Just lecture cards

Question 1

Biological Vulnerabilities to negative mood states

Answer 1

Irritable, Tension

Question 2

Specific Psychological Vulnerability to negative mood states

Answer 2

Somatic preoccupations, panic symptoms

Question 3

General Psychological Vulnerability

Answer 3

Low confidence, low self-esteem, low self-efficacy

Question 4

If someone has a vulnerability under certain circumstances, what will it develop into?

Answer 4

Anxiety

Question 5

Common comorbidities with physical disorders (anxiety)

Answer 5

Thyroid Disease → Hypo-thyroid
Respiratory Disease → overlaps with gastro.
Gastrointestinal disease
Arthritis
Migraine
Headaches
Allergies
Pain disorders can also create comorbidities with anxiety.
If you have a particular disorder that could account for anxiety, it is not diagnosed. For example, vestibular disorder and panic attack vertigo and panic.

Question 6

Generalized anxiety disorder DSM5

Answer 6

Defined by excessive worry and avoidance to solve that worry.

Question 7

Etiology of Generalized Anxiety

Answer 7

• About 3% of the populations meet the criteria
• genetic evidence in mono-zygotic twins (But-genetics seems to be more about anxiety rather than GAD specifically therefore it is not compelling and can be explained by anxiety specific/neuroticism).
• Less physical reactivity to stress but higher muscle tension.
• Slower heart rate, less sweating, slower respiration, lower blood pressure than non-GAD
• They avoid, engage in frantic, non-imagery based worrying to avoid feared outcomes and manage to avoid facing the fear and solving it (This involves lots of cognitive activity and muscle tension)
• avoidance maintains the disorder - tunes out specifics “just something bad”

Question 8

Poly genetics of GAD

Answer 8

Like rumination → no problem solving going on. (Not a bad problem solver- just impossible conditions)
Frantic intense thoughts are the impossible conditions for problem solving. (Where does this come from?)
Afraid of uncertainty “intolerance of uncertainty”
Avoid the present moment → habitual
Challenges as threats

Question 9

GAD Treatments

Answer 9

• Benzodiazepines but risky and medium effect sizes – short-term benefit
• SSRIs like Paxil are safer and more beneficial but are not long-lasting
• CBT is as effective as the SSRIs and the treatment effects are more durable (Newman et al., 2011)
• Tolerance of Benzo’s occur long-term even though they are most used?
• SSRIs’ –> not tolerant but as soon as you stop, it doesn’t work
• CBT –> More durable overall

Question 10

What is CBT-G?

Answer 10

Highly effective (large effect sizes; Borkovec & Ruscio, 2001) Provides a model of intolerance of uncertainty, unhelpful thoughts and avoidance (Dugas et al., 1998)
Use cognitive techniques to consider alternative thoughts and thinking styles
Avoid avoidance
Teach relaxation skills

Question 11

The model of therapy

Answer 11

Situation → what if ? Wouldn’t it be terrible if? → worry → anxiety → Demoralization/Exhaustion

Question 12

Panic Disorder (PD) and the DSM5

Answer 12

“The consequences of panic can constitute a more serious problem than the panic itself” Overall, it is Fear of panic.

Question 13

Treatment for PD

Answer 13

Benzodiazepines work quickly, but dependence and cog and motor issues
Most frequently used; 90% relapse rate upon discontinuation
SSRIs and SNRIs effective
Pills are effective for 60% but relapse is high (50%)
CBT-P (Craske et al., 1991) highly effective (large effect sizes) and advantages remain even at two years post-treatment
Combining CBT and Drugs is also a potential.

Question 14

CBT for panic disorder:

Answer 14

Introduction to panic and anxiety
Anxiety symptoms are functional and not dangerous (activates body in emergencies)

Psychoeducation about panic
Normal (i.e., harmless) physiologic changes in breathing, heart rate, muscle activity are perceived → mistaken for a problem → arousal → panic attack

Breathing retraining for over-breathers
Physiologic consequences of shallow breathing

Cognitive restructuring:
Overestimation of danger (e.g., cardiac arrest or suffocation)

Question 15

Panic mechanism for PD

Answer 15

Physical sensations during panic –> very strong sensitivity to those sensations –> fear of the sensations of arousal.

Question 16

Cognitive restructuring

Answer 16

“What is the evidence for…?”
“What is the actual likelihood of …?”
“How could you cope with these sensations if they happened?”

Question 17

Behavioural Elements of PD

Answer 17

Identification of feared/avoided activities
Cease safety of behavior/avoidance (Avoid avoidance)
Interoceptive exposure (to panic, feared sensations)
Experiences of those situations without anxiety or panic
Expose them to the sensations…
Our body burns out → gets bored of being anxious etc.,

Question 18

Interoceptive exposures

Answer 18

For example, someone that is afraid to throw up –> spinning in place for 60 seconds to allow them to feel the sensations

Question 19

Nocturnal Panic (NP)

Answer 19

Nocturnal panic in up to 70% of those with panic disorder but only half experience nocturnal panic regularly
Sleep loss lowers panic thresholds
Insomnia complaints are common in panic disorder particularly those with NP
Evidence of residual insomnia after panic disorder

Question 20

CBT-NP Treatment

Answer 20

Understand that panic attacks occur due to the excessive fear of the sensations of arousal
Accept that the sensations pose no real threat → expose to anxiety-provoking sensations
Through acceptance, patient becomes:
Less anxious (with ↓ arousal there is ↓ panic)
Less sensitive to the sensations (↓ attention)
Address insomnia – improving sleep will reduce arousal and ↓ likelihood of panic
Same as daytime protocol but nocturnal rationale and exposures

Question 21

DSM5- Agoraphobia

Answer 21

Fear of marketplace (wide open space with busy/no escape)
Marked anxiety in situations in which escape may be difficult
Could have a fear of having a panic attack out in public and not being able to be helped
DSMIVTR Used to group panic disorder with agoraphobia
Now seperated from panic disorder
Gender role perspective → housewives developing agoraphobia

Question 22

Social Anxiety Disorder

Answer 22

A marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others

Question 23

Are we all naturally inclined towards anxiety?

Answer 23

Responses conditioned to angry faces: Directed toward the subjects showed significant resistance to extinction

Responses conditioned to angry faces: Directed away extinguished immediately during extinction

Question 24

Social Anxiety Treatments

Answer 24

Cognitive Therapy (Clark et al., 2003): challenging the danger assumption of negative social evaluation and helping with social skills → CT challenges the cognitive assumptions of danger → when disaster → not safe…

Superior to Prozac

SSRIs are also effective (Stein et al., 1998)

Question 25

Specific Phobia DSM5

Answer 25

Marked fear/anxiety about a specific object/situation

Phobic situation/object almost always provokes immediate fear or anxiety

Phobic situation/object is actively avoided or endured with intense fear or anxiety

The fear/anxiety is out of proportion to the actual danger posed by the phobic situation/object

The fear/anxiety/avoidance is persistent (6 months or more)

The fear/anxiety/avoidance causes distress or impairment

Not better explained by another mental disorder

Question 26

Subtypes for specific phobia

Answer 26

Animal (e.g., spiders)
Natural environment (e.g., heights)
Blood-injection injury (e.g., needles—more likely to faint)
Situational (e.g., enclosed spaces)
Other (e.g., clowns)

Question 27

What are the names of specific phobias for: spiders, heights, open spaces, the cold, flying, dark, closed spaces, holes

Answer 27

ear of spiders → Arachnophobia
Fear of heights → Acrophobia
Fear of open spaces → Agoraphobia
Fear of the cold → Frigophobia
Fear of flying → Aviophobia
Fear of the dark → Scotophobia
Fear of closed spaces → Claustrophobia
Fear of darkness is also called achluophobia
Fear of the cold is mainly seen in Chinese culture . Yin is energy sapping and associated with the cold. When experiencing cold, there is an imbalance of yin and yang and ruminate over the loss of heat, dressing in layers on hot days.
Trypanophobia is fear of holes in nature 60% of people have this phobias Not in the DSM5

Question 28

What are the most common phobias in order?

Answer 28

Agoraphobia, heights, illness, animals, death, storms

Question 29

Phobia development

Answer 29

Experiential
Vicarious
Alarm

• What if you are watching your friend get attacked by a dog: It is possible for you to have alarm systems that go off. It can also be generalized (I.e., little albert)
• Informational transmission = If you are warned about danger, you can begin to fear that situation or object.

Question 30

Recipe for a phobia:

Answer 30

Scary experience/situation
Genetic predisposition
Post experience is focused on whether it will recur.

Question 31

Treatment to specific phobias: Exposure

Answer 31

Develop a hierarchy of fearful situations (What is the most scary for them to the least, starting with the least)
Expose, fear decreases – paired with neutral experience

Question 32

Virtual Reality Exposure Therapy

Answer 32

Supported for flight, public speaking anxiety, school phobia, fear of falling, dental phobia, arachnophobia, social anxiety, ptsd, gad, and panic disorder.

Question 33

Post traumatic stress disorder and the DSM5

Answer 33

A.Exposure to actual or [threatened death, serious injury or sexual violence] = trauma - in one or more of the following ways:

B. [Intrusive symptoms] Presence of one or more of the following intrusion symptoms.

C. [Avoidance] Persistent avoidance of stimuli associated with the traumatic event

D. [Cognitive Emotional] Negative alterations in mood and thoughts associated with the trauma, beginning or worsening with the trauma as evidenced by two or more of:

E. [Hyperarousal] Marked alterations in arousal and reactivity as evidenced by two or more of the following:

Question 34

PTSD Treatments

Answer 34

Prolonged exposure therapy (PE; Foa, McLean, Capaldi, & Rosenfield, 2013)

CBT → Frontline treatment

Eye Movement Desensitization and Reprocessing (EMDR; Shapiro, 1995): client thinks about trauma while following therapists moving finger with eyes –Some good data, but slightly less effective
Criticism: exposure therapy with nonsense.
Theory about what is going on, but the theory gets discredited.
No more effective than relaxation therapy.

PE superior to EMDR, which was no different than relaxation therapy (Taylor et al., 2003); all three treatments showed some improvement in symptoms, but PE helped with avoidance, thoughts and quicker recovery
SSRIs

** CBT and PE are the best for PTSD treatments **

Question 35

Psycho-education for PE

Answer 35

Fear structures: a template for escaping danger
Adaptive in most cases: Mobilize and self preserve → SP = endure but survive.
Fear structures contain information about:
The feared stimuli (what we are scared of)
The fear responses (different ways that people respond when they are very scared)
The meaning of stimuli and responses

Question 36

Fear structure

Answer 36

A trauma memory is a type of fear structure which contains:
Stimuli during the trauma (e.g., alone, smells gas)
Physiological and behavioral responses during the trauma (e.g., freezing, screaming)
Meaning of the responses (e.g., “I’m too blame” “I’m incompetent”)
Erroneous associations between symptoms and competence → we need to disentangle this
Erroneous associations between stimuli and danger → become overgeneralized → we have to claim back, too generalized (i.e., you can’t be afraid of every tall bald man)

Question 37

Cognitive and Prolonged exposure therapy

Answer 37

No cognitive work necessary → all exposure.
Exposures challenge beliefs such as:
The world is an extremely dangerous place and people cannot be trusted
I am extremely incompetent and should have been able to prevent the trauma. My PTSD symptoms are a sign of weakness.

Question 38

Rationale for a client with Prolonged exposure therapy

Answer 38

There are two common ingredients in a persistent trauma reaction:
Avoidance: of any part of the trauma memory (e.g., sleeping with light on, don’t go out)
Avoidance maintains these beliefs.
Unhelpful beliefs such as, “the world is dangerous” or “I am incompetent, to blame” etc.
This is what makes persistent trauma occur
Avoidance maintains the unhelpful beliefs (if we were to experience the trauma reminders, we would see they are not inherently dangerous)
Neutral responses to these experiences with exposure to erode that belief to make you think that that stimulus should be feared.

Question 39

How do we fix the rationale for a client in PE therapy?

Answer 39

Bring the avoided to surface
Process the information
Correct the unhelpful and untrue beliefs
World has shrunk due to avoidance, now the client can navigate freely (feared stimuli not part of the trauma structure any longer)
Remove something from the feared structure
Give back the stimuli to people so their world isn’t that small anymore.

Question 40

Relaxation skills

Answer 40

Learn relaxation techniques (in session) and practice them daily, sometimes using a CD (practice is tracked daily with a diary)
Progressive Muscle Relaxation
Breathing retraining
Shallow breathing is common in trauma → disentangle this.

Question 41

Imaginal Exposure

Answer 41

Revisiting (Repeatedly) and describe in first person
Experiencing and telling the trauma is not the same thing.
Make sense of the trauma, rather than shutting down processing
Learn that thinking about the trauma is not dangerous
Intrusiveness and how activating that is.
You will get used to it.
Imaginal exposure results in habituation, so that eventually it can be remembered without all the symptoms
Self-efficacy –> False alarm.

Question 42

Typical instructions for the imaginal exposure therapy

Answer 42

Recall the trauma memory vividly, with eyes closed
Visualize the trauma as it is happening nw
Engage the feelings elicited by the memory
Describe the trauma in present tense
Include details of event, thoughts and feelings
Repeat narrative as many times as necessary in allotted time
Review in session → write it out between sessions
EMDR connection to this → review session.

Question 43

Therapist during the imaginal exposure

Answer 43

Keep comments to a minimum, usually just to express empathy
Ideally it shouldn’t be a conversation - avoidance
Just listening.
Period reassurance of safety, “this is hard, but you are safe here. You are doing a great job, stay with it..”
To prevent avoidance. (Coaching to stay in the moment)

Question 44

In-vivo Exposure

Answer 44

Develop a list of situations that have been avoided since the trauma
Inquire about safety (i.e., it is possible that they actually live in an unsavory neighborhood)
Exposures aren’t just being in the situation
Sensitization → just exposing is not good… worsen. (Burning out of the emergency response)
Most distressive thing to the least distressive thing
Start with the low or moderate distressive thing (rate out of 20 or how many they have).
Chipping away at the fear structure, getting back that stimulus.

Question 45

In-vivo homework for client

Answer 45

Get client to rate the anticipated subjective unit of distress for each situation and rank them
Start with easier exposures (moderate SUDS of 40-60)
Emphasize staying in the exposure for about 30 minutes or until SUDS falls by 50%

Question 46

Obsessive Compulsive Disorder

Answer 46

Presence of obsessions, compulsions or both Obsessions:
Typically have both.

Question 47

Examples of obsessions and compulsions

Answer 47

Obsessions:
Harming: if I forget to say goodbye, they’ll die
They know it doesn’t make sense, not psychotic. Like a superstition.
Contamination/disease: germs
Inappropriate/unacceptable behaviour: sex acts, worrying about going out in public nude
Really common
Constant things that are persistent and disturbing.
Doubts about safety/memory: leaving things like the iron on
Checking

Compulsions:
Ordering things
Repeating rituals
Repeated washing
Saving objects with no real value

Question 48

How do obsessions and compulsions start?

Answer 48

Can be out of the blue.
The obsession almost never happens (The iron isn’t usually on when people go back to check).
You have to make an association with the anxiety symptom in the presence of something = makes it feared.
You get the alarm, and it is reinforced, and then avoidance occurs.
If you find something that avoids it, it strengthens it.
If you use compulsions against it, strengthens it (avoidance)
Natural for us to have this occur to us, judge ourselves, and then thought suppression.
Acceptance allows it to go away and neutralize us.

Question 49

OCD Treatments

Answer 49

Exposure and response prevention
Expose to triggers (e.g., contaminants) and prevent the response (no washing)
Client learns that no harm occurs – rituals don’t matter
Drugs are less effective and people relapse when off them
Not as good as PE or CBT
People relapse as soon as they go off of them.
No advantage to pairing drugs and ERP
Surgery (lesion of the cingulate bundle) is a desperate last resort.
Only about a third benefit and there are side effects of this approach

Question 50

Related disorders to OCD

Answer 50

Body dysmorphia, Trichotillomania Disorder, Excoriation Disorder, Hoarding Disorder

Question 51

Sleep problems

Answer 51

Problems associated with sleepiness (e.g., obstructive sleep apnea)
Problems associated with sleeplessness (e.g., insomnia disorder)
Other sleep problems (e.g., nightmare disorders)
Involuntary and typically embarrassing

Question 52

Excessive Sleepiness

Answer 52

Fall asleep unintentionally outside of the sleep period, includes dozing, nodding off
There are lots of reasons why people fall asleep: voluntary sleep restriction example with the common reason in students
Occur while you are sleeping and disrupt your sleep so you don’t get the proper amount, thus falling asleep during the day.

Problems causing sleepiness (not exhaustive)
Voluntary sleep restriction
Sleep apnea
Narcolepsy
Shift work
Periodic Limb Movement Disorder

Question 53

Hypersomnolence Disorder

Answer 53

Self-reported sleepiness despite a sleep period of at least 7 hours with at least one of the following: Recurrent periods of sleep or lapses into sleep within the same day
Prolonged main sleep period of 9 hours or more that is non-restorative
Difficulty being fully awake when awoken abruptly
The hyper-somnolence occurs at least three times a week for at least three months
Distress or functional impairment
Not better accounted for or does not occur exclusively during another disorder
Not attributable to a condition or a substance
Co-existing mental or medical disorder does not adequately explain
Epworth sleepiness scale.

Question 54

Multiple sleep latency test

Answer 54

Objective Test
4 or 5 nap opportunities.
For most normal sleepers → won’t fall asleep on these nap opportunities, or after lunch (dip in body temperature after lunch)
Fall asleep after 10 mins → sleepy
Normal sleepers fail to nap in these opportunities after 20 mins has passed.
Under 5 minutes to fall asleep across the nap opportunities → nap

Question 55

Treatment of daytime sleepiness

Answer 55

Address cause if known (e.g., apnea, narcolepsy)
Can’t always do this.
If we can’t, we make sure they have the best habits they can.
Ensure proper sleep-wake habits (e.g., Harvey et al., 2015)
Increase daytime alertness (stimulant medications)
Manage sleepiness behaviourally (naps)
Safety assessment

Question 56

Obstructive Sleep Apnea (OSA)

Answer 56

Obstruction in the airway for 10 seconds → at least 15 times
Cardiovascular traumas
Disrupts sleep → you code and the brain wakes up to resuscitate you.
Not conscious of this.
This is why they become sleepy (constantly woke up)
Disorders categorized by sleepiness
Hunger chemicals increase, stress chemicals increase, satiety chemical decrease, ability to process insulin slows, metabolism slows.
Very difficult to lose weight.
Accidents are more fatal than drunk drivers.

Question 57

Correlates of obstructive sleep apnea

Answer 57

Obese, age (older than 50), neck size 40cm, gender (male) → correlates of apnea

Question 57

Correlates of obstructive sleep apnea

Answer 57

Obese, age (older than 50), neck size 40cm, gender (male) → correlates of apnea

Question 58

OSA

Answer 58

Theta wave activity → disruption (arousal) wakeful ekgs → alpha-waves now.
Before the alpha wave → breathing flatlined or blunted
Slow resume → waking
When positive airway pressure is obstructed → folds → leads to partial inflation or deflation.
Need a blast to get the pressure back → if the blast isn’t occurring → the brain will wake you → then cause that desaturation.

Question 59

Gold standard PAP therapy

Answer 59

Positive Airway Pressure (PAP) therapy eliminates events and can reverse the diseases apnea causes
BUT, up to 40 % are going to have issues with it
Some will feel claustrophobic using the mask- have to do exposure therapy with the mask (Conditioned arousal)
Some won’t believe it is useful
Some won’t believe the results of the test
Some will find it uncomfortable (e.g., air leakage)

Question 60

Narcolepsy

Answer 60

Recurrent periods of an irrepressible need to sleep (sleep attacks) within the same day (at least 3 times per week for at least 3 months)

Question 61

Cataplexy

Answer 61

Cataplexy is a loss of muscle tone in response to increased emotional arousal.
Occurs in around two thirds of those with the diagnosis (Bassetti & Aldridge, 1996).
The loss of tone may result in total collapse onto the floor or mild buckling of the legs such that the patient can continue to stand. The head and jaw often slump forward and the arms often collapse to their sides.
Can be dramatic → pass out
Partial → parts of your face
Or the knees buckle out and hang there.
Very distressing disorder.
Usually happens in response to something ie. being excited or scared.

Question 62

Emotional Triggers of Cataplexy

Answer 62

Common emotional triggers include laughing, being frightened, or being angered.
The person remains aware throughout the attack which can frighten them and leave them vulnerable to prolonged symptoms.
This can be a life-threatening condition
Sleep paralysis can become a part of narcolepsy
Sleep onset hypnagogic

Question 63

Mechanisms of cataplexy

Answer 63

Cataplexy appears to have a genetic basis: a gene turns on an autoimmune response that attacks hypocretin cells.
Colony of hypocretin-knockout Doberman Pinschers raised at Stanford.
Chocolate is a highly palatable food that excites mice, and in mice whose hypocretins are knocked-out, the introduction of chocolate is associated with increased activity in the medial prefrontal cortex (mPFC) and resultant cataplexy (Oishi et al., 2013) .
During the cataplexy, there was also increased activity in parts of the limbic system, namely the hypothalamus and amygdala.
Blocking mPFC activity in these mice resulted in a reversal of the chocolate-induced cataplexy; thus, emotional areas and the mPFC are likely critical for cataplexy.
mPFC + emotional conditions (know both)

Question 64

Cataplexy treatment

Answer 64

The most common treatment approaches are to:
facilitate adrenergic activity with selective reuptake inhibitor (SSRIs) antidepressant medications such as fluoxetine or fluvoxamine
Antidepressants are not really getting rid with depression - what it really does is modulates emotions
(Blunting emotional responses)
Use gamma hydroxybutyrate (GHB) to consolidate REMS
Potent, dangerous drug
Measure out doses and leave by bed
Highly regulated
An extreme way, but also give stimulants during the day
a patient can consolidate sleep by taking this medication and it has been shown to help with other narcolepsy symptoms too (U.S. Xyrem Multicentre Study Group, 2004

Question 65

Hallucinations

Answer 65

Hypnopompic hallucinations occur upon awakening whereas hypnagogic hallucinations occur while falling asleep.
most often visual hallucinations involving shapes and colors on the wall but it can also include sounds or music or perception of someone touching the body.
Like sleep paralysis, hypnopompic or hypnagogic hallucinations can occur in the normal population (Ohayon, Priest, Caulet, & Guilleminault, 1996).
There are no hallucination-specific interventions except for psychoeducation to reassure the patient of the normalcy of this experience
There is no intervention for this, tell people it is normal to reduce anxiety.
Dart the eyes back and forth (because it is the one muscle you can move) to hasten waking up.

Question 66

Nightmare disorder

Answer 66

Repeated, extended dysphoric, well-remembered dreams (usually threats to survival, security or physical integrity, typically in the second half of the night)

Not a sleep terror = where you don’t remeber what is happening
REM sleep - half awake anyway.

Upon awakening from the bad dream, they are alert
Distress or impairment in functioning
Not attributable to a substance
Co-existing condition is not enough to explain the nightmare
Comorbid and PTSD.

Question 67

Nightmares and Trauma

Answer 67

Most people who have nightmares following trauma eventually stop having them. Nightmares gradually change into less disturbing dreams. This process was not enacted in PTSD, but IRT can start that process.
In some cases of PTSD → doesn’t happen → IRT allows it. (retraumatize if they don’t use IRT)
IRT = essentially write out their nightmare in first person, whole thing out (exposure) and then they can change the dream → but change the trauma, and then they close their eyes and imagine that new dream. Do this a couple of times a day (influence dream content)
If they start with other nightmare content, it intrudes the original nightmare
Large effect sizes for the most part,
But can have small effect sizes too.
Can be helpful, but it is inconsistent.
Over time, nightmares take on a life of their own. Move beliefs towards nightmares being caused by habit over trauma.
Imagery Rescripting and Rehearsal Therapy (IRT) produces large effects on nightmare frequency/intensity and PTSD symptoms (Davis et al., 2011; Krakow et al., 200

Question 68

Insomnia Disorder

Answer 68

It is about being chronic → not getting a bad sleep.
Difficulty sleeping (initiating and/or maintaining sleep* OR nonrestorative sleep)
Difficulty functioning: contemporary views of insomnia conceptualize it as a 24-hour disorder (daytime component) and/or distress
At least 3 nights per week
>3 months duration
Occurs despite adequate opportunity for sleep
Not better explained by drug, medical/mental/sleep-wake disorder – ID is usually comorbid)

Question 69

Wakefulness and Sleepiness: a competing process

Answer 69

The biological systems that promote wakefulness and sleep are distinct
Process S: Homeostat → responsive to behavior
Process C: Circadian/Body Clock → responsive to genetics.

Question 70

Process S

Answer 70

→ Build, build build, fall.
The moment you wake, building of adenosine
Homeostatic system is associated with adenosine → by-product of cells working.
Makes up for lost sleep.
We don’t make up for lost sleep with more sleep
We make up for sleep with deep sleep.
At the begging of sleep → deep sleep
Growth hormone released → restores tissue.
If you don’t have this, you don’t feel refreshed, and tissues don’t repair, get aches and pains.
Build up adenosine gets flushed into the body, and sets off the growth hormones.
Not in relation to clock time, in relation to your body activity.
When you stay up later → you get more adenosine build up and you would have a greater amount of deep sleep.

Question 71

Building sleep drive and sleeping deeply

Answer 71

Staying active, deep sleep = restoration
How you make up for lost sleep
Always monitoring how active you are.
Less activity = less sleep buildup.
People in pain = don’t have the same sleep drive = don’t get deep sleep or restoration.

Question 72

Process C

Answer 72

The body clock
TIMING
Clock determines timing of sleep especially REM sleep
timing AND timing of alertness
SCN → the thing that coordinates all these clocks.
This system is incredibly important to alertness → determines orexin levels, important to REM, and mood.
MANAGING DRIFT → requires input → can adapt when there are different signals in the environment.
There is drift in our clock because it is longer than 24 hours
Regular bedtimes, regular rise times and regular light exposure
Many people aren’t regular.
“set” the clock and manage drift
Jet-lag is a mismatch between the environmental cues and the time that is occurring.

Question 73

Circadian Signals (24hrs)

Answer 73

Conventional person → not on the extremes.
Post lunch dip.
Peak in the evening and then fall. → melatonin releases → allows the signal to fall.
Taking more melatonin in bed is a placebo effect. (It has already been released).
Few hours of calm before bed.
Someone who gets into bed early → going before the melatonin release.
The alerting signal is high (it may be at its maximal peak)
You need a strong sleep drive with the outer system to overpower this system.
When it starts to fall → then you feel sleepy.
Going to bed early → cuts off your drive for deep sleep.
Specific to the person → not generalized.
Drop in the early hours → REM sleep
When you are getting REM sleep → wakefulness/dreaming
You can usually fall asleep after this due to the lack of alerting signals in those early hours.

Question 74

Chronic Insomnia

Answer 74

Precipitating Factor → stressor
We use disruption instead of maladaptive behaviour because what they are doing while they are suffering with this disorder is not maladaptive.
Most often, it is conditioned arousal.
These are not pathological
A single factor doesn’t have to cause insomnia → it has to be all three.

Question 75

Acute insomnia

Answer 75

Is normal
Different etiologies → clock s
Different physiologies → clock c
Different interventions → what causes the disorder.
At the beginning of insomnia, start to feel tired during the day.
Then find it difficult to fall asleep.
Different interventions.

Question 76

Homeostatic perpetuating factors

Answer 76

We need to “build” sleep drive to have continuous and quality sleep, therefore behaviors that will have a negative impact on this build-up will be:
Spending increased time in bed relative to how much sleep you can currently produce
Napping; Sleeping-in; Going to bed early
Inactivity (Carney et al., 2006)

Question 77

Going to sleep early means:

Answer 77

Less sleep build up, less deep sleep, meaning more lighter sleep, more time awake, and less restoration

Question 78

Sleep in or lay in means:

Answer 78

Less sleep build up, lighter sleep, more time awake, less restoration

Question 79

Naps mean:

Answer 79

Less sleep build up, lighter sleep, more time awake, less restoration

Question 80

We nap for sleepiness never for sleep

Answer 80

Can help: even as short as 15 minutes (Dinges, Orne, Whitehouse & Orne, 1987).
The briefer and earlier in the day, the less sleep disruptive
Helpful when not a chronic insomniac
Has a negative effect on sleep if you are a poor sleeper.

Question 81

Napping with insomnia

Answer 81

They already have low deep sleep drive
They fear not being able to cope and need to face that fear
It’s poor stimulus control to sleep outside the sleep window

Question 82

Process C: Circadian Perpetuating factors

Answer 82

Optimal sleep is produced during a dynamic, idiosyncratic timing window, therefore the following behaviours would have a negative impact on sleep:
Variable timing of going to bed and getting out of bed (consistent everyday is what is best)
If you are experiencing insomnia this exacerbates this.
Sleeping outside of your optimal window (i.e., keeping late hours if you are a lark or getting up early if you are an owl)

Question 83

Do we stimulate jet-lag habits

Answer 83

Jet lag is not about getting on the plane, it is actually about the internal clock being set at your time and then getting out of the plane → the environmental cues are very discrepante to our internal clock
Our body reorganises → this reorganisation causes bad symptoms → overlaps with anxiety.

Question 84

Delayed and advanced chronotypes (Genetic clocks)

Answer 84

Delayed sleep phase during puberty. (You don’t typically get sleepy until after 12 am)
This causes problems (same with advanced sleep phase → falling asleep before 10pm).
Young adults shift out of this as they approach young adulthood. (Become early birds).
There is a western bias for the early birds.

Question 85

The third process: The arousal system

Answer 85

The arousal system can trump the sleep promoting system
allows us adequate respond to dangerous threats
When overactive, the arousal system interferes with the processes controlling sleep. Hyperarousal issues:
Conditioned arousal
The most common for insomnia disorder
“The switch”
Bell should not make a bell drool → but if you pair it with meat → overtime the association will work.
If bed is paired with wakefulness (bedroom, bedtime routine, sleeplessness, tossing, turning, upset).
Cognitive arousal
Physiological arousal

Question 86

Conditioned arousal in the bedroom

Answer 86

“The switch”
Bell should not make a bell drool → but if you pair it with meat → overtime the association will work.
If bed is paired with wakefulness (bedroom, bedtime routine, sleeplessness, tossing, turning, upset).

Question 87

Cognitive model for insomnia

Answer 87

Attentional bias → out to look for signs, scanning the environment, that confirm your worst fear (now I’m never going to get to sleep) (dog barking, stomach pain).
All or none thinking → I am never going to be able to sleep
Leads to coping behaviours that we engage in that tend to reinforce those beliefs. (low-sleep self efficacy)

Question 88

Sleep medications

Answer 88

Sleep medications, approved by Health Canada (Canada) are effective treatment options for insomnia. → This is important to know.
benzodiazepine or non-benzodiazepine zolpidem drugs (GABA agonists that increase drowsiness) ** EXAM ** increase GABA → increase sleepiness, decrease GABA decrease in sleepiness.
Downsides include daytime sedation, psychological dependence, unwanted involuntary sleep-walking or sleep-sex behaviours
More at risk for car accidents.
The half-life refers to the time it takes for the drug to lose half of its action (half of the drug is used up).
long half-life effective for people with problems staying asleep throughout the night (e.g., dalmane) but increased sedation throughout the day
Short half-life is most commonly used for those with sleep onset insomnia only. The short half-life would limit the leftover effects of the medication the next day but such drugs would not help the patient if they woke up in the middle of the night.
Two shorts equal a long.

Question 89

CBT v. Meds

Answer 89

Both are effective
Short term is the same.
CBT is incredibly durable.
Augmenting approach often preferred but data is mixed for this practice
Unlike hypnotic treatment, gains achieved during CBT-I endure months to years after the end of active therapy
If you compare behaviour therapy (CBT) to drugs (PCT) across meta-analyses, you see that CBT is better on sleep onset latency and drugs are better on total sleep time, but there the same on everything else

Question 90

CBT-1 and physiology

Answer 90

CBT-I improves neurophysiology (what is happening in your brain right now) of sleep: ↓high frequency & ↑ slow wave activity in the EEG (Cervena,Dauvilliers, Espa, et al., 2004) → we want slow activity: (This is what happens with CBT).
Also get more growth hormone with CBT → better respiration.
Does operate on physiology.

Question 91

OTC and Melatonin

Answer 91

No melatonin problems in insomnia
It is already in your brain when you go to sleep.
Oral melatonin is somewhat effective in Delayed Phase Circadian Rhythm Disorder because melatonin release occurs much later and thus, sleep onset is delayed. Melatonin not delayed in insomnia
Melatonin taken before bed would have a placebo effect only; taking melatonin when melatonin already present in the brain does nothing—signal was already sent.
During the day, the brain responds by increasing sleepiness several hours later because no melatonin present in the brain when the pill was taken
You have to take it hours (1.5) before you go to bed. (when melatonin is not there)
If you take melatonin when it is already there (nothing will happen).
Buscemi and colleagues’ (2007) meta-analysis, melatonin’s hypnotic effects were negative when given before bed. Thus, melatonin is not used for insomnia in sleep settings despite the belief by many that it is helpful for insomnia

Question 92

Complementary medicines in Insomnia

Answer 92

In sum, there is a lack of efficacy evidence for any alternative or complementary medicine approach for insomnia (Meoli et al., 2005).
National Centre for Complementary and Alternative Medicine (NCCAM)

Question 93

What is CBT-1

Answer 93

An evidence-based treatment developed from biological and learning principles:
Stimulus Control (Bootzin, 1972): a set of sleep rules to address conditioned arousal.
Sleep Restriction (Spielman et al., 1987): a technique to increase sleep drive by matching the time spent in bed with current sleep production time.
Stimulus control and sleep restriction are the most effective “ingredients”
Sleep Hygiene: a set of rules designed to address sleep-interfering habits or substances.
Cognitive Therapy: a set of techniques to modify beliefs about sleep and fatigue that cause or exacerbate insomnia
There is not good evidence that is effective on its own.
Helpful for appearance (to function).

Question 94

Stimulus control

Answer 94

If wakefulness and the bed have become associated, re-associate bed with sleep by:
Going to bed only when sleepy → conditioned arousal. → not tired (sleepy is falling asleep on the couch or in your chair).
Getting out of bed when unable to sleep (better to go to bed later to build sleep drive) → do whatever you need to do to fall asleep. (go back to watching TV).
Getting out of bed at a consistent time each morning (irrespective of how you slept) → this is going to have positive effects 1. Increasing deep sleep drive that you can use the next night, if you stay in bed you don’t bank this sleep drive. 2.
Using the bed and bedroom only for sleep (and sex)
Refraining from daytime nap

Question 95

Sleep Restriction therapy (SR) or Time-in-bed Restriction

Answer 95

To restore homeostatic sleep drive:
Match time-in-bed with current average sleep production (add 30 minutes for normal sleep onset latency)
Time in bed restriction → you don’t get less sleep, over two weeks you get more sleep and deep sleep.
Once sleep normalises and there is sleepiness (self-reported or a mean sleep onset latency 10 min or less or a sleep efficiency above 90%) we extend time-in-bed in 15 or 30 minute increments – sleep extension.
Sleep extension
Happens with one of three signs of sleepiness ** Exam **
Actively falling asleep in the day
Fall asleep (sleep latency) on average less than 10 minutes (that is a sign that you need to spend more time in bed = sleep extension).
Sleep efficiency (proportion of time of sleep in bed) is above 90% (need more time in bed)

Question 96

Sleep Hygiene: Focused on Lifestyle factors that are not implicated Insomnia

Answer 96

Caffeine – timing and reduction
Nicotine reduction/elimination
You will get insomnia when trying to quit smoking
Prescribed exercise - timing
Light bedtime snack (milk, peanut butter)
Avoid middle of the night eating
Reduce alcohol, marijuana & other substances
Optimise environment: light, noise, temperature
American Academy of Sleep Medicine recommends against using sleep hygiene on its own (Edinger et al., 2021)
Used as a behavioural placebo in clinical trials (e.g. Carney et al., 2017)
Findings that were in the basic sleep literature that affect sleep architecture.
Sleep effort increases insomnia.

Question 97

Summary for insomnia

Answer 97

We have two main efficacious treatments for insomnia:
Hypnotic medications (benzo and non-benzo)
Cognitive behaviour therapy for insomnia (CBT-I)
Hypnotic medications are less effective than CBT-I long-term and have a number of side effects that can make them undesirable.
CBT-I is comprised of: Stimulus Control, Sleep Restriction, Sleep Hygiene and Cognitive Therapy
Stimulus Control helps to disassociate the bed with wakefulness (i.e., conditioned arousal)
Sleep Restriction increases the drive for deep sleep
Sleep Hygiene is sometimes necessary but rarely sufficient to address insomnia
Cognitive Therapy modifies sleep-interfering belief

Question 98

Impact of eating disorders

Answer 98

Up to 20% of people with anorexia die from their disorder (5% within a decade, e.g., Franko et al., 2013)
More than any disorder
This is more than any other disorder, including depression
The rate of suicide is 50 X higher than in the general population Arcelus et al., 2011)

Question 99

Bulimia Nervosa in the DSM5

Answer 99

Recurrent episodes of binge eating, meaning:
Eating, in a discrete amount of time an amount of food (e.g., within 2 hours), definitely larger than most people would eat in a similar amount of time
Sense of lack of control over eating during the episode
Recurrent inappropriate compensatory behaviours to prevent weight gain (vomiting, exercise, laxatives, diuretics)
Occurs at least once a week for at least 3 months
Self-evaluation is unduly influenced by body shape and weight → a key factor
Self worth gets wrapped up in this (pre-occupation)
Doesn’t occur exclusively during episodes of anorexia nervosa
Eating Disorders didn’t appear as their own category until DSM IV!

Question 100

Bulimia Side Effects

Answer 100

Facial distortions from salivary gland enlargement (vomiting)
Loss of and damage to teeth from vomiting
Potentially fatal cardiac arrhythmia or kidney failure, from electrolyte imbalances
Subsequent substance abuse, smoking, (von Ranson, Iacono & McGue, 2002) and depression (Steiger et al., 2013)
Weight gain (Ludescher et al., 2009) - laxatives and vomiting are not effective. Most are within 10% of their normal body weight when they start.
A distortion.
Colon damage or constipation from laxative use
Lose their ability to normally produce bowel movements

Question 101

Anorexia Nervosa

Answer 101

Intense fear of obesity
Distorted sense of their body size: Pick your body shape.
They answer with gross overestimation (McCabe, McFarlane, Polivy & Olmstead, 2001); they believe they look “fat”
Other observers would estimate the same person’s shape accurately, and would recognize that they look sickly
They can binge/purge too (eating without control albeit far smaller amounts of food than those with bulimia and an immediate purge)
They expect continual weight loss. Weight maintenance, even at dangerously low levels, is anxiety provoking

Question 102

Etiology Social Gender of Anorexia Nervosa

Answer 102

Greater sex prevalence in females
Those whose assigned sex at birth does not match their gender identity, are more likely than cisgender people (assigned sex at birth matches gender identity) are more likely to engage in disordered eating. The odds of past year ED and past month ED symptoms are significantly higher than the odds of these behaviors in cisgender males (Watson, Veale, & Saewyc, 2017)
Gender nonconforming people assigned a female sex at birth have increased risk of EDs relative to people who are male-to-female or female-to-male (Diemer et al., 2018)

Question 103

Etiology and culture of Anorexia Nervosa

Answer 103

Overweight men depicted on tv are 2-5 X more common; magazine portrayals of women since the 70s have had decreasing weight
Frequent portrayals of women dieting, making disparaging remarks about their bodies
Previously thin ideals were achieved via corsets not dieting
An examination of Ebony magazine had less representations of thin women; there is a lower rate of ED in black women

Question 104

Etiology Family Contributions for Anorexia Nevosa

Answer 104

More likely to have perfectionistic, dieting mom
Dad’s can say stuff too → “you have meat on ya”
Families with preoccupation with others’ sizes
Having a family member with an ED is stressful and creates family strife

Question 105

Dieting leads to:

Answer 105

People who don’t diet, don’t develop eating disorders
Teen girls who diet, are 8 x more likely to develop EDs
Dieting leads to weight gain, which increases preoccupation/concern
Boring food, after exposure to junk food, leads to anxiety in rats – when you give them junk food, anxiety decreases – reinforcement
We are all exposed to media images of thin women, why is the rate of eating disorders less than 1%

Question 106

Etiology Biological of eating disorders

Answer 106

Heritability of AN of .56 (Bulik et al., 2006) but WHAT is being inherited?
Also no adoption studies, just twin studies
Isn’t this the case across all of our disorders?
A nonspecific biological vulnerability which could be sensitivity to distress?
Drive for control under uncertainty?
Responsivity to stress?
Tendency towards a negative mood?
Low levels of serotonin?

Question 107

Etiology psychological

Answer 107

Our models have focused on general psychological vulnerability
What are they?
Perfectionism
Anxiety sensitivity
Need for control
Low self-efficacy
Eating Disorder specific?
Distortions on body image
Intolerance of negative mood states
Fear of becoming fat

Question 108

Treatment for eating disorders

Answer 108

Treatment seeking is not as common as you would think, given that AN is the
most fatal
Develop a loli-pop head → skeletal body with a disproportionate head.
It is more common to seek treatment for the comorbid condition, e.g., MDD

Question 109

Treatment options for eating disorders

Answer 109

SSRIs help some with bulimia but not long-term so they are combined with
CBT, if used at all (Reas & Grillo, 2014); SSRIs not helpful with anorexia
(Kruger & Kennedy, 2000)
CBT-E (Fairburn, 2008) is a transdiagnostic treatment with good efficacy and an approach that addresses the common factors across disorders eating
Interpersonal Psychotherapy (IPT) focuses solely on interpersonal issues and is as effective as CBT (Fairburn et al., 1993; Agras et al., 2000)
Even in CBT, there is family involvement/counselling re: communication around food, having structured and reinforcing meals, attitudes towards body shape.
Motivational interviewing may be helpful before therapy to enhance readiness for change (Dunn, Neighbours & Larimer, 2006).
Used before treatment.

Question 110

Cognitive behaviour therapy for eating disorders

Answer 110

In a nutshell:
Normalise eating behaviours
In bulimia and BED, there are frequent scheduled small meals and in anorexia they are hospitalised until safe weight is achieved
Continued nutritional counselling
Identify environmental triggers that precipitate the behaviour
Identify unhelpful thoughts or moods that precipitate bingeing or purging or urges towards restriction.
Modify beliefs about weight and self-esteem and control

Question 111

Treatment for restricted eating

Answer 111

Restricted eating
Ingesting insufficient calories (i.e., below body’s needs)
Restrained eating (be able to eat foods that are good for us, satisfy our needs, and our goals)
Attempting to follow demanding, rigid, perfectionistic rules to try to experience sense that one is in control of their eating
Creates a preoccupation/obsession with food
Ironically attempts to control eating deprive them of a true ability to control eating
Makes eating anxiety provoking, guilt-ridden experience

Question 112

Targeting for restrained eating

Answer 112

Identify dietary restraint rules: What foods do you fear? If you were at a dinner party, what situations would cause anxiety?
They learn why restrained eating doesn’t work, the adverse consequences and how ineffective laxatives and vomiting are as strategies
Connect the motivation to the behaviour. What would happen if?….
Make a plan for breaking rules, by creating low stakes situations (coping plan to prevent binges/purges). Repeat exposures until guilt and anxiety decrease
CBT-E prescribes 6 small “meals” at no more than 3 hour intervals to reduce over eating or restricting and prevention of compensatory behaviours

Question 113

Targeting maladaptive beliefs

Answer 113

There is nothing inherently good about resisting eating
There are no bad foods. Quantity and balance takes care of this.
Goal is not to eat crappy foods—just to have freedom to choose from a range of foods
Eating should not be restrictive; its something we do to be healthy
Rules about eating less are like developing rules to breathe less than others
The right amount of food is the amount needed to maintain a healthy weight and follow nutritional guideline

Question 114

Depressant disorders

Answer 114

Decrease central nervous system activity (the action)
Alcohol, hypnotics, anxiolytics
Symptoms: relaxation
Withdrawal: agitation, anxiety (always opposite to the action)
Underlined is the exam layout of these questions.
Long-term withdrawal: delirium tremens, vomiting, hallucinations, death

Question 115

Alcohol related disorders

Answer 115

Statistics on Use and Abuse
23% Canadians exceed low-risk guidelines for alcohol consumption
Binge consumption frequent among college students
Men drink more than women
Single males most likely to be heavy drinkers
Cultural differences exist.
Influences several neuroreceptor systems: GABA, inhibitory neurotransmitter, causes blackouts)
Delirium Tremens (DTs): frightening hallucinations and body tremors
Fetal Alcohol Syndrome (FAS): affects child whose mother drank while she was pregnant
Liver disease

Question 116

Stimulants disorders

Answer 116

(make us alert and give us energy = action, withdrawal = sleepy)
Increase central nervous system activity (enhance GLU, NE, DA)
Caffeine, nicotine, amphetamines, cocaine
Symptoms: alertness, energy
Side effects: impaired judgement/functioning, paranoia, heart racing, chills, nausea, vomiting , respiratory depression, seizures, coma
Withdrawal: fatigue, in cocaine: apath

Question 117

Opiod disorders

Answer 117

Block pain experiences, provides rush of endorphins
Oxycodone, morphine, heroin
Symptoms: euphoria, drowsiness, slowed breathing, analgesia
Withdrawal: nausea and vomiting, aches, chills, diarrhea, insomnia, prolonged (many days) and painful

Question 118

Cannabis disorders

Answer 118

Altered perception, mood swings, in large doses hallucinations and paranoia – wide variations in report of symptoms
Concentration, sleep, memory, motivation, interpersonal and occupational problems can occur in long term use
Withdrawal: diminished appetite, irritability, headaches, loss of focus, cold sweats, chills, depression and anxiety
Long-term problems include insomnia
No growth hormone (pain) due to change in structures in cannabinoid structures.
There are medicinal products being tested for medical problems such as cancer pain, which typically have low tetrahydrocannabinols (THC)

Question 119

Hallucinogen depressant

Answer 119

LSD – a fungus associated with hallucinations, perceptual changes, depersonalization (outside of yourself, observing yourself), dilated pupils, sweating, rapid heartbeat and blurred vision

Question 120

Biological aspect of substance disorders

Answer 120

Agonist substitution
Methadone

Antagonist treatments
Naltrexone

Aversive treatment
Antabuse

Question 121

Psychosocial

Answer 121

Inpatient facilities
Expensive; assist through
Alcoholics Anonymous (AA)
Social support
Controlled use/ Harm reduction/Controlled drinking
Safe injection sites (SISs)
Component therapy (coping skills, contingencies, community)
Motivational enhancement to increase readiness for change
Very common treatment to make them ready for change because most are ambivalent.