Psych Flashcards
what is parasuicide
an act that looks like suicide but does note result in death.
Parasuicide can be tantamount to attempted suicide but not necessarily – may just be a cry for help
how would you carry out a suicide assessment?
first thing is to ensure medical safety and fitness
history
- event leading up to the suicide
- planned?
- did they leave a note?
- precaution against discovery?
self-harm incident
- what method? violent vs non-violent
- intoxicated?
- alone?
- what was going through their head?
- who found them? found by chance?
after the incident - how did the patient feel? - did they seek help after the event? - how did they get to A&E? - how do they feel about the event now? regret?
perform a full risk assessment
- current suicidal ideations and mental state
- screen fore depression/psychosis/alochol dependency/anorexia
- previous attemtps?
- outlook for futures? what will they do when thy get home
- any protetct factors?
management for suicide attempt
• Acute management
o Ensure patient is medically safe and stable
o Complete a full assessment
• Long term management will depend upon:
o Level of risk
o Comorbidities
Anxiety and depression need appropriate management
o Was it an impulsive act?
Acts that are genuinely regretted in adults often do not need long term follow up
o Part of a pattern of repeated self-harm?
• In most cases patient can be discharged back into the community
o Especially if strong social support network and no current suicidal thoughts
o Safety plan (see prevention below):
o Crisis Team information
o Refer to GP for follow up – in some cases also the CMHT
If already under the care of CMHT contact their care co-ordinator as soon as possible
what is dementia
a syndrome due to disease of the brain that is chronic or progressive in nature. Involves disturbances of higher cortical function
• Should be present for at least 6 months
what are the main types of dementia?
- Alzheimer’s – most common
- Atrophy of the cerebral cortex, ↓ Ach, senile (β amyloid) plaques, ↑ neurofibrillary Tau protein tangles
- Lewy Body
- Lewy bodies = intracellular eosinophilic inclusions – consist of abnormally phosphorylated neurofilament proteins, aggregated with ubiquitin and alpha synuclein → neuronal loss → ↓ Ach. Senile plaques may also be seen
- Fronto-temporal (Pick’s disease)
- Selective, asymmetrical knife blade atrophy in the frontal and temporal areas. Pick cells = ballooned neurons. Pick bodies = Tau +ve neuronal inclusions.
- Vascular
- Thrombotic event = deterioration. Stepwise progression
clinical features of dementia
- Diagnosis based upon cognition is impaired & activities of daily living are affected
- No clouding of consciousness
- Memory Loss - short term memory affected more than long term. I.e. difficult to learn new things & commonly disorientated
- Impaired Thinking - concrete thinking, poor judgement, reduced fluency, struggles to make plans, may have delusions, sundowning (confusion worse in the evening)
- Agnosia - inability to recognise things: visual, auditory, prosopagnosia (inability to recognise faces)
- Language - expressive (Broca’s - frontal) / receptive dysphasia (Wernicke’s - parietal)
- Lexical anomia - word finding difficulty (i.e forgetting that a phone is called a phone)
- Personal Functioning - severe senile self neglect (Diogennes Syndrome); tendency to hoard rubbish
- Personality & Behaviour - euphoria, emotional lability (rapid changes); apathy, irritable, frustrated, disinhibition in social setting - can lead to aggression
- Hallucinations – mostly visual
- Motor impairment – apraxia, spastic paresis, urinary incontinence
what are the 5 As of alzheimer’s
Amneis aphasia agnosia apraxia associated behvaiours. psychological, delusions
psychological - delusions, hallucinations, depression, anxiety
behavioural - aggression, wandering, agitation
clinical features of Lewy body dementia
- Marked fluctuations in cognitive impairment and alertness
- Vivid visual hallucinations (70%) – occurs earlier than any other dementia
- Early parkinsonism (70%)
- Frequent faints and falls
clinical features of fronto-temporal dementia
- Insidious onset and gradual progression
- Early decline in social interpersonal conduct
- Early impairment in regulation of personal conduct
- Early emotional blunting
- Early loss of insight
what are some risk assessment of confused older adults are there?
to self
- wandering
- leaving the gas on
- leaving keys in the door
- abuse
- neglect by self or others
- falls
to others
- driving - have to inform DVLA and unable to drive
- aggression
- risk behaviors
what are some investigations for dementia
MMSE/Addenbrook’s
bloods = FBC, U&Es, TFT< LFT, b12, folate, ca, mg, serum cholesterol, serum glucose
cxr
ct head
mri - 1st chocie for suspected fronto-temporal disease
SPECT (Dat) - Lewst body
differentials for dementia
- Drugs, delirium
- Emotions/depression
- Metabolic disorders
- Eye and ear impairment
- Nutritional disorders
- Tumours, toxins, traumas
- Infections
- Alcohol, arteriosclerosis
management of dementia
- Memory aids e.g. clocks, calendars, photographs
- Try and keep at home for as long as possible
- Psychological:
- Emotional support
- CBT
- Social
- Carer support
- Occupational therapy
- Biological
- Alzheimers
- AchEI e.g. donepezil, rivastigmine. SE: stomach ulcers, N+V
- Diazepam/lorazepam for anxiety
- SSRI’s for depression
- Mementine (NMDA receptor) – 2nd line
- Risperidone (antipsychotic) for agitation
- Lewy body – AchIn e.g. rivastigine. AVOID antipsychotics
- Diazepam/lorazepam for anxiety
- SSRI’s for depression
- Mementine (NMDA receptor) – 2nd line
- Vascular – Stop smoking, healthy eating, exercise, anticoagulants
- Fronto-temporal – AVOID AchEI’s
what is an adjustment disorder?
A protracted (lasting longer than usual) response to a significant life change or event (within the last 3 months)
how long does acute adjustment disorder need to be?
< 6 months
how long does chronic adjustment disorder need to be?
> 6 months and causes disruption to a person’s life
what is acute stress reaction?
o Acute response to highly threatening or catastrophic experience
o Anxiety dies down within hours/days
clinical features of acute stress reaction?
traumatic event
dazed
amnesia or denial to the events
overactivity or withdrawal
somatic symptoms eg tachycardia, sweating, flushed, “dazed”
clinical features of adjustment disorder
significant life changes longer period of time, symptoms fluctuates depression, anxiety preoccupation with events angry outburst, disturbed
some somatic symptoms
management of acute stress reaction
remove stress, reassurance, support, short course benzodiazepine
management of adjustment disorder
- Usually self resolving
- Psychological interventions may be useful: problem solving psychotherapy, crisis intervention
- Biological: antidepressants/Anxiolytics rarely required
what is bereavement
objective state of having experienced a loss
what is grief
the subjective state of experiencing the psychological and physiological reaction to loss
what is complicated/pathological grief
failure to return to a pre-loss level of performance or state of emotional wellbeing
often > 6 months
what are the stages of normal bereavement?
< 12 months
DAB DA
Denial - may include auditory/visual psuedohallucinations
Angry
Bargaining
Depression
Acceptance
what is considered normal bereavement
< 12 months
sadness,anxiety, apathy, hallucinations
no functional impairment
wants to be with the deceased - inc wanting to die specifically to be with them
what is abnormal bereavement
> 12 months
sadness, anxiety, apathy, hallucinations
functional impairment
suicidal ideations with no intentions of it being just to be with the loved one
management of normal bereavement
- 3C’s – Comfort, Consultation, Coping (restitution)
- CBT
- Medications e.g. depressive, anxiety symptoms
- Individual counseling
- Group therapy
what is the management of abnormal bereavement
- 3C’s – Comfort, Consultation, Coping (restitution)
- CBT
- Medications e.g. depressive, anxiety symptoms
- Individual counselling
- Group therapy
- Complicated grief treatment
- Residential inpatient management/ outpatient grief rehabilitation programmes
what is somatisation
Physical symptoms that cannot fully be explained by other medical, neurological or psychiatric disorders
aetiology of somatisation
- Female
- Hx of life stressors
- Recent life stressors
- Anxiety
- Depression
clinical features of somatisation
- Multiple physical SYMPTOMS present for a long time (>2 years) that cannot be accounted for with a physical disorder
- Symptoms that are distressing or result in significant disruption of daily life eg abdo pain, headahce, aching muscles, fatigue, neuro symptoms
- Excessive thoughts, feelings, or behaviours related to the somatic symptoms or associated health concerns as manifested by at least one of the following:
- Disproportionate and persistent thoughts about the seriousness of one’s symptoms
- Persistently high levels of anxiety about health or symptoms; excessive time or energy devoted to these symptoms or health concerns
- Even if any one somatic symptom is not continuously present, the state of being symptomatic is persistent (typically more than 6 months)
what other conditons are included in somatization?
somatoform disorder
hypochondriacal disorder - – worrying that you are going to DEVELOP a serious medical condition despite medical reassurance to the contrary
conversion disorder - conversion anxiety into more tolerable symptoms that attack benefits of the sick role
what is anxiety?
A state consisting of psychological & physical symptoms brought out by a sense of apprehension by a perceived threat
what are some neurochemical theory of anxiety?
inc noradrenergic and seratonergic neurons & GABA may contribute to symptoms of anxiety disorders
what are the different types of anxiety disorder
phobia
- agoraphobia -Fear of places that are difficult or embarrassing to escape from
- social phobia - fear of being judged by pthers & being embarrased or humiliated. can be in spefici social situations
- specific phobia
GAD
PTSD
Panic Disorder
aetiology of anxiety disorder
- Young adulthood
- Women
- Endocrine: hyperthyroid, Cushing’s pheochromocytoma, hypoglycaemia
- Genetic: neurotic personality traits
- Environmental: can be triggered by stressful events, particularly those involving threat. Also results from stressful/traumatic events in childhood e.g. parental indifference/ physical abuse
- Drug/alcohol intoxication/withdrawal
what are some clinical features of anxiety disorder
biological
- palpitations, tachycardia, chest pain
- dry mouth, globus hsytericus, abdo discomfort, frequent/loose motions
- hyperventilation, difficulty catching breath, chest tightness
- urinary frequency, failure of erection, amenorrhoea
- hot flushes,cold chils, tremour, sweating, headhcales, muscle pains, numbness
psychological
- the feeling of impending doom, restlessness, startle response, poor concentration, insomnia, night terrors, depersonalisation, derealisation
what are some GAD specific symptoms
long-standing anxiety that may fluctuate but is neither situational or episodic, free-floating
> 6 months of worry without prominet tension
worry about everyday events
autonomic arousal irritability poor concentration muscle tension tiredness sleep disturbance depressive symptoms
what are the clinical features of panic disorder?
rapid onset of severe anxiety lasting 20-30 minutes
can occur unexpectedly
panic disorder = panic attack occurs recurrently
ICD criteria - 4 of the following - palpitations - dizziness - feeling of choking - chest pain \+ 1 autonomic arousal symptoms \+ 4 panic attacj in 4 weeks --> each lasting > 10 minutes
investigations for anxiety disorder
mainly clinical and make sure no other organic causes
GAD-7
identify social anxiety - mini SPIN
what is the management for GAD?
GAD – work in a stepwise fashion:
1) Education on the condition, self help resources for both patient and family, active monitoring of the person’s symptoms and functioning
2) Individual non facilitated self help (self help + minimal therapist contact), Individual guided self help (CBT in written form, facilitated by a trained practitioner and face to face/telephone consultations), psychoeducational groups
3) CBT/applied relaxation + SSRI/SNRI
4) Specialist care
management of phobias
Phobia: • Avoid TCA/benzos • Do not routinely offer mindfulness-based interventions 1) CBT with graded exposure 2) SSRI/SNRI 3) Short term psychodynamic therapy
management of panic disorder
Mild to moderate: Individual non facilitated self help (self help + minimal therapist contact), Individual guided self help (CBT in written form, facilitated by a trained practitioner
2) Moderate to severe: CBT AND/OR SSRIs/TCAs
3) 2 interventions tried together and not successful = specialist referral
• Benzodiazepines can be used short term
clinical features of PTSD
re-experiencing of the event (flashbacks)
avoidance
hyperarousal - hypervigilance, anger, irritability
emotional numbing/dysregulation
dissociation
-ve self perception
management of PTSD?
• Avoid benzodiazepines due to high risk of dependence
1) Peer support groups
1) Within 1 month of the event with subthreshold symptoms: active monitoring
1) Within 1 month of the event and symptomatic:
• Trauma focused CBT
• Eye movement desensitisation and reprocessing
• Supported trauma focused computerised CBT
2) Venlafaxine/SSRI
3) Risperidone – consider in addition to psychological therapies if severe hyperarousal/psychotic symptoms
how long does the symptoms of PTSD must be present in order for a diagnosis to be made?
> 1 month
what is obsessional compulsive disorder
• Can be classified as predominantly obsessional thoughts, compulsive acts or mixed obsessional compulsive
pathophsiology of OCD
• Pathology in the caudate nucleus fails to suppress signals from the orbitofrontal cortex → hypothalamus becomes overexcited & sends strong signals back to orbitofrontal cortex
what are some aetiology of OCD
Fhx of OCD
PANDAS - paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection
male
clinical features of OCD
obsessional thought
- recurrent idea, image or impulse that is perceived as being sensless
- intrusive thought doesn’t leave quickly
- unsuccessfully resisted & that results in marked anxiety/distress
- common obsessional thoughts - contamination, safety, orderliness, physical symptoms, sex, aggression
compulsive act
- a recurrent stereotyped behaviour that is not enjoyable or useful, however, reduced anxiety & distress temporarily
- usually perceived as being senseless. however is unsuccessfully resisted
- behaviour is repeated again and agina
- time-consuming> 1 hour per day
- common compulsive actions - washing & cleaning, counting, arranging & ordering, repeating a phrase, checking
what are some investigation for obsessional compulsive disorder
Yale Brown Obessive Compulsive scale
differentials for OCD
obsessive compulsive personality disorder delusional disorder Austim/ Asperger's Tourette's other anxiety disorder psychotic disorder depressive disorder
management of OCD
Mild impairment:
1) CBT → exposure & response prevention (Self-help/individual by phone/group)
Moderate impairment:
1) CBT → exposure & response prevention (Self-help/individual by phone/group)
2) High dose SSRI fluxoxetine or sertraline, clomipramine (TCA specific for OCD)
Severe impairment – specialist input after trial of clomipramine and 2 different SSRI
what is section 2 for?
detainment for assessment and treatment of a MH condition up to 28 days
treatment can only be given if it is aimed at diagnosing and treating the mental disorder or complications arising directly from the mental disorder
who can revoke or challenge section 2?
may be revoked at any time by clinician in charge, hospital managers or the nearest relatives
• Patients can also appeal the section within the first 14 days – done via a tribunal panel
when can a section 3 be used?
after a conclusive period under section 2 OR when there is already a diagnosis of a mental disorder that has been made, with no doubt of the diagnosis
how long can you be detained under section 3 for?
up to 6 months
• Section 3 can be done back to back an unlimited number of times
when can a patient appeal aginst section 3
can appeal twice within the first 6 months & then yearly after that
what is the aim of section 3
for treatment of a mental disorder
what is the aim of section 5(2)
Doctors Holding Power
- A holding power of up to 72 hours so that a MHA assessment can be carried out
- CANNOT be used to treat mental health disorder or any physical health problems
what is the aim of section 5(4)
however, an application can be recommended by a mental health nurse on a psychiatric ward
• Holding powers last up to 6h
• Patient cannot appeal and treatment cannot be given without consent
what is the aim of Section 135
Police’s ability to enables the removal of a person from their home/premises to a place of safety. Can be detained for up to 72h
what is the aim of Section 136
Enables the removal of a person from a public place to a place of safety. Can also be used to keep someone in A&E. Can be detained for up to 24h (sometimes 36h)
what are the different types of anorexia nervosa
- Restrictive type = reduced oral intake in order to cause weight loss
- Binge-purge = individuals eat large amounts of food in one sitting, followed by purging that food either by vomiting/taking laxatives
aetiology of anorexia nervosa
female
westernised countries - culture bound syndrome
Fhx
misuse of insulin
poor self-sesteem, perfectionist personality
premorbid anxiety or depressive disorder
stress eg changing schools, exams
clinical features of anorexia nervosa
restriction of energy, leading to very low weight
intense fear of weight gain
body dysmorphia
biological symptoms - yellow pigment of the skin (carotenemia), bradycardia, lanugo hair, low BP, dry skin/lips, pale conjunctiva, absent periods, constipation, diarrhoea, bloating, abdo pain
if severe - cardiac arrest, heart failure, IDA, infertility, kidney failure, osteopenia, osteoporosis
what are the severity of anorexia nervosa according to BMI?
mild - 18.5-17.5
moderate 17-16
severe 16-15
extreme < 15
investigation for anorexia nervosa
Gs and Cs raised - growth hormones, glucose, salivary glands, cortisol, cholesterol, carotinaemia
bloods - FBC (dec WBC and platelet), haematocrits, U&Es (dec phosphate), glucose, cortisol
ECG - cardiac arrest due to hyperkalaemia
BMI
assessment of muscle wasting/strength - sit up-squat-stand test
SCOFF screening questions
- S - feel SICK because you feel uncomfortably full?
- C - lost CONTROL over how much you eat?
- lost more than ONE stone in a 3 month period?
- yourself to be FAT when others say you are too thin?
- say that FOOD dominates your life?
management of anorexia nervosa
Consider emergency medical/psychiatric admission for anyone at risk of serious psychical complications/suicide/serious self harm • Weight loss >1kg a week • CV instability • Hypothermia • Abnormal bloods • Acute mental health risk • Lack of support at home Otherwise referral to CMHT/CAMHS/specialist eating disorder unit
MANTRA – Helps people to understand what causes their anorexia and encouraging a change in behaviour
1) Individual eating disorder focused CBT
1) SSCM (Specialist support of counselling and management)
1) Other: family therapy & psychotherapy to combat distorted views of their body
1) Encourage refeeding → ~3000kcal per day (needs to be done gradually to avoid refeeding syndrome)
what is bulimia nervosa
excessive overeating past he point of fullness, followed by compensatory behaviour eg vomiting/laxatives/excessive exercise
what are the different types of bulimia nervosa
purging type
non-purging type - episodes of binging followed by compensatory behaviour such as fasting & excessive exercise but not self induc vomiting
what is the time frame for bulimia nervosa?
at least an episode once a week over 3 months
aetiology of bulimia nervosa
female age around 20s
models/gymnasts/dnacers/male
diagnostic criteria of typical bulimia nervosa according to ICD-10?
• There are recurrent episodes of overeating (at least twice a week over a period of 3 months) in which large amounts of food are consumed in short periods of time.
• There is persistent preoccupation with eating, and a strong desire or sense of compulsion to eat (craving).
• The patient attempts to counteract the fattening effects of food by ≥1 of the following:
o Self-induced vomiting
o Self-induced purging
o Alternating periods of starvation
o Use of drugs such as appetite suppressants, thyroid preparations, and diuretics; when bulimia occurs in diabetic patients they may choose to neglect their insulin treatment
• There is a self-perception of being too fat, with an intrusive dread of fatness (usually leading to underweight)
diagnostic criteria of atypical bulimia nervosa according to ICD-10?
- Some of the features of bulimia nervosa are fulfilled, but the overall clinical picture does not justify that diagnosis. For instance, there may be recurrent bouts of overeating or overuse of purgatives without significant weight change, or the typical over-concern about body shape and weight may be absent.
- BMI is often within normal limits
what are other biological symptoms of bulimia nervosa
CVD - Arrhythmias, diet pill toxicity (palpitations, hypertension), valve prolapse, peripheral oedema
endocrine - Thyroid abnormalities, incomplete development of secondary sexual characteristics, impaired temperature regulation
Amenorrhoea, irregular menes, hypoglycaemia, osteopenia
GI - Acute gastric dilation, oesophageal rupture, Mallory-Weiss tears, enlargement of the parotid glands
Dehydration, electrolyte disturbance, obesity related complications
Aspiration pneumonitis
Erosion of tooth enamel
Russell’s sign: knuckle calluses from inducing vomiting (Russell probs wants to punch me)
investigation of bulimia nervosa
- BMI
- Temperature, pulse, BP
- Hydration status
- Assessment of muscle wasting/strength: Sit up-Squat-Stand test
- Person lies flat on a firm surface and has to sit up without using their hands
- Person has to rise from a squatting position without using their hands
- FBC (↓ RBC/WCC/platelets), U&Es (↓ K/Na), TFT, glucose, Ca, Mg, B12/folate,
- ECG
- SCOFF screening question:
management of bulimia nervosa
Consider emergency medical/psychiatric admission for anyone at risk of serious psychical complications/suicide/serious self harm • Weight loss >1kg a week • CV instability • Hypothermia • Abnormal bloods • Acute mental health risk • Lack of support at home Otherwise referral to CMHT/CAMHS/specialist eating disorder unit 1) Bulimia focused guided self help 1) Bulimia focused CBT/family therapy 1) Fluoxetine 60mg
what is pseudodementia
cognitive deficit in depression that mimics dementia
is pseudodementia curable?
yes - when depression is managed
clinical features of pseudodementia
- Short and abrupt onset
- Anterograde (making new memories) and retrograde (past memories) memory affected equally
- Amnesia of emotional events
- Loss of social skills – early sign
- Patient answers with ‘don’t know’ to memory testing
- Little effort in performing tasks
- Will not respond to dementia treatment [see condition]
management of pseudodementia
CBT/IPT
SSRIs
what is dysthymia
a chronic state of low mood, that is usually insidious in onset and lasts for at least 2 years
definition of BAD
at least 2 episodes of depression and mania
what is hypomania
differentiated from mania in that the mood elevation is mild, does not disrupt social activity, nor is there any psychosis
what is hypomania
differentiated from mania in that the mood elevation is mild, does not disrupt social activity, nor is there any psychosis
what is cyclothymia
mild chronic bipolar affective disorder, recurrent milk episodes elation and mild depressive symptoms, not sufficiently severe or prolonged to meet criteria for bipolar affective disorder or recurrent depressive disorder
what is rapid cycling bipolar
at least four affective episodes in a 12 month period
criteria of depression according to ICD-10?
depressive symtpoms must be > 2 weeks
what is the definition of mild depression
4 symptoms - 2 must be core
what is the definition of moderate depression
5-6 symptoms - 2 must be core
what is the definition of severe depression
7 or more symptoms - 2 must be core
what are the different types of depression according to ICD-10
mild
moderate
severe
psychotic
aetiology of depression
Monoamine Hypothesis → suggests depression results from the depletion of certain monoamine neurotransmitters, i.e. noradrenaline, serotonin, dopamine.
clinical features of depression
core symptoms - 3
1) anhedonia
2) low mood
3) aergia
psychological symptoms
1) poor concentration
2) poor self esteem
3) guilt
4) pessimism
somatic symptoms
1) sleep disturbance
2) early morning waking
3) morning depression - diurnal variation of mood
4) loos of appetite/weight loss
5) loss of libido
6) agitations
at times, in severe depression - psychotic symptoms eg nihilistic delusion/Cotard’s syndrome, delusion of guilt/poverty
investigation for depression
clinical diagnosis
PHQ-9
FBC, U&Es, LFT, TFT (to rule out hypo), ESR, vit b12 + folate (rule out anaemia)
what is the management of depression
antidepressants –> lithium –> ECT
Mild
1) Individual guided self help/computerised CBT
1) IAPT/group based CBT
2) Alternative antidepressant
Moderate
1) Antidepressant + CBT/IPT/behavioural activation/couples therapy
2) Alternative antidepressant
Severe
1) Antidepressant + CBT/IPT/behavioural activation/couples therapy
2) Alternative antidepressant
3) Consider psych referral for ECT (if treatment resistant depression)
Severe with psychosis
1) Psych referral + emergency care (benzo/ECT) + antidepressant + antipsychotic
THEN Antidepressant + ECT + antipsychotic
in those patient with suicidal ideations, which antidepressants would you not give?
TCA or MAOIs
how long should you give antidepressants before it start showing signs of effectiveness?
1 month
and upon recovery, antidperessants should be gradually reduced
pt should continue taking the same dose for 6 months before reducing
what neurochemical does a TCA target?
serotonin and noradrenaline
what neurochemical does a SSRI target?
serotonin only
what neurochemical does a NARI target?
noradrenaline
what neurochemical does a SNRI target?
serotonin and noradrenaline
what neurochemical does a NaSSA targert?
noradreanlien and specific serotonin
example of TCA
amitriptyline
imipramine
clopramine
Secondary –
Notriptyline
Dothiepin
Lothepramine
example of SSRI
fluoxetine citalopram sertaline fluvoxamine ezcitalopram
example of NARI
reboxetine
example of an SNRI
venlafaxine
example of a NaSSa
Mirtazepine
what is special characteristic of fluoxetine?
longest 1/2 life - 1st chocie for compliance issue
can not give with bleeding disorder
which antidepressants best given with hepatic/renal impariment
citalopram
SE of SSRI
nausea, vomiting, diarrhoea, dry mouth, weight loss & anorexia
headaches, drowsiness, anxiety, dizziness, sexual dysfunction
withdrawal symptoms of SSRI
headahce anxiety dizziness sweating lethargy insomnia mood changes shcok like senstation in head, neck and spine
complications of SSRI
hyponatraemia
serotonin syndrome
what are the symptoms of serotonin syndrome?
psych - agitation, confusion
neuro - nystagmus, myoclonus, tremors and seizures
hyperpyrexia, autonomic instability - breathing/HR
side effect of TCA
anticholinergic - dry mouth, blurred vision, constipation, sedation, urinary retention
antihistamien - sedative + weight gain
noradrenergic - postural hypotension + sedative
antiserotonin - weight gain, sexual dysfunction
when is TCA contra-indicated?
- manic phase of BAD
- if pt is suicidal
- if pt is elderly or severely ill
- glaucoma
when is SNRI used the most
venlafaxine has slightly better efficacy in severe depression
what are some examples of monoamine oxidase inhibitors
reversible - moclobemide, phenelzine
irreversible - phenelzine is ocarboxacid, tranylcypromine
what is the biggest side effect of MAOIs?
hypertensive crisis - can lead to subarachnoid hemorrhage
what is the advise regarding antidepressant during pregnancy?
- SSRIs should not be used in pregnancy unless benefit outweighs risk
- Fluoxetine is SSRI with lowest risk during pregnancy
why is lithium so difficult to use?
narrow theraputic range and need to avoid drugs that reduce lithium excretion eg ACEi, NSAIDs, diuretics
side effects of lithium
early
- dry mouth
- metallic taste
- Nauses
- tremor
- fatigue
- polyuria
- polydipsia
late
- diabetes insidious
- hypothyroidism
- arrhythmias
- dysarthria
what are the 2 medications used to prepare a patient for ECT
propofol
suxamethonium - muscle relaxant
what are the different subtype of BAD
bipolar 1 - consist of episodes of major depression and mania
bipolar 2 - consists of episodes of major depression and hypomania
what is the criteria of mania
> 1 week
severe enough to cause marked impairment in social/occupational functioning/necessitate hospitals
incl psychotic features such as delusions or hallucinations
what are some RF for BAD?
genetic
higher socioeconomic class
early life stress, childhood abuse/neglect
cannabis/cocaine
clinical features of mania
- Abnormally elevated mood
- Grandiose delusions
- Hallucinations
- Decreased need for sleep/↑ energy
- More talkative/↑ pressure of speech
- Flight of ideas
- Distractibility
- Agitated
- Risky behaviours e.g. spending large amounts of money
management of BAD?
current manic
- consider stopping the antidepressant
- antipsychotic (olanzapine/haloperidone/risperidone)
+/- benzos
if currently depressed
- olanzapine +/- fluoxetine
ECT
mood stabilizer during recovery period - lithium, sodium valproate
side effect of valporate
nausea, tremor, sedation, weight gain, alopecia, blood dyscrasias (blood and bone marrow disorder), hepatotoxicity, pancreatitis.
teratogenic
side effect of carbamazepine
much more serious SE than valproate so less commonly used
nausea, headache, dizziness, sedation, diplopia, ataxia, skin rashes, blood dyscriasis, hepatotoxicity
what is borderline personality disroder
efforts to avoid real or imagined abandonment
unstable interpersonal relationship which alternates between idealization and devaluation
unstable self image
impulsivity in potentially seld damaging area - spending, sex, substance abuse
recurrent suicidal behaviour
chronic feeling of emptiness
