2. Depression Flashcards
What can cause depression?
- Stress
- Bereavement
- Divorce
- Illness
- Redundancy
- Financial concerns
- Postnatal
Physical disorders = thyroid dysfunction, vit B12 def, heart + lung disease, kidney disease, liver disease
Outline the pathophysiology of depression
Not clearly defined
1) Monoamine hypothesis = def of monoamine neurotransmitters (NA, serotonin 5-HT). Monoamine oxidase inhibitors (MAOIs) block the enzyme monoamine oxidase from destroying neurotransmitters
2) Receptor hypothesis = abnormality in receptors for monoamine transmission leads to depression
3) Gene expression = problem within the molecular events distal to the receptor
What are the S+S of depression? and outline the ICD-10 classification
Continual for >2w:
- mild = 2 core + 2 other
- moderate = 2 core + 3/4 other
- severe = 3 core + >4 other
- severe + psychosis
Core Sx = low mood, anhedonia, fatigue
Biological Sx = decreased appetite, weight loss, sleep disturbance (feeling more tired but getting less sleep, EMW – early morning waking), reduced libido, psychomotor retardation, diurnal variation in mood (worse in morning)
Cognitive Sx = suicidal thoughts, hopelessness, worthlessness, guilt, hypochondriacal thoughts, poor concentration
How should depression be investigated?
Patient Health Questionnaire-9 (PHQ-9) = 9-item depression scale; each item is scored from 0-3, providing a 0-27 severity score
Beck Depression Inventory (BDI) = 21-question symptom-rating scales providing a 0-63 severity score
BDI for primary care = 7-question scale adapted from the BDI.
Bloods: FBC (anaemia), TFT (hypo), U+Es, LFTs, Ca, glucose
MRI/CT: where presentation is atypical, ?lesion
How is depression best managed?
- Sick note
- Suicide risk assessment
BIO: (make sure not bipolar)
1st LINE) SSRI’s (serotonin selective reuptake inhibitor) = fluoxetine (<18), citalopram (high risk QT-p), sertraline (common 1st line, safest in cardiac disease)
- after 2-4w should be some response
- after 4-6w should be significant response
2nd) alternate SSRI
3rd) SNRI’s (serotonin/noradrenergic reuptake inhibitor) = venlafaxine, duloxetine, mirtazepine (drowsiness, weight gain)
4th)
- TCAs (tricyclic Antidepressants) = nortriptyline, imipramine (dry mouth, blurred vision), clomipramine (dry mouth, weight gain)
- MAOI’s (monoamine oxidase inhibitor) = phenelzine
- **for depression if there is no benefit at a typical dose, no point increasing, or if significant SEs = switch
- for anxiety = increase dose first
- ECT
PSYCHO: counselling, CBT, cognitive, behavioural, psychodynamic, group, play/art, IPT
SOCIAL: family/friend support, hobbies/enjoyments, social support
What is the role of serotonin in the brain and where is it produced?
Produced in the brain stem - raphe nuclei
Sleep
Impulse control
Appetite
Mood
What is the mechanism of SSRIs?
Citalopram, sertraline (safest in CVD), fluoxetine, paroxetine
Inhibit the reuptake of serotonin into the presynaptic cell = increased serotonin the synaptic cleft
Leads to down regulation of post-synaptic receptors
- should be stopped gradually over 4w
- SSRI + NSAID = increased GI bleeding risk - give PPI
- should be continued 6m after Sx remission
What are the SEs of SSRIs?
Restlessness, agitation
Nausea, diarrhoea, weight changes (give PPI)
Headache
Sexual dysfunction
Increased risk of bleeding
Overdose = reasonable safe on its own
- citalopram = QT prolongation
- fluoxetine = serotonin syndrome (vague Sx, fluids + monitoring)
- paroxetine = discontinuation syndrome (shorter than half-life, bigger the prob: sweating, shakes, insomnia, headaches, N+V, paraesthesia, clonus) - slowly stop
What is the mechanism of TCAs?
Amitriptyline (old), lofepramine, nortriptyline
*** used at low doses for neuropathic pain
Blocks serotonin transporter (SERT) + norepinephrine transporter (NET) = elevation of synaptic cleft neurotransmitters + enhancement of neurotransmission
What are the SEs of TCAs?
CNS – sedation, lower seizure threshold
ANS – reduction in glandular secretions
CVS – tachycardia, postural hypotension, impair myocardial contractility
GI - constipation
Urinary - anticholinergic effect may lead to urinary retention, overflow incontinence
Overdose = Seizures, tachycardia, elevated temperature (pyrexia), death (QT prolongation, arrhythmias)
What is the mechanism of SNRIs?
Venlafaxine, duloxetine
Developed as SSRIs with property of noradrenaline uptake inhibition grafted on
What are the SEs of SNRIs?
Anorexia, nausea, diarrhoea
Sleep disturbance, increased BP, dry mouth, hyponatraemia, sedation, sexual dysfunction
Give a DDx for depression
Psychiatric = bipolar, schizophrenia, anorexia, anxiety
Substance misuse
Dementia
Delirium
Sleep disorders
Physical illness
Medication SEs
What is psychotic depression
Depression +
- hallucinations (often auditory)
- delusions (hypochondrial, guilt, nihilistic, persecutory)
Outline post-natal depression
10-15% of women, usually within 1-2m post partum
At most extreme = thoughts of harming baby
RF = personal/FH, older age, single mother, unwanted preg, poor social support, previous PND
Mx:
- self-help strategies = partner, friends and family, exercise, healthy eating, good sleep
- therapy = CBT, IPT
- medication = antidepressants (some you cant while breastfeeding)
