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Neuroscience > Wk 9.1 Depression and Anxiety > Flashcards

Wk 9.1 Depression and Anxiety Flashcards

1
Q

What is the most common psychiatric disorder and what genetic component is most likely to obtain it?

A

Depression
Concordance ratefor monozygotic twins with bipolar may reach 80%

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2
Q

What are the two types of Depression?

A

Unipolar- major depression
Bipolar- Episodes of mania

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3
Q

What are the subtypes of unipolar depression and what symptoms do they show?

A

-Melancholic depression=Depression with diurnal variations in mood, Insomnia, Anorexia, Loss of interest and Loss of capacity for joy

-Atypical depression= Depression with diurnal variations in mood, Weight gain, Anxiety and Loss of interest in activities but cheer up temporarily when good things happen

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4
Q

What are the symptoms of Bipolar depression?

A

-Alternating euphoria and depression

-Depression similar to that of unipolar type

  • Manic episodes: elevated, expansive mood over-talkativeness,increased energy and libido, decreased need for sleep. Can also include hallucinations and delusions.
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5
Q

What are the two types of bipolar and what is the difference between them?

A

Type I: at least 1 full manic episode and atleast 1 episode of major depression

Type II: at least 1 episode of hypomania and1 episode of major depression

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6
Q

What cause disruptions?

A
  • Monoamine hypothesis= dopamine, 5HT,NA and A
  • Neurotrophic hypothesis of depression= BDNF-1, NP,NM,Growth factors
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7
Q

What is the Evidence of brain regions involved in mood disorders?

A

-Enlargement of amygdala

  • Hippocampal atrophy in depression-correlated to amount and duration of priorepisodes of depression

-Feedback mechanisms within HPA axis areimpaired – lack of inhibition of cortisol

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8
Q

How does MAOI work?

A

-Dopamine is released to the synaptic cleft and gets reuptake, and by specific dopamine transporters

-The presynpatic terminal converts into 3-4 dihydroxyphenyl acetic acid and it metabolised

  • MAOI inhibits MAO which is used for the conversion of dopamine to other intermediates making it more persisant
  • Dopamine is reuptaked to the presynaptic cleft and is degraded by 1. MAO coverting D=-4 dihydroxyphenyl acetic acid and 2. Catechol-O-methyl transferase converting D= 3 methyoxytryamine
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9
Q

What do both intermediated get coverted to in the end?

A

Hamolalignic acid

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10
Q

what is the Evidence of monoamine disruption?

A

Reserpine- used to treat Hypertension and mental disorders

  • Induces depression

-Produced depression-like syndrome,motor retardation and sedation in animals

-Thought to inhibit vesicular storage of severalneurotransmitters (mainly 5HT and NE)

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11
Q

What is the production of serotonin?

A

-Tryptophan–tryptophan hydroxylase= 5-Hydroxy-Tryptophan

-Hydroxy-Tryptophan–Aromatic amino acid decarboxylase= 5-Hydroxy-Tryptamine

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12
Q

What is the production noradrenaline?

A

-Tyrosine– Tyrosine hydroxylase= L-dopa

-L-Dopa– Aromatic amino acid decarboxylase= Dopamine

-Dopamine– Dopamine-β-hydroxylase= Noradrenaline

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13
Q

What does depression involve?

A

Depression involves a decrease in availability of monoamines

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14
Q

What does depression medication known as SSRI & SSNI stop?

A

Stops reuptake the the neurotransmitter allowing it to bind to the receptors on the post synpatic and increase monoamines in the synpatic cleft

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15
Q

What are environmental componenet of depression and what do they effect?

A

-Chronic stress, early-life experiences, lack of maternal care, physical abuse and parental violence

-Affect the resilience against adverse effects andincrease the likelihood to develop depression

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16
Q

What is the HPA axis

A
  • hypothalamic and pituitary gland axis known the reaction to stress
  • Used to regulate stress response
  • It contains group of hormone screting glands from NS
17
Q

How does HPA axis work?

A

1.Hormones from the pituitary gland travel to the kidenys and influence secreation of hormones= adrenal glands

2.In stressful situtation the hypothalamus releases a hormone called corticotrophin- releasing hormone (CRH)

3.CRH signlas pituitary gland to secrete adrenocorticotropic hormone (ACTH)

4.ACTH travels doen to the adreanl glands and stimulates the release of cortisol hormone from the cortex

5.Release of cortisol causes changes that help the body deal with stress e.g mobilise glucose for the body to have enough energy to cope with prolonged stressor

6.High cortisol levels are sensed by receptors in the hippo and hypo which leads to shutting the stress (Negative FBM)

18
Q

In overactive HPA axis what does cortisol cause?

A

Symptoms associated with depression e.g insomnia

19
Q

What is the anxiety epidemology?

A
  • One of the most common mental illness in theUS
  • 40 million (18%) of the adult US population affected
  • Cost $ 42 billion a year
  • People with anxiety are 6 times more likely to be hospitalized for psychiatric disorders than non-sufferers.
  • Commonly co-occur with other mental or physical illnesses, including alcohol or drug
20
Q

What are some examples of Anxiety disorders?

A
  • Panic disorder
  • Post-traumatic stress disorder (PTSD)
  • Generalized anxiety disorder (GAD)
  • Social anxiety disorder (SAD)
  • Simple phobias
  • Obsessive-compulsive disorder (OCD)
21
Q

Information about panic attacks?

A
  • Brief episodes of terror
  • Unexpected
  • Overactivation of sympathetic nervous system
  • Recurring panic attacks – panic disorder
  • 50% patients with panic attacks also have depression
  • Successfully treated with tricyclics and MAOI’s– but mainly SSRI’s
  • Involves prefrontal cortex, LC and Limbic system
22
Q

Information about PTSD?

A
  • Occurs after extremely stressful event
  • Involves an increase in noradrenergic transmission
  • Noradrenaline and adrenaline are released from the adrenal medulla during exposure to a stressor
  • Exhibit increased heart rate, BP, andNE levels when challenged with traumatic reminders
  • Yohimbine causes panic attacks in these patients
  • Propanolol
23
Q

Information about GAD?

A

*Excessive worry lasting continuously for 6 months or longer

  • Motor tension

*Autonomic hyperactivity

  • Exaggerated startle response
  • Benzodiazapines
24
Q

Information about SAD?

A
  • Fear in social situations
  • Patients normally feel self-conscious and fear of how others will perceive them –cognitive distortions
  • Trembling,sweating nausea
  • Associated with Amygdala overactivation
  • Cognitive behavioural therapy and SSRI’s
25
Q

What does the amygdala do in anxiety?

A

Activated in response to stimuli that induce fear

26
Q

What is Benzodiazepines and what are the problems with it?

A

-It is a GABA A medication which helps with anxiety

  • Side effecrs due to lack of sensitivity

Neuroscience (16 decks)

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