Lecture 18 - management of sleep disorders and insomnia Flashcards
what are the 5 stages of sleep?
Stage 1: ~5-10 mins. Transition from awake to sleep (loss of muscle tone, easily aroused).
Stage 2: ~20 mins. Light sleep (50% of total), movement stops, HR and body temp drop.
Stages 3 & 4: ~30 mins each, deep or slow wave sleep (restorative)
Stage 5: REM (rapid eye movement). 25% of total time. brain activity (dreaming). Processing and consolidation of information and emotions.
Stages 1-5 make up the sleep cycle lasting about 90mins. Cycle is repeated 5-6 times a night.
descried the neurotransmitters that are used in sleep
High neuronal activity in histaminergic, noradrenergic and serotonergic pathways during wakefulness – descreaseduring non REM and almost stops during REM sleep.
Cholinergic activity slows during non REM but increase in REM- dreaming?
Dopamine in the transition from awake to sleep
GABA – (inhibitory transmitter) induces relaxation and sleep
Melatonin: released from pineal gland (regulates circadian rhythm)
Orexins- from hypothalmus regulate sleep –wake cycle
what is sleep disorders and different types of sleep disorders?
Characterised by disturbances of usual sleep patterns or behaviours that cause distress and impair daytime functioning.
Affects 10-37% of the population
Insomnias: initiating & maintaining sleep (i.e quality & quantity)
Parasomnias: disturbance of arousal-sleep maintenance mechanisms (polysomnography PSG often required)
Sleep apnoea: restriction of airflow, interrupts breathing, (poor sleep quality)
Narcolepsy : neurological disorder where the brain is unable to regulate the sleep-wake cycle
describe insomnia
insomnia Is a Symptom not a Disorder
1 in 5 complain of insomnia
Inability to get to sleep
Inability to stay asleep
Waking too early
Unsatisfying sleep (e.g tiredness during the day – assume that it caused by inadequate sleep the previous night)
Sleep disturbance alongside significant daytime dysfunction
Total time asleep declines with age- less active, daytime napping BUT should NOT dismiss as very common in those with a psych disorder- persistent, disabling, contributes to poorer outcomes and lower quality of life.
how is sleep disorders and insomnia managed?
Treat underlying condition e.g depression, coughs/itch/pain/ frequency of urination
Sleep hygiene – change in behaviours prior to sleep, sleep diary
Psychological therapies- e.g Cognitive Behaviour Therapy (CBT)
Complementary Therapies – acupuncture, herbal remedies
Medication to increase brain inhibition via GABA/BZ receptor OR decrease excitation by blocking 5HT or histamine receptors
give advice on sleep hygiene
Maintain an environment conducive to sleep ( noise, heat in bedroom).
Avoid caffeine drinks ( alcohol intake)
Relaxation (avoid exercise later in day, but partake daytime)
Bed time routines (prepare body for sleep)
Body awareness i.e the rest – activity cycle. Take cues from the environment e.g as we asleep, there is a drop in body temperature. The temperature rises as the body gears up in its physiological function- leads to waking up.
what are the effecst of medicatiosn used to target sleep disorders?
Medication (hypnotics e.g BZP or Z drugs, melatonin, chlormethiazole) decrease time to sleep onset
and episodes of waking,
BUT get an increase total sleep time- short term use only i.e 6wks.
Goal: to restore normal restful sleep without a residual hangover and to return to normal sleep pattern
describe the mechanism of action of benzodiazepines
Bind to GABA A receptor and enhance inhibitory effect of GABA - activation of the GABA receptor leads to influx of Cl- ions into the neuron reduces its excitability- thereby reducing activity in the brain- sedation, induces sleep.
BZs supress stages 4 (deep sleep) and lower of REM
Z drugs lower stage 1 but increase stage 2, little effect on stages 3,4 and REM
describe the kinetics of benzodiazepines
Rapidly absorbed from GI tract & extensively metabolised by oxidation in the liver-some active metabolites e.g oxazepam.
Long, medium and short acting BZs- based upon plasma t1/2 and duration of action.
Substrates for several CYP enzymes- caution when co-prescribed with inhibitors or induces
Additive or synergic effects with other psychotropic drugs- impairment of motor/intellectual function or worsen respiratory depression.
Various formulations- oral, IM and IV for acute/rapid sedation (agitation/pre-operatively) and for emergency treatment of seizures. Low water solubility so administered with solvents or as emulsion.
describe benzodiazepines hypnotics
Induce sleep within 30mins (Stages 1-3).
Residual effect likely, esp with nitrazepam – caution in the elderly.
Side effects: headache, confusion, blurred vision, amnesia, affect driving performance, disinhibition, respiratory depression (IV route)
Driving offence- All benzodiazepines can impair driving ability but clonazepam, diazepam, lorazepam named.
See DVLA website
what are adverse effects of taking benzodiazepines?
Short term use (max 6 weeks) for severe, disabling insomnia
Tolerance - in effect despite continued administration
Dependence – a need for repeated doses to maintain wellbeing or prevent withdrawal symptoms. Dependence can be psychological or physical
Psychological- a craving or compulsion to maintain wellbeing
Physical: depends on extent of dependence/period of use
Mild - irritability, tremor, headache, nausea
Moderate - flu like symptoms, appetite, abnormal sensation of movement
Severe – seizures, psychosis
what are safety issues in benzodiazepines use for hypnotics or anxiolytics
high propensity for dependance. 2 weeks acute treatment is the ideal but definitely not reality
high propensity for tolerance so need to increase dose or prescribe an alternative
require a tapered withdrawal treatment regime to avoid withdrawal effects
Shorter acting BZs tend to be more problematic
To withdraw or stop – best to convert to diazepam and then gradually reduce by 1/8th (or 1/6th) of total daily dose every fortnight/week – over 6-12 months. (not an exact science- depends on symptoms)
describe what Z drugs mechanism of action and how they differ from other drugs
zopiclone, zolpidem and zaleplon
Alternative to BZs- lower risk of dependence / tolerance and abuse – debatable??
Agonist at α1 subunit of GABA receptor ( GABA mediated Cl- influx into the cell= inhibits neurotransmission)
Rapid onset and relatively short duration – hangover effect, cognition function etc.
SE: metallic taste (mainly zopiclone), GI disturbance, dizziness, headache.
what are OTC products for management of sleep
Sedative antihistamines (diphenhydramine, promethazine)
or
Herbal products (valerian, lavender, CBD/cannabidiols)
For short term use only –
Understand patients motives: psychosocial issues, anxiety – worries, stress,
Addressing the underlying cause is more effective than sleeping tablets-
what antihistamines can be used ?
Only those that cross the BBB –i.e antagonists at the H1 receptor thereby causing sedation
Primarily used in children (lack of alternatives)
Promethazine (5-10mg at night). However, has a long t1/2, but low abuse potential
Diphenydramine (25-50mg at night). potential for abuse - affects cognitive function
Also available as OTC products e.g Nytol
