Antidepressants Quiz: Mechanisms and Effects
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Questions and Answers

What is the primary mechanism through which tricyclic antidepressants (TCAs) exert their therapeutic effects?

  • They increase the production of neurotransmitter molecules in the presynaptic terminal.
  • They activate presynaptic receptors, enhancing neurotransmitter release.
  • They block the reuptake of serotonin and noradrenaline from the synaptic cleft. (correct)
  • They inhibit the release of neurotransmitters from the presynaptic terminal.

    • Which class of antidepressants specifically targets serotonin reuptake without affecting noradrenaline levels?

  • Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)
  • Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs)
  • Tricyclic Antidepressants (TCAs)
  • Selective Serotonin Reuptake Inhibitors (SSRIs) (correct)

    • What neurotransmitter is primarily affected by Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs)?

  • GABA
  • Glutamate
  • Serotonin
  • Dopamine (correct)

    • Which of the following represents a potential consequence of blocking reuptake at serotonergic and noradrenergic synapses?

    <p>Increased activation of postsynaptic receptors over time.</p> Signup and view all the answers

    Which of the following is a commonly known tricyclic antidepressant?

    <p>Imipramine</p> Signup and view all the answers

    What role does propranolol play in exposure therapy for phobias?

    <p>It helps reduce physical anxiety symptoms.</p> Signup and view all the answers

    How does propranolol influence the recall of fear memories according to the content provided?

    <p>It decouples fear memories from emotional responses.</p> Signup and view all the answers

    Which of the following neurotransmitters is primarily associated with inhibitory synapses in the brain?

    <p>GABA</p> Signup and view all the answers

    The activation of GABAA receptors primarily leads to which of the following physiological changes?

    <p>Hyperpolarization of the membrane due to chloride influx.</p> Signup and view all the answers

    What is the primary function of GABAB receptors in the nervous system?

    <p>To inhibit synaptic release presynaptically.</p> Signup and view all the answers

    What is a key therapeutic outcome when propranolol is used in exposure therapy for PTSD?

    <p>Reducing the emotional intensity during recall of traumatic memories.</p> Signup and view all the answers

    Which of the following statements about exposure therapy is accurate?

    <p>It systematically desensitizes individuals to fear through gradual exposure.</p> Signup and view all the answers

    What might be a potential effect of propranolol when used effectively in therapy sessions?

    <p>It makes it easier for individuals to engage with their fears.</p> Signup and view all the answers

    What is a potential severe complication of prolonged lithium treatment?

    <p>Serious renal tubular damage</p> Signup and view all the answers

    Which antiepileptic drug is noted for having fewer side effects compared to lithium in the treatment of bipolar disorder?

    <p>Carbamazepine</p> Signup and view all the answers

    What neurological symptoms may indicate acute lithium toxicity?

    <p>Confusion and motor impairment</p> Signup and view all the answers

    How do many antiepileptic drugs exert their effect on sodium channels?

    <p>By blocking channels in the deactivated state</p> Signup and view all the answers

    What condition can arise due to lithium treatment, apart from neurological effects?

    <p>Hypothyroidism</p> Signup and view all the answers

    Which of the following statements accurately describes a characteristic of cognitive symptoms in schizophrenia?

    <p>They reduce the ability to think clearly and perform daily tasks.</p> Signup and view all the answers

    What is the main difference between positive and negative symptoms in schizophrenia?

    <p>Negative symptoms show a reduction or loss in function, whereas positive symptoms are characterized by exaggeration.</p> Signup and view all the answers

    Which antipsychotic drug is classified as a first-generation or typical antipsychotic?

    <p>Chlorpromazine</p> Signup and view all the answers

    Catatonia is often associated with psychosis. Which of the following behaviors best exemplifies catatonia?

    <p>Exhibiting extreme immobility or lack of response.</p> Signup and view all the answers

    Which subtype of dopamine receptor is NOT included in the classification of antipsychotic agents?

    <p>D6</p> Signup and view all the answers

    What is a common misconception about the symptoms of schizophrenia?

    <p>All individuals with schizophrenia will experience all types of symptoms.</p> Signup and view all the answers

    Which aspect of schizophrenia is characterized by disorganized thoughts and delusions?

    <p>Positive symptoms</p> Signup and view all the answers

    Among the following, which symptom is NOT typically associated with schizophrenia?

    <p>Consistent logical reasoning</p> Signup and view all the answers

    Which adverse effect is primarily associated with the use of typical antipsychotics that block D2 receptors?

    <p>Extrapyramidal symptoms</p> Signup and view all the answers

    What is a common symptom of pseudoparkinsonism associated with typical antipsychotic use?

    <p>Tremors at rest</p> Signup and view all the answers

    Which of the following is an effect of hyperprolactinaemia caused by typical antipsychotics?

    <p>Amenorrhea</p> Signup and view all the answers

    Which condition represents a risk factor for typical antipsychotic medications at higher doses?

    <p>Higher incidence of extrapyramidal symptoms</p> Signup and view all the answers

    What is primarily responsible for the effective management of symptoms in schizophrenia with aripiprazole?

    <p>Partial agonism at D2 receptors</p> Signup and view all the answers

    Which symptom is indicative of acute dystonia due to typical antipsychotic usage?

    <p>Muscle spasms of the tongue</p> Signup and view all the answers

    Which second-generation antipsychotic is considered the most effective for treating negative symptoms of schizophrenia?

    <p>Cariprazine</p> Signup and view all the answers

    In comparison to lower-potency agents, high-potency typical antipsychotics are more likely to cause which of the following?

    <p>Extrapyramidal symptoms</p> Signup and view all the answers

    What is a common side effect that necessitates regular blood monitoring for patients on clozapine?

    <p>Neutropenia</p> Signup and view all the answers

    Which of the following is a behavioral symptom of akathisia related to typical antipsychotic medications?

    <p>Restlessness and pacing</p> Signup and view all the answers

    Which of the following correctly describes the receptor activity of cariprazine?

    <p>Partial agonist at D2 and D3 receptors with higher affinity than aripiprazole</p> Signup and view all the answers

    Chlorpromazine differs from haloperidol mainly in its:

    <p>Potency level and incidence of EPS</p> Signup and view all the answers

    What characterizes the risk of extrapyramidal symptoms (EPS) associated with D2 antagonism?

    <p>Causes severe EPS</p> Signup and view all the answers

    What are the potential heart-related risks early in clozapine treatment?

    <p>Myocarditis and cardiomyopathy</p> Signup and view all the answers

    Why might some schizophrenic patients be classified as treatment resistant?

    <p>They fail to improve with any antipsychotic therapy</p> Signup and view all the answers

    Which of the following side effects is associated with the use of clozapine?

    <p>Metabolic syndrome</p> Signup and view all the answers

    Study Notes

    Anxiety

    • Fear is a complex physiological, behavioral, and cognitive response to a threatening stimulus
    • It's an adaptive response to real threats and is usually transient
    • The normal fear response to a threatening stimulus includes defensive behaviors, autonomic reflexes, arousal and alertness, corticosteroid secretion, and negative emotions
    • Anxiety is meant to increase the likelihood of survival in dangerous situations
    • Symptoms of anxiety include increased arousal, hypervigilance, tachycardia, and physical preparedness (activation of the sympathetic nervous system)
    • Anxiety is a longer-lasting response to danger that may have a specific cause related to something that can signal danger
    • Anxiety may be caused by events thought or anticipated to have adverse consequences
    • When anxiety persists beyond a genuine risk, or produces a response out of proportion to the possible threat, it's an anxiety disorder
    • Currently recognized anxiety disorders include generalized anxiety disorder, panic disorder, post-traumatic stress disorder, social anxiety disorder, simple phobias, and obsessive-compulsive disorder
    • Therapeutic strategies for anxiety disorders include benzodiazepines for acute anxiety and SSRIs/SNRIs for chronic anxiety
    • Benzodiazepines provide a rapid onset of action and are suitable for acute anxiety; antidepressants/buspirone are slower-onset anxiolytics that require longer treatment periods to show a therapeutic effect
    • Propranolol is a beta-blocker traditionally used for hypertension and arrhythmias but is also used in exposure therapy for phobias and PTSD
    • Propranolol can reduce the physical symptoms of anxiety (like increased heart rate and tremors) by blocking the effects of adrenaline
    • Propranolol can influence the emotional component of memories, potentially making it easier to engage with fear
    • Exposure therapy is a psychological approach that gradually exposes individuals to phobic imagery, and systematically desensitizes them to feared stimuli
    • Exposure therapy may occur in a virtual reality environment
    • Propranolol may help patients engage more effectively in exposure therapy by reducing the physical symptoms of anxiety during the session
    • Propranolol may reduce anxiety during exposure by mitigating the emotional response during the recall and confrontation of fear memories, decoupling the memory from the associated emotional and physical response

    GABA

    • GABA is the major inhibitory neurotransmitter in the brain
    • Most inhibitory synapses in the brain use GABA as a neurotransmitter
    • GABA receptors include GABAA and GABAB receptors
    • GABAA receptors are found postsynaptically
    • GABAB receptors are found presynaptically and can inhibit synaptic release
    • GABAA receptors mediate inhibitory synaptic transmission throughout the central nervous system (CNS)
    • GABAA receptors are permeable to Cl− ions
    • Upon activation, Cl− influx hyperpolarizes the membrane and inhibits action potentials
    • GABAB receptors are associated with second messenger systems rather than Cl− channels
    • Second messenger systems often result in opening K+ channels, leading to hyperpolarizing current
    • Decreases GABA release and drugs that activate GABAB receptors can cause seizures
    • Decreased GABA activity can cause seizures and high anxiety/panic
    • Slightly decreased GABA activity can cause increased anxiety
    • Normal GABA activity leads to no significant behavioral effects
    • Benzodiazepines enhance the effect of GABA, leading to central nervous system depression
    • Examples of benzodiazepines include diazepam (Valium), lorazepam (Ativan), alprazolam (Xanax), and clonazepam (Klonopin)
    • Higher GABA activity leads to sedation and marked sedation sleep
    • Each of the five sub-units of the GABAA-benzodiazepine receptor complex is a different protein
    • The principal families of GABAA receptor sub-units have been coded as α, β, and γ sub-units
    • GABA binds to the β sub-unit

    Benzodiazepines

    • Benzodiazepines are used to treat acute anxiety
    • Those used to treat anxiety have a long biological half-life and are no longer used in long-term therapy
    • Benzodiazepines are often co-administered during SSRI use
    • Benzodiazepines act as positive allosteric modulators on GABAA receptors
    • Benzodiazepines bind to a modulatory site distinct from the GABA binding site, facilitating the opening of GABA-activated chloride channels
    • This enhances the inhibitory response to GABA
    • For the GABA-A receptor, several sites allow modulation of channel opening
    • Benzodiazepines increase the affinity of the GABA binding site for GABA, meaning GABA is able to activate the channel at a higher rate, increasing chloride transmission
    • Some long-acting benzodiazepines (e.g., diazepam and chlordiazepoxide) are converted to a long-lasting active metabolite (nordazepam)
    • The tendency of benzodiazepines to produce cumulative effects and long hangovers when repeatedly given is due to the long half-life of nordiazepam
    • Adverse effects of benzodiazepines include sedation, dizziness, ataxia, impaired coordination and balance, cognitive impairment (anterograde amnesia), psychomotor slowing, motor impairment, dependence and withdrawal (with long-term use), tolerance (with long-term use), and overdose risk, especially with alcohol. Short-acting benzodiazepines are mainly used for insomnia and pre-op anxiety, medium acting ones for anxiety, and long-acting ones for anxiety, seizures, or alcohol withdrawal
    • The benzodiazepine binding site subtypes include BZ1 and BZ2

    Z-drugs

    • Z-drugs are non-benzodiazepine hypnotics primarily used for treating insomnia
    • Z-drugs act on GABAA receptors
    • Z-drugs are prescribed for short-term insomnia
    • Clinical notes for Z-drugs include recommendations for short-term use and monitoring for abuse potential
    • Zolpidem, zopiclone, and zaleplon are examples of Z-drugs

    Flumazenil

    • Flumazenil blocks benzodiazepines from binding, having no effect by itself
    • Flumazenil is used to reverse or partially reverse the central sedative effects of benzodiazepines
    • Flumazenil is used for termination of hypnosedative effects in general anaesthesia
    • Flumazenil is used for diagnosis and treatment of benzodiazepine intoxications or overdose

    Reuptake Inhibitors

    • SSRIs (selective serotonin reuptake inhibitors) and SNRIs (serotonin-norepinephrine reuptake inhibitors) are useful for long-term management of anxiety disorders
    • SSRIs and SNRIs are sometimes ineffective at the start of therapy and can initially make anxiety worse, but effects develop gradually over a period of 2 to 4 weeks
    • Examples of SSRIs include fluoxetine (Prozac), paroxetine (Paxil), citalopram (Celexa), escitalopram (Lexapro), and sertraline (Zoloft)
    • Examples of SNRIs include venlafaxine XR (Effexor XR), duloxetine (Cymbalta), and desvenlafaxine (Pristiq)
    • SSRIs are highly lipophilic
    • Fluoxetine has been found to be not toxic at doses up to 1500mg
    • SSRIs and SNRIs can precipitate mania, particularly in patients with unipolar depression
    • SSRI/SNRIs use caution due to the potential of inducing mania and/or hypomania, especially if not used with a mood stabilizer or antipsychotic
    • First-line agents for anxiety treatment, especially major depressive disorder, include benzodiazepines for immediate effectiveness and SSRIs/SNRIs for long-term management
    • Benzodiazepines and SSRIs/SNRIs are also sometimes used in combination

    Ketamine

    • Small clinical trials suggest a single intravenous, sub-anaesthetic dose of ketamine, a non-competitive NMDA channel blocker produces a rapid but short-lasting decrease in depressive symptoms lasting from a few hours up to 14 days
    • Esketamine is a nasal spray analogue of ketamine, it has less side effects and can be used with other oral antidepressants for treatment-resistant cases

    ECT (Electroconvulsive Therapy)

    • ECT is highly effective against depression
    • ECT is relatively safe, and remains the single most effective treatment for serious major depression
    • ECT is mainly used on patients who do not respond to other medications

    TMS (Transcranial Magnetic Stimulation)

    • TMS is a non-invasive neuromodulation technique that utilizes magnetic fields to stimulate specific areas of the brain
    • TMS involves placing a coil over the scalp, generating a magnetic field that influences neuronal activity in the targeted brain region
    • TMS has been approved for the treatment of MDD, particularly when patients do not respond to first-line pharmacological treatments (treatment-resistant depression)

    Schizophrenia

    • Schizophrenia affects about 1% of the population, predominantly in young people, with an average age of onset at 18 for men and 25 for women
    • Psychosis, or loss of contact with reality, is manifested in a variety of mental or psychiatric disorders, and can be acute (caused by drugs or toxins) or a chronic disorder
    • Psychosis is usually characterized by multiple symptoms such as difficulty processing information, disorganized thoughts, distortion of reality, delusions, hallucinations, incoherence, catatonia, and aggressive/violent behavior
    • Symptoms of schizophrenia are divided into: cognitive symptoms (impaired attention/concentration, working memory, executive function, reasoning/problem-solving), positive symptoms (exaggeration of normal function, incoherent speech, hallucinations, delusions, paranoia), and negative symptoms (poverty/simplicity of speech, blunted affect, poor self-care, social withdrawal)
    • Treatment approaches depend on predominant symptoms and their severity.

    Antipsychotic Drugs

    • Two main categories of antipsychotic drugs exist: first-generation and second-generation
    • First-generation antipsychotics (typical or conventional) block the D2 dopamine receptor
    • Examples include chlorpromazine, haloperidol, and fluphenazine
    • First-generation drugs have a higher risk of extrapyramidal side effects (EPS) and tardive dyskinesia (TD) and are less effective in treating negative symptoms
    • Second-generation antipsychotics (atypical) block D2 dopamine, 5-HT2A, and other receptors
    • Examples include risperidone, olanzapine, quetiapine, aripiprazole, and clozapine
    • Second-generation drugs have a lower risk of EPS and TD, and usually more effective for negative symptoms
    • Clozapine is a high-affinity D4 partial agonist, low-affinity D2 partial agonist, and high-affinity 5-HT2A full antagonist
    • Clozapine is often the treatment of choice for treatment-resistant schizophrenia, but it's not the first choice because it has serious drawbacks and requires blood monitoring
    • Atypical antipsychotics usually have a lower risk of EPS and tardive dyskinesia
    • Side effects of atypical antipsychotics include weight gain, diabetes, and dyslipidemia
    • Aripiprazole is an atypical antipsychotic that is a partial agonist at D2, D3 and 5HT-1a receptors, and an antagonist at the 5HT-2a receptor

    Bipolar Disorder

    • Bipolar disorder involves swings between manic (euphoric) and depressive (dysphoric) moods
    • Bipolar disorder usually appears in early adult life
    • Bipolar disorder is less common than major depression, and there's a strong hereditary tendency, though no specific genes have been identified
    • Treatment goals include preventing manic episodes, alleviating depressive symptoms, and avoiding rapid cycling
    • Mood stabilizers, like lithium and antiepileptic drugs (e.g., carbamazepine, valproate, and lamotrigine), are commonly used to treat bipolar disorder
    • Lithium has a calming effect but can cause memory loss and confusion; it is often administered as Lithium Carbonate; and patient compliance is often an issue
    • Lithium toxicity (prolonged treatment) includes serious renal tubular damage and thyroid enlargement, sometimes associated with hypothyroidism
    • Antidepressants (SSRIs and SNRIs) can induce mania
    • Antidepressants should not be used as a standalone treatment in bipolar disorder but should be paired with mood stabilizers or antipsychotics

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    Description

    Test your knowledge on the mechanisms and effects of various classes of antidepressants, including tricyclics and NDRIs. This quiz covers key concepts related to neurotransmitter action and clinical implications. Perfect for psychology students and anyone interested in mental health pharmacology.

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