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Applied Pathophysiology > Sleep & Anxiety Disorders > Flashcards

Sleep & Anxiety Disorders Flashcards

1
Q

Wellness..

A

is based upon the integrated and coordinated function of many Neurotransmitter systems

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2
Q

Disorder =

A

IMBALANCE SIGNIFICANTLY impairing Function and Quality of Life

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3
Q

What are the research targets?

A

Molecular, Biochemical, Cellular, Neuronal, & Behaviour areas

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4
Q

What are the meaningful outcomes?

A

functional status & QOL

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5
Q

______ <–> ________

A

Mental

Physical Health

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6
Q

What are the key features of NS?

A

BALANCE & Adaptation (when physical/mental health is good we are better able to adapt to things like COVID)

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7
Q

What is 1 of the biggest reasons why we don’t know exact pathophys of the disorder?

A

because it contains MANY neurons with MANY connections

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8
Q

What should Health Care Practitioners draw upon for optimal outcomes?

A

more than clinical & scientific skills
- combo of both pharmaceutical & other is ideal

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9
Q

What are the factors for discussion?

A
  • PRECISE pathophys is unknown
  • Neuronal receptor mech’s are vital
  • Evidence-based research is critical
  • Definitions of illnes/disorders
  • Overall impact of dysfunction
  • Societal impact of disorders
  • Outcome - focused perspectives
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10
Q

What is imp. about Anxiety/Sleep Disorders?

A
  • Co-occurrence is VERY HIGH (if anxiety is high, sleep is probs disrupted & vice versa)
  • Overgeneralizing: An excess of “stimulating” neural flow relative to “Calming” neural flow
  • Considerable overlap of symptoms, pathophys, persistence, & treatment approaches
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11
Q

Autonomic (Involuntary) Nervous System:

A
  • directs the action of skeletal muscle, cardiac muscle & gland secretion
  • consists of SNS & PNS - balanced for optimal body function
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12
Q

What underlies mental health conditions such as: Anxiety, Depression & Chronically feeling “Stressed”?

A

OVERACTIVE Sympathetic/UNDERACTIVE Parasympathetic

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13
Q

What are the Neurochemical Models of Anxiety?

A
  • NORADRENERGIC model
  • GABA model
  • SEROTONIN model
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14
Q

NORADRENERGIC model:

A

ANS is HYPERsensitive or OVERactive –> excessive NE, Glutatmate, Locus Ceruleus (alarm center for brain) firing

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15
Q

GABA model:

A

normalizing (HIGH) GABA can favorably impact 5HT, NE, DA

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16
Q

Serotonin model:

A

increasing/normalizing Serotonin (5HT) reduces Locus Ceruleus firing & NE “excess”, hence reducing overstimulation

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17
Q

What is the presentation of an Anxiety disorder?

A
  • often present as PHYSIOLOGIC or SOMATIC COMPLAINTS (often pt doesn’t straight up say they have anxiety)
  • Headaches, upset stomach, high BP, pain sensitivity
  • IMPAIRMENT of sleep, ability to relax, & of appetite are common features
  • PERSISTENT WORRIES about health & wellbeing of self & of others
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18
Q

What is anxiety good?

A

allow us to prepare for or react to environmental changes
- part of us, should be ADAPTIVE & TRANSIENT (a healthy surge of STIMULATION)

19
Q

When is anxiety bad?

A

when EXCESSIVE
- becoming severe, persistent & impair function

20
Q

What type of arousal is anxiety?

A

psychologic/phyiologic

21
Q

What are high comorbidities of anxiety?

A
  • medical illness
  • depression
  • schizophrenia
  • bipolar disorder
22
Q

What is the etiology of increased anxiety/anxiety disorders?

A
  1. Medical causes (CV, Endo, Neural, Resp etc,)
  2. Psychiatric (Depn, SZP, BpD, Alz, Subst)
  3. Drugs - Antidepressants, Bronchiodilators, Steroids, Thyroid, Stimulants, Herbals etc.
  4. Drugs - withdrawal from Sedatives (rebound after discontinuing sedatives)
  5. Life stressors
  6. Endogenous factors (ex: why 1 fam is anxious & another isn’t)
23
Q

What is the Anxiety tx?

A

Thorough Assessment to define condition and focus reduction of Reversible factors must clarify Symptomatic target and Chronic vs. Transient nature of Symptoms

GOAL - reduce duration & severity of Sx & to improve overall functioning

24
Q

What are Anxiety’s symptoms?

A
  1. Physical
    - restlessness, fatigue, muscle tension, sleep disturbances, irritability
  2. Psychologic/cognitive
    - HIGH anxiety, worries hard to control, on EDGE, poor concentration
25
Q

What are the Physical symptoms for anxiety?

A
  • Respond quickly to GABAa Agonists - Benzodiazepines
  • Antidepressants have superior LONG-TERM benefits, but can INCREASE PHYSICAL SYMPTOMS at 1st & benefits take time (*worse before better)
  • Rapid effectiveness of BZD contributes to DEPENDENCE liability, esp. with FAST ONSET & RAPID ELIMINATION ex: Lorazepam
26
Q

What are the Psychologic symptoms for anxiety?

A
  • Some quick “easing” with BZD, not sustained (like temporary dulling of headache pain)
  • Antidepressants work more slowly but are treatment of choice for chronic anxiety symptoms - transient increase in symptoms may challenge adherence
  • Psychoeducation, psychotherapy, meditation, exercise, etc are often VITAL for optimal management

(SHOULD BE MEDICATION + OTHER –> best answer for long-term)

27
Q

Benzodiazepines:

A

All have Muscle Relaxant, Anxiolytic, Sedative/Hypnotic, and Anticonvulsant properties

All ↓ CNS Excitability via enhancing GABA {GABA Agonists}

Onset speed correlates with Lipid Solubility

Variable Half-Lives

28
Q

Benzodiazepines

Slower Drug Elimination =

A

LONGER half-life……INCREASE hangover effect

(might help them fall asleep, but might wake up feeling off)

29
Q

Benzodiazepines

Faster Drug Elimination =

A

SHORTER half-life (Lorazepam, Diazepam)…..INCREASE rebound symptoms, elevated risk of dependency

30
Q

Benzodiazepine dependency:

A
  • UNAUTHORIZED dosage increase & potential for dependency is a concern
  • Lorazepam & Alprazolam - Short t1/2
  • Diazepam - Rapid onset
  • Highest risk for Dependency with quick onset & accelerated clearance or metabolism (liver induction)
31
Q

What about Antidepressants for Anxiety?

A

mech not fully understood

Modulation of 5HT, NE, and DA normalizes gene expression → → more BDNF, less CRF (↓ Cortisol)

5HT modulation ( Short & Long-term)

NE modulation ( Indirect & Direct )

DA modulation ( Indirect & Direct)

Antidepressants don’t work super fast

32
Q

Sleep Disorders:

A

Insomnia may be related to Endogenous, Situational, Medical, Psychiatric, or Pharmacologic factors

  • transient, short-term (up to 3 weeks) or chronic insomnia
  • improvement WITHOUT MEDICATION is ideal
33
Q

Subtypes of Sleep Disorders:

A
  • difficulty in falling asleep
  • difficulty in maintaining sleep
  • or non-restorative sleep
34
Q

“ Normal “ Sleep Cycles & Circadian Rhythm

A
  • stage 3 & 4 are REM
  • delta sleep - most RESTORATIVE sleep, difficult to arouse, muscle atonia (3&4)
35
Q

What do most sleep medications do?

A

alter sleep cycles

36
Q

Wakefulness/alertness associated with…

A
  • NE
  • DA
  • ACH
  • Histamine
  • Substance P
  • Corticotropin Releasing Factor –> CORTISOL
37
Q

What are Sleep Hygiene & Stimulus Control?

A
  1. Establish REGULAR TIMES to wake up & got to sleep
  2. Sleep only as much as needed to feel rested
  3. Go to bed only when sleepy (avoid long periods of wakefulness in bed)
  4. If you do not fall asleep within 20-30 mins, leave the bed & do something relaxing
  5. Avoid daytime naps
  6. Schedule worry time during the day. Do not take your troubles to bed
  7. Exercise routinely, but not close to bedtime
  8. Minimize sensory stimulation in the bedroom (light, sound, temp, etc)
  9. Reduce use of alcohol, caffeine, & nicotine - esp. in the evening
  10. Avoid large quantities of liquids in the evening
  11. Do something relaxing & enjoyable before bedtime

(Address these 1st BEFORE adding medications to pt)

38
Q

What are the reversible causes of insomnia treatment?

A
  • Situational (stressors, jet lag, shift work)
  • Medical (CV, pain, pregnancy etc.)
  • Psychiatric - all disorders, incl substance abuse
  • Medications (ex on slides)
39
Q

What are the treatment targets in insomnia?

A

Address Reversible Causes & Utilize Sleep Hygiene techniques!
- before adding medications

Enhance (restore) GABA, Serotonin

Inhibit (normalize) Histamine, Ach, NE, Da, Substance P, CRF - Cortisol

40
Q

What are the current treatments of insomnia?

A
  • through assessment, non-pharm techniques (ex: stress, sleep hygiene), careful use of sedative hypnotics)
  • BZD - GABAa agonists
  • NonBenzo GABAa agonists - Zopiclone etc
  • Antihistamines
  • Antidepressants (esp if pt has or is prone to depression) incl. Trazodone (least disruptive to sleep - don’t cause bad impact on sleep)
  • Melatonin & related agonists, Valerian (natural compounds)
41
Q

What is an ex of a medication that helps sleep but also causes sleep problems?

A

Benzodiazepines - GABAa agonists
- suppress REM sleep
- when they stop taking it, their REM has been suppressed so they have REM REBOUND –> it causes lots of dreams etc.
- lasts a few nights
- can be done but has to be slowly & carefully

42
Q

Dimenhydinate (Gravol)

A
  • most effective for motion sickness
  • an Antihistamine, also Anticholinergic
  • acts as a CNS depressant, often causing drowsiness & sedation as SE’s

(*good for pt with upset stomach & has sleep problems but should be monitored)

  • off-label use as a sleep aid
43
Q

Sleep / Anxiety Disorders &
Pharmacists:

A

Educate about:
- non-drug strategies
- importance of thorough assessment & of appropriate pharmacologic strategies
- appropriate time-frames for response, & minimizing SE’s

Promote:
- ADHERENCE to a therapeutic plan, incl. “Do not increase dose without discussing with prescriber”

Applied Pathophysiology (34 decks)

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