NBME Flashcards
Narcolepsy pathophys?
Narcolepsy is a chronic sleep disorder characterized by [daytime sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis. Narcolepsy arises from deficient production of orexins in the hypothalamus], which may result from genetic or autoimmune causes. [Orexins typically induce the secretion of monoamines such as norepinephrine throughout the brain to promote wakefulness. As a result, patients suddenly and inappropriately transition into sleep during the day]. Further, [REM sleep features (eg, cataplexy, hypnagogic hallucinations, sleep paralysis) occur during wakefulness]. Cataplexy refers to a sudden loss of muscle tone and usually occurs in response to positive emotion. [Because of orexin dysfunction, nighttime sleep is frequently fragmented with regular awakenings.] The clinical diagnosis should be confirmed by polysomnography (to confirm the [rapid transition into REM sleep, known as decreased REM latency] and rule out other causes of daytime sleepiness) and a multiple sleep latency test (to confirm decreased sleep latency). Treatment includes a regular sleep schedule, avoidance of daytime naps, and in patients with severe daytime sleepiness, modafinil. Modafinil has an unclear mechanism of action that involves increasing orexin and monoamine availability.
Schizoaffective disorder
According to the DSM-5, patients with schizophrenia spectrum disorders (eg, schizophrenia or schizoaffective disorder) demonstrate at [least two of the following five symptoms: delusions, hallucinations, disorganized speech, disorganized behavior, and negative symptoms (eg, flat affect, apathy, or alogia). To meet diagnostic criteria, patients must demonstrate functional deficits, and the total duration of symptoms must exceed 6 months. Patients with schizoaffective disorder must demonstrate mood episodes (eg, major depressive episodes or manic episodes) for a substantial portion of the duration of the illness. ] Manic episodes typically include a euphoric or irritable mood, a decreased need for sleep, increased energy, grandiose thinking (as in this patient), and increased goal-directed activity. By definition, [patients with schizoaffective disorder also experience psychotic symptoms (eg, delusions, hallucinations) in the absence of mood symptoms for at least 2 weeks,]as in this patient. Management requires antipsychotic medication and may also include adjunctive antidepressant medication (if depressive episodes are predominant) or mood stabilizing medication (if manic episodes are predominant).
Malingering
Malingering refers to patients [consciously producing symptoms (eg, purposely injuring themselves or faking a fever by eating something warm) or falsifying symptoms for a conscious purpose. This conscious purpose is known as secondary gain and includes motives such as obtaining disability payments, missing work, or being released from jail]. Diagnosis is supported by [inconsistencies in the history and/or physical examination, and the presence of a tangible benefit of an escalation in care. The distribution of this patient’s numbness does not correlate with any peripheral nervous system or central nervous system (CNS) distribution, and he has a possible motivation of release from jail or missing his upcoming trial. ]Unnecessary diagnostic tests should be avoided. [The physician should explain the scientific reasoning for not escalating care without accusing the patient of feigning symptoms.]
Marijuana intoxication
Marijuana is a hallucinogen that causes [euphoria, anxiety, perception of slowed time, impaired judgement, cognitive slowing, and increased appetite. Tachycardia and hypertension are likely to be seen on examination. Conjunctival injection and dry mucosa] are also commonly seen in marijuana intoxication. Patients with marijuana [intoxication can present with paranoia, anxiety, social withdrawal, and hallucinations. ] This patient’s anxiety, physical examination findings, and sense of euphoria and slowed time are consistent with marijuana intoxication.
Anorexia nervosa physiological changes.
(Decreased serum albumin concentration is the most likely explanation for her lower extremity edema). Laxatives are sometimes employed for weight loss purposes in individuals with anorexia nervosa. (Severe anorexia with profound caloric restriction can, in itself, lead to significant electrolyte disturbances) and physiologic derangements, but laxative abuse can further exacerbate these findings. Common findings include (orthostatic hypotension from volume depletion, hypokalemia with a metabolic alkalosis, and hypoalbuminemia). There are various types of laxatives that can impair protein and fat absorption and, when combined with the caloric restriction frequently seen in anorexia nervosa, can lead to severe hypoalbuminemia. As albumin is one of the primary osmotically active constituents of blood, loss of albumin can lead to fluid extravasation out of the vasculature and into the surrounding peripheral tissues, which is manifest most readily as lower extremity edema. All patients with severe complications of anorexia should be hospitalized for treatment. Nutrient replacement should be initiated cautiously as there is a risk for refeeding syndrome, which can result in hypokalemia, hypophosphatemia, rhabdomyolysis, and heart failure.
Normal physical/ cognitive /social development in teenager
This patient’s presentation is consistent with normal adolescent development. [Boys typically enter puberty between the ages of 9 and 12. Puberty is associated with a variety of physical and psychological changes associated with increased sex hormone production driven by follicle-stimulating hormone], including development of secondary sexual characteristics (eg, pubic and axillary hair), increased stature, increased bone growth, and changes in body fat composition and lean muscle mass. [Mood instability and psychological stress associated with these changes is common.]
Ethylene glycol toxicity
Patients that ingest ethylene glycol may present [similarly to patients with alcohol intoxication, including central nervous system effects such as disorientation and altered mental status. ]Ethylene glycol is metabolized by alcohol dehydrogenase to toxic metabolites including glycolate, glyoxylate, and oxalate. These metabolites are directly toxic to the kidneys through tubular damage as well as oxalate crystal precipitation causing tubule obstruction, resulting in acute kidney injury. [Oxalate crystals are seen on urine microscopy. These metabolites also contribute to an anion-gap metabolic acidosis.] Management of ethylene glycol poisoning involves the administration of fomepizole, an alcohol dehydrogenase inhibitor that prevents the metabolism of ethylene glycol to its toxic metabolites. For severe ingestions, hemodialysis to remove ethylene glycol and its metabolites from the serum may be necessary.
Delirium tremen, tx?
This patient is potentially developing delirium tremens, a serious complication of alcohol withdrawal. Alcohol increases the central nervous system activity of γ-aminobutyric acid (GABA), the main inhibitory neurotransmitter. [Abrupt discontinuation of alcohol therefore leads to sympathetic overdrive]. Uncomplicated alcohol withdrawal typically presents with tremors, anxiety, restlessness, headache, nausea, and diaphoresis, which can occur hours after the cessation of alcohol use. Delirium tremens, the most concerning and life-threatening complication of alcohol withdrawal, involves [severe confusion and disorientation, fluctuations in consciousness, agitation, visual hallucinations, and autonomic instability (fluctuations in pulse and blood pressure with hyperthermia). As in this patient, delirium tremens can begin 2 to 5 days after the patient’s last alcoholic drink]. Patients with delirium tremens are at risk for death from associated dysrhythmias or respiratory failure. Delirium tremens is managed supportively with [benzodiazepines, such as lorazepam, to address agitation and prevent the symptoms of withdrawal, as well as with fluids, nutritional supplementation, and frequent assessment including vital sign checks. ]Other complications of alcohol withdrawal include alcoholic hallucinosis (auditory or visual hallucinations without confusion or autonomic instability) and seizures
Down syndrome
Trisomy of an autosomal chromosome (21) is the mechanism behind Down syndrome. In most cases, this is caused by a meiotic nondisjunction but may also be caused by a Robertsonian translocation (4%). It is the most common trisomy and a frequent cause of developmental delay. It is associated with advanced maternal age, as in this case, with the [incidence increasing significantly after a maternal age of 40]. Down syndrome is characterized by unique facial features, including a [flat facial profile, enlarged tongue, low-set ears, and up-slanted eyes with prominent epicanthal folds. Single palmar creases are often present.] Patients with Down syndrome have increased rates of [atlantoaxial instability, Hirschsprung disease, duodenal atresia, and congenital heart disease. Intellectual disability] is a prominent feature, though severity may range. Later in life, patients with Down syndrome are at an increased risk for developing Alzheimer disease, acute lymphocytic leukemia, and hypothyroidism.
Substance induced psychotic disorders caused by amphetamine
Methamphetamine and other amphetamines are central nervous system stimulants and sympathomimetics, and [intoxication is characterized by euphoria, grandiosity, increased wakefulness and attention, agitation, anorexia, and paranoia]. On examination, patients can present with signs of [sympathomimetic toxicity including hypertension, tachycardia, tachypnea, diaphoresis, and dilated pupils]. Because of [increased synaptic dopamine, hallucinations and paranoia can occur]. Though [appetite suppression and weight loss] are common, electrolyte disturbances would be atypical. Methamphetamine abuse can lead to methamphetamine-induced psychotic disorder, which features delusions, paranoia, and hallucinations. Chronic methamphetamine use may lead to cognitive impairment. Treatment for acute methamphetamine intoxication is supportive, and benzodiazepines have been shown to be effective for the management of agitation or seizures in these patients.
Akathisia caused by prochlorperazine / tx?
Prochlorperazine is a [first-generation antipsychotic medication that is commonly utilized as an antiemetic]. Its antidopaminergic activity may lead to extrapyramidal symptoms (eg, acute dystonic reaction, parkinsonism, or akathisia). This patient is likely experiencing [akathisia, a neuropsychiatric syndrome featuring inner restlessness that may be associated with intense anxiety and a compulsion to move. ]The pathophysiology of akathisia is incompletely understood but may be related to an imbalance in dopaminergic and cholinergic activity (similar to other extrapyramidal symptoms). Management typically includes [β-adrenergic blockers or benzodiazepines, though anticholinergic medications (eg, benztropine) are second-line treatments. Alternatively, the offending agent may be decreased or discontinued.]
Cocaine abuse
[Cocaine blocks the presynaptic reuptake of dopamine, serotonin, and norepinephrine,] which increases the concentration of these substances in the synaptic cleft. Cocaine is an addictive recreational drug that typically causes [euphoria, restlessness, and increased sympathetic tone leading to tachycardia, hypertension, hyperreflexia, and pupillary dilation. Increased synaptic serotonin leads to euphoria, while increased synaptic dopamine leads to addiction (and in severe cases, hallucinations and paranoia). ][Withdrawal from cocaine can cause depressed mood, fatigue, and slowing of activity. The patient’s daily mood swings are likely caused by cocaine intoxication and withdrawal, and chronic cocaine use can lead to paranoia.]
Tardive dyskinesia pathophys
[The chronic use of dopamine-2 (D2) antagonists (particularly high potency D2 antagonists such as risperidone) may upregulate D2 receptors in the basal ganglia, leading to dopamine receptor hypersensitivity and consequent tardive dyskinesia]. Tardive dyskinesia is a syndrome of involuntary movements (eg, lip smacking, choreoathetoid movements of the tongue). When D2 antagonists are discontinued, dopaminergic signaling increases and transiently worsens tardive dyskinesia. Since tardive dyskinesia is not fully reversible for some patients, patients on antipsychotic medication or metoclopramide should be closely monitored for the development of tardive dyskinesia (or alternative agents should be selected). Management involves reducing the dose of the offending medication and/or switching to a medication that does not cause potent D2 antagonism. Vesicular monoamine transporter-2 inhibitors (eg, tetrabenazine) can also improve tardive dyskinesia by depleting dopamine stores.
Panic disorder tx?
Panic attacks feature acute fear or anxiety that peaks within minutes and are associated with four additional physical symptoms or associated mental states. These additional symptoms may include heart palpitations or tachycardia, shortness of breath, chest pain, dizziness, the sensation of choking, gastrointestinal distress, paresthesias, sweating, chills, trembling, derealization, the fear of dying, or the fear of losing control. In patients with an initial episode of panic symptoms, a thorough history and physical examination along with a basic laboratory workup and, potentially, ECG should be performed. Panic disorder is a relatively common psychiatric disorder characterized by recurrent panic attacks that are unexpected and associated with worry about future panic attacks or avoidance of panic attack triggers. Treatment of panic disorder typically includes [antidepressant medication and/or cognitive behavioral therapy (CBT)]. In CBT, patients are typically exposed to feared situations or sensations (utilizing approach instead of avoidance behaviors), which teaches the patient that they can cope with the feared situation. Further, the patient is taught to restructure their cognitions to appreciate risks and decrease catastrophic thought patterns.
Evaluation for dementia
When patients or patients’ family members report a subjective concern about the patient’s memory, the first diagnostic step is to administer a short cognitive screen such as the Mini-Mental State Examination. This patient’s current cognitive function appears decreased compared to his cognitive baseline of being able to execute his instrumental activities of daily living. The differential for cognitive impairment in an older individual is broad and includes [primary dementia, pseudodementia secondary to major depressive disorder, and delirium] (less likely given the patient’s alertness on examination and the subacute, rather than acute, onset). Dementia can be caused by [neurodegenerative proteinopathies (eg, Alzheimer dementia, Lewy body dementia, Parkinson dementia, or frontotemporal dementia), focal neurologic processes (eg, stroke or subdural hematoma), nutritional deficiencies (eg, vitamin B12), or endocrine disease (eg, hypothyroidism)]. All patients with confirmed cognitive impairment on cognitive screening should undergo thorough [histories and physical examinations, depression screenings, laboratory workup to include vitamin B12 and thyroid function tests, and neuroimaging]
MAOI adverse effect? Tx?
Phenelzine is a nonselective monoamine oxidase inhibitor (MAOI). It was previously commonly used in the treatment of major depressive disorder, particularly with atypical features, but its use has declined with the advent of newer agents, such as selective serotonin reuptake inhibitors that have a more favorable adverse effect profile. Monoamine oxidase’s (MAO) primary role in the central nervous system is the breakdown of dopamine, norepinephrine, and serotonin, so inhibition of this enzyme leads to increased availability of these amine neurotransmitters. [A hypertensive crisis can occur in patients taking MAOIs when they consume foods containing tyramine, such as wine, cured meats, and aged cheeses ]because tyramine is also metabolized by MAO. When tyramine is present in large amounts, it can displace norepinephrine, serotonin, and dopamine from presynaptic vesicles. This release, particularly of norepinephrine, [leads to vasoconstriction and marked hypertension. The primary treatment for an MAOI-induced hypertensive crisis is phentolamine, ]which is a non-selective α-adrenergic blocker that leads to vasodilation and decreases blood pressure
Normal sleep changes in elderly
Older adults typically experience several sleep-related changes as they age. A [slightly decreased total sleep duration (eg, 6.5 to 7 hours), slightly increased sleep latency, increased nighttime awakenings (three per night is normal), and a decreased proportion of time spent in the deep sleep and REM sleep stages is typical]. The increase in nighttime awakenings can be attributed to less time spent in deep sleep and nocturia (a result of age-related changes in the urinary system). Management should include [reassurance, and counseling on sleep hygiene can help patients optimize their sleep patterns.]
Tx for Tardive dyskinesia
This patient with a history of auditory hallucinations, delusions, and suicide attempts likely has a diagnosis of schizophrenia. Patients with schizophrenia typically demonstrate clusters of positive symptoms (delusions, hallucinations, or disorganized thinking and behavior) and negative symptoms (loss of affect, volition, or speech). Treatment for schizophrenia consists of antipsychotics, such as haloperidol, chlorpromazine, olanzapine, and risperidone. Use of typical antipsychotics, such as haloperidol or chlorpromazine, is associated with numerous adverse effects, such as acute dystonia, akathisia, bradykinesia or Parkinson-like effects, and tardive dyskinesia. Tardive dyskinesia potentially occurs with the long-term use of typical antipsychotics and is a syndrome of involuntary movements (eg, lip smacking or choreoathetoid movements of the tongue). [Treatment involves discontinuing the typical antipsychotic and switching to an atypical antipsychotic, such as olanzapine or risperidone]
Lithium toxicity and risk factors
Acute lithium toxicity typically manifests with [gastrointestinal (eg, nausea, vomiting, or diarrhea), cardiac (eg, QTc prolongation or bradycardia), and neurologic symptoms. ]Neurologic symptoms typically include [somnolence, confusion, ataxia, and nystagmus, along with signs of neuromuscular excitability such as coarse tremors, fasciculations, and myoclonus]. Severe toxicity leads to [seizures]. Lithium is removed from circulation by the kidney. (It is not metabolized by the liver.) As such, one [risk factor for increased serum lithium concentrations is hypovolemia (eg, from excessive exercise, heat, vomiting, or diuretic medication),] which promotes compensatory renal tubular sodium and lithium reabsorption (since lithium is approximately the same charge and size as sodium). [Another risk factor is decreased renal function. Nonsteroidal anti-inflammatory drugs (NSAIDs) ]prevent prostaglandins from dilating the afferent arteriole, leading to a decreased glomerular filtration rate and consequent increases in serum lithium concentrations. [Angiotensin-converting enzyme inhibitors] similarly decrease the glomerular filtration rate (by preventing the vasoconstriction of the efferent arteriole) and may increase serum lithium concentrations. Management of acute lithium toxicity requires fluid resuscitation and hemodialysis in patients with decreased consciousness, seizures, or serum lithium concentrations greater than 5 mEq/L.
MDD vs. adjustment d/o
Adjustment disorder (Choice A) is characterized by anxiety, depressed mood, or inappropriate behavior in response to a profound life change. Adjustment disorder is diagnosed when the patient does not meet criteria for another psychiatric disorder. In this case, the[ patient meets criteria for major depressive disorder instead, so while her depression may be influenced by her having recently given birth, it does not qualify as adjustment disorder.]
Synthetic opioid notable negative effects?
Synthetic opioids have been found to be contaminated with [MPTP, a neurotoxin associated with acute, irreversible parkinsonism]. [The toxic metabolite of MPTP has a high affinity for dopamine transporters. This metabolite is transported to dopaminergic nerve terminals in the substantia nigra, leading to neuronal damage]. Parkinsonism manifests with muscle rigidity, bradykinesia, resting tremor, and postural instability. Drooling secondary to bradykinesia and poor motor control of the tongue may occur. Some patients with MPTP-associated parkinsonism have been treated with carbidopa-levodopa, which may improve symptoms but does not cure the disease.
Wernicke and Karsarkoff
Patients who chronically abuse alcohol typically demonstrate a significant vitamin B1 (thiamine) deficiency because of poor nutritional intake, thiamine malabsorption, and impaired cellular utilization of thiamine. Over time, thiamine deficiency can result in damage and atrophy of the mammillary bodies, visible on MRI of the brain, which manifests as Wernicke encephalopathy. The typical clinical presentation of [Wernicke encephalopathy is a triad of acutely altered mental status, ophthalmoplegia or nystagmus, and ataxia.] Patients may present with [physical examination and laboratory findings consistent with liver cirrhosis, as evidenced by this patient’s gynecomastia and palmar erythema (both related to impaired liver metabolism of estrogen).] The symptoms of Wernicke encephalopathy are reversible but increase the risk for developing Wernicke-Korsakoff syndrome in chronic alcohol users if not immediately treated with intravenous thiamine. [Wernicke-Korsakoff syndrome is an irreversible condition that features anterograde and retrograde amnesia along with the consequent tendency to confabulate, ]or verbalize false stories or memories, to compensate for the inability to remember.
Sexual dysfunction vs. performance anxiety
[Psychological factors such as performance anxiety or marital conflict can exert a strong influence on sexual function in both men and women. ]In men, anxiety can lead to decreased libido, decreased ability to obtain or maintain an erection, premature ejaculation, or decreased ability to ejaculate. New sexual partners are a risk factor for performance anxiety. Patients with sexual dysfunction secondary to performance anxiety typically continue to experience nocturnal tumescence and emissions and lack anatomical abnormalities of the genitalia on physical examination. Treatment strategies include cognitive behavioral therapy, mindfulness meditation training, or pharmacotherapy (eg, serotonergic anxiolytic medications or phosphodiesterase inhibitors).
Anticholinergic toxicity? causes and risk factors? Tx?
This patient’s [newly started fluoxetine has likely increased the serum concentration of doxepin, a tricyclic antidepressant (TCA) medication, via inhibition of CYP2D6. TCAs demonstrate strong anticholinergic activity]. Acetylcholine activity in the brain mediates attention and motivation, and peripheral acetylcholine mediates smooth muscle contraction. Anticholinergic agents commonly cause cognitive impairment (as evidenced by this patient’s strange behavior) and delirium (as evidenced by this patient’s disorientation) along with smooth muscle dysfunction (decreased function of sweat glands and pupillary muscles lead to this patient’s flushed skin and mydriasis, respectively). [Anticholinergic toxicity typically manifests as sedation, delirium, hallucinations, ataxia, mydriasis, visual disturbances (cycloplegia, or loss of accommodation), dry mouth, tachycardia, urinary retention, constipation, and flushed skin. TCA toxicity causes an anticholinergic toxidrome along with cardiovascular toxicity (eg, conduction abnormalities such as atrioventricular block, QRS prolongation) and seizures. In patients demonstrating anticholinergic or TCA toxicity, the offending medication should be discontinued. In patients with TCA toxicity and a QRS interval greater than 100 ms or a ventricular arrhythmia, sodium bicarbonate should be administered]
When to admit suicidal patient involuntarily
This patient possesses several acute risk factors for suicide. Most concerningly, he was found after a likely [suicide attempt] (jumping off a bridge with rocks to go for a swim does not make logical sense). He denies that the incident was a suicide attempt and declines a psychiatric admission, which may indicate he [still wishes to attempt suicide and is not willing or able to make a safety plan]. Other acute suicide risk factors possessed by this patient include a [depressive episode (as evidenced by weight loss indicating a decreased appetite, decreased energy, and tearful affect), social isolation, and increased substance use]. Other acute suicide risk factors include acute [anxiety, feeling like a burden, and command auditory hallucinations]. In patients with several acute suicide risk factors, the physician should assess the patient’s willingness to be hospitalized and pursue voluntary hospitalization if the patient is willing. In this scenario, if the patient declines hospitalization, the physician should involuntarily hospitalize the patient because of the probable presence of continued active suicidal ideation with intent and the patient’s unwillingness to make a safety plan.
Generalized tonic clonic seizure
Generalized tonic-clonic seizures are characterized by a [sudden loss of consciousness followed by a stiffening of all of the muscles of the arms, legs, chest, and back (tonic phase), progressing to jerking or twitching of all of the muscles (clonic phase). After the seizure, postictal confusion is common]. Although the parents’ description of the episodes is limited, the spells that the parents describe are likely seizures, and a [postictal state is likely the cause of this patient’s vacant expression and confusion after he awakens. ][The definitive diagnosis of seizures and epilepsy is completed through EEG]. Treatment is with anti-epileptic medication.
Bipolar
Bipolar disorder is a mood disorder that features acute episodes of mania. Acute mania typically manifests with euphoric or irritable mood, increased energy, a decreased need for sleep, increased goal-directed activity, rapid speech and thinking (as evidenced by this patient’s pressured speech with a flight of ideas), irresponsibility (as evidenced by this patient’s out-of-character spending), and grandiose thinking (as evidenced by this patient believing that God is talking to him). Some patients demonstrate associated psychotic symptoms (eg, paranoid delusions or hallucinations). Type 1 bipolar disorder is this patient’s most likely diagnosis. Though patients with type 1 bipolar disorder need to demonstrate a history of mania to meet diagnostic criteria, patients with type 2 bipolar disorder must demonstrate major depressive episodes in addition to hypomanic episodes (less severe and shorter episodes of mania without psychotic features). Management requires mood stabilizing therapy (eg, mood stabilizers or mood stabilizing antipsychotics) for acute mania. Once acute mood episodes resolve, patients with bipolar disorder should continue mood stabilizing maintenance therapy to prevent future episodes of mania or depression.
OCD tx?
Obsessive-compulsive disorder (OCD) manifests as recurrent, intrusive urges or thoughts that the patient tries to relieve or neutralize by repetitive rituals, which leads to significant dysfunction in social and personal life. It often presents in early adulthood, as in this case. OCD can be distinguished from obsessive-compulsive personality disorder by being ego-dystonic or recognized by the patient as abnormal and undesirable. In contrast, obsessive-compulsive personality disorder is ego-syntonic, meaning that patients do not see their behaviors as problematic. Treatment of OCD includes pharmacotherapy, [cognitive behavioral therapy with relaxation techniques, and patient education. First-line pharmacotherapy is a selective serotonin reuptake inhibitor (SSRI) such as sertraline based on its efficacy in large clinical trials]. Clomipramine, a tricyclic antidepressant, and venlafaxine, a serotonin-norepinephrine reuptake inhibitor, have also been shown to be efficacious.
Specific phobia
Specific phobia is a psychiatric disorder featuring [anxiety about a certain situation or object that leads to avoidance behavior. Common phobias include flying, animals, and enclosed spaces. To meet diagnostic criteria, the anxiety symptoms must be persistent (lasting greater than 6 months), and patients must demonstrate distress or social or occupational impairment]. The anxiety may center around exposure to or anticipation of the stimulus. Long-term cognitive-behavioral therapy psychotherapy is the most effective treatment, though short-term benzodiazepines may be utilized in certain patients whose feared situations occur infrequently.
Mood disorder due to medical condition
Obstructive sleep apnea (OSA) features repetitive obstruction of the pharyngeal airway during sleep and typically occurs in patients with obesity because of a combination of structural, vascular, and neuromuscular factors. Though older males are most commonly affected, younger and female patients may also be affected. [Patients commonly experience hypoxemia several times nightly with fragmented sleep leading to daytime sleepiness, fatigue, poor concentration, and irritability. ]Snoring, related to airway obstruction, is commonly associated with OSA. Because of overlapping symptoms, OSA may be confused with depression. Alternatively, because of abnormal sleep architecture or intermittent nocturnal hypoxemia, [OSA may cause depression. In patients with depression secondary to OSA], treatment should include continuous positive airway pressure, which addresses OSA and consequently treats the associated depression symptoms.
Causes of Catalonia? Tx?
This patient has had a recent traumatic experience and is now demonstrating dissociative symptoms including a flat affect and catatonia. [Catatonia can occur in the context of many underlying psychiatric disorders and may present, as in this case, with mutism, immobility, and stupor]. [It may be malignant, if accompanied by fever and vital sign instability, or non-malignant, ]as in this case, which impacts treatment approach. In this case, the patient’s [catatonia is induced by his recent traumatic experience. Taken together, these findings suggest a diagnosis of acute stress disorder.] Acute stress disorder presents similarly to post-traumatic stress disorder, with symptoms of intrusive thoughts, hyperarousal, dissociation, avoidance, and/or depressed mood. However, acute stress disorder typically lasts between 3 days and 1 month following a traumatic event whereas post-traumatic stress disorder lasts for more than a month after the event. [A benzodiazepine such as lorazepam is warranted in the treatment of non-malignant catatonia. Malignant catatonia is treated with benzodiazepine and urgent electroconvulsive therapy. ]However, in some cases of acute stress disorder with only mild symptoms, pharmacotherapy is not needed.
Pathophys of MDD?
This patient meets criteria for major depressive disorder (MDD). Symptoms of MDD include 2 or more weeks of at least five of the following symptoms: depressed mood, anhedonia, guilt or worthlessness, difficulty concentrating, suicidal thoughts, and neurovegetative symptoms (decreased energy, sleep disturbance, appetite disturbance). These symptoms disrupt everyday functioning. Though some patients are able to express a depressed mood, others (particularly women, elderly patients, and African American patients) may primarily endorse somatic or neurovegetative symptoms. [MDD is postulated to result from dysregulation of the hypothalamic-pituitary-adrenal axis, particularly in response to stress, and consequent hypercortisolemia (increased serum cortisol concentration). Cortisol promotes changes in serotonin receptors, mediating mood changes.] Treatment of MDD should include psychotherapy and antidepressant medication.
MDD vs. somatic symptoms disorder
This patient meets criteria for major depressive disorder (MDD). Symptoms of MDD include 2 or more weeks of at least five of the following symptoms: depressed mood, anhedonia (eg, decreased interest in socializing), guilt or worthlessness, difficulty concentrating, suicidal thoughts, and neurovegetative symptoms (decreased energy, sleep disturbance, appetite disturbance). These symptoms disrupt everyday functioning. This patient has poor appetite, guilt, low energy, difficulty concentrating, and anhedonia. [Though some patients are able to express a depressed mood, others (particularly women, elderly patients, and African American patients) may present with primarily somatic symptoms. Depression and somatic symptoms (especially pain symptoms) commonly co-occur], which is postulated to arise from a common descending pain pathway. Patients may [interpret their depression symptoms as being related to physical disease to normalize the symptoms, which is related to the stigma of mental illness]. Treatment of MDD should include psychotherapy and antidepressant medication.
In somatization disorder (Choice E), more commonly known as somatic symptom disorder, the patient is [excessively preoccupied with one or more somatic symptoms such that these symptoms disrupt the patient’s daily life. Patients persistently devote excessive time and energy to these symptoms or related health concerns (eg, repeatedly going to the doctor). This patient does not demonstrate preoccupation or maladaptive care-seeking behaviors related to her symptoms].
Dissociative disorder vs. adjustment disorder
Dissociative disorder occurs when [consciousness, memory, identity, or awareness of self and surroundings are disrupted]. [Depersonalization, detachment from one’s self, and derealization, the sense of the world being strange or unreal], are also features. Within the umbrella of dissociative disorder are several [subtypes: dissociative identity disorder, dissociative amnesia, and depersonalization-derealization disorder]. [Acute trauma], such as in this case, is a characteristic cause of dissociative amnesia, depersonalization, and derealization. Chronic trauma, severe stress, substance abuse, and underlying psychiatric disorders are additional potential triggers. When dissociation occurs acutely secondary to trauma, it also frequently remits acutely. If it does persist, however, the cornerstone of treatment is psychotherapy. If psychotherapy is not effective, an atypical antipsychotic or antiepileptic such as lamotrigine may be used.
Adjustment disorder (Choice A) is characterized by anxiety, depressed mood, or inappropriate behavior in response to a profound life change. [Adjustment disorder is only diagnosed when the patient does not meet the diagnostic criteria for another psychiatric disorder]. In this case, the patient meets criteria for dissociative disorder instead.
Tx for specific phobia
A specific phobia is a fear of an object or situation. It is an anxiety disorder that significantly impairs functioning because it leads to behavior directed at avoiding the object or situation, which can often be excessively time-consuming, as in this patient. Common phobias include heights, animals, enclosed spaces, and needles or injections. According to the DSM-5, diagnostic criteria include marked fear or anxiety that is out of proportion to and consistent in response to the stressor, avoidance behaviors, and significant distress or impairment in functioning. [First-line treatment consists of cognitive behavioral therapy with exposure to the patient’s specific phobia]. This therapy is designed to assist the patient in developing cognitive and behavioral strategies to modify their approach to the phobia. Exposure occurs in repeated and graded amounts, which decreases the fear through extinction. [Medication can be used if cognitive behavioral therapy is not sufficient. Medications used include benzodiazepines and selective serotonin reuptake inhibitors.]
