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Depression and bipolar Flashcards

1
Q

Outline the two main types of depression

A

Unipolar: low mood

Bipolar: also known as manic. low mood with periods of mania

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2
Q

Define dysthymia

A

Low grade but long term depression

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3
Q

What type of depression may be accompanied by delusions

A

Psychotic or major depression

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4
Q

What is lifetime prevalence of major depression?

A

4% in males 8% in females

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5
Q

Why is there a gender difference in depression and antidepressant efficacy?

A

Sramek et al., 2016: there is sex difference in antidepressant efficacy - body fat, hormone levels impact pharmacokinetics of drugs.

Females: harsher symproms, increased weight gain, younger onset, greater anxiety.

Theory: due to oestrogen and progesterone (as incidence of depression in women post menopause is similar to that of men). PET showed decreased serotonin synthesis in females.

SSRIs: females respond better than men and postmenopausal females have diminished response compared to younger females.

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6
Q

State the difference between reactive and endogenous depression

A

Reactive: depression due to external factors such as death, 75%.
Endogenous: due to biochemical reasons, 25%. No external factors

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7
Q

State the differences between treatment of endogenous and reactive depression

A

There is no differentriation in drug treatment.

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8
Q

How is depression diagnosed and what criteria is used?

A

DSM-IV Criteria for Major Depressive Disorder

Depressed mood/loss of interest or pleasure in daily activities for over 2 weeks.
Mood changes from person’s baseline.
Impaired functionality (social, occupational, educational).

Significant distress is caused.

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9
Q

Define anhedonia

A

Reduced ability to feel pleasure.

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10
Q

List symptoms of depression

A

Depressed mood or irritability (misery, apathy and pessimism)
Loss of motivation
Significant weight change
Insomnia or hypersomnia
Fatigue
Guilt, low self esteem feeling worthless
Loss of libido
Suicidal thoughts

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11
Q

State brain system/s associated with anhedonia and reduced drive and describe

A

Reward system (VTA, NAcc)

Decreased level of mesolimbic DA to VTA implicated, could also be due to decreased hippocampal activity via NAcc to VTA.

The NAcc generates behaviour aimed at acquiring rewards and activity of this region imporves hedonic tone (Willner et al., 2012)

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12
Q

State brain system/s associated with reduced energy and describe

A

HPA axis

Chronic stress induced adrenal exhaustion caused by activation of HPA axis (Herman et al., 2016)

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13
Q

State brain system/s associated with memory problems and describe

A

Hippo

Poor memory for positive and potentiated memory for negative events.

Possibly via stress mediated suppression of hippocampal neurogenesis (Dillon and Pizzagalli., 2018)

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14
Q

State brain system/s associated with attention and cognitive impairment and describe

A

PFC and ACC

Decreased ACC volume observd in depressed patients.

DBS therapy 50% of patients showed improved DSM-VI scores one year later (Willner et al., 2012).

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15
Q

State brain system/s associated with anxiety and describe

A

HPA

Again chronic stress

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16
Q

Explain evidence that shows that antidepressant treated brains are different to normal brains

A

Willner et al., 2012:
When successfully treated depressed patients are administered a DA blocker depressed mood returns.

People in normal state show slight improvement in mood when same block administered.

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17
Q

Do different antidepressants all work on different targets?

A

yes and no: will all have different primary effects but all known increase responsiveness of DA D2 receptors in NAcc and CREB expression in the hippocampus (Willner et al., 2012)

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18
Q

Is CREB expression anti or pro-depressant?

A

Both…

Hippo is anti
NAcc is pro

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19
Q

What does chronic administration of BDNF into hippocampus cause?

A

Increases neurogenesis.

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20
Q

What does chronic activation of HPA axis lead to?

A

Chronic CRH release - neurotoxic to hippocampal cells causing loss of glucocorticoid receptors in granule cells.

This leads to less BDNF production and atropy of dendrties.

Spatial memory in rodents and verbal declarative memory then impaired in humans.

Willner et al., 2012.

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21
Q

State reason why some people may be predisposed to depression

A

Negative experiences in early life such as abuse.

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22
Q

What hormone does CRH stimulate the release of and what does it do?

A

ACTH (adrenocorticotrophic releasing hormone) from the pituitary gland.

Causes secretion of cortisol from the adrenal glands and via negative feedback it inhibits release of CRH.

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23
Q

What impact does cortisol secretion have on ACTH?

A

Inhibits release via negative feedback.

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24
Q

Describe differences to do with HPA axis that depressed patients show

A

High levels cortisol, CRH.
Increased number of CRH-secreting neurons.
CRH binding sties reduced in frontal cortex.
Dysregulated circadian cortisol patterns.

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25
Q

What does blockade of CRF1 receptors produce?

A

Reduction in anxiety and depression symptoms.

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26
Q

What does admin of CRH produce?

A

Symptoms that resemble depression:
Decreased appetite
Sleep disruption
Decreased libido
Increased anxiety
Neophobia.

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27
Q

Define neophobia:

A

irrational fear of new or unknown.

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28
Q

Why are animal models of depression hard to design?

A

animals do not show human symptoms such as: guilt, suicidality… (Krishnan and Nestler, 2011)

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29
Q

What depressive symptoms can you measure in animals?

A

Anhedonia, helplessness and alterations in sleep and appetite(Krishnan and Nestler, 2011)

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30
Q

Outline evolutionary perspective of ‘depression’ in animals

A

(Krishnan and Nestler, 2011): depression is an analog of involuntary defeat strategy.

Animals percieve defeat in heirarchical struggle for resources.

NB: this is adaptive as use less energy and therefore not pathological.

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31
Q

Name and describe the three different types of validity in animal models. What needs to be taken into account regarding depression?

A

1) face: symptomatic homology
2) construct: similar cause
3) pharmacological: reversal via antidepressants.

1) anthromorphisation cannot be excessive
2) not possible due to incomplete etiology of depression.
3) in this model are we only treating depression that is monoamine sensitive?
(Krishnan and Nestler, 2011)

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32
Q

What is the fourth type of validity that needs to be developed

A

Same pathology in brain via postmortem examination of human…

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33
Q

Outline acute stress animal models

A

Forced swim: inescapable cylinlder of water, initial struggle then immobile.

Tail suspension.

In both of the above, increase immobility = more depressed.
(Krishnan and Nestler, 2011)

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34
Q

How do antidepressants impact acute stress models

A

Decrease immobility with no therapeutic delay (NB: antidepressants take over 2 weeks to work in humans)

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35
Q

What are SERT KO mice and how do they react to acute stress models of depression?

A

Serotonin transporters (reuptake): diff mouse strains show differential effects, both pro and anti.

V strange as would expect anti for all.

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36
Q

What effect does Isotretinoin have on animals and humans?

A

Also known as Accutane: acne treatment that increases risk of depression and suicide in humans.

In animals mice show increased immobility and decreased neuronal proliferation.

(Krishnan and Nestler, 2011)

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37
Q

Outline the learned helplessness model of depression

A

Exposure of animal to uncontrollable and inescapable stress such as footshocks.

When same animal introduced to same stress with easy escapse they either escape quickly or completely fail. Depressed fail.

Rats show: weight loss, altered sleep, loss of spinal synapses in hippocampus after this model.

(Krishnan and Nestler, 2011)

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38
Q

Describe social stress models for depression

A

Dominant animal: hard to replicate in lab and only in males

Social isolation: v easy

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39
Q

Give animal model of secondary depression

A

HPA axis dysfunction implicated in depression which causes altered glucocorticoid function.

Glucocorticoid receptor KO mice developed: increased acute stress immobility which is reversable with antidepressants.
(Krishnan and Nestler, 2011)

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40
Q

Outline the monoamine hypothesis

A

Depression: lack of amines
Mania: excess of amines

NADR/5-HT affecting drugs could help stabilise/elevate mood.

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41
Q

Support for monoamine hypothesis

A

MAOi’s increase concentration of amines by inhibition of catabolism are effective antidepressants.
Reserpine depletes monoamines and exacerbates depression.
Reuptake inhibitors increase concentration and time in synaptic cleft are effective antidepressants.

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42
Q

Problems with monoamine hypothesis

A

Pharmacological effects are correlated with blood plasma concentrations but therapeutic effects are delayed at least 2 weeks.
Some effective atypical antidepressants do not alter monoamine levels in the synaptic cleft.
Cocaine inhibits reuptake of DA, NA, 5HT but is not an effective antidepressant.
Precursor amino acids increase amine levels but are not effect antidepressants.

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43
Q

What could explain the therapeutic delay seen with antidepressants?

A

Synaptic plasticity…
Hours: increase 5HT, NA and trigger the start of signalling cascades.
Weeks: increased BDNF, increased synaptic proteins and increased dendritic sprouts etc.

44
Q

In the monoamine hypothesis what are the main antidepressant targets?

A

Inhibition of reuptake (TCAs and SSRIs)
MonoAmine Oxidase Inhibitors (MAOi’s)

45
Q

Why is there a time lag in traditional antidepressant agents but not with novel agents such as ketamine?

A

Traditional: takes weeks to increase BDNF levels

Ketamine: directly activates mTOR and increases BDNF release from post synaptic
(Duman and Voleti, 2012)

46
Q

Outline evidence that explains ketamine mechanism of action

A

mTOR blockage prevents antidepressant effects of Ket.(Duman and Voleti, 2012)

mTOR pathway goes on to increase BDNF.

47
Q

Why can depression be viewed as a mild neurodegenerative disorder?

A

Postmortem: reduces size of pyramidal, decreased number of GABAergic interneurons.
Above has also been observed in rodent studies.
(Duman and Voleti, 2012)

Chronic stress causes a decrease in hippocampal volume, possibly via inhibition of neurogenesis ( Lang and Borgwardt, 2013)

48
Q

Why can depression be viewed as a metabolic disorder?

A

Lang and Borgwardt 2013

Depression increases risk of type 2 diabetes by 60%…
Leptin levels in gut implicated in depressed mood, sleep disturbances etc. The leptin receptor is colocalised to glucocorticoid (linked to insulin resistance) in hippo neural progenitor cells. Furthermore, leptin converges on GSK3 to decrease basal DA secretion.

Carbs suppress grehlin whose feedback regulates mood, feeding and acts as an antidepressant.

NB: chronic stress can release gre which generates anxio to help cope.

49
Q

What does BDNF deletion do to metabolism?

A

Implicated in obesity, increased abdominal white adipose tissue. Has been implicated in mediating food intake.
(Land and Borgwardt, 2013)

50
Q

Outline the link between depression and light deprivation

A

Exposure to light = secretion of melatonin which modulates circadian rhythm, vit D and increases 5HT in platelets.
Bright light therapy improves mood and leads to better sleep.
New antidepressant agomelatin is melatonin analog.

BDNF serum conc is correlated to sunlight.

Superior remission rates in chromotherapeutic strategy vs exercise.

Lang and Borgwardt 2013.

51
Q

Outline how depression can be viewed as a inflammatory disorder

A

Inflammatory cytokines such as interleukin 1beta are stress mediated.

Increased concentrations of proinflammatory agents such as TNF-alpha are found in depressed patients. (opposite has also been reported).

Sesamol is potent cytokine inhibitor and reversed chronic stress in mice. Chronic stress said to ‘cause’ depression due to HPA axis link

Lang and Borgwardt, 2013

52
Q

Outline how chronic stress can be thought of as an endocrine disorder

A

Chronic stress = chronic HPA activation = chronic corticosteroid relesase = impaired corticosteroid receptor signalling.

Clinical depression occurs in 40% of hypothyroid sufferers and increased chance of hyper being diagnosed. conc of free thyroxine in blood increased in 30% of depression cases (this seen in hyper).

Land and Borgwardt 2013

53
Q

Outline how depression can be seen as a issue with glutamate regulation

A

Ketamine is anti and NMDAR antagonist.

Other anti raise brain magnesium levels which also inhibits NMDAR.

Lang and Borgwardt 2013

54
Q

Why is depression sometimes regarded as a deficiency state?

A

Omega 3 intake is inversely associated with depression.

Folic acid deficiency is seen in psychiatric conditions (depression and bipolar). Treatment with folic, vita6 and 12 reduces risk of major depressive episode by 50%.

Lang and Borgwardt. 2013

55
Q

What is the link between depression and cardiovascular disorders?

A

MDD: increased risk of coronary heart disease.

Increased sympathetic tone associated with higher prevalence of depressive disorders.

In depressed patients there is increased blood coagulation.

Lang and Borgwardt 2013

56
Q

Outline stepped care management of depression

A

Mild is generally not treated with drugs etc as the risk to benefit ratio is very poor. CBT and self help (exercise) are first line treatments.
Moderate to severe depression often requires both pharmacological and CBT. It is important to remember that therapeutic effects of the drugs are delayed…

57
Q

Why can some antidepressants initially worsen symptoms?

A

SSRIs: serotonergic neurons co-release glutamate.

Thought that initial effect due to reduction of glutamatergic signal component.

Fischer et al 2014

58
Q

What are TCAs and how do they work?

A

Tricyclic Antidepressants: such as chomipramine inhibit amine reuptake and therefore increase concentration in the synaptic cleft.

Further later changes: reduction of presynaptic alpha2 receptor sensitivity. So enhanced efficacy of release.

CLOMIPRAMINE

59
Q

State side effects of TCAs

A

antimuscarinic: blurred vision, dry mouth, urinary retention, constipation and excessive perspiration.

Cardiovascular: block of HERG K+ channels causes postural hypotension, tachycardia and palpatations.

Antihistamine: sedation and weight gain.

Alpha2: postural hypotension

60
Q

Why are patients only given a 1 week supply of TCAs?

A

Toxic levels are obtained at 10X therapeutic dose so only one week to prevent overdose.

61
Q

What drugs should TCAs not be given with?

A

alcohol, anaesthetics, hypotensive, MAOis and NSAIDs.

62
Q

What are MAOis and how do they work?

A

MAOA is implicated in depression as preferentially metabolises 5HT. NB: MAOB selective no anti.

63
Q

State difference between selective and non selective MAOis

A

phenelzine (non): hypersensitive response to tyramine containing foods - cheese reaction (can be fatal).

moclobemide: reversible and selective so side effects less severe.

64
Q

State side effects of MAOis

A

Weight gain
CNA stimulation: insomnia, restlessness, acute overdose.
Hypertensive crisis in irreversible inhib.

65
Q

What should MAOis not be given with?

A

SSRIs, TCAs, pethidine

66
Q

Why are SSRIs most prescribe antidepressants?

A

Similar efficacy to TCAs, less acute toxicity to TCAs and MAOIs as specifically target 5HT

67
Q

State side effects of SSRIs

A

Nausea
insomnia
sexual dysfunction
increased anxiety in early phase
Serotonin syndrome; when combo with MAOi - confusion, hypothermia, cardiovascular collapse.

68
Q

What can compliance issues cause in antidepressants?

A

Compliance problems: cause of non-response.

Sudden discontinuation symptoms when stopped.

69
Q

What should be done if there is no improvement in symptoms after one month of anti?

A

As response unlikely new treatment should be started.

70
Q

What is maintenance treatment?

A

maintain on therapeutic dose to reduce reccurence for those with 2+ episodes.

71
Q

Continuiation of anti for 6 month?

A

Halves relapse rate.

72
Q

How is ECT used in depression?

A

Electroconvulsive therapy: recommended treatment for treatment resistant depression.
Involves: induction of epileptic seizures under general anaesthesia 3 times weekly for 8 weeks. (Israel-Elgali et al., 2021).

Developed as schizo patients had decreased glial number whereas epilepsy had increased. Actual mechanism is uncertain.
Regional blood floow increased in seizure areas and hypometabolism observed in depression and bipolar.
BBB transient breakdown which increases BDNF conc, shown in rodents.
Human MRI studies reported increased hippo volume prior to treatment. (Singh and Kar 2017)

73
Q

How is DBS used in depression?

A

Deep brain stimulation

Optimisation is not complete but:
NAcc: the more severe the anhedonia the smaller the nucleus, after DBS reduced hamilton depression rating scale (HDRS) and immediate increase in reward seeking thoughts.

BNST: amygdala output pathway that regulates stress response. One study found 2/7 in remission and other 5 all responded well to treatment 3 years after initial.

There is a possibility for personalised treatment with DBS
(Drobisz and Damborka 2019)

74
Q

How is TMS used in depression?

A

Transcranial Magnetic Stimulation

10Hz delivered to left dorsolateral PFC for 4-6 weeks daily. expensive and time consuming. (Sonmez et al., 2019)

Protocol is not optimised but transient current flow and neuronal depol in cortical tissue directly beneath stimulation site, this will effect downstream circuits.
Thought to modulate synaptic strength and functional connectivity.
fMRI in depressed showed hyperactivity in DMN corrected after treatment but hypo in CEN not…

DMN (default mode network), PFC: rumination, episodic memory retrieval. Hyperactive in depression.
CEN (central executive network), DLPFC: attention, working memory, descision making. Hypoactive in depression.

75
Q

How is VNS used in depression?

A

Vagus Nerve stimulation: links gut microbiome and brain.

Increased amygdala-DLPFC connectivity (decreases depression severity).
Anti-inflam: suppresion of proinflam cytokines such as interleukin 6. This verified by plasma levels.

Liu et al., 2020

76
Q

Outline experiment about vulnerability to stress and depression

A

Rat model (Bouvier et al., 2017)

First stress: social defeat, 40% of animals then classed as vulnerable

Second: chronic mild, only those vulnerable before develop depressed phenotype.

Shows that natural predisposition as same stresses applied to all.

In vulnerable: persistant state of oxidative stress found. This is due to low BDNF which prevents Nrf2 translocation and therefore less antioxidant enzymes.

77
Q

What role does GSK3 play in depression?

A

Is inhibited via phosphorylation by antidepressants (lithium, ketamine and SSRIs): when inhibited beta-catenin levels are increased and gene transcription is increased, inflammation is decreased.

78
Q

How does lithium inhibit GSK3?

A

phosphorylation via akt pathway.

79
Q

How do SSRIs inhibit GSK3?

A

phosphorylation via activation of 5HT1A receptors.

80
Q

How does Ketamine inhibit GSK3?

A

Ketamine activates akt which phosphorylates and inhibits GSK3.

81
Q

How does ketamine exert antidepressant effects?

A

Activates mTOR and increases BDNF release from post.
Must act via mTOR as mTOR blockage prevents antidepressant effects of ketamine.

Non-selective NMDAR antagonist, increases spine number and AMPAR insertion. If pretreated with AMPAR antagonist then no effect (Duman and Voleti)

82
Q

What role does BDNF play in depression?

A

Antidepressive: increase in presynaptic pool of vesicles in active zones. Upregulation of synaptic proteins such as synapsin. Mutation = impaired dendritic transport and decreased hippo volume. ERK-MAPK pathway activation.

Binds to TrKB: akt pathway stim which inhibits GSK3…

SNP (Val66met) blocks trafficking of BDNF to dendrites. Leads to decreased hippocampal volume and targeted BDNF deletion in hippo causes depression in female mice.

83
Q

What plasticity causes antidepressant?

A

Increased AMPAR insertion, increased number of spines and increased spine function along with increased BDNF release from post.

84
Q

Outline role of Wnt in depression

A

Upstream GSK regulator whose activation leads to GSK3 inhibition.

ECS and SSRIs increase Wnt2 expression in hippo which produces anti in sucrose preference tests.

85
Q

Outline role of CREB in depression

A

activated by camKII and increases BDNF levels (anti)

CamKII is activated by NMDAR activation which is interesting as ket is anti and also antagonist.

86
Q

Why can bipolar disorder be hard to diagnose?

A

Patients enjoy manic or hypomanic episodes and therefore may only visit GP when depressed.

Furthermore, symptoms can be confused with anxiety or schizophrenia

87
Q

If a doctor suspects you have bipolar what sort of questions will be asked and how?

A

Questionnaire:
Have you ever found yourself to be abnormally talkative and speaking very quickly.
Have you ever been so manic that people thought you were not yourself?

88
Q

State symptoms of mania

A

Overly good euphorica mood
Increased energy, activity and restlessness
Racing thought s that jump from one idea to the next (also seen in speech)
Provocative, intrusive or aggressive behaviour
Needs little sleep
Unrealistic belief in one’s abilities or powers
Increased libido
Abuse of drugs
Denial that anything is wrong.

89
Q

List all potential phases of bipolar from most manic to most depressive, state cycling.

A

Severe mania
Hypomania
Normal mood
Mild to moderate depression
Severe depression

Think about sin waveform. Bipolar will often cycle through above phases in pattern.

90
Q

Define rapid cycling

A

4 or more episodes (cycles - one wavelength)

In 12 months

91
Q

State difference between bipolar I and bipolar II

A

I: recurrent episodes of mania and depression (depression in most cases).

II: recurrent episodes of hypomania and depression.

92
Q

Why should antidepressants not be given to bipolar patients?

A

Treatment aim should be to bring patients to baseline normal mood or as close to normal as possible.

Antidepressants: Would raise whole waveform so that ‘trough’ was closer to norm and that most severe mania that patient used to feel is now further down waveform and no longer peak.

93
Q

What are the main two types of pharmacological treatment of bipolar?

A

Short term control of acute mania (olanzapine - neuroleptic, valproate, carbamazepine both of which are anticonvulsants)

Long term prophylatic treatment to maximise time interval between cycling (lithium).

94
Q

What drug is used for treatment if overt mania?

A

Neuroleptic olanzapine: via block of Da D2 receptors and 5HT receptors

95
Q

What anticonvulsants are used to treat bipolar disorder and how

A

Valproate: restrictions in women of childbearing age. Increase GABA

Carbemazepine: greater risk of cardiotoxicity and increased propensity for drug interactions. Enhance Na channel inactivation

96
Q

Is the therapeutic effect of mood stabilisers delayed?

A

Yes

97
Q

What is the long term prophylatic drug used to treat bipolar

A

Lithium: inhibits GSK3 via akt phosphorylation. This is main mechanism of action but are more.

At a neuronal level, lithium reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission

98
Q

Outline patient care in bipolar treatment

A

Teaching patients to recognise early symptoms of manic relapse.
Compliance with lithium treatment important.
Monitoring of lithium blood conc after one week then every three months

99
Q

What are therapeutic plasma levels of Li+ associated with?

A

GI discomfort and nausea.
Neurological symptoms (often dissipate): fatigue, malaise, muscle weakness.
Decreased water reabsorption by kidney
Weight

100
Q

What is moderate Li+ conc in blood? State symptoms

A

1.5-2.0 mmol/L

GI: vomiting, dry mouth, abdominal pain.

Neurological: ataxia, dizziness, slurred speech, lethargy, muscle weakness.

101
Q

What is blood conc severe of Li+ and symptoms?

A

2-2.25 mmol/L

GI: anorexia nervosa, persistent vomiting

Neurological: blurred vision, delirium, clonic limb movements, muscle fasciculum, convulsions, syncope, coma, circulatory failure

102
Q

What percentage of patients cannot tolerate the adverse side effects of lithium?

A

30%

103
Q

How does increased monoamine concentration lead to plasticity

A

Increased 5HT (monoamine) leads to increased cAMP, which increases CREB. CREB goes on to increase BDNF which exerts anxiolytic and antidepressant effects.

Increases AMPAR insertion, more spines etc

104
Q

Onset and prevalence of bipolar

A

Prevalence: 4% with higher rates in women

Onset: late teens

105
Q

Aetiology of bipolar

A

Highly genetic

106
Q

Depression new theories citation

A

Lang and Borgwardt 2013

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