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Year 5 😊✌🏼 > Psych > Flashcards

Psych Flashcards

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
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2
Q

What are the 3 core symptoms of depression?

A

anhedonia
low mood
low energy

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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

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4
Q

What MHA are we currently using?

A

1983

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5
Q

What does the MHA challenge

A

Human rights act ( article 5) - right to liberty

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6
Q

Where can you use section 5(2) of the MHA?

A

in inpatient ssettings

not in A&E!!

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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

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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

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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 β€˜place of safety’- S136 suite

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10
Q

Section 135

A

like section 136 but when a person is removed from home rather than a public area

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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

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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

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13
Q

5 Principles of MCA / Capacity

A
  1. Assumption of capacity - they have capacity until proven otherwise
  2. Assist with decision-making process (prior to assessment of capacity)
  3. Unwise decisions (may be a reason to set aside assumption of capacity and to test capacity)
  4. Best interests
  5. Least restrictive alternative (if person assessed as lacking capacity)
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14
Q

Which antihypertensives can cause low mood?

A

beta-blockers

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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

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16
Q

How long should a second episode of depression be treated for?

A

at least 2 years following remission.

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17
Q

Father of CBT

A

Aaron Beck

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18
Q

Negative cognitive triad

A

Negative views about oneself
Negative views about the world
Negative views about the future

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19
Q

Define ECT

A

a small electrical pulse is passed through the brain using electrodes, triggering a generalised tonic-clonic seizure

under GA

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20
Q

What are the indications for ECT?

A
  • severe depressive illness (more)
  • Uncontrolled Mania
  • Catatonia
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21
Q

What is the preferred antidepressant in children and adolescents?

A

Fluoxetine (SSRI)

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22
Q

Example of tricyclic antidepressants

A

amitryptyline
nortiptyline
clomipramine
lofepramine

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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

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24
Q

Complications of serotonin syndrome

A

DIC
Rhabdomyolysis,
renal failure/Metabolic acidosis
seizures

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25
Q

Symptoms of serotonin syndrome

A
  • restlessness
  • tachycardia
  • mydriasis (pupil dilation)
  • sweating
  • myoclonus
  • hyperreflexia
  • confusion / altered mental status
  • nausea, diarrhoea, vomiting
  • fits

Complications: rhabdomyolysis

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26
Q

Examples of SSRIs

A

Sertraline
fluoxetine
Ctalopram
Escitalopram
fluvoxamine
dapoxetine
paroxetine

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27
Q

Symptoms of opioid withdrawl

A

generalised muscle and joint pains
abdominal cramps
fever
β€˜everything runs’ (diarrhoea, lacrimation, vomiting, rhinorrhoea)
agitation
dilated pupils (mydriasis)
goosebumps

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28
Q

What drug type are heroin and methadone?

A

opioids

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29
Q

delirium tremens

A
  • 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
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30
Q

Symptoms of benzodiazepine withdrawal

how soon after last exposure to benzos?

A

sweating
insomnia
headache
tremor
nausea
psychological features (anxiety, depression and panic attacks)

occurs within several hours of last exposure to short acting benzo

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31
Q

How do you manage benzodiazepine addiction?

A

give these patients diazepam (long acting benzo) and taper the dose down gradually over months

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32
Q

symptoms of cocaine intoxication

A

euphoria

tachycardia
nausea
hypertension
dilated pupils
haluctinatioins

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33
Q

How many h

A
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34
Q

How are antipsychotics classified?

A

Typical (1st generation) and atypical (2nd generation)

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35
Q

List some atypical antipsychotics

A

amisulpride
aripiprazole
olanzapine
quietapine
risperidone
clozapine

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36
Q

list some typical antipsychotics

A

chlorpromazine
haloperidol

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37
Q

When would you prescribe clozapine? What do you have to be careful about and how do you monitor it?

A
  • 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
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38
Q

Indications for prescribing antipsychotics

A

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)

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39
Q

How do antipsychotics work?

A

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.

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40
Q

What receptors do antipsychotics interact with and how?

A

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

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41
Q

Stopping antipsychotics

A

taper medications over at least 3 weeks

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42
Q

How long should antipsychotics be taken for?

A

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

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43
Q

What monitoring is required for antipsychotics?

A
  • weight, height (for BMI) and waist circumference
  • ECG
  • bloods (FBC, U&Es, blood lipids, LFTs, glucose, HbA1c, PRL)
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44
Q

Side effects of antipsychotics

A
  • 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
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45
Q

What are the different type of ESPEs?

A

Acute dystonia and Parkinsonism

Akathisia

tardive dyskinesia

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46
Q

What medications are likely to cause ESPEs?

A

typical / 1st gen antipsychotics

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47
Q

How do antipsychotics cause ESPEs?

A

due to DA blockade in the the nigrostriatal pathway

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48
Q

What is acute dystonia?

A
  • reflects drug induced DA/ACh imbalance
  • an involuntary, painful, sustained muscle spasm (e.g. oculogyric spasm, torticollis)
  • treated with anticholinergic drugs e.g. procyclidine
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49
Q

Akathisia

A
  • unpleasant feeling of restlessness
  • ESPE
    -pts often have to pace around or jiggle their legs
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50
Q

Management of ESPE: Akathesia

A

decrease dose or chnage drug

propanolol or benzodiazepine can also be used to treat

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51
Q

ESPE: parkinsonism Sx and Mx

A

triad: resting tremor, ridigity and bradykinesia (RTRB)

Mx: decrease dose or change antipsychotic; anticholinergic e.g. procyclidine

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52
Q

ESPE: tardive dyskinesia

A

rhythmic involuntary movements of the mouth, face, limbs, and trunk.
Pts may grimace, make chewing and sucking movements, or excessively blinking.

Often irreversible

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53
Q

Is tardive dyskinesia reversible?

A

it is often irreversibel

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54
Q

Mx of ESPE tardive dyskinesia

A

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

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55
Q

What is lithium in priegnaing associated with?

A

About 1 in 1000 babies exposed in first trimester to lithium have Ebstein’s Anomaly, a serious cardiac anomaly.

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56
Q

What is 1st trimester benzodiazepine use associated with?

A

Cleft lip

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57
Q

Is lithium safe in breastfeeding women?

A

No.

Lithium is found in high concentrations in breast milk and is hence contraindicated.

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58
Q

What are delusions?

A

fixed, unshakable, irrational beliefs

(e.g. I can fly)

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59
Q

What are hallucinations?

A

Perceptions in the absence of an external stimulus

can be auditory (most common) but also visual, somatic and olfactory

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60
Q

When are visual hallucinations most common>

A

In physical health issues (check this)

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61
Q

How common are delusions in schizophrenia?

A

occur in around 50% people with schizophrenia

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62
Q

What are the different types of schizophrenia according to ICD-10?

A
  1. Paranoid Schizophrenia
    a. Relatively stable paranoid delusions accompanied by auditory hallucinations
    1. Catatonic Schizophrenia
      a. Prominent psychomotor disturbance (hyperkinetic or stupor)
    2. Residual Schizophrenia
      a. Chronic negative Sx, dominate with poor self care and social performance
    3. Persistent delusional disorder
      a.
    4. 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.
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63
Q

Key features of schizophrenia

A
  • 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)
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64
Q

What are Schneider’s first rank Sx?

A
  • 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)
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65
Q

Negative Symptoms in schizophrenia

A
  • social withdrawal
  • reduction in speech production
  • apathy
  • anhedonia
  • defects in attention
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66
Q

Cognitive Sx in schizophrenia

A

not diagnostic

but pts with schizophrenia often have them.

memory, attention, executive dysfunction

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67
Q

Hypnagogic and hypnopompic hallucinations

A

when you go to sleep and when you wake up

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68
Q

Epidemiology in schizophrenia

A
  • lifetime prevalence 1.5%
  • more common in men
  • later onset in women
  • peak onset in late adolescence and early adulthood
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69
Q

Prognosis of schizophrenia

A

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
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70
Q

Why do people with schizophrenia have reduced life expectancy?

A
  • CVD (19 years lower)
  • 5-10% die by suicide (depressive Sx, hopelessness, higher IQ, alcohol misuse, esp in perdiod following discharge)
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71
Q

Cannabis use and Schizophrenia

A
  • 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
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72
Q

DDx for Schizophrenia

A
  • affective psychosis
  • drug-induced psychosis
  • delirium
  • personality disorders
  • physical health conditions
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73
Q

What physical health conditions can cause psychosis?

A
  • metabolic disturbacnes
  • systemic infection
  • stroke
  • endocrine
  • neurodegenerative diseases
  • drug treatments
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74
Q

Investigations for Schizophrenia

A
  • 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)
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75
Q

How long do you have to monitor patients on antipsychotics?

A
  • 2 years following slow discontinuation
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76
Q

What antipsychotics are more likely to cause sedation>

A

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)

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77
Q

What medication do you usually use in first onset psychosis?

A

aripiprazole

lowest SE profile

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78
Q

Who would you not prescribe risperidone?

A

in young males (because it is more likely to cause sexual SE)

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79
Q

What antipsychotic would you prescribe to a patient that struggles with sleep too?

A

olanzapine becarse the sedation SE is higher with it, so it could also help people with sleep

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80
Q

How long would you trial and antipsychotic before switching? (due to not helping)

A

6-8 weeks

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81
Q

normal QTc interval

A

440 ms in men
460 ms in women

above that is abnormal

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82
Q

Adherence with antipsychotics

A
  • 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
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83
Q

Which antipsychotics can be given as a depot?

A

xx

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84
Q

Why can people be non-adherent to medication?

A
  • SE
  • thinking they do not need it
  • trading medication for e.g. drugs
  • stigma
  • family environment
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85
Q

How does CBT in psychosis work

A

β€œhere and now”

  • normalisation of the psychotic experience / reduction of stigma

recommended for all adults with psychosis or schizophrenia (NICE) - however only 46% attend

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86
Q

β€˜High expressed emotion’ or β€˜schizophrenogenic mother’ in schizophrenia

A

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

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87
Q

Physical health interventions in psychosis/schizophrenia

A
  • smoking cessation (some antipsychotics are procoagulant; smoking also impacts levels of clozpeine in the blood)
  • lifestyle
  • weight control
  • exercise
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88
Q

What medication do you have to be very careful about smoking with?

A

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

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89
Q

Psychosis/Schizophrenia Management: employment and education

A
  • reintegration into society
  • crime prevention
  • future goals

monitor more closely at stressful periods in their life

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90
Q

Do you usually use one or more antipsychotics?

A

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.

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91
Q

Which antipsychotic could you use in pregnancy?

A

olanzapine

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92
Q

Attachment vs Bonding

A

attachment: flows from infant to caregiver (develops over first year)

bonding: flows from the caregiver to the infant (develops rapidly)

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92
Q

Attachment vs Bonding

A

attachment: flows from infant to caregiver (develops over first year)

bonding: flows from the caregiver to the infant (develops rapidly)

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93
Q

What is the leading cause of directs deaths within a year after the end of pregancy?

A

maternal suicide

-> low threshold for mental health assessment at this time

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94
Q

Incidence of postnatal psychosis

A

2 in 1000

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95
Q

How common are past mental health issues in postnatal psychosis?

A

50% are a first presentation of mental health illness

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96
Q

Features of postnatal psychosis

A

mania
paranoid psychosis
rapidly changing mood
perplexity
rapid progression and chaining β€˜kaleidoscopic’ picture

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97
Q

Perinatal red flags

A

insert here

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98
Q

Management of postnatal psychosis

A
  • 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
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99
Q

RFs for postpartum psychosis

A
  • 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.
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100
Q

Infanticide act (1922)

A
  • very strict criteria
  • when a mother killed her baby in the early period (under 12 months)
  • ## legally differentiates infanticide from manslaughter or murder
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101
Q

Postnatal depression RFs

A
  • 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
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102
Q

incidence of baby blues

A

50-80%

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103
Q

How long do baby blues last?

A

up to 48 h

occurs within first 10 days (peaks around 4-5) and subsides

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104
Q

Maternal OCD - features and examples

A
  • 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

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105
Q

Drug risks at different times of pregnancy

A

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

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106
Q

Which SSRI do you not use in pregnancy?

A

paroxetine

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107
Q

Which antipsychotic should be avoided in pregnancy?

A

risperidone

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108
Q

Which mood stabiliser CANNOT be given in pregnancy?

A

valproate

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109
Q

What should women that take mood stabilisers in pregnancy be advised to do?

A

take folic acid!

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110
Q

Breastfeeding: RID

A

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

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111
Q

What is another term for antipsychotics?

A

neuroleptics

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112
Q

What was the first antipsychotic?

A

chlorpromazine

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113
Q

How do antipsychotics cause lactation?

A

DA suppresses PRL release

antipsychotics are D2R antagonists

tuberoinfundibulnar pathway

more suppression -> increased prolactin

> 1000 mU/L

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114
Q

How to antipsychotics work?

A

block the D2 receptors within the mesolimbic pathway

modern atypical work as partial agonists

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115
Q

Why do atypical have lower rates of ESPEs?

A
  • as downstream effect of blocking 5HT-2A -> nigrostriatal pathway
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116
Q

Depot antipsychotics - when?

A

= 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

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117
Q

Which antipsychotics can be given as a depot and how frequently?

A

= 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

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118
Q

How long does it take antipsychotics to work?

A
  • sedative effects rapidly, within minutes to hours
  • begin exerting clear antipsychotic effects after 1-2 weeks, maximum benefit generally seen within 6 weeks
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119
Q

What is rapid tranquillisation (RT)?

A

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 β€˜as required’ to manage acutely agitated
- olanzapine and haloperidol are commonly used
- pre treatment ECG needed for haloperidol
- monitor for respiratory depression

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120
Q

How do you medically manage an acutely agitated patient when de-escalation was not successful?

A

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.

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121
Q

HDAT

A

=high dose antipsychotic therapy

> 100% of the BNF dose

mostly in treatment resistant populations

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122
Q

Difference in presentation in Parkinsonism from antipsychotics and Parkinson’s disease?

A

in PD the pill rolling tremor usually starts unilaterally, in medication induced Parkinsonism it is usually bilateral

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123
Q

What dangerous behaviour is akathisia associated with?

A

increased risk of suicide

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124
Q

Sx of hyperprolactinaemia

A

Women: reduced libido, amennorhoea, galactorrhea, osteoporosis, ?increased risk of breast cancer

Men: erectile dysfunction, gynaecomastia ????

125
Q

What is the main risk of QTc prolongation?

A

cardiac arrhythmias (esp. torsades de pointes)

126
Q

What antipsychotic is most risky in terms of QTc?

A

haloperidol

127
Q

Neuroleptic malignant syndrome (make into multiple Fcs)

A
  • 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
Q

Investigations for NMS

A

bloods (raised Ck, leukocytosis, deranged liver function, deranged renal function (secondary to rhabdomyolysis from raised CK)

129
Q

management of NMS

A
  • 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
Q

Hypothyroidism is a se of lithium - true or false?

A

True

131
Q

Is depression more common in men or women?

A

Women (2:1 f:m)

132
Q

Is bad more common in males or females?

A

1:1

133
Q

Heritability of depression and BPAD?

A

Depression: 35-50%

BPAD: 80-90%

134
Q

Triggers for manic episodes

A

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
Q

Organic causes of depression

A

Physical illness and clronicpain predispose;

Cushing’s syndrome
Hypothyroidism
Stroke
Parkinson’s disease
MS
Hyperparathyroidism
Beta blockers
Substance misuse (alcohol, cocaine)

136
Q

Organic causes for mania

A

Cushing syndrome;
Head injury
MS
Steroids
antidepressants
Stimulants

137
Q

Summarise beck’s negative cognitive triad;

A

Negative thoughts on the self the world, and the future β†’ helpless, hopeless, worthess/guilty

138
Q

Neurochemical theory _ what would the levels of monoamines in the brain be?

A

Low/deficient

139
Q

Observations supporting the monoamine hypothesis.

A
  • Most antidepressants increase 5-ht and na.
  • meds that deplete monoamines (e.g. Reserpine) cause depression;
  • reduced plasma tryptophan (5-ht precursor)
  • reduced CSI homoοΏΌvanillic 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
Q

N euro transmitters playing aro6 in depression

A
  • 5-HT
  • NA
  • DA

Newer studies also suggest
- GABA
- glutamate
- NMDA
- substance P
- brain derived neurotrophic factor

141
Q

Monoamine theory in mania

A
  • 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
Q

What are the 5 theories for depression?

A
  • 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
Q

Classifiications of depression

A

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
Q

Pseudodementia

A

In older people the memory loss associated with depression can resemble dementia but it resumes with treatment of depression.

145
Q

DDX for depression

A
  • 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
Q

Dysthymia

A

Chronic low mood for more days than not, lasting years not continuous enough to diagnose depressionοΏΌ

147
Q

Normal vs abnormal grief

A

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
Q

Why are SSRIs prescribed first line for depression?

A
  • rel. Mild SE
  • less dangerous in overdose
149
Q

How long should you continue antidepressants for?

A

-6-9 months after recovery (to prevent renission)
- in recurrent depression at least 2 years

150
Q

Most important risk of antidepressants?

A

Î suicide risk in the first 2 weeks β†’ warn!

151
Q

Do you give antidepressants to patients with mania/ hypomania?

A

You avoid them due to the risk of β€˜switching’ from depression to mania.

People who respond too well to antidepressants may be my switching to mania (undiagnosed bpad).

152
Q

Regimen for ECT

A

2x/week for 6-12 weeks

Continuation after each session.

153
Q

What exercise can you prescribe for people with depression?

A
  • Couch to 5k
  • Park run
  • cycle commuting

β†’ increases activity while connecting with people.

154
Q

Antidepressant discontinuation Sx

A
  • flu-like Sx
  • β€˜electric shock’ sensations
  • dizziness
  • headache
  • vivid dreams
  • irritability

-> taper over a few weeks

155
Q

What is cross-tapering?

A

When switching from one drug to another, reduce the dose of the old one whilst increasing the dose of the new one

156
Q

Considerations when switching from one antidepressant to another

A

Dangerous interactions of antidepressants of different classes are possible

  • some need cross-tapering
  • some need drug-free β€˜washout’ period.
157
Q

Augumentation therapies with antidepressants

A
  • lithium
  • second-generation antipsychotics (lower doses than for psychosis)
  • T3
  • combining two antidepressantts
158
Q

Mirtazapine drug class

A

NASSA (noradrenergic and specific serotonin antidepressant)

159
Q

Mirtazapine common side effects

A

sedation
appetite/weight gain
oedema
headache

sexual side effects are relatively uncommon in NASSAs

160
Q

Mocobemide drug class

A

RIMA (reversible inhibitors of monoamine oxidase A)

161
Q

With which drugs duo you have to avoid tyramine rich foods?

A

MAOIs

RIMAs

to avoid hypertensive crisis

162
Q

Issues with TCAs?

A
  • infrequently used due to cardio toxicity
  • even small overdoses can be fatal
163
Q

Amitriptyline drug class

A

TCA

164
Q

Clomipramine drug class

A

TCA

165
Q

Imipramine drug class

A

TCA

166
Q

Lofepramine drug class

A

TCA

167
Q

Venlaflaxine drug class

A

SNRI

168
Q

Duloxetine drug class

A

SNRI

169
Q

Examples of MAOIs

A

Phenelzine
Tranylcypromine

170
Q

Investigations for depression

A
  • 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
Q

Trazodone drug class

A

SARI (serotonin antagonist and reuptake inhibitor)

172
Q

Psychoogical Interventions for depression

A
  • CBT
  • psychodynamic psychotherapy
  • interpersonal therapy (IPT)
  • mindfulness based cognitive therapy (MBCT)
173
Q

regimen and duration of CBT

A

usually 1/week for 8-24w

174
Q

common thinking errors examples(CBT)

A
  • generalisation (i always mess everything up)
  • minimisation (i only passed by chance, I am not actually clever)
175
Q

Negative automatic though types (NATs)

A

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 (β€˜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
Q

How does psychodynamic psychotherapy work in depression?

A
  • 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
Q

Risk of recurrence following depressive episode

A

50%

Risk of recurrence increases significantly with each subsequent episode

178
Q

Prognosis of depression with psychotic Sx

A
  • worse prognosis than without psychotic Sx
  • better response to ECT
  • higher risk of suicide
179
Q

Risk of suicide in depressioin

A

up to 15% people with depression die by suicide

180
Q

Manic episode (definition)

A

extreme mood state lasting at least a week (unless shortened by treatment)

181
Q

Hypomanic episode

A

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
Q

What is a mixed episode?

A

mixture or rapid alteration between manic and depressive Sx on most days for at least 2 weeks

183
Q

BPAD Type 1 and Type 2 diaganosis

A

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
Q

rapid cycling BPAD

A

4 or more episodes in 1 year

commoner in women

185
Q

cognitive sx of mania

A
  • 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 (β€˜flight of ideas’)
186
Q

biological symptoms in mania

A

decreased sleep
increased appetite (but may be β€˜too busy to eat’)
increased energy
increased libido

187
Q

psychotic sx in mania

A

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
Q

Risks in mania

A
  • 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
Q

Why is a collateral hx in hypomania important?

A

it is possible to mask hypomania in a short assessment

190
Q

Ddx for BPAD/mania/hypomania

A
  • organic causessuch as delirium, intoxication (e.g. amphetamines, cocaine), dementia, frontal lobedamage, cerebral infection (e.g. HIV), and β€˜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
Q

Ix in mania

A
  • 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
Q

Management of mania (goals)

A

risk containment
mood stabilisaton

long term treatment is required even after a single episode (future episodes are potentially devastating)

193
Q

Acute management of mania and hypomania

A

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
Q

What are cotard delusions?

A

believing that one is dead, non-existent or rotting

195
Q

What are delusions when a patient thinks that they are dead, non-existent or rotting called?

A

cotard delusions

196
Q

typical biochemistry results in anorexia nervosa

A
  • hypokalaemia
  • low sex hormone levels (FSH, LH, oestrogen and testosterone)
  • raised GH and cortisol levels
  • hypercholesterolaemia
197
Q

List mood stabilisers

A

lithium

valproate
carbamazepine
lamotrigine

(last 3 are anticonvulsants)

198
Q

How do mood stabilisers work?

A

Not fully understood

anticonvulsants may work through sodium channels and the inhibitory neurotransmitter GABA

199
Q

What are the different formulations of lithium?

A

lithium citrate (usually liquid) and lithium carbonate (usually tablet)

switching between them requires care, they contain different amounts of lithium

200
Q

What meds can be used in BPAD?

A

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
Q

Lamotrigine

A
  • 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
Q

Monitoring of lithium

A
  • 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
Q

therapeutic plasma range of lithium

A

0.6-1.0 mmol/L

levels taken 12h post dose

204
Q

Lithium toxicity

A

> 1.2 mol/L
- life threatening

  • diarrhoea
  • N&V
  • drowsiness
  • ataxia
  • slurred speech
  • gross tremor
  • fits
  • renal failure
205
Q

Management of lithium toxicity

A
  • stop lithium
  • transfer for medical care (rehydration, dialysis)
206
Q

triggers for lithium toxicity

A
  • electrolyte changes due to low salt diets, dehydration, diarrhoea and vomiting
  • drugs interfering with lithium excretion (NSAIDs. thiazide diuretics, ACEi)
  • OD
207
Q

Are antidepressants prescribed in BPAD?

A
  • 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
Q

Stopping mood stabilisers

A

stopping suddenly (especially lithium) can trigger a manic episode

209
Q

Psychoeducation in BPAD/Mania

A
  • 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
Q

Therapy for BPAD

A

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
Q

Social intervention for BPAD/Mania

A
  • 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
Q

%people with BPAD dying by suicide

A

up to 15% (although long terrm treatment with lithium reduces risk to that of gen pop)

213
Q

Depression in children and adolescents

A
  • 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
Q

What is the first line treatment for depression in children and adolescents?

A

after persisting 4w: CBT

215
Q

What is the first line medication for depression in children and adolescents?

A

fluoxetine

medication given alongside psychological therapy

216
Q

Anxiety disorders in children and adolescents

A
  • period prevalence: 9-32% during childhood and adolescence
  • M:F 1:1
  • many anxiety disorders commence in adolescence
  • may present with somatic Sx
217
Q

self-harm in children and adolescents - consideration in hispitals

A

must be reviewed by aa CAMHS specialist before discharge and admitted to a paeds inpatient ward if necessary to facilitate this

218
Q

Eating disorders in children - presentation difference to adults

A
  • may present with faltering growth or delayed puberty
219
Q

Psychosis in children and adolescents

A
  • rare in children before puberty
  • poor prognosis with disrupted social development
  • important to exclude ASD and organic causes (e.g. autoimmune disease)
220
Q

Separation anxiety disorder

A
  • excessive fear of separation from attachment figures, usually parents
  • at least several months
  • causing significant emotional distress or functional impairment
221
Q

Sx of school refusal in children

A
  • typically tummy pains before school but not on weekends or holidays
  • many different causes
222
Q

Enuresis in children facts

A

> 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
Q

What is the medical term for repeated defecation in inappropriate places above the age of faecal continence (4y)?

A

Encopresis

224
Q

Encopresis

A

epeated defecation in inappropriate places above the age of faecal continence (4y)

225
Q

Most common cause of encopresis

A

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
Q

What is selective mutism and who does it more commonly affect?

A

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
Q

prevalence of selective mutism

A

4 in 1000 children

228
Q

How many children in the UK are affected by ASD?

A

1%

229
Q

m:f ration of ASD

A

4:1

230
Q

What drugs are occasionally prescribed in ASD?

A

Antipsychotics and mood stabilisers ( for severe aggression not or hyperactivity not responding to behavioural interventions.

231
Q

Asperger syndrome

A

No longer considered distinct from ASD

used to be the term for Autism without intellectual and language impairment

232
Q

Are antidepressants more effective in adults and children?

A

Antidepressants are less effective in children

233
Q

What medication is used for OCD in children?

A

Sertraline

234
Q

Is personality disorder commonly diagnosed in children?

A

No.

Because the personality is still developing in children

235
Q

prognosis of anxiety in children

A

most child anxiety do not persist into adulthood

most adult anxiety are preceded by an anxiety disorder in adolescence.

236
Q

Depression in children NICE guidelines

A
  • 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
Q

Admission criteria in childhood depression

A
  • high risk
  • poor home supervision/support
  • intensive assessment required

admission is last resort, usually you try to avoid it.

238
Q

How do you differentiate ADHD and bipolar in children?

A

in ADHD you have continuous symptoms

239
Q

Age-appropriate experiences and behaviours that are not psychosis in children

A
  • 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
Q

useful therapeutic method in substance abuse (incl. in children)

A

Motivational interviewing

pointing out that their values are not in line with their behaviours

241
Q

Triad of ADHD

A

Inattention
Impulsivity
Hyperactivifty

242
Q

ICD-11 ADHD

A

> 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
Q

Hyperkinetic disorder vs ADHD

A
  • hyperkinetic disorder has a higher level of impairment
244
Q

prevalence of ADHD and hyperkinetic disorder

A

1% hyperkinetic disorder
5% ADHD

245
Q

M:F ratio in ADHD

A

M:F 3:1

but may be under diagnosed in females because they present differently

246
Q

Comorbidity associated with ADHD

A
  • ODD 50% / CD 25%
  • anxiety 25% / depressive disorder 15%
  • ## learning difficulties 30% (including reading difficulties)
247
Q

How does medication for ADHD work?

A

it readdresses prefrontal underactivity

e.g. ritalin (methylphenidate)

248
Q

Drug classes for ADHD

A

stimulants: methylphenidate (ritalin); block presynaptic DAT + agonistic at postsynaptic DRD4

non-stimulants e.g. amoxetine (NA reuptake inhibitor)

249
Q

Side effects of ADHD meds

A
  • effects on height, weight, sleep and mood
250
Q

Which medication can help with ADHD and tics?

A

Guanfacine

251
Q

SE of stimulant meds for ADHD.

A

Nausea, diarrhoea, hypertension, tachycardia, appetite suppression, insomnia

252
Q

What proportion of ADHD cases persist into adulthood?

A

Up to 50% retain symptoms into adulthood and up to 30% retain the diagnosis.

253
Q

Management of ADHD

A
  • 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
Q

Prevalence of ADHD

A

2% of UK children

(higher in countries using DSM i.e. 6% in USA)

255
Q

Heritability of ADHD

A

75% or 60-90%

however unknown cause

256
Q

RFs for ADHD

A
  • 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
Q

Maximal treatment duration with benzodiazepines in psych

A

2-4 weeks

258
Q

Russel sign

A

calluses on fingers (metacarpophalangeal joints)

due to inducing vomiting

seen in AN

259
Q

commonest cause of death from refeeding syndorme

A

cardiac arrhythmia

260
Q

Are anxiety disorders commoner in males or females?

A

usually females but OCD is the only one with equal prevalence

261
Q

Mental illnesses with highest mortality rate

A

eating disorders

262
Q

Key differences between AN and BN?

A

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
Q

What electrolyte imbalance may be seen in AN or BN?

A

Vomiting β†’ hypokalaemia β†’ arrhythmias
Laxative use β†’ hyponatraemia β†’ convulsions

264
Q

Refeeding syndrome - what is the underlying pathology?

A

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

β†’low potassium, phosphate and magnesium

This risks life threatening arrhythmias and sudden electrolyte depletion

265
Q

Psychological interventions for AN

A
  • motivational interviewing
  • family therapy
  • ED focused CBT
  • Focal psychodynamic therapy
266
Q

ED charity (AN)

A

BEAT

provide information and support for people with AN, their families, healthcare professionals and the general public

267
Q

ED screening

A

SCPFF

β€’ Do you make yourself Sick because you feel uncomfortably full?
β€’ Do you worry you have lost Control over how much you eat?
β€’ Have you recently lost One stone in a 3 month period
β€’ Do you believe yourself to be Fat when others say you are thin
β€’ WouldyousayFooddominatesyourlife?

If yes to 2 then suspect ED, or if yes to 1 and high suspicion

268
Q

Management of bulimia nervosa

A

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
Q

% deaths by suicide in eating disorders

A

20%

270
Q

Disorders falling under anxiety disorders in ICD-10

A
  • GAD
  • specific phobias
  • social anxiety disorder
  • PTSD
  • panic disorder
  • OCD
  • agoraphobia
  • BDD
270
Q

Disorders falling under anxiety disorders in ICD-10

A
  • GAD
  • specific phobias
  • social anxiety disorder
  • PTSD
  • panic disorder
  • OCD
  • agoraphobia
  • BDD
271
Q

CDD commoner in boys or girls

A

4X commoner in boys

272
Q

socialised vs unsocialised CDD

A

socialised CDD occurs in peer groups

in unsocialised CDD, children are rejected by other children, often making them more isolated and hostile

273
Q

DDX for CDD

A
  • 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
Q

What is the difference between CDD and ODD?

A
275
Q

Management of CDD

A
  • 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
Q

Prognosis of CDD

A

up to 50% children with CDD Develop substance use or dissociality in adult life

277
Q

What are tics?

A

sudden, rapid, non-rhythmic, recurrent movements and vocalisations

278
Q

are tics commoner in boys and girls

A

3x commoner in boys

279
Q

what worsens tics?

A

stress and stimulant medication

280
Q

What medications can help with tics?

A

clonidine (an adrenergic agonist) or antipsychotics

281
Q

(Gilles de la)Tourette syndrome

A

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
Q

What is the puerperium?

A

from 0 to 6 weeks after childbirth

a time within the postpartum period

283
Q

How common are baby blues?

A

600 in 1000 women

(60%)

284
Q

How common is postpartum psychosis?

A

2 in 1000

285
Q

how common is mild-moderate postpartum depression?

A

125/1000

286
Q

how common is severe PPD?

A

30 in 1000

287
Q

how common is PSTD postpartum?

A

30 in 1000

288
Q

What services does the perinatal psychiatry team offer?

A
  • 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
Q

Anxiety disorders (perinatal)

A
  • 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
Q

Management of OCD in postpartum women

A
  • 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
Q

Presentation of baby blues

A
  • normal
  • strarting a few days after the birth
  • last around a week
  • new mothers feel weepy, irritable, muddled; mood β€˜all over the place’ (labile), and may have trouble sleeping
292
Q

Management of baby blues

A

explanation and reassurance

severe babyblues occasionally progress to postpartum depression

293
Q

Risk factors for PPD

A
  • personal or family hx of PPD, depression or BPAD
  • younger maternal age
  • stressful life events
  • marital discord
  • poor social support
294
Q

When may hospital admission be necessary in PPD?

A
  • high risk cases
  • not eating
  • suicidal
  • unable to care for baby
295
Q

Why is effective treatment important in PPD?

A
  • PPD can affect attachment
  • PPD can affect long term family health and well-being
296
Q

Does PPD increase risk of depression?

A

No.

It increases the risk of PPD but not depression per se.

297
Q

Risk factors for PPP

A
  • personal or FHx of PPP or BPAD
  • puerperal infection
  • obstetric complications (Incl. c-section)
  • first delivery
298
Q

When is a time where BPAD is more likely to relapse?

A

BPAD is 8x more likely to relapse in the puerperal period

299
Q

What is PPP?

A

postpartum psychosis

may be a variant of BPAD in which childbirth is the trigger

300
Q

What is PPP?

A

postpartum psychosis

may be a variant of BPAD in which childbirth is the trigger

301
Q

onset of PPP

A
  • usually rapid
  • within 2 weeks of delivery
  • often beginning with insomnia, restlessness and perplexity.
302
Q

Management of PPP

A
  • 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
Q

Prognosis for PPP

A
  • 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
Q

define pesonality

A

an individual’s characteristic way of behaving, experiencing life, and of perceiving and interpreting other people and events.

305
Q

Define PD

A

`marked disturbance in personality functioning, which is nearly always associated with considerable personal and social disruption (ICD-11)

306
Q

What are the differences between NMS and SS?

A

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
Q

What is serotonin syndrome?

A

life threatening condition caused by serotonergic overactivity in patients with exposure to serotonergic drugs

308
Q

Name serotonergic drugs

A

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
Q

serotonin abbreviation

A

5-HT

310
Q

RFs for serotonin syndrome

A

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

Year 5 😊✌🏼 (53 decks)

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