psych Flashcards
define mood disorder
disturbance of mood severe enough to impair ADLs, characterised by distorted excessive or inappropriate moods/emotions for a sustained period of time
define affect
transient flow of emotions in response to stimulus
define mood
sustained experienced emotional state over a period of time which can be described subjectively or objectively as dysthymic, euthymic or elated
how can primary mood disorders be classified?
unipolar - depressive disorder (mild, mod, severe, psychotic) or dysthymia
bipolar - bipolar affective disorder (1 or 2), cyclothymia
list causes of secondary mood disorder
physical - anaemia, hypothyroid, malignancy, cushings/addisons, MS, Parkinsonism
psych - schizophrenia, alcoholism, dementia, personality disorder
drug induced - interferon a, corticosteroids, digoxin, AED, b-blocker, antidepressant
define depressive disorder
mood disorder characterised by persistent low mood (2wks+), lack of energy and/or anhedonia accompanied by emotional cognitive and biological symptoms
what is the hypothesised pathophysiology underlying mood disorder?
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
risk factors for depressive disorder?
FF, AA, PP, SS family history, female alcohol, adverse events past depression, physical comorbidity social support low, SES low
biological clinical features of depression
psychomotor retardation, EMW, diurnal variation in mood, low appetite and weightloss, loss of libido
cognitive sx of depression
suicidal ideation, poor concentration, guilt, Becks triad of negative thoughts about self/world/future
core sx depression
anhedonia, anergia, persistent low mood lasting for at least 2 weeks
How is severity of depressive disorder classified?
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
Ddx for depression
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.
Ix for ?depression
PHQ9, HADS, Beck’s depression inventory
FBC, U+Es, LFTs, TFTs, calcium, glucose
atypical/?SOL = CT/MRI head
Mx of depression
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 long should someone continue SSRI after resolution of depressive episode?
at least 6 months if first episode, 2 years if recurrence
ECT indications
treatment resistant depression/mania
psychosis features inc catatonia
rapid response required
severe depression which is life threatening
Contraindications to ECT
only absolute - raised ICP
MI <3m ago, major unstable fracture
cerebral aneurysm
stroke <1m ago, hx status epilepticus, severe anaesthetic risk
side effects of ECT
short term - cardiac arrhythmia, headache, nausea, short term memory impairment, muscle aches, status epilepticus
long term -anterograde and retrograde amnesia
define bipolar affective disorder
chronic episodic mood disorder characterised by at least 1 episode of hypo/mania and a further episode of mania/depression.
Risk factors for BPAD?
3As, 3Ss
Age early 20s, anxiety disorder, after depression
strong family hx, substance misuse, stressful life events. Also seems more common in BAME groups
Sx of mania
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 does hypomania differ from mania?
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
What is the difference between Bipolar 1 and 2 disorder?
bipolar 1 depression and mania
bipolar 2 severe depression and hypomania
what is rapid cycling bipolar affective disorder?
at least 4 episodes of mania and depression in one year with no intervening asymptomatic periods. poor prognosis
How would you investigate ?BPAD
FBC, U&Es, LFTs, TFTs, Ca, HbA1c, glucose
urine drug test
CT head to r/o SOL if ?
Ddx for bipolar disorder
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 would you manage BPAD
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
Driving rules in mental health
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
When would you start lithium in a first presentation mania?
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
Baseline investigations before starting lithium
U+Es, TFTs, ECG and pregnancy test
S/E of lithium use within therapeutic window (and define that)
TW - 0.5-1mmol/l
polydipsia/polyuria, weight gain, oedema, fine tremor, hypothyroidism, impaired renal function, memory problems, teratogenic in pregnancy
sx of lithium toxicity and what level constitutes toxicity?
toxicity >1.5mmol, severe >2
coarse tremor, N+V, ataxia, muscle weakness, apathy, nystagmus, dysarthria, hyperreflexia, oliguria, hypotension, seizures, coma
how would you monitor someone on lithium therapy?
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
Schneiders first rank symptoms
Delusional perception
3rd person auditory hallucinations (usually running commentary)
Thought interference - withdrawal/broadcast/insertion
Passivity phenomenon
define delusions
fixed false belief held firmly despite evidence to the contrary, which goes against the individuals normal cultural/social belief system
define hallucination
perception in the absence of external stimuli, can be auditory/visual/olfactory/gustatory/somatic
what is thought disorder
impairment in the ability to form thoughts from logically connected ideas
How does circumstantiality differ to tangentiality
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
ddx for psychosis
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 does persistent delusional disorder present differently to schizophrenia?
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.
what is schizophrenia?
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
what is the underlying pathology of schizophrenia?
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
match the dopamine pathways in the brain to the effect they are responsible for in relation to schizophrenia as hypothesised by the dopamine hypothesis
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)
Positive sx of schizophrenia
Delusions (inc ideas of reference), hallucinations, formal thought disorder (knights move thinking, tangentiality, word salad, neologism), thought interference, passivity phenomenon
Negative sx schizophrenia
6As Alogia Anhedonia Attention deficit Avolition Asocial behaviour Affect blunted
Ix ?schizophrenia
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
Mx schizophrenia
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
In treating schizophrenia, your firstline antipsychotic doesn’t work, next step?
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
define anxiety disorder
Anxiety = unpleasant emotional state characterised by subjective feat and somatic symptoms. Disorder when this becomes excessive or inappropriate and impacts functioning.
Most common anxiety disorders?
specific phobia > social phobia > GAD > agoraphobia > panic disorder > OCD
psychiatric sx of anxiety disorders
inappropriate/excessive worries or fears, commonly depressive sx, feeling of impending doom, increased startle response, restlessness, poor concentration and attention, irritability, depersonalisation and derealisation
physical sx of anxiety disorders
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 can anxiety disorders be classified?
Paroxysmal - situation dependent (phobic anxiety disorder - specific/social/agora) or independent (panic disorder)
Continuous - GAD
describe generalised anxiety disorder
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 do paroxysmal anxiety disorders tend to present (vs GAD)?
abrupt onset of severe anxiety with strong autonomic symptoms but usually short lived (typically 1hr) which may occur in response to specific threats
conditions associated with anxiety disorders
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
risk factors for GAD
female, family hx, personality type, living alone/divorced/single parent, stressful life events, unemployment, relationship problems, illness
clinical features specific to GAD
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)
Ix ?anxiety disorder
FBC (infection, anaemia), TFT(hyper), glucose (hypo), ECG (arrhythmia/sinus tachycardia), GAD-2/7, Becks anxiety inventory
Mx GAD
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
define phobia
intense and irrational fear of an object/place/person/situation that is recognised as excessive or unreasonable
define agoraphobia
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
define social phobia
fear of social situation which may lead to humiliation, criticism or embarrassment
clinical features which differentiate phobic anxiety disorders from GAD
specific situations
anticipatory anxiety
attempted avoidance
Mx phobic anxiety disorders
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
what is a panic disorder?
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
risk factors for panic disorders
family hx, major life events, age 20-30, recent trauma, female, other mental disorder, white, asthma, smoker, medication (e.g. benzo withdrawal)
sx of panic disorders
PANICS Disorder Palpitations Abdominal distress Numbness/nausea Intense fear of death Choking sensation/chest pain Sweating/SOB/shaking Depersonalisation/derealisation
how does the associated behaviour and cognitions differ in GAD, panic disorder and phobic anxiety disorder?
GAD = irritable, constant worry panic = escape, fear of sx phobic = avoid, fear of situation
Mx of panic disorder
SSRIs (no improvement after 12wk consider TCA)
CBT
bibliotherapy, support group, encourage exercise
what is PTSD
intense prolonged delayed reaction following exposure to an exceptionally traumatic event
what is abnormal bereavement
loss overwhelms coping capacity in a grief reaction that has delayed onset, is prolonged (6m) and more intense
risk factors for PTSD
exposure to major traumatic event, perceived threat to life
hx mental illness/trauma/childhood abuse
female
low SES, life stressors, poor social support
Clinical features of PTSD
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
mx PTSD
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
what is OCD
syndrome characterised by recurrent obsessional thoughts ± compulsive acts which are present most days for at least 2 weeks.
what are obsessions in the context of OCD?
recurrent, intrusive and distressing thoughts/mental images/urges that are egodystonic and recognised by the patient as a product of their own mind.
what are compulsions in the context of OCD?
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.
clinical features of OCD
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
Ddx ?OCD
epilepsy, head injury, dementia
ED/anankastic PD/body dysmorphic disorder
Mainly O - anxiety/depression/hypochondria/schizophrenia
Mainly Cs - Tourettes/kleptomania
Mx OCD
CBT with exposure and response prevention component
SSRI (fluoxetine, paroxetine, sertraline, citalopram) or clomipramine if severe
How does somatisation disorder present?
multiple physical sx present for at least 2 years, patient refuses to accept reassurance or negative test results
how does hypochondriacal disorder present?
patient has a persistent belief they have serious underlying disease e.g. cancer, refuses to accept reassurance or negative test results
How does conversion disorder present?
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.
how would you mx medically unexplained sx?
psych - CBT + coping strategies
bio - anti-depressant/physical exercise
social - stress releasing activity, involve family as appropriate
What is anorexia nervosa?
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
defining clinical features of anorexia nervosa
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
what other clinical features of anorexia are seen apart from ICD10 criteria FEED?
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
Give the main ways in which anorexia nervosa can be distinguished from bulimia nervosa
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)
List ix you would perform in a person with ?anorexia nervosa
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
Ddx for AN
Anorexia, bulimia, ED-Not Otherwise Specified, schizophrenia, depression, OCD, anankastic PD
diabetes, hyperthyroid, malignancy
alcohol/substance misuse
Mx of anorexia nervosa
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
Describe the pathophysiology of refeeding syndrome?
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
complications of anorexia nervosa
hypokalaemia, hypotension, hypothermia, anaemia, cardiac failure, hypoglycaemia, osteoporosis, acute renal failure.
what is bulimia nervosa?
ED characterised by repeated episodes of uncontrolled binge eating followed by compensatory weightloss behaviours and overvalued ideas regarding ‘ideal body shape/weight’
how is the epidemiology of BN different to AN?
AN seen predominantly in higher SES, BN equal SES distribution
AN has a clear genetic proponent, unclear in BN
common comorbidities in BN?
depression, anxiety, DSH, substance misuse, EUPD
ICD10 clinical features of BN?
‘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
List possible consequences of the repeated vomiting and hypokalaemia seen in BN
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.
Ix in BN?
FBC, U&Es, TFTs, amylase, glucose, lipids, Mg, Ca, P, VBG
ECG - arrhythmia, increased PR interval, flattened/inverted t waves, prominent u waves.
how would you mx BN?
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
What are the defining clinical features of substance dependence syndrome?
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
How would someone withdrawing from opioids present?
3 of: craving, lacrimation, rhinorrhoea, myalgia, abdo cramps, N+V, diarrhoea, piloerection, pupillary dilatation, increased HR/BP
how would someone withdrawing from benzodiazepines present?
tremor (hands, tongue, eyelid), N+V, tachycardia, postural hypotension, headache, agitation, malaise, transient illusions/hallucinations, paranoid ideation, grand Mal seizure
Mx of substance misuse?
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
how do you calculate the number of units of alcohol in a drink?
ABV (%) x volume (ml) / 1,000
Alcohol dependence features
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
how would you screen for alcohol dependence?
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)
how does alcohol withdrawal present?
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)
What is wernickes encephalopathy?
neuropsychiatric disorder seen in thiamine (B1) deficiency. sx confusion, ophthalmoplegia + nystagmus, ataxia, hypothermia + delirium. Rx IV pabrinex (PO thiamine after IV/prophylaxis)
what is Korsakoff syndrome?
sequelae of untreated wernickes encephalopathy, profound and irreversible short-term memory loss, characterised by retrograde and anterograde amnesia, and confabulation, ± disorientation to time
mx of alcohol abuse
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.
what is a personality disorder?
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.
risk factors for personality disorder
low SES, genetics, poor parenting and parental deprivation, childhood abuse
what are the cluster A personality disorders?
schizoid and paranoid
what are the cluster B personality disorders?
histrionic, EUPD, antisocial
what are the cluster C personality disorders?
anxious, dependent, anankastic
how does schizoid personality disorder present?
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
how does paranoid personality disorder present?
SUSPECTS Suspicious Unforgiving Spousal fidelity questioned Perceives attack Envious Cold affect/criticism not liked Trust in others reduced Self reference
how does EUPD present?
AM SUICIDE Abandonment feared Mood instability Suicidal behaviour Unstable and Intense relationships Control of anger poor Impulsivity Disturbed sense of self Emptiness (chronic)
how does histrionic personality disorder present?
PRAISE Provocative behaviour Real concern for physical attractiveness Attention seeking Influenced easily Superficial/seductive inappropriately Egocentric/exaggerated emotion
how does antisocial personality disorder present?
CORRUPT Callous Others to blame Reckless disregard for safety Remorseless Underhanded Poor planning (impulsive) Temper/tendency to violence
how does dependent personality disorder present?
RELIANCE reassurance needed expressing disagreement is difficult lack self-confidence initiating project difficult abandonment feared needs others to assume responsibility companionship sought exaggerated fears
how does anxious personality disorder present?
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
how does anankastic personality disorder present?
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
Mx personality disorder
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.
risk factors for DSH
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
Motives for DSH
DRIPS Death wish Relief - temporary escape form pain Influence others to change views/behaviour Punishing self Seek attention/help
Mx DSH
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
risk factors for suicide
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
risk factors for suicide following DSH
Note left behind Planned Attempts to avoid discovery Afterwards help not sought Violent method Final acts - organising finances, writing will etc.
Aim of CBT
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
Why are SSRIs first line for depression?
better tolerated + work more quickly + less risk of inducing mania
others are more effective but less tolerable/safe
how long does it take for antidepressants to take effect?
1wk, but 4-6 weeks til clinically detectable benefit
What type of anti-depressant is citalopram?
SSRI
what type of anti-depressant is venlafaxine?
SNRI - serotonin + noradrenaline reuptake inhibitor
what type of anti-depressant is mirtazapine?
NASSA - Noradrenaline and specific serotonergic antidepressants
what type of anti-depressant is reboxetine?
NARI - NA reuptake inhibitor
what type of anti-depressant is trazodone?
SARI - serotonin antagonist and reuptake inhibitor
what type of anti-depressant is amitriptyline?
TCA
what type of anti-depressant is clomipramine?
TCA
what type of anti-depressant is dosulepin?
TCA
what type of anti-depressant is phenelzine?
MAOI
what type of anti-depressant is moclobemide?
irreversible MAOI specific to MAOI-A so no diet restriction
what group is fluoxetine most commonly used in?
adolescents and children
MoA of SSRIs
inhibits reuptake of serotonin from the synaptic cleft to the presynaptic membrane increasing concentration in synaptic cleft
Side effects of SSRIs
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
What conditions are cautions when prescribing SSRIs
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
when should you review a patient after starting SSRIs
1 wk if <30 or increased risk suicide, 2 weeks otherwise
how does serotonin syndrome present and how would you manage it?
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
what is discontinuation syndrome?
suddenly stop SSRI - chills insomnia, hypomania, anxiety and restless with GI sx so taper dose down over 4wks don’t just stop
MoA of SNRIs
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)
S/E SNRIs
nausea, dry mouth, headache, headache, dizziness, sexual dysfunction, htn
CI for SNRIs
mania, any condition with high risk of arrhythmia, uncontrolled htn (regular BP monitoring starting venlafaxine)
what group is mirtazapine most commonly used in?
depression where pt would benefit from weight gain and is struggling with insomnia
MoA of NASSAs
weak NA reuptake inhibiting effect, anti-histaminergic, a1 + a2 blocker effect causes increased appetite and sedation
S/E of mirtazapine
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
S/E NARIs
nausea, dry mouth, constipation, anorexia, tachycardia, palpitations, vasodilatation, postural hypotension, headache, insomnia, dizziness, chills, impotence, urinary retention, impaired visual accommodation, sweating and hypokalaemia
MoA of TCAs
inhibit reuptake of serotonin and noradrenaline in synaptic cleft, affinity for cholinergic and 5HT2 receptors causes side effects
S/E of TCAs
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
CI for TCAs
arrhythmia, recent MI, mania, severe liver disease, agranulocytosis (not normal but also someone with high risk suicide - OD potential)
MoA of MAOIs
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
S/E MAOIs
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.
what is the main side effect of typical and atypical antipsychotics by class?
typicals - EPSEs
atypicals - less EPSEs but more metabolic syndrome due to serotonergic activity which treats affective + negative symptoms.
at what point should clozapine be considered for use in a patient on antipsychotics?
3rd line rx - start on atypical, assess over 2wks, change as needed to atypical/typical, assess over 2wks, check compliance/change to clozapine
Describe the activity of each dopaminergic pathway in the schizophrenic brain, and thus the side effects it produces during rx antipsychotic
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)
side effects specific to clozapine
hyper salivation, agranulocytosis, constipation and bowel obstruction
what are EPSEs and when do they develop relative to starting rx?
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
how are EPSEs treated in psych?
procyclidine
how does neuroleptic malignant syndrome present?
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.
how would you investigate and manage ?neuroleptic malignant syndrome
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
baseline investigations for starting pt on antipsychotics?
Baseline - pregnancy test, ECG, FBC, U+Es, LFTs, fasting glucose, lipids, CK, PRL; ECG; weight and BP
how would you monitor a patient on clozapine?
weekly FBC for 18wks, then fortnightly until 1yr, then monthly to ensure no agranulocytosis
how long should a patient continue on antipsychotics following an acute episode and how would they stop?
stay on for at least 1-2yrs after episode (some recommend 5yrs), taper dose over 3wks
side effects of lithium
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)
sx lithium toxicity
coarse tremor, oliguric renal failure, ataxia, hyperreflexia, confusion, convulsions, coma
how would you monitor someone starting lithium?
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
side effects of valproate
teratogenicity, weight gain, aggression, LFTs up, thrombocytopenia, reversible hair loss, peripheral oedema, ataxia, tremor/tiredness, vomiting
s/e carbamazepine
GI disturbance, dermatitis, dizziness, hyponatraemia, leukopenia/thrombocytopenia
MoA of carbamazepine
reduces neuronal excitability by blocking voltage-gated sodium channels to reduce neuronal firing/glutamate release/dopamine and NA turnover
what makes LTG so different from its mood stabilising counterparts?
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)
MoA of benzodiazepines
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
S/E benzodiazepines
hangover effect - drowsiness and lightheadedness morning after
paradoxical increase in aggression
confusion, ataxia, amnesia, dependence, muscle weakness, respiratory depression
how does benzodiazepine overdose present and how would you rx it?
ataxia, dysarthria, nystagmus, somnolence, resp depression, coma; mx - A to E assessment and IV flumazenil
how does benzodiazepine withdrawal present?
up to 3wks after, insomnia, anxiety, reduced appetite, tremor, sweating, mydriasis, headache, mood swings, tinnitus, perceptual disturbance
drugs which reduce seizure threshold
lithium, antipdepressants and antipsychotics
indications for ECT
prolonged or severe mania
severe depression - life-threatening/treatment resistant/risk to self or others
catatonia
S/E ECT
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
CI to ECT
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
what is capacity
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.
If someone has been deemed to lack capacity what are your next steps?
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
advanced care planning consists of what 3 major steps?
appoint LPA, advanced statements, advanced directive
what is the difference between an advance directive and an advance statement?
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
what is a deprivation of liberty safeguard?
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
who can a section be used on?
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.
Describe section 2 uses, duration, application, appeals
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
Describe section 3 uses, duration, application, appeals
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.
Describe section 4 uses, duration, application, appeals
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.
Describe section 5(2) uses, duration, application, appeals
72h holding order where doctor can legally detain a voluntary inpatient (not A+E), for conversion to S2/S3, cannot appeal
Describe section 5(4) uses, duration, application, appeals
6h nurses holding order voluntary inpatient
Describe section 135
court order allows police to enter a persons home to remove to place of safety for assessment
Describe section 136
24h - police remove person from public place to place of safety for assessment
