Depression Flashcards

1
Q

What is Psychiatry?

A
  • Branch of medicine, diagnosis & treatment of disorders that affect the mind or psyche
  • Disorder of thought, moods and fears considered outside the reach of neuroscience
  • Now hope that neuroscience will help identify causes and treatment of mental illnesses (Anxiety, scz, depression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do you think of mental illness and the brain?

A
  • Human behaviour is the product of the brains activity
  • The brain is the product of genetics and environment
  • Experience
  • Genetic make-up and experience can interact, making a person more or less susceptible to future experience
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give some facts about mental illnesses

A
  • In 2020, estimated about 971 mil ppl living with mental or behavioural disorders
  • 1 in 4 British adults experience at least one diagnosable mental health problem in any year
  • Depression affects 1 in 5 older people living in the community
  • More than 70% of prison population has two or more mental health disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the characteristics of affective disoders

A
  • Disorders of mood rather than thought/cognition
  • Most common is depression
  • Major cause of premature death and disability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List the 2 different types of depression

A
  • Unipolar Depression
  • Bipolar depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe unipolar depression

A
  • Mood swings in one direction
  • Most common depressive illness
  • 75% cases REACTIVE (induced by environmental factors)
  • 25% cases are ENDOGENOUS (genes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe Bipolar depression

A
  • Oscillation between depression and mania
  • Mania: Excessive exuberance, enthusiasm, self confidence
  • Type 1: More mania episodes with or without depression
  • Type 2: Hypomania and always episodes of major depression (0.6%)
  • Onset usually in adult life
  • Strong hereditary tendency (no genes found yet)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the criteria for being diagnosed with depression?

A
  • Depressed mood most of the day, nearly everyday
  • Markedly diminished interest or pleasure in all, or almost all activities most of the day
  • Significant weight loss when not dieting or weight gain or decrease/increase in appetite nearly everyday
  • A slowing down of thought and a reduction of physical movement
  • Fatigue or loss of energy nearly everyday
  • Feelings of worthlessness or excessive or inappropriate guilt nearly everyday
  • Dimished ability to think or concentrate or indecisiveness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is required in order to be diagnosed with depression?

A
  • 5 or more of the following symptoms have to be present during the same 2 week period and represent a change from the previous functioning
  • Atleast one of the symptoms being a depressive mood or loss of interest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can the symptoms of depression be split into?

A
  • Emotional symptoms
  • Biological symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List some biological symptoms of depression

A
  • Loss of appetite
  • Loss of sleep
  • Loss of libido
  • Reduced activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List some Emotional symptoms of depression

A
  • Apathy, Negativity
  • Low self esteem, feeling guilty
  • Loss of motivation
  • Indecisiveness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the other medical conditions that can coincide with depression (Co-morbidity)?

A
  • Terminal illness
  • Chronic illness
  • Thyroid dysfunction
  • Stroke
  • Drug abuse
  • Parkinson’s disease
  • Anxiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the monoamine theory of depression?
Discuss evidences for the theory

A

Evidence for
- Overall reduced activity of central noradrenergic and/or serotonergic systems
- Reserpine depletes brain of NA and 5 HT induces depression
- Main antidepressants drugs (amines) in brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the monoamine theory of depression?
Discuss evidences against the theory

A
  • Difficult to show deficits in the brain (NA) & (5-HT) and functioning results from CSF, plasma in depressed individuals respond better to one AD than another
  • Most antidepressant drugs take several weeks for therapeutic effect but ã in amines acute
  • Some antidepressants weak/no effect on amine uptake/ no increase in 5HT or NA but antidepressants
  • Cocaine blocks amine uptake but has no antidepressant effect
  • Decrease in 5HT in dipolar linked to aggression rather than depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the neuron doctrine theory of depression?

A
  • NAergic & 5HT neurons input to hypothalamus
  • Hypothalamus releases corticotropin releasing hormone
  • CRH acts on pituitary, release of adrenocorticotrophic hormone
  • Cortisol release from adrenal cortex in response to ACTH in blood
17
Q

What is the evidence for the neuron doctrine theory of depression?*

A
  • There is evidence of hyperactivity of HPA in depressed patients
  • Corticol plasma in depressed patients
  • [CRH] I’m the cerebrospinal fluid
  • There is clear evidence that genes and environment can contribute to this hyperactivity and as such could offer an explanation for how genes x environment interaction can predispose ppl to mental health conditions
18
Q

Describe the neuroendocrine in more detail

A
  • ‘d hippocampal feedback in depression
  • ’d glucocorticoid receptors (cortisol receptors) in hippocampus
  • Glucocorticoid receptor gene expression regulated by early experience
  • Tactile stimulation just after birth activates 5-HT pathways to hippocampus
  • 5-HT triggers long-lasting  in expression of glucocorticoid receptor gene
  •  in glucocorticoid receptors in hippocampus
  • SSRIs  glucocorticoid receptors in the hippocampus
19
Q

Describe the neuroplasticity & neurogenesis theory of depression

A
  • Evidence of neuronal loss and  neuronal activity in hippocampus and prefrontal cortex (decision making centres)
  • Antidepressants and electroconvulsive therapy (ECT) promote neurogenesis in these regions
  • 5-HT promotes neurogenesis during development (BDNF)
  • Increase in Glutamate in Cx of depressed people (NMDA antagonists potential for depression treatment e.g. ketamine)
20
Q

Describe the brain activity in depressed patients

A

Depressed patients tend to have lower levels of activity’s in all areas of the brain

21
Q

List and describe the different types of treatments for Depression

A
  • Cognitive behavioural therapy (CBT): Based on helping depressed individuals to recognise and change their negative cognitive processes and thus improve their mood & their counterproductive behaviours
  • Pharmacotherapy: Assumes that depression is multi factorial but that interpersonal difficulties play a central role in maintaining depressive symptoms
22
Q

List some pharmacological treatment

A
  • Tricyclic antidepressants
  • Monoamine oxidase inhibitors
  • Selective serotonin reuptake inhibitors
23
Q

Describe the use of SSRI’s

A
  • NICE recommends SSRI’s for the pharmacological treatment of depression
  • Selectively inhibit the reuptake of serotonin in the synapse
  • Because they’re more selective in the molecules to which they bind, they do not bind to receptors on other classes of neurons
24
Q

List some long term neurochemical antidepressants

A
  • Monoamine Oxidase inhibitors (MAOIs)
  • Tricyclic Antidepressant Drugs (TCAs)
  • Selective Serotonin Re-uptake Inhibitors (SSRIs)
  • Other mixed 5HT/NA reuptake inhibitors (SNRIs)
  • NA reuptake inhibitors
  • Monoamine receptor antagonists
  • Downregulation a2, 5HT1A, b1, b2, 5HT2A, 5HT3
25
Q

Describe the mechanism of action of MAOI’s

A
  • Inhibition of MAO A correlates with anti depressive activity
  • MAO-A 5-HT > Na
  • MAOIs rapidly increase [5HT] > [Na] > [DA]
  • Increase in Na -> increased Euphoria -> increase motor activity
26
Q

Describe MAO I

A
  • Associated with food and drug interactions
  • Tyramine acts as indirect sympathomimetic and increase Na release
  • Excess Na destroyed by MAO, if blocked then Na will accumulate
  • Na accumulation increases headaches, intracranial haemorrhage-> elevation in BP -> severe hypertension
  • MAOI’s not specific, reduce metabolism of opioid analgesics and alcohol
27
Q

Describe Reversible MAOI’s (RIMA)

A
  • One example is moclobemide
  • Accumulation of NA displaces the RIMA allowing degradation of excess NA
  • RIMAs sager and selective RIMAs better tolerated
28
Q

What is a side effect of MAOI’s?

A
  • MAO is inhibited in the gut
  • Dietry amines such as tyramine can get into the circulation
  • Foods include cheese,yoghurt,meat,wine,yeast products
  • All contain high concentrations of tyramine
  • Tyramine acts as an indirect sympathomimetic displacing noradrenaline from vesicles
29
Q

Describe the mechanism of action of Tricyclic antidepressants

A
  • Main therapeutic affects are: Na reuptake inhibitor, 5HT reuptake inhibitor
  • Initially increase [NA] & [5HT] in synaptic cleft
  • Chronic treatment down regulation of (B1) & 5HT2
  • ⍺2, 5-HT1A/1D (autoR)
  • Also affect mACh, HR, 5HTR