psych Flashcards

1
Q

define mood disorder

A

disturbance of mood severe enough to impair ADLs, characterised by distorted excessive or inappropriate moods/emotions for a sustained period of time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define affect

A

transient flow of emotions in response to stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

define mood

A

sustained experienced emotional state over a period of time which can be described subjectively or objectively as dysthymic, euthymic or elated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how can primary mood disorders be classified?

A

unipolar - depressive disorder (mild, mod, severe, psychotic) or dysthymia
bipolar - bipolar affective disorder (1 or 2), cyclothymia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

list causes of secondary mood disorder

A

physical - anaemia, hypothyroid, malignancy, cushings/addisons, MS, Parkinsonism
psych - schizophrenia, alcoholism, dementia, personality disorder
drug induced - interferon a, corticosteroids, digoxin, AED, b-blocker, antidepressant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

define depressive disorder

A

mood disorder characterised by persistent low mood (2wks+), lack of energy and/or anhedonia accompanied by emotional cognitive and biological symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the hypothesised pathophysiology underlying mood disorder?

A

monoamine hypothesis - depressive disorder caused by deficiency of monoamines (NA, dopamine, serotonin) - supported by use of anti-depressants which increase [monoamine] in the synaptic cleft and relieve sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

risk factors for depressive disorder?

A
FF, AA, PP, SS
family history, female
alcohol, adverse events
past depression, physical comorbidity
social support low, SES low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

biological clinical features of depression

A

psychomotor retardation, EMW, diurnal variation in mood, low appetite and weightloss, loss of libido

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cognitive sx of depression

A

suicidal ideation, poor concentration, guilt, Becks triad of negative thoughts about self/world/future

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

core sx depression

A

anhedonia, anergia, persistent low mood lasting for at least 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is severity of depressive disorder classified?

A

Mild - 2 core + 2 other sx
Moderate - 2 core + 3-4 other sx
Severe - 3 core + 4+ other sx
Depression with psychosis - presence of psychotic sx e.g. hallucinations and delusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ddx for depression

A

physical - anaemia, hypothyroidism
mood disorder - bipolar affective disorder (hx mania), schizoaffective disorder, dysthymia,
other psych - substance abuse, psychosis, anxiety, adjustment disorder, personality disorder
normal bereavement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ix for ?depression

A

PHQ9, HADS, Beck’s depression inventory
FBC, U+Es, LFTs, TFTs, calcium, glucose
atypical/?SOL = CT/MRI head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mx of depression

A

Risk assess, consider psych referral if high risk suicide, severe depression, recurrent, or does not respond to rx
Mild-mod = computerised CBT + self help, support groups and exercise, only med if hx mod-sev depression/long lasting/failure of other mx.
Mod-severe = SSRI (e.g. citalopram), CBT + psychoeducation, social support group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How long should someone continue SSRI after resolution of depressive episode?

A

at least 6 months if first episode, 2 years if recurrence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ECT indications

A

treatment resistant depression/mania
psychosis features inc catatonia
rapid response required
severe depression which is life threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Contraindications to ECT

A

only absolute - raised ICP
MI <3m ago, major unstable fracture
cerebral aneurysm
stroke <1m ago, hx status epilepticus, severe anaesthetic risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

side effects of ECT

A

short term - cardiac arrhythmia, headache, nausea, short term memory impairment, muscle aches, status epilepticus
long term -anterograde and retrograde amnesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

define bipolar affective disorder

A

chronic episodic mood disorder characterised by at least 1 episode of hypo/mania and a further episode of mania/depression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Risk factors for BPAD?

A

3As, 3Ss
Age early 20s, anxiety disorder, after depression
strong family hx, substance misuse, stressful life events. Also seems more common in BAME groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Sx of mania

A
I DIG FASTER
Irritability
Distractibility/disinhibition
Insight impaired/increased libido
Grandiose delusions (psychotic sx)
Flight of ideas
Activity/appetite increased
Sleep decreased
Talkative (pressured speech)
Energy increased/elated mood
Recklessness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does hypomania differ from mania?

A

Hypomania usually 3-4d, mania lasts 7d+
hypomania may still be able to function socially/work though they are elated, mania unable to function in everyday life
hypomania symptoms are generally less intense than mania, no psychosis
hypomania may retain partial insight, unlikely to require hospitalisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the difference between Bipolar 1 and 2 disorder?

A

bipolar 1 depression and mania

bipolar 2 severe depression and hypomania

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is rapid cycling bipolar affective disorder?

A

at least 4 episodes of mania and depression in one year with no intervening asymptomatic periods. poor prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How would you investigate ?BPAD

A

FBC, U&Es, LFTs, TFTs, Ca, HbA1c, glucose
urine drug test
CT head to r/o SOL if ?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Ddx for bipolar disorder

A

mood disorder - cyclothymia, hypomania, mixed episode
psychotic - schizophrenia, schizoaffective
medical - thyroid dysfunction, cushings, stroke, cerebral tumour. S/E corticosteroids, anti-depressants,
other psych - Illicit drug ingestion/withdrawal, histrionic/EUPD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How would you manage BPAD

A

risk assess and hospitalise if risk to self/others, sig psychotic sx, impaired judgement, psychomotor agitation
Bio - acute antipsychotic (olanzapine, risperidone, quetiapine - or haloperidol), prophylaxis mood stabiliser (lithium first line); ECT if severe uncontrolled
Psych - CBT, psychoeducation
Social - support group, self-help group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Driving rules in mental health

A

Depression - problems with memory / concentration / agitation / behavioural disturbance or risk of suicide
Mania/psychosis - no during acute episode, well for 3/12 and on rx that does not cause S/E impairing driving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

When would you start lithium in a first presentation mania?

A

4 weeks after resolution of acute episode/when they regain insight as want them to be on it long term, if they have insight when taking it more likely to be compliant, build up therapeutic levels so not suitable for acute mx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Baseline investigations before starting lithium

A

U+Es, TFTs, ECG and pregnancy test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

S/E of lithium use within therapeutic window (and define that)

A

TW - 0.5-1mmol/l
polydipsia/polyuria, weight gain, oedema, fine tremor, hypothyroidism, impaired renal function, memory problems, teratogenic in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

sx of lithium toxicity and what level constitutes toxicity?

A

toxicity >1.5mmol, severe >2
coarse tremor, N+V, ataxia, muscle weakness, apathy, nystagmus, dysarthria, hyperreflexia, oliguria, hypotension, seizures, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how would you monitor someone on lithium therapy?

A

measure lithium levels 12h after first dose, then weekly until stable within therapeutic window for 4 weeks. Move to 3-monthly.
U+Es every 6months
TFTs every 12months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Schneiders first rank symptoms

A

Delusional perception
3rd person auditory hallucinations (usually running commentary)
Thought interference - withdrawal/broadcast/insertion
Passivity phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

define delusions

A

fixed false belief held firmly despite evidence to the contrary, which goes against the individuals normal cultural/social belief system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

define hallucination

A

perception in the absence of external stimuli, can be auditory/visual/olfactory/gustatory/somatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is thought disorder

A

impairment in the ability to form thoughts from logically connected ideas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does circumstantiality differ to tangentiality

A

circumstantiality - provides excessive, unnecessary detail but eventually returns to the point
tangentiality - wanders from the topic when answering a question and does not return to the original point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ddx for psychosis

A

non-organic - schizophrenia (1m+), acute and transient episode psychosis (<1m), schizoaffective disorder, mood disorder with psychosis, delusional disorder, puerperal or post natal psychosis
organic - drug-induced psychosis, iatrogenic (steroids, levodopa/methyldopa, antimalarials), complex partial epilepsy, dementia, delirium, SLE, Huntington’s, syphilis, cushings, b12 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how does persistent delusional disorder present differently to schizophrenia?

A

PDD - a single/set of delusions for 3m+ is the only or most prominent sx of psychosis; other areas of thinking and functioning are well preserved, may appear well in superficial conversation until challenged on beliefs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is schizophrenia?

A

most common psychotic disorder, characterised by hallucinations delusions and formal thought disorder which lead to functional impairment, in the absence of underlying organic disease or drug/alcohol induced disorder and is not secondary to elevated/depressed mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is the underlying pathology of schizophrenia?

A

schizophrenia is secondary to the overactivity of mesolimbic dopamine pathways in the brain supported by use of D2 receptor antagonists to rx psychosis positive sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

match the dopamine pathways in the brain to the effect they are responsible for in relation to schizophrenia as hypothesised by the dopamine hypothesis

A

mesolimbic pathway hypothesised to cause positive sx, mesocortical pathway causes negative sx, nigrostriatial causes EPSEs and tardive dyskinesia, tuberoinfundibulnar pathway causes hyperprolactinaemia (which causes osteoporosis by suppressing oestrogen and testosterone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Positive sx of schizophrenia

A

Delusions (inc ideas of reference), hallucinations, formal thought disorder (knights move thinking, tangentiality, word salad, neologism), thought interference, passivity phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Negative sx schizophrenia

A
6As
Alogia
Anhedonia
Attention deficit
Avolition
Asocial behaviour
Affect blunted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Ix ?schizophrenia

A

for causes - FBC (anaemia, infection), TFTs (either can cause psychosis), vit B12 and folate (deficiency), urine drug test
for baseline before rx - U+Es, LFTs, HbA1c, ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Mx schizophrenia

A

Bio - atypical antipsychotic, adjuvant - mood stabiliser/anti-depressant
Psych - CBT, psychoeducation, art rx/social skills training
Social - support groups Rethink and SANE, peer support worker, supported employment programme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

In treating schizophrenia, your firstline antipsychotic doesn’t work, next step?

A

Consider compliance - what S/E is discouraging this and work around that, may ?need for depot
1st line - atypical
2nd line - a different atypical or a typical
3rd line - clozapine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

define anxiety disorder

A

Anxiety = unpleasant emotional state characterised by subjective feat and somatic symptoms. Disorder when this becomes excessive or inappropriate and impacts functioning.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Most common anxiety disorders?

A

specific phobia > social phobia > GAD > agoraphobia > panic disorder > OCD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

psychiatric sx of anxiety disorders

A

inappropriate/excessive worries or fears, commonly depressive sx, feeling of impending doom, increased startle response, restlessness, poor concentration and attention, irritability, depersonalisation and derealisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

physical sx of anxiety disorders

A

GI - ‘butterflies’, abdo pain, loose stools, nausea, dry mouth, dysphagia
resp - hyperventilation, cough, chest tightness
CVS - palpitations, chest pain
GUM - urinary frequency, ED, menstrual discomfort
neuromuscular - tremor, myalgia, headache, paraesthesia, tinnitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How can anxiety disorders be classified?

A

Paroxysmal - situation dependent (phobic anxiety disorder - specific/social/agora) or independent (panic disorder)
Continuous - GAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

describe generalised anxiety disorder

A

persistent widespread worries about normal life events that is not triggered by a particular situation/object. patient recognises this as excessive or inappropriate. It is present most days for at least 6months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how do paroxysmal anxiety disorders tend to present (vs GAD)?

A

abrupt onset of severe anxiety with strong autonomic symptoms but usually short lived (typically 1hr) which may occur in response to specific threats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

conditions associated with anxiety disorders

A

medical - any chronic condition (e.g. CCF, COPD), anaemia, hyperthyroidism, hypoglycaemia, cushings disease, phaeochromocytoma, cancer
substance related - intoxication (caffeine, alcohol, cannabis), withdrawal (caffeine, alcohol, Benzos) or side effects (steroids, thyroxine, adrenaline)
psych - ED, somatoform disorder, depression, schizophrenia, OCD, PTSD, adjustment disorder, anxious personality disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

risk factors for GAD

A

female, family hx, personality type, living alone/divorced/single parent, stressful life events, unemployment, relationship problems, illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

clinical features specific to GAD

A

WATCHERS
Widespread + uncontrollable worry, excessive
Autonomic hyperactivity (sweating, mydriasis, tachycardia)
Tremor/tension in muscles
Concentration difficulty/chronic aches
Headache/hyperventilation
Energy loss
Restlessness
Startled easily/sleep disturbed (difficult getting to sleep, then intermittent waking + nightmares)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Ix ?anxiety disorder

A

FBC (infection, anaemia), TFT(hyper), glucose (hypo), ECG (arrhythmia/sinus tachycardia), GAD-2/7, Becks anxiety inventory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Mx GAD

A

Risk - suicide, depression, substance/alcohol misuse
Bio - 1yr+ of SSRI sertraline (antidepressant + anxiolytic); 2nd SNRI
Psych - psychoeducation, CBT and applied relaxation techniques
Social - self-help methods, support group, exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

define phobia

A

intense and irrational fear of an object/place/person/situation that is recognised as excessive or unreasonable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

define agoraphobia

A

fear of public spaces or fear of entering a public space from which immediate escape would be difficult in the event of a panic attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

define social phobia

A

fear of social situation which may lead to humiliation, criticism or embarrassment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

clinical features which differentiate phobic anxiety disorders from GAD

A

specific situations
anticipatory anxiety
attempted avoidance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Mx phobic anxiety disorders

A

screen for substance abuse/depression/PD
agoraphobia - CBT graded exposure techniques + SSRI
social phobia - CBT with graduated exposure + SSRI/SNRI/MAOIs; psychodynamic psychotherapy
specific phobia - exposure through self help methods or more formally through CBT. May use Benzes in short term for exceptional circumstance e.g. CT + claustrophobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is a panic disorder?

A

recurrent, episodic and severe panic attacks which are unpredictable, not restricted to any particular situation or circumstance. symptoms usually peak within 10min rarely persist beyond 1hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

risk factors for panic disorders

A

family hx, major life events, age 20-30, recent trauma, female, other mental disorder, white, asthma, smoker, medication (e.g. benzo withdrawal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

sx of panic disorders

A
PANICS Disorder
Palpitations
Abdominal distress
Numbness/nausea
Intense fear of death 
Choking sensation/chest pain
Sweating/SOB/shaking
Depersonalisation/derealisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

how does the associated behaviour and cognitions differ in GAD, panic disorder and phobic anxiety disorder?

A
GAD = irritable, constant worry
panic = escape, fear of sx
phobic = avoid, fear of situation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Mx of panic disorder

A

SSRIs (no improvement after 12wk consider TCA)
CBT
bibliotherapy, support group, encourage exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is PTSD

A

intense prolonged delayed reaction following exposure to an exceptionally traumatic event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what is abnormal bereavement

A

loss overwhelms coping capacity in a grief reaction that has delayed onset, is prolonged (6m) and more intense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

risk factors for PTSD

A

exposure to major traumatic event, perceived threat to life
hx mental illness/trauma/childhood abuse
female
low SES, life stressors, poor social support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Clinical features of PTSD

A

within 6months of event -
RELIVING - persistent intrusive and involuntary flashbacks / nightmares / vivid memories when reminded of the traumatic event
AVOIDANCE - avoid reminders of trauma (assoc people locations), ruminating, unable to recall aspects of it
HYPERAROUSAL - exaggerated startle response, irritability/outbursts, difficulty concentrating/sleeping, hypervigilance
EMOTIONAL NUMBING - feeling of detachment, difficulty experiencing emotion, negative thoughts about self, giving up previously enjoyed activities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

mx PTSD

A

RISK ASSESS
within 3/12 trauma + sx - trauma focused CBT, rx sleep disturbance. if mild sx <3/12 - could watchful waiting
3/12 after trauma + sx - CBT with eye movement desensitisation + reprocessing, ± mirtazapine/paroxetine (amitriptyline or phenelzine) if comorbid depression/severe arousal/little benefit from CBT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what is OCD

A

syndrome characterised by recurrent obsessional thoughts ± compulsive acts which are present most days for at least 2 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what are obsessions in the context of OCD?

A

recurrent, intrusive and distressing thoughts/mental images/urges that are egodystonic and recognised by the patient as a product of their own mind.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what are compulsions in the context of OCD?

A

repetitive and stereotyped behaviours/mental acts which may be overt or covert that the patient feels driven to perform to neutralise anxiety provoked by the obsession.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

clinical features of OCD

A

O - most commonly contamination, C - checking/cleaning/washing. O + C must share all the following features (FORD Car)
Failure to resist
Origin of own mind
Repetitive
Distressing
Carrying out the obsessive thought or compulsive act is not in itself pleasurable but reduces anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Ddx ?OCD

A

epilepsy, head injury, dementia
ED/anankastic PD/body dysmorphic disorder
Mainly O - anxiety/depression/hypochondria/schizophrenia
Mainly Cs - Tourettes/kleptomania

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Mx OCD

A

CBT with exposure and response prevention component

SSRI (fluoxetine, paroxetine, sertraline, citalopram) or clomipramine if severe

83
Q

How does somatisation disorder present?

A

multiple physical sx present for at least 2 years, patient refuses to accept reassurance or negative test results

84
Q

how does hypochondriacal disorder present?

A

patient has a persistent belief they have serious underlying disease e.g. cancer, refuses to accept reassurance or negative test results

85
Q

How does conversion disorder present?

A

typically a loss of motor/sensory function, patient does not consciously feign sx but it is a transformation of emotional distress or conflict into physical sx. often seen during stressful period of life.

86
Q

how would you mx medically unexplained sx?

A

psych - CBT + coping strategies
bio - anti-depressant/physical exercise
social - stress releasing activity, involve family as appropriate

87
Q

What is anorexia nervosa?

A

eating disorder characterised by an intense fear of fatness, distorted body image, deliberate weightloss and endocrine disturbance; typically with onset in mid adolescence in a female

88
Q

defining clinical features of anorexia nervosa

A

FEED for at least 3 months
fear of fatness
emaciated - >15% below expected body weight / BMI <17.5
endocrine disturbance - amenorrhoea in women, ED and loss of sexual drive in men
distorted body image/deliberate weight loss
ABSENCE OF cravings, recurrent episode binge eating

89
Q

what other clinical features of anorexia are seen apart from ICD10 criteria FEED?

A

physical - fatigue, hypothermia, bradycardia, arrhythmia, peripheral oedema (hypoalbuminaemia), headaches, lanugo hair
preoccupation with food - dieting, preparing elaborate meals for others
socially isolated, sexuality feared, may have sx depression + obsessions

90
Q

Give the main ways in which anorexia nervosa can be distinguished from bulimia nervosa

A
AN = underweight, BN = normal/overweight
AN = more likely to see endocrine disturbance
AN = no cravings, BN = cravings
AN = no recurrent binge eating, BN = recurrent bingeing
AN = restriction of food intake is main method of control, can have other compensatory weight loss behaviours excluding purging. BN = may restrict food intake but compensatory weight loss behaviours predominate (inc purging)
91
Q

List ix you would perform in a person with ?anorexia nervosa

A

FBC (pancytopenia), U&Es (low K, Mg, Ca, P; high urea creatinine if dehydrated), LFTs (low alb), glucose (low), cortisol (up), lipids (high cholesterol), sex hormones (low FSH, LH, oestrogen and progesterone), amylase (?pancreatitis - common complication); VBG (met alk if vomiting, met acid if laxative);
?osteoporosis = dexa
ECG - sinus Brady, QTc prolongation

92
Q

Ddx for AN

A

Anorexia, bulimia, ED-Not Otherwise Specified, schizophrenia, depression, OCD, anankastic PD
diabetes, hyperthyroid, malignancy
alcohol/substance misuse

93
Q

Mx of anorexia nervosa

A

Risk assess - suicide, medical complications
?hospitalisation - severe electrolyte imbalance, BMI<14, suicidal. Risk of refeeding syndrome?
Bio - rx medical complications, weight gain (0.5-1kg/wk), SSRI for comorbid depression/OCD
Psych - psychoeducation, at least 6m of CBT adults/family therapy young people; other options CAT/IPT
Social - voluntary organisations, self help groups

94
Q

Describe the pathophysiology of refeeding syndrome?

A

prolonged period of starvation leads to severe deficiencies of phosphate, magnesium and potassium. 1st episode of eating causes massive insulin surge which drives phosphate levels further down and causes cardiac failure

95
Q

complications of anorexia nervosa

A

hypokalaemia, hypotension, hypothermia, anaemia, cardiac failure, hypoglycaemia, osteoporosis, acute renal failure.

96
Q

what is bulimia nervosa?

A

ED characterised by repeated episodes of uncontrolled binge eating followed by compensatory weightloss behaviours and overvalued ideas regarding ‘ideal body shape/weight’

97
Q

how is the epidemiology of BN different to AN?

A

AN seen predominantly in higher SES, BN equal SES distribution
AN has a clear genetic proponent, unclear in BN

98
Q

common comorbidities in BN?

A

depression, anxiety, DSH, substance misuse, EUPD

99
Q

ICD10 clinical features of BN?

A

‘bulimia patients fear obesity’
Behaviours to prevent wt gain (compensatory ) e.g. self induced vomiting, laxatives, diuretics, amphetamine, thyroxine, periods starvation, excessive exercise
Preoccupation w/eating - cravings (sense of compulsion)
Fear of fatness - inc self perception of being too fat
Overeating at least 2 episodes a week for 3/12

100
Q

List possible consequences of the repeated vomiting and hypokalaemia seen in BN

A

arrhythmia, peripheral oedema, mallory Weiss tears, parotid swelling, dehydration, renal stones/failure, enamel erosion on teeth, menstrual abnormalities, hypoglycaemia, osteopenia, Russell sign (callus on knuckles/back of hand), aspiration pneumonitis, cognitive impairment, peripheral neuropathy, seizures, cardiac arrhythmia.

101
Q

Ix in BN?

A

FBC, U&Es, TFTs, amylase, glucose, lipids, Mg, Ca, P, VBG
ECG - arrhythmia, increased PR interval, flattened/inverted t waves, prominent u waves.

102
Q

how would you mx BN?

A

Risk assess - suicide, electrolyte abnormalities, comorbid substance misuse, depression/anxiety; need for hospitalisation? (usually good insight and motivation to get well)
Bio - fluoxetine (reduces freq of binge + purge), rx medical complications and comorbidities
Psych - CBT-BN, or IPT, psychoeducation
Social - food diary to track behaviours, techniques to avoid binging, small + regular meals, self help programme

103
Q

What are the defining clinical features of substance dependence syndrome?

A

at least 3 of the following features occur over 1 month ‘Drug Problems Will Continue To Harm’
Desire (compulsion) to consume
Preoccupation with substance use
Withdrawal sx
Control of substance taking impaired
Tolerance
Harmful effects acknowledged but continue to use

104
Q

How would someone withdrawing from opioids present?

A

3 of: craving, lacrimation, rhinorrhoea, myalgia, abdo cramps, N+V, diarrhoea, piloerection, pupillary dilatation, increased HR/BP

105
Q

how would someone withdrawing from benzodiazepines present?

A

tremor (hands, tongue, eyelid), N+V, tachycardia, postural hypotension, headache, agitation, malaise, transient illusions/hallucinations, paranoid ideation, grand Mal seizure

106
Q

Mx of substance misuse?

A

motivational interviewing
establish therapeutic alliance with a key worker
CBT, self help groups, refer to turning point, contingency management
opioid addiction - consider methadone, buprenorphine, naltrexone

107
Q

how do you calculate the number of units of alcohol in a drink?

A

ABV (%) x volume (ml) / 1,000

108
Q

Alcohol dependence features

A
SAW DRINk
Subjective awareness of compulsion
Avoidance/relief of withdrawal sx
Withdrawal sx
Drink seeking behaviour
Reinstatement drinking after attempted abstinence
Increased tolerance
Narrowed drinking repertoire
109
Q

how would you screen for alcohol dependence?

A

CAGE
have you ever felt you needed to Cut down your drinking?
do you get Annoyed by people criticising your drinking?
have you ever felt Guilty about your drinking?
do you ever have a drink early in the morning to wake you up or steady your nerves (Eye opener)

110
Q

how does alcohol withdrawal present?

A

6-12h - malaise, nausea, insomnia, tremor, transient hallucination, auton hyperactivity (sweating, tachycardia)
36h - peak incidence of seizures
72h - peak incidence delirium tremens - coarse tremor, confusion, delusions, auditory + visual hallucinations, fever, tachycardia (physical illness predisposes)

111
Q

What is wernickes encephalopathy?

A

neuropsychiatric disorder seen in thiamine (B1) deficiency. sx confusion, ophthalmoplegia + nystagmus, ataxia, hypothermia + delirium. Rx IV pabrinex (PO thiamine after IV/prophylaxis)

112
Q

what is Korsakoff syndrome?

A

sequelae of untreated wernickes encephalopathy, profound and irreversible short-term memory loss, characterised by retrograde and anterograde amnesia, and confabulation, ± disorientation to time

113
Q

mx of alcohol abuse

A

inpatient Hospitalisation if in acute withdrawal/risk of DT or seizure
rx PO chlordiazepoxide (lorazepam if hepatic failure) + taper dose down; + IV pabrinex (initially, then PO thiamine)
long term - disulfiram, naltrexone, Motivational Interviewing ± CBT, Alcoholics Anonymous.

114
Q

what is a personality disorder?

A

deeply ingrained and enduring pattern of internal experience and behaviour that deviates markedly from expectations in the individuals culture and causes impairment or distress. it is pervasive and inflexible, with onset in adolescence/early adulthood and staying stable over time.

115
Q

risk factors for personality disorder

A

low SES, genetics, poor parenting and parental deprivation, childhood abuse

116
Q

what are the cluster A personality disorders?

A

schizoid and paranoid

117
Q

what are the cluster B personality disorders?

A

histrionic, EUPD, antisocial

118
Q

what are the cluster C personality disorders?

A

anxious, dependent, anankastic

119
Q

how does schizoid personality disorder present?

A
DISTANT
Detached affect
Indifferent to criticism/praise
Sexual drive reduced
Tasks performed alone
Absence of close friends
No emotion (cold)
Takes pleasure in few activities
120
Q

how does paranoid personality disorder present?

A
SUSPECTS
Suspicious
Unforgiving
Spousal fidelity questioned
Perceives attack
Envious
Cold affect/criticism not liked
Trust in others reduced
Self reference
121
Q

how does EUPD present?

A
AM SUICIDE
Abandonment feared
Mood instability
Suicidal behaviour
Unstable and Intense relationships
Control of anger poor
Impulsivity
Disturbed sense of self
Emptiness (chronic)
122
Q

how does histrionic personality disorder present?

A
PRAISE
Provocative behaviour
Real concern for physical attractiveness
Attention seeking
Influenced easily
Superficial/seductive inappropriately
Egocentric/exaggerated emotion
123
Q

how does antisocial personality disorder present?

A
CORRUPT
Callous
Others to blame
Reckless disregard for safety
Remorseless
Underhanded
Poor planning (impulsive)
Temper/tendency to violence
124
Q

how does dependent personality disorder present?

A
RELIANCE
reassurance needed
expressing disagreement is difficult
lack self-confidence
initiating project difficult
abandonment feared
needs others to assume responsibility
companionship sought
exaggerated fears
125
Q

how does anxious personality disorder present?

A

CRIES
Certainty of being liked needs before becoming involved with people
Restricted lifestyle to maintain security
Inadequacy felt
Embarrassment potential prevents involvement in new activities
Social inhibition

126
Q

how does anankastic personality disorder present?

A
LAW FIRMS
Loses point of activity preoccupied with detail
Ability to complete task compromised by perfectionism
Workaholic at the expense of leisure
Fussy
Inflexible
Rigid
Meticulous attention to detail
Stubborn
127
Q

Mx personality disorder

A

Written crisis plan! identify and rx psych disorders /substance misuse, risk assess, help patients deal with situations that provoke problem behaviours/traits, support to pt + family to reduce anxiety and tension
Psych - DBT, CBT, psychodynamic psychotherapy
Bio - mood stabilisers may help e.g. EUPD, antipsychotics as needed, small role for antidepressants
Social - support groups, substance misuse services.

128
Q

risk factors for DSH

A
DSH Largely Comes Via Self-Poisoning
Divorced/single/living alone
Severe life stressors
Harmful drug/alcohol use
Less than 35y/o
Chronic physical health problems
Violence (domestic) or childhood maltreatment
Socioeconomic disadvantage
Psych illness e.g. psychosis, depression
129
Q

Motives for DSH

A
DRIPS
Death wish
Relief - temporary escape form pain
Influence others to change views/behaviour
Punishing self
Seek attention/help
130
Q

Mx DSH

A

Risk assess - ? hospitalisation ± MHA or crisis team, follow up within 48h discharge
Bio - suture lacerations/antidote for OD, if within 1h OD then activated charcoal to reduce absorption, consult toxbase. psych - counselling, CBT (depression), psychodynamic (PD). social - social services input, voluntary organisation

131
Q

risk factors for suicide

A
IM A SAD PERSON
institutionalised
mental illness
alone (lack support)
sex - male
age - middle
depression
previous attempt
ethanol use
rational thinking lost
sickness
occupation - vets, farmers, doctors, nurses
no job - unemployed
132
Q

risk factors for suicide following DSH

A
Note left behind
Planned
Attempts to avoid discovery
Afterwards help not sought
Violent method
Final acts - organising finances, writing will etc.
133
Q

Aim of CBT

A

identify and change automatic negative thoughts, modify abnormal underlying core beliefs that lead to maladaptive behaviours e.g. address becks cognitive distortions such as all or nothing thinking, selective abstraction, overgeneralisation

134
Q

Why are SSRIs first line for depression?

A

better tolerated + work more quickly + less risk of inducing mania
others are more effective but less tolerable/safe

135
Q

how long does it take for antidepressants to take effect?

A

1wk, but 4-6 weeks til clinically detectable benefit

136
Q

What type of anti-depressant is citalopram?

A

SSRI

137
Q

what type of anti-depressant is venlafaxine?

A

SNRI - serotonin + noradrenaline reuptake inhibitor

138
Q

what type of anti-depressant is mirtazapine?

A

NASSA - Noradrenaline and specific serotonergic antidepressants

139
Q

what type of anti-depressant is reboxetine?

A

NARI - NA reuptake inhibitor

140
Q

what type of anti-depressant is trazodone?

A

SARI - serotonin antagonist and reuptake inhibitor

141
Q

what type of anti-depressant is amitriptyline?

A

TCA

142
Q

what type of anti-depressant is clomipramine?

A

TCA

143
Q

what type of anti-depressant is dosulepin?

A

TCA

144
Q

what type of anti-depressant is phenelzine?

A

MAOI

145
Q

what type of anti-depressant is moclobemide?

A

irreversible MAOI specific to MAOI-A so no diet restriction

146
Q

what group is fluoxetine most commonly used in?

A

adolescents and children

147
Q

MoA of SSRIs

A

inhibits reuptake of serotonin from the synaptic cleft to the presynaptic membrane increasing concentration in synaptic cleft

148
Q

Side effects of SSRIs

A
GI + STRESS
GI sx (nausea, dyspepsia, bloating, flatulence, diarrhoea and constipation), Sweating, Tremor, Rash, EPSEs (uncommon), Sexual dysfunction/somnolence/increased suicidal ideation in first few days
149
Q

What conditions are cautions when prescribing SSRIs

A

IHD (post-MI = sertraline)
Hx bleeding disorders/anticoag - avoid in warfarin/heparin
hx GI bleeding - avoid co-prescribing NSAIDs, but if you do give gastroprotection
epilepsy
hepatic/renal impairment

150
Q

when should you review a patient after starting SSRIs

A

1 wk if <30 or increased risk suicide, 2 weeks otherwise

151
Q

how does serotonin syndrome present and how would you manage it?

A

increased serotonin activity usually within minutes of taking medication, cognitive sx - confusion, headache, agitation, hypomania, hallucinations + coma. Autonomic - shivering, sweating, hyperthermia, htn, tachycardia. Somatic - myoclonus, hyperreflexia, tremor.
Mx - stop offending drug (SSRI/TCA/lithium), supportive rx

152
Q

what is discontinuation syndrome?

A

suddenly stop SSRI - chills insomnia, hypomania, anxiety and restless with GI sx so taper dose down over 4wks don’t just stop

153
Q

MoA of SNRIs

A

inhibits reuptake of NA and 5HT by presynaptic membrane (more effective and rapid onset than SSRIs), but does not block cholinergic receptors (less S/E than TCAs)

154
Q

S/E SNRIs

A

nausea, dry mouth, headache, headache, dizziness, sexual dysfunction, htn

155
Q

CI for SNRIs

A

mania, any condition with high risk of arrhythmia, uncontrolled htn (regular BP monitoring starting venlafaxine)

156
Q

what group is mirtazapine most commonly used in?

A

depression where pt would benefit from weight gain and is struggling with insomnia

157
Q

MoA of NASSAs

A

weak NA reuptake inhibiting effect, anti-histaminergic, a1 + a2 blocker effect causes increased appetite and sedation

158
Q

S/E of mirtazapine

A

increased appetite, drowsiness and fatigue, abnormal dreams, oedema, weight gain, dry mouth, postural hypotension, tremor, confusion, anxiety, insomnia, arthralgia, myalgia. Uncommon - mania, syncope, hallucinations. Rarely - pancreatitis, aggression, myoclonus

159
Q

S/E NARIs

A

nausea, dry mouth, constipation, anorexia, tachycardia, palpitations, vasodilatation, postural hypotension, headache, insomnia, dizziness, chills, impotence, urinary retention, impaired visual accommodation, sweating and hypokalaemia

160
Q

MoA of TCAs

A

inhibit reuptake of serotonin and noradrenaline in synaptic cleft, affinity for cholinergic and 5HT2 receptors causes side effects

161
Q

S/E of TCAs

A

S/E + toxicity in OD big reason why not used!
Anticholinergic (urinary retention, blurred vision, dry mouth, constipation, confused), cardiac - arrhythmia, postural hypotension, tachycardia, syncope, sweating, hypersensitivity (urticaria, photosensitivity), metabolic (increased appetite and weight gain, blood glucose dysregulation), hypomania/mania, confusion, delirium; headache, sexual dysfunction, tremor; endocrine - testicular enlargement, gynaecomastia, galactorrhea; neuropathy - convulsions, movement disorder, dysarthria, paraesthesia, taste disturbance, tinnitus

162
Q

CI for TCAs

A

arrhythmia, recent MI, mania, severe liver disease, agranulocytosis (not normal but also someone with high risk suicide - OD potential)

163
Q

MoA of MAOIs

A

inactivate monoamine oxidase enzymes to prevent breakdown of 5HT, NA, dopamine and tyramine. inactivation of MAO-A enzyme produces positive effects, MAO-B causes interactions with food

164
Q

S/E MAOIs

A

arrhythmia, postural hypotension, drowsiness, insomnia, headache, increased appetite and weight gain, anorgasmia, LFTs raised, hypertensive reaction with non-selective MAOIs and tyramine containing foods (cheese, marmite, bovril, liver, some red wines). Interactions with opiates, insulin, SSRI, TCAs, AEDs.

165
Q

what is the main side effect of typical and atypical antipsychotics by class?

A

typicals - EPSEs
atypicals - less EPSEs but more metabolic syndrome due to serotonergic activity which treats affective + negative symptoms.

166
Q

at what point should clozapine be considered for use in a patient on antipsychotics?

A

3rd line rx - start on atypical, assess over 2wks, change as needed to atypical/typical, assess over 2wks, check compliance/change to clozapine

167
Q

Describe the activity of each dopaminergic pathway in the schizophrenic brain, and thus the side effects it produces during rx antipsychotic

A

Mesocortical - responsible for negative sx
Mesolimbic - responsible for positive sx
Nigrostriatal - responsible for EPSEs in rx
Tuberoinfundibular - responsible for hyperprolactinaemia in rx (which causes osteoporosis, anovulation, a/oligo-menorrhoea, galactorrhea, gynaecomastia)

168
Q

side effects specific to clozapine

A

hyper salivation, agranulocytosis, constipation and bowel obstruction

169
Q

what are EPSEs and when do they develop relative to starting rx?

A

Dystonia - within days - torticollis, oculogyric crisis
Parkinsonism - weeks-months - bradykinesia, rigidity, tremor
Akathisia - first few months - restlessness
Tardive dyskinesia - years - choreoathetoid movement, most commonly pouting and chewing

170
Q

how are EPSEs treated in psych?

A

procyclidine

171
Q

how does neuroleptic malignant syndrome present?

A

rare but life threatening, seen within hrs-days of starting atypical antipsychotic (can be on cessation of dopaminergic drug e.g. levodopa). Sx - pyrexia, muscle rigidity, confusion, autonomic lability (tachycardia, fluctuating BP, htn, tachypnoea), fluctuating consciousness and agitated delirium.

172
Q

how would you investigate and manage ?neuroleptic malignant syndrome

A

Ix - FBC (leukocytosis) CK (up), LFTs (deranged)
Mx - stop antipsychotic, monitor obs, IV fluid to prevent AKI, cooling ± dantrolene/bromocriptine. Complications = PE, renal failure, shock

173
Q

baseline investigations for starting pt on antipsychotics?

A

Baseline - pregnancy test, ECG, FBC, U+Es, LFTs, fasting glucose, lipids, CK, PRL; ECG; weight and BP

174
Q

how would you monitor a patient on clozapine?

A

weekly FBC for 18wks, then fortnightly until 1yr, then monthly to ensure no agranulocytosis

175
Q

how long should a patient continue on antipsychotics following an acute episode and how would they stop?

A

stay on for at least 1-2yrs after episode (some recommend 5yrs), taper dose over 3wks

176
Q

side effects of lithium

A

GI (N+V, diarrhoea), leukocytosis, polydipsia, polyuria, fine tremor, impaired renal function, hypothyroidism, hair loss, weight gain and fluid retention, metallic taste, teratogenicity in pregnancy (floppy baby, neonatal thyroid abnormality, CHD commonly ebsteins anomaly)

177
Q

sx lithium toxicity

A

coarse tremor, oliguric renal failure, ataxia, hyperreflexia, confusion, convulsions, coma

178
Q

how would you monitor someone starting lithium?

A

baseline - pregnancy test, U+Es, TFTs, ECG, discuss contraceptive use, avoid NSAIDs, regular fluid intake, 1-2u alcohol a day, takes 3-6m to establish.
lithium levels - take 12h post-dose weekly until stable in TW (0.5-1mmol/l) for 4 weeks, then 3-monthly
U+Es 6 monthly
TFTs annually

179
Q

side effects of valproate

A

teratogenicity, weight gain, aggression, LFTs up, thrombocytopenia, reversible hair loss, peripheral oedema, ataxia, tremor/tiredness, vomiting

180
Q

s/e carbamazepine

A

GI disturbance, dermatitis, dizziness, hyponatraemia, leukopenia/thrombocytopenia

181
Q

MoA of carbamazepine

A

reduces neuronal excitability by blocking voltage-gated sodium channels to reduce neuronal firing/glutamate release/dopamine and NA turnover

182
Q

what makes LTG so different from its mood stabilising counterparts?

A

stabilises mood by lifting! Good for BPAD with prominent depression/adjunct for depression, but does not rx mania. also less teratogenic and tends to be better tolerated (GI sx, rash)

183
Q

MoA of benzodiazepines

A

potentiate the inhibitory effect of GABA by acting as a positive allosteric modulator at GABA-A receptors to increase frequency of chloride channels opening and allowing inflow of Cl- and thus hyper polarising neuronal membrane

184
Q

S/E benzodiazepines

A

hangover effect - drowsiness and lightheadedness morning after
paradoxical increase in aggression
confusion, ataxia, amnesia, dependence, muscle weakness, respiratory depression

185
Q

how does benzodiazepine overdose present and how would you rx it?

A

ataxia, dysarthria, nystagmus, somnolence, resp depression, coma; mx - A to E assessment and IV flumazenil

186
Q

how does benzodiazepine withdrawal present?

A

up to 3wks after, insomnia, anxiety, reduced appetite, tremor, sweating, mydriasis, headache, mood swings, tinnitus, perceptual disturbance

187
Q

drugs which reduce seizure threshold

A

lithium, antipdepressants and antipsychotics

188
Q

indications for ECT

A

prolonged or severe mania
severe depression - life-threatening/treatment resistant/risk to self or others
catatonia

189
Q

S/E ECT

A

short-term - status epilepticus, cardiac arrhythmia, headache, short term memory loss/confusion, myalgia, anaesthetic risks (N+V, sore throat, laryngospasm), oral and dental trauma, peripheral nerve palsy
long-term - anterograde and retrograde amnesia

190
Q

CI to ECT

A

only absolute = raised ICP (e.g. SOL, intracranial bleed)

MI <3m ago, stroke <1m ago, cerebral aneurysm, status epilepticus, major unstable fracture, severe anaesthetic risk

191
Q

what is capacity

A

the ability to make a decision, requires ability to understand information, retain it long enough to process it and use it to make a decision which they can then communicate (verbal, signed, etc), it is time-specific and decision-specific.

192
Q

If someone has been deemed to lack capacity what are your next steps?

A

defer to advanced directive/lasting power or attorney

if no LPA or NOK then appoint an independent mental capacity advocate and treat patient in best interest

193
Q

advanced care planning consists of what 3 major steps?

A

appoint LPA, advanced statements, advanced directive

194
Q

what is the difference between an advance directive and an advance statement?

A

advance directive - legal document with specific refusal of rx in a pre-defined future situation in which they lack capacity. Can refuse care but not demand it, cannot refuse basic care need (e.g. nutrition)
advance statement - can be verbal or written, allows patient t make general statement about wishes and preference for future, more general e.g. where to be cared for, what food they’d like, etc; not legally binding

195
Q

what is a deprivation of liberty safeguard?

A

ensures people in care homes/hospital who lack capacity are cared for in the least restrictive way that does not inappropriately restrict freedom. Hospital/care home applies for authorisation of DoLS. Used in situations in which patient is closely monitored, restrained, given sedating medication

196
Q

who can a section be used on?

A

individuals 16+ who will not be admitted voluntarily for assessment/treatment of a mental health disorder, it excludes patients where the problem is due to intoxication with alcohol/drugs.

197
Q

Describe section 2 uses, duration, application, appeals

A

28d assessment order made by AMHP on recommendation of two doctors, one of whom is an approved clinician. Cannot be renewed. Pt may appeal to tribunal within first 14d, and to hospital manager at anytime. Pt cannot refuse treatment

198
Q

Describe section 3 uses, duration, application, appeals

A

6m treatment order made by AMHP + 2 dr both of whom have seen pt in last 24h. Can be renewed. Pt can appeal to tribunal once during first 6m, again in second 6m, then yearly. Can be treated against their will for the first 3m at which point second opinion appointed doctor for assessment. Entitled to aftercare under s117.

199
Q

Describe section 4 uses, duration, application, appeals

A

72h emergency section where section 2 would constitute unacceptable delay, often converted to section 2 on arrival at hospital. GP + AMHP/NR. No right to appeal.

200
Q

Describe section 5(2) uses, duration, application, appeals

A

72h holding order where doctor can legally detain a voluntary inpatient (not A+E), for conversion to S2/S3, cannot appeal

201
Q

Describe section 5(4) uses, duration, application, appeals

A

6h nurses holding order voluntary inpatient

202
Q

Describe section 135

A

court order allows police to enter a persons home to remove to place of safety for assessment

203
Q

Describe section 136

A

24h - police remove person from public place to place of safety for assessment