-
what is it called when manic and depressive symptoms COEXIST?
mixed affective episode
-
what is the lifetime risk of BPAD?
1%
-
what is average age of onset of BPAD?
20-30s
-
what is sex ration of BPAD?
m=f
-
which socioeconomic groups is BPAD assoc with and urban/rural?
-
what 3 categories can you split symptoms of mania into and give eg
- 1. biological:
- less need for sleep (not assoc with fatigue)
- increased energy (spending, risky business)
- increased interest in sex (disinhibition)
- general: psychomotor excitation
- 2. cognitive:
- self esteem, grandiose
- poor concentration, easily distractible
- accelerated thinking: flight of ideas, pressured speech
- impaired judgement and insight
- 3. psychotic
- thought form disorder: circumstantiality (lots of detail eventually to the point), tangentiality (never to the point),
- thought content disorder: secondary delusions (grandiose and persecutory) - mood congruent,
- abnormal perceptions: auditory hallucinations (2nd person) and sensory distortions (hyperacusis or visual hyperaesthesia)
-
what is the main difference between hypomania and mania?
- in mania there has to be 1 week duration of symptoms
- COMPLETE DISRUPTION OF WORK AND SOCIAL LIFE (whereas in hypomania it is not complete)
-
what is the differential diagnosis of elevated or irritable mood?
- MOOD DISORDERS: hypomania, mania, depression (after AD or ECT) or agitated depression
- SECONDARY TO GENERAL MEDICAL CONDITIONS: brain tumour, infarct, infection, cushiness disease, huntington's disease, hyperthyroid, MS, temporal lobe epilepsy
- PSYCHOACTIVE SUBSTANCE USE: amphetamines, antidep, cocaine, steroids, hallucinogens
- PSYCHOTIC DISORDERS: schizoaffective disorder (may be similar to mania with psychosis, but delusions are mood INCONGRUENT), schizophrenia
- PERSONALITY DISORDERS
- DELIRIUM OR DEMENTIA
-
what is the immediate biological treatment of bipolar / mania? (4marks)
- RISK ASSESSMENT: where what who treat (OP, CC, IP)
- 1. mood stabilisers: lithium, anti-convulsants (sodium valproate, carbamazapine, lamotrigine)
- 2. anti psychotic: olanzapine
- 3. prophylaxis: if had 2 episodes
- 4. depression: anti-depressants (but may cause secondary mania) use SSRI with mood stabiliser
-
how is lithium administered?
as a chemical salt - carbonate or citrate, sulphate
-
what is the distribution and MOA of lithium?
- small so cross BBB into CNS
- interacts with receptors to decrease noradrenaline release and increase serotonin synthesis
-
what needs to be done before starting lithium?
- 1. establish diagnosis
- 2. discuss need for prolonged treatment
- 3. renal and thyroid function, weight
- 4. pregnancy test (Ebsteins heart defect)
- 5. tell patient must use contraception if on Lithium as don't want to accidentally have baby then its got defect
-
what is the starting dose of lithium and at what time of day?
- 600-800mg nocte
- then can gradually increase dose
-
when do levels of lithium need to be checked again?
after 5-7 days from first starting
-
what is the level of lithium that is aimed for in the blood?
0.5-1.0 mmol/l
-
what are the benefits of lithium in mania?
- 1. reduce the risk of manic episodes by 30-40%
- 2. reduce the length and severity of manic episodes
-
how is lithium treatment monitored?
- 1. monitor mood - mood diary?
- 2. adherence or concordance with treatment?
- 3. any SE from lithium
- 4. Li level every 3 months (note every time change dose of Li, check after a week)
- 4. Renal function every 6 months
- 5. Thyroid function every 12 months
- 6. Discontinue Li slowly - otherwise risk of manic relapse
-
what are the SE of lithium?
- thirst- polydipsia
- polyuria
- metallic taste
- GI disturbance
- sedation
- mild tremor
-
at what levels of lithium do signs of Li toxicity appear?
above 1.3mmol/l
-
what are the early signs of lithium toxicity?
-
what are the late signs of lithium toxicity?
- disorientation
- dysarthria
- convulsions
- coma
- severe bloody diarrhoea
-
what are the causes of death in Li toxicity?
- cardiac effect
- pulmonary complications
-
who is susceptible to Li toxicity at therapeutic levels?
- elderly
- also as many on diuretics which dehydrates
-
what is the MOA of anticonvulsant drugs?
- enhances the actions of GABA
- may have effects on membrane excitability
-
give 4 indications of carbamazepine in psychiatry
- 1. treatment resistant mania or depression
- 2. treatment resistant schizophrenia
- 3. adjunct to lithium in prophylaxis of BPAD
- 4. rapid-cycling BPAD: multiple episodes >4/year
-
what are the adverse effects of carbamazepine? think systems…
- CNS: headache, drowsiness, diplopia
- Liver: elevation of GGT, hepatitis, cholestatic jaundice
- Other GI: N&V
- Blood dyscrasias
- Skin rashes
- Teratogenic effects - folate deficiency (spina bifida, anencephalcy)
-
how does carbamazepine affect other drugs?
- hepatic enzyme inducer
- so induces metabolism of:
- anticoagulants, AD, AP, OCCP, Steroids
-
what are the 5 MOA of sodium valproate?
- inhibit GABA transaminase
- inhibit calcium channel current
- increase GABA binding in hippocampus
- reduce action of NA at alpha2 receptors
- inhibit formation of protein kinase C
-
what are the indications of sodium valproate? (6)
- 1. refractory mania
- 2. rapid cycling BPAD
- 3. may have benefit in prophylaxis
- 4. epilepsy
- NB: most effective in non-psychotic patients
- may have benefit in prophylaxis
-
what are the SE of sodium valproate?
- WHAT
- weight gain
- hepatotoxicity
- alopecia
- tremor, teratogenic
- N&V
-
what is MOA of lamotrigine?
- stabilise sodium channels
- inhibits glutamate release
-
what is the use of lamotrigine in bipolar?
- it is an anti-depressant in bipolar depression
- (mood stabiliser)
-
what are the SE of lamotrigine?
- rash
- GI problems
- CNS problems
-
what are the 2 major SE to be worried about in anti-psychotics?
- tardive dyskinesia
- neuroleptic malignant syndrome (medical emergency)
-
what are extra-pyramidal SE?
- acute dystonia: torticollis
- spasm of any muscle group esp head and neck
- akathesia: inner disccomfort and restlessness
- signs of parkinsons disease
- tardive dyskinesia: repetitive, involuntary, purposeless actions eg lip smacking, grimacing, tongue protrusion. tardive=slow onset
-
what are the psychosocial treatments of bipolar disorder?
- 1. bipolar prodromes: recognise early signs and symptoms
- 2. life events monitoring, diary
- 3. regulate social and sleep routines (disruption of circadian rhythms)
- 4. structured short term problem-focused therapies eg cognitive to develop new coping skills
- teach to reject negative thoughts
-
what are the SE of risperidone?
sexual dysfunction especially in men
-
what are the SE of olanzapine?
-
whats the median duration of a manic episode?
4 months
-
what is the median duration of a depressive episode?
6-12 months
-
what % of pts get chronic mania with deteriorating course?
10-15%
-
how does mania change with age?
- remissions are shorter
- episodes more severe
-
which is more common mania or depression in middle aged?
depression more common and longer
-
who experiences more mixed affective and depressive episodes?
women
-
what is rapid cycling mania? who gets it more
- 4 or more episodes per year
- women more
-
what are 5 poor prognostic factors of mania/bipolar?
- young age onset
- more severe symptoms
- co-morbid: Personality disorder
- Co-morbid substance misuse
- treatment avoidance
-
what are the type of delusions found in depression with psychotic symptoms?
- worthlessness\
- guilt
- ill health
- poverty
- nihilistic delusions: pt believe something important has ceased to exist eg family no longer exists, bowel disintegrated
-
what is depressive stupor?
- severe depression
- slowing of movement
- poverty of speech
- motionless
- mute
-
what are the cognitive features of depression?
negative patterns of thinking about the present, future, past and the world.
-
which physical medical conditions can present as depression?
- hypothyroidism
- cushings
- dementia
- hypoparathyroidism
- medications eg antiHTN or steroids
-
what are the at risk groups for depression?
- women
- unemployed
- low socioeconomic class
- certain occupational groups eg doctors
- single men
- women with children
- chronically physically ill or disabled
- prisoners
- people with other psychiatric disorders or substance misuse
-
what is the risk of depression for a 1st degree relative if a person has major depression?
2-4 fold
-
what are the etiological factors for depression?
- genetics
- early environment eg childhood trauma, separation
- divorced parents
- poor relationship with parents
- childhood sexual abuse
- any loss events
-
what are the 3 psychological theories for depression?
- 1. psychodynamic theory: repressed sense of loss and anger turned inwards, excessive dependence on others
- 2. learning theory: seligman - learned helplessness: cannot control the stresses that presented to you - learned passive acceptance
- 3. cognitive theory: negative feelings follow from illogical negative beliefs about self.
- Becks triad: self, future, world. negative interpretation of events
-
which endocrine abnormality is found in depression?
- stress response
- hypothalamic pituitary adrenal axis
-
which areas of the brain are found to have underactivity and overactivity in PET scans of depressed people?
- underactivity: frontal and temporal cortices
- overactivity: limbic
-
what % of people hospitalised for depression will commit suicide?
15%, highest in first 7 days of leaving hospital
-
give the immediate social intervention for depression?
- RISK assessment
- 1. suicide
- 2. self neglect
- 3. self harm
- 4. insight and compliance
- 5. psychotic symptoms
- 6. ongoing stressors
- decide - need inpatient/outpatient or crisis team care??
-
what is the intermediate social intervention for depression?
- minimise adverse life events: finance, house, relationship, work
- contact with key worker - CPN or SW
- admit to day hospital
-
what is the long term social intervention for depression?
- social network
- access to help: debt, jobs, relationships
- structured activities
- regular exercise
-
what are the 2 main types of IMMEDIATE biological interventions for depression?
- antidepressant drugs
- ECT - in an emergency
-
what are the 5 main classes of AD drugs? give examples
- 1. TCA: amitriptyline, imipramine
- 2. SSRI: fluoxetine, sertraline, citalopram, paroxetine
- 3. MAOI: phenelzine, moclobemide
- 4. SNRI: venlafaxine
- 5. NASSA: mirtazapine
-
what are the actions of 5HT1A receptors?
- anti-depresant
- anti anxiety
- anti obsessive
-
what are the actions of 5HT2 receptors?
- agitation
- anxiety
- insomnia
- sexual dysfunction
-
what are the actions of 5HT3 receptors?
- nausea
- GI symptoms
- headaches
-
what is the effect of alpha 1 receptors on 5HT release?
increase 5HT release
-
what is the effect of alpha 2 receptors on 5HT release?
decrease 5HT release
-
what are the anticholinergic SE of most AD?
- constpiation
- dry mouth
- blurred vision
- drowsy
- delirium
-
what are the alpha 1 adrenergic SE of AD?
-
what are the anti histamine SE of AD? and give eg of a drug that especially causes that
- weight gain
- sedative - drowsy
- eg mirtazepine (NaSSA)
-
what are the SE of SSRI?
- 5HT2 actions:
- anxiety (early - will resolve with time)
- agitation (early - will resolve with time)
- insomnia
- sexual dysfunction
- 5HT3 actions:
- GI irritation: N&V (early - will resolve with time)
- headache
- discontinuation effects: body becomes used to having a drug on a receptor, if stop abruptly - body isn't used to not having it, get flu like effects for a week
-
what are the SE of TCAs?
- anticholinergic:
- dry mouth
- constipation
- urinary retention
- blurred vision
- drowsy
- alpha adrenergic block:
- postural hypotension - dizzi, syncope
- histamine block: wt gain, sedation
- cardiotoxic: long QT, ST elevation, heart block, arrhythmias
-
what are the 2 main SE of mirtazapine?
- weight gain
- sedation
- so good if skinny and tired!
-
what are the NICE guidelines for using AD?
use ONE antidepressant if possible as they can interact, more SE, harder to remember to take them, £££
-
what things need to be explained to a patient when initiating an AD?
- 1. AD are effective on basis of evidence
- 2. NICE: 1st line SSRI (fewer SE, safer than TCA, esp if heart probes)
- 3. warn there are many SE, many are temporary SE eg GI, anxiety will resolve
- 4. not addictive
- 5. delayed therapeutic onset,
- 6. treatment for 6-8 months after recovery
- 7. risk of discontinuation syndrome in some
- ***DOCUMENT THE DISCUSSION***
-
if there is no response after 4-6 weeks of starting an AD, what needs to be checked and done?
- 1. dosage
- 2. duration
- 3. adherence
- 4. SE
- consider SWAPPING
- 2nd line: SSRI (citalopram, fluoxetine), mirtazapine, reboxetine or TCA
- 3rd line: venlafaxine
- if still no response:
- lithium augmentation
- ECT
-
name 3 main indications for ECT according to NICE?
- 1. severe depressive illness including psychotic depression
- 2. catatonia (schizophrenia): immobile, mute
- 3. prolonged or severe manic episode
-
when is ECT used as an emergency?
where rapid symptom relief is required eg not eating or drinking, suicide risk
-
what % of depressed pts improve on ECT?
71-78%
-
what is the mechanism of ECT?
- electric current passed briefly across brain via electrodes
- to produce GENERALISED seizure
-
what risk of ECT must be monitored?
mania
-
what may the effect of ECT be mediated by?
increased turnover of NA, DA, 5HT
-
what are the SE of ECT?
- headache
- feel muzzy for short period
- short term memory loss both anterograde and retrograde
- possible loss of long term episodic memory
-
what is the mortality of ECT?
same as GA for minor surgery
-
what is the definition of treatment resistant depression?
severe depression that has failed to repined to treatment trials with 2 or more anti depressant for an adequate time and dose
-
what are the CI for ECT?
- 1. any significant medical condition where there is a very high anaesthetic risk
- 2. if had an MI: within 3 months there is an increased risk of arrhythmias
- 3. if had stroke within 3 months - risk of rebelled
- 4. pre-existing brain pathology eg tumour.
- always have to balance these with the patient not eating or drinking due to the depression, so ECT may really be needed.
-
after a first episode of depression, what % of patients will go on to have a second?
50-85%
-
what % of those who have a second depressive episode go on to have a 3rd?
80-90%
-
what are NICE recommendations for continuing Rx if people have had 2+ episodes?
continue Rx for 2 years
-
what is the most important part of the IMMEDIATE psychological intervention
- for depression?
- psychoeducation (after secured a confiding relationship)
- 1. explain that it is common
- 2. can be treated, will improve
- 3. lifestyle changes help: no alc or drug, more social support, exercise
- 4. clear info about Rx
- 5. sleep hygiene (keep work apart from bedroom, sleep early, horlicks)
-
what are the INTERMEDIATE psychological interventions for depression treatment?
- 1. counselling
- 2. problem solving therapy: identify and resolve current life difficulties, good for major depression in primary care and self harm
- 3. supportive psychotherapy: mild depression
- 4. CBT
- 5. interpersonal thearpy (IPT)
- 6. short term psychodynamic psychotherapy
-
what is the principle of CBT?
- examines connections between THOUGHTS, EMOTIONS and BEHAVIOURS
- structured approach: homework
- addresses cognitive distortions -eg arbitrary inference (everything focussed on self - all bad things)
-
what is the principle of interpersonal therapy?
- explores ORIGINS of depression in terms of interpersonal lOSSES, role disputes
- deficits in social skills
-
what are the long term psychological interventions for Rx of depression?
- patient themselves using CBT approaches
- supportive relationship with GP or keyworker
|
|