Lecture 5: Everyday life Flashcards
What are the two main types of affective/mood disorder?
Unipolar depression and bipolar depression. It’s when severe dejection alters daily functioning
Describe the prevalence of unipolar depression
15% of people have a severe episode at some point. Twice as many women have it but they tend to have it in a milder form. There is no sex differences in children. It’s dramatically increased in younger people. At ages 30-65, white people are more at risk than afro-american. Two thirds recover in 6 months but most have recurrent episodes.
List the symptoms of unipolar depression
Intense sadness, dejection, feeling empty, crying, angry, anxious, little pleasure, loss of humour, motivation, sex drive and energy. Paralysis of will, lethargic, self blame, hopelessness, poor memory, headaches, indigestion, constipation, dizziness pain, appetite and sleep disturbance. They perform as well as everyone else but they think they have done worse. Up to 15% commit suicide.
How is unipolar depression diagnosed?
Severely disabling, lasts at least 2 weeks, must have at least 5 of the symptoms. Drugs, medicine and grief must be ruled out as a cause. Some people have psychotic symptoms like hallucinations. Single episode means it’s the first episode they’ve had with no mania. After that it’s considered recurrent.
What is SAD? What is catatonic? Postpartum? Melancholic? Dysthymia? NOS?
Seasonal affective disorder, it means you’re depressed in the winter.
It can mean either motor disability or excessive motor activity
Unipolar depression 4 weeks after birth
When someone is unaffected by pleasurable events, suffers motor disturbances, feels guilt and has a loss of appetite and sleep
It’s when someone has less than five symptoms for more than 2 years, the recovery rate is 40%
Not otherwise specified is when someone has unipolar depression that doesn’t fully meet the previous criteria
What is SAD? What is catatonic? Postpartum? Melancholic? Dysthymia? NOS?
Seasonal affective disorder, it means you’re depressed in the winter.
It can mean either motor disability or excessive motor activity
Unipolar depression 4 weeks after birth
When someone is unaffected by pleasurable events, suffers motor disturbances, feels guilt and has a loss of appetite and sleep
It’s when someone has less than five symptoms for more than 2 years, the recovery rate is 40%
Not otherwise specified is when someone has unipolar depression that doesn’t fully meet the previous criteria
Describe the life events of most people with unipolar depression
They’ve had a greater number of traumatic life events prior to an episode
If they’re isolated and there are multiple stressors then they’re more likely to become depressed
30% don’t report a traumatic event before the onset of depression
Internal and situational components interact with each other
Describe the different hypotheses for the etiology of unipolar depression
Psychodynamic: Hostility turned inward, oral fixation, anal and phallic problems and loss of self esteem
Harlow: His monkeys showed that isolation and separation causes it, it’s a despair reaction.
Loss of a parent before age 6 can increase your chances
Lewinsohn: lower performance of positive behaviours which results in decreased reward, as the rate of reinforcement rises, the depression improves.
Beck: Negative cognitions like maladaptive attitudes or errors in thinking (arbitrary inference, selective abstraction, overgeneralisation, magnification/minification and personalisation) are the true cause of unipolar depression. Emotional, motivational, behavioural and somatic aspects of depression are caused by cognitive processes. Well supported.
Cognitive triad: Negative interpretations of experiences, oneself and one’s future.
Ruminative responses during a depressed mood is linked to a longer depressed mood
Seligman: Learned helplessness
Genetics: 20% of relatives are depressed compared to 5% of general population. Monozygotic= 43% concordance, dizygotic= 20%. Deficiency of norepinephrine, serotonin or both.
Describe the different hypotheses for the etiology of unipolar depression
Psychodynamic: Hostility turned inward, oral fixation, anal and phallic problems and loss of self esteem
Harlow: His monkeys showed that isolation and separation causes it, it’s a despair reaction.
Loss of a parent before age 6 can increase your chances
Lewinsohn: lower performance of positive behaviours which results in decreased reward, as the rate of reinforcement rises, the depression improves.
Beck: Negative cognitions like maladaptive attitudes or errors in thinking (arbitrary inference, selective abstraction, overgeneralisation, magnification/minification and personalisation) are the true cause of unipolar depression. Emotional, motivational, behavioural and somatic aspects of depression are caused by cognitive processes. Well supported.
Cognitive triad: Negative interpretations of experiences, oneself and one’s future.
Ruminative responses during a depressed mood is linked to a longer depressed mood
Seligman: Learned helplessness
Genetics: 20% of relatives are depressed compared to 5% of general population. Monozygotic= 43% concordance, dizygotic= 20%. Deficiency of norepinephrine, serotonin or both.
Genes and the environment interact, 4+ stressful life events and a short/short allele at highest risk
Describe the different hypotheses for the etiology of unipolar depression
Psychodynamic: Hostility turned inward, oral fixation, anal and phallic problems and loss of self esteem
Harlow: His monkeys showed that isolation and separation causes it, it’s a despair reaction.
Loss of a parent before age 6 can increase your chances
Lewinsohn: lower performance of positive behaviours which results in decreased reward, as the rate of reinforcement rises, the depression improves.
Beck: Negative cognitions like maladaptive attitudes or errors in thinking (arbitrary inference, selective abstraction, overgeneralisation, magnification/minification and personalisation) are the true cause of unipolar depression. Emotional, motivational, behavioural and somatic aspects of depression are caused by cognitive processes. Well supported.
Cognitive triad: Negative interpretations of experiences, oneself and one’s future.
Ruminative responses during a depressed mood is linked to a longer depressed mood
Seligman: Learned helplessness
Genetics: 20% of relatives are depressed compared to 5% of general population. Monozygotic= 43% concordance, dizygotic= 20%. Deficiency of norepinephrine, serotonin or both.
Genes and the environment interact, 4+ stressful life events and a short/short allele at highest risk
Describe antidepressant treatments
Before 1950s: Amphetamines increased activity but didn’t help depression itself.
MAO inhibitors and tricyclics: Monoamine oxidase inhibitors like phenelzine prevents the destruction of norepinephrine and serotonin. However, MAO is an essential enzyme, for example it controls blood pressure. It stops its production in the liver and instestine, allowing tyramine to accumulate. Patients must watch their tyramine consumption (bananas, cheese). Tricyclics like imipramine, are more common and help unipolar patterns. Up to 50% chance of relapse within 6 months without drug but 20% chance with it if the drugs are taken for several months after there are no depressive symptoms. They act on reuptake mechanisms and alter the sensitivity of norepinephrine and serotonin receptors. Less dangerous and more effective than MAO but can cause dizziness, blurred vision and dry mouth.
Describe antidepressant treatments
Before 1950s: Amphetamines increased activity but didn’t help depression itself.
MAO inhibitors and tricyclics: Monoamine oxidase inhibitors like phenelzine prevents the destruction of norepinephrine and serotonin. However, MAO is an essential enzyme, for example it controls blood pressure. It stops its production in the liver and instestine, allowing tyramine to accumulate. Patients must watch their tyramine consumption (bananas, cheese). Tricyclics like imipramine, are more common and help unipolar patterns. Up to 50% chance of relapse within 6 months without drug but 20% chance with it if the drugs are taken for several months after there are no depressive symptoms. They act on reuptake mechanisms and alter the sensitivity of norepinephrine and serotonin receptors. Less dangerous and more effective than MAO but can cause dizziness, blurred vision and dry mouth.
Second generation antidepressants: For example, maprotiline, they alter the sensitivity of norepinephrine and serotonin receptors. SSRI’s, selective serotonin reuptake inhibitors, fluoxetine, alter serotonin activity. Equally as effective as tricyclics but less side effects. Most research focuses on the synaptic site.
When are MAO inhibitors most effective?
What about tricyclics?
Overeating, oversleeping, intense anxiety
Slow movement, insomnia, loss of appetite
When are MAO inhibitors most effective?
What about tricyclics?
Overeating, oversleeping, intense anxiety
Slow movement, insomnia, loss of appetite
Is electro-convulsive therapy more effective than tricyclics and MAO inhibitors?
When is ECT used?
Yes but without medication relapse is very likely
When someone has severe depression and doesn’t respond to other treatments, they must also be at high suicide risk