Psychological Disorders - Exam 7 Flashcards
(80 cards)
1
Q
Every ___ to _____ minutes we cycle through 5 stages of sleep.
A
90 to 100 minutes
2
Q
True or false: the 5 stages of sleep we cycle through are easily detected by an EEG
A
True
3
Q
What would an EEG show if you were awake and alert?
A
Beta
4
Q
What would an EEG show if you were awake but relaxed?
A
Alpha
5
Q
How does electrical activity in the brain change as you drift into sleep?
A
Relatively random electrical activity in the
brain gradually synchronizes as we drift into
sleep and continues to synchronize as we get into deeper and deeper stages of sleep.
6
Q
What does an EEG show during stage 1 of sleep?
A
Sleep is marked by the slow and irregular brain waves of stage 1. Hallucinations are likely here.
7
Q
What does an EEG show during stage 2 of sleep?
A
Stage 2 lasts about 20 minutes. Sleep spindles are common in this stage- bursts of rapid, rhythmic brain activity
8
Q
What does an EEG show during stages 3 and 4 of sleep?
A
Stages 3 and 4 feature increasingly larger and slower delta waves. Lasts for about 30 minutes. Difficult to wake at this point.
9
Q
Describe stage 5 of sleep (REM)
A
Almost all muscles are relaxed, except the eyes, which move rapidly. Lasts for about 10 minutes. Characterized by elevated heart rate, rapid and irregular breathing, and momentary bursts of eye movement. Paradoxical sleep is characterized by genital arousal but almost complete muscle relaxation; the body is internally aroused, but externally calm
10
Q
True or false: as the night progresses, stage 3 & 4 sleep get shorter and REM sleep lengthens
A
True
11
Q
Staying awake and aroused requires what two things?
A
Reticular formation and the hypothalamus
12
Q
Calming down requires what part of the brain?
A
Parts of the basal forebrain
13
Q
How does the reticular formation keep us awake and aroused?
A
- Pontomesencephalon – releases glutamate (excitation) and acetylcholine
- Locus Coeruleus (inside the pons) – releases norepinephrine to keep one alert.
- This area is at rest while sleeping
14
Q
How does the hypothalamus keep us awake and aroused?
A
Hypothalamus – releases histamines and orexin (without these we become really drowsy – indeed, its how you feel when you take anti-histamines!)
15
Q
How do parts of the basal forebrain help us calm down for sleep?
A
Calming down for sleep requires parts of the Basal forebrain - which release GABA (inhibition)
16
Q
We spend an average of _____ years sleeping
A
25
17
Q
What is the purpose of sleep?
A
•Reduces energy expenditure so our bodies can focus on tissue growth and repair
•Important for the organization and
consolidation of memories
•But… neuronal connections deteriorate
quickly if not used
> We cycle between deep sleep and periods of intense activity – REM sleep
18
Q
Define insomnia
A
Inadequate sleep
19
Q
What are potential causes of insomnia?
A
Caused by a number of factors: • Noise • Stress • Diet and medication • Dependence on sleeping pills or alcohol and shifts in the circadian rhythms can also result in insomnia
20
Q
Define narcolepsy
A
A sleep disorder characterized by frequent periods of sleepiness
21
Q
True or false: narcolepsy attacks of sleepiness can be either gradual or sudden
A
True
22
Q
What causes narcolepsy?
A
Caused by lack of hypothalamic cells that
produce and release orexin
23
Q
How is narcolepsy treated?
A
Primary treatment is with stimulant drugs (i.e., Ritalin), which increase wakefulness by
enhancing dopamine and norepinephrine activity
24
Q
Why does feeling blue not always equal depression?
A
We all experience days where we feel blue, but because those feelings are temporary they do not indicate major depression
25
What is persistent depressive disorder?
Persistent Depressive Disorder is a mood disorder that is extremely long-lasting. Down-in-the-dumps mood or MDD-like symptoms everyday for 2 years or more
26
What is dysthymic disorder?
Dysthymic Disorder: Down-in-the-dumps mood everyday for 2 years or more
27
Feeling blue = ?
Extremely temporary
28
What is major depressive disorder (MDD)?
Cognitive, behavioral, and mood changes
| everyday for 2 weeks or more
29
What is anhedonia?
A loss of the ability to experience pleasure and the absence of happiness
30
What are some symptoms of major depressive disorder (MDD)?
• Absence of happiness is more reliable than presence of sadness
> Anhedonia: Loss of the ability to experience pleasure; absence of happiness
• Irritability
• Difficulties in concentration, memory, decision making about little things
• Body movements are “slowed down” and/or agitated
• Negative thinking
> Minimises positive information
> Person pays attention only to negative information, exaggerates them
> Gives rise to hopelessness
31
Describe negative thinking
• Negative thinking
Minimises positive information
Person pays attention only to negative information, exaggerates them
Gives rise to hopelessness
32
What should one watch out for when diagnosing MDD?
These symptoms cannot be fully accounted for by another medical or psychological problem (e.g., substance use withdrawal; hypothyroidism). They also must cause significant distress and/or impairment in the person’s life.
33
What percent of adults experience major depression at some point in their lives?
5-15%
34
Is major depression more common in women or men? In newer generations or older?
It is 2 times more common in women than in men, and symptoms are often more severe in women. It is found more than ever in young people.
35
True or false: MDD episodes (2 weeks or more) come and go
True
36
How do MDD episodes happen?
```
MDD episodes (remember: 2 weeks or
longer) come and go
> First episode tends to be linked to a specific stressor
> Later episodes = less likely to identify a trigger
```
37
What causes MDD?
Genetics, hormones, and always the brain and neurotransmitters
38
Describe the genetic component of major depression
Moderate degree of heritability
• Early onset depression (before 30) – linked to depression, anxiety, OCD in family
• Later onset depression (after 45) – linked to circulatory problems in family
39
Describe the hormonal component of major depression
Stress and cortisol release
| Postpartum depression – sudden drop in estrodiol and progesterone
40
Describe the brain/ neurotransmitter component of major depression
Norepinephrine, serotonin dysregulation
Instability, desynchronization, abnormal reactivity at a neural level
> ....which can be shaped by bio-psycho-social factors
41
Clinical scientists emphasize a ____ model for many disorders
bio-psycho-social
42
One hypothesis for the cause of MD is a
functional deficiency of _________,
particularly norepinephrine.
catecholamines
43
What are the hypotheses of causes of major depression?
One hypothesis for the cause of MD is a
functional deficiency of catecholamines,
particularly norepinephrine.
Insufficient activity of other amines (serotonin, dopamine and epinephrine) in the brain have also been linked to depression
These hypotheses are supported by evidence that shows that a depletion of tryptophan, the serotonin precursor, produces a relapse in depression
However, drugs that agonize serotonin (SSRIs) do not work immediately (it takes up to 4 weeks for some patients) and so
it is possible that another explanation exists.
44
The first drug to treat depression was actually designed to treat what?
Tuberculosis
45
Describe monamine oxidase inhibitors as a treatment for major depression
-Monoamine oxidase is involved in enzymatic degradation of the neurotransmitters norepinephrine,
serotonin, and dopamine. MAOIs
prevent this from happening.
-Monoamine oxidase inhibitors (MAOIs) were the first type of antidepressant developed; replaced by antidepressants that are safer and cause fewer side effects.
46
Describe tricyclic antidepressants as a treatment for major depression
Class of drugs used to treat depression; inhibits reuptake of norepinephrine and serotonin but also affects other neurotransmitters; named for molecular structure
47
Describe SSRIs as a treatment for major depression
Antidepressant drug that specifically inhibits reuptake of serotonin without affecting reuptake of other neurotransmitters
48
Describe SNRIs as a treatment for major deprssion
Norepinephrine and Serotonin Reuptake Inhibitors are an antidepressant drug that specifically inhibits reuptake of norepinephrine and serotonin without
affecting reuptake of other neurotransmitters
49
Describe the side effects of tricyclic antidepressants
Blocks transporter proteins that reabsorb
serotonin, dopamine, & norepinephrine.
SIDE EFFECTS: blocks histamine, ACh
(causes dry mouth, difficulty urinating) and
sodium (heart irregularities).
50
Describe the side effects of SSRIs
Blocks transporter proteins that reabsorb
serotonin.
Milder side effects with same effectiveness!
51
Describe the side effects of monoamine oxidase inhibitors
```
Blocks enzyme that breaks down
catecholamines and serotonin.
This makes more serotonin available.
SIDE EFFECTS: Increased blood
pressure with certain foods (cheese, etc)
```
52
Are anti-depressants agonists or antagonists?
They're agonists, because they work to increase amount of catecholamine (serotonin, dopamine, norepinephrine) and their effect is gradual. Sometimes the full effect requires weeks of exposure.
53
What are some non-drug treatments for depression?
St. John’s Wort - Some report equal benefits but taking this homeopathic remedy makes other drugs less effective (read: be careful if you are using birth control / heart medications / antibiotics etc...)
Aerobic exercise also helps calm anxiety and uplift
depressed mood
54
What percent of people show positive responses to antidepressant drugs?
50%
55
Who do antidepressants work best for?
Those with moderate to severe depression
56
True or false: About 50% of people respond well to psychological therapy, which is about the same percent that respond well to antidepressants
True
57
What percent of people with depression respond to a placebo?
About 30%
58
A combination of both drugs and therapy benefits only a _____ ____ percentage
slightly higher
59
Why don't SSRIs work immediately?
Antidepressants alter synaptic activity quickly but behavior doesn’t change for several weeks.
• This means that depression can’t be solely the result of low serotonin levels (otherwise the drugs would work immediately).
Antidepressant drugs perhaps increase the release of brain derived neurotropic factor (BDNF) which promotes neuron growth and survival and requires a few weeks of sustained serotonin levels to become plentiful.
• If so, that would mean that medications have a similar mechanism as another depression therapy – ECT, electroconvulsive therapy.
60
What does CBT focus on?
CBT focuses on the here-and-now, agena-driven, lasts about 12 weeks on average, and is the gold-standard psychotherapy for many (but not all) psychological disorders
61
What is an important part of CBT?
“Homework” is an important part—kind of like going to the gym to practice strength exercises, in-between personal trainer sessions
62
Describe the therapies under the umbrella term CBT
CBT is an umbrella term for a philosophy and set of therapeutic techniques. It could include one or both of these:
Cognitive: Harmful automatic thinking styles and biased, negative beliefs about the self, others, and/or world that drive persistent negative emotions
• Addressed by helping the patient to notice these automatic thinking patterns and replacing them with more balanced, realistic patterns
Behavioral: Harmful behaviors, such as avoidance, that keep the vicious cycle of symptoms going are replaced
• Examples include safe assignments for facing illogical fears or for planning activities for depressed patients
63
Describe electro-convulsive shock therapy as a treatment for depression
Electro-Convulsive Shock Therapy
First introduced in the ‘30s
Tends to get a biased and scary rep in movies and TV shows
Patient is shocked with 100V to the brain while awake
Produced whole body convulsions and brief unconsciousness
Now is used under general anesthetic with muscle relaxers
Limited for severe cases of depression where nothing else works
Quite successful but no one knows HOW it works – likely by increasing BDNF
64
What does the word schizophrenia come from?
Schizo (a split or schism) and phrenos (the mind)
65
Describe the common features of schizophrenia
• Separation from what the person wants to communicate & the reality of what is actually being communicated
• Delusions: false beliefs that have no basis and that are not influenced by reality
• Hallucinations: reports of sensory stimulation when no such stimulation is present
Auditory are most common
• Disturbances in affect (feeling)
Flat affect (a lack of emotion) strongly predicts a poor prognosis
66
What are the diagnostic criteria for schizophrenia?
• Deteriorated everyday functioning and symptoms for at least 6 months
• 2 or more of the following:
Delusions (unjustifiable beliefs)
Hallucinations (false experiences of one or more of the 5 senses; usually auditory and visual)
Disorganized speech (e.g., hard to follow)
Disorganized or catatonic behavior
Negative symptoms
• Symptoms are not due to drugs, medications, medical illness (e.g., brain tumor), etc.
67
Define positive symptoms
Something that is present (generally). Associated with a better outcome with medication.
68
Describe negative symptoms
Something that is absent (generally)
69
What are the positive symptoms (what is generally present) of schizophrenia?
Disturbances of thought and language
Delusional thinking
Perceptual disturbances
Indicate a better outcome with medication
70
What are the negative symptoms (what is generally absent) of schizophrenia?
- Psychomotor disturbances
- Impaired interpersonal relationships
- Inappropriate/odd-fitting affect (i.e.,
emotions) to the situation
- Lack of pleasure / motivation
71
True or false: Due to the multiple ways of combining symptoms to meet diagnostic criteria, schizophrenia can look a bit different for different patients, and severity can range as well
True
72
Define diathesis
Genetic vulnerability
73
What are the causes of schizophrenia?
• Clearly, schizophrenia is related to genetics.
However identical twins, who share 100%
genetic code, have about 50% concordance in diagnosis. Therefore, the diathesis - stress theory is widely supported.
Note: diathesis-stress model kind of falls under “biopsychosocial” approaches to understanding causes
Diathesis: genetic vulnerability – necessary, but not sufficient by itself to cause the disease
• 50% concordance in monozygotic (identical) twins
• More concordance in dizygotic (fraternal) twins than non-twin siblings
• Suggests a potential role of prenatal environment
Stress: Environment / Events /Circumstances shape the development of the organism (and possibly the expression of genetic vulnerabilities)
74
Describe how the neurodevelopmental hypothesis of schizophrenia relates to prenatal development
1) Schizophrenia may begin with abnormalities
prenatally.
Some evidence exists for:
• Maternal malnutrition: premature birth, low birth weight
• Maternal exposure to extreme stress
• Season-of-birth: babies born in winter are at increased risk
due to possible exposure to viral infections – cytokines, fevers
etc...
• Exposure to toxins: toxoplasma gondii
75
Describe the neurodevelopmental hypothesis of schizophrenia
1) Schizophrenia begins with abnormalities
prenatally.
2) The abnormalities prenatally lead to the brain becoming more vulnerable to other disturbances.
3) This could eventually result in brain abnormalities:
1) Enlarged ventricles
2) Smaller thalamus
3) Reduced blood flow in frontal lobes (this is associated with negative symptoms and is more difficult to treat)
76
What is the correlational evidence for the neurodevelopmental hypothesis of schizophrenia?
• Behavioral Marker: Eye movement dysfunction
>• Subjects visually follow a moving spot of light
>• Pattern of eye movement is different in patients with schizophrenia
• Marker: Dopamine Regulation in frontal lobes and limbic system
>• Hypothesis that schizophrenia involves an excess of dopamine
>• Associated with positive symptoms
>• For example, one possible side effect of high doses of L-Dopa includes hallucinations/delusions
77
Define the dopamine hypothesis of schizophrenia
The positive symptoms associated with schizophrenia may exist because of excess dopamine activity. Either neurons
release too much or synthesize too much to replace what’s not been reabsorbed.
78
What is the evidence for the dopamine hypothesis of schizophrenia?
```
Some evidence is that most effective
drugs for treating schizophrenia work by
blocking dopamine receptors
• Chlorpromazine
• Haloperidol
```
79
What is the glutamate hypothesis of schizophrenia?
It suggests that schizophrenia symptoms exist because of a deficiency in glutamate
activity, especially in the prefrontal cortex.
80
What is the problem with the glutamate hypothesis?
Dopamine typically inhibits glutamate
release
• So, drugs that block dopamine – will ALSO stimulate glutamate.
