NURS 660 Exam 3 Study Guide
1. Describe different types of insomnia/sleep disorders and identify which medications are best
indicated to treat different types of insomnia/sleep disorders.
Insomnia
o Suggested criteria for defining insomnia
Average sleep latency > 30 min
Wakefulness after sleep onset (WASO) > 30 min
Sleep efficiency < 85%
Total sleep time < 6.5 hours o Hyperarousal at night
o Neuroanatomical abnormalities
Reduced gray matter in left orbitofrontal cortex and hippocampus o Neurobiological abnormalities
Decreased GABA levels in occipital and anterior cingulate cortices
Reduced nocturnal melatonin secretion
Increased glucose metabolism
Attenuated sleep-related reduction in glucose metabolism in wake-promoting regions
Decreased BDNF
o Autonomic Nervous System Abnormalities
Heart rate elevations and variability
Increased metabolic rate
Increased body temperature
HPA axis activation
Increased NE o Systemic inflammation o Genetic factors
CLOCK gene polymorphisms
GABA-A receptor gene polymorphisms
Serotonin reuptake transporter (SERT) gene polymorphisms
Human leukocyte antigen (HLA) gene polymorphisms
Epigenetic modifications affecting genes involved in the response to stress
Circadian Rhythm Disorders
o Shift Work Disorder
Insomnia or excessive sleepiness temporarily associated with a recurring work schedule that overlaps with the usual time for
sleep
Symptoms associated with shift work schedule are present for at least 1 month
Sleep log or actigraphy monitoring (with sleep diaries) for at least 7 days demonstrates disturbed sleep (insomnia) and circadian
and sleep-time misalignment
Sleep disturbance is not due to another current sleep disorder, medical disorder, mental disorder, substance use disorder, or
medication use
o Advanced Sleep Phase Disorder
Go to bed to early and wake up to early
Increasingly common as you age
Treatment: early morning melatonin and evening light
Can help reset the SCN so that the sleep/wake switch stays off longer
o Delayed Sleep Phase Disorder – “Night owls”
Stay up late and sleep in late
Patients with MDD and teenagers
Use melatonin at night and light in the morning
, o Non-24
Blind patients who cannot see light o Disrupted sleep/wake cycle can decrease leptin (appetite inhibiting) hormone and
increase ghrelin (appetite stimulating) hormone; this increase in ghrelin is hypothesized to contribute to the increased risk of obesity,
diabetes, and CV disease
• Narcolepsy: rapid, unwanted
transition from wakeful state to
sleep state o Lack of orexin
neurons in hypothalamus plays a
role in narcolepsy
Orexin – active during wakefulness, reinforces the arousal system, stabilizes o In narcolepsy, loss of orexin’s stabilizing
influence causes abrupt switch from one state of consciousness to another
“floppy sleep switch” o SCN has few direct projections to VLPO and orexin neurons o
Dorsomedial nucleus of hypothalamus (DMH) – 3rd system that controls sleep/wake
SCN – active during the day
VLPO – active at night
DMH – intermediate step, receives projections from SCN and sends projections to VLPO
DMH affects – eating, temperature, corticosteroid cycles, sleep, and arousal o FDA approved medications: amphetamine,
methylphenidate (d,l)
o Off-label medications: lisdexamfetamine, methylphenidate (d), modafinil, sodium
oxybate
• To promote sleep
o Enhance GABA (threshold 25%), or o Inhibit
Hypocretin/orexin (threshold 65%)
Acetylcholine
Dopamine
Norepinephrine
Serotonin
Histamine (threshold 80%)
• To promote wakefulness o
Inhibit GABA o Enhance
Hypocretin/orexin
Acetylcholine
Dopamine
Norepinephrine
Serotonin
Histamine
2. Distinguish among beta fiber neurons, delta fiber neurons, and C-fiber neurons.
Beta Fiber Neurons (non-noxious mechanical stimulus – tickled with a feather)
o Dampen the pain (gate theory of pain) through activation of inhibitory interneurons in the dorsal horn, which results in a much
smaller signal being conveyed to the brain.
This explains why rubbing an injury seems to reduce pain (rationality of using a tens unit) o
Centralization of pain makes the non-noxious mechanical stimuli hurt
C-Fiber neurons (noxious heat and chemical stimuli – chili pepper/fire) o Unmyelinated, so they send much slower signals and
response to dull pain. o The duller pain signal of the C
fibers becomes the most troublesome in chronic pain
Delta Fiber Neurons (noxious mechanical stimulus – getting hit with a hammer)
o Myelinated axons that act quickly and send the first sharp signals of pain
3. Explain peripheral neuropathy pain.
1. Describe different types of insomnia/sleep disorders and identify which medications are best
indicated to treat different types of insomnia/sleep disorders.
Insomnia
o Suggested criteria for defining insomnia
Average sleep latency > 30 min
Wakefulness after sleep onset (WASO) > 30 min
Sleep efficiency < 85%
Total sleep time < 6.5 hours o Hyperarousal at night
o Neuroanatomical abnormalities
Reduced gray matter in left orbitofrontal cortex and hippocampus o Neurobiological abnormalities
Decreased GABA levels in occipital and anterior cingulate cortices
Reduced nocturnal melatonin secretion
Increased glucose metabolism
Attenuated sleep-related reduction in glucose metabolism in wake-promoting regions
Decreased BDNF
o Autonomic Nervous System Abnormalities
Heart rate elevations and variability
Increased metabolic rate
Increased body temperature
HPA axis activation
Increased NE o Systemic inflammation o Genetic factors
CLOCK gene polymorphisms
GABA-A receptor gene polymorphisms
Serotonin reuptake transporter (SERT) gene polymorphisms
Human leukocyte antigen (HLA) gene polymorphisms
Epigenetic modifications affecting genes involved in the response to stress
Circadian Rhythm Disorders
o Shift Work Disorder
Insomnia or excessive sleepiness temporarily associated with a recurring work schedule that overlaps with the usual time for
sleep
Symptoms associated with shift work schedule are present for at least 1 month
Sleep log or actigraphy monitoring (with sleep diaries) for at least 7 days demonstrates disturbed sleep (insomnia) and circadian
and sleep-time misalignment
Sleep disturbance is not due to another current sleep disorder, medical disorder, mental disorder, substance use disorder, or
medication use
o Advanced Sleep Phase Disorder
Go to bed to early and wake up to early
Increasingly common as you age
Treatment: early morning melatonin and evening light
Can help reset the SCN so that the sleep/wake switch stays off longer
o Delayed Sleep Phase Disorder – “Night owls”
Stay up late and sleep in late
Patients with MDD and teenagers
Use melatonin at night and light in the morning
, o Non-24
Blind patients who cannot see light o Disrupted sleep/wake cycle can decrease leptin (appetite inhibiting) hormone and
increase ghrelin (appetite stimulating) hormone; this increase in ghrelin is hypothesized to contribute to the increased risk of obesity,
diabetes, and CV disease
• Narcolepsy: rapid, unwanted
transition from wakeful state to
sleep state o Lack of orexin
neurons in hypothalamus plays a
role in narcolepsy
Orexin – active during wakefulness, reinforces the arousal system, stabilizes o In narcolepsy, loss of orexin’s stabilizing
influence causes abrupt switch from one state of consciousness to another
“floppy sleep switch” o SCN has few direct projections to VLPO and orexin neurons o
Dorsomedial nucleus of hypothalamus (DMH) – 3rd system that controls sleep/wake
SCN – active during the day
VLPO – active at night
DMH – intermediate step, receives projections from SCN and sends projections to VLPO
DMH affects – eating, temperature, corticosteroid cycles, sleep, and arousal o FDA approved medications: amphetamine,
methylphenidate (d,l)
o Off-label medications: lisdexamfetamine, methylphenidate (d), modafinil, sodium
oxybate
• To promote sleep
o Enhance GABA (threshold 25%), or o Inhibit
Hypocretin/orexin (threshold 65%)
Acetylcholine
Dopamine
Norepinephrine
Serotonin
Histamine (threshold 80%)
• To promote wakefulness o
Inhibit GABA o Enhance
Hypocretin/orexin
Acetylcholine
Dopamine
Norepinephrine
Serotonin
Histamine
2. Distinguish among beta fiber neurons, delta fiber neurons, and C-fiber neurons.
Beta Fiber Neurons (non-noxious mechanical stimulus – tickled with a feather)
o Dampen the pain (gate theory of pain) through activation of inhibitory interneurons in the dorsal horn, which results in a much
smaller signal being conveyed to the brain.
This explains why rubbing an injury seems to reduce pain (rationality of using a tens unit) o
Centralization of pain makes the non-noxious mechanical stimuli hurt
C-Fiber neurons (noxious heat and chemical stimuli – chili pepper/fire) o Unmyelinated, so they send much slower signals and
response to dull pain. o The duller pain signal of the C
fibers becomes the most troublesome in chronic pain
Delta Fiber Neurons (noxious mechanical stimulus – getting hit with a hammer)
o Myelinated axons that act quickly and send the first sharp signals of pain
3. Explain peripheral neuropathy pain.
