MOOD DISORDERS GENERAL + DEPRESSION Flashcards
(196 cards)
1
Q
What are the different types of manic episodes?
A
Hypomania
Mania without psychotic symptoms
Mania with psychotic symptoms
2
Q
What is hypomania?
A
persistant mild elevation of mood, increased energy and activity, and usually marked feelings of well-being and both physical and mental efficiency. Increased sociability, talkativeness, over-familiarity, increased sexual energy, and a decreased need for sleep are often present but not to the extent that they lead to severe disruption of work or result in social rejection.
Lasts at least 4 days
3
Q
What is mania?
A
Mood is elevated out of keeping with the patient’s circumstances and may vary from carefree joviality to almost uncontrollable excitement. Elation is accompanied by increased energy, resulting in overactivity, pressure of speech, and a decreased need for sleep. Attention cannot be sustained, and there is often marked distractibility. Self-esteem is often inflated with grandiose ideas and overconfidence. Loss of normal social inhibitions may result in behaviour that is reckless, foolhardy, or inappropriate to the circumstances, and out of character.
Lasts at least 7 days
4
Q
What psychotic symptoms may occur with mania?
A
delusions (usually grandiose)
hallucinations (usually of voices speaking directly to the patient) are present
Pressured or disorganised thoughts and speech
5
Q
What are mood congruent delusions?
A
the content of a person’s delusions or hallucinations aligns with the person’s mood state.
6
Q
What is an example of a mood congruent delusion during a bout of mania?
A
a person believing they have superpowers or are best friends with a celebrity
7
Q
What is bipolar defective disorder characterised by?
A
2 or more episodes in which the patient’s mood and activity levels are significantly disturbed, this disturbance consisting on some occasions of an elevation of mood and increased energy and activity (hypomania or mania) and on others of a lowering of mood and decreased energy and activity (depression). Repeated episodes of hypomania or mania only are classified as bipolar.
8
Q
How do we describe bipolar affective disorder in its different states?
A
Current episode hypomanic
Current episode manic without psychotic symptoms
Current episode manic with psychotic symptoms
Current episode mild or moderate depression
Current episode severe depression without psychotic symptoms
Current episode severe depression with psychotic symptoms
Current episode mixed
Currently in remission
9
Q
How do we diagnose depression?
A
PHQ2:
During the last month, have you often been bothered by feeling down, depressed, or hopeless?
During the last month, have you often been bothered by having little interest or pleasure in doing things?
If the person answers ‘yes’ to one of the questions and symptoms have been present most days, most of the time, for at least 2 weeks, ask about associated symptoms of depression:
Disturbed sleep
Decreased or increased appetite and/or weight.
Fatigue or loss of energy.
Agitation or slowing down of movements and thoughts.
Poor concentration or indecisiveness.
Feelings of worthlessness or excessive or inappropriate guilt.
Recurrent thoughts of death, recurrent suicidal ideas, or a suicide attempt or specific plan.
Do the PHQ9
10
Q
How do we determine the severity of the depressive episode?
A
Mild - 4 symptoms
Moderate 5-6 symptoms
Severe 7+ symptoms
(Depressed mood, loss of interest, reduction in energy, loss of self confidence, feelings of guilt, recurrent thoughts of death, not being able to concentrate, change in psychomotor activity, sleep disturbance, change in appetite and weight)
11
Q
When can depression present with psychotic symptoms?
A
In moderate or severe depressive episodes
12
Q
What psychotic symptoms does severe depression usually cause?
A
Hallucinations (most common is auditory)
Delusions
Psychomotor agitation or retardation
13
Q
What is atypical depression?
A
A specific type of depression in which the symptoms vary from the traditional criteria. One symptom specific to atypical depression is a temporary mood improvement in response to actual or potential positive events (mood reactivity)
14
Q
What is recurrent depressive disorder?
A
A disorder characterized by repeated episodes of depression as described for depressive episode, without any history of independent episodes of mood elevation and increased energy (mania).
There may, however, be brief episodes of mild mood elevation and overactivity (hypomania) immediately after a depressive episode, sometimes precipitated by antidepressant treatment.
15
Q
What category does seasonal depression fall under?
A
Recurrent depressive disorder
16
Q
What are the different types of recurrent depressive disorder?
A
Current episode mild
Current episode moderate
Current episode severe without psychotic symptoms
Current episode severe with psychotic symptoms
Currently in remission
17
Q
What are the 2 most common persistant mood disorders?
A
Cyclothymia
Dysthymia
18
Q
What is Cyclothymia?
A
A persistent instability of mood involving numerous periods of depression and mild elation, none of which is sufficiently severe or prolonged to justify a diagnosis of bipolar affective disorder or recurrent depressive disorder.
Some patients with cyclothymia eventually develop bipolar affective disorder.
19
Q
Which group of people is Cyclothymia frequently found in?
A
in the relatives of patients with bipolar affective disorder
20
Q
What is dysthymia?
A
A chronic depression of mood, lasting at least several years, which is not sufficiently severe, or in which individual episodes are not sufficiently prolonged, to justify a diagnosis of severe, moderate, or mild recurrent depressive disorder.
21
Q
Outline the epidemiology of depression?
A
4th leading cause of disability worldwide
1/5 will experience it at some point in their life
3rd most frequent reason for consulting a GP
22
Q
What are the 3 core symptoms of depression?
A
Persistent low mood
Loss of interests/pleasure
Fatigue/low energy
23
Q
What are the 3 main options for classification of depressive episodes?
A
Depressive episode
Bipolar affective disorder
Recurrent (unipolar) depressive disorder
24
Q
What are the 2 whooley questions/PHQ2 used to screen for depression in primary care?
A
During the last month have you often been bothered by feeling down, depressed or hopeless?
During the last month have you often been bothered by having little interest or pleasure in doing things?
25
What are the known risk factors of depression?
Female sex.
Older age.
PHx of depression.
Personal, social, or environmental factors, such as relationship issues or breakdown, bereavement, stress, poverty, unemployment, homelessness, social isolation, or past history of child maltreatment.
Postpartum period.
FHx of depressive illness or suicide.
History of other mental health conditions and/or substance misuse.
Other chronic physical health conditions associated with functional impairment
26
Outline how a FHx of depression is a risk factor for depression?
first-degree relatives of a person with a 'major' depressive episode have a three-fold increased risk of depression
Hereditability is 40-70%
27
What chronic physical illnesses increase your risk of depression?
Diabetes mellitus, COPD, CVD, chronic pain syndromes, epilepsy, stroke disease
28
What is the monoamine theory of depression?
Depression is due to a shortage of noradrenaline, serotonin and potentially dopamine.
29
What evidence supports the monoamine theory of depression?
Pt with low levels of serotonin metabolite were found to be more likely to have committed suicide
drugs that deplete monoamines can cause depression
TCAs and MAOIs increase monoamines and are known to treat depression
30
What evidence does not support the monoamine theory of depression?
it takes 2-3 weeks for antidepressant drugs to effectively treat depression but if the monoamine theory is true then depression should decrease as levels of neurotransmitters rise - shold not have a delayed therapeutic effect onset
31
What are the somatic symptoms of depression?
sleep disturbance, appetite disturbance, and fatigue or loss of energy.
32
What proportion of those with depression report multiple unexplained physical symptoms?
50%
33
What brain changes have been seen with bipolar?
Enlarged cerebral ventricles on CT scan
34
How do we treat depression conservatively?
Education
Lifestyle changes e.g. sleep hygiene, diet, exercise, substance use
Improve physical health
Problem solving e.g. sorting out debt and divorces
35
How do we treat mild depression?
Watch and wait for 2 weeks
Lifestyle changes
Group exercise
Self help - books, online CBT, self help groups
36
How do we treat mild to moderate depression?
Talking therapies e.g. CBT, counselling, behavioural activation, interpersonal psychotherapy
37
How do we treat moderate to severe depression?
Antidepressant medication and talking therapy (combination therapy)
Or individual CBT orBA
Or individual medication
38
What is CBT?
Based on the cognitive model - it focuses on identifying and changing negative through patterns and behaviours that can contribute to depression
39
What are the ‘levels’ of CBT?
Self help materials
Assisted self help e.g. computerised CBT
Specific CBT interventions
Formulation driven CBT (1:1 weekly sessions)
40
Which patients are likely to be good candidates for CBT?
Can recognize and capture thoughts in different situations
Can recognize and differentiate emotions
Accepts personal responsibility to change
Understands cognitive model
Can form good therapeutic relationship
Onset of problems is recent (e.g. within 6 months)
Can stay focussed ‘on task’
Doesn’t use defence mechanisms
Optimistic about outcome
Problems are not very severe
41
Whats the CBT model of depression?
Underlying beliefs centre around being helpless or unloveable because of early experiences
Trigger events typically involve loss or ‘failure’
This produces negative cognitions about self/ future/world which reinforce underlying beliefs, and affect mood and behaviour
These negative thoughts are maintained by distorted information processing (e.g. overgeneralization, personalization, selective abstraction)
42
Whats the evidence base for CBT?
CBT is highly effective compared to controls and shows equivalence to medication except in severe cases
43
What is behavioural activation therapy?
Therapy aiming to increase a pt’s engagement in positive rewarding activities
It’s based on the ideas that depression is maintained by a lack of positive reinforcement
44
What is counselling?
Individual sessions delivered by a practitioner with therapy-specific training and competence.
Usually consists of 12-16 regular sessions
Focus is on emotional processing and finding emotional meaning, to help people find their own solutions and develop coping mechanisms.
Provides empathic listening, facilitated emotional exploration and encouragement.
Collaborative use of emotion focused activities to increase self-awareness, to help people gain greater understanding of themselves, their relationships, and their responses to others, but not specific advice to change behaviour.
45
Who is counselling suitable for?
May be useful for people with psychosocial, relationship or employment problems contributing to their depression.
May suit people who do not like talking about their depression in a group.
46
What is psychodynamic psychotherapy?
Therapy thataims to resolve unconscious conflitcts and early childhood experiences that may underlie depression
47
What is interpersonal psychotherapy?
a talking treatment that helps people with depression identify and address problems in their relationships with family, partners and friends.
This is based on the idea thta depression can be exacerbated bu issues in interpersonal relationships
48
Why do we choose SSRIs first line?
all antidepressants have a similar efficacy for the treatment of depression so we choose SSRIs as they are better tolerated as have less side effects and are safer in overdose
49
During the first few weeks of treatment with antidepressants, how is the pt likely to feel?
increased potential for agitation, anxiety, and suicidal ideation.
50
Outline the options for antidepressants?
SSRI
Another SSRI or SNRI
TCAs
MAOIs
Addition of other antidepressant
Use of augmenting agent
51
How long should antidepressant treatment be tried for. Before considering switching to another antidepressant ?
4 weeks at least (6 in elderly)
52
How long should you continue using an antidepressant for if it has bought on remission of symptoms?
Continued at full dose for 6 months at least
53
Long term use of which antidepressants have been linked to an increased risk of developing type 2 diabetes?
SSRIs and TCAs
54
Outline how serotonin is released into synaptic clefts?
Presynaptic serotonergic neurones use tryptophan to synthesise serotonin (5-Hydroxytryptophan) which is then stored in vesicles. When an action potential reaches the presynaptic membrane, vesicles fuse with the membrane and release serotonin into the synaptic cleft. Serotonin can bind to 5HT2 receptors on the postsynaptic neurone and this causes a new action potential. On the presynaptic membrane there are serotonin reuptake transporters which facilitate the uptake of serotonin.
55
Outline the moa of SSRIs?
SSRIs bind to serotonin reuptake transporters and inhibit them which increases the serotonin level within the synaptic cleft.
56
How long do SSRIs take to work? And why?
4-6 weeks before improvements seen
These meds are slow acting as it takes time for serotonin to accumulate within the synaptic cleft.
57
What can SSRIs treat?
Chronic anxiety
PTSD
OCD
Major depressive disorder
Bulimia nervosa
58
What are the side effects of SSRIs?
Body weight increase
Anxiety and agitation
Dizziness (+ other anticholinergic side effects e.g. blurred vision and dried mouth)
Serotonin syndrome
Sad tummy (nausea, vomititng, indigestion, diarrhoea, constipation)
Reproductive and sexual dysfunction
Insomnia
59
What are side effects specific to citalopram?
Arrhythmias due to prolongation of QT interval
60
What are side effects specific to paroxetine?
Congenital heart defects if taken in pregnancy
61
Which SSRI drugs inhibit CYP450 and reduce the rate of elimination of other drugs causing, potentially toxic, effects?
Fluoxetine, norfluoxetine and paroxetine
62
What is serotonin syndrome?
Serotonin accumulation which causes overstimulation of the nervous system. It usually happens when using a combination of SSRIs and other antidepressants that increase serotonin levels.
63
What are the symptoms of serotonin syndrome?
Shivering
Hyperreflexia and myoclonus (most prominent in lower extremities. Differentiates from NMS which has lead pixie rigidity)
Increased temp (in severe cases)
Vital sign abnormalities (tachypnoea, tachycardia, labile bp)
Encephalopathy (mental state changes, confusion, delirium, agitation)
Restlessness
Sweating
64
How do we treat serotonin syndrome?
withdrawal of medication and supportive care. In moderate to severe cases we may consider cyproheptadine
65
Whats the moa of cyproheptadine?
competing with free histamine and serotonin for binding at their respective receptors.
66
What are the effects of serotonin?
Serotonin plays a key role in such body functions as…
mood - more focused, emotionally stable, happier and calmer
sleep - promotes wakefulness and inhibits REM sleep. Also a precursor to melatonin
digestion - inhibits gastric acid secretion and increases gut motility to facilitate absorption after feeding
Appetite - suppresses appetite
nausea - too much serotonin can cause nausea
wound healing - causes proliferation and migration of fibroblasts
bone health - gut derived serotonin reduces the osteoblast proliferation and thus leads to bone loss and brain derived serotonin decreases sympathetic output and thus favors bone formation
blood clotting - induces constriction of injured blood vessels and enhances platelet aggregation
Inhibitory modulator of sexual desire
67
How do we get tryptophan in the body?
Through diet e.g. meat, dairy products, eggs and nuts
68
Why do SSRIs cause anxiety?
Its thought to be because of fluctuating serotonin levels during the early days of treatment
69
Why do SSRIs cause nausea?
stimulation of 5-HT3 receptors in the vomiting centre, CTZ
70
Why do SSRIs cause insomnia?
SSRIs regulate sleep-wake cycle
71
Why do SSRIs cause diarrhoea or constipation?
As they can disrupt the gut motility and gastric acid secretion = disrupts normal functioning of digestive tract
72
Why do SSRIs cause loss of appetite and weight loss?
Serotonin suppresses appetite
Loss of emotional eating as antidepressant starts to work
73
Why do SSRIs cause hyponatraemia?
Serotonin causes increase of ADH release = SIADH
74
Which population is SIADH secondary to SSRI use most likely in?
Why?
Elderly population - more vulnerable to diffiuclties in fluid level regulation
75
What are symptoms of mild and more severe hyponatraemia?
Mild symptoms include nausea, headache, muscle pain, reduced appetite, confusion.
More severe hyponatraemia can cause fatigue, disorientation, agitation, psychosis and seizures and even coma.
76
What are the contraindications of SSRIs?
manic phase of bipolar disorder.
poorly controlled epilepsy.
77
What are contraindications specific to citalopram?
With known QT interval prolongation, or congenital long QT syndrome
Concurrent use of drugs known to prolong the QT interval
78
What are contraindications specific to sertraline?
severe hepatic impairment
79
Who should you prescribe SSRIs with caution to?
A history of bleeding disorders (especially gastrointestinal bleeding).
A history of mania.
Cardiac disease.
Diabetes mellitus.
Epilepsy (discontinue if convulsions develop).
Susceptible to angle-closure glaucoma.
Hepatic impairment (prolonged half-life) — manufacturer advises dose reduction or increasing dose interval in mild to moderate impairment.
Renal impairment (citalopram and escitalopram).
Risk factors for QT-interval prolongation (citalopram and escitalopram) or hyponatraemia.
Undergoing concurrent electroconvulsive therapy.
80
With which drug combination does the most severe cases of serotonin syndrome occur?
an MAOI and an SSRI.
81
What are some possible drug interactions for SSRIs?
Antiepileptics
Antidiabetic drugs
Aspirin, NSAIDs, anticoagulants, and antiplatelets
Carbamazepine
Cocaine
Grapefruit juice
HIV protease inhibitors
Lithium
Monoamine oxidase inhibitors (MAOIs)
SNRIs (venlafaxine, duloxetine)
Tamoxifen
Other sedative drugs (alcohol, barbiturates, benzodiazepines)
Other drugs, which if taken with SSRIs may increase the risk of serotonin syndrome or neuroleptic malignant syndrome, include opioids, St John’s wort (avoid concurrent use), triptans, vortioxetine.
Drugs that cause QT interval prolongation
Concurrent use with drugs associated with hyponatraemia
82
Why do you have to be careful when using SSRIs with antiepieptics?
can reduce the seizure threshold.
83
Why do you need to be careful when prescribing an SSRI in a diabetic?
SSRIs can affect diabetic control. Monitor blood glucose when starting or stopping an SSRI.
84
What do you need to be wary of when prescribing an SSRI concurrently with anticoagulant, warfarin, aspirin, antiplatelets etc?
increased risk of bleeding if taken concomitantly with SSRIs. Consider additional INR monitoring with warfarin.
85
What happens if you take carbamazepine with sertraline?
Can decrease sertraline levels and therefore its effects
86
How can cocaine interfere with SSRIs?
possibly an increased risk of bleeding with citalopram. Prescribers should enquire about illicit drug use before prescribing SSRIs.
87
How does grapefruit juice interferes with SSRI levels?
levels of sertraline may be modestly increased.
88
What are the efefcts of using HIV protease inhibitors concurrently with SSRIs?
efficacy of SSRIs may be reduced. Monitor and adjust dose of SSRI if required.
89
What are the concerns with using lithium concurrently with SSRIs?
concurrent use with SSRI may cause serotonin syndrome or neuroleptic malignant syndrome.
In addition, lithium has been associated with QT prolongation and concomitant use may increase this risk.
90
What are the concerns with using MAOIs concurrently with SSRIs?
concurrent use is contraindicated.
Fatal reactions may occur (serotonin syndrome or neuroleptic malignant syndrome)
91
What are the concerns with using SNRIs concurrently with SSRIs?
increased risk of serotonin syndrome or neuroleptic malignant syndrome when given concomitantly with an SSRI.
Venlafaxine may also increase the risk of QT interval prolongation if taken concomitantly with an SSRI.
92
What are the concerns with using tamoxifen concurrently with SSRIs?
avoid concurrent use with fluoxetine or paroxetine.
Fluoxetine and paroxetine are potent inhibitors of the liver enzyme CYP2D6 and may reduce the plasma concentration of tamoxifen, leading to reduced efficacy
93
What are the concerns with using alcohol/barbiturates/benzos concurrently with SSRIs?
SSRIs are sedating and co-administration with other sedating drugs may have a synergistic effect.
94
What are the concerns with using opioids, st joins worts, Triptans and vortioxetine concurrently with SSRIs?
may increase the risk of serotonin syndrome or neuroleptic malignant syndrome
95
What are the concerns with using anti arrythmics/antipsychotics/sildenafil/TCAs concurrently with SSRIs?
QT interval prolongation — some SSRIs are associated with QT interval prolongation and torsade de pointes. Concurrent use with other drugs that prolong the QT interval drugs may increase the risk.
96
What are the concerns with using diuretics/NSAIDs/antipsychotics/carbamazepine/calcium channel blockers/ACEi/laxatives concurrently with SSRIs?
Hyponatraemia — increased risk if concurrent use with other drugs known to be associated with hyponatraemia
97
What are the indications for TCAs?
major depressive disorder (MDD), dysthymic disorder, chronic neuropathic pain, and migraine or tension-type headache, phobic disorders
98
What are additional indications for clomipramine?
OCD
99
What are additional indications for imipramine?
Nocturnal enuresis
100
Why are TCAs not used first line for major depressive disorder? When are they used?
Severe side effects and more dangerous in overdose
Used when other antidepressants have not worked
101
Whats the difference between secondary and tertiary TCAs?
Secondary are selective and only inhibit norepinephrine transporters
Tertiary are non-selective and inhibit serotonin transporters and norepinephrine transporters
102
What are examples of secondary/specific TCAs?
Desipramine
Protriptyline
Nortriptyline
103
What are examples of tertiary TCAs?
Amytriptyline
Imipramine
Clomipramine
Trimipramine
Doxepin
104
Which TCAs are sedating?
Desipramine
Amytryptiline
Clomipramine
Trimipramine
Doxepin
105
How long does it take after starting TCAs for improvements to be seen?
2-4 weeks
It takes time for serotonin and norepinephrine to accumulate in the synaptic cleft
106
What are the adverse effects of TCAS?
Tachycardia
Cardiac effects (QTc prolongation, arrhythmias)
Anticholinergic effects
Sexual dysfunction and sedation
107
Why do TCAs cause sedation, increased appetite, weight gain, and confusion?
As they also block H1 receptors = increased histamine
108
Why do TCAs cause orthostatic hypotension and dizzziness?
As TCAs also act as competitive antagonists on post-synaptic alpha 1 cholinergic receptors
109
What are the 3 most common side effects of TCAs?
Dry mouth
Dizziness
Constipation
110
Why do TCAs cause blurred vision, constipation, xerostomia, confusion, urinary retention, and tachycardia?
As they are competitive antagonists for cholinergic receptors
111
Whats a SE of TCAs which only affects under 24 year olds?
an increased risk of suicidal ideation and behavior in individuals age 24 or less
112
When starting a TCA what should you be screened for?
screening for pre-existing cardiac conditions, including prolonged QTc intervals, heart disease, and a family history of arrhythmias
worsening depressive symptoms or new-onset suicidal thoughts or behaviors
113
Which group of antidepressants should TCAs not be used with because of a risk of developing serotonin syndrome?
MAOIs
114
What are the 3 most common causes of death when taking TCAs?
Convulsion
Coma
Cardiotoxicity
115
Why should TCAs be used in caution in elderly?
As they can worsen dementia, narrow angle glaucoma, cardiac conduction abnormalities, prostatitis and urinary retention
116
Although all dangerous in overdose, which TCA has the best safety profile?
Lofepramine
117
What are the contraindications of TCAs?
arrhythmias, heart block
immediate recovery period after MI
severe hepatic impairment
manic phase of bipolar
when taking MAOI
severe renal impairment (lofepramine)
acute porphyria (lofepramine)
118
When should you prescribe TCAs with caution?
history of bipolar or psychosis
increased risk of suicide
CVD
older age
chronic constipation
epilepsy
DM
hepatic impairment
hyperthyroidism
susceptibility to angle-closure glaucoma
phaeochromocytoma
prostatic hypertrophy
urinary retention.
119
Why should you prescribe TCAs with caution to people with hyperthyroidism or phaeochromocytoma?
Both have a risk of arrhythmias
120
What are the possible drug interactions associated with TCAs?
Clonidine
lithium
MAOIs
other sedative drugs
phenothiazines
SSRIs and SNRIs
Tramadol
warfarin
drugs which prolong QT interval
drugs which increase levels of TCAS
drugs which decrease levels of TCAs
121
Which drugs can increase levels of TCAs?
Antifungal, bupropion, climetidine, diltiazem, verapamil, HIV protease inhibitors
122
What drugs can reduce the levels of TCAs?
carbamazepine, phenobarbital and rifampicin
123
Which drugs can prolong the QT interval and therefore should be a contraindication for considering taking TCAs?
Antiarrhythmics
Antipsychotics
Olanzapine
Clozapine
Domperidone
Hydroxyzine
Mizolastine
Sotalol
124
How might TCAs interact with clonidine?
Antihypertensive effects may be reduced
125
How might TCAs interact with lithium?
Neurotoxicity
Serotonin syndrome
Neuroleptic malignant syndrome
QT interval prolongation
Tornadoes de pointes
126
How might TCAs interact with other sedative drugs?
TCAs are sedating and co-administration with other sedating drugs may have a synergistic effect.
127
How might TCAs interact with phenothiazines?
Concentrations of both drugs may be increased, increasing the risk of tardive dyskinesia and antimuscarinic adverse effects. In addition, risk of QT interval prolongation if both drugs are taken concomitantly.
128
How might TCAs interact with SSRIs?
TCA concentrations may be increased leading to adverse effects. SSRIs and SNRIs are also associated with QT interval prolongation, possibly increasing the risk of arrhythmias
129
How might TCAs interact with Tramadol?
Increases risk of serotonin syndrome
130
How might TCAs interact with warfarin?
May affect prothrombin time
131
Why are MAOIs not used as first line treatment for depression?
due to safety and tolerability concerns and the need for dietary restrictions
132
Which type of depression are MAOIs particularly good at treating?
Atypical depression
Phobias
133
Whats the function of monoamine oxidase A?
Metabolises the neurotransmitters serotonin, epinephrine, norepinephrine, and dopamine
134
Whats the function of monoamine oxidase B?
Metabolises dopamine
135
Whats the function of monoamine oxidase inhibitors?
They inhibit MAO A and/or MAO B = prevents metabolism of neurotransmitters = increased levels of serotonin, NE, epinephrine and dopamine
136
What are non-selective MAOIs?
inhibit MAO A and MAO B so increase serotonin, NA and dopamine levels.
137
What are selective MAOIs and what are they used to treat?
Inhibits MAO B only = increases dopamine levels
Used to treat Parkinson’s disease and alzheimers
138
How long do you have to have stopped MAOIs for before staring another antidepressant?
2 weeks
3 weeks if clomipramine or imipramine
139
What are the side effects of MAOIs?
Muscarinic (anticholinergic side effects)
Anxiety/agitation
Orthostatic hypertension
Insomnia
140
Which MAOIs are approved to treat depression?
Isocarboxazid (Marplan)
Phenelzine (Nardil)
Selegiline (Emsam)
Tranylcypromine (Parnate)
141
When is hypertensive crisis caused by MAOIs usually seen?
When MAOIs are combined with tyramine rich food and drinks e.g. aged cheese, red wine, fermented soy products
142
Why can MAOIs cause a hypertensive crisis?
Usually, within the gut wall, monoamine oxidase A and B break down tyramine so when these are inhibited, more tyramine is absorbed and concentration increases. tyramine promotes the efflux of catecholamines from the sympathetic nervous system and the adrenal medulla increasing arterial blood pressure and heart rate by peripheral vasoconstriction, resulting in hypertensive crisis.
143
What is a hypertensive crisis?
a sudden, severe increase in blood pressure. The blood pressure reading is 180/120 millimeters of mercury (mm Hg) or greater. A hypertensive crisis is a medical emergency. It can lead to a heart attack, stroke or other life-threatening health problems.
144
What are examples of augmenting agents for depression?
lithium, lamotrigine, or triiodothyronine
Or…
Specialist drug options include combining an antidepressant with a second-generation antipsychotic (such as aripiprazole, olanzapine, quetiapine, risperidone)
145
Why does lithium require close monitoring?
It has a very narrow therapeutic widow
Check every 5 days at the start and then every 3 months - check thyroid and renal function
146
In which situations is it very easy to overdose on lithium?
Impaired renal function
Using drugs that decrease GFR e.g. ACEi, NSAIDs, diuretics
As lithium is almost exclusively eliminated by the kidneys so wont be eliminated efficiently
147
What are the side effects of lithium?
Leukocytosis
Insipidus (polyuria and polydypsia)
Tremor (fine) and tired
Hypothyroidism and hyperparathyroidism
Increased weight
Upset tummy (nausea, vomiting, diarrhoea)
Metallic taste (+dry mouth) and muscle weakness (rhabdomyolysis)
148
Why can lithium cause nephrogenic diabetes insipidus ?
Chronic lithium use can damage renal tubules in collecting ducts = resistance to ADH
149
Why can lithium cause hypothyroidism?
Lithium is concentrated by the thyroid and inhibits thyroidal iodine uptake. I
t also inhibits iodotyrosine coupling, alters thyroglobulin structure, and inhibits thyroid hormone secretion
150
Why can lithium cause hyperparathyroidism?
Lithium elevates parathyroid hormone by raising the threshold of the calcium sensing receptor
151
Why is lithium not safe in pregnancy?
As it increases the risk of congenital heart defects
152
What are the effects of lithium toxicity?
diarrhoea, vomiting, anorexia, muscle weakness, lethargy, dizziness, ataxia, lack of coordination, tinnitus, blurred vision, coarse tremor of the extremities and lower jaw, muscle hyper-irritability, choreoathetoid movements, dysarthria, and drowsiness.
Severe - hyper-reflexia and hyperextension of limbs, syncope, toxic psychosis, seizures, polyuria, renal failure, electrolyte imbalance, dehydration, circulatory failure, coma, and occasionally death.
153
What is tryptophan licensed for?
Treatment-resistant depression
154
What is vortioxetine?
An antidepressant that directly modulates serotonergic receptor activity and inhibits the re-uptake of serotonin. Suitable for those whose condition has responded inadequately to 2 antidepressants within the current episode
155
What is St. John’s wort and why do doctors not recommend it?
herbal treatment (botanical name is Hypericum perforatum) that may help mild to moderate depression. There amount of active ingredients varies among individual brands and batches so its not recommended by doctors.
156
How do you stop antidepressants and why?
Slowly over 4 weeks to prevent withdrawal symptoms
157
What are withdrawal symptoms of antidepressants?
Flu-like sympotms (sweating, GI upset)
Imbalance/unsteady
Nausea
Insomnia
Sensory disturbance (hallucinations or strange dreams)
Hyperarousal (agitation and anxiety)
these symptoms usually come on within 5 days of stopping the medicine and generally last 1-2 weeks but they can last months.
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What are indications for inpatient admissions for depression?
• distressing hallucinations or delusions or other psychotic phenomena
• Active suicidal ideation or planning, especially if suicide has previously been attempted or many risk factors for suicide are present
• Lack of motivation that has led to self neglect
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What is IAPT?
Improving access to psychological therapy - provide evidence-based psychological therapies to people with anxiety disorders and depression.
160
What are the indications of ECT for the treatment of depression?
Acute treatment for severe depression that is life-treating and when a rapid response is required, or when other treatments have failed.
161
When should you consider a repeat trial of ECT after depression has not responded well to a previous course of ECT?
After…
reviewing the adequacy of the previous treatment course and considering all other options and discussing the risks and benefits with the person and/or, where appropriate,
their advocate or carer.
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What do you have to consider discussing with the pt when considering ECT for treating depression
Risks associated with a general anaesthetic
Potential adverse events
Risks associated with not recieving ECT
163
In which group should you exercise particular caution when considering ECT and why?
Older people
As risks are greater
164
Outline the difference with bilateral and unilateral ECT?
bilateral ECT is more effective than unilateral ECT but may cause more cognitive impairment
with unilateral ECT, a higher stimulus dose is associated with greater efficacy, but also increased cognitive impairment compared with a lower stimulus dose.
165
Outline monitoring needed with ECT?
Assess clinical status after each treatment
Stop treatment when remission has been achieved
Stop if side effects outweighs potential benefits
Assess cognitive function before first ECT and monitor at least every 3/4 treatments and at the end of a course of treatment
If there is evidence of significant cognitive impairment consider changing from bilateral to unilateral electrode placement, reduce the stimulus dose, stopping treatment
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What should assessment of cognitive function in ECT monitoring include?
orientation and time to reorientation after each treatment
measures of new learning, retrograde amnesia and subjective memory impairment
(most do Addenbrooke’s cognitive assessment)
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What are advantages of ECT?
Effective when other treatments don’t work
Most effective with most severe illness
168
What are disadvantages of ECT?
Multiple brief anaesthetics
Acute confusional states
Memory impairment: anterograde and retrograde
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Whats the problem with a dose being too low in ECT?
Ineffective or confusion
170
Whats the problem with a dose being too high in ECT?
Less effective
Confusion
171
What is the seizure threshold?
defined as the minimum amount of electrical energy that is required to induce cerebral seizure activity of a defined length
172
Which groups of people have a higher seizure threshold?
men and older people
173
Which medicines interfere with ECT?
Anticonvulsants and lithium
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What are the short term adverse effects of ECT?
Headache
Muscle aches
Nausea
Distressed, tearful, frightened
Temporary loss of memory
Confusion
Damage to tongues, teeth, lips due to contraction for jaw muscles
175
What are the long term adverse effects of ECT?
Memory problems - 1/10
Feelings that their personalities have changed, lost skills, no longer the person they were before
176
What proportion of people with severe depression commit suicide?
15%
177
Whats the difference between mood and affect?
mood refers to a more pervasive and sustained emotional 'climate', whereas, affect refers to more fluctuating changes in the emotional 'weather'.
178
Whats the mean age of onset for mood disorders?
17
179
Whats the average length of a depressive episode?
6-8 months
180
How long must you have a depressed mood for for a diagnosis of dysthmia?
2 years
181
What sleep disorders are common in depression?
Insomnia
HYPERSOMNIA - more common in young adults
Early morning wakening
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What are common delusions in depression?
Delusions of ill health
Delusions of guilt
Nihilistic delusions
Delusions of enormity
183
What are the 3 depressive disorderS?
Single episode depressive disorder
Recurrent depressive disorder
Dysthymia disorder
184
How do depression symptoms tend to vary in the day?
Normally worse in the morning - diurnal variation
185
How does depression tend to present in developing countries and why?
As somatic preoccupation because of the stigma and taboo surrounding mental illness
186
What is catatonic depression?
Severe depression with mutism and stupor i.e. they do not respond to what is happening around them, may be silent and motionless
187
What is double depression?
A complication of dysthymic disorder where the pt experiences worsening symptoms leading to the onset of a full syndrome of major depression superimposed on their dysthymic disordet
188
How is SAD diagnosed?
your depression occurs at a similar time each year for at least 2 years
the periods of depression are followed by periods without depression
189
What are the aetiological factors fo depression?
Biological - genetics, neurological, hormonal, immunological and neuroendocrinological
Psychoglocial - negative patterns of thinking, deficits in coping skills, judgement kills, impaired emotional intelligence
Social - experiencing traumatic situations, early separation, lack of social support, or harassment (bullying)
190
What are the Brown and Harris vulnerability factors for depression?
Risk factors
- early maternal loss
- lack of a confiding realtionship
- >3 children under the age of 14 at home
- unemployment
191
What is learned helplessness theory?
the view that clinical depression and related mental illnesses may result from a real or perceived absence of control over the outcome of a situation
192
What is becks cognitive triad?
thoughts about self, world, and future. In all the three instances, depressed individuals tend to have negative views
193
What is selective abstraction?
type of cognitive bias or distortion in which a detail is taken out of context and believed while everything else in the context is ignored.
E.g. Someone attends a party and afterward focuses on the one awkward look directed her way and ignores the hours of smiles.
194
What is selective magnification/minimisation ?
Exaggerating the negative and minimising the positive (blowing things out of proportion or shrinking their importance)
195
What is the neurotrophic hypothesis of depression?
depression results from decreased neurotrophic support (i.e. low BDNF), leading to neuronal atrophy, decreased hippocampal neurogenesis and loss of glia
196
What is mindful-based cognitive therapy?
A therapy that teaches mindfulness techniques to allow the pt to be more aware of their thoughts and emotions
It’s based on the idea that depression is maintained by negative thought processes
