Mood Disorders

What are mood disorders

psyc disorders involving mood or one’s emotional state

also called affective disorders

types: Clinical Depression,, Bipolar Disorder

Clinical Depression

a severe type of depression that goes on for a long time, the person cannot control their depressed mood

more bodily than circumstansial

Bipolar Disorder

episodes of depression and mania, different variations

What percentage of people experience MAD

14% of canadians

how many Canadians die annually from suicide

4500 canadians

men more likely to suicide, indigenous too

women more likely to self harm

How many Canadians experience bipolar disorder

3.4% of canadians

What are common warning risks of people who are suicidal?

feel hopeless

withdraw from friends, familiy

has no purpose

threatens or talks about hurting or kill themselves

seeks ways to kill themselves

talks,, writes about death more than normal

what is Beck Hopelessness Scale (BHS)

a scale for hopelessness that uses 20 t/f questions

measures negative expectations about the future, their goals,, lack of control over the future

hopelessness is one of the key predictors of suicide

how much of suicides are due to impulses

about 40% of suicides are done impulsively in the moment, why those without a disorder. if stoped once its likely they wont commit again

What is the most common mood disorder?

Major Depressive disorder

what gender is most likely to develop depression?

women

what are the key symptoms of MAD and DSM symptom criteria

low mood, lack of pleasure in activies

appeitie

hyper/insomnia

fatigue

poor concentration

physical agitation, retardation

thoughts of death

5 or more sympoms for a two week period, 1 needs to be mood, pleasure related

How genetic/hereditary is depression, is there one gene invovled?

twin studies reveal it is more genetic: identical twins vs fraternal

there is no one gene involved there are many that contribute also plus environmental trigger (but D2 receptors keep in mind)

What do PET scans of depressed people reveal

compared to control condition depressed brains have more blood flow to the PFC and amygdala

the hippocampus is smaller and has less activity

and less flow to posterial temporal cortex,, parietal cortex,, and anterial cingulate

What are the treatments (antidepressants) for Depressions

MAO inhibitors
Tricyclics

SSRIS
(experimental: ketamine,, psychedelics which target opioid receptors)

Monoamine Oxidase Inhibitors (MAO)what? how does it work, what does it do, hypothesis?, side effects

first generation of antidepressents developed,

it inhibits monoamine oxidase so monoamines stay intact (not broken down) and attach to receptors

this means theres now more monoamines in the synapse

it works to improve mood, base for monoamine hypothesis (for depression)

side effects: toxic to liver, cant eat certain foods

Tricyclic Antidepressents what? how does it work, what does it do, hypothesis?, side effects

the second generation of antidepressents

it prevents the reuptake of serotonin and norephinephrine so there is more avalible in the synapse

over time this med will better ones mood. (follows monoamine hypo)

side effects: the meds will begin blocking or binding to other things besides whats intended (low selectivity)

muscarinic Ach antagonists: blunts rest and digest/ParaNS

dry mouth, blurr vision, urinary retention, etc (Anticholeinergic)

what is the Monoamine Hypothesis of Depression and evidences (2)

proposes that when one or more monoamine (such as serotonin) had less actitivty it would cause depression

evidence: Mao and tricyclic help depression

and reserprine which reduce norepinephrine and serotonin create massive depression

SSRIs (what, how does it work, result/findings, risks)

3rd gen of antidepressants selective serotonin reuptake inhibitors

it blocks the reuptake of serotonin NTs at serotonergic synapses
result it works like mao,, tricyclics but less side effects

only danger is serotonin syndrome: have too much and you can die esp if combined with MAOs, other drugs

what is the mechanism of MAO inhibitors

these drugs prevent Norepinephrine and serotonine (5-HT monoamine) from being broken down by enzymes and thus allows more of them to exist and be used

what is the mechanism behind Tricyclics

this medicaiton stops the reuptake of serotonin 5HT and Norepinephrine specifically

SSRIS

blocks reuptake of only serotonin (selectively serotonin)

what is wrong with monoamine hypothesis?

serotnin cannot be the direct cause of depression because antidepressents are not effective immediately

instead its likely that downstream changes due to serotonin are responsible for improvement

its possible that if one has fewer monoamines that there is a bigger overall dysregulation behind it

SNRIs (what is it, how does it work, what disorders does it help, how long to take effect, is it better than ssri?,, what are its symptoms

inhibitits the reuptake of norepinenephrine

helps anxiety disorders and depression

takes few weeks to take effect

less side effects, creates sexual dysfunction (not so diff from ssri)

what is the Diathesis - Stress Model

Diathesis means biological or pyschological vulnerability

+ Stress (life event)

exists because for some if they become stressed past a point they can develop a disorder

this stress can be accumulative appear subtle

how is the HPA axis involved in depression

high glucocortisol levels (like cortisol) is linked with depression

Dexamethasone Supression Test

Dexmethasone is used to suppress cortisol via neg feedback and it does not supress for people who are Depressed

how effective are antidepressants

statically they are effective, but improvements are small

on avg (possibly due to mixed responses)

more effective for severely depressed people

Electroconvulsive therapy ECT

shocks brain under anesthesia to disrupt neural networks, and increase neuroplasticity

maybe release monoamines

used in cases other stuff hasnt worked

Repetitive Transcanial Magnetic Stimulation

like ect but with magetic stimulation. less invasive

Vagus nerve stimulation

like ECT but electrodes are implanted. used for people who are resistant to other depression treatments

Deep brain stimulation

also uses surgically implanted electrodes, with mild stimulation may have same efficacy as a placebo

learned helplessness

when an animal cant escape a stimulus time and time again the animal learns to helpless. this is linked to less serotonin funciton and dopamine

SAD: Seasonal Affective Disorder

seasonal depression usually when wonter comes around

and circadian rhythm is disrupted. bright light therapy can help treat but

evidence is not 100 because of spring suicide peaks etc

a specifier: has to have Bipolar or MDD with seasonal pattern 2 yrs min

Bipolar Disorder

mania and depressive states

mania

elevated, irritable mood,, impaired judgement, uninhibitied

hypomania

a mild form of mania without impaired judgement or performance

How is the brain different for those with Bipolar Disorder

those with the disorder have enlarged ventricles at limbic structures like amygdala. (less brain volume)

during manic episodes brain activity increases

How does Bipolar overlap with Schizophrenia

they share unipolar depression/MDD

manic symptoms (grandiosity, speech) that seem psychotic

both are more heritable (family studies showed)

LIthium

used to treat Bipolar

the exact mechanism is not fully understood

but we know it disrupts second messenger systems after entering through neurons’ sodium channels

effects the brain vastly, and helps neural plasticity,, and BDNF protein (neuron growth, survival)

what gender is more affected in Bipolar disorder, age of onset

equally affected,, onset is earlier than MDD