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121 Cards in this Set
- Front
- Back
40 y/o with insomnia after death of his brother. ANSS without OSA or PLMD. Dx?
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Adjustment sleep disorder.
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Effect of benzos on sleep stages? Non-benzo hypnotics?
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Benzos increase stage II. Decrease REM, SWS. Non BZ agents do not decrease SWS or REM.
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Morning anxiety in patient using triazolam?
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Rebound anxiety can be seen with shorter acting agents.
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Nefazodone (Serzon) mechanism?
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Blocks 5HT2 and serotonin reuptake.
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Mirtazapine (Remeron) mechanism?
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Alpha-2 blocker (increases NE and serotonin), 5HT2, 5HT3 blocker.
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Hypnotic agent for mid-cycle awakenings?
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Sonata - shortest half-life.
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30 y/o woman with several year hx of sleep init/maintenance insomnia. Sleeps okay when traveling. Has normal ANSS. Why?
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Psychophysiological insomnia. If less than 6 monhs, this is adjustment sleep disorder. Normal ANSS cold also indicate sleep state misperception.
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Reverse first night effect?
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Good night sleep in the lab. Suggests psychophysiological insomnia or problem with home sleep environment.
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Cyclic activity in chin EMG suggests this dx.
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Bruxism
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Prevalence in kids and adults. Risk factors?
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20-88% in kids (before adult teeth come in). Approx 3% of adults over 60. Smokers may have more bruxism.
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Medications causing bruxism? Other possible causes?
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Levodopa, SSRIs. Stress, tooth malocclusion.
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Associated sx?
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Headache, TMJ pain,
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Bruxism most common in which stages?
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II, REM (tonic)
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Treatment for bruxism?
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Nothing proven in clinical trial. Mouthguard may help. Many meds tried: levodopa, benzos, muscle relaxants, relaxation therapy, biofeedback, hypnosis.
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Typical EMG pattern in bruxism?
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"Checkerboard" pattern.
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Percent of seizure occuring only during sleep?
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10-40%
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Order of seizure threshold from low to high in wakefulness, REM, NREM sleep?
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REM, wake, NREM. (Highest chance of a seziure in NREM sleep.)
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EEG pattern for seizures? Usual direction of initial deflection?
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Spike and wave. Negative (up).
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Correct way to amplify a nasal pressure signal on PSG?
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DC signal or AC with long time constant or very small low filter setting (<=0.01).
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Three factors influencing degree of O2 desat in OSA patients.
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Waking supine PaO2, amount of sleep spent in apnea, and ERV.
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Causes of a false negative sleep study?
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Abstinence from usual alcohol or sedative use. Mild OSA can show more night to night variability. Lack of REM or supine sleep.
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Minimum amount of sleep required for diagnostic portion of split night study.
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Two hours.
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Minimum AHI for split study.
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AHI > 20 with desats; > 40 if no associated findings.
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Shape of expiratory flow curve in a central apnea?
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Round.
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No change in body position with fluctuating level of recorded leak - probably source of leak?
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Mouth
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"Symptomatic" according to Medicare guidelines for CPAP treatment.
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EDS, HTN, ischemic heart dz, stroke, insomnia, mood disorder.
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Does sham nasal CPAP improve subjective daytime sleepiness?
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Yes. Placebo effect documented in 1999 Lancet article.
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Medicare definition of hypopnea.
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>=30% reduction in airflow with 4% desat. Does not include arousals without desats.
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Do split night studied over- or underestimate OSA severity.
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Usually underestimate. Don't record as much supine/REM sleep.
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Possibly useful types of positive airway pressure for patient who has trouble tolerating high pressures needed in specific position or sleep stage.
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BiPAP or Auto-CPAP
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Usual method of titrating BiPAP.
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Keep IPAP=EPAP and increase both until apneas resolve. Then increase IPAP until hypopnea and snoring resolves. Or, start at 6/4 and sequentially increase IPAP then EPAP to desired effect.
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BiPAP helpful for mouth leak?
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Yes. Not studied, but sometimes you can get away with less pressure.
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If there are persistent apnea, do you adjust IPAP or EPAP? And for persistent hypopneas?
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Increase EPAP for apneas, IPAP for hypopneas (and snore).
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Potential cause of hypoxia during REM immediately after adequate CPAP titration?
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Can have more REM d/t rebound, with hypoventilation during REM.
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How to treat hypoxia/hypercapnia in obese pts. with OSA? Is it permanent?
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Consider bilevel pressure or volume cycled mode. Ventilation usually improves after few weeks on CPAP.
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Patients that do best with UPPP?
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Those with upper airway narrowing limited to retropalatal area.
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Failed UPPP cases: most common site of failure?
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Retropalatal area.
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Less common but severe cause of failure post UPPP?
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Nasopharyngeal inlet stenosis.
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Post-op UPPP complications?
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Pain. Velopharyngeal incompetence (snarfing). Change in voice. Globus. Worsened OSA.
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Poor candidates for oral appliance?
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Pre-existing TMJ. Not in book but according to Dr. Rosen: very large neck.
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Two major types of oral appliance?
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Tongue retaining device and mandibular advancing device.
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Criteria for safety clearnace using MWT?
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None have been established.
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"Normal" MWT results?
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Stay awake more than 19 minutes on a 40 minute test or 11 minutes on a 20 minute test.
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Things that worsen simple snoring?
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Anything that narrows upper airway, increases nasal resistance, decreases upper airway muscle tone: sedatives, supine position, nasal congestion.
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Prevalence of habitual snoring over age 40?
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Some studies suggest 60% men 40% women.
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Intensity of snoring and stage of sleep?
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Loudest in SWS, quietest in REM.
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Do thermistors detect snoring?
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No. But nasal pressure xducer or pneumotachograph can.
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EMG chin pattern sometimes seen with snoring?
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Increase in chin EMG activity at inspiration.
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Stage of sleep with loudest snoring?
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Stage IV
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Can you have UARS without excess daytime somnolence?
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No
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Why would someone with Prader-Willi have prolonged elevation of transcutaneous CO2 and hypoxia without frank obstructive events?
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Markedly blunted hypoxic ventilatory response, especially in peripheral chemoreceptors. The hypercapneic response can be blunted, mainly in the obese.
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Chromosome usually affected in Prader Willi?
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15
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Are hypnotics safe in patients with COPD?
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Minimal effect on breathing if stable COPD (not overlap syndrome) with normal daytime CO2.
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Does nocturnal O2 cause CO2 retention?
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Should not as long as there is no sleep apnea present.
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DDx of nocturnal awakenings in patients with asthma?
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Diurnal reduction in airflow vs. OSA. FEV1 hits nadir at 4am. Treating OSA can also help control the asthma.
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Timing of arousal in Cheyne Stokes vs. idiopathic central apnea?
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C-S apnea - arousal usually at peak ventilatory effort. Idiopathic - usually at apnea termination.
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Tx of idiopathic central sleep apnea?
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Debatable. CPAP, oxygen, triazolam, inhaled CO2, acetazolamide all listed.
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Two top causes of Cheyne Stokes breathing?
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CHF and stroke
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Prevalence of C-S apneas in severe CHF?
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"As high as" 40-50%
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Difference in daytime pCO2 in CHF patients with or without Cheyne Stokes?
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Lower pCO2 in Cheyne Stokes patients.
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Difference in hypercapneic ventilatory drive in CHF patients with or without Cheyne Stokes breathing (CSB)?
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Higher drive in CSB patients.
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Difference in LV filling pressure in CHF patients with or without Cheyne Stokes?
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Higher LV filling pressure in CSB.
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Effect of higher filling pressures on ventilation?
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Can stimulate lung receptors, lead to increased ventilation.
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Why does CPAP help CSB? Three reasons (in theory).
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Improve LV function, increase O2 stores (less desat), and slightly increase pCO2.
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How does adaptive servo ventilation work?
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During hypoventilation, the IPAP/EPAP difference widens. Narrows during increased ventilation. Usually maintains minimum of EPAP 5. Can have back up rate.
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Usual PSG finding in congenital central hypoventilation?
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Reduced tidalvolume and respiratory rate. Central apneas not common.
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Why would ventilation be worse in NREM sleep for CCHS patients?
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Metabolic control of ventilation occurs during NREM; durin REM, there is less related to hypoxic/hypercapenic input.
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Two disease associationg seen with CCHS?
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Hirschsprung dz and neuroblastomas.
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Are peripheral chemo-receptors functional in CCHS?
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Yes. (AK - One study showed passive pedaling of legs during sleep reduced pCO2 in these patients.)
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Are leg movements associated with apnea termination counted towards the PLMI?
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No.
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If there is a periodic movement in the left leg >5 seconds after onset of a periodic movement in the right leg, are the events counted as one or two?
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Two. More than 5 secs apart and they're separate events.
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Difference between a leg movement and a periodic leg movement?
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PLM has to be part of 4 repetitive movements, not associated with apnea termination or after an arousal.
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Criteria for counting a leg movement?
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Lasts 0.5 to 5 secs and is at least 25% amplitude seen in the biocal. These criteria can vary.
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ICSD categorization of PLMs into mild, mod, severe?
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5-24 mild; 25-49 moderate; > 50 severe. PLMA index > 25 is severe. Not based on any data.
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Frequency of augmentation when RLS treated with carbidopa? If PLMS tx'd with crabidopa?
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Up to 80% in RLS and 30% in PLMS.
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First step if you see augmentation with Mirapex?
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Treat earlier in the evening.
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Side effects seen in Mirapex?
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Nausea, hypotension, somnolence, headache, and rare lower extremity edema.
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If you get nausea or augmentation with mirapex, what advice do you give?
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Try splitting dose - half at 6p half at 8p.
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Requip side effects?
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Nausea, somnolence, postural hypotension.
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Mechanism of clearnace in requip? In Mirapex?
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Requip = hepatic; mirapex = renal.
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% of narcolepsy patients with cataplexy
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70%
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Concordance in twins?
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25-30%
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% of narcolepsy cases starting over age 50?
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5%
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Percent of narcoleptics with the tetrad (cataplexy, hypnagogic hallucination, sleep paralysis, sleep attacks)?
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10-15%
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Is cataplectic weakness ever asymmetric?
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No.
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Abnormally low REM latency? Percent of narcoleptics wit this PSG finding?
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Less than 20 mins. 40-50%.
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Probablility of a positive MSLT (two REM naps and mean sleep latency < 5 mins) in a narcoleptic?
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70-80%
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Generic name of Dexedrine? Dexosyn? Ritalin?
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Dextroamphetamine. Methamphetamine. Methylphenidate.
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Major toxicity of pemoline?
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Liver
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Nonpharmacologiscal methods to treat narcolepsy?
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Sleep hygiene, scheduled naps, adequate sleep time.
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Most common side effect of Provigil? How to avoid it?
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Headache. Can start at 100mg for a few days before increasing dose.
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Important warning for women taking Provigil?
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Reduced efficacy of birth control meds.
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Alternative therapy to stimulants in narcoleptics?
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Selegiline - alerting and anticataplectic properties. Irreversible MAO type B inhibitor. Has non-selective MAO inhibition abotve 20mg dose. Need low tyramine diet.
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Does negative HLA DQB1*602 rule out narcolepsy? How many narcoleptics are negative?
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No. 1-5%.
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Approach to persistent sleepiness in OSA?
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Check compliance, rule out concurrent sleep disorders. MSLT with CPAP can show narcolepsy in right clinical scenario.
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Other haplotypes associated with narcolepsy?
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HLA-DR2. HLA-DR15 (negative in 40% of African Americans).
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Familial cases of idiopathic hypersomnia associated with which HLA?
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HLA-Cw2
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Associated symptoms in familial IH?
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Autonomic dysfunction - hypotension, Raynaud's, syncope.
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Hypersomnia after head injury?
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Posttraumatic hypersomnia develops 6-18 months after accident.
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Clue to depression on PSG?
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REM latency less than 60 mins.
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Things to rule out prior to making diagnosis of IH?
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Depression, hydrocephalus, meds/abuse, insufficient sleep, UARS or OSA, PLMS.
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MSLT findings in IH?
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Latency < 10 mins, less than two REM naps.
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Stage of sleep associated with bruxism?
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Stage II
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Does sleepwalking require a psych eval?
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No. Usually not associated with psychopathology. Book says "at least" 50% of adults who sleepwalk don't have psychpathology. Sounds like a lot of psychopathology to me.
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When does sleepwalking occur?
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Classically in SWS (first third of night), especially in kids. Can occur in stage II, so it may be seen in 2nd half of night.
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Sleepwalking triggers?
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Sleep deprivation, fevers, meds (lithium, phenothiazenes [compazine, thorazine], tricyclics).
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Reasons to get sleep study in suspected parasomnia?
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Injury, medico-legal issues, high frequency of events, daytime somnolence.
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Prevalence of bruxism over age 60? In kids?
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About 3%. 20-88% of kids.
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Usual rate of bruxism?
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About 1 per second.
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Appropriate paper speed for examining rhytmic EEG activity?
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30mm/sec (10 second epoch)
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Probablility of seizure in REM, NREM, wake.
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NREM > Wake > REM
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Mimics of spike and wave?
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Bursts of theta or delta (no spikes); electrode popping (usually slower frequency than spike and wave).
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Difference between interictal spike and wave activity versus ictal (or seizure) activity?
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Interictal is isolated. Ictal occurs in bursts.
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Percentage of seizure occuring primarily or only in sleep?
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10-40%
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Insomnia at home, but relatively normal sleep in the lab or when away from home?
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Psychophysiological insomnia.
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Psychophysiological insomnia of less than 6 months?
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Adjustment sleep disorder
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Three GABA-benzo receptor subtypes, BZ1, 2, and 3. Which is responsible for hypnotic effect?
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BZ-1.
BZ-2 and -3 induce muscle relaxant, anti-seizure and anxiolytic effects. |
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Presentation of delayed sleep phase syndrome?
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Sleep onset insomnia.
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Two antidepressants that increase REM sleep?
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Bupropion and nefazodone.
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Mechanism of mirtazapine?
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Blocks 5HT-2, 5HT-3, histamine type 1, alpha-2 receptors.
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Kleine-Levin syndrome?
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Recurrent hypersomnia. At leas 1-2 times per year, 3-21 day episode of voracious appetite, hypersexuality, disinhibition. Can just be hypersomnolence.
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