Psych Flashcards
(312 cards)
1
Q
rise Why do psychiatrists want an ECG before staring meds?
A
- to establish the baseline QT interval
- certain drugs (e.g. tricyclines, antipsychotics) can lead to QT-interval prolongation / long QT syndrome
2
Q
What are the 3 core symptoms of depression?
A
anhedonia
low mood
low energy
3
Q
What is the difference between illusions and hallucinations?
A
Hallucinations are perceptions in the absence of a stimulus
Illusions are misperceptions of stimuli
4
Q
What MHA are we currently using?
A
1983
5
Q
What does the MHA challenge
A
Human rights act ( article 5) - right to liberty
6
Q
Where can you use section 5(2) of the MHA?
A
in inpatient ssettings
not in A&E!!
7
Q
Summarise section 5(2)
A
for 72h
used to temporarily detain a person who is trying to leave
acts as a MHAA
can be used on any ward
completed by approved clinician (consultant) or their deputy
cannot be done by FY1, you need to have a full GMC license
has to be completed by the team caring for the patient
does not authorise treatment for mental disorder
8
Q
What is section 4 of the MHA for?
A
For 72h
needs 1 doctor and one AAMP
for MHAA
when there is not sufficient manpower (i.e. no 2 doctors) -> often converted too section 2
9
Q
Section 136
A
Emergency power that Police have to remove a suspected mentally ill person from a public place to a place of safety for further assessment.
Can result in 24 hour detention for assessment
Appears to be suffering from Mental Disorder
Individual is in a place to which the public have access to e.g. front garden, A&E, carpark, street.
Taken to ‘place of safety’- S136 suite
10
Q
Section 135
A
like section 136 but when a person is removed from home rather than a public area
11
Q
What is the CTO?
A
an order for supervised treatment in the community, and rapid recall if conditions not met
Must have been on a Section 3
Set conditions e.g. regular assessments, medication adherence (depot), blood tests (clozapine)
simplifies the process of getting them to hospital
12
Q
Summarise the MCA
A
Mental capacity is the ability to make decisions…….
MCA is a framework for decision-making on behalf of people who lack capacity
Identifies how best interests are determined
Applies to people aged 16 and over
13
Q
5 Principles of MCA / Capacity
A
- Assumption of capacity - they have capacity until proven otherwise
- Assist with decision-making process (prior to assessment of capacity)
- Unwise decisions (may be a reason to set aside assumption of capacity and to test capacity)
- Best interests
- Least restrictive alternative (if person assessed as lacking capacity)
14
Q
Which antihypertensives can cause low mood?
A
beta-blockers
15
Q
Minimum treatment duration of depression
A
6 months
There are suggestions that older patients may benefit from a minimum of 1 year’s treatment
16
Q
How long should a second episode of depression be treated for?
A
at least 2 years following remission.
17
Q
Father of CBT
A
Aaron Beck
18
Q
Negative cognitive triad
A
Negative views about oneself
Negative views about the world
Negative views about the future
19
Q
Define ECT
A
a small electrical pulse is passed through the brain using electrodes, triggering a generalised tonic-clonic seizure
under GA
20
Q
What are the indications for ECT?
A
- severe depressive illness (more)
- Uncontrolled Mania
- Catatonia
21
Q
What is the preferred antidepressant in children and adolescents?
A
Fluoxetine (SSRI)
22
Q
Example of tricyclic antidepressants
A
amitryptyline
nortiptyline
clomipramine
lofepramine
23
Q
What dose of sertraline is used in depressive disorders?
A
start with 50 mg OD
increase by 50mg in intervals of 1w if required.
max 200 mg / day
50 mg OD maintanence dose
24
Q
Complications of serotonin syndrome
A
DIC
Rhabdomyolysis,
renal failure/Metabolic acidosis
seizures
25
Symptoms of serotonin syndrome
- restlessness
- tachycardia
- mydriasis (pupil dilation)
- sweating
- myoclonus
- hyperreflexia
- confusion / altered mental status
- nausea, diarrhoea, vomiting
- fits
Complications: rhabdomyolysis
26
Examples of SSRIs
Sertraline
fluoxetine
Ctalopram
Escitalopram
fluvoxamine
dapoxetine
paroxetine
27
Symptoms of opioid withdrawl
generalised muscle and joint pains
abdominal cramps
fever
'everything runs' (diarrhoea, lacrimation, vomiting, rhinorrhoea)
agitation
dilated pupils (mydriasis)
goosebumps
28
What drug type are heroin and methadone?
opioids
29
delirium tremens
- a form of alcohol withdrawal
- occurring 48-96h after last alcohol exposure
- delirium, seizures, tremors, agitation, visual, auditory and tactile hallucinations (e.g. seeing little people or animals or feeling insects crawling over the skin) and autonomic dysfunction
30
Symptoms of benzodiazepine withdrawal
how soon after last exposure to benzos?
sweating
insomnia
headache
tremor
nausea
psychological features (anxiety, depression and panic attacks)
occurs within several hours of last exposure to short acting benzo
31
How do you manage benzodiazepine addiction?
give these patients diazepam (long acting benzo) and taper the dose down gradually over months
32
symptoms of cocaine intoxication
euphoria
tachycardia
nausea
hypertension
dilated pupils
haluctinatioins
33
How many h
34
How are antipsychotics classified?
Typical (1st generation) and atypical (2nd generation)
35
List some atypical antipsychotics
amisulpride
aripiprazole
olanzapine
quietapine
risperidone
clozapine
36
list some typical antipsychotics
chlorpromazine
haloperidol
37
When would you prescribe clozapine? What do you have to be careful about and how do you monitor it?
- prescribed when two other antipsychotics have not achieved symptom control; superior efficacy to oder antipsychotics, decreases suicide and therefore death rates in schizophrenia)
- dangerous SE: fatal agranulocytosis
- monitor FBC 1x/week for 18 weeks, then every 2/52 then every 1/12
- also risk of seizures; VTE, myocarditis, cardiomyopathy
38
Indications for prescribing antipsychotics
schizophrenia and other psychoses (e.g. mania, psychotic depression)
- acute mania
- mood stabilisation in BAPD
- violent/agitated behaviour that is not responsive to de-escalation; often in combination with a benzodiazepine.
- tourettes (at lower doses)
39
How do antipsychotics work?
abnormal DA transmission can result in a false sense of having seen or heard something or not having done so (mesolimbic pathway for +ve sx)
it is thought that antipsychotics improve psychosis by blocking the DA D2/3 receptors.
40
What receptors do antipsychotics interact with and how?
D2/D3 (all antipsychotics reduce transmission, almost all are antagonist, aripiprazole is a partial D2 agonist; typical have higher affinity than atypicals)
5HT (most atypical antipsychotics are potent antagonists)
adrenergic
cholinergic
histaminergic
-> typical antipsychotics are potent antagonists for these 3
41
Stopping antipsychotics
taper medications over at least 3 weeks
42
How long should antipsychotics be taken for?
At least 2 years after 1st episode of psychosis; 98% relapse after discontinuation after 2 years, therefore many recommend that they are continued for 5 years
43
What monitoring is required for antipsychotics?
- weight, height (for BMI) and waist circumference
- ECG
- bloods (FBC, U&Es, blood lipids, LFTs, glucose, HbA1c, PRL)
44
Side effects of antipsychotics
- movement disorders
- sedation
- weight gain
- sexual dysfunction
- ESPEs (more common in typical antipsychotics due to more potent DA-ergic effects)
- raised PRL (more common in typical antipsychotics due to more potent DA-ergic effects)
- metabolic SE and insulin resistance are more common in atypical antipsychotics; sexua; dysfunction is also more common in 2nd gen
45
What are the different type of ESPEs?
Acute dystonia and Parkinsonism
Akathisia
tardive dyskinesia
46
What medications are likely to cause ESPEs?
typical / 1st gen antipsychotics
47
How do antipsychotics cause ESPEs?
due to DA blockade in the the nigrostriatal pathway
48
What is acute dystonia?
- reflects drug induced DA/ACh imbalance
- an involuntary, painful, sustained muscle spasm (e.g. oculogyric spasm, torticollis)
- treated with anticholinergic drugs e.g. procyclidine
49
Akathisia
- unpleasant feeling of restlessness
- ESPE
-pts often have to pace around or jiggle their legs
50
Management of ESPE: Akathesia
decrease dose or chnage drug
propanolol or benzodiazepine can also be used to treat
51
ESPE: parkinsonism Sx and Mx
triad: resting tremor, ridigity and bradykinesia (RTRB)
Mx: decrease dose or change antipsychotic; anticholinergic e.g. procyclidine
52
ESPE: tardive dyskinesia
rhythmic involuntary movements of the mouth, face, limbs, and trunk.
Pts may grimace, make chewing and sucking movements, or excessively blinking.
Often irreversible
53
Is tardive dyskinesia reversible?
it is often irreversibel
54
Mx of ESPE tardive dyskinesia
Stop the drug or reduce the dose and switch to an atypical or clozapine
avoid anticholinergics because they can worsen the problem
tetrabenazine is used for moderate/severe
55
What is lithium in priegnaing associated with?
About 1 in 1000 babies exposed in first trimester to lithium have Ebstein’s Anomaly, a serious cardiac anomaly.
56
What is 1st trimester benzodiazepine use associated with?
Cleft lip
57
Is lithium safe in breastfeeding women?
No.
Lithium is found in high concentrations in breast milk and is hence contraindicated.
58
What are delusions?
fixed, unshakable, irrational beliefs
(e.g. I can fly)
59
What are hallucinations?
Perceptions in the absence of an external stimulus
can be auditory (most common) but also visual, somatic and olfactory
60
When are visual hallucinations most common>
In physical health issues (check this)
61
How common are delusions in schizophrenia?
occur in around 50% people with schizophrenia
62
What are the different types of schizophrenia according to ICD-10?
1. Paranoid Schizophrenia
a. Relatively stable paranoid delusions accompanied by auditory hallucinations
2. Catatonic Schizophrenia
a. Prominent psychomotor disturbance (hyperkinetic or stupor)
3. Residual Schizophrenia
a. Chronic negative Sx, dominate with poor self care and social performance
4. Persistent delusional disorder
a.
5. Acute and transient psychotic disorders
a. Acute onset of psychotic Sx - delusions, hallucinations, disruption of ordinary behaviour. Complete recovery usually within days (up to a few months), often associated with acute stress.
63
Key features of schizophrenia
- positive symptoms (delusions, hallucinations)
- negative symptoms (attention, memory, executive function)
- negative syndrome (affective flattening, alogia, avolition, anhedonia)
- disorganisation (formal thought disorder)
- dysphoria/depressive features (suicidality, hopelessness)
- disturbed behaviour (social withdrawal, thought disturbance, antisocial behaviour)
- impaired social cognition
- neurocognitive dysfunction (attention, memory, executive function)
64
What are Schneider's first rank Sx?
- They are not diagnostic! Good for remembering :)
Mnemonic:
- auditory hallucinations (3rd person, running commentary, thought echo)
- passivity experiences
- thought withdrawal
- thought insertion
- delusional perception (linking normal perception to bizarre conclusions)
65
Negative Symptoms in schizophrenia
- social withdrawal
- reduction in speech production
- apathy
- anhedonia
- defects in attention
66
Cognitive Sx in schizophrenia
not diagnostic
but pts with schizophrenia often have them.
memory, attention, executive dysfunction
67
Hypnagogic and hypnopompic hallucinations
when you go to sleep and when you wake up
68
Epidemiology in schizophrenia
- lifetime prevalence 1.5%
- more common in men
- later onset in women
- peak onset in late adolescence and early adulthood
69
Prognosis of schizophrenia
at 5 years
- 25% completely recover
- 40% have periods or intervals of recovery lasting several years
- 10% sustained deterioration with reduced social functioning and negative symptoms
- remainder episodic
- prognosis worse if early onset
- shorter duration of untreated psychosis predict better resins to antipsychotic medication
- better in resource-poor countries
- reduced life expectancy
70
Why do people with schizophrenia have reduced life expectancy?
- CVD (19 years lower)
- 5-10% die by suicide (depressive Sx, hopelessness, higher IQ, alcohol misuse, esp in perdiod following discharge)
71
Cannabis use and Schizophrenia
- not fully understood what the link is
- may be responsible for 12% of psychosis in Europe and 30% in the UK
- associated with increased +ve Sx and violence and aggression
- associated with poorer response to antipsychotics and lower adherence to medications
72
DDx for Schizophrenia
- affective psychosis
- drug-induced psychosis
- delirium
- personality disorders
- physical health conditions
73
What physical health conditions can cause psychosis?
- metabolic disturbacnes
- systemic infection
- stroke
- endocrine
- neurodegenerative diseases
- drug treatments
74
Investigations for Schizophrenia
- Hx and MSE (incl. collateral)
- physical exam (neural, CV, weight, BP)
- urine drug screen
- bloods (FBC, electrolytes, HbA1c, lipids, endocrine tests)
- EEG when investigating TLE or post-octal Sx
- MRI/CT if indicated (exclude e.g. tumour/stroke)
75
How long do you have to monitor patients on antipsychotics?
- 2 years following slow discontinuation
76
What antipsychotics are more likely to cause sedation>
first generation
therefore take them before going to bed so they can help going to sleep and don't make you too drowsy during the day)
77
What medication do you usually use in first onset psychosis?
aripiprazole
lowest SE profile
78
Who would you not prescribe risperidone?
in young males (because it is more likely to cause sexual SE)
79
What antipsychotic would you prescribe to a patient that struggles with sleep too?
olanzapine becarse the sedation SE is higher with it, so it could also help people with sleep
80
How long would you trial and antipsychotic before switching? (due to not helping)
6-8 weeks
81
normal QTc interval
440 ms in men
460 ms in women
above that is abnormal
82
Adherence with antipsychotics
- only 50% are adherent in the first year
- 10 days following discharge are partially non-adherent
- adherence with long-acting injectables (e.g. risperidone) - 75% adherence and 30% lower rate of relapse
83
Which antipsychotics can be given as a depot?
xx
84
Why can people be non-adherent to medication?
- SE
- thinking they do not need it
- trading medication for e.g. drugs
- stigma
- family environment
85
How does CBT in psychosis work
"here and now"
- normalisation of the psychotic experience / reduction of stigma
-
recommended for all adults with psychosis or schizophrenia (NICE) - however only 46% attend
86
'High expressed emotion' or 'schizophrenogenic mother' in schizophrenia
very anxious mother, over involved, overcaring
packs lunch every day, there all teh time, intrusive, claustrophobic, wants to know what happens, the mom will be calling the ward, panicking about medication, joins appointments
-ve impact on people with schizophrenian psychosis; increased relapse, increased hospitalisation, worse adherence to medications
Family intervention can target this and increase independence of patients
87
Physical health interventions in psychosis/schizophrenia
- smoking cessation (some antipsychotics are procoagulant; smoking also impacts levels of clozpeine in the blood)
- lifestyle
- weight control
- exercise
88
What medication do you have to be very careful about smoking with?
CLOZAPINE
if they reduce how much they smoke -> reduce dose of clozapine (otherwise higher risk of the dangerous SE)
if they start smoking more - increase the dose
89
Psychosis/Schizophrenia Management: employment and education
- reintegration into society
- crime prevention
- future goals
monitor more closely at stressful periods in their life
90
Do you usually use one or more antipsychotics?
Usually you only treat with one due to SE.
cross-titrate when switching form one to another.
sometimes you can also give a mood stabiliser if indicated.
in very rare and treatment resistant cases you might use more than one antipsychotic.
91
Which antipsychotic could you use in pregnancy?
olanzapine
92
Attachment vs Bonding
attachment: flows from infant to caregiver (develops over first year)
bonding: flows from the caregiver to the infant (develops rapidly)
92
Attachment vs Bonding
attachment: flows from infant to caregiver (develops over first year)
bonding: flows from the caregiver to the infant (develops rapidly)
93
What is the leading cause of directs deaths within a year after the end of pregancy?
maternal suicide
-> low threshold for mental health assessment at this time
94
Incidence of postnatal psychosis
2 in 1000
95
How common are past mental health issues in postnatal psychosis?
50% are a first presentation of mental health illness
96
Features of postnatal psychosis
mania
paranoid psychosis
rapidly changing mood
perplexity
rapid progression and chaining 'kaleidoscopic' picture
97
Perinatal red flags
insert here
98
Management of postnatal psychosis
- urgent treatment with antipsychotics +/- tranquillisation (olanzapine, haloperidol)
- home treatment is usually not an option here
- admission to psych mother and baby unit
- 2-1 or 1-1 nursing
- consider PICU
99
RFs for postpartum psychosis
- FH of mental health problems, particularly a family
- history of postpartum psychosis
- diagnosis of bipolar disorder or schizophrenia
- traumatic birth or pregnancy
- experienced postpartum psychosis before.
100
Infanticide act (1922)
- very strict criteria
- when a mother killed her baby in the early period (under 12 months)
- legally differentiates infanticide from manslaughter or murder
-
101
Postnatal depression RFs
- personal or FHx of PND
- PMH of depression
- traumatic delivery
- younger age
- unemployment
- attachment with own parents
- childhood abuse
- socially prescribed perfectionism
- previous pregnancy loss
- longer time for conception
- depression in fathers
- poor partner relationship
- lack of social support
102
incidence of baby blues
50-80%
103
How long do baby blues last?
up to 48 h
occurs within first 10 days (peaks around 4-5) and subsides
104
Maternal OCD - features and examples
- Recurrent, unwelcome thoughts, images, ideas or doubts (Obsessions)
- Related behavioural or mental acts (Compulsions) to suppress or neutralise the distress or prevent a feared outcome
- Significant functional impairment in a number of domains
E.g.
Fear of contamination e.g. perceives a high risk of infection or of being poisoned
Thoughts or images of them harming their child
Thoughts or images of others harming their child
Thoughts or images of child being harmed by an accident e.g dropping their baby, baby drowning in the bath
Repeatedly checking baby’s breathing or waking a sleeping baby for reassurance
105
Drug risks at different times of pregnancy
Timing of exposure:
Early pregnancy – Major structural defects
Later pregnancy – Minor structural defects, functional defects, premature delivery, abnormal fetal growth
Before delivery – Neonatal toxicity, neonatal withdrawal
Developmental effects – Intelligence, behaviour, motor and social development
106
Which SSRI do you not use in pregnancy?
paroxetine
107
Which antipsychotic should be avoided in pregnancy?
risperidone
108
Which mood stabiliser CANNOT be given in pregnancy?
valproate
109
What should women that take mood stabilisers in pregnancy be advised to do?
take folic acid!
110
Breastfeeding: RID
relative infant dose
1-5% (up to 10% regarded as acceptable)
encourage women to breastfeed should they wish to do so and are able to
do not give lithium when breast-feeding
111
What is another term for antipsychotics?
neuroleptics
112
What was the first antipsychotic?
chlorpromazine
113
How do antipsychotics cause lactation?
DA suppresses PRL release
antipsychotics are D2R antagonists
tuberoinfundibulnar pathway
more suppression -> increased prolactin
>1000 mU/L
114
How to antipsychotics work?
block the D2 receptors within the mesolimbic pathway
modern atypical work as partial agonists
115
Why do atypical have lower rates of ESPEs?
-
- as downstream effect of blocking 5HT-2A -> nigrostriatal pathway
116
Depot antipsychotics - when?
= long acting injectables (given IM)
can be used in patients with poor oral compliance
a feature of psychosis is a loss of insight, therefore some patients may be unwilling to participate in treatment planning b/c they do not believe that they are unwell.
Not all tablet APs are available as depots but some are
117
Which antipsychotics can be given as a depot and how frequently?
= LAIs (long acting injectable antipsychotics)
Zuclopenthixol (Clopixol) – Given every 1-4 weeks
Flupentixol (Depixol) Given every 1-4 weeks
Haloperidol (Haldol) – Given every 4 weeks
Olanzapine (Zyprexa) – Given every 2-4 weeks
Paliperidone (risperidone metabolite) – Available as 4 weekly, 3 monthly (Trevicta) and soon to be 6 monthly (Hafyera)
Aripiprazole (Abilify) – Given every 4 weeks
118
How long does it take antipsychotics to work?
- sedative effects rapidly, within minutes to hours
- begin exerting clear antipsychotic effects after 1-2 weeks, maximum benefit generally seen within 6 weeks
119
What is rapid tranquillisation (RT)?
Use of medications to manage agitated patients when other methods have not worked.
1st and 2nd line are benzodiazepines and promethazine
3rd line: antipsychotics used 'as required' to manage acutely agitated
- olanzapine and haloperidol are commonly used
- pre treatment ECG needed for haloperidol
- monitor for respiratory depression
120
How do you medically manage an acutely agitated patient when de-escalation was not successful?
1st line: Benzodiazepines
2nd line: promethazine (antihistamine)
3rd line: antipsychotics (Olanzapine and haloperidol are most commonly used, PO/IM)
Accuphase (Zuclopenthixol Acetate) - nor rapid. used for severely agitated patients who have had needed multiple IM injections.
good to have a baseline ECG to make sure that the Qtc is not prolonged if using haloperidol.
Always check local guidelines.
121
HDAT
=high dose antipsychotic therapy
>100% of the BNF dose
mostly in treatment resistant populations
122
Difference in presentation in Parkinsonism from antipsychotics and Parkinson's disease?
in PD the pill rolling tremor usually starts unilaterally, in medication induced Parkinsonism it is usually bilateral
123
What dangerous behaviour is akathisia associated with?
increased risk of suicide
124
Sx of hyperprolactinaemia
Women: reduced libido, amennorhoea, galactorrhea, osteoporosis, ?increased risk of breast cancer
Men: erectile dysfunction, gynaecomastia ????
125
What is the main risk of QTc prolongation?
cardiac arrhythmias (esp. torsades de pointes)
126
What antipsychotic is most risky in terms of QTc?
haloperidol
127
Neuroleptic malignant syndrome (make into multiple Fcs)
- clinical emergency, cute life threatening complication
-
muscle rigidity
- confusion
-etc
- RFs: high dose typically, rapid dose changes, male gender, younger age
- seen in 1% patients
128
Investigations for NMS
bloods (raised Ck, leukocytosis, deranged liver function, deranged renal function (secondary to rhabdomyolysis from raised CK)
129
management of NMS
- stop causative antipsychotics
- transfer to hospital/ITU under medics
- supportive care and fluids
- pain management (e..g benzos)
- Benzodiazepines (relax muscles and manage agitation)
- Bromocriptine (dopamine agonist) and Dantrolene (muscle relaxant)
130
Hypothyroidism is a se of lithium - true or false?
True
131
Is depression more common in men or women?
Women (2:1 f:m)
132
Is bad more common in males or females?
1:1
133
Heritability of depression and BPAD?
Depression: 35-50%
BPAD: 80-90%
134
Triggers for manic episodes
Childbirth; sleep deprivation; flying across time zones;
Both positive and negative life events can precipitate mania but environmental triggers are less important in established BPAD.
135
Organic causes of depression
Physical illness and clronicpain predispose;
Cushing's syndrome
Hypothyroidism
Stroke
Parkinson's disease
MS
Hyperparathyroidism
Beta blockers
Substance misuse (alcohol, cocaine)
136
Organic causes for mania
Cushing syndrome;
Head injury
MS
Steroids
antidepressants
Stimulants
137
Summarise beck's negative cognitive triad;
Negative thoughts on the self the world, and the future → helpless, hopeless, worthess/guilty
138
Neurochemical theory _ what would the levels of monoamines in the brain be?
Low/deficient
139
Observations supporting the monoamine hypothesis.
- Most antidepressants increase 5-ht and na.
- meds that deplete monoamines (e.g. Reserpine) cause depression;
- reduced plasma tryptophan (5-ht precursor)
- reduced CSI homovanillic acid (dopamine metabolite)
-PET studies show reduced 5- ht transporter binding sites in midbrain and amygdala and decreased availability of 5-ht receptors in main brain areas.
- degeneration of dopamine striata projections in PD is associated with depression;
140
N euro transmitters playing aro6 in depression
- 5-HT
- NA
- DA
Newer studies also suggest
- GABA
- glutamate
- NMDA
- substance P
- brain derived neurotrophic factor
141
Monoamine theory in mania
- mania is associated with monoamine overactivity
- bromocriptine (da-agonist), L-dopa, amphetamine,and cocaine can induce mania symptoms
- antipsychotics (DA antagonists) treat mania.
- antidepressants can trigger mania
- glutamate C the main excitatory NT) overactivityis-thought to play a role in BPAD and many mood stabilisers decrease gentamate activity).
142
What are the 5 theories for depression?
- cognitive behavioural theory (Beck's cognitive triad)
- psychoanalytic theory (superego buying ego into despair)
- neurochemical theories (5-HT, NA, and DA. low levels of monoamines leading to depression, this is targeted by antidepressants)
- neuroendocrine abnormalities (high baseline cortisol, loss of negative feedback)
- neuroanatomical abnormalities (left anterior cingulate cortex abnormalities, ?cause/effect, targeted by deep brain stimulation for treatment resistant depression)
143
Classifiications of depression
mild
moderate
severe
severe with psychotic symptoms
-> depends of number and severity of symptoms and the impact they have on a person's day to day functioning
144
Pseudodementia
In older people the memory loss associated with depression can resemble dementia but it resumes with treatment of depression.
145
DDX for depression
- Organic causes (hypothyroid, hypoactive delirium, addisons, dementia)
- sadness/ bereavement
- adjustment disorder (mild affective Sx after stressful event)
- dysthymia
- BPAD
- Substance misuse
- postpartum depression
- burnout
146
Dysthymia
Chronic low mood for more days than not, lasting years not continuous enough to diagnose depression
147
Normal vs abnormal grief
Normal stages:
-Numbness
- pining
- depression
- recovery
Feeling slightly better than at first is encouraging
Abnormal features:
- prolonged (>6 months without any relief)
- extremely intense clanging for the deceased or persistent preoccupation withintense emotional pain).
- exceeds expected social, cultural or religions norms
- significantly impairs functioning
148
Why are SSRIs prescribed first line for depression?
- rel. Mild SE
- less dangerous in overdose
149
How long should you continue antidepressants for?
-6-9 months after recovery (to prevent renission)
- in recurrent depression at least 2 years
150
Most important risk of antidepressants?
Î suicide risk in the first 2 weeks → warn!
151
Do you give antidepressants to patients with mania/ hypomania?
You avoid them due to the risk of 'switching' from depression to mania.
People who respond too well to antidepressants may be my switching to mania (undiagnosed bpad).
152
Regimen for ECT
2x/week for 6-12 weeks
Continuation after each session.
153
What exercise can you prescribe for people with depression?
- Couch to 5k
- Park run
- cycle commuting
→ increases activity while connecting with people.
154
Antidepressant discontinuation Sx
- flu-like Sx
- 'electric shock' sensations
- dizziness
- headache
- vivid dreams
- irritability
-> taper over a few weeks
155
What is cross-tapering?
When switching from one drug to another, reduce the dose of the old one whilst increasing the dose of the new one
156
Considerations when switching from one antidepressant to another
Dangerous interactions of antidepressants of different classes are possible
- some need cross-tapering
- some need drug-free 'washout' period.
157
Augumentation therapies with antidepressants
- lithium
- second-generation antipsychotics (lower doses than for psychosis)
- T3
- combining two antidepressantts
158
Mirtazapine drug class
NASSA (noradrenergic and specific serotonin antidepressant)
159
Mirtazapine common side effects
sedation
appetite/weight gain
oedema
headache
sexual side effects are relatively uncommon in NASSAs
160
Mocobemide drug class
RIMA (reversible inhibitors of monoamine oxidase A)
161
With which drugs duo you have to avoid tyramine rich foods?
MAOIs
RIMAs
to avoid hypertensive crisis
162
Issues with TCAs?
- infrequently used due to cardio toxicity
- even small overdoses can be fatal
163
Amitriptyline drug class
TCA
164
Clomipramine drug class
TCA
165
Imipramine drug class
TCA
166
Lofepramine drug class
TCA
167
Venlaflaxine drug class
SNRI
168
Duloxetine drug class
SNRI
169
Examples of MAOIs
Phenelzine
Tranylcypromine
170
Investigations for depression
- collateral hx
- physical exam
- bloods (TFTs, FBC, Glucose/HbA1c, Vit D, Vit B12, calcium, plus any indicated by hx and exam)
- rating scales (BDI, HADS, PHQ-9)
- cognitive assessment (if dementia/pseudo-dementia are ddx)
- CT/MRI head (not routine. In suspected cerebral pathology)
171
Trazodone drug class
SARI (serotonin antagonist and reuptake inhibitor)
172
Psychoogical Interventions for depression
- CBT
- psychodynamic psychotherapy
- interpersonal therapy (IPT)
- mindfulness based cognitive therapy (MBCT)
173
regimen and duration of CBT
usually 1/week for 8-24w
174
common thinking errors examples(CBT)
- generalisation (i always mess everything up)
- minimisation (i only passed by chance, I am not actually clever)
175
Negative automatic though types (NATs)
Beck:
- personalisation (taking responsibility for things one has no control over)
- overgeneralisation (making sweeping conclusions based on a single event)
- minimisation (downplaying the importance of a positive emotion, thought or event)
- magnification ('making a mountain out of a mole hill')
- selective abstraction (drawing conclusions based on one of many elements in a situation)
- arbitrary interference (drawing conclusions where there is little or no evidence)
https://en.wikipedia.org/wiki/Beck%27s_cognitive_triad
176
How does psychodynamic psychotherapy work in depression?
- focus on developing relationship between person and their therapist
- patient's past experiences cause them to behave (unconsciously) in certain ways e.g. thinking the therapist will let them down
- the therapist can pick up the distorted transference and draw it to the person's conscious through interpretations and comments
- articulating these feelings allows the person to recognise and re-evaluate them, changing the way they see themselves and others influencing their behavioiur outside therapy
- typically over a year pr more, but a focussed course over 16-20 weeks is also possible
177
Risk of recurrence following depressive episode
50%
Risk of recurrence increases significantly with each subsequent episode
178
Prognosis of depression with psychotic Sx
- worse prognosis than without psychotic Sx
- better response to ECT
- higher risk of suicide
179
Risk of suicide in depressioin
up to 15% people with depression die by suicide
180
Manic episode (definition)
extreme mood state lasting at least a week (unless shortened by treatment)
181
Hypomanic episode
Persistent mood state lasting at least several days, whose symptoms are less severe and don't cause marked impairment in the person's work of social functioning.
182
What is a mixed episode?
mixture or rapid alteration between manic and depressive Sx on most days for at least 2 weeks
183
BPAD Type 1 and Type 2 diaganosis
Type 1: one or more manic/mixed episodes, often alternating with depressive episodes
Type 2: one or more hypomanic episodes and at least one depressive episode, without manic/mixed episodes
184
rapid cycling BPAD
4 or more episodes in 1 year
commoner in women
185
cognitive sx of mania
- elevated self-esteem and confidence
- feels more capable than usual
- thinks optimistically about the future, ignoring potential pitfalls of their many ideas
- thoughts and concentration may feel clearer than ever before but they are objectively distractable with poor concentration and racing thoughts which change topic rapidly ('flight of ideas')
186
biological symptoms in mania
decreased sleep
increased appetite (but may be 'too busy to eat')
increased energy
increased libido
187
psychotic sx in mania
in severe mania the person can experience delusions and hallucinations (typically mood congruent)
- auditory hallucinations of religious figures or celebrities praising them/instructing them
- grandiose delusions (wealth, fame, special purpose, talent)
- sometimes persecutory delusions (e.g. being hated because others envy them)
188
Risks in mania
- impulsive behaviour
+/- disinhibition
- taking risks without considering the consequences (e.g. overspending, gambling, driving recklessly, drug/alcohol misuse)
- sexual disinhibition: placing themselves and others at risk (unsafe sex, exploitation, assault)
- irritability -> verbal/physical aggression
- self-harm or suicide can occur in moments off sudden despair
- death from dehydration and physical exhaustion are possible if untrteated
189
Why is a collateral hx in hypomania important?
it is possible to mask hypomania in a short assessment
190
Ddx for BPAD/mania/hypomania
- organic causessuch as delirium, intoxication (e.g. amphetamines, cocaine), dementia, frontal lobedamage, cerebral infection (e.g. HIV), and 'myxo-edema madness' (paradoxical state of hyperactivity in
extreme hypothyroidism)
- schizoaffective disorder (psychotic and affective sx evolve simultaneously)
- EUPD: labile mood and impulsivity can mimic mania, but will be persistent traits, not episodic symptoms.
- Perinatal disorders
- ADHD: can be hard to distinguish from emerging BAD in young people, but ADHD is more persistent and develops earlier (by the age of 6).
191
Ix in mania
- collateral hx
- physical exam
- bloods (FBC, TFTs, CRP, ESR; other tests as per hx, e.g. HIV)
- urinary drug screen
- CT/MRI head for intracerebral causes if indicated (e.g. abrupt Sx, change in consciousness, focal neurological signs)
- consider LP if encephalitis is suspected
192
Management of mania (goals)
risk containment
mood stabilisaton
long term treatment is required even after a single episode (future episodes are potentially devastating)
193
Acute management of mania and hypomania
hypomania can be managed in the community but mania usually requires hospital admission
- stop exacerbating meds (e.g. antidepressants, steroids, DA agonists)
- limit access to drugs an alcohol where possible
- monitor food/fluid intake to prevent dehydration
- consider short course of benzodiazepines/hypnotics
- start/optimise mood stabilisers: SGA or mood stabiliser or SGA+mood stabiler for severe sx/poor response
- rarely consider ECT (life-threatening overactivity and exhaustion despite medication)
194
What are cotard delusions?
believing that one is dead, non-existent or rotting
195
What are delusions when a patient thinks that they are dead, non-existent or rotting called?
cotard delusions
196
typical biochemistry results in anorexia nervosa
- hypokalaemia
- low sex hormone levels (FSH, LH, oestrogen and testosterone)
- raised GH and cortisol levels
- hypercholesterolaemia
197
List mood stabilisers
lithium
valproate
carbamazepine
lamotrigine
(last 3 are anticonvulsants)
198
How do mood stabilisers work?
Not fully understood
anticonvulsants may work through sodium channels and the inhibitory neurotransmitter GABA
199
What are the different formulations of lithium?
lithium citrate (usually liquid) and lithium carbonate (usually tablet)
switching between them requires care, they contain different amounts of lithium
200
What meds can be used in BPAD?
mood stabilisers
- lithium
- anticonvulsants (valproate, carbamazepine, lamotrigine)
antipsychotics (SGA e.g. olanzapine, initiated during a manic episode and may be continued for long-term prophylaxis)
201
Lamotrigine
- anticonvulsant
- good for depressive Sx, often used in BPAD type 2
- carefully titrate dose when starting to prevent Stevens-Johnson syndrome (flu like sx, blistering mucous membranes, rash)
202
Monitoring of lithium
- check plasma level 1 week after starting / changing dose
weekly monitoring until steady therapeutic level, then every 3 months
- monitor U&Es, calcium, TFTs every 6 months (risk of renal impairment/hypothyroidism)
203
therapeutic plasma range of lithium
0.6-1.0 mmol/L
levels taken 12h post dose
204
Lithium toxicity
>1.2 mol/L
- life threatening
- diarrhoea
- N&V
- drowsiness
- ataxia
- slurred speech
- gross tremor
- fits
- renal failure
205
Management of lithium toxicity
- stop lithium
- transfer for medical care (rehydration, dialysis)
206
triggers for lithium toxicity
- electrolyte changes due to low salt diets, dehydration, diarrhoea and vomiting
- drugs interfering with lithium excretion (NSAIDs. thiazide diuretics, ACEi)
- OD
207
Are antidepressants prescribed in BPAD?
- depression in BPAD s difficult to treat because antidepressants can cause switch from depression to mania
- only prescribed with mood stabiliser/antipsychotic and the patient is monitored for signs of mania
208
Stopping mood stabilisers
stopping suddenly (especially lithium) can trigger a manic episode
209
Psychoeducation in BPAD/Mania
- identify relapse indicators (e.g. insomnia, increased energy)
- strategies:
- daily routine
- sleep hygiene
- healthy lifestyle
- limiting excessive stimulation/stress
- addressing substance misuse
- medication changes
210
Therapy for BPAD
CBT reduces relapse frequency and duration as well as number of inpatient admissions
-psychoeducation with opportunities to test and challenge grandiose thoughts and regain perspective
211
Social intervention for BPAD/Mania
- family therapy (family and friends play a vital role in managing BPAD)
- interpersonal and social rhythm therapy (IPSRT)
- support groups
- encouragement to maintain education/career and be in touch with occupational health with plan
212
%people with BPAD dying by suicide
up to 15% (although long terrm treatment with lithium reduces risk to that of gen pop)
213
Depression in children and adolescents
- affects 1-2% children and 8% adolescents
- M:F 1:1 until puberty than girls more than boys
- often presents as physical Sx (e.g. headaches, tummy pains) or teachers noticing irritability/worsening performance at school
214
What is the first line treatment for depression in children and adolescents?
after persisting 4w: CBT
215
What is the first line medication for depression in children and adolescents?
fluoxetine
medication given alongside psychological therapy
216
Anxiety disorders in children and adolescents
- period prevalence: 9-32% during childhood and adolescence
- M:F 1:1
- many anxiety disorders commence in adolescence
- may present with somatic Sx
217
self-harm in children and adolescents - consideration in hispitals
must be reviewed by aa CAMHS specialist before discharge and admitted to a paeds inpatient ward if necessary to facilitate this
218
Eating disorders in children - presentation difference to adults
- may present with faltering growth or delayed puberty
219
Psychosis in children and adolescents
- rare in children before puberty
- poor prognosis with disrupted social development
- important to exclude ASD and organic causes (e.g. autoimmune disease)
220
Separation anxiety disorder
- excessive fear of separation from attachment figures, usually parents
- at least several months
- causing significant emotional distress or functional impairment
221
Sx of school refusal in children
- typically tummy pains before school but not on weekends or holidays
- many different causes
222
Enuresis in children facts
>5yo (age when urinary continence should be achieved)
- often Fix of similar problems
- nocturnal enuresis more common in boys, diurnal in girls
secondary is usually stress related i.e. new school
223
What is the medical term for repeated defecation in inappropriate places above the age of faecal continence (4y)?
Encopresis
224
Encopresis
epeated defecation in inappropriate places above the age of faecal continence (4y)
225
Most common cause of encopresis
constipation -> overflow incontinence (dehydration, painful defecation (e.g. due to anal fissures), fear of punishment, toilet fears (e.g. monsters in toilet), hirschprung disease)
226
What is selective mutism and who does it more commonly affect?
consistent selective speech in specific social situations but not others
more than 1 month
more common in girls
talkative at home but extremely shy elsewhere
227
prevalence of selective mutism
4 in 1000 children
228
How many children in the UK are affected by ASD?
1%
229
m:f ration of ASD
4:1
230
What drugs are occasionally prescribed in ASD?
Antipsychotics and mood stabilisers ( for severe aggression not or hyperactivity not responding to behavioural interventions.
231
Asperger syndrome
No longer considered distinct from ASD
used to be the term for Autism without intellectual and language impairment
232
Are antidepressants more effective in adults and children?
Antidepressants are less effective in children
233
What medication is used for OCD in children?
Sertraline
234
Is personality disorder commonly diagnosed in children?
No.
Because the personality is still developing in children
235
prognosis of anxiety in children
most child anxiety do not persist into adulthood
most adult anxiety are preceded by an anxiety disorder in adolescence.
236
Depression in children NICE guidelines
- offer psychoeducation
- advice on sleep, exercise and diet
- manage the environment (work with schools, family etc)
Mild depression: watchful waiting for 2w by GP. counsellor, social worker; if no improvement psychological therapy (self hep, CBT, counselling, group intervention therapy)
Moderate-to-severe depression: Review by CAMHS; 3 months CBT, family therapy, psychodynamic psychotherapy -> then switch psychological therapy or fluoxetine combined
237
Admission criteria in childhood depression
- high risk
- poor home supervision/support
- intensive assessment required
admission is last resort, usually you try to avoid it.
238
How do you differentiate ADHD and bipolar in children?
in ADHD you have continuous symptoms
239
Age-appropriate experiences and behaviours that are not psychosis in children
- sleep-related perceptual phenomena (i.e. hearing someone say their name when they are waking up)
- imaginary friends/ fantasy figure
- child's understanding and expression of religious/cultural beliefs and concepts
240
useful therapeutic method in substance abuse (incl. in children)
Motivational interviewing
pointing out that their values are not in line with their behaviours
241
Triad of ADHD
Inattention
Impulsivity
Hyperactivifty
242
ICD-11 ADHD
> 6 months
inattention and/or hyperactivity-impulsivity
pervasive across different situations
onset <7years (starts in early to mid childhood)
significant distress or social impairment
243
Hyperkinetic disorder vs ADHD
- hyperkinetic disorder has a higher level of impairment
244
prevalence of ADHD and hyperkinetic disorder
1% hyperkinetic disorder
5% ADHD
245
M:F ratio in ADHD
M:F 3:1
but may be under diagnosed in females because they present differently
246
Comorbidity associated with ADHD
- ODD 50% / CD 25%
- anxiety 25% / depressive disorder 15%
- learning difficulties 30% (including reading difficulties)
-
247
How does medication for ADHD work?
it readdresses prefrontal underactivity
e.g. ritalin (methylphenidate)
248
Drug classes for ADHD
stimulants: methylphenidate (ritalin); block presynaptic DAT + agonistic at postsynaptic DRD4
non-stimulants e.g. amoxetine (NA reuptake inhibitor)
249
Side effects of ADHD meds
- effects on height, weight, sleep and mood
250
Which medication can help with ADHD and tics?
Guanfacine
251
SE of stimulant meds for ADHD.
Nausea, diarrhoea, hypertension, tachycardia, appetite suppression, insomnia
252
What proportion of ADHD cases persist into adulthood?
Up to 50% retain symptoms into adulthood and up to 30% retain the diagnosis.
253
Management of ADHD
- parent training and education programmes
- educational psychologist assessment of child's classroom needs
- group CBT and social skills training
- social support and self-help for families e.g. ADDISS
- Medication:
a) stimulant meds (methylphenidate, dexamfetamine, lisdexamfetamine)
b) non-stimulant medication e.g. atomoxetine and guanfacine
lack of evidence but many parents report children benefitting from dietary chanegs
254
Prevalence of ADHD
2% of UK children
(higher in countries using DSM i.e. 6% in USA)
255
Heritability of ADHD
75% or 60-90%
however unknown cause
256
RFs for ADHD
- prematurity
- very low birth weight
- prenatal tobacco and lead exposure
- foetal alcohol syndrome
associated with:
- paternal dissocial behaviour
- maternal depression
- lower socioeconomic status
- some food additives
257
Maximal treatment duration with benzodiazepines in psych
2-4 weeks
258
Russel sign
calluses on fingers (metacarpophalangeal joints)
due to inducing vomiting
seen in AN
259
commonest cause of death from refeeding syndorme
cardiac arrhythmia
260
Are anxiety disorders commoner in males or females?
usually females but OCD is the only one with equal prevalence
261
Mental illnesses with highest mortality rate
eating disorders
262
Key differences between AN and BN?
AN: BMI <18.5; no binging; endocrine dysfunction is common
BN: BMI >18.5; binging; endocrine dysfunction is uncommon
Both have deliberate weight loss, purging and body image distortion
263
What electrolyte imbalance may be seen in AN or BN?
Vomiting → hypokalaemia → arrhythmias
Laxative use → hyponatraemia → convulsions
264
Refeeding syndrome - what is the underlying pathology?
Potentially fatal complication of feeding extremely malnourished people
Switch from fat (in starvation) to carbohydrate (when feeding) metabolism increases insulin secretion causing electrolytes to move rapidly from blood into intracellular stores
→low potassium, phosphate and magnesium
This risks life threatening arrhythmias and sudden electrolyte depletion
265
Psychological interventions for AN
- motivational interviewing
- family therapy
- ED focused CBT
- Focal psychodynamic therapy
266
ED charity (AN)
BEAT
provide information and support for people with AN, their families, healthcare professionals and the general public
267
ED screening
SCPFF
• Do you make yourself Sick because you feel uncomfortably full?
• Do you worry you have lost Control over how much you eat?
• Have you recently lost One stone in a 3 month period
• Do you believe yourself to be Fat when others say you are thin
• WouldyousayFooddominatesyourlife?
If yes to 2 then suspect ED, or if yes to 1 and high suspicion
268
Management of bulimia nervosa
Medication: SSRIs can reduce binging and purging by anhancing impulse control
Psychological interventions:
- BN-focused guided self-help programmes
- adapted CBT-ED
BN-focused family therapy
- longer term psychotherapy
Social interventions:
- family, education, employment support, charities
- dental care to manage complications of frequent vomiting
269
% deaths by suicide in eating disorders
20%
270
Disorders falling under anxiety disorders in ICD-10
- GAD
- specific phobias
- social anxiety disorder
- PTSD
- panic disorder
- OCD
- agoraphobia
- BDD
270
Disorders falling under anxiety disorders in ICD-10
- GAD
- specific phobias
- social anxiety disorder
- PTSD
- panic disorder
- OCD
- agoraphobia
- BDD
271
CDD commoner in boys or girls
4X commoner in boys
272
socialised vs unsocialised CDD
socialised CDD occurs in peer groups
in unsocialised CDD, children are rejected by other children, often making them more isolated and hostile
273
DDX for CDD
- ODD (persistent pattern (6 months or more)of markedly defiant, disobedient, provocative or spiteful behaviour...)
- ADHD (comorbid with CDD in at least 1/3 of the cases)
- Depression (some young people externalise distress, presenting with dissocial behaviour)
274
What is the difference between CDD and ODD?
275
Management of CDD
- education: understanding as well as limiting reinforcing responses
- parent management training
family therapy
- educational support
- anger management
- treatment of comorbid disorders (e.g. ADHD)
276
Prognosis of CDD
up to 50% children with CDD Develop substance use or dissociality in adult life
277
What are tics?
sudden, rapid, non-rhythmic, recurrent movements and vocalisations
278
are tics commoner in boys and girls
3x commoner in boys
279
what worsens tics?
stress and stimulant medication
280
What medications can help with tics?
clonidine (an adrenergic agonist) or antipsychotics
281
(Gilles de la)Tourette syndrome
chronic (>1year) tic disorder featuring birth motor and vocal tics with onset in childhood
it tends to worsen in adolescence and persist into adulthood
282
What is the puerperium?
from 0 to 6 weeks after childbirth
a time within the postpartum period
283
How common are baby blues?
600 in 1000 women
(60%)
284
How common is postpartum psychosis?
2 in 1000
285
how common is mild-moderate postpartum depression?
125/1000
286
how common is severe PPD?
30 in 1000
287
how common is PSTD postpartum?
30 in 1000
288
What services does the perinatal psychiatry team offer?
- prepregnancy planning in women with a hx of MH problems (especially regarding medication use)
- care planning and monitoring of pregnant women at a high risk of relapse of known MH problems
- assessments of women on maternity wards with acute mental illness
- arranging MBU admission
- community FU after the birth (often up to a year)
289
Anxiety disorders (perinatal)
- postpartum period can trigger or exacerbate anxiety disorders e.g. PTSD in response to traumatic labour or stillbirth
- Mx: CBT ist first line, some women may need antidepressants
- OCD is especially common in women with a hx of OCD or anankastic personalty traits
290
Management of OCD in postpartum women
- reassurance and support from relatives and/or CBT therapists to face their fears (e.g. to hold and wash their baby)
- an antidepressant e.g. sertraline may help
291
Presentation of baby blues
- normal
- strarting a few days after the birth
- last around a week
- new mothers feel weepy, irritable, muddled; mood 'all over the place' (labile), and may have trouble sleeping
292
Management of baby blues
explanation and reassurance
severe babyblues occasionally progress to postpartum depression
293
Risk factors for PPD
- personal or family hx of PPD, depression or BPAD
- younger maternal age
- stressful life events
- marital discord
- poor social support
294
When may hospital admission be necessary in PPD?
- high risk cases
- not eating
- suicidal
- unable to care for baby
295
Why is effective treatment important in PPD?
- PPD can affect attachment
- PPD can affect long term family health and well-being
296
Does PPD increase risk of depression?
No.
It increases the risk of PPD but not depression per se.
297
Risk factors for PPP
- personal or FHx of PPP or BPAD
- puerperal infection
- obstetric complications (Incl. c-section)
- first delivery
298
When is a time where BPAD is more likely to relapse?
BPAD is 8x more likely to relapse in the puerperal period
299
What is PPP?
postpartum psychosis
may be a variant of BPAD in which childbirth is the trigger
300
What is PPP?
postpartum psychosis
may be a variant of BPAD in which childbirth is the trigger
301
onset of PPP
- usually rapid
- within 2 weeks of delivery
- often beginning with insomnia, restlessness and perplexity.
302
Management of PPP
- depends on presentations
- antipsychotics, antidepressants or mood stabilisers
- benzodiazepines may help with agitation
- in severe cases ECT may be life-saving
- inpatient admission is often required (preferably MBU)
303
Prognosis for PPP
- recovery within 6-12 weeks
- psychosis recurs in 50% women having another baby and in over 50% women at another time (unrelated to childbirth)
304
define pesonality
an individual's characteristic way of behaving, experiencing life, and of perceiving and interpreting other people and events.
305
Define PD
`marked disturbance in personality functioning, which is nearly always associated with considerable personal and social disruption (ICD-11)
306
What are the differences between NMS and SS?
NMS
- caused by antipsychotics
- symptoms:
- complications:
- management:
SS:
- caused by antidepressants
- symptoms: autonomic d/f (sweating, tachhy, HTN, mydriasis), Neuromuscular excitability (can lead to hyperthermia, hyperreflexia, myoclonus, clonus, horizontal ocular clonus, rigidity); altered mental status (delirium, psychomotor agitation); other: N&V, diarrhoea, seizure, hypotension
- complications:
- management:
307
What is serotonin syndrome?
life threatening condition caused by serotonergic overactivity in patients with exposure to serotonergic drugs
308
Name serotonergic drugs
Antidepressants (MAOIs, SSRIs, SNRIs, TCAs)
Anxiolytics (busiprone)
anticonvulsants (valproate)
opioids
NMDA R antagonists
5-HT3 R antagonists e.g. ondansetron
serotonin receptor agonists (e.g. triptans, ritonavir)
ABx (linezolid)
herbals (St johns wort, ginseng, tryptophan)
recreational dx (MDMA, cocaine)
309
serotonin abbreviation
5-HT
310
RFs for serotonin syndrome
concurrent use of
- two or more serotonergic drugs (e.g. MAOI and SSRI)
- one or more serotonergic drugs with certain CYP450 inhibtors (e.g. ciprofloxacin)
switching from one serotonergic drug to another without tapering
accidental or intentional OD
patient specific pharmacokinetic or pharmacodynamic factors
