W4 Daytime Sleepiness Flashcards
Daytime sleepiness
Causes
Background
Insomnia
Obstructive Sleep Apnea
RSL Syndrome / Limb Movement DIsorder
Poor Sleep / Sleep Hygiene
Narcolepsy
Depression / Anxiety
Sleep Terror
Medications
Stages of sleep
Background FYI
Based on the measure of electrical activity occurring in the brain.
Measured by an EEG (electroencephalogram) — can be used as well to detect seizure activity
The EEG measures voltage fluctuations resulting from ion current within the neurons of the brain via electrodes placed on the scalp.
Sleep has 4 stages: Don’t memorise
1.Stage 1: high frequency, low amplitude waves (light sleep; “dozing off”)
2.Stage 2: represented by sleep spindles and K-complexes (light sleep)
3.Stage 3: low frequency, high amplitude (delta/deep sleep; restfulness)
4.Stage 4: return to sage 2 and 1 prior to entering rapid eye movement (REM) : muscles relaxed but eyes moving rapidly; dream stage.
Following REM, repeat each cycle 1-4 on average 4-5x per night with each total cycle lasting 90-110 minutes. Less sleep, duration in each stage is less
Benefits of sleep
Background — FYI
Restoration: body metabolic processes are reduced and harmful by-products (free radicals) are removed
Growth hormone is released (raises testosterone levels); reduces obesity
Improve immune system
Reduces cortisol stimulation; if elevated, associated with higher risk of cardiovascular disease. A lot of MIs happen in the morning when cortisol is release
Improved long term memory
Poor sleep associated with mood disorders (depression)
Sleep hygiene
Background — FYI
Creating an environment and behavioral routine to ensure consistent, uninterrupted sleep
Assess in all patients with complaints of insomnia. Can ask during clinical interview and have patient record a sleep diary.
Goal is 8 hours of sleep per night.
Recommendations:
—Consistent schedule; in balance with circadian rhythm
—Create a routine with a relaxing activity 30 minutes prior to bed : meditation, stretching, reading
—Reduce blue light from devices that reduce melatonin levels in your body
—Daily exercise; avoid 1-2 hours prior to sleep
Insomnia
Three main groups who suffer from insomnia
Defined:
Subjective perception of difficulty with sleep initiation, duration, consolidation, or quality that occurs despite adequate opportunity for sleep, and that results in some form of daytime impairment.
Women are more likely to experience insomnia with the higher prevalence attributed to hormonal changes (pregnancy as well as after menopause)
Other higher risk patients:
>65 years of age
—menopausal women
—Comorbidities including pulmonary disease, heart failure, neurologic disease, and chronic pain
Insomnia
Treatments
What is first line?
FIrst line therapy is NON-pharmacologic (sleep hygiene)
PHARMACOLOGIC
1. Melatonin Agonists
—Melatonin regulates sleep-wake cycle and a disruption of timing of release or decreased production can cause insomnia
—Worsens with age, shift work, and switching time zones
—Ramelteon (Rozerem) = melatonin agonists: modest effectiveness but few adverse effects and no habit forming properties
—Controlled release melatonin at 3.5 - 5 mg nightly (decreased sleep latency by 7 minutes, increased total time by 8 minutes, and improved overall quality)
2. GABA AGONISTS — stay away from these
Nonbenzodiazepine Sedative Hypnotics
—“Z-medications” (Zolpidem = ambien, Zaleplon = sonata, EsZopiclone = lunesta); all are schedule IV medications due to risk of abuse
—‼️Can cause memory loss, disinhibition, and hallucinations
Benzodiazepines
—(not first line given physical dependence as well as chronic use disrupts the sleep cycle)
—Risk of dependence is high (15-40%) with possibility of severe withdrawal with either rebound insomnia or symptoms from discontinuation
3. TRICYCLIC Antidepressants:
—have a sedative effect related to antagonism of the histamine H1 receptor
—prescribed a lot, esp. in hospital. Generally safe. Bill recommends this and melatonin
—Doxepin, Trazodone, Remeron, Elavil
4. Antihistamines:
—Diphenhydramine (benadryl) and Doxylamine are available OTC; sleep hangover.
—Recommended for pregnancy related insomnia due to safety profile and some benefit with nausea.
5. Antipsychotics:
—off label for insomnia; include Olanzapine (Zyprexa), quetiapine (Seroquel), and risperidone (Risperdal)
6. Orexin Receptor Antagonist:
—Suvorexant (belsomra) is now FDA approved; the orexin system regulates sleep arousal and wakefulness. The 20 mg dose reduced sleep latency by 22 minutes.Most common side effect was daytime somnolence but otherwise well tolerated.
7. Antiepileptics:
—Gabapentin (Neurontin) and Pregabalin (Lyrica) improve sleep but by an unknown mechanism.
—Improved sleep time 45-60 minutes.
Insomnia
approach to management
—⭐️Behavioral interventions are first and then pharmacologic ⭐️
—If the initial pharmacologic intervention is ineffective, a different agent in the same call or a different class should be considered
—‼️Caution if use a combination strategy ‼️
—If have ISA or respiratory disease, consult a sleep specialist due to the risk of respiratory depression associated with some sedating medications
—❌ Benzodiazepines are the last choice and should be utilized for a short amount of time given the risk of dependence
—❌Avoid use of benzodiazepines, Z-drugs, and atypical antipsychotics in geriatric
Obstructive Sleep Apnea (OSA) — will be on the exam
What is it?
Associated with?
3 classifications
First two causes?
Most common?
Sleep apnea is a common medical disorder causing intermittent hypoxia (apnea >10secs), intermittent hypercapnia, sympathetic activation, and sleep fragmentation.
Leads to metabolic dysregulation, endothelial dysfunction, systemic INFLAMMATION, oxidative stress, hypercoagulation, and neurohormonal changes.
Associated with morbidities:
—Arrhythmias (atrial fibrillation)…Sleep apnea should always be a consideration for causing afib
—Pulmonary Vascular Disease : pulmonary hypertension
—Ischemic Heart Disease and Heart Failure
—Cerebral Vascular Disease
Classified as:
OBSTRUCTIVE — most common
—repetitive intermittent collapse of the upper pharyngeal airway during sleep which causes apnea that is then terminated by partial arousal
—Overweight
—Enlarged Tonsils or Adenoids / Deviated Nasal Septum
—Excessive Overbite
—Large Neck Circumference / Enlarged tongue size
CENTRAL
—defined by a lack of respiratory effort
—repetitive absent or diminished respiratory efforts that occur intermittently or in a CYCLICAL pattern predominantly during sleep
—Hyperpnea (rapid breathing) -> causes hypocapnic (decreased CO2)
—Apnea then ensues to increase CO2 levels
—Hypercapnia (elevated CO2) results causing hyperpnea (rapid breathing)
—Very familiar to cheyne’s-stokes
—Associated with high altitude, narcotics, CNS disease (stroke), heart failure, parkinson’s disease, or idiopathic
MIXED
—combination of both
Apnea is an episode of breathing cessation lasting 10 seconds in duration
Obstructive Sleep Apnea - control of respiration 3 centres
Obstructive Sleep Apnea - control of respiration
1. Medullary Respiratory Center: composed of ventral and dorsal groups:
—Dorsal : responsible for inspiration and movement of diaphragm
—Ventral : responsible for rhythmicity of breathing
-
Pontine Respiratory Center:
—works with medulla to assist with rhythm of inspiration/expiration
Impulses from above are sent via neurons to the muscles of respiration: diaphragm and intercostal muscles
PERIPHERAL CHEMORECEPTORS
CENTRAL CHEMORECEPTORS:
PERIPHERAL CHEMORECEPTORS
—(aortic arch, carotid bodies): Main regulator; a decrease in oxygen or pH or an increase in CO2 will stimulate chemoreceptors to stimulate the pontine and medullary respiratory centers
CENTRAL CHEMORECEPTORS:
—located in the medulla; perform same function of detection and resulting stimulation/depression
(Ignore below — Bill removed from PPP)
HIGHER CENTER OF BRAIN: voluntary control that can affect respiratory rate by stimulation or depression of pontine and medullary respiratory centers
CHEMORECEPTORS IN MUSCLES: stimulated during exercise to stimulate respiratory system (increase O2 and decrease CO2/byproducts/acidosis)
STRETCH RECEPTOR in lung: suppress respiration to prevent over inflation of lung
OSA
Risk factors
S/S
—Male
—OBESITY: pharyngeal fat deposits narrow the airway
—Craniofacial and Upper Airway Abnormalities: large neck circumference, increased size of adenoids/tongue, maxillomandibular defects
—Acromegaly
—Familial Link
—Alcohol and Sedatives
—Polycystic Ovary Syndrome (PCOS): combination of high levels of androgenic hormones and obesity increases risk of OSA 30x
S/S
—Typically an obese middle aged man presenting because of snoring and daytime somnolence. If have a sleep partner, they report episodes of apnea
—Excessive daytime sleepiness
—Snoring
—Poor sleep quality
—Morning headaches
—Decreased libido
—Decreased cognitive performance
OSA
Exam
Differential
Diagnostics
What is mild/moderate and severe
EXAM:
Overweight
Large neck circumference (> 40 cm)
Hypertension (> 50% of cases)
DIFFERENTIAL:
Inadequate sleep time
Shift work
Excessive caffeine/stimulants/drugs
Depression
Physical illness/chronic pain
Narcolepsy
Diagnostics:
🔸Polysomnography (gold standard) 🔸
The diagnosis is based upon the presence of symptoms and the measured frequency of respiratory events during sleep (apnea, hypopnea, and respiratory effort related to arousal) as measured by the test. Formulates an apnea-hypopnea index (AHI) based on the number of apnea and hypopnea spells per hour of sleep.
OSA
Management
Management:
—Weight loss
—Change sleep position
—Avoid alcohol/sedatives
—Medical Intervention: Positive airway pressure (CPAP or Bipap)
—Surgical Therapy: tonsillectomy,uvulopalatopharyngoplasty
Pharmacology: for patients with continued daytime somnolence despite above therapy can use adjunctive medications to stimulate the respiratory drive: Theophylline and Acetazolamide
no need to memorise these
Theophylline:
—a xanthine derivative chemically similar to caffeine that relaxes bronchial smooth muscle and pulmonary blood vessels.
—Also binds to adenosine and prevents bronchoconstriction. —Typically used to treat asthma and bronchoconstriction.
Acetazolamide:
—inhibitor of carbonic anhydrase enzyme that results in reduction of hydrogen ion secretion at the renal tubule and increased excretion of sodium, potassium, water, and bicarbonate.
—Normally diuretic or to treat glaucoma.
—But also INHIBITS carbonic anhydrase in the CNS to minimize abnormal and excessive discharge form neurons.
OSA
Complications
COMPLICATIONS:
Pulmonary Hypertension
Hypertension
Arrhythmias
Increased cardiovascular diseases including heart failure
Depression
Cognitive dysfunction
Impaired glucose metabolism
Pregnancy hypertensive complications
With treatment, prognosis is good with improvement in alertness, quality of life, mood, cognitive dysfunction, and a reduction in cardiovascular events
Some evidence of reduced work or driving related events
Restless Leg Syndrome (RLS)
Primary vs secondary
Mechanism
RLS: urge to move the legs often associated with an uncomfortable sensation to move the legs or occasionally other body parts
PRIMARY RLS: idiopathic and runs in families; onset is < 45 years of age with a progressive pattern/worsens over time
SECONDARY RLS: associated with other underlying medical conditions or medications; onset typically > 45 years of age
Other associated medical conditions -> iron deficiency, smoking, Parkinson’s disease, peripheral neuropathy, renal failure, obesity, pregnancy
Medication effects: antidepressants, antiemetics, antipsychotics, antihistamines, and CCB
MECHANISM:
—Not well understood (unknown)
—Genetic; higher prevalence in females
—CNS: possibly related to iron deficiency; results in imparied oxygen transport, impaired myelination, and abnormal signaling in neurotransmitter systems, specifically dopamine. Drugs that increase dopamine signaling improve RLS symptoms.
Peripheral Nervous System: abnormal A fibers and microvasculature
