotonergic activity in the CNS and is characterized by neuromuscular abnormalities, altered mental state, and autonomic dysfunction. On the other hand, Neuroleptic Malignant Syndrome is a rare acute disorder of thermoregulation and neuromotor control that is almost exclusively caused by antipsychotics. The symptoms of both syndromes can overlap, but there are some distinguishing clinical features. Hyperreflexia, ocular clonus, and tremors are more prominent in Serotonin Syndrome, while Neuroleptic Malignant Syndrome is characterized by uniform ‘lead-pipe’ rigidity and hyporeflexia. Symptoms of Serotonin Syndrome usually resolve within a few days of stopping the medication, while Neuroleptic Malignant Syndrome can take up to 14 days to remit with appropriate treatment. The following table provides a useful guide to the main differentials of Serotonin Syndrome and Neuroleptic Malignant Syndrome.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 23 - What is the maximum duration of a normal QTc interval in an adult...

    Correct

    • What is the maximum duration of a normal QTc interval in an adult male?

      Your Answer: 440

      Explanation:

      While the upper limit technically reaches 439, it is evident that 440 is the optimal choice among the options provided.

      Amantadine and QTc Prolongation

      Amantadine is a medication used to treat Parkinson’s disease and influenza. It has been associated with QTc prolongation, which can increase the risk of Torsades de points. Therefore, caution should be exercised when prescribing amantadine to patients with risk factors for QT prolongation. If a patient is already taking amantadine and develops a prolonged QTc interval, the medication should be discontinued and an alternative treatment considered. It is important to monitor the QTc interval in patients taking amantadine, especially those with risk factors for QT prolongation.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 24 - What is a true statement about thiamine? ...

    Correct

    • What is a true statement about thiamine?

      Your Answer: It is required for carbohydrate catabolism

      Explanation:

      A lack of vitamin C is commonly linked to gum inflammation and bleeding.

      Thiamine Deficiency and Alcohol-Related Brain Disease

      Thiamine deficiency is a well-known cause of a neurological disorder called Wernicke-Korsakoff syndrome (WKS) in individuals with alcohol use disorder. Thiamine, also known as vitamin B1, is an essential nutrient that cannot be produced by the body and must be obtained through the diet. Thiamine is required for the proper functioning of enzymes involved in the metabolism of carbohydrates, the synthesis of neurotransmitters, nucleic acids, fatty acids, and complex sugar molecules, and the body’s defense against oxidative stress.

      Three enzymes that require thiamine as a cofactor are transketolase, pyruvate dehydrogenase (PDH), and alpha ketoglutarate dehydrogenase (KGDH), all of which participate in the breakdown of carbohydrates. Thiamine deficiency leads to suboptimal levels of functional enzymes in the cell, which can cause cell damage in the central nervous system through cell necrosis, cellular apoptosis, and oxidative stress.

      Alcoholism can contribute to thiamine deficiency through inadequate nutritional intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired utilization of thiamine in the cells. Giving thiamine to patients with WKS can reverse many of the acute symptoms of the disease, highlighting the importance of this nutrient in the prevention and treatment of alcohol-related brain disease.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 25 - Which of the following factors does not increase the risk of QTc prolongation?...

    Correct

    • Which of the following factors does not increase the risk of QTc prolongation?

      Your Answer: Male gender

      Explanation:

      Some additional risk factors for QTc prolongation include being female and having a slow heart rate (bradycardia).

      Amantadine and QTc Prolongation

      Amantadine is a medication used to treat Parkinson’s disease and influenza. It has been associated with QTc prolongation, which can increase the risk of Torsades de points. Therefore, caution should be exercised when prescribing amantadine to patients with risk factors for QT prolongation. If a patient is already taking amantadine and develops a prolonged QTc interval, the medication should be discontinued and an alternative treatment considered. It is important to monitor the QTc interval in patients taking amantadine, especially those with risk factors for QT prolongation.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 26 - Which of the options below is the least probable cause of a notable...

    Correct

    • Which of the options below is the least probable cause of a notable increase in a patient's prolactin levels?

      Your Answer: Clozapine

      Explanation:

      Hyperprolactinemia is a potential side effect of antipsychotic medication, but it is rare with antidepressants. Dopamine inhibits prolactin, so dopamine antagonists, such as antipsychotics, can increase prolactin levels. The degree of prolactin elevation is dose-related, and some antipsychotics cause more significant increases than others. Hyperprolactinemia can cause symptoms such as galactorrhea, menstrual difficulties, gynecomastia, hypogonadism, and sexual dysfunction. Long-standing hyperprolactinemia in psychiatric patients can increase the risk of osteoporosis and breast cancer, although there is no conclusive evidence that antipsychotic medication increases the risk of breast malignancy and mortality. Some antipsychotics, such as clozapine and aripiprazole, have a low risk of causing hyperprolactinemia, while typical antipsychotics and risperidone have a high risk. Monitoring of prolactin levels is recommended before starting antipsychotic therapy and at three months and annually thereafter. Antidepressants rarely cause hyperprolactinemia, and routine monitoring is not recommended. Symptomatic hyperprolactinemia has been reported with most antidepressants, except for a few, such as mirtazapine, agomelatine, bupropion, and vortioxetine.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 27 - Who is the originator of the term 'cheese effect' in reference to the...

    Incorrect

    • Who is the originator of the term 'cheese effect' in reference to the negative effects associated with MAOI antidepressants?

      Your Answer: Kuhn

      Correct Answer: Blackwell

      Explanation:

      A Historical Note on the Development of Zimelidine, the First Selective Serotonin Reuptake Inhibitor

      In 1960s, evidence began to emerge suggesting a significant role of serotonin in depression. This led to the development of zimelidine, the first selective serotonin reuptake inhibitor (SSRI). Zimelidine was derived from pheniramine and was marketed in Europe in 1982. However, it was removed from the market in 1983 due to severe side effects such as hypersensitivity reactions and Guillain-Barre syndrome.

      Despite its short-lived availability, zimelidine paved the way for the development of other SSRIs such as fluoxetine, which was approved by the FDA in 1987 and launched in the US market in 1988 under the trade name Prozac. The development of SSRIs revolutionized the treatment of depression and other mood disorders, providing a safer and more effective alternative to earlier antidepressants such as the tricyclics and MAO inhibitors.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 28 - At what percentage of occupancy of striatal D2 receptors is the risk of...

    Correct

    • At what percentage of occupancy of striatal D2 receptors is the risk of extrapyramidal side-effects expected to increase?

      Your Answer: 80%

      Explanation:

      Extrapyramidal side-effects (EPSE’s) are a group of side effects that affect voluntary motor control, commonly seen in patients taking antipsychotic drugs. EPSE’s include dystonias, parkinsonism, akathisia, and tardive dyskinesia. They can be frightening and uncomfortable, leading to problems with non-compliance and can even be life-threatening in the case of laryngeal dystonia. EPSE’s are thought to be due to antagonism of dopaminergic D2 receptors in the basal ganglia. Symptoms generally occur within the first few days of treatment, with dystonias appearing quickly, within a few hours of administration of the first dose. Newer antipsychotics tend to produce less EPSE’s, with clozapine carrying the lowest risk and haloperidol carrying the highest risk. Akathisia is the most resistant EPSE to treat. EPSE’s can also occur when antipsychotics are discontinued (withdrawal dystonia).

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 29 - Which medication, prescribed for individuals with Alzheimer's disease, functions as an NMDA antagonist?...

    Correct

    • Which medication, prescribed for individuals with Alzheimer's disease, functions as an NMDA antagonist?

      Your Answer: Memantine

      Explanation:

      Memantine is an NMDA antagonist that reduces glutamate mediated excitotoxicity and is recommended by NICE guidelines for managing Alzheimer’s disease in patients with moderate of severe disease who are intolerant of of have a contraindication to acetylcholinesterase inhibitors. Donepezil and galantamine are reversible acetylcholinesterase inhibitors, while rivastigmine is both a reversible acetylcholinesterase inhibitor and butyrylcholinesterase inhibitor. Tacrine, which is not licensed in the UK, has been associated with hepatotoxicity and limited cognitive benefits. Treatment should only be initiated and continued by specialists in dementia care, with regular reviews and assessments of patient benefits. Specialists include psychiatrists, neurologists, and care of the elderly physicians.

    • This question is part of the following fields:

      • Psychopharmacology
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  • Question 30 - What is a true statement about Torsades de pointes? ...

    Incorrect

    • What is a true statement about Torsades de pointes?

      Your Answer: It is a form of supraventricular tachycardia

      Correct Answer: It is often transient

      Explanation:

      Torsades de pointes may not be present on an ECG even if the patient experiences recurring episodes, as it has a tendency to appear and disappear.

      QTc Prolongation: Risks and Identification

      The QT interval is a measure of the time it takes for the ventricles to repolarize and is calculated from the beginning of the QRS complex to the end of the T wave. However, the QT interval varies with the heart rate, making it difficult to use a single number as a cut-off for a prolonged QT. Instead, a corrected QT interval (QTc) is calculated for each heart rate using various formulas. A QTc over the 99th percentile is considered abnormally prolonged, with approximate values of 470 ms for males and 480 ms for females.

      Prolonged QT intervals can lead to torsade de pointes (TdP), a polymorphic ventricular tachycardia that can be fatal if it degenerates into ventricular fibrillation. TdP is characterized by a twisting of the QRS complexes around an isoelectric line and is often asymptomatic but can also be associated with syncope and death. An accurate diagnosis requires an ECG to be recorded during the event. It is important to note that an increase in the QT interval due to a new conduction block should not be considered indicative of acquired LQTS and risk for TdP.

    • This question is part of the following fields:

      • Psychopharmacology
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SESSION STATS - PERFORMANCE PER SPECIALTY

Psychopharmacology (22/30) 73%
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