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Block 3: Pathophysiology and pharmacology > Depression > Flashcards

Depression Flashcards

1
Q

What are the two patterns of depressive states?

A

Unipolar [low level of mood affecting quality of life]

Bipolar [recurrent episodes of mania and depression]

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2
Q

How is a unipolar depressive state generally treated?

A

CBT

Antidepressants

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3
Q

How is a bipolar depressive state generally treated?

A

Antipsychotics

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4
Q

What is dysthymia?

A

Mild, chronic depression

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5
Q

What is cyclothymia?

A

Cycle of mild depression and and elevated mood

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6
Q

What are the 2 forms of bipolar depression?

A 
Bipolar disorder (periods of mania and depression)
Cyclothymia (periods of hypomania and mild depression)
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7
Q

What are the ‘core’ symptoms of depression?

A

Persistent low mood
Anhedonia (lack of pleasure)
Anergia (abnormal lack of energy)

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8
Q

What other symptoms present in people with depression?

A 
Disturbed sleep
Change in appetite/ weight 
Fatigue 
Agitation 
Poor concentration 
Feelings of worthlessness/ guilt 
Suicidal thoughts
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9
Q

What areas of the brain show decreased activity in depression?

A

Prefrontal cortex

Hippocampus

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10
Q

What areas of the brain show increased activity in depression?

A

Amygdala

Hypothalamus

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11
Q

What are the theories of depression?

A

Neurotransmitter (monoamines)
Neurohormonal (steroids, HPA axis)
Immune (e.g. autoimmune)
Circadian

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12
Q

What is the main site of production of Serotonin?

A

Raphe Nuclei (Brainstem)

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13
Q

What functions is Serotonin involved in?

A 
Mood/ agitation 
OCD 
Anxiety 
Appetite
Insomnia 
Sexual functioning 
Nausea/ vomiting
GI function
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14
Q

What are the main sites of noradrenaline production?

A 
Locus Coeruleus (Pons) 
Lateral Tegmental Area (Brainstem)
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15
Q

What are the functions of Noradrenaline?

A 
Depression 
Attention 
Energy homeostasis
Agitation 
Emotions
Blood pressure/ Heart rate 
Bladder control
Motor function
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16
Q

How does Serotonin and Noradrenaline interact?

A

Interactions in the brainstem speed activity
Interactions in the cortex slow activity
Depends on the distribution of adrenergic receptors on the dendrites/ presynaptic terminal which makes responses variable

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17
Q

What is the role of inflammation in depression?

A

Inflammatory mediators lead to microglia activation, cell dysfunction and cell death which can lead to a spectrum of disorders.
Damage occurs in CNS and only crosses blood-brain barrier if there is a point of weakness.

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18
Q

What is the gut-brain axis?

A

Inflammation in the gut can trigger altered brain activity.
Altered microbiota can lead to breakdown of protection known as ‘leaky gut’.
Probiotics have been shown to reduce anxiety and improve mood.

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19
Q

What is the role of neurogenesis in depression?

A

Depression associated with decreased dendritic arborisation, a decreased number of synapses and overproduction of receptors.

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20
Q

What treatments options are available for depression?

A 
CBT 
Pharmacological 
Transcranial Magnetic Stimulation (TMS) 
Transcranial Direct Current Stimulation (TDCS) 
Electroconvulsive Therapy (ECT)

[Nb. important to consider exercise and lifestyle changes in all patients with mental health problems]

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21
Q

What pharmacological treatments are available for depression?

A

SSRIs
Tricyclic antidepressants
Monoamine Oxidase Inhibitors
Atypical antidepressants

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22
Q

What is the placebo effect?

A

Beneficial effect produced by placebo drug/ treatment that cannot be attributed to the placebo itself and therefore must be due to patient’s belief in the treatment.
30% of patients respond to placebo treatment and can change in neuronal activity levels.

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23
Q

What are the advantages of Transcranial Magnetic Stimulation?

A
  1. Can be effective in patients who do not respond to antidepressants
  2. Less stigma than ECT
  3. Fewer side effects
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24
Q

Where in the brain does TMS target?

A

Prefrontal cortex

Limbic system

25
Q

How do SSRIs work?

A

Increases 5HT levels by inhibiting re-uptake pump

26
Q

What are the common SSRIs used to treat depression?

A

Sertraline

Citalopram

27
Q

What is serotonin syndrome?

A 
Group of symptoms associated with SSRI use, including: 
Hyperthermia
CV problems
Aggression 
Tremor
Rigidity
28
Q

What is a common norepinephrine reuptake inhibitor?

A

Reboxetine [works the same way as SSRIs]

29
Q

What is a common Serotonin Norepinephrine Reuptake Inhibitor?

A

Venlafaxine

30
Q

How do 5HT partial agonists work?

A

Reduce activity in order to increase transmitter levels

31
Q

What is a common 5HT partial agonist?

A

Buspirone

32
Q

What are the advantages of 5HT partial agonists?

A

Fewer side effects

No sedation or loss of coordination

33
Q

What is Agomelatine?

A

A melatonin agonist
Works by increasing slow wave sleep
Currently used as treatment for depression

34
Q

What are the 5 main actions of tricyclic antidepressants?

A
  1. 5HT reputake blocker
  2. NA reuptake blocker
  3. alpha1 adrenoreceptor antagonist
  4. H1 receptor antagonist
  5. M1 receptor antagonist
35
Q

What are the side effects of tricyclic antidepressants?

A 
Accumulation can lead to slowly developing side effects, including: 
Sedation 
Postural hypotension 
Confusion 
Visual problems 
Cardiac dysrhythmia 
Mania

Also drug interactions (e.g. with aspirin and alcohol)

36
Q

How do monoamine oxidase inhibitors work?

A

Increases NA/5HT levels by inhibiting enzymatic breakdown

37
Q

What is the most common MOAI?

A

Moclobemide

38
Q

What are the side effects of MOAIs?

A

Similar side effects to TCAs
Drug interactions (cannot be used with SSRIs or TCAs)
Postural hypotension
Restlessness
Convulsions
Sleep disorders
‘Cheese reaction’ [acute hypertension when cheese is consumed whilst on MOAIs - reaction with Tyramine]

39
Q

How do alpha-adrenoreceptors modulate NA and 5HT release?

A

alpha-1 receptors increase transmitter release

alpha-2 receptors slow transmitter release

40
Q

What is a common alpha-2 antagonist?

A

Mirtazapine [works by increasing transmission of NA/ 5HT]

41
Q

What are the side effects of alpha-2 antagonists?

A 
Decreased vascular flow to extremities
Postural hypotension 
Fatigue 
Bronchoconstriction 
Cardiac failure
Bradycardia 
Sleep disorders
Impotence
Depression
42
Q

What are the aims of CBT?

A
  1. Identify thinking that causes problematic feelings/ behaviour
  2. Question negative feelings in order to enable positive change
  3. Plan goals to achieve change
43
Q

How can dysfunctional thoughts arise in people with depression?

A

‘Shoulds’ (set of expectations concerning behaviour of self and others)
Catastrophising (expecting the worst, interpreting situations as looming disaster)
Filtering (focusing on negatives, ignoring positives)
Polarisation (insistence on extreme views)
Over-generalisation (reaching conclusions with minimal evidence)
Personalisation (comparing to others, assumption of negative feelings from other people)
Mind-reading
Heaven’s reward (feeling that pain/ suffering will be rewarded)

44
Q

What is the CBT process?

A
  1. Problem identification
  2. Goal selection
  3. Exploring options
  4. Consideration of consequences
  5. Plan of action
  6. Implementation
  7. Evaluation
45
Q

What conditions can CBT be beneficial for?

A 
Depression 
Anxiety
Addiction 
OCD
Eating disorders
Phobias
Chronic Fatigue Syndrome
46
Q

What are the benefits of CBT?

A

Can be used instead of/ in conjunction with medication
Can be provided in different formats (e.g. individual, group, online etc.)
Practical strategies for every day life
Can be completed in a shorter time than other therapies

47
Q

Who may CBT not be suitable for?

A

Those with complex mental health needs or learning disabilities
Those who are not ready to pursue change

48
Q

What techniques are involved in CBT?

A 
Challenging irrational beliefs
Reframing 
Thought stopping 
Graded exposure
Assertiveness
Social skills training 
Problem solving training 
Relaxation techniques
49
Q

What is the ABCD approach used in Rational Emotive Behaviour Therapy (a form of CBT)?

A 
A = activating event 
B = belief (about event) 
C = consequences (of event) 
D = disputing belief
50
Q

What are alternative counselling approaches to CBT?

A 
Psychodynamic therapy
Humanistic approach
Systemic approach
Transactional analysis
Integrative approach
51
Q

What are the 3 forms of unipolar depression?

A 
Dysthymia (mild, chronic depression)
Major depression (more severe but less chronic than dysthymia) 
Atypical depression (patient may experience improved mood with pleasurable events e.g. no anhedonia)
52
Q

What 2 classification tools are used for depression?

A

ICD-10 (at least 1 core symptom for >2 weeks)

DSM-V

53
Q

How long would symptoms have to be present for to be classed as chronic depression?

A

2 years

54
Q

What does the monoamine theory of depression state?

A

Result of altered activity of monoamines (e.g. NA, 5HT)

55
Q

What does the neurohormonal theory of depression state?

A

Result of a dysregulated HPA axis function and impaired cortisol feedback
Increased levels of inflammatory markers and thus inflammation, leading to cell dysfunction and death

56
Q

What does the immune theory of depression state?

A

Cytokines (e.g. IL-1) can activate the HPA axis, modulating immune response and causing inflammation, leading to cell dysfunction and death

57
Q

What does the circadian theory of depression state?

A

Light input affects many factors such as internal temperature regulation, hormone production (incl. cortisol and melatonin) and organ function

58
Q

What is ECT?

A

Induces seizures under general anaesthetic using electrodes

Gold standard for treatment of severe depression

59
Q

What are 2 potential side effects of ECT?

A

Muscle aches

Memory loss

Block 3: Pathophysiology and pharmacology (16 decks)

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