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Depression Flashcards

1
Q

Affective disorders

A

Set of psychiatric disorders, also called mood disorders.

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2
Q

Main types of affective disorders

A

Depression

Bipolar disorders

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3
Q

Major depression

A

Major depressive disorder (MDD), is a mental disorder characterised by at least two weeks of low mood that is present across most situations. It is often accompanied by low self-esteem, loss of interest in normally enjoyable activities, low energy, and pain without a clear cause.

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4
Q

Monoamine hypothesis of affective disorders

A

Predicts that the underlying pathophysiologic basis of depression involves deficits of in the levels of serotonin, noradrenaline and/or dopamine in the central nervous system

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5
Q

Diathesis-stress hypothesis of affective disorders

A

Suggests that exaggerated or hypersensitivity of the hypothalamic-pituitary-adrenal axis is at the centre of the neurobiology of this disorder

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6
Q

Electroconvulsive therapy (ECT)

A

Procedure, done under general anaesthesia, in which small electric currents are passed through the brain, intentionally triggered a brief seizure. ECT seems to cause changes in brain chemistry that can quickly reverse symptoms of certain mental illnesses.

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7
Q

Clinical Neurology

A

A branch of medicine involved in the treatment of nervous system disorders such as MS and paralysis

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8
Q

Psychiatry

A

A branch of medicine involved in treatment of disorders that affect the mind or psyche.

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9
Q

What is human behaviour a product of?

A

Product of brain activity

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10
Q

What is brain activity caused by?

A
  • Product of genetics and environment
  • Experience (trauma/disease)
  • Genetic make-up and experience can interact, making a person more or less susceptible to future experience
    - > Genetic mutation or under severe stress will detrimental effects to the brain.
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11
Q

What explains psychiatric disorders?

A

By the genetics and environment e.g. chronic stress from abusive relationship

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12
Q

Treatment of Mental Health Disorders

A
  • Non-therapeutic e.g. cognitive behavioural
  • Psychosocial support
  • Pharmacotherapy
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13
Q

What type of disorder is depression?

A

Depression is characterised as an affective disorder

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14
Q

Affective disorder

A

A disorder of mood rather than thought/cognition.

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15
Q

What psychiatric disorder can cause premature death and disability?

A

Depression

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16
Q

Unipolar depression

A
  • Mood swings in one direction
  • Most common depressive illness
  • 75% of cases reactive = induced by environmental factors
  • 25% of cases endogenous = genetic
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17
Q

Bipolar depression

A
  • Oscillation between depression and mania
  • Less common
  • Onset usually in adult life
  • Strong hereditary tendancy
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18
Q

What is mania?

A

Excessive exhuberance, enthusiasm, self-confidence, impulsive actions, aggression, irritability, delusions of grandiose

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19
Q

How is depression diagnosed?

A
  • Diagnosed through the DSM IV
  • If 5 or more of the following symptoms have been presented during the same 2-weeks is diagnosed as depression:
    • > Depressed mood nearly every day
    • > Markedly diminished interest or pleasure in all or almost all, activities most of the day
    • > weight loss
    • > insomnia
    • > retardation
    • > fatigue or loss of energy
    • > feelings of worthlessness of excessive or inappropriate guilt
    • > diminised ability to think or concentrate, or indecivisness nearly every day
    • > recurrent thoughts of death, recurrent suicidal ideation without a specific plan or a suicide attempt or a specific pain for committing suicide
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20
Q

What are depressive symptoms split into?

A

Emotional and biological symptoms

21
Q

Emotional symptoms

A
  • Apathy, pessimism, negativity
  • Low self esteem, feeling guilty
  • Loss of motivation
  • Indecisiveness
22
Q

Biological symptoms

A
  • Reduced activity
  • Loss of libido
  • Sleep disturbance
  • Loss of appetite
23
Q

What is the age of first depressive episode?

A

Usually late adolescence of early adulthood

24
Q

Why has the age of depression onset decreased?

A
  • Life may be more stressful
25
Q

What is comorbidity?

A
  • Depression being comorbid with other psychiatric conditions (e.g. withdrawal from drugs and abuse)
  • Can link with terminal illnesses/chronic illnesses, thyroid dysfunction (hypothyroidism), stroke, neurological disease, drug abuse, Parkinson’s disease, anxiety
26
Q

What causes depression?

A
  • Depression is both influenced by genetic predisposition and environmental factors.
  • Genetic predispostion is supported by twin studies that show that if one twin suffers from depression than the other twin has a 50% chance of also suffering
  • Depression can affect individuals environmentally through loss of family member, environmental stressors and social isolation
27
Q

Major theories for causes of depression

A
  • Monoamine Theory
  • Neuroendocrine theory
  • Neuroplasticity and Neurogenesis
28
Q

What is the monoamine theory of depression?

A
  • Depression is caused due to deficits of monoamines in the brain.
  • Overall reduced activity of central noradrenergic and or serotonergic systems
  • Evidence for this system is injection of reserpine will deplete stores of NA and 5-HT = induces depression
29
Q

What are the problems of the monoamine theory of depression?

A

Patients have a high variability of monoamine levels in plasma and cerebrospinal fluid and low levels of serotonin is linked to violence.
- Antidepressants also increase monoamine levels however, they take 2 weeks to kick in which also questions the theory.

30
Q

What is the neuroendocrine theory of depression?

A
  • Depression is caused due to hypersensitivity of the HPA axis.
  • NAergic and 5-HT neurons will input to the hypothalamus
  • Hypothalamus will release CRH (corticotrophin releasing hormone)
  • CRH will act on pituitary and stimulate release of ACTH
  • Cortisol release from adrenal cortex (zona fasciculata) in response to increased ACTH in blood. Increase incortisol = high in plasma
31
Q

Evidence for the neuroendocrine theory

A
  • CRH mimics some depression symptoms
  • Evidence of hyperactivity of HPA in depressed patients
    • > Increased cortisol in depressed patients
    • > Increased CRH in CSF
  • Genes and environment can contribute to this hyperactivity
    • > Evidence of reduced hippocampal feedback
    • > Decreased hippocampal glucocorticoid receptors
32
Q

What do projections of the amygdala and the hippocampus do to the HPA axis?

A
  • High activity of the amygdala will activate HPA axis to release cortisol
  • High activity of the hippocampus will suppress HPA axis to stop the release of cortisol
33
Q

Explain the negative feedback mechanism of cortisol

A

Cortisol released will act on the glucocorticoid receptors on the hippocampus to suppress the HPA axis in a negative feedback mechanism.

34
Q

What regulates the HPA axis?

A

Good balance between amygdala and hippocampal activity

35
Q

What is important for HPA activity to start?

A

The development of the glucocorticoid receptor in the hippocampus after birth.

  • Tactile stimulation just after birth will activate the 5-HT pathways to the hippocampus
  • 5-HT triggers long lasting increase in expression of glucocorticoid receptor gene.
  • Increase in glucocorticoid receptor in hypothalamus.
  • Negatively regulate cortisol release by inhibiting CRH neurons hence reducing depression.
36
Q

What are the negative complications of children suffering from stress?

A

Glucocorticoid receptors are not developing, no negative feedback = increase of cortisol which can lead to mental health conditions later on in life.

37
Q

What do SSRIs do in the hippocampus?

A

Increase glucocorticoid receptors

38
Q

What can cause depression? - relating to neuroplasticity and neurogenesis

A

Evidence of neuronal loss and decreased neuronal activity in hippocampus and prefrontal cortex

39
Q

What drugs can prevent neurogenesis in the hippocampus and frontal cortex?

A

Antidepressants and electroconvulsive theory (ECT)

40
Q

What is the key molecule for the induction of neurogenesis and has an antidepressant effects?

A

Brain derived neurotophic factor (BDNF)

41
Q

When do BDNF levels increase?

A

Increase during exercise

42
Q

What do high levels 5-HT promote?

A

Promote neurogenesis

43
Q

Why is high glutamate linked to depressed people?

A
  • Glutamate will bind to NMDA receptors that can cause excitotoxicity leading to neuronal and cell death.
  • This can lead to depression.
  • Ketamine can block the NMDA receptor and has been a suggested treatment in depression.
44
Q

Pathophysiology of depression

A
  • Chronic stress over a long period of time will cause an activation of the HPA axis.
  • This will cause an increase in cortisol from the adrenal cortex and stimulate the detrimental gene transcription response which will cause neuronal apoptosis and depression.
45
Q

Effect of chronic stress increasing glutamate

A

Cause hyperactivation of the NMDA receptor causing excitotoxicity and depressive symptoms

46
Q

How does the monoamine theory support the idea of a detrimental gene?

A

Noradrenaline and serotonin will activate the alpha receptor and 5HT1A receptor respectively. This will promote beneficial gene transcription response and inhibit detrimental gene transcription response which will inhibit depressive symptoms hence low levels.

47
Q

Treatments of depression

A

Electroconvulsive Therapy (ECT)

  • Localised electrical stimulation
  • Some evidence of neurogenesis, possible involvement of hippocampus
  • Adverse effect: Memory loss

Psychotherapy

  • Mild to moderate depression
  • Overcome negative views

Monoamine oxidase inhibitors

  • Inhibit the breakdown of noradrenaline and serotonin - accumulate in the synaptic mealier.
  • Used on people who suffer from severe depression

Tricyclic antidepressants

  • Increase NA and serotonin by blocking the NA and serotonin transporter - causes elevation of monoamine levels in the synaptic bouton.
  • Also has CVS effects e.g. increased BP

SSRIs

  • Most commonly used: fluoxetine, citalopram, Prozac
  • Selectively block the serotonin transporter = increased serotonin
  • Safer than monoamine oxidases and tricyclic antidepressants as they don’t have severe CVS effects
  • Side effects like diarrhoea and insomina
  • If they do not work, might go onto TCAs or monoamine oxidases
48
Q

How do drugs used to treat depression normally work?

A

Act to increase monoamine levels (serotonin and noradrenaline)

Neuro (20 decks)

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