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MTB x > week 10 part 2 > Flashcards

week 10 part 2 Flashcards

1
Q

What does dysfunction of specific areas in the brain give rise to?

A

Neurobiological and behavioural changes

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2
Q

Definition of a mental disorder?

A

A psychological disorder characterised by elevation or lowering of a person’s mood

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3
Q

What are examples of mental disorder?

A
  1. Major depression
  2. Bipolar disorder
  3. Panic/Anxiety disorder
  4. Eating disorder
  5. Schizophrenia
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4
Q

According to WHO-2019, what is depression characterised for?

A

low mood for a constitutive period of mood more than 2 weeks

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5
Q

What is depression?

A

Leading cause of ill health and disability worldwide

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6
Q

What is lifetime risk for major depression?

A

15% of the population (varies on country)

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7
Q

Who suffers from depression once in your life?

A

1 in every 10 will suffer from depression

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8
Q

What is the incidence of depression?

A

women: 10-25% in women
Men: 5-10%
men are 3X as likely to take their own lives than wimen

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9
Q

what are the symptoms of major depression?-

A

Atleast 2 weeks if:

  1. Depressed mood
  2. Rumination
  3. Feelings of worthlessness
  4. Anhedonia - decreased ability to experience pleasure of normal activity
  5. Diminished ability to think or concentrate
  6. Weight gain or weight loss (>5% change in a month)
  7. Insomnia or hypersomnia
  8. Fatigue
  9. Thoughts of dead and suicide
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10
Q

What are examples of severe and chronic life stressors?

A
  1. Death of relative/Divorce
  2. Loss of social status
  3. Chronic illness
  4. Poverty
  5. Illness
  6. Hormonal upheaval
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11
Q

What are the leading cause of major depression?

A
  1. Severe and chronic life stressors
  2. Certain medications/drugs - drugs for diabetes/cancer
  3. Genetic vulnerability
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12
Q

What was the treatment for depression?

A

'’Shock’’ therapy

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13
Q

What is shock therapy?

A
  1. treatment of chronic mental conditions by electroconvulsive therapy or by inducing physiological shock
  2. ECT invented in italy in 1930
  3. ECT works by using electricity to induce seizures
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14
Q

What did psychiatrist discover?

A

Inducing seizures could relieve symptoms of mental illness

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15
Q

What was ECT used as?

A

Treatment for homosexuality

  1. No evidence it did alter anyone’s sexuality
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16
Q

What is the world’s first antidepressant?

A

Iproniazid

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17
Q

What does Iproniazid have?

A

Antimicrobial effects: Orginally developed for the treatment as an antimicrobial therapy for people suffering from tuberculosis

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18
Q

Why does Iproniazid have?

A
  1. Historic value

2. Helped establish the relationship between psychiatric disorders and the metabolism of neurotransmitters

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19
Q

What was Iproniazid?

A

Monoamine oxidase inhibitory

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20
Q

when did pharmacological characterisation of drugs start?

A

The modern era of the pharmacologic treatment of psychiatric disorders

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21
Q

Where did monoamine hypothesis originate from?

A

Early clinical observations

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22
Q

What was other compounds used to treat depression originally been designed to treat?

A

Parkinson’s or TB

for non-psychiatric conditions (Parkinson’s)

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23
Q

What did the compounds do?

A

Enhance concentration of central serotonin or norepinephrine transmission

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24
Q

What was the monoamine hypothesis of depression?

A

Depression is caused by the imbalance or deficiency of monoamine neurotransmitters”

  1. Dopamine
  2. Serotonin
  3. Norepinephrine
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25
Q

What does the imbalance of monoamine neurotransmitter explain?

A

Different symptoms of depression

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26
Q

What is the hypothesized pathophysiology appear to be supported by?

A

the mechanism of action of antidepressants: agents that elevate the levels of these neurotransmitters in the brain have all been shown to be effective in the alleviation of depressive symptoms

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27
Q

What are antidepressant responses?

A

Transiently reversed, with the results being dependent on the class of antidepressants

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28
Q

What is there a large diversity of?

A

Neurotransmitters in the brain

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29
Q

What are neurotransmitters?

A

Abundant and associated with many different brain areas

some are associated with specific neural networks

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30
Q

What does 3 neurotransmitters send projection to?

A

Rest of the brain - reaches cortex and limbic system and therefore explains mood changes and motivation changes seen in depression

31
Q

What is Iproniazid?

A

An inhibitor of monoamine oxidase a and b molecules

a and b are in the presynaptic space

32
Q

What is monoamine oxidase?

A

Enzymes involved in the breakdown of bioamines: dopamine, serotonin, norepinephrine

contributes to recycling of neurotransmitter

33
Q

What does recycling of neurotransmitter contribute to?

A

Production of more molecules of these neurotransmissions

34
Q

What does inhibition of monoamine oxidase results in?

A

Increased levels of bioamines and increase MOOD

35
Q

What does serotonin imbalance cause?

A

mood differences in depression

36
Q

What are the modern antidepressants?

A

Selective serotonin reuptake inhibitors (SSRI) - 40 years old

37
Q

What is the most prescribed antidepressant, well known SSRI?

A

Prozac

38
Q

What is the mechanism of action SSRI?

A
  1. Blocks serotonin re-uptake transporters

2. Decreased uptake of serotonin

39
Q

what has antidepressant allowed?

A

Revolutionised mental health care

40
Q

What doesn’t depression improve?

A

cellular and molecular characteristic of mood/health outcomes

41
Q

What does SSRI allow?

A

Deinstitutionalisation

42
Q

What has discoveries of drugs allowed patients to be?

A

Dehospitalised

43
Q

What gives clues about cause?

A
  1. Brain imaging

2. Postmortem studies

44
Q

What are the affected brain areas?

A
  1. Frontal cortex - cognition, attention procesisng
  2. Hippocampus - working memory, cogntive function
  3. Amygdala - fear, anxiety, aggression
  4. Hypothalamus - sleep, apetite, sexual desire
  5. Thalamus - processing of thoughts, movement
  6. Stratium - Reward
45
Q

What does these affected brain areas have?

A

Changes in size or activity in depressed patients

46
Q

How long does it take for antidepressant effect to take place?

A

3-4 weeks

47
Q

What is the possible explanation for why there is a disconnect between onset of treatment and onset of resolution of treatment?

A
  1. • Acute increases in the amount of synaptic monoamines induced by antidepressants produce secondary neuroplasticity effects:
  2. • function on a longer timescale
  3. • involve transcriptional and translational changes -EPIGENETIC
  4. • SSRI mediate molecular and cellular plasticity
48
Q

What do you use to study depression?

A
  1. Human genetics
  2. Scan of human brain
  3. Postmortem brain and animal model
49
Q

What suggested the plasticity and neurogenesis hypothesis?

A
  1. Genetics
  2. Environment
  3. Neurotrophic processes
50
Q

What are trophic factors?

A

• Signal molecules to allow neurons first to migrate to destiny of fate, they contribute to maintenance and survival of neuron – one neuron attaches to another neurons and exchange NTF and keep eachother healthy

51
Q

What are signal factors called?

A

NGF

52
Q

What are examples of neurotrophic factors or NTF?

A
  1. NGF
  2. Neurotrophins (NT-3,4,5)
  3. BDNF
  4. CNTF
  5. Ephrins
53
Q

What is the plasticity and neurogenesis hypothesis?

A
  1. Decrease in the volume of hippocampus and other forebrain regions observed in subsets of depressed patients
  2. Also in post mortem theres a reduction of formation of synapse in hippocampus
54
Q

What is plasticity?

A

Changes and formation of synapses

55
Q

What is adult neurogenesis?

A

Proliferation

56
Q

What lead to depression hypothesis?

A

the findings of damage to hippocampus

57
Q

What is depression caused by?

A

Decreases in neurotrophic factors

58
Q

Neurotrophic factors

A

neurodevelopmentally expressed growth factors that promote neuronal survival and regulate plasticity within adult brain → in hippocampus

59
Q

What is hippocampus in depressed patient?

A

Atrophy

60
Q

What does precursors in the basal subgranular zone give?

A

Rise to postmitotic neuroblasts

61
Q

Where does neuroblasts translocate to?

A

Apical zones

62
Q

What does neuroblasts differentiate?

A

Produce dendrites and axons

63
Q

What is decreased in depression?

A

Neurogenesis

64
Q

What increases adult hippocampal neurogensis?

A

Chronic antidepressant treatment

65
Q

What is neurogenesis associated with?

A

Plasticity of the brain

66
Q

What does reduced neurogenesis in depression involve?

A

Trophic factors

67
Q

What does stress reduce?

A

BDNF signalling in the hippocampus

68
Q

What is consequences of reduced BDNF signalling in the hippocampus?

A

Reduced proliferation and plasticity in hippocampus

Reduced hippocampal formation

69
Q

What is Antidepressant therapy?

A
  1. Antidepressant increases BDNF signalling
  2. Neural progenitors in the hippocampus divide mitotically to form new neurons that differentiate
  3. Hippocampal circuitry and output increases
70
Q

What does BDNF lead to?

A
  1. loss of plasticity
71
Q

What is BDNF polymorphism associated with?

A

short-term episodic memory impairment and mood disorder and schizophrenia

72
Q

What does stress reduce ?

A

BDNF

73
Q

What is the effect of antidepressant on neurogenesis?

A
  1. Antidepressant growth factors
  2. Adult hippocampal neurogenesis
  3. Hippocampal circuitry
  4. Output: amygdala, stratium, prefrontal cortex

MTB x (15 decks)

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