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Biological Psychology > Lecture 8: Depression > Flashcards

Lecture 8: Depression Flashcards

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1
Q

at least 1 of the symtpoms of major depressive disorder (MDD)

A
  • depressed mood
  • loss of interest or pleasure
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2
Q

other symptoms of MDD

A
  • weight loss or weight gain
  • increase/decrease in appetite
  • insomnia or hypersomnia
  • psychomotor agitation or delay
  • fatigue or loss of energy
  • feelings of worthlessness or guilt
  • reduced ability to think or concentrate
  • recurring thoughts of death, suicidal thoughts, or plan/attempt
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3
Q

prevalence

A

refers to the number of people with the disorder at a given time or during a given period
- depression is more prevalent in women (diagnosed 1.7 times more often than men)

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4
Q

how many people have mood disorders

A
  • UK: 4 million +
  • Europe: 33 million +
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5
Q

recovery from MDD

A
  • 54% of patients are likely to recover within 6 months
  • 81% within 2 years
  • relapse is highly likely (58% relapse within the next 10 years)
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6
Q

depressive symptoms

A

different from depressive disorder
- may be transient and occur in response to stressful life events without developing into a depressive disorder

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7
Q

unipolar depression

A

a purely depressive disorder

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8
Q

bipolar depression

A

bipolar patients have depression that alternates with periods of mania

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9
Q

bipolar I vs bipolar II

A
  • bipolar I is the classic manic depression
  • bipolar II is a milder variant
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10
Q

symptoms of a manic episode

A
  • inflated sense of self-worth or grandeur
  • decrease in need for sleep
  • more talkative than usual or feels pressure to keep talking
  • lost of ideas or feeling like thoughts are racing
  • quickly distracted
  • increased in purposeful activity or psychomotor agitation
  • increased involvement in activities that are highly likely to produce pain
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11
Q

hypomania

A

a marked period of abnormally and persistently elevated, expansive, or irritable mood and increased goal-directed activity or energy
- lasting at least 4 days and present most of the day

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12
Q

endogenous depression

A

occurs for no apparent reason
- potentially caused by an underlying neurochemical imbalance as the critical neuropathology
- tends to respond well to pharmacotherapy

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13
Q

reactive depression

A

can be seen as a result of a stressful life event
- responds better to psychological interventions (e.g. cognitive-behavioral therapy)

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14
Q

factors which can cause depression

A
  • family history
  • abuse
  • trauma and stress
  • death or loss
  • pessimistic personality
  • major life events
  • physical conditions
  • social isolation
  • lack of exposure to sunlight
  • hormones
  • other mental disorders
  • drug abuse
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15
Q

twin studies of depression

A

estimate the heritability of depression in monozygotic twins at 40/50%

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16
Q

equifinality

A

the idea that multiple different causes or processes (e.g. genetic, environmental, or psychological factors) can lead to the same outcome, such as the development of depression

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17
Q

effect of the hypothalamic-pituitary-adrenal axis (HPA) for depression

A

norepinephrine, acetylcholine, serotonin, and GABA are mobilized in response to stress
- activates cortisol

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18
Q

stress diathesis model of depression

A

integrates environmental experiences (e.g. stressors), with genetic predisposition (diathesis)

19
Q

stress theory of depression

A

emphasizes the role of a dysregulated HPA axis in depression

20
Q

noradrenergic hypothesis

A

depression results from reduced norepinephrine (noradrenaline) activity

21
Q

reserpine

A

a drug that depletes norepinephrine in the brain
- depletion leads to depressive symptoms that can be reversed by antidepressants

22
Q

amphetamine

A

increases norepinephrine levels and produces a euphoric high
- increases monoamine levels

23
Q

monoamine oxidase inhibitors (MAOIs)

A

among the first successful treatments for depression
- block the action of MAO, an enzyme that breaks down norepinephrine and other neurotransmitters
- increases availability of norepinephrine at the synapses

24
Q

tricyclic antidepressants (TCAs)

A

work by inhibiting the reuptake of serotonin and norpinephrine into the presynaptic neuron
- increases the concentration of norepinephrine in the synapse, allowing it to exert its effects for a longer period of time
- tend to have more side effects than other types of antidepressants (dry mouth, blurred vision, constipation, and sedation)

25
Q

alpha-2 autoreceptors

A

are on the presynaptic neurons and inhibit norepinephrine release when activated
- acted upon by drugs such as clonidine
- chronic use of antidepressants block these autoreceptors, reducing their inhibitory effect

26
Q

serotonin hypothesis

A

proposes that low serotonin levels contribute to depression
- serotonin is critical for mood regulation

27
Q

selective serotonin reuptake inhibitors (SSRIs)

A

work by preventing the reuptake of serotonin, thereby increasing its availability at the synapse
- e.g. fluoxetine (Prozac) and sertaline (Zoloft)
- relatively low side effects compared to TCAs
- may cause gastrointestinal disturbances or sleep issues

28
Q

inflammation theory

A

suggests that elevated levels of pro-inflammatory cytokines are associated with depression
- inflammation in the brain can cause symptoms that resemble sickness behavior (fatigue, social withdrawal, loss of appetite)

29
Q

neuroplasticity theory

A

links depression to reduced neuroplasticity (brain’s ability to adapts and reorganize
- in depression, levels of brain-derived neurotrophic factor (BDNF), a key protein involved in neuroplasticity, are lower

30
Q

atypical antidepressants

A

include a variety of drugs that do not fit into other categories but are still effective in treating depression
- may target different neurotransmitter systems such as norepinephrine and dopamine (e.g. Bupropion)

31
Q

selective norepinephrine reuptake inhibitors (SNRIs)

A

inhibit reuptake of both serotonin and norepinephrine
- used to treat depression, anxiety, and chronic pain
- e.g. venlafaxine (Effexor)

32
Q

dual-action antidepressants

A

drugs that target both the serotonin and norepinephrine systems to increase their availability
- may include atypical antidepressants and SNRIs, targeting multiple neurotransmitter pathways to address symptoms of depression

33
Q

lithium

A

primarily used in the treatment of bipolar disorder, particularly in management of manic episodes
- effective in reducing the frequency and severity of mania, but also used in combination with other antidepressants to treat the depressive phase
- increases serotonin and stabilizes mood through several mechanisms

34
Q

electroconvulsive therapy (ECT)

A

a treatment for severe depression that has not responsed to other treatments
- involves inducing seizures through electrical stimulation of the brain
- can be very effective in treatment-resistant depression and severe cases

35
Q

psychotherapy

A

cognitive behavioral therapy (CBT) and other therapeutic interventions are often used to treat depression
- helps patients identify and change negative thought patterns and behaviors that contribute to their depression

36
Q

vagus nerve stimulaiton (VNS)

A

the stimulation of the vagus nerve with electrical impulses
- typically delivered through an implanted device
- used for treatment-resistant depression and has shown promise in reducing symptoms in some patients

37
Q

light therapy

A

often used to treat seasonal affective disorder (SAD)
- patients are exposed to bright artificial light
- helps regulate mood by affecting the production of melatonin and serotonin

38
Q

St. John’s wort (hypericum perforatum)

A

a herbal remedy often used as an alternative treatment for mild to moderate cases of depression
- thought to work by increasing serotonin levels
- still under debate

39
Q

depression and co-occuring somatic disorders

A

depression is often associated with somatic illnesses (40-60% of depressed patients
- can reduce effectiveness of medical treatments
- 85% of patients with mild and 60% of patients with severe depression go unrecognized by primary care physicians (complaints are often not taken seriously leading to inadequate care)

40
Q

psychosocial aspects to somatic conditions

A

patients deal with loss, trauma, limitations in self-care, work, and social or family life
- unpredictability of certain illnesses can increase likelihood of depression

41
Q

psychobiological aspects to somatic conditions

A

depression can result from neurological damage, hormonal imbalances, or as a side effect of certain medications

42
Q

conditions leading to increased risk of depression

A

conditions with eleveated cytokine levels, such as autoimmune diseases, chronic infections, obesity, diabetes mellitus, and cardiovascular disease increase the risk of depression

43
Q

medications leading to increased risk of depression

A

medications for conditions such as hypertension, hormone treatments, and drugs such as alpha-interferon are known to contribute to the onset of depression

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