Psychpedia

Dear learners looking to deepen your #psychiatry knowledge and build practical, exam-ready skills, @psychpedia is here for you. We offer 2,800+ board-style MCQs covering psychopharmacology, neurocognitive disorders, child psychiatry, forensic psychiatry, and more. Our questions are written by clinicians and designed to support preparation for ABPN certification, PRITE, and the psychiatry shelf. Psychpedia currently supports learners in: 1. Saudi Arabia 2. UAE 3. Bahrain 4. Kuwait 5. Oman 6. Qatar 7. United States 8. Canada 9. United Kingdom We’re actively working to expand access to more countries.

Antisocial Personality Disorder, by itself, does not satisfy the mental disease or defect prong in any major U.S. standard; pairing it with another qualifying disorder requires careful attribution of which symptoms drove the act. Continue reading: psychpedia.com/articles/crimi…

Narcissistic personality disorder vs. others: separating it from other personality disorders, mood and psychotic illnesses, and substance- or medically-induced mimics. psychpedia.com/articles/narci…

"GRANDIOSE" is a mnemonic for Narcissistic Personality Disorder. Continue reading: psychpedia.com/articles/narci…

Spotting neuroleptic-induced parkinsonism versus other causes — read the full overview: psychpedia.com/articles/neuro…

Tremor, Rigidity, Akinesia/bradykinesia, Postural instability — the four cardinal signs shared with idiopathic Parkinson disease.

A new psychiatric presentation in a patient over 40, especially with visual hallucinations, fluctuating consciousness, or abnormal vital signs, is delirium until medical workup proves otherwise.

Infection, Withdrawal, Acute metabolic, Trauma/Toxins, CNS pathology, Hypoxia, Deficiencies (thiamine, B12), Endocrinopathies, Acute vascular, Toxins/heavy metals, Heavy metals/Heart failure — a broad differential for the precipitant of delirium.

Metoclopramide-induced TD often presents in older patients prescribed the drug for gastroparesis or chronic nausea; cumulative exposure beyond 12 weeks should prompt reassessment.

Laryngeal dystonia can cause airway obstruction within minutes. Treat as an airway emergency: call for help, administer parenteral anticholinergic or antihistamine, and prepare for advanced airway management if no rapid response.

Anticholinergics worsen tardive dyskinesia and impair cognition in older adults. Avoid benztropine in patients over 65 when possible, and never combine with another anticholinergic agent.

Recurrent hypokalemia in a young woman without an obvious medical cause should prompt screening for self-induced vomiting or diuretic misuse, even when the patient is normal weight.

High-yield offending agents that could induce depressive symptoms/disorder. Continue reading: psychpedia.com/articles/subst…

Behavior, Affect, Sensation, Knowledge — the four channels along which dissociation can split experience, useful when probing what the patient does and does not remember from a given event.

Treating a stimulant-induced manic presentation with high-potency first-generation antipsychotics can worsen agitation through and is best avoided when a second-generation agent or benzodiazepine is available.

Do not start antidepressant monotherapy in suspected cyclothymic disorder without first evaluating for hypomanic history; antidepressant monotherapy may induce activation, mixed states, or accelerated cycling.

A patient on sertraline or any other SSRI agent, who develops new fatigue, headache, nausea, or confusion has hyponatremia until proven otherwise. Check for sodium levels before assuming the symptoms are depressive relapse.

Ketamine in #Depression: For decades, depression treatment focused on monoamines — serotonin, noradrenaline, dopamine. SSRIs work, but slowly, and around a third of patients fail two or more adequate trials, meeting criteria for Treatment-Resistant Depression (TRD). A different mechanism Ketamine and its S-enantiomer esketamine (Spravato) antagonise NMDA glutamate receptors. This triggers BDNF release and mTOR pathway activation, rapidly promoting synaptogenesis in the prefrontal cortex — rebuilding synaptic connections lost in chronic depression. The result is antidepressant effect within hours, not weeks. Clinically Esketamine is FDA (2019) and NICE (TA693, 2021) approved for TRD. It’s given intranasally in supervised settings, alongside an oral antidepressant, twice weekly for 4 weeks then tapered. Patients can’t drive on treatment days. Watch for dissociation, raised BP, and nausea acutely; long-term bladder toxicity is a concern with chronic use. The bigger picture Ketamine’s success challenged monoamine dogma and demonstrated that rapid, profound antidepressant responses are biologically possible — now driving research into psilocybin and other psychoplastogens.

Why do SSRIs take 2–6 weeks to work — if serotonin reuptake is blocked within hours? This is one of the most important questions in psychopharmacology, and the answer reframes how we understand antidepressant action entirely. Acute SSRI administration does block the serotonin transporter (SERT) rapidly — yet clinical response is delayed by weeks. The explanation lies in autoreceptor desensitization. Presynaptic 5-HT1A somatodendritic autoreceptors act as a negative feedback brake. When serotonin accumulates acutely, these receptors fire — suppressing serotonergic neuron firing and partially offsetting the reuptake blockade. Net synaptic serotonin increase is therefore blunted initially. With sustained SSRI exposure over 2–4 weeks, these autoreceptors downregulate and desensitize → inhibitory feedback diminishes → serotonergic neurons increase tonic firing → net synaptic 5-HT rises meaningfully. This is why buspirone (partial 5-HT1A agonist) and pindolol (5-HT1A antagonist) have been studied as augmentation agents to accelerate this desensitization — with modest but real evidence supporting pindolol augmentation in particular. Clinical implication: Patients who discontinue SSRIs in the first 1–2 weeks citing “no effect” are abandoning treatment before the therapeutic mechanism has even fully engaged. Psychoeducation on this timeline is a direct clinical intervention. Board note: The same autoreceptor desensitization model applies to SNRIs. For TCAs, additional alpha-2 adrenergic autoreceptor downregulation contributes to delayed noradrenergic effects.