SPN, Pleural Disease, Sleep Flashcards
Differentiate benign vs. malignant patterns of calcification for a solitary pulmonary nodule
Suggests benign etiology (ex: hamartoma) if calcification if diffuse (think granuloma), popcorn (think hamartoma) central, or laminar/concentric
Beware of malignant if stippled (dotted) or eccentric
Name features of a benign solitary pulmonary nodule
-calcification, more specifically diffuse popcorn concentric or central (think hamartoma, granuloma)
-fat containing (think hamartoma)
-vessel running in and out as you scroll (think AVM)
Hounsefeld units of
(a) Air
(b) Water
(c) Fat
(d) Bone
(e) Lung parenchyma
Hounsefield units- universal units for CT scan, based on arbitrary delineation of water as 0 and air as -1,000
So scale generally runs from -1,000 (air, all black) to +2,000 (bone or metal, all white)
(a) Air: -1,000
(b) Water: 0
(c) Fat: -35 to -40 Hu
(d) Bone: +2,000
(e) Lung parenchyma: -600 to -700 (has a lot of air in it…)
Aside from granuloma or hamartoma, what are other etiologies of solitary pulmonary nodules
-pulmonary AVMs (see vessels running in and out)
-lipoid PNA (fat containing)
-intrapulmonary lymph node (often peripheral, can be triangular shaped)
For what specific type of nodules do the Fleischner Society Guidelines refer to?
-incidentally found (so NOT for nodules found on lung cancer screening CT)
-not for immunocompromised
-not if have a feature suggesting benign nature (calcification, fat, vessel, peripheral and triangular)
So incidentally found solitary pulmonary nodules
Guideline recs for f/u of solitary solid pulmonary nodule incidentally-found based on size
Fleischner Society Guidelines for incidentally found solitary pulmonary nodule
Under 6mm: NTD (can continue annual cancer screening for those at high risk)
6-8mm: CT chest at 6-12 months for both low and high-risk groups
Over 8mm: F/u CT chest at 3 months vs. PET vs. tissue sampling
Guideline recs for f/u of multiple solid pulmonary nodule incidentally-found based on size
Multiple nodules:
Still if under 6mm no f/u needed, if high risk optional at 12 mo
Anything over 6mm: f/u in 3-6 months (so faster than SPN which is 6-12 mo)
Guideline recs for f/u of solitary ground glass vs. sub-solid pulmonary nodule incidentally-found based on size
Both ground glass and subsolid nodule: again if under 6mm: no f/u needed
If ground glass over 6mm: f/u 6-12 months (want to trend the solid component)
If part solid over 6mm: CT at 3-6 months
Give a Ddx for nodules based on 3 different types of distribution of CT
3 distributions of nodules
- centilobular- think HP, bronchiolitis (infectious or respiratory from smoking)
- perilymphatic- think sarcoid
- random- think hematogenous spread of either miliary infection (Tb or fungal) or metastasis
How to narrow diagnosis for multiple random nodules on CT chest
Random nodules
-homogeneous and tiny (1-3mm): think miliary Tb
-heterogeneous maybe ground glass or solid mixed think metastases
Describe classic nodular pattern of sarcoidosis on CT
(a) Galaxy sign
Perilymphatic nodules- so along interlobular septa, fissures, aka where the lymphatics go
(a) Nodules (representing granulomas) can coalesce into mass-like consolidations = galaxy sign
Describe the type of nodules seen here:
(a) Likely diagnosis
Centrilobular- spares periphery, hazy, in the middle of the lobule, equally separated b/c standard size of secondary lobule (smallest unit visible on CT chest)
(a) acute HP = diffuse centrilobular nodules
What is this pattern on CT?
(a) Location of the nodules
(b) Likely etiology
Y-shaped branching centrilobular nodules c/w tree-in-bud opacification due to bronchiolar obstruction causing dilation/impaction of the centrilobular nodule
(a) Tree-in-bud if a form of centrilobular nodules
(b) Mucoid impaction- can be from any acute infection, seen in asthma, MAI
Distinguish halo sign and reverse halo sign on chest CT
(a) Imaging features
(b) Buzzword diagnoses
Halo sign:
(a) central consolidation with surrounding ground glass classically representing hemorrhage
(b) angioinvasive aspergillus (or other fungal infection)
Reverse-halo sign = Atoll sign
(a) Central ground glass (central clearing) with denser consolidation crescenting around at least 3/4 circumference
(b) Organizing PNA, fungal infection, GPA, pulmonary infarct
What is Atoll sign on chest imaging?
Reverse-halo sign = Atoll sign
(a) Central ground glass (central clearing) with denser consolidation crescenting around at least 3/4 circumference
(b) Organizing PNA, fungal infection, GPA, pulmonary infarct
When may a pleural effusion due to CHF be exudative?
CHF effusion may be falsely exudative in s/o diuresis
-check out the albumin ratio to serum, aka likely that serum albumin is also reduced
Explain how can have a hepatic hydrothorax w/o ascites
Yes due to oncotic pressure pushing ascites up through diaphragmatic defects, but also can be due to negative intrapleural pressure (lungs draw in fluid from abdomen)
Diagnostic criteria for spontaneous bacterial pleuritis
(b) Mgmt
The other SBP = complication of hepatic hydrothorax
Diagnosis: either + culture with more than 250 nucleated cells (neutrophils)
or negative culture w/o evidence of PNA and more than 500 nucleated cells (neutrophils)
(a) Typically just need abx, don’t require drainage
What dx to consider if pt with nephrotic syndrome presents with exudative pleural effusion?
Think of pulmonary embolism
-high risk (about 20%) of PE in pts w/ nephrotic syndrome due to acquired protein S deficiency
Differentiate pleural manometry of normal vs. trapped lung
Pleural manometry in trapped lung- big pressure drop with removal of small amount of fluid
What is pleural elastance?
Pleural elastance- change in pressure of the pleural space per certain amount of volume removed
= dP/dV
ex: High pleural elastance in trapped lung where with small volume removal there is a big change in pleural pressure
-while normal needs a large volume removed to get a change in pressure
Differentiate trapped vs. entrapped lung
(a) Which may be reversible
Trapped = abnormally high pleural elastance due to fibrous thickening of the visceral pleura causing the pleural space to be irreducible
(a) Typically not reversible, may require decortication if pt very symptomatic
Entrapped = initially normal elastance (dP/dV) that becomes abnormally high as pleural fluid is removed, typically due to restriction of the visceral pleura from acute inflammation
(a) May resolve with treatment of the active pleural process
Describe physiology of transudative vs. exudative pleural effusion
Transudative- low protein fluid pushed against intact capillary membrane due to increase in hydrostatic pressure inside the capillaries
Exudative- fluid pushed against defective capillary membrane (due to inflammation- think infection, malignancy, rheumatologic) => allowing protein and cells (neutrophils, hence elevated LDH) to cross
Rare causes
(a) Parapneumonic effusion with high pH
(b) Transudative effusion w/ low pH
(a) Proteus PNA uniquely causes a parapneumonic effusion w/ elevated pH while other parapneumonic effusions will have low pH
(b) Urinothorax (urine in the pleural space) due to an obstructive uropathy = only cause of low pH transudative pleural effuison
Etiology of pleural effusion will cause what to pleural glucose
(a) Low
(b) Super low
(b) Normal
Pleural glucose typically mirrors pleural pH
(a) Low (under 60)- malignancy, infection, rheumatologic (lupus, rheumatoid), Tb
(b) Very low, like undetectable- think rheumatoid pleurisy or empyema
(c) Normal (mirrors serum) in transudative
3 most common causes of a lymphocytic pleural effusion
Malignancy, Tb pleuritis, and post-CABG
What is the typical cause of eosinophilic effusions (when eos are more than 10% of nucleated cells)
Nonspecific finding typically from trauma- reflecting blood (hemothorax) or air (penumothorax) in the pleural space
Positive beta-2 transferrin in pleural fluid is diagnostic for what?
(a) Clinical context
Beta-2 transferrin positive in duropleural fistula = fistula between subarachnoid space and pleural space (aka CSF in the pleural space)
(a) After trauma, spinal or CT surgery, or malignancy
Expected composition of pleural effusion due to perforated esophagus
L-sided effusion typically exudative with signs of inflammation (low pH, glucose under 60, LDH over 1000)
-L sided, very low pH (under 7.0), high salivary amylase (not pancreatic amylase)
Differentiate simple vs. complicated parapneumonic effusion
(a) pH
(b) Pleural glucose
(c) Pleural LDH
Simple parapneumonic effusion:
(a) pH over 7.2
(b) Glucose over 60 (more similar to serum)
(c) LDH under 1,000
Complicated parapneumonic
(a) pH under 7.2
(b) Glucose under 60- mechanism presumed that bacteria using up the glucose
(c) Pleural LDH over 1,000
MIST-1 vs. MIST-2 trial results
MIST-1: no improved outcomes with intrapleural tPA for empyema
MIST-2: tPa/DNase superior to either alone for empyema- reduced hospital LOS (by almost a week), reduced surgical referral, improved fluid drainage
Characteristics of pleural effusion associated with
(a) Pulmonary embolism
(b) Tb
(c) Pancreatitis
Pleural effusion
(a) PE- exudative, not uncommon (book says up to 20-50%), thought to be due to increased permeability
(b) Tb- exudative, low glucose, lymphocytic
(c) Pancreatitis- exudative, elevated amylase, typically L-sided
LIkelihood of AFB culture positivity in pleural fluid from TB pleuritis
Under 40% (so low sensitivity)
ADA is pretty sensitive (90%), use PCR
Pleural fluid studies to differentiate RA and SLE pleuritis
RA is uniquely low pH (under 7.2) and low glucose (under 60)
While SLE pleurisy expect normal pH and normal glucose (similar to serum)
Definition of hemothorax
Hemothorax: pleural fluid hematocrit at or above 50% serum Hct
Most common causes of cholesterol pleural effusion (pseudochylothorax)
Cholesterol effusion typically due to long-standing pleurisy (pleural inflammation) from Tb pleuritis or RA pleurisy
Chylothorax vs. cholesterol effusion
(a) Mechanism
(b) How to differentiate on pleural fluid studies
Both can look milky/opalescent but very different mechanisms, differentiate objectively by TG and chylomicrons
Chylothorax
(a) Lymphatic fluid (chyle) spills into pleural space due to damage or obstruction of thoracic duct
(b) Diagnostic TG over 110 with presence of chylomicrons
Cholesterol effusion from (a) chronic pleural inflammation (Tb or RA)
(b) No chylomicrones, TG under 110, total cholesterol over 220
Chylothorax vs. cholesterol effusion
(a) Main causes
Chylothorax (chyle in pleural effusion)- due to damage to or obstruction of lymphatic duct- iatrogenic (procedure) or malignancy
-characteristic presence of chylomicrons in pleural fluid
-pleural fluid cholesterol under 200
Cholesterol effusion (cholesterol in pleural effusion) due to chronic inflammation of pleural space, (a) typically Tb or RA pleurisy
-fluid cholesterol > 200
Differentiated more by cholesterol:TG ratio- higher it is, more likely cholesterol effusion vs. chylothorax
List causes of elevated amylase in pleural fluid
Amylase in pleural fluid-
-pancreatitis (acute or chronic), typically L-sided effusion
-esophageal perforation
-pulmonary malignancy
Triad of yellow nail syndrome
- Yellow/discolored, hardened nails
- Lung disease- typically pleural effusion but can be bronchiectasis or chronic sinusitis
- Lymphedema => swelling
Name 3 findings of benign asbestos-related pleural abnormalities
Asbestos-related pleural disease
- (15-20 year latency) benign asbestos- pleural effusion- often bloody, exudative, occasionally with eos
- 20 yr latency- pleural plaques, do not correlate with mesothelioma risk
- Rounded atelectasis- infolding of redundant pleura, can appear mass-like
Typically what is the earliest pleural finding of asbestos exposure?
- (15-20 year latency) benign asbestos- pleural effusion- often bloody, exudative, occasionally with eos
- 20 yr latency- pleural plaques, do not correlate with mesothelioma risk, calcifies over time (30+ years)
Comet tail sign on CT chest
Comet tail sign of rounded atelectasis- pulling of bronchovascular bundle leading to peripheral mass-like appearing consolidation of collapsed lung due to infolding of redundant pleura
-classically 2/2 asbestos exposure
-also pulmonary infarct, parapneumonic effusion, Tb
Normal intrapleural pressure at FRC
(a) Normal increase in intrapleural pressure with 2L pleural fluid in the hemithorax
Intrapleural pressure at FRC (RV + ERV, end of tidal exhale) is about -5
(a) Pleural pressure can increase to about +10
Differentiate lung entrapment from trapped lung
(a) Etiology
(b) Pleural pressure change
(c) Reversibility
Entrapped lung (b) Can remove some pleural fluid with normal drop in pleural pressure, but then when remove a lot get a precipitous drop in pleural pressure
(a, c) typically more reversible etiology of pleural inflammation like infection causing thickening of visceral pluera, also from endobronchial obstruction
vs.
Trapped lung (b) with removal of just 500cc get precipitous drop in intrapleural pressure
(a,c) Chronic more difficult to reverse process, typically visceral pleural scarring
Explain how to use pleural manometry to reduce risk of re-expansion pulmonary edema
Normal intrapleural pressure at FRC is around 0 to neg 5, when accumulates fluid can rise to ~+10
While draining fluid stop when pleural fluid starts to approach -3 to -5 to prevent re-expansion pulmonary edema.
If yoiu stop by pleural manometry or when pt reports chest pain there is very low risk of reexpansion pulmonary edema
Explain how to use pleural manometry to predict risk of pneumothorax ex vacuo
PTX ex vacuo when the lung cannot re-expand- see a drastic drop in intrapulmonary pressure with removal of not a lot of fluid. So if see intrapleural pressure on manometry drop to way below -5 esp with removal of just 500-750cc of fluid think PTX ev vacuo
For an exudative pleural effusion differentiate meaning of elevated protein vs. elevated LDH (what do they signify about the effusion)
Elevated protein indicates broken capillary barrier => proteins can leak
Elevated LDH indicates high inflammation => lots of cells and turnover
What additional pleural fluid test can be helpful to differentiate heart failure effusions falsely classified as exudates?
Up to 25% of transudative effusions can be falsely classified as exudative, especially in s/o diuresis
Can use pleural fluid cholesterol to help differentiate, pleural fluid cholesterol over 55 suggests exudative
Things that can falsely change the pH of pleural fluid
(a) Falsely increase pH
(b) Falsely lower pH
(a) Falsely increase pH (reduce sensitivity for complicated effusion) in excess air in the syringe and excess time until processing
(b) Lidocaine can falsely lower pH detection
Tricks to improve accuracy of pleural pH measurement
(a) What measure may be used as a surrogate?
Put on ice, push out air bubbles, get to lab within an hour. (air and time in syringe can falsely increase pH). Try to avoid lidocaine in syringe (can falsely drop pH)
(a) Glucose can potentially be used as a surrogate b/c low glucose often seen in same things that have low pH (empyema)
Pleural fluid studies diagnostic for spontaneous infection of hepatic hydrothorax (spontaneous bacterial pleuritis)
Either
-ANC over 250 with positive culture, or
-ANC over 500 with negative culture
What determines whether chylothorax will be R or L sided?
Depends where the injury (or obstruction) is to the thoracic duct. Around level of T5 thoracic duct migrates from R to L
so below T5 => R chylothorax
above T5 => L chylothorax (then thoracic duct drains into L subclavian
Pleural fluid studies to differentiate lupus from rheumatoid pleuritis
Mostly differentiate by LDH and glucose
RA: expect LDH over 1,000, strikingly low glucose often under 30
elevated RF
What syndrome to suspect when pt with uterine fibroids presents with pleural effusion
Meig’s syndrome: pleural effusion, ascites, benign ovarian mass (fibroma), often elevated CA-125
-association of adnexal mass with ascites and pleural effusion
Tx = remove the adnexal mass to resolve the ascites and pleural effusion
Differentiate characteristics of early vs. late post-CABG pleural effuions
Early (within first 30 days) expect bloody and possible eosinophilic
Late (after 30 days) expect lymphocytes, non-bloody
Most common bugs causing pleural infection
(a) community acquired
(b) nosocomial
(a) 85% pleural infections community acquired
-most common (70%) strep
-2nd with 15% staph
(b) 15% hospital acquired
-Most common (40%) staph, then 25% gram negatives
Outcomes of MIST-2 trial
MIST-2 NEJM 2011: tPA + DNase superior to either alone for reducing surgical referral, hospital LOS, and improving drainage/radiographic outcomes for pts with complicated parapneumonic effusions or empyema
-not reduced mortality
What marker can be added to pleural ADA to increase specificity of TB pleuritis to nearly 100%?
IL-27
What disease to consider in pt with spontaenous PTX and the following skin finding
Fibrofolliculomas (benign hamartomas of hair follicles) + cystic lung disease (25% risk of pneumothorax)- think Birt-Hogg-Dube due to autosomal dominant mutation in folliculin gene
folliculin gene mutation => loss of function of tumor suppressor gene
Per guidelines which PTX can potentially be discharged from the ED?
Primary spontaneous PTX that is small
-primary only, not secondary: so no underlying lung disease. underlying lung disease => should get admitted
-small meaning under 3cm from apex to cupola
Can manage by watching in ED for 3-6 hrs then sending home w/ f/u CXR next day
Primary spontaneous PTX
(a) At what size requires drainage?
(b) Recurrence rate
(c) When to consider procedure to prevent recurrence
Primary spontaneous PTX
(a) Over 3cm from apex to cupola (top of chest wall to top of lung) requires admission and drainage- under 3cm can consider expectant management and d/c home
(b) Recurrence rate 25-50% in the first year
(c) Don’t pleurodese after the first, consider after the second
Clinical story hint to consider thoracic endometriosis in patient with spontaneous pneumothorax
Catamenial symptoms- so chest pain and PTX during time of menses
Which carries higher risk of PTX: Birt-Hogg-Dube vs. LAM?
BHD- about 25% risk of PTX
-folliculin gene mutation
-associated skin fibrofolliculomas and kidney tumors
vs.
LAM- about 50% lifetime risk of PTX
-TSC gene mutation
-associated renal angiomyolipomas
Top 3 most common cancers causing malignant pleural effusion
Lung –> breast –> lymphoma
Describe process of talc pleurodesis
First drain all fluid (want the pleural surfaces as together as possible)
Then talc pleurodesis- mix 4g talc with normal saline, inject into chest tube (can be either small or large bore) then keep it clamped for an hour. (can have patient shift around to try to distribute talc) then unclamp and let drain to suction, then take out chest tube when drainage low for 24 hrs
Describe mechanism by which medical pleurodesis is supposed to work
Thought is to cause inflammation/fibrosis that adheres the visceral and parietal pleura together
First line- talc
Others- doxycycline, bleomycin
TIME-1 trial:
(a) NSAIDs vs. opiates for chest tube analgesia
(b) Small vs. large bore chest tube for empyema
TIME-1 trial for chest tube placement
(a) No difference in pain scores or rates of pleurodesis for NSAIDs vs. opiates
-try to use NSAIDs before opiates
(b) Small bore obviously less pain, trend towards noninferior but not significant
What did the ASAP trial (AJRCCM 2017) tell us about best frequency of pleurX drainage
ASAP trial- compared q24 hr to q48 hr of pleurX fluid drainage- showed more frequent drainage (q24h) had better rate of pleurodesis
-median time to autopleurodesis was 54 days
=> standard of care is daily drainage for median of 54 days
What did the IPC-Plus trial (NEJM 2018) tell us about talc via intrapleural catheter vs. placebo for rate of pleurodesis
IPC-Plus: for patients with intrapleural catheter in place, put talc in vs. placebo, pts who got talc had double the rate of pleurodesis
So can put talc through a pleurX! (assuming not a trapped lung)
Differentiate the two types of asbestos forms
(a) which more carcinogenic?
Asbestos refers a group of silicates that exist in a fibrous form, 2 types
(a) Serpentine- spiral shaped and pliable, accounts for large majority (90+%) of exposures in the US, less carcinogenic
(b) vs. amphiboles- rigid, needle-like, can penetrate through lung into pleural surface
more carcinogenic
Environmental risk factors for asbestos exposure
Ship building, plumbers, pipefitters, mechanical engineer, ship/boat building,
Typical latency period for
(a) pleural plaques
(b) asbestos-related pleural effusion
(c) mesothelioma
(a) pleural plaques- 20ish years
(b) asbestos-related pleural effusions can have the shortest latency period, can develop within 1-20 yrs of exposure
(c) Mesothelioma after typically 30+ yrs
Preferred management for trapped lung causing malignant pleural effusion
For trapped lung due to malignant cause can still consider intrapleural catheter (pleurX) b/c then patient can drain fluid gradually and stop at any pain (when pleural pressure gets too negative)
Main advantage of intrapleural catheter over talc pleurodesis
IPC- outpatient procedure, vs. 6-7 day LOS stay for pleurodesis
-similar improvement in quality of life, dyspnea, similar cost (given initial hospital costs offset by pleurX supply catheters)
In hospital acquired parapneumonic effusion what is the most commonly identified organism
Staph
(in community acquired is strep)
Where are the pleural lymphatics located?
(a) Visceral vs. parietal
(b) Mediastinal vs. distal/peripheral flow
(a) pleural fluid drains via openings directly from the parietal pleura
- while visceral lymphatics drain the lung parenchyma, not generally the pleural space
(b) Drains medially/through mediastinum
Dosing of intrapleural medications for empyema per MIST-2 trial
MIST-2: NEJM 2011, tPA (10mg) + DNase 5mg twice a day x3 days
MIST-2 trial outcomes
Intrapleural tPA (10mg) + DNase (5mg) BID x3 days (so max 6 doses)
improved primary outcome of radiographic improvement
also reduced hospital LOS and need for surgical consult
Stage of sleep
(a) Most of night spent in
(b) K-complexes
(c) Delta waves
(d) Sleep spindles
Sleep stages
(a) Most of the night spent in N2 sleep (K-complexes, sleep spindles)
(b) K-complexes = stage 2
(c) Delta waves = stage 3
(d) Sleep spindles = stage 2
What happens to the duration of REM as the night goes on
REM duration increases throughout the night, REM periods occur every 90-120 minutes and become longer as the night goes on
With age which of the sleep stages change?
(a) Which RTS?
With age: N3 (deep) sleep declines and is replaced by N1 sleep
(a) REM remains relatively constant at 15-25% of sleep
How to distinguish REM on polysomnogram?
(a) EEG waves
(b) EOG
(c) Chin EMG
REM
(a) EEG with mixed frequency ‘sawtooth’ waveforms, low voltage
(b) EOG = electro-oculogram showing eye movements, rapid eye movements- eyes gazing left then right
(c) Flat chin EMG b/c of muscle atonia (no chin movement)
CNS structure that regulates circadian rhythm in humans
(a) Location
Suprachiasmatic nucleus
(a) Anterior hypothalamus
Track path of light to the brain to regulate circadian rhythm
Light through the retinohypothalamic tract which acts as the afferent connection to the suprachiasmatic nucleus in the anterior hypothalamus
Deficiency in what hormone is implicated in narcolepsy with cataplexy
Hypocretin deficiency => narcolepsy with cataplexy
Key neurotransmitter for
(a) Generating rapid eye movements in REM
(b) Blocked by caffeine
(c) Blocked by haldol
Neurotransmitter for
(a) Generating REM- ACh (acetylcholine)
(b) Caffeine blocks adenosine receptor => blocking CNS inhibition
(c) Haldol = dopamine antagonist
More or less responsive to CO2 and O2 in NREM or REM?
Reduced responsiveness to both CO2 and O2 in non-REM, then even further reduction in responsiveness to both in REM (compare to wake)
What neurotransmitter
(a) amphetamine is an agonist of
(b) Main CNS excitatory
(c) Main CNS inhibitory
Neurotransmitter
(a) Amphetamine - dopamine agonist (CNS)
(b) Main CNS excitatory nt = glutamate
(c) Main CNS inhibitor nt = GABA
Where is melatonin synthesized?
(a) When is it secreted in highest amount
Melatonin- secreted by pineal gland
(a) At night to promote sleep
What is most effective in shifting circadian rhythm?
Most effective is light exposure- more effective than melatonin
Respiratory system changes during sleep (vs. wake)
(a) MV
(b) TV
(c) RR
Respiratory system changes
(a) Reduced minute ventilation
(b) Decreased tidal volume
(c) Respiratory rate remains about the same
Respiratory physiology changes during sleep (vs. wake)
(a) PaO2
(b) SpO2
(c) PCO2
Respiratory changes
(a, b) PaO2 and SpO2 drop during sleep
(c) pCO2 rises b/c minute ventilation falls (due to drop in tidal volume, while RR remains constant)
What sleep phase?
Wake!
-over 50% of epoch (30 second interval) is showing alpha rhythm (red arrows) = drowsy with eyes closed = 8-13 Hz
-high chin tone (differentiate from REM)
What sleep phase?
N1
-alpha activity (8-13 Hz) diminished or disappeared)
-low amplitude, mixed frequency (4-7 Hz) waves for more than 50% of epoch, black arrow
-slow rolling eye movements (red arrow)
-vertex waves may be present (sharp negative waves of 4-7 Hz frequency)
-chin EMG lower than wake phase (green arrow)
What sleep phase?
N2
-presence of K-complexes (sharp negative wave followed by slower positive component)
and/or sleep spindles (short rhythmic waveform clusters in 12-14 Hz range)
What sleep phase?
N3
- over 20% of epoch with low frequency, high amplitude delta waves (0.5-2 Hz, nice big wide waves)
What characteristic EEG waveforms define N2 sleep?
-K complexes = sharp negative wave with slower positive component
-Sleep spindles = short rhythmic waveforms with clusters in 12-14 Hz range
Differentiate definition of apnea vs. hypopnea
Apnea = 90% or greater drop in flow (thermal sensor amplitude of flow) for at least 10 seconds
-definition does not include desat!
Hypopnea = 30% or greater drop in flow for at least 10 seconds accompanied at least 3% drop in SpO2 OR arousal from sleep (insurance requires 4% but for boards definition it’s 3%)
What type of apnea shown here?
For time that flow is absent- in the beginning no thorax/abdominal movements, then second part of the no flow start to see some thorax movement
= mixed apnea = central event followed by obstructive event
Differentiate the three types of apneas
Apneas:
-obstructive apnea = abd/thorax movement but no flow
-central apnea = no flow but no abd/thorax movement (no effort)
-mixed apnea = central apnea followed by obstructive, so get no effort w/ no flow followed by some effort still w/o flow
Differentiate definition of AHI and RDI (respiratory disturbance index)
AHI = apnea hypopnea index, apneas plus hypopneas per hour
RDI = respiratory disturbance index = apneas + hypopneas + respiratory effort-related arousals per hour of sleep
Grade sleep disordered breathing by AHI
AHI
Normal: 0-5
Mild OSA: 5-15
Moderate OSA: 15-30
Over 30 = severe OSA
What score on Epworth Sleepiness scale indicates excessive daytime sleepiness?
How likely are you to fall asleep during certain activities: 0 (never) to 3 (high chance)
Score 10 or above = excessive daytime sleepiness
Multiple sleep latency test vs. maintenance of wakefulness test
(a) Instructions
(b) Prerequisite
(c) Sensitivity for detecting sleepiness
MSLT
(a) Instructed to fall asleep every 2 hrs in a quiet setting
(b) Requires polysomnogram the night before (ensure adequate sleep night before)
(c) Much better for detecting daytime sleepiness
vs.
Maintenance of wakefulness test more used as work screening tool
(a) Instructed to stay awake in a quiet setting
(b) PSG not required
(c) Less sensitive, ppl can still have significant sleepiness with normal maintenance of wakefulness
Explain multiple sleep latency test
(a) Instructions
(b) Helpful for diagnosis of what
MSLT
(a) Pt instructed to fall asleep every 2 hrs, measure sleep onset latency (SOL, abnormal if under 8 minutes) and SOREMPS (REM within 15 minutes of sleep onset)
Requires PSG the night before
(b) To diagnose narcolepsy, SOREMPs also seen in sleep deprivation
Name two defining features of narcolepsy on PSG with MSLT
-decreased sleep onset latency (fall asleep in under 8 minutes)
-at least two SOREMPS (sleep-onset REM periods) on PSG + MSLT (asked to fall asleep every 2 hrs for 4-5 naps)
so can have 1 on PSG and 1 on MSLT
Despite symptoms, when may treat mild OSA?
Mild OSA (AHI 5-15) treat obv if symptoms (improve daytime sleepiness, improve QOL) but also as adjunctive anti-hypertensive therapy
-no great data to show PAP reduces CV risk other than HTN (even reduces BP in ppl w/o HTN)
When is home sleep study good enough for diagnosis of OSA? (vs. when should get an in lab study)
Can do home sleep study for high pre-test probability and low concern for comorbid condition (OHS, central sleep apnea, significant cardiovascular disease/stroke, COPD c/f hypoxia)
What result on sleep study correlates best with increase in CV risk in OSA patients?
SpO2
Desat correlates better than AHI to cardiovascular risk
Who with OSA should get treated? (ex: AHI of 7?)
Treat moderate OSA so AHI over 15 regardless of symptoms
-or mild OSA (5-15) with symptoms (daytime sleepiness, memory/moood problems, depression) or comorbidities (CV disease, HTN, depression)
What is the definition of CPAP compliance?
CPAP compliance = at least 4 hrs a night for at least 70% of observed nights (5/7 nights)
What is the best historic predictor of OSA?
Witnessed apneas is the most sensitive predictor
While daytime sleepiness is the most common but absent in up to 50%
Differentiate end-tidal for pts with Cheyne-Stokes respirations vs. opiate-induced hypoventilation
Cheyne-stokes respirations => eucapneic central sleep apnea
-increased ventilatory response to hypercapnia
while opiate-induced hypoventilation in sleep from chronic opiates is a form of hypercapnic central sleep apnea
Tx options for normocapnia central sleep apnea
Normocapnic CSA ex: cheyne-stokes respiration treatments
1st line- treat heart failure (ACEi)
2nd line- ASV (adaptive servo ventilation) where ventilatory support adjusts pressure to meet a set tidal volume if EF > 45%
Explain adaptive servo ventilation
ASV- best as treatment for central sleep apnea
-adjusts TV or RR to maintain a set minute ventilation
-will increase inspiratory pressure to maintain tidal volume during periods of apnea or hypopnea
How are ghrelin and leptin affected by sleep deprivation?
With sleep deprivation- ghrelin (hunger hormone) increases, leptin (fullness hormone) decreases
What determines the cycle length in Cheyne-Stokes breathing
(a) Average cycle length
Cycle length (crescendo-decresendo) typically 60-90 seconds
-proportional to circulation time
-inversely proportional to LVEF (lower the EF, longer the circulation tiem)
Mechanism of Cheyne-stokes respiration
-hyperactive chemosensor of CO2 (so causes hyperventilation to normal level of CO2)
-delayed circulatory time due to low cardiac output
During what part of the cheyne-stokes respiratory cycle does arousal occur?
Arousal occurs during peak hyperpnea (when breathing is the fastest) b/c the desat and relative hypercapnia are delayed (due to slower circulatory time)
-cycle lasts about 40-90 seconds (correlates to circulatory cycle)
Diagnostic criteria for OHS
BMI over 30 with elevated awake pCO2 over 45
Proposed mechanism of narcolepsy
Narcolepsy- thought to be due to orexin/hypocretin (same thing) deficiency or destruction (autoimmune?) of hypocretin-containing neurons
-hypocretin is associated with alertness and inhibition of REM sleep
Narcolepsy symptoms
(a) Most sensitive
(b) Most specific
Narcolepsy symptoms
(a) Everyone has daytime sleepiness (if not sleepy during the day it’s likely not narcolepsy unless really significant cataplexy)
(b) Cataplexy pathognmonic
Describe manifestations of sleep fragmentation seen in narcolepsy
Core feature of narcolepsy = discontinuation of wakefulness with features of REM intruding into wakefulness
Examples of the sleep fragmentation:
-cataplexy
-hypogogic and hypnopompic hallucinations
-sleep paralysis
Differentiate two types of sleep hallucinations
GO to sleep
POP awake
Hypnoogogic hallucinations upon falling asleep
Hypnopompic hallucinations upon awakening
MSLT diagnostic cutoff for
(a) Narcolepsy
(b) Idiopathic hypersomnia
Multiple sleep latency test
(a) Narcolepsy: mean sleep onset time under 8 minutes (told every 2 hrs to fall asleep) with at least 2 SOREMPs (sleep onset REM periods)
(b) Idiopathic hypersomnia: mean sleep onset time under 8 minutes with one or less SOREMP
Clinical features differentiating narcolepsy from idiopathic hypersomnia
Narcolepsy
-cataplexy may be present (doesn’t have to be but if it is it’s narcolepsy)
-sleep and daytime naps are refreshing
Idiopathic hypersomnia
-No cataplexy
-Sleep and daytime naps are not refreshing
Non-pharmacologic treatment for narcolepsy
Narcolepsy- regimented sleep schedule, schedule naps (= strategic napping, b/c naps are refreshing and helpful)
Pharmacologic treatment for daytime sleepiness in narcolepsy
Daytime sleepiness
-first line = stimulants (modafinil)
-second line = amphetamines
Pharmacologic treatment for cataplexy in narcolepsy
Cataplexy
Can try SSRIs (suppress REM)
Sodium oxybate (GHB, ‘date rape drug’) which is a GABA metabolite => GABA agonist
Pts with REM sleep behavior disorder are at high risk of developing which condition?
High association between REM sleep behavior disorder (loss of atonia in REM => act out dreams) and neurodegenerative disorders such as Parkinsons
40% of pts with REM-sleep behavior disorder go on to develop a neurodegenerative disorder
Clinical features of restless leg syndrome
RLS = uncomfortable leg sensations at rest relieved with movement
Need to be confirmed by PSG (polysomnogram) with periodic leg movements
Proposed mechanism of restless leg syndrome
Thought to be due to iron deficiency in the CNS therefore inhibiting dopamine synthesis b/c iron is a co-factor in the rate limiting step of dopamine synthesis
=> tx of RLS includes dopmaine agonists
Restless leg syndrome
(a) 1st line Tx
(b) 2nd line Tx
RLS treatment
(a) First line-
1. Iron supplementation if ferritin under 50
2. dopamine agonists = pramipexole, ropinirole (dopamine receptor agonists)
(b) Second line = gabapentin, opiates (long acting- methadone), carbidopa/levodopa
What are parasomnias?
Examples?
Parasomnias = abnormal body movements during sleep
Sleep walking, sleep talking
Are parasomnias more likely to occur in first or second half of the night?
Parasomnias more likely to occur during non-REM sleep (since typically there is muscle atonia in REM) => more likely to happen in first half of the night (b/c REM duration increases throughout the night)
Clinical description of night terrors
Night terrors- typically little kids (boys over girls) sit up in bed screaming, appear panicked, are difficult to awaken and have no memory/recollection of the event
Typically much scarier for parents then kids
What is REM sleep behavior disorder?
REM sleep behavior disorder = loss of atonia during REM => act out dreams
Can be very dangerous to self (falling off bed) and bed partner (kicking/punching)
High association with development of neurodegenerative disease (Parkinsons)
Clinical features that differentiate night terrors from REM sleep behavior disorder
Night terrors- typically in kids, difficult to awaken, amnesia/don’t remember events
REM-sleep behavior disorder typically in elderly M, easy to awaken, remember events
Tx of sleep terrors
Supportive
Reassure parents
Tx of REM-sleep behavior disorder
(a) Pharmacologic
(b) Nonpharmacologic
REM-sleep behavior disorder = loss of atonia during REM => act out dreams
(b) Nonpharmacologic- safe sleep environment, sometimes have to put mattress on the floor so don’t fall out of bed, remove bed partner if kicking/punching
(a) Pharmacologic = clonazepam
Treating the sleep behavior does not reduce risk of progression to neurodenegerative disease (40% risk of progression to neurodeg such as Parkinsons)
Differentiate delayed vs. advanced sleep phase syndrome
Delayed sleep phase syndrome = daytime sleepiness or impairment when go to sleep too late so wake up later
vs.
Advanced sleep phase syndrome = impairment or symptoms when go to sleep super early and wake up super early (like 3am and can’t go back to sleep), typically in elderly
Describe actigraphy for Free running disorder (also known as non-24 hr disorder)
Non-24: in 40% of blind patients b/c no light input to regulate circadian rhythm
On actigraphy see sleep-wake cycle get progressively delayed each night
Two mainstay treatments for circadian rhythm disorders
Either delayed or advanced phase syndrome, two main parts of treatment
- Chronotherapy = using light to inhibit melatonin when you want to promote wakefulness
ex: in delayed sleep phase syndrome use light therapy in AM - Melatonin when want to promote sleepiness
ex: melatonin early in AM when want to put elderly pt w/ advanced sleep phase syndrome to sleep
Differentiate classic progression of paralysis in GBS vs. myasthenia gravis
GBS = acute demyelinating polyneuropathy
Typically presents with bilateral lower extremity symmetric muscle weakness that is ascending
Myasthenia gravis = autoimmune disorder of the neuromuscular junction
Starts up top then descends (bulbar and ocular hallmark)
At what NIF/MIP to be worried about impending respiratory failure/consider elective pre-emptive intubation
At NIF/MIP less than -30 cm H2O get worried about impending respiratory failure
Differentiate nerve stimulation test results for myasthenia gravis vs. lambert eaton
Myasthenia gravis = autoimmune disorder of the neuromuscular junction
-weakness/fatigue worsens throughout the day
-repetitive nerve stimulation with incremental reduction in action potential
vs.
Lambert-Eaton = paraneoplastic associated with small cell lung CA
-repetitive nerve stimulation with incremental increase in action potential amplitude, so strength generally improves w/ mild to moderate activity
Mechanism of botulism-toxin paralysis
Botulism toxin irreversibly binds presynaptic membrane of the cholinergic synapse => blocks cholinergic signaling
Respiratory failure in GBS vs. MG- which would you consider pulse steroids?
GBS- steroids can worsen, stick to plasmapheresis and/or IVIG
Myasthenia gravis- autoiimune, so pulse steroids (or other immunosuppression) can be used in crisis
Clinical features of organophosphate toxicity
Organophosphate toxicity (typically from pesticide exposure) => cholinergic excess
SLUDGE
salivation
lacrimation
urination
defecation
GI upset
emesis
What exposure causes organophosphate toxicity
Typically from pesticide exposure- cholinergic excess = SLUDGE
salivation
lacrimation
urination
defecation
GI upset
emesis
ALS
(a) Typical presenting clinical feature
(b) Cause of death
Amyotrophic lateral sclerosis
(a) Typically with asymmetric limb weakness as initial presentation
(b) Invariably progresses to respiratory failure from respiratory muscle weakness within 5ish yeras
Indications for NIV in ALS patients
In the beginning of disease track disease progression with FVC every 306 onths, then as they lose ability to tightly form seal around mothpiece use MIP/NIF
Start noninvasive:
-MIP/NIF under -60 cmH2
-pCO2 over 45
-FVC under 50% predicted
What outcomes has CPAP treatment shown to improve?
CPAP treatment reduces blood pressure, even in non-hypertensive patients
-No proven reduction in ACS, stroke, or neurocognition
CPAP of 5, then drops by 1-2 mmHg during early phase of exhalation for comfort
What is cataplexy?
Transient episode of muscle atonia or hypotonia precipitated by intense emotion (laughter, anger, stress, sex)
-memory and consciousness unaffected => aware of what’s going on
-recovery is immediate and complete, typically under 2 minutes
Differentiate type 1 and type 2 narcolepsy
Both have diagnostic criteria for narcolepsy met with average SOL under 8 minutes and at least 2 SOREMPs (REM within 15 minutes sleep onset),
If cataplexy present = type 1
- reduced hypocretin in CSF (under 110)
type 2 = cataplexy absent and hypocretin in CSF normal (over 110)
Describe adaptive-servo ventilation
ASV- constant EPAP to relieve obstruction
-then IPAP is adjusted to maintain minute ventilation or flow = variable inspiratory PAP
ex: if pt breathing deeper than baseline, IPAP minimized
ex: if pt breathing less than baseline, IPAP increases to augment the breath
ASV (adaptive servo ventilation) should be used for which of the following?
(a) Cheyne-stokes
(b) Central apnea in s/o methadone use
(c) OHS
(d) Treatment-emergent CSA
(e) Neuromuscular disease
ASV should be used for
Central sleep apneas except in Cheyne-Stokes with EF under 45% (ASV then had increased CV mortality)
(a) ASV can be helpful for Cheyne-Stokes if EF over 45% (but try CPAP first)
(b) Yes use in central apnea from chronic opiate use
(c, e), ASV not to be used when hypercapnia at baseline since the ASV adjusts to patient’s baseline => not for use in OHS or neurmoscular disease
(d) ASV ideal for treatment-emergent CSA when central sleep apnea is revealed when obstruction is relieved, typically resolves spontaenously with 3 months of CPAP but not always
Pt with PSG-proven Cheyne-stokes: why important to get TTE before starting empiric treatment for CSA?
SERVE-HF trial: EF under 45% treated with ASVV had reduction in central apneas but increased all-cause and CV mortality to those not treated w/ ASV
=> decides treatment
Secondary triggers for myasthenia crisis
Can be primary, or secondary to
- Infection (not C. Jejuni that’s guillan-barre)
- Meds: fluoroquinolones (cipro), macrolides, beta-blockers
Indications for hypoglossal nerve stimulator
(a) Age
(b) BMI
(c) AHI
(d) Type of soft-airway collapse
Hypoglossal nerve stimulator as second line tx for OSA
(a) Age over 22
(b) BMI under 32 (do worse if more obese)
(c) AHI 20-65
(d) Candidates undergo endoscopy during sleep to determine anatomy of soft palate- complete concentric collapse is a contraindication to procedure, while anterior posterior collapse is what the procedure can help (by activating geniogloccus muscle in synchrony with inspiration)
Describe mechanism by which sleep-disordered breathing in pt with OSA can worsen significantly at high altitude
High altitude induces periodic breathing with central apnea, so do to the central apnea not worsening of obstruction
Hypoxia overstimulates ventilation => reduced CO2 reserve and enhanced chemosensitivity causes ventilatory overshoot => periodic breathing with central apneas
Pt with OHS and severe OSA- first line treatment?
Start first with CPAP
-CPAP noninferior to noninvasive for improving QOL and mortality, more cost effective
If CPAP fails for some reason then can return to sleep lab for repeat PAP titration to establish efficacy and superiority of NIV over CPAP
Key is to discharge these pts home with CPAP- reduces readmission and mortality
What diagnosis is this PSG showing?
(a) First-line treatment
Treatment-emergent central apnea = OSA that upon initial of CPAP central apneas occur
(a) CPAP- 85-90% of treatment-emergent central sleep apnea self-resolve within 3 months of CPAP therapy, so don’t have to jump straight to Bilevel ST or ASV
Differentiate Bilevel S from Bilevel ST
Bilevel S = bipap spontaneous, no backup rate, just augments ventilation with patient-triggered breaths
Bilevel ST = bilevel spontaneous timed = has back up rate
GBS vs. MG
(a) Mechanism
(b) Associated symptoms
Guillain-Barre:
(a) Progressive demyelinating neuropathy
(b) Typically starts with bilateral symmetric lower extremity weakness then ascends
Myasthenia Gravis
(a) AUtoimmune against AChR in the neuromuscular junction
(b) Typically starts ocular/bulbar and can progress downward, classically associating with fatiguing weakness (worse w. more use or at end of the day)
Which neuromuscular disorder is associated with (ALS, MG, vs. GBS)
(a) Autonomic instability
(b) hyperreflexia and fasiculations
(c) thymoma
(d) C. jejuni infection
Neuromuscular disorder
Guillain-Barre: progressive demyelinating neuropathy typically starting with lower extremity weakness and ascending
(a) GBS is associated with autonomic instability- fluctuations in HR/BP, diaphoresis
(d) C. jejuni (diarrheal illness) infection associated with GBS
(b) Hyperreflexia and fasiculations = UMN and LMN involvement typical of ALS
(c) Thymoma typically associated with production of antibodies seen in myasthenia gravis
Which neuromusclar disorder is associated with (GBS, MG, ALS, L-E)
(a) Elevated protein in CSF
(b) presentation of asymmetric limb weakness
(c) improved strength with mild-moderate activity
Neuromuscular disorder
(a) CSF protein elevated = GBS (progressive demyelinating neuropathy)
(b) Asymmetric limb weakness is the most common presentaiton of ALS
(c) Lambert-Eaton = paraneoplastic syndrome, abnormality at nmj, action potential amplitude increases with repetitive stimulation (aka strength improves with mild/moderate exercise)
Severe OSA adequately treated with CPAP (AHI resolves to under 5) but daytime sleepiness persists- next step?
Add wake-promoting agent such as modafinil and armodafinil- RCTs show improved daytime sleepiness in OSA pts highly adherent to CPAP and improved QOL
-don’t increase BP and HR like stimulants (methylphenidate)
-but do make OCPs ineffective so watch out in F of child-bearing age
Differentiate sleep patterns associated with opioid-induced central apnea vs. cheyne-stokes breathing
Cheyne-stokes has classic crescendo-decrescendo pattern
While opioid-induced central apnea has distinct respirtaory patterns
-ataxic breathing = high variability in RR, TV, and duration of central events (aka the pattern is not having a pattern)
-cluster breathing = run of several deep breaths then intervening central apneas or variable lenth
Pt with Parkinsons whose wife can’t sleep in the bed b/c of kicking during dreams
(a) Diagnosis
(b) Key parts on PSG
(a) REM-sleep behavior disorder
(b) See rapid eye movements on E1 and E2, then see tons of R leg movement- which shouldn’t happen b/c should have peripheral muscle atonia during REM
Contraindications to use of clonazepam for treatment of REM-sleep behavior disorder
(b) Second line pharmacologic agent
Clonazepam containdicated if hypersensitivity (or hypersomnolence/bad reaction) to any benzo in the past
AND
acute angle glaucoma, significant liver disease
(b) Second line tx = melatonin
Chest tube placed for L PTX (see below) with persistent large PTX- management? Place a second chest tube on L vs. remove chest tube
Need to place a second chest tube first so can quantify PTX/hemothorax
-if significant bloody output once intraparenchmal tube removed, consider surgical exploration
Once second chest tube placed then can consider removing initial chest tube w/o leaving pt vulnerable to PTX and hemothorax
28M with prior primary PTX resolved with needle compression 8 years ago presented with another moderate-sized primary spontaneous PTX
Chest tube with observation vs. chest tube then VATS with pleurodesis
Any recurrence- definitive treatment to prevent another event is indicated
=> even though it was 8 yeras ago and you can focus on smoking cessation, answer is chest tube with plan for VATS/medical thorascopy with pleurodesis
ADA cutoff normal in pleural effusion
(a) Most likely dx
(b) Other possible dx
ADA over 40 is abnormal
(a) over 80% sensitive and specific for pleural Tb
(b) but can be mildly elevated in empyema or parapneumonic effusion- in which case look for pleural neutrophila
Cutoff for eosinophilic pleural effusion
(a) Main causes
Eosinophilic pleural effusion if over 10% eos
-commonly trauma (air or blood in pleural space causing inflammatory response) ex: after PTX
-drug-induced: warfarin, PTU, nitrofurantoin
-malignancy
-benign asbestos pleural effusion
Differentiate RERA (respiratory effort related arousal) from hypopnea
RERA = 10sec or more of flattening of nasal pressure (flow) despite increased respiratory effort leading to an arousal
-but doesn’t meet criteria for apnea (not 90% or greater reduction in flow) or hypopnea (no 3% desat)
Differentiate the 4 events shown on this PSG epoch
- RERA- leads to arousal but no desat and not over 90% drop in flow
2,3. Mixed apneas- cessation of flow with beginning no thor/abd flow but then some at the end
- reduction in flow but not completely flat nasal pressure and 4% drop in SpO2
STAR trial for hypoglossal nerve stimulation- what outcome?
SubQ implant with sensing lead on chest to detect breaths then stimulation lead around hypoglossal nerve to push tongue out of the way
STAR trial showed reduced AHI from 29 to 9 despite stable BMI, also improved QOL and reduced sleepiness
Benefit of auto-PAP
Reduced mean PAP required
-not shown to have sig improvedCA compliance or any better outcomes, just less PAP
Can OHS exist without OSA?
Yes! Typically co-exist, 90% of pts with OHS have OSA
but 10% of pts with OHS don’t have OSA
Treatment of insomnia- best short and long term outcomes
Insomnia treatment:
-meds (hypnotics ex: zolpidem) best in short term but then CBT-I has better long term results
What sleep phase to adults spend the most time in?
NREM 2 (stage 2 with sleep spindles and K-complexes)
What does STOP-BANG stand for?
STOP
Snoring
Tiredness (fatigue)
Observed apneas
Pressure (HTN)
BANG
BMI over 35
Age over 50
Neck circumference over 17
Gender (M)
Answer- (A) Narcolepsy type 1, doesn’t matter how many SOREMPs if CSF hypocreti is under 110
Differentiate mechanism of meds to treat daytime sleepiness in narcolepsy
(a) Solriamfetol
(b) Pitolistant
(a) Solriamfetol = dopamne and norepi reuptake inhibitor
to treat daytime sleepiness in narcolepsy, also residual daytime sleepiness in OSA
(b) Ptiolistant = H3 receptor antagonist
Which narcolepsy medication is also approved for treatment of OSA-related daytime sleepiness?
(solriamfetol vs. pitolistant)
Solriamfetol (dopamine and NE reuptake inhibitor) also approved in OSA for residual sleepiness despite adequate treatment
-While pitolistant (H3 receptor antagonist) not approved in OSA
Answer- (C) 1am, want to limit time in bed and then once sleep efficiency (time spent sleeping / time in bed) increases to above 90% can extend time in bed
Differentiate mechanism of suvorexant and eszopiclone in sleep-maintenance insomnia
Suvorexant = orexin antagonist = blocks wakefulness promoting neuropeptide orexin
Eszopiclone (Lunesta) is a non-benzo GABA agonist for sleep onset and latency insomnia
Which hyponotic agent used for tx of insomnia can have a rare side effect of cataplexy?
Suvorexant (orexin antoagnist) can cause REM dyscontrol including cataplexy and sleep paralysis
For restless leg syndrome- why check both ferritin and iron panel?
B/c ferritin can be an acute phase reactant so falsely elevated
Presumed mechanism for iron deficiency causing RLS
What is Kleine Levin syndrome (hint: sleep disorder)
Kleine Levin = recurrent hypersomnia, unclear mechanism/pathogenesis
-recurrent hypersomnia associated with irregular cognitive behavioral disturbance (prominent apathy, derealization)
-other disorders in same category = narcolepsy type 1, 2 and idiopathic hypersomnia
Describe RLS augmentation
(a) Mgmt
Restless leg syndrome tx with dopamine agonists- can make symptoms worse (restlessness spreads to arms, symptoms occur earlier in the day), most classically when increasing the dopaminergic agent
(a) Reduce the dopaminergic agent (pramiprexole, ropinerole)
What is the most common arrhythmia/irregular rhythm that occurs during sleep?
PVCs/PACs (ectopy)
More common than AFib in sleep
During sleep, what HR is considered
(a) Bradycardia
(b) Tachycardia
(a) Bradycardia in sleep is sustained HR under 40
(b) Tachycardia = sustained HR over 90
Are REM-related sleep disorders more likely to have symptoms in beginning or towards end of the night?
REM occurs every cycle (90ish mins) and duration increases throughout the night, so more time spent in REM at the end of the night = expect more symptoms then
Why is so little time typically spent in N1 sleep?
N1 = transition from wake to sleep, about 5% of the night
see slow rolling eye movements
Describe the EEG waves seen in REM sleep
EEG in REM- low amplitude mixed frequency waves, saw tooth
Differentiate the shape of K-complexes from delta waves
K-complexes (like PVCs of the brain)- sharp up and slow down
While delta waves are more symmetric, and more copious (more of them in an epoch)
Describe main change in sleep stages seen in pts taking SSRI/SNRIs
SSRI/SNRIs reduce REM sleep
-to the point where it can be hard/impossible to diagnose narcolepsy in a pt taking SSRI/SNRIs
Notable PSG finding in pts taking benzos
Benzos increase sleep spindles in stage 2 sleep
So if see tons of sleep spindles- consider UTox
Why may AHI be underestimated by home sleep study?
Home sleep studies don’t have a way of measuring duration of sleep, so denominator is length of the sleep study (time measured), not sure if all of that time is spent actually sleeping
