psychiatry Flashcards
Section 2
Duration
Professionals
Evidence
Assessment
28 days (not renewable)
TWO doctors (one S12 approved)
ONE approved mental health professional (AMHP)
When a px is suffering a mental disorder of a nature that warrants detention in hx for assessment (+ they are not consenting)
When a px needs to be detained for their own/others safety
Section 3
Duration
Professionals
Evidence
Treatment
6 months (renewable)
TWO doctors (one S12 approved)
ONE approved mental health professional (AMHP)
When a px is suffering a mental disorder of a nature that makes it appropriate for them to receive tx in hx (+ they are not consenting)
Their tx is in the interests of theirs/others health + safety
There must be appropriate tx available
Section 4
Duration
Professionals
Evidence
Emergency order - urgent necessity to hold px until assessment by S12 doc
72 hrs
ONE doctor, ONE AMHP
There is not enough time for a second doctor to attend
Section 5 (4)
Duration
Professionals
Evidence
For a px already admitted (can be under psych or general hx) + is wanting to leave
6 hrs
NURSES holding power until a doctor can attend
Cannot be tx coercively whilst under this section
Section 5 (2)
Duration
Professionals
Evidence
For a px already admitted (can be under psych or general hx) + is wanting to leave
72 hrs
DOCTORS holding power
Allows time for a section 2/3 assessment
Section S136
Police section
Person suspected of having a mental disorder in a public place (A&E counts!)
24 hrs
Section S135
Police section
Needs court order to access px home + remove them
36 hrs
what are the factors assoc w poor prognosis in schizophrenia
strong FHx
gradual onset
low IQ
prodromal phase of social withdrawal
lack of obvious precipitant
what are first rank sx
thought alienation
passivity phenomena
3rd person auditory hallucinations (he/she)
delusional perception
risk of developing schizophrenia if
monozygotic twin has it
parent
sibling
none
50%
10-15%
10%
1%
RFs for dev schizophrenia (in order of biggest to lowest)
FHx
Black caribbean
Migration
Urban environments
Cannabis use
risk factors for suicide
SAD PERSONS
Sex - male 2.0
Age - <19, >45
Depression
Prev attempt
Excess alcohol/substance use
Rational thinking loss
Social support lacking
Organised plan
No spouse
Sickness
depression sx
fatigue
low mood
anhedonia
mild depression
> 2 wks sx, 2/3 main sx, 5+ generalised sx
how to end SSRIs if gd response
continue for 6 months after remission to decrease relapse risk
then reduce dose over 4 wk period (don’t need to w fluoxetine)
when to avoid citalopram
if taking meds that cld prolong QT interval, check hx cardiac disease
will need to do ECG monitoring
what does paroxetine have increased incidence of
discontinuation sx
which SSRI to used post MI/unstable angina
sertraline
electrolyte abnormality to observe for w SSRIs
hyponatraemia
be careful in elderly especially
which SSRI to use in children
fluoxetine
what to check before starting SNRI
BP as can dev HTN
side effects of mirtazapine (SNRI)
weight gain + sedation
SEs of tricyclic antidepressants
can’t pee, can’t see, can’t shit, can’t spit
weight gain
long QT
SNRI egs
mirtazapine
duloxetine
venlafaxine
what to do if on SSRI + NSAID
take PPI as increased bleeding risk
tricyclic antidepressant (amitriptyline) OD
confusion
seizure
tachy
hypotension
dilated pupils
metabolic acidosis
long QT, wide QRS
tx tricyclic antidepressant (amitriptyline) OD
IV sodium bicarbonate
triad in wernicke’s encephalopathy
nystagmus
ophthalmoplegia
ataxia
korsakoff’s syndrome
untreated wernicke’s encephalopathy
- antero + retrograde amnesia
confabulation
what is wernicke’s encephalopathy
neuro dis caused by thiamine (v B1) deficiency
most common in alcoholics
tx wernicke’s encephalopathy
give thiamine (pabrinex)
what is Disulfiram
alcohol detox drug
to Discourage
give you unpleasant sx within 20-30 mins of drinking alcohol
what is alcomposate
alcohol detox drug
enhancing GABA transmission
anti-craving
what is naltrexone
alcohol detox drug, an opioid antagonist
decreases cravings + pleasurable ex
6-12 hrs alcohol withdrawal
sweaty
tremor
tachy
anxiety
peak incidence of seizures in alcohol withdrawal
36 hrs
what is delirium tremens
48-72 hrs after alcohol withdrawal
coarse tremor
confusion
delusions
auditory + visual hallucinations
fever
tachy
tx delirium tremens
long acting benzos - chlordiazepoxide
what is malingering
faking sx for material gain
what is munchausens / factitious disorder
self inflicted sx / fabricated illness
you create sx
can be by proxy
what is somatisation
multiple physical sx for 2+ yrs w no medical explanation
px refuses to accept reassurance/-ve tests
what is hypochondriasis
persistent belief in presence of underlying serious disease (usually focuses on one body system / cancer)
px refuses to accept reassurance/-ve tests
what is conversion disorder
loss of motor/sensory function with no neuro cause
may be caused by stress
Don’t consciously feign/seek gain
what is akathisia
inner restlessness, inability to keep still
difference between depersonalisation + derealisation
depersonalisation is yourself derealisation is everything around you
what is hoover’s sign
used to differentiate organic from non-organic leg paralysis
If non-organic will feel oressure under paretic leg when lifting normal leg against pressure (invol contra hip extension)
PTSD sx + when is it dx
re-experiencing - flashbacks, nightmares
avoidance
hyperarousal - hyper vigilance, sleep probs
4 wks after event (b4 4 wks it is acute stress disorder)
emotional detachment
PTSD tx
eye movement desensitisation + reprocessing therapy
acute stress disorder tx
trauma focused CBT
SEs clozapine
decreases seizure threshold
agranulocytosis (need FBC monitoring)
neutropenia
constipation
myocarditis (take baseline ECG b4 starting tx)
hypersalvation
when to give clozapine in schizophrenia
if it does not respond to 2 consecutive trials of antipsychotics
what to do if clozapine doses missed for >48 hrs
re titrate again slowly
clozapine + smoking
smoking cessation can cause an increase in clozapine levels
when would you get an abnormal grief reaction
6+ months after
when do you have chronic insomnia
3+ months 3/7 nights a week
tx chronic insomnia
sleep hygiene
hypnotics only if daytime impairment is severe - short acting benzos/nonbenzos - zopiclone
lowest effective dose for shortest time
review after 2 wks + consider CBT
features assoc w insomnia
Female gender
Increased age
Lower educational attainment
Unemployment
Economic inactivity
Widowed, divorced, or separated status
RFs insomnia
Alcohol and substance abuse
Stimulant usage
Medications such as corticosteroids
Poor sleep hygiene
Chronic pain
Chronic illness: patients with illnesses such as diabetes, CAD, hypertension, heart failure, BPH and COPD have a higher prevalence of insomnia than the general population.
Psychiatric illness: anxiety and depression are highly correlated with insomnia. People with manic episodes or PTSD will also complain of extended periods of sleeplessness.
knights move
unexpected and illogical leaps from one idea to another w no logical assoc
feature of schizophrenia
flight of ideas
leaps from one topic to another but with discernible links between them
feature of mania
clang associations
when ideas are related to each other only by the fact they sound similar or rhyme
neologisms
new word formations, which might include the combining of two words
word salad
completely incoherent speech where real words are strung together into nonsense sentences
Tangentiality
wandering from a topic without returning to it
Circumstantiality
excessive, unnecessary detail but the person does eventually return to the original point
derailment
series of unrelated ideas
Perseveration
repetition of ideas or words despite an attempt to change the topic
Echolalia
repetition of someone else’s speech, including the question that was asked
lithium therapeutic range
0.4-1.0 mmol/L
lithium SEs
N&V, diarrhoea
fine tremor
nephrotoxicity: polyuria, secondary to nephrogenic diabetes insipidus
thyroid enlargement, may lead to hypothyroidism
ECG: T wave flattening/inversion
weight gain
idiopathic intracranial hypertension
leucocytosis
hyperparathyroidism and resultant hypercalcaemia
lithium monitoring requirements
when checking lithium levels, the sample should be taken 12 HOURS POST DOSE
after starting lithium LEVELS should be performed WEEKLY and after each dose CHANGE until concentrations are STABLE
once established, lithium blood LEVEL should be checked EVERY 3 MONTHS
after a CHANGE in dose, lithium LEVELS should be taken a WEEK later and WEEKLY until the levels are stable.
THYROID AND RENAL FUNCTION should be checked every 6 MONTHS
patients should be issued with an information booklet, alert card and record book
what can precipitate lithium toxicity
dehydration
renal failure
drugs: diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor blockers, NSAIDs and metronidazole.
features of lithium toxicity
coarse tremor (a fine tremor is seen in therapeutic levels)
hyperreflexia
acute confusion
polyuria
seizure
coma
mx lithium toxicity
mild-moderate toxicity may respond to volume resuscitation with normal saline
haemodialysis may be needed in severe toxicity
sodium bicarbonate is sometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion
what can lithium cause in preg
Ebstein’s abnormality (where tricuspid valve is in the wrong position)
so stop in 1st trim
when would you use ECT
severe depression refractory to medication (e.g. catatonia) those with psychotic symptoms
absolute CI to ECT
raised intracranial pressure
SEs ECT
short term:
headache
nausea
short term memory impairment
memory loss of events prior to ECT
cardiac arrhythmia
long term:
impaired memory
tx for acute dystonia 2ndary to antipsychotics
procyclidine
what is acute dystonia
sustained muscle contraction (e.g. torticollis, oculogyric crisis)
example of a extrapyramidal SEs of antipsychotics
what is tardive dyskinesia
late onset of choreoathetoid movements, abnormal, involuntary
most common is chewing and pouting of jaw
tardive dyskinesia tx
tetrabenazine
mechanism of action of typical antipsychotics
Dopamine D2 receptor antagonists, blocking dopaminergic transmission in the mesolimbic pathways
(can get prolactinaemia as SE)
mechanism of action of atypical antipsychotics
Act on a variety of receptors (D2, D3, D4, 5-HT)
warnings when antipsychotics are used in elderly patients
increased risk of stroke
increased risk of venous thromboembolism
SEs typical antipsychotics
eg Haloperidol
Chlopromazine
Extrapyramidal side-effects (EPSEs)
antimuscarinic: dry mouth, blurred vision, urinary retention, constipation
sedation, weight gain
raised prolactin
may result in galactorrhoea
due to inhibition of the dopaminergic tuberoinfundibular pathway
impaired glucose tolerance
neuroleptic malignant syndrome: pyrexia, muscle stiffness
reduced seizure threshold (greater with atypicals)
prolonged QT interval (particularly haloperidol)
Extrapyramidal side-effects (EPSEs)
Parkinsonism
Acute dystonia
Akathisia (severe restlessness)
Tardive dyskinesia
SEs atypical antipsychotics
weight gain
clozapine is associated with agranulocytosis (see below)
hyperprolactinaemia
Examples of atypical antipsychotics
clozapine
olanzapine: higher risk of dyslipidemia and obesity
risperidone
quetiapine
amisulpride
aripiprazole: generally good side-effect profile, particularly for prolactin elevation
palilalia
automatic repetition of own words / phrases
echopraxia
meaningless repetition/imitation of movements of others
othello syndrome
pathological jealousy where a person is convinced their partner is cheating on them without any real proof. This is accompanied by socially unacceptable behaviour linked to these claims.
Delusional parasitosis
fixed, false belief (delusion) that they are infested by ‘bugs’
Cotard syndrome
patient believes that they (or in some cases just a part of their body) is either dead or non-existent
De Clerambault’s syndrome / erotomania
a form of paranoid delusion with an amorous quality. The patient, often a single woman, believes that a famous person is in love with her.
capgras syndrome
delusional/misidentification syndrome
px believes someone significant in their life has been replaced by an identical imposter
fregoli syndrome
px believes multiple ppl are the same person
charles bonnet syndrome
px w vision loss have hallucinations
these px have insight
ekbom syndrome
px believes they are infested w parasites
sx B12 def?
anorexia physiological abnormalities
hypokalaemia
low FSH, LH, oestrogens and testosterone
raised cortisol and growth hormone
impaired glucose tolerance
hypercholesterolaemia
hypercarotinaemia
low T3
anorexia features
reduced body mass index
bradycardia (long QT)
hypotension
enlarged salivary glands
metabolic consequences of refeeding syndrome
hypophosphataemia
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance
who is high risk of refeeding syndrome
ONE + of:
BMI < 16 kg/m2
unintentional weight loss >15% over 3-6 months
little nutritional intake > 10 days
hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
TWO + of:
BMI < 18.5 kg/m2
unintentional weight loss > 10% over 3-6 months
little nutritional intake > 5 days
history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids
Russell’s sign
calluses on the knuckles or back of the hand due to repeated self-induced vomiting
acid base in bulimia
hypokalaemic metabolic alkalosis
MOAs with tyramine containing foods (cheese, pickled herring, bov + marmite, oxo, broad beans)
causes hypertensive reactions
tx heroin withdrawal
lofexidine (alpha 2 receptor agonist)
sx mx - benzos, antiemetics, loperamide (immodium)
Semantic dementia
form of fronto temporal dementia
55-65 yrs
px has a fluent progressive aphasia.
The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.
pick’s disease
type of fronto temporal dementia
characterised by personality change and impaired social conduct.
Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours.
Pick’s disease ix
Focal gyral atrophy with a knife-blade appearance
Macroscopic changes:-
Atrophy of the frontal and temporal lobes
Microscopic changes:-
Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques
what is creutzfeldt-Jakob disease (CJD)
rapidly progressive neurological condition caused by prion proteins
causes misfolded proteins leading to cell death
features CJD
rapidly progressive dementia
myoclonus
CJD ix
CSF is usually normal
EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
MRI: hyperintense signals in the basal ganglia and thalamus
stages of AI encephalitis
early sx:
fever
headaches
diarrhoea
URTIs
2nd stage:
confusion
paranoid
word finding
later:
seizures
rigid
temp dysreg
causes of serotonin syndrome
monoamine oxidase inhibitors
SSRIs
- St John’s Wort, often taken over the counter for depression, can interact with SSRIs to cause serotonin syndrome
- tramadol may also interact with SSRIs
ecstasy
amphetamines
multiple antidepressants
features serotonin syndrome
neuromuscular excitation
- hyperreflexia
- myoclonus
- rigidity
autonomic nervous system excitation
- hyperthermia
- sweating
altered mental state
- confusion
presents in hrs
what is neuroleptic malignant syndrome
are but dangerous condition seen in patients taking antipsychotic medication.
It may also occur with dopaminergic drugs (such as levodopa) for Parkinson’s disease, usually when the drug is suddenly stopped or the dose reduced.
dopamine blockade induced by antipsychotics triggers massive glutamate release and subsequent neurotoxicity and muscle damage
features of neuroleptic malignant syndrome
within hours to days of starting an antipsychotic and the typical features are:
pyrexia
muscle rigidity
autonomic lability: typical features include hypertension, tachycardia and tachypnoea
agitated delirium with confusion
RAISED CREATININE KINASE
AKI if severe
leukocytosis
pxs at an increased risk of developing hepatotoxicity following a paracetamol overdose
patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)
malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days
paracetamol OD tx
<1hr ago + does >150mg/kg = activated charcoal
staggered OD/ ingestion >15 hrs ago = n-acetylcysiene asap
ongestion <4hrs ago = wait 4 hrs to take a level + tx w n-acetylcysiene based on level
ingestion 4-5 hrs ago = immediate level based on nonogram + tx
n-acetylcysiene adverse effects
commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release). Anaphylactoid reactions to IV acetylcysteine are generally treated by stopping the infusion, then restarting at a slower rate
infused over 1 hour
what is semantic paraphasia
words are inappropriately substituted; e.g. ‘I baked the cake in the dustbin, then I put the butter back in the dog’
SSRI discontinuation symptoms
increased mood change
restlessness
difficulty sleeping
unsteadiness
sweating
gastrointestinal symptoms: pain, cramping, diarrhoea, vomiting
paraesthesia
overview of refeeding syndrome + how it happens
- sudden introduction of glucose after prolonged starvation
- causes insulin to be released which pushes glucose into cells
- causing demand for phosphate, potassium, magnesium
- leading to them all being low
Clinical Consequences of Hypophosphatemia:
Cardiac Dysfunction
Respiratory Failure - due to muscle weakness as needed for ATP prod
Neurological Complications
Haematological Effects - hypoxia + haemolysis
Rhabdomyolysis
