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Year 4 Psych > Affective Disorders > Flashcards

Affective Disorders Flashcards

1
Q

How common is depression?

A

Prevalence 2-5%

1/5 will suffer at some point in their lives

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2
Q

Is depression more common in F or M?

A

2:1 F:M

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3
Q

What is the pathophysiology of depression?

A

Monoamine (MA) theory - depression associated with reduced noradrenaline or serotonin in brain

Antidepressants inhibit breakdown of MA rapidly but clinical improvements can take weeks

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4
Q

List the monoamine neurotransmitters

A

Imadazoleamines - histamines

Catecholamines - adrenaline, noradrenaline, dopamine

Indolamines - serotonin, melatonine

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5
Q

What are the core symptoms of depression?

A

1) Depressed mood for most of the day, every day
- Little variation in mood despite changes in time, circumstances or activity
- Possible diurnal variation (worse in morning and improving throughout day)

2) Anhedonia
3) Fatigue

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6
Q

What are the typical symptoms of depression?

A

Biological:
1) Poor appetite with marked unintentional weight loss
- >5% in past month
(Rarely inc appetite and weight gain)
2) Disrupted sleep
- Initial insomnia with early waking (3+ hrs)
3) Psychomotor retardation eg sluggish thought processes, limited spontaneous movement or restlessness
4) Decreased libido
5) Inability to concentrate

Plus:

6) Feelings of worthlessness or inappropriate guilt
7) Recurrent thoughts of death, suicidal ideation or suicide attempts

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7
Q

What is needed to diagnose depression?

A

At least 2 core symptoms + 2/more typical symptoms

Symptoms present every or nearly every day without significant changes throughout the day for over 2 weeks

Must represent a change from normal personality without alcohol/drugs, medical disorders or bereavement

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8
Q

List the ICD-10 categories for mild, moderate, severe depression

When should this be used?

A 
Mild = 2 x core + 2 x typical
Moderate = 2 x core + 3(+) typical
Severe = 3 x core + 4(+) typical

First episode (further depressive episodes classified as recurrent depressive disorder)

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9
Q

List some ddx for depression

A

Psych - dysthymia, bipolar disorder, schizophrenia, anorexia nervosa, anxiety

Neuro - dementia, PD, HD, MS, stroke

Metabolic - hypoglycaemia, hypercalcaemia

Haem - anaemia

Inflammatory - SLE

Infections - syphilis, Lyme disease, HIV encephalopathy

Medications - anti-HTN, steroids, H2 blockers, sedatives, antipsychotics

Substance misuse - alcohol, BDZ, opiates

Sleep disorders

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10
Q

What psychotic symptoms may someone with depression suffer from?

A

Delusions eg poverty, guilt over things which could not be their fault, punishment, nihilism

Hallucinations eg auditory (accusatory, cries for help), olfactory (rotten food, faeces), visual (demons, corpses etc)

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11
Q

What investigations should be done for depression?

A

Bloods

  • FBC: anaemia
  • ESR
  • B12/ filate
  • TFTs
  • Glucose
  • Calcium
Urine toxicity
Syphilis serology
HIV
Dexamethasone suppression test
ACTH stimulation
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12
Q

What is the dexamethasone suppression test?

A

Dexamethasone reduces ACTH release in normal people

Thus taking dexamethasone should reduce ACTH and lead to decreased cortisol

Cortisol is measured either overnight (more common) or standard (3 days) after administration of dexamethasone

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13
Q

Why may pt with depression present with an abnormal dexamethasone suppression test?

A

NA inhibits corticotropin releasing factor, thus decreasing ACTH secretion by the pituitary, and in turn, cortisol secretion by the adrenal glands

Deficiency of brain NA can lead to both depressive symptoms and increased cortisol production

Episodes fo cortisol secretion are longer and more frequent in depressed patients, and the circadian rhythm of cortisol release is altered

Dexamethasone does not suppress plasma cortsol levels in pts cvs normal subjects

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14
Q

What is ACTH stimulation?

A

aka cosyntropin test / syncathen test

Measures the response of adrenal glands to ACTH (should release cortisol)

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15
Q

List some biological causes of depression (7)

A

1) Genetic serotonin transporter gene (FH++)
2) Abnormal concentrations of serotonin and other NTs
3) Disregulation of the HPA axis
- Inc cortisol in 50%
- Linked to adrenal hypertrophy and failed dexamethosone suppression test

4) Hypothyroidism
5) Postnatal
6) Chronic pain
7) Medications

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16
Q

List some psychological causes of depression (7)

A

1) Childhood trauma
2) PTSD
3) Low self esteem
4) Stress, lack of coping, lack of resilience
5) Attitudes and beliefs
6) Anxiety and guilt
7) Burden of chronic disease / comorbities

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17
Q

List some social causes of depression (8)

A

1) Isolation
2) Bereavement
3) Stress
4) Abuse
5) Relationships
6) SES
7) Homelessness
8) Education

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18
Q

List antidepressants which may be used in the management of depression

A

SSRIs = first line
SNRI - Serotonin noradrenaline re-uptake inhibitors
NARI - Noradrenaline re-uptake inhibitor
TCA - Tricyclics
MAOIs - Monoamine oxidase inhibitors
NASSA - Nonadreneric and specific serotonergic antidepressants

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19
Q

Give some examples of SSRIS

A 
Fluoxetine
Citalopram
Escitalopram
Sertraline
Fluvoxamine
Paroxetine
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20
Q

In which populations are SSRIs more commonly used?

A

Elderly
Anxiety
OCD

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21
Q

What are some side effects of SSRIs?

A

Nausea and vomiting common
Agitation
Sexual dysfunction - 70% affected and difficult to treat

Also dizziness, dry mouth, blurred vision

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22
Q

Which SSRIs prolong the QT interval?

A

Citalopram

Escitalopram

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23
Q

What is serotonin syndrome?

A

Acute toxic syndrome due to increased 5HT activity

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24
Q

How does serotonin syndrome present?

A 
Confusion
Myoclonic jerks and hyperreflexia
Pyrexia and sweating
GI symptoms
Mood changes and mania
Convulsions
Death
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25
Q

When can serotonin syndrome occur?

A

Within a few hours of SSRI dose or dose changes

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26
Q

How is serotonin syndrome managed?

A

Symptomatic support

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27
Q

Give some examples of TCAs

A

Amitriptyline
Imipramine
Lofepramine
Dosulepin

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28
Q

How do TCAs work?

A

5HT and NA reuptake inhibition
Anticholinergic effects
Antihistaminergic effects

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29
Q

What are some side effects of TCAs?

A

Cardiotoxic:

  • QT prolongation
  • ST elevation
  • AV block

Alpha adrenergic blockade:

  • Postural HTN
  • Sedation
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30
Q

What are some risks of TCAs?

A

Increased risk of manic switch in bipolar disorder

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31
Q

In which populations are TCAs less useful?

A

Elderly
Physically ill
Overdose risk pt

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32
Q

What is the mechanism of action of MAOIs?

A

Inhibition of MAO-A and MAO-B

MAO-A metabolises NA, 5HT and tyramine

MAO-B metabolises DA and tyramine

Thus increase storage and release of 5HT and NA

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33
Q

Give some examples of MAOIs

A

Phenelzine

Tranylcypromine

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34
Q

What are some side effects of MAOIs?

A 
Postural HTN
Restlessness
Oedema
Nausea
Sexual dysfunction
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35
Q

What interaction is important to note for those taking MAOIs?

A

Interaction with tyramine containing foods

  • Cheese
  • Yeast extracts
  • Hung game
  • Some alcoholic drinks eg red wine
  • Pickled herring
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36
Q

What is tyramine?

A

Naturally occurring monoamine compound and trace amine derived from the amino acid tyrosine

It is a catecholamine releasing agent

Unable to cross BBB thus is can only lead to non-psychoactive peripheral sympathomimetic effects

However a HTN crisis can result from ingestion of tyramine rich foods in conjunction with MAOI

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37
Q

What happens when someone taking MAOIs ingests foods rich in tyramine?

A

Tyramine is not inactivated by MAO

Tyramine causes catecholaime release = tachycardia, sweating, HTN, arrythmias, stroke, death

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38
Q

What are venlafaxine and duloxetine?

A

Serotonin and NA reuptake inhibitors

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39
Q

How do SNRIs work?

A

Dual action reuptake inhibitors

NA reuptake is only seen at higher doses

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40
Q

Which SNRI can cause HTN at higher doses?

A

Venlafaxine

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41
Q

Compare SNRIs and TCAs

A

SNRIs = ‘cleaner’ and safer in OD than TCAs

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42
Q

What is mirtazapine?

A

Noradrenergic and specific serotonergic antedepressant (NASSAs)

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43
Q

How does mirtazazapine work?

A

Presynaptic alpha 2 autoreceptor antagonist = thus enhances NA transmission

More sedative at LOWER doses due to its antihistaminergic effect predominating over its noradrenergic effects - useful in pt who cannot sleep

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44
Q

What are some side effects of mirtazapine?

A

Stimulates appetite, causes weight gain (may be useful in some pt), sedation classic (take at night)

LACKS CV and anticholinergic side effects

Less incidence of sexual dysfunction

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45
Q

What is the onset of action of antidepressants?

A

Myth that they do not exert effects for 2-4wks

ALL antidepressants show a pattern of response where rate of improvement is highest during weeks 1-2 and lowest during weeks 4-6

If no effect by 3-4 weeks, consider switching

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46
Q

What does the term discontinuation symptoms describe? When do they occur?

A

Used to describe symptoms experienced on stopping prescribed durgs that are not drugs of dependence = NOT WITHDRAWAL

Onset usually within 5 days of stopping treatment

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47
Q

List classic discontinuation symptoms

A 
Flu-like symptoms
Insomnia
Agitation
Irritability
Shock-like sensations
Vivid dreams
48
Q

Which drugs most commonly cause discontinuation symptoms?

A

Drugs with shorter half lives

Eg immediate release venlafaxine, paroxetine

49
Q

How can discontinuation symptoms be avoided?

A

Discontinue antidepressant slowly - ie over 4 week period

50
Q

How should antidepressants be swapped / stopped?

A

Avoid abrupt withdrawal

Cross-tapering is preferred = old drug is slowly reduced and the new one is slowly increased

  • Speed judged by pt tolerability
  • Not always necessary eg when switching from one SSRI to another (if you cross-tapered there would be a risk of serotonin syndrome)
  • Not appropriate sometimes eg MAOIs to TCAs
51
Q

What must be warned to pt starting antidepressants?

A

Motivation improves before mood and this leads to a period of increased risk where people might suddenly have the motivation to act on suicidal ideation

52
Q

What is the electrolyte risk with antidepressants? Who is more at risk?

A

Hyponatraemia

Inc risk in older, thin females in the summer with poor renal function

53
Q

What length of treatment is recommended for antidepressants?

A

Don’t have to be on it forever

Usually recommended person stays on it for 6-9mnths following recovery

If it is not the first time then consider being on it for 2yrs

54
Q

Other than antidepressants, what biological treatment options are available for depression?

A

Augmentation of antidepressants with:

  • Lithium
  • Other antidepressants (combination therapy)
  • Antipsychotics

Thyroxine
ECT

55
Q

What are the indications for lithium?

A

Mania - treatment and prophylaxis
Bipolar affective disorder
Recurrent depression
Aggressive or self-mutilating behaviour

56
Q

What are the pharmacokinetics of lithium?

A

Clearance is via kidney thus clearance depends on renal function, fluid intake and sodium intake

  • Should monitor levels 12hrs after last dose
57
Q

What baseline investigations should be performed before starting lithium?

A 
Weight
U&Es
Renal function
TFTs
Calcium
ECG
Pregnancy test
58
Q

How frequently should lithium levels be monitored?

A

Check 5 days after 1st dose
Then check every week until levels have been stable for 4 weeks
After than check every 3 months

Renal function, U&Es, thyroid and calcium should be checked every 6 months

59
Q

What are some side effects of lithium?

A

Early:

  • Dry mouth
  • Metallic taste
  • Nausea
  • Fine tremor
  • Fatigue
  • Polyuria
  • Polydipsia

Late:

  • Nephrogenic diabetes insipidus
  • Kidney damage with long term treatment
  • Hypothyroidism
60
Q

What drug interactions are associated with lithium?

A

Narrow therapeutic index (0.4-1mmol/L)

Most clinically significant interactions are with drugs that affect sodium handling:

  • ACEi
  • NSAIDs
  • Thiazide diuretic
61
Q

What is the mechanism of action of lithium?

A

Only partially understood

Increases synthesis and release of 5HT

Range of effects on CNS

Handled by body in similar way to sodium

May have neuroprotective effects

Takes approx a week to work

62
Q

What are symptoms of lithium toxicity?

A

Early:

  • Blurred vision
  • Anorexia
  • N&V&D
  • Coarse tremor
  • Ataxia
  • Dysarthria

Late:

  • Confusion
  • Renal failure
  • Fits
  • Delirium
  • Death
63
Q

What is ECT?

A

Electroconvulsive therapy

Very good evidence base

Electrical currents sent through brain to induce seizures

A short acting GA and muscle relaxant administered

64
Q

How often is ECT performed?

A

2 x weekly therapies for 6 weeks

65
Q

What are some side effects of ECT?

A

Headache
Nausea
Muscle pain
Memory loss around time of seizure (both retrograde and anterograde)

66
Q

What are some psychological management options for depression?

A

Mainly for mild-moderate (medication not indicated):

  • Advice on sleep hygiene
  • Physical exercise
  • CBT
  • Self help books

Moderate-severe:

  • CBT (8-12 sessions over 2-3 months)
  • IPT (interpersonal therapy)
  • Combination of psychosocial and biological management
67
Q

What is IPT? How many sessions are recommended?

A

Aims to help the person with their relationship with others - how they are interacting with and relating to other people

Brief = 16-20 session

68
Q

What is CBT?

A

Based on cognitive behavioural model - it is not the event that causes problems but instead how we respond to it

Tries to spot patterns in behaviour and attitudes that might lead to the symptoms of depression and then try to break these patterns down by changing things that CAN be controlled

  • ie your behaviour when you experience a certain trigger
  • Try and change the response so that you’re not feeding into the negative pattern of behaviour
69
Q

List some cognitive biases

A

1) Catastrophising
2) Jumping to conclusions
3) All or nothing view
4) Personalising (it went wrong and it must have been something I did)
5) Generalising (one bad thing going wrong means everything will go wrong)

70
Q

What are some social management options for depression?

A

Friends and family education
Community and voluntary organisations
Selt help
IAPT = Improving access to psychological therapies

71
Q

What are the tiers of making a referral to secondary care for depression?

A

Tier 1 - GP
Tier 2 - Primary care mental health worker (PCMHW)
Tier 3 - Community mental health team (CMHT)
Tier 4 - Inpatient or home treatment

Exceptions - risk to self or others, severe functional impairment, indication for specialist treatment

72
Q

What is the prognosis of depression?

A

Average depressive episode = 6 months

80% pt have recurrent episodes

Approx 10% have manic episodes and become bipolar

Suicide 13%

73
Q

What are some medical causes of mania? (14)

A 
Cerebral neoplasms, infarcts
Trauma, infection (inc HIV)
Cushing's disease
Huntington's disease
Hyperthyroidism
MS
Renal failure
SLE
Temporal lobe epilepsy
Vit b12 and niacin deficiency
74
Q

What are some substances which can cause mania? (11)

A

1) Amphetamines
2) Anticholinergics
3) Antidepressants
4) Antiviral drugs
5) Antimalarials
6) Captopril (ACEi)
7) Cimetidine
8) Cocaine
9) Corticosteroids
10) Hallucinogens
11) L-dopa

75
Q

How does mania present? (timeframe)

A

Usually begins abruptly with 3/more characteristic symptoms of mania lasting for > 1 week

76
Q

What are some biological symptoms of mania?

A

Decreased need for sleep

  • Usually one of the earliest warning signs
  • Can be a few hrs to no sleep
  • Not associated with fatigue

Increased energy

  • Increased goal directed activity
  • When coupled with impaired judgement can lead to reckless behaviour, inc risk taking eg gambling, drugs, sexual encounters
77
Q

What are some cognitive symptoms of mania?

A

Elevated mood

  • Lability likely
  • “Finally seeing things clearly”
  • “On top of the world”

Elevated sense of self or grandiosity
- Hypomanic pt may overestimate abilities or social / financial status

Poor concentration
- Can be identified in thought content, thoughts may not be linear and going off on tangents

Accelerated thinking

  • When thoughts are associated but expressed rapidly in.a stream of ideas = flight of ideas
  • Pressurised speech

Impaired judgement and insight

78
Q

What are some psychotic symptoms of mania?

A

Disordered thought form:

  • Most commonly circumstantiality = focus of conversation drifting, over-inclusion of details but often coming back to the point
  • Tangentiality = initial train of thought is diverted from but does not come back to the point

Secondary delusions = ones that develop in response to another psychopathological state (abnormal mood). It is understandable how the delusion occurred when one examines the pt mental state
- Eg grandiose delusions in pt with elevated mood

Perceptual disturbance

  • Things appearing louder = hyperacusis
  • Colours seem brighter = visual hyperaesthesia
79
Q

What is a distinguishing symptom between mania and hypomania?

A

Psychotic symptoms such as auditory and visual hallucinations

80
Q

What is hypomania?

A

A lesser degree of mania with 3 / more symptoms lasting at least 4 days

Not severe enough to interfere with social / occupation or require hospital admission

No psychotic symptoms

81
Q

Outline MSE findings in someone presenting with mania

A

A&B

  • Bright unusual combination of clothing
  • Hyperactive, aggressive, flirtatious or overfamiliar behaviour

Speech
- Pressurised speech, neologisms

Mood
- Euphoric, irritable, labile

Thought form
- Racing, flight of ideas, loosening of associations, tangential

Thought content
- Optimistic, grandiose delusions

Perceptions
- Hallucinations if severe

Cognition

  • Intact
  • Poor attention and concentration

Insight
- Very poor

82
Q

What is the biological management of mania?

A

Compulsory admission

1st line = Lithium
- 80% response rate for mood stabilisation

Antipsychotics

  • Olanzapine or respiradone
  • Useful in severely agitated pt to allow recovery before starting them on long term mood stabiliser

BDZs
- May stabilise pt without need for antipsychotics

Stop antidepressants

Anticonvulsants eg carbamazepine / valproate

ECT if drug resistance

83
Q

What is the psychosocial management of mania?

A

Education to recognise the importance of lifestyle changes

  • Avoid triggers
  • Sleep well
  • Importance of compliance
84
Q

What is the prognosis of mania?

A

Average length of manic episode is 4 months

85
Q

What assessment should be done for someone presenting with mania?

A

If already on lithium - check blood level for adherence

Bloods - FBC, U&Es, TFT, LFT, Vit B12, folate

CT head and EEG

Urine - dip and drugs screen

Assess risk - suicide, self harm, to others, from others

86
Q

How common is bipolar affective disorder (BAD)?

A

Approx 1%

87
Q

Is BAD more common in M or F?

A

M=F

88
Q

How do first episodes of BAD differ in M and F?

A

M first episode usually manic

F first episode usually depressive

89
Q

What is the mean age of onset of BAD?

A

21yrs

>51yrs = more likely to have an organic cause

90
Q

What is the aetiology of BAD?

A

Neurochemical abnormalities (monoamine theory)

  • Inc levels of NA, DA, 5HT can cause neuronal insults
  • Thus cocaine and amphetamines exacerbate mania
  • Environemtal stressors and exogenous steroids can affect hormones = thus glucocorticoids may be implicated

Genetics

  • First degree relative have 7x risk od developing
  • Children of bipolar parents have 50% chance of psychiatric disorder

Seasonal
- More onset in late spring and summer

91
Q

What is the ICD-10 criteria for BAD?

A

1) Elevated mood, irritable mood, lability
2) Inc energy levels, over-activity
3) Distractibility, reduced concentration, constant change of plans
4) Perceived reduced NEED for sleep
5) Inflated self-esteem / grandiosity
6) Overfamiliarity / disinhibition
7) Reckless behaviour / overspending
8) Inc in sex drive
9) Flight of ideas
10) Psychotic symptoms

= 2 x episodes of seriously seriously disturbed mood

92
Q

What is bipolar I and II?

A

Bipolar I - one or manic episodes with/without one or more depressive episodes

Bipolar II - one or more depressive episodes with AT LEAST ONE manic / hypomanic episode

93
Q

How long should a manic, hypomanic or depressive episode last in BAD?

A

Manic = 1 week

Hypomanic = 4 days

Depressive = 2 weeks

NB patients with manic or hypomanic episodes can be diagnosed with BAD even in the absence of depressive episodes

94
Q

What is a mixed episode in BAD?

A

Contain both manic / hypomanic and depressive symptoms in a single episode, lasting at least 2 weeks:

  • Depression plus overactivity / pressured speech
  • Mania plus reduced energy / libido
95
Q

What is rapid cycling in BAD? More common in F or M?

A

4 / more episodes in a year

More common in F

96
Q

What is cyclothymia?

A

Usually begins in early adulthood and follows a chronic course with intermittent periods of wellness in between

Characterised by instability of mood resulting in alternating periods of mild elation and mild depression that are not severe or long enough to meet criteria for either a hypomanic or depressive episode

97
Q

What is the management of BAD?

A

Depends on nature of presenting episode

Mania - antipsychotics to stabilise followed by mood stabiliser

Depressive - antidepressants augmented by a mood stabiliser (use with caution as risk of inducing manic episode and / or rapid cycling)

Follow up 4 weeks after

Psychosocial therapies can help to identify trigger factors for relapse

Psychosocial therapies can help to identify trigger factors for relapse eg CBT

Hospital admission if severe

98
Q

What is a mood stabiliser?

A

Term applied to lithium, anticonvulsant drugs and some atypical drugs used to treat BAD

Refers to the ability of a drug to treat one or both poles of bipolar disorder without causing a switch to the other pole

99
Q

List 4 mood stabilisers

A

1) Lithium
2) Carbamazepine
3) Sodium valproate
4) Lamotrigine

100
Q

How does carbamazepine work?

A

Blocks voltage dependent sodium channels thus inhibiting repetitive neuronal firing

Reduces glutamate release and decreases turnover of DA and NA

Similar structure to TCAs

101
Q

What interactions does carbamazepine have?

A

Hepatic enzyme inducer so lots of interactions

Both carbamazepine and clozapine can cause agranulocytosis

102
Q

What are some side effects of carbamazepine?

A 
Dizziness
Diplopia
Drowsiness
Ataxia
Nausea
Headaches
Blood dycrasias
103
Q

How does sodium valproate work?

A

Inhibits catabolism of GABA

104
Q

When is sodium valproate used?

A

Effective in treatment of mania and thought to reduce aggression in other psychiatric disorders

105
Q

What is a benefit of sodium valproate?

A

No routine plasma level monitoring

106
Q

What are some side effects of sodium valproate?

A 
Blood dycrasias
Weight gain
Hair loss with curly regrowth
Pancreatitis
Sedation
Dose related tremor
Thrombocytopenia - unusual bleeding / bruising

+ MAJOR human teratogen so not really used in women of childbearing age

107
Q

What is a risk associated with lamotrigine?

A

SJS

108
Q

What is a standard starting and max dose of:

1) Sertraline
2) Citalopram

A

1) Sertaline - 50mg OD (can increase in 50mg incrrements up to 200mg)
2) Citalopram - 20mg up to max 40mg

109
Q

Outline the ATHLETICS pneumonic for drugs counselling

A 
Action
Timeline
Length of treatment
Effects (time before felt)
Tests
Important SE
Complications and Contraindications
Supplementary advice
110
Q

Outline ATHLETICS for SSRIs

A

A - Antidepressants alter the balance of some of the chemicals in the brain (neurotransmitters). SSRI antidepressants mainly affect a neurotransmitter called serotonin. An altered balance of serotonin and other neurotransmitters is thought to play a part in causing depression and other conditions
T - OD
H - Tablet
L - stop 3-6 months after feeling better (taper off)
Effect - 4-6wks
T - none
I - GI (n&v&d), headaches, drowsiness (can take at night), anxiety for 2w, withdrawal, hyponatraemia
C - CI if suicide risk of past psych illness
Caution in pregnancy
S - mind.org.uk

111
Q

What must be warned for pt starting SSRIs <30yr?

A

Motivation increases before mood

Increased risk of suicide / impulsive behaviours in first few weeks

112
Q

Outline ATHLETICS for lithium

A

A - Mood stabiliser. Exact mechanism unknown.
Thought to enter the cells and interfere with neurotransmitter release and second messenger systems
T - One or twice daily depending on brand
H - Tablet, capsule or syrup
L - lifelong (if works, regular reviews by psychiatrist)
E - 1-2 weeks
T - Before starting = FBC, U&Es, TFTs, beta-HCG, ECG
Check lithium after 5 days, then every week until stable for 4 weeks, then every 3 months
Check TFTs, U&Es, calcium every 6mnths
I - GI (abdo pain, nausea), metallic taste, fine tremor, water symptoms (thirst, polyuria, impaired urinary conc, weight gain, oedema)
- Lithium toxicity = GI (anorexia, d&b), NM (dysarthria, dizziness, ataxia, muscle twitching, tremor), drowziness, apathy, restlessness
C - complications = renal toxicity, nephrogenic diabetes insipidus, hypothyroidism
CI - 1st trimester pregnancy, BF, cardiac disease, significant renal impairment, Addison’s disease, low Na diets, untreated hypothyroidism
S - bipolaruk.org.uk

113
Q

What are the concerns surrounding SSRIs in pregnancy?

A

Particularly in third trimester

Can increases risk of persistent pulmonary HTN of newborn

Paroxetine increases risk of congenital malformations

114
Q

What substances can be added to SSRI therapy to make it more effective?

A

Lithium

Atypical antipsychotics:
Quetiapine
Risperidone
Ariprprazole

115
Q

What are some important drug interactions with SSRIs? (12)

A

1) NSAIDS - give PPI if alternatives not found
2) Warfarin or heparin
3) SSRIs
4) ‘Triptan’ drugs for migraine
5) Monoamine oxidase B inhibitors
- Eg selegiline and rasagiline
6) Theophylline
7) Clozapine
8) Methadone
9) Tizamide
10) Flecainide
11) Propafenone
12) Atomoxetine

116
Q

What are some side effects of SNRI?

A

Similar to SSRIs as they block serotonin - weight change, insomnia, appetite changes, drowsiness, dizziness, fatigue, headache

Also inc NA and so can cause additional SE:

  • Inc HR
  • Inc BP (measure BP before starting and ensure well controlled)
  • Anxiety

QT prolongation

Year 4 Psych (10 decks)

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