Sleep Medicine Flashcards
What are the features used to Dx restless legs syndrome?
URGE pneumonic
- Urge to move limb
- Rest (inactivity) worsens or precipitates the symptoms
- Getting up and moving improves the symptoms
- Evening or bedtime worsens or precipitates symptoms
Restless legs can be primary or secondary. Describe the phenotype of primary onset restless legs?
What are some causes of secondary restless legs?
Primary
- younger pts
- Slowly progressive / stable disease
Family Hx or idiopathic
Some causes of secondary inc
- Iron def, ESRF on HDx, preg, medication induced
What medicaitons can induce restless legs?
antidepressants, antihistamines, lithium and dopamine receptor blockers
What is the only pathological abnormality than can be identified in pts with restless legs?
Decreased iron store in the brain
Pt noted to have Periodic limb movements during sleep. What condition?
restless legs
- 80% of restless legs pts have PLMS
Medications of restless legs?
Dopamine agonists
Pregalablin, pregabalin (dont have augmentation or impulse control issues)
Opioids
What is the main issue with Rx restless legs with dopamine agonists? What to do if this occurs?
Augmentation
- symptoms actually get worse on dopamine agonists (usually initially improve)
- Aim to wean off Dop agonists and switch to another agent
Impulse control
- Dopamine agonists can cause issues with impulse control
What is a broad classification of parasomonias?
Sleep wake transition disorders
Non-REM parasomnias
REM parasomnias
What are risk factors for NREM parasomnias?
Priming factors (things that occur before sleep that make it more likely to occur that night)
- alcohol
- emotional stress
- sleep deprivation
- Zolpidem
Triggering factors (things that occur during sleep that can precipitate it. Basically anything that causes abrupt wake ups)
- OSA
- GORD
- SInus symptoms
What are some types of NREM sleep disorders?
Sleep walking
Confessional arrousals
Sleep terrors
How are NREM sleep parasomnia’s managed?
Conservatively
- prevent sleep deprivation
- Address exacerbating factors (ie etoh, sinus issues, OSA)
- Re-aasureance
- Safe environment
Pharm ( there is no RCTs in this space)
- Clonazapam has most evidence for NREM parasomnia in general
- Toperimatre for sleep related eating disorder
How does night eating syndrome differ from sleep related eating disorder?
Night eating syndrome is a psych condition, pts are aware of eating.
Linked to eating disorders
Sleep related eating disorder is a parasomnia, pts arent aware and have no recollection of the events
When do NREM parasomnias happen (sleep stage)?
Occur during non rem sleep by definition, usually N3 but sometimes N2 sleep
Usually first third of the night
What is the hallmark failure in a person with rem sleep behaviour disorder?
Loss of the usual REM sleep atonia
- this is why they can act out dreams in REM sleep
What is the main risk in pts with RBD?
pts with rem sleep behavior disorder are at very high risk of developing a alpha synucleinopathy in the future (parkinsons, LBD, parkinsons plus syndrome etc).
How is RBD Dx?
Requires re-enacting dreams
AND
Documentation of loss of atonia during REM sleep (polysomnography)
What is teh characterisitic features of acting out dreams due to REM sleep behaviour disorder?
Physically acting out dream
Impaired consciousness (ie pt is asleep)
Rapid return to baseline post waking (oriented and alert)
Pt can usually say they were dreaming, and can describe the dream (often correlates to the action ie fight = kicking and punching)
How does loss of atonia manifest on a leep study?
Chin and limb EMG activity during REM seel (evident rapid eye movements) on a sleep study
Management of rem sleep behaviour disorder?
Safe environ
- SLeep separately from people
- SLeep on the ground (ie not in high bed)
- SLeep in sleeping bag
- Wear restraints (lol)
Pharm:
- CLonazapam (usually respond very well to this)
- malatonin (only short acting is effective)
What are some sleep changes that are characteristic of Narcolepsy?
- The fall asleep fast
- Have early REM / REM sleep intrusions
- Often cycle sporadically though sleep stages with a greater proportion of REM sleep
WHo is most affected by narcolepsy?
Teenagers
How is narcolepsy T1 and T2 distinguished?
Narcolepsy type 1 is narcolepsy with catoplexy
- Low CSF hypocretin (AKA orexin) levels
Narc T2 is Narc without catoplexy
- Have normal CSF hypocretin levels
What is the clinical course of NT1, and NT2?
NT1 - usually stable does not resolve or get better
NT2 - can improve with time, can get worse or develop into type 1
Pt with elevated levels of hypocretin (orexin) in CSF. What condition?
NT2
- levels can be normal or high or low
NT1 only has low levels
What are some characteristic clinical features of NT1 and NT2?
NT1/2:
- Day time sleepiness
- Falling asleep sporadically throughout the day (sleep attacks)
- Automatic behaviors - doing things without realizing
- Sleep hallucinations when waking up from sleep
- Sleep paralysis (intrusion of REM sleep)
NT1 only:
- Catoplexy - partial or complete loss of muscle tone. Pt is awake and aware
What HLA is associated with NT1?
HLA DQB1 06:02
What are Dx criteria for Narcolepsy?
Mean sleep latency <8mins
At least 2 sleep onset REM periods
Catoplexy = NT1
How is narcolepsy managed?
Scheduled naps
Regular sleep schedule and hygine
School and work consideration
Pharm:
- Modafinil (contra in preg, can reduce effectivness of OCP)
- Amphetamine
How is catplexy treated?
Antidepressants
Sodium Oxybate
How is primary insomnia characterised?
Insomnia is charactgerised based on which specific part of slepe is affected
- Sleep initiation
- Duration of sleep
- COnsolidation of sleep
- Quality of sleep
How is insomnia treated? What medicaitons are used?
Primarily psychology driven ie stimulus control therapy, sleep restriction therapy, Relation therapy, CBT etc
Medicaitons can be used but should try to be avoided
Most are depressants so have issues like sedation, addiction, toelrance
Medications dont address the root problem either
How is the pathohysiology of OSA best understood?
The primary issue is colapse of teh upper airways during sleep
- there is an imbalance between the colapsing forces and the patency forces
RIsk factors for OSA? what is most predictive of OSA?
Middle aged men
Commercial driver
Obesity
Post menopausal women
Central obesity is most predictive
What are the main complications of OSA in the long term?
Cardiovascular complications
What does OSA look like on sleep capnography?
Respeated short duraiton desaturaitons (spiky appearance of graph with O2 sats on Y axis)
Treatment of OSA?
Conservative:
- Weight loss and exersise
- Supine avoidance (worse Sx wehen supine because gravity)
- Nasal decongestants or surgery (partial nasal blokcage results in relativly more negative intraairway pressure required which promotes col.,lapsing)
- Smoking cessation, avoid sedative drugs and etoh
Definitive managment?
- CPAP (fixed vs autoset)
- Oral appliance (Mandibular advancement device) - brace that moves your lower jaw forwards)
- Surgery
What is the main advantage and disadvantage of mandibular advancement devices vs CPAP?
CPAP is better managment but worse tolerated
MASD is worse managment but better tolerated
Does CPAP Rx for OSA reduce the risk of secondary cardiovascular events?
Unclear
Large RCT showed nil difference with CPAP, however there were strict exclusion criteria that make interpretation of this result difficult.
Regardless should treat people even if just for symptomatic control
What is signs of OSA on sleep study?
the thorasic and abdo bands show movement (ie effort to breath), but there is no flow of air on the flow meter
THis correlates with drop in O2 sats
Pt is a truck driver. He is very sleepy, often hjas near misses (ie almost falls asleep at the wheel). Can he drive?
No, should recommend nil driving until Dx and Rx issue
What is a more severe form of OSA?
If OSA is severe it can also involve hypoventialation
- OSA + obesity hypoventiualation overlap
How is obesity hypoventilation Dx?
Evidence of hypoventilation during wakefulness (PaCO2 >45)
Presence of obesity
Hypoventilation is not due to other lung disease or airway disease etc
WHat are the two pattern of OHS presentation?
Acute on chronic resp failure
- 30-70% of first presentations-
- High incidence of needing ICU
- Most were Dx with COPD (given the prominent hypercaponea) despite having nil restriction on PFTs
Chronic (stable) OHS
- usually found on routine assessment of OSA
- Dx late and Dx when end stage
What is treatment for OHS?
Weight loss
Lifestyle (similar to OSA)
If have significant or severe OSA (often teh case)
- CPAP to treat the OSA. THis willm often normalise the CO2 and solve teh issue
If pts fail CPAP then will need NIV (ie BiPAP)
Pt suspected to have obestiy hypoventialation. Being DC from hospital. SHould they be DC from hospital on NIV prior to having been formally Dx with OHS?
Yes, DC hosp with NIV
Then OP Sleep study to Dx issue
What are the causes of central sleep aponea?
Primary (idiopathic)
Secondary:
- CCF (most important cause)
- Drugs (Opioids)
- Stroke, neuromuscular condition, CNS conditions
How does OSA differ from central aponea on sleep study?
OSA will show action in abdo and thorasic bands
Central aponea wont
What are some conditions under the banner of sleep related hypoventiaslation and hypoixaemic syndromes?
- Obestiy hypoventilation syndrome
- Severe COPD (often hypoventilates at night)
- Severe OSA
- Neuromuscular disorders (esp during REM sleep because accesory muscles are parylysed)
- CNS disorders
- COngenital central hypoventialation syndrome (PHOX 2B gene)
Severe COPD comes in with resp failure requiring NIV in hosp. How do you decid if they need long term NIV?
Most COPD pts with acute resp failkure are no longer hypercaponeic once acute exacerabtion has resolved
therefore DC then blood gas in 2 week to see if baseline hyp[ercaponic
If baseline hypercaponic then evidence to say that NIV will reduce hospitalisaitons and is gerenally good
