Lecture 4.2 Flashcards

(52 cards)

1
Q

How does the DSM-5 define depression?

A

An ‘affective’ or ‘mood’ disorder.

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2
Q

What is meant by ‘depressed mood’?

A

Pervasive negative affective state present for the majority of the day, nearly every day, for at least 2 weeks.

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3
Q

What is anhedonia?

A

Loss of interest or pleasure in previously enjoyable activities.

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4
Q

What are examples of appetite/weight disturbances?

A

Increased appetite and weight gain, or decreased appetite and weight loss.

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5
Q

What are examples of psychomotor disturbances?

A

Restlessness or slowed movements. Slowing of thoughts and behaviours. Agitation.

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6
Q

What is fatigue?

A

Persistent low energy and tiredness.

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7
Q

What are examples of feelings of guilt and/or worthlessness?

A

Excessive self-blame or unrealistic negative evaluations of oneself.

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8
Q

What does concentration and/or memory impairments refer to?

A

Difficulty focusing, remembering, or making decisions.

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9
Q

How may suicidal ideation be defined?

A

Thoughts of death or suicide, with or without a specific plan.

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10
Q

What is the Kindling Effect?

A

The phenomenon where future depressive episodes are more likely to occur after previous episodes.

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11
Q

What are monoamines?

A

Neurotransmitters, including serotonin, dopamine, and norepinephrine.

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12
Q

What is serotonin involved in?

A

Mood regulation, sleep, appetite, and pain.

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13
Q

What is dopamine involved in?

A

Reward, motivation, and motor control.

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14
Q

What is norepinephrine involved in?

A

The stress response, alertness, and concentration.

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15
Q

What is the Monoamine Hypothesis?

A

The theory that depression is caused by a deficiency in monoamine neurotransmitters in the brain.

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16
Q

What is reserpine?

A

A drug that depletes monoamines, historically used to treat high blood pressure.

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17
Q

What is iproniazid?

A

The first monoamine oxidase inhibitor (MAOI) antidepressant.

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18
Q

What are monoamine oxidase inhibitors (MAOIs)?

A

Drugs that inhibit the enzyme monoamine oxidase, thus increasing monoamine availability.

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19
Q

What are depletion protocols?

A

Experimental procedures designed to temporarily reduce monoamine levels in the brain.

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20
Q

What is therapeutic delay?

A

The lag time between the start of antidepressant treatment and the onset of therapeutic effects.

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21
Q

What is mirtazapine?

A

An atypical antidepressant that enhances norepinephrine and serotonin neurotransmission.

22
Q

Clinically, how are classes of drugs classified?

A

By their primary mechanism of action.

23
Q

What are some examples of depressive disorders?

A

Major depressive disorder, persistent depressive disorder (dysthymia).

24
Q

What are some examples of affective-related disorders?

A

Bipolar disorder and cyclothymic disorder.

25
What are the 9 symptoms of depression?
Depressed mood. Anhedonia. Appetite/weight disturbances. Psychomotor disturbances. Fatigue. Feelings of guilt/worthlessness. Concentration/memory impairments. Suicidal ideation. Sleep disturbances.
26
How many symptoms of depression need to be present for a diagnosis?
Five or more symptoms.
27
What 3 things can symptoms not be due to for a depression diagnosis?
Substance use, another medical condition, or bereavement.
28
What does dichotomy mean in terms of certain depression symptoms?
Symptoms present as opposite extremes (e.g., increased or decreased appetite).
29
The substantial heterogeneity in depression symptom profiles accounts for what?
The variability in clinical presentation and treatment response.
30
What are the number of potential presentations that can qualify for a depression diagnosis? What is this caused by?
227, caused by interaction between aetiological factors and symptoms.
31
What are the 2 depressogenic subtypes?
Melancholic and atypical.
32
What is the prevalence of the melancholic subtype?
The most common subtype, affecting about 67% of depressed individuals.
33
What is the melancholic subtype characterized by?
□ Non-reactive mood. □ Pervasive anhedonia. □ Blunted emotional responses. □ Appetite/weight loss. □ Insomnia. □ Loss of libido.
34
What is the atypical subtype characterized by?
□ Low mood reactivity. □ Appetite/weight gain. □ Hypersomnia. □ Leaden paralysis. □ Sensitivity to interpersonal rejection.
35
What are the unique features of the melancholic subtype?
□ Diurnal variations in mood. □ Higher completion rates of suicide. □ Higher comorbidity with psychosis. □ Overactive HPA axis.
36
What are the unique features of the atypical subtype?
□ Underactive HPA axis. □ Prevalence increasing – obesogenic environments. □ Increased risk of chronic health conditions.
37
What is the prevalence of the atypical subtype?
About 15-50% of depressed individuals.
38
Depression is __ and __? What are the significant predictors of this?
Recurrent and progressive; symptom severity/duration
39
When should the Kindling Effect be considered?
When considering long-term management and prevention of recurrence.
40
How prevalent are depressive episodes?
All of the above; median duration of depression in 24 weeks
41
What are the 3 monoamines?
Serotonin, dopamine, and norepinephrine.
42
What were the 3 lines of evidence that led to the Monoamine Hypothesis?
Reserpine's effects, iproniazid's effects, and post-mortem studies.
43
What effect did reserpine have on monoamines?
Depleted monoamine levels.
44
How was the mechanism of action for antidepressants founded?
Through observing the effects of drugs like iproniazid.
45
What did post-mortem studies show about monoamines?
Decreased levels of monoamines or their metabolites in the brains of depressed individuals.
46
What are the 5 contradictory evidence for the Monoamine Hypothesis?
Therapeutic delay. Depletion protocol findings. Drugs blocking serotonin reuptake not being effective. Antidepressant efficacy vs. placebo not explaining much. Drug responsivity being influenced by many factors.
47
Why is measuring synaptic monoamine concentrations not really feasible?
Because lumbar punctures are too invasive and may not show the original levels in the brain.
48
How do depletion protocols work?
By using the blood-brain barrier to cross/block monoamines precursors.
49
What does the therapeutic delay account for?
The time lag between drug administration and clinical improvement, suggesting that changes beyond neurotransmitter levels are involved.
50
What drugs that block serotonin reuptake but aren't effective in treating depression?
Mitrazapine. Cocaine. Amphetamines.
51
Antidepressant efficacy, although better than placebos, doesn't explain what?
No responses/delay with antidepressants.
52