March 23 - Psychiatric Disorders

Question 0

What is a psychiatric disorder?

Answer 0

Psychiatric disorders are central nervous system diseases characterized by disturbances in emotion, cognition, motivation and socialization. As a result of their high prevalence (1 in 5 people), early onset and persistence, they contribute substantially to the burden of illness worldwide

Question 1

What is wellness based on?

Answer 1

Upon the integrated and coordinated function of many neurotransmitter systems

Question 2

What makes psychiatric disorders unique?

Answer 2

They have very heterogenous syndromes, lacking bona fide biological markers. Diagnosis is made solely on clinical observations and criteria (DSM-V)

Question 3

Describe the relationship between mental health and physical health

Answer 3

Mental health issues and physical health issues look very different. Overall health is a dynamic, malleable, integration of domains. Connection between physical and mental health is two-way, and perpetual. We try to use what we know about microfactors (tiny things) and how we try to translate that to improve the global function of the individual

Question 4

How many neurons are found in the brain? How many connections?

Answer 4

The brain contains 100 billions neurons, with 1000 trillion connections

Question 5

Where does controversy lie with regards to psychiatric disorders?

Answer 5

Abnormality vs illness (where do we draw the line between someone who is odd vs someone with a mental health problem)
Holistic approach vs specific targets
Psychosocial vs pharmaceutical
Autonomy vs specialized care

Question 6

Describe the co-occurrence of anxiety and sleep disorders

Answer 6

Co-occurrence is very high
A patient will have an excess of “stimulating” neural flow relative do the “calming” neural flow
There is a considerable overlap of symptoms, pathophysiology and treatment approaches

Question 7

What is anxiety?

Answer 7

Anxiety allows us to prepare for or react to environmental changes. It’s essential. It should be adaptive and transient. We’re supposed to able to move on and put the anxiety behind us. When anxiety is excessive, it can become persistent, severe, and impair function.

Question 8

What is the diagnostic criteria to diagnose someone as having a generalized anxiety disorder (GAD)?

Answer 8

Excessive anxiety and worry, occurring more days than not for at least 6 months, about a number of issues. The person finds it difficult to control the worry, and both are associated with three (or more) of the following symptoms: restlessness or feeling keyed up or on edge, being easily fatigued, difficulty concentrating or mind going blank, irritability, muscle tension, sleep disturbance

Question 9

What is dimenhydinate? What is it used for?

Answer 9

Dimenhydinate aka Gravol is an antihistamine, anticholinergic. It acts as a CNS depressant, causing drowsiness and sedation. It is most effective for motion sickness. It’s used off-label as a sleep aid

Question 10

Describe the target sleep architecture

Answer 10

There are four stages: stage I, stage II, stage III and stage IV. Stage III and IV are known as delta sleep, a deeper sleep characterized by muscle atonia. It is the most restorative sleep. Ideally, a person will go through 4-6 cycles (stage I to stage IV). There is a gradual decline in the quality of sleep with age

Question 11

What controls the circadian rhythm?

Answer 11

The suprachiasmic nucleus

Question 12

How do sleep aids affect the sleep cycle?

Answer 12

Most sleep medications alter the sleep cycles; the patient may fall asleep faster but the sleep won’t be as restorative

Question 13

What controls non-REM sleep?

Answer 13

NREM sleep is enabled by primary serotonergic tracts in the medulla and the dorsal Raphe nucleus

Question 14

What controls REM sleep?

Answer 14

REM sleep is turned on by cholinergic tracts and turned off by noradrenergic areas

Question 15

What neurotransmitters cause wakefulness (stimulating effect)? What is the importance of these neurotransmitters in sleep disorders?

Answer 15

Dopamine has an ‘altering’ effect. Wakefulness is also associated with norepinephrine, acetylcholine, histamine, substance P and corticotropin releasing factor -> cortisol.
People with sleep disorders tend to have a relative excess of one or more of these neurotransmitters

Question 16

What causes insomnia? How does it present?

Answer 16

Insomnia may be related to situational, medical, psychiatric or pharmacological factors
May present as difficulty falling asleep, difficulty in maintaining sleep or non-restorative sleep (spending a large period of time in stage II)
Sleep disorders may be transient, short-term (up to three weeks) or chronic

Question 17

Good sleep hygiene and stimulus control is the ideal way to treat insomnia. How is good sleep hygiene achieved?

Answer 17

1. Establish regular times to wake up and to go to sleep
2. Sleep only as much as necessary 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 minutes, leave the bed and do something relaxing
5. Avoid daytime naps
6. Schedule worry time during the day (e.g., don’t do finances right before bed). Do not take your troubles to bed
7. Exercise routinely, but not close to bedtime
8. Minimize sensory stimulation in the bedtime (lights, sound, temperature, etc.)
9. Reduce the use of alcohol, caffeine and nicotine, especially in the evening
10. Avoid large quantities of liquids in the evening
11. Do something relaxing and enjoyable before bedtime

Question 18

What are reversible causes of insomnia?

Answer 18

Situational (stressors, jet lag, shift work)
Medical (cardiovascular, respiratory, pain, endocrine, GI, neurologic, pregnancy)
Psych (all disorders including substance abuse)
Pharmacological (anticonvulsants, adrenergic blockers, diuretics, SSRIs, steroids, stimulants)

Question 19

Explain the relationship between anxiety, sleep disorders, chronic pain and depression

Answer 19

These are four different issues that people can have, and if a patient has one of these issues, there is a greater chance that they will develop another one. So a patient who has anxiety and sleep disorders is more likely to develop chronic pain and/or depression relative to a patient without these disorders. Having said this, if a patient has anxiety and sleep disorders, directly improving one of these issues will most likely indirectly improve the other one (e.g., improving the patient’s sleep will likely decrease their anxiety)

Question 20

What are the treatment targets in insomnia?

Answer 20

Address the reversible causes and utilize sleep hygiene techniques
Enhance (restore) GABA, serotonin
Inhibit (normalize) Histamine, acetylcholine, norepinephrine, dopamine, substance P, corticotropin releasing factor (cortisol)

Question 21

What are some pharmacological treatment options for insomnia?

Answer 21

Benzodiazepines (GABAa agonists)
Non-benzo GABAa agonists (zopiclone)
Antihistamines
Antidepressants (Trazodone, at lower doses)
Melatonin agonists (Valerian)

Question 22

What are causes of anxiety?

Answer 22

Medical causes (cardiovascular, endocrine, neurological, respiratory, etc.)
Psychiatric (depression, schizophrenia, bipolar disorder, Alzheimer’s, substance abuse)
Drugs (antidepressants, bronchodilators, steroids, herbals, thyroid, stimulants, and others)
Drugs - withdrawal from sedatives
Stressors
Endogenous factors

Question 23

Describe the different neurochemical factors (models) that can lead to anxiety

Answer 23

Noradrenergic model - autonomic nervous system is hypersensitive/overactive, which causes an excess of norepinephrine, glutamate, and locus ceruleus firing (alarm centre of our brain)
GABA model - natural regulation of serotonin, norepinephrine, dopamine, etc is under-performing
Serotonin model - increasing/normalizing serotonin reduces locus ceruleus firing and norepinephrine excess

Question 24

Describe the treatment of anxiety

Answer 24

Thorough assessment to define condition and focus reduction of reversible factors; must clarify symptomatic target and chronic vs transient nature of symptoms. The goal is to reduce the duration and severity of symptoms and improve overall functoning

Question 25

What is the prevalence of anxiety disorders?

Answer 25

There is high prevalence; approx 18% of people/year. Less than 25% of patients receive appropriate treatment

Question 26

What are the symptoms of anxiety disorders?

Answer 26

Physical symptoms - restlessness, fatigue, muscle tension, sleep disturbances, irritability
Psychologic/cognitive symptoms - increased anxiety, worries are hard to control, on edge, poor concentration

Question 27

How do the physical symptoms of anxiety respond to treatment?

Answer 27

They respond quickly GABAa agonists
Antidepressants may have superior long-term benefits but can increase physical symptoms at first and benefits take time
Effectiveness of benzodiazepines contributes to dependance liability, especially with fast onset and rapid elimination (e.g., lorazepam)

Question 28

How do the psychological symptoms of anxiety respond to treatment?

Answer 28

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

Question 29

Describe benzodiazepines

Answer 29

They are all muscle relaxants, anxiolytics, sedative/hypnotic and anticonvulsant properties.
They all reduce CNS excitability via enhancing GABA (GABA agonists)
Onset of speed correlates with lipid solubility
They have variable half-lives; the longer their half life, the more likely to have a hangover effect. The shorter their half life, the more likely to have rebound symptoms and develop dependance

Question 30

Benzodiazepine dependancy: do they work too well?

Answer 30

Unauthorized dosage increase and eventual dependancy - common to all
Lorazepam and alprazolam both have short half lives
Diazepam - rapid onset
Highest risk for dependancy with quick onset and accelerated clearance (liver induction)

Question 31

How do antidepressants work in anxiety?

Answer 31

The mechanism is not fully understood. Modulation of serotonin, norepinephrine and dopamine normalizes gene expression, which results in more brain derived neurotrophic factor and less corticotropin releasing factor (decreasing cortisol)

Question 32

What is the role of a pharmacist in the treatment of anxiety and sleeping disorders?

Answer 32

Educate about non-drug strategies
Educate about the importance of thorough assessment and appropriate pharmacological strategies
Educate about appropriate time-frames for response and minimizing side effects
Promote adherence to a therapeutic plan