Psychiatry Flashcards
Tell me abit about ADHD
aetiology
when do sx start?
persistent inattention and/or hyperactivity/impulsivity.
in kids - developmental delay.
for kids - 6 of features present
17 + - 5 features
twice common in boys than girls.
genetic
pregnancy related - maternal smoking, premature birth, low birth weight
environmental factors
sx start in childhood. consistent across settings.
Diagnostic Features of ADHD
inattention
hyperactivity/impulsivity
inattention:
- doesnt follow instructions
- easily distracted
-finds it difficult to sustain tasks
- finds it difficult to organise tasks/activities
- loses things necessary for tasks or activities
- doesnt seem to listen when spoken directly
Hyperactivity:
- talks too much
- cant play quietly
- on the go
- interruptive/intrusive
- answer prematurely
- run and climb in situations where not appropriate
- doesnt wait their turn
screening tool for adult adhd
adult adhd self-report scale (ASRS)
How would you manage ADHD? kids
ten week watch and wait for a child.
refer to CAMHS.
drug last resort. only 5+
mild/moderate sx: parents attend education and training programmes.
then
methylphenidate 1st line in kids. - 6 week trial. cns stimulant acting on dopamine/norepinephrine reuptake inhibitor.
if dont work : switch to lisdexamfetamine.
dexamfetamine if benefit from lisdex but cant tolerate side effects
side effect of methylphenidate adhd - kids and also rules for taking
6 week trial initially
abdo pain
nausea
dyspepsia
weight and height to be monitored every 6 months
how would you manage adult adhd?
positive approach, routine, clear boundaries, physical activity, healthy diet
methylphenidate or lisdexamfetamine - 1st line.
switch between drugs if no benefit.
adhd treatment drugs main issue and what to do because of this?
cardiotoxic
do baseline ecg. before tx.
refer to cardiology if any pmh or fhx.
What is depression?
Pathophysiology of it
disorder of persistent feelings of low mood low energy and reduced enjoyment of activities.
disturbance in neurotransmitter activity in cns, particularly serotonin (5-ht). tx are serotonin booster essentially.
Causes of depression
life events ie loss of loved one.
genetic, psychological, biological and environmental factors.
physical health conditions like stroke mi ms parkinsons
What tools would you use to assess for depression?
hospital anxiety and depression - had
14 qus 7 for anxiety 7 for depression, each scored 0-3. total 21. 0-7 normal 8-10 borderline , 11+ cse.
answer quickly.
patient health questionaire (PHQ-9)
last 2 weeks, bothered by any of these problems?
9 items 0-3 scoring. thoughts of self harm.
less than 16 on phq-9 - less severe depression
score of 16 or more - severe depression
dsm-5 - criteria for diagnosing major depressive disorder.
tell me about dsm-5
major depressive disorder -5 or more of these during same 2 week period , at least 1 is either depressed mood or loss of interest or pleasure.
depressed mood most the day, nearly every day.
marked diminished interest or pleasure
significant weight loss /apetite
insomnia/hypersomnia
fatigue/loss of energy
feelings of worthlessness or guilt
cant think concentrate or decide
recurrent thoughts of death suicide
psychomotor agitation or retardation
all of these are nearly everyday
what 2 questions can i ask to screen for depresion
during last month have you been bothered by feeling down depressed or hopeless
during last month bothered by having little interest or pleasure in doing things?
presentation of depression
emotional
cognitive
physical
low mood
anhedonia - lack of pleasure or interest in activity
emotional:
- anxiety
-irritability
-low self esteem
-guilt
-hopelessness about future
cognitive:
- poor concentration
-slow thoughts
-poor memory
physical:
- low energy
-abnormal sleep
-poor apetite or overeating
-slow movements
when taking a depression history what factors should you ask about?
caring responsibilities
alcohol
drug use
forensic hx - violence/abuse
self neglect, self harm, harm to others, suicide
how would you manage depression?
phq less than 16 - less severe :
guided self help, cbt, group behavioural activation, group exercise, mindfullness, IPT, SSRIs, counselling, short term psychodynamic psychotherapy
more severe:
cbt and antidepressant (ssri or snri)
counselling
stpp
interpersonal psychotherapy - ipt
guided self help
group exercise
rules in switching antidepressants in depression tx
direct switch if you want for the following ssris: citalopram, sertraline, paroxetine, excitalopram
if fluoxetine to another ssri: stop leave 4-7 day gap then start low dose alternative ssri
ssri to tca: - cross tapering recommended.
unless fluoxetine stop way 4-7 days then low dose.
switch from citalopram,escitalopram,sert,parox to venlafaxine - be careful with paroxetine otherwise direct switch no problems
fluox to venlafaxine - stop that start venla at low dose 4-7 days later
how does depression differ from dementia?
favour depression over dementia :
short hx rapid onset
weight loss sleep disturbed
pt worried about memory
dont wanna ake tests dissapointed with results
mmse: variable
global memory loss - dementia is recent
name 3 specialist treatments for unresponsive or severe depression
antipsychotic meds : olanzapine or quetiapine
lithium
electroconvulsive therapy - twice weekly for 4 weeks . general anesthesia electrodes place on pt head , give electrical current, short generalised seizure trigged for 30 secs.
se: headache muscle ache short term memory loss
tell me the symptoms of psychotic depression
treatment
sx of psychosis:
delusions
hallucination
thought disorder - disorganised thoughts causing abnormal communication/behaviour
give antipsychotics olanzapine or quetiapine and antidepressants.
ect is an option too
What is autism spectrum disorder?
when sx start?
who can get it?
epidemiology
neurodevelopmental condition
spectrum of aspergers, autistic disorder, pervasive developmental disorder) - dsm def
qualitative impairment in social interaction and communication and repetitive stereotyped behaviour, interests and activities
sx in early childhood
association with any general intellectual learning ability
ranges from subtle understanding issue to impaired social function and severe disability.
no cure.
3-4* more likely in boys than girls. 50% of kids with it have intellectual disability
Clinical Features of Autism Spectrum Disorder
notice these things before 2-3 yrs old
Impaired Social Communication and interaction:
- kid plays alone, uninterested in being with other kids
- cant regulate social interaction by cues like eye gaze, facial expression, gestures
- cant form appropriate relationships, become socially isolated
- lack of eye contact,delay in smile
Repetitive behaviours,interests,activities:
- stereotyped and repetitive motor mannerisms, inflexible adherence to nonfunctional routines or rituals.
- certain way of going about activities.
intellectual impairement, language impairement.
adhd 35% association
epilepsy 18% association
higher head circumference to brain volume ratio.
How would you manage autism spectrum disorder?
no cure
start early , to increase functional independence and quality of life.
non pharm:
- applied behavioural analysis
- asd preschool programme
- treatment and education of autistic an communication related handicapped children/structured teaching method (TEACCH)
- early start denver model (ESDM)
- joint attention symbolic play engagement and regulation (JASPER)
Pharm: no evidence showing improves social communication
ssri: helps reduce sterotyped behaviour, anxiety, ,aggression
antipsychotics drug: reduces aggression, self-injury
methylphenidate: for adhd
family support: parental education
what communication delays are evident in autism pt?
language development
repetitive use of word/phrases
difficulty in imaginative or imitative behaviour
lack of appropriate nonverbal communication
what deficits in behaviour evident in autism?
greater interest in objects numbers or patterns than ppl
repetitive behaviour nd fixed routines
anxiety and distress with experiences outside of regular routine
strict food preferences
stereotypical movements - self-stimulating, hand-flapping or rocking
intense/deep interests persistent and rigid
What is bipolar?
types of it
chronic mental health recurrent episodes of depression and mania/hypomania.
usually start under 25 yrs. high rate of suicide.
manic episode: excessively elevated mood and energy, impact normal function like caring/working responsibilities. SEVERE FUNCTIONAL IMPAIREMENT OR PSYCHOTIC SX FOR 7 DAYS OR MORE
hypomanic: milder than manic without significant impact on their function. DECREASED/INCREASED FUNCTION FOR 4 DAYS OR MORE
mixed: mix of sx or rapid cycling between mania and depression
deprressive episodeS: low mood , anhedonia, low energy.
type 1 : mania and depression - MC
type 2: hypomania and depression
difference between hypomania and mania bipolar
delusions of grandeur or auditory hallucination - suggesting mania
how would you manage bipolar disorder?
ACUTE MANIC EPISODE:
antipsychotic meds - olanzapine,quetiapine, risperidone or haloperidol - 1st line
other options: lithium, sodium valproate
existing antidepressatn tapered and stopped
for acute depressive episode:
olanzapine+ fluoxetine
antipsycotic meds - olanzapine or quetiapine
lamotrigine
long term mx:
- lithium!! (alternative sodium valproate and olanzapine)
serum lithium levels monitered make sure dose is correct - take 12 hrs after most recent dose. target is 0.6-0.8 mmol/L. you can get lithium toxicity if levels are too high.
what potential adverse effects can you get with lithium? - long term bipolar tx
fine tremor
weight gain
ckd
hypothyroidism and goitre
hyperparathyroidism and hypercalcaemia
nephrogenic diabetes insipidus
ecg: t wave flattening/inversion
idiopathic intracranial hypertension
benign leucocytosis
what do i need to know about sodium valproate ? (bipolar tx)
teratogenic
neural tube defects
developmental delay if used in pregnancy.
VALPROATE PREGNANCY PREVENTION PROGRAMME - ensure effective contraception and annual risk acknowledgement form.
with bipolar what conditions are there an increased risk for? and by how much?
2-3 times increased risk
diabetes
cv disease
copd
tell me the spectrum of conditions for postpartum mental health issues
when is it seen?
baby blues - 1st week after birth - more common in primips
post natal depression - 3 months after months
puerperal psychosis - few weeks after birth
tell me the presentations of baby blues and why it might happen
tell me tx too.
when should it resolve
no tx
resolves within 2 weeks of delivery
sx: mild few days - mother anxious tearufl and irritable
- mood swings
-low mood
-anxiety
-irritability
-tearfulness
why it can happen:
- hormonal change
-recovery from birth
-fatigue, sleep deprivation
-establishing feeding
-responsibility of caring for neonate
how do you assess for postnatal depression?
edinburgh postnatal depression scale
10 item questionaire, max 30 score- asks how mother felt previous week. over 13 is depressive illness of varying severity. sensitivity and specificity over 90%. includes qu about self harm.
tell me about postnatal depression
10% of women
start within a month and peaks at 3 months.
similar to depressive features. triad: low mood, anhedonia,low energy
cbt
ssri - sertraline and paroxetine (good bc of low milk/plasma ratio) - if sx severe. secreted in breast ilk but not harmful to infant.
mild- self help
moderate - ssri and cbt
severe - specialist psych, rarely inpatient and mother and baby unit
tell me about puerperal psychosis
sx
tx
onset within first 2-3 weeks after birth.
severe swings in mood - similar to bipolar
and disordered perception - auditory hallucinations
admission to hospital - mother and baby unit
25-50% chance of recurrence
sx:
delusions
hallucination
depresion
mania
confusion
thought disorder
tx:
mother and baby unit
cbt
meds - antidepressants , antipsychotics, mood stabilisers
ECT
potential side effect of giving SSRI during pregnancy?
neonatal abstinence syndrome - withdrawal basically
few days after birth presents : irritability and poor feeding.
supportive management.
What is PTSD?
examples of traumatic events
mental health condition due to traumatic experiences with ongoing distressing symptoms
increases risk of depression anxiety substance misuse and suicide.
witnessing or experiencing:
- violence
- major car accidents
-major health events
-natural disasters
-military combat and war zone events
presentation of ptsd
re-experiencing : flashbacks, nightmares,repetitive and distressing intrusive images
avoiding: people, situations, circumstances resembling
hyperarousal: hypervigilance, exaggerated startle response, sleep issue, irritable, difficulty concentrting
emotional numbing - lack fo ability to experience feelings, feeling detached
derealisation - feeling the world isnt real
Diagnosis of PTSD - how?
screening tools
trauma screening questionaire - tsq
diagnosis based on the following criteria:
diagnostic and statistical manual of mental disorders (DSM-5)
International Classification of Diseases (ICD-11)
How would you manage PTSD?
watchful waiting - mild sx less than 4 weeks
trauma focused cbt or eye movement desensitisation and reprocessing (EMDR) therapy in severe cases.
drugs not 1st line .
if used : venlafaxine or ssri like sertraline.
in severe cases: risperidone
what is eye movement desensitisation and reprocessing (emdr)?
processing traumatic memories while performing specific eye movements.
basically reprocessing traumatic memories in a normal way so they dont cause negative emotion and distress.
Name the types of learning disabilities
dyslexia - specific difficulty in reading, writing, spelling
dysgraphia - specific difficulty in writing
dyspraxia - developmental co-ordination disorder.
auditory processing disorder
non-verbal learning disability - difficulty processing it, such as body language facial expressions.
profound and multiple learning disability - severe difficulties across multiple areas, need help daily life.
how to classify learning disabilities?
iq :
55-70 mild
40-55 moderate
25-40 severe
under 25 - profound
causes of learning disability
fhx.
environmentals - abuse neglect psychological trauma and toxins.
certain conditions:
- genetic disorders such as downs
- autism
-epilepsy
- problems in early childhood eg meningitis
- antenatal problems eg - fetal alcohol syndrome and maternal chickenpox
- problems at birth eg prematurity and hypoxic ischaemic encephalopathy
mdt involved in managing learning disability
health visitor
social worker
school
educational psychologist
paediatrician gp nurses
OT
speech and language therapist
to have capacity pt must demonstrate the ability to ?
understand - decision needs to be made
retain - information long enough to make decision
weight up - options and implications
communicate- decision
what is psychosis?
features of psychosis?
person experiencing things different from those around them
hallucinations - auditory
delusions
thought disorganisation
- alogia - little info conveyed by speech
- tangentiality - answers diverge from topic
- clanging - rhyming
- word salad: link words incoherently - nonsensical content
give some associated features of psychosis
agitation and aggression and depression and thought of self harm
neurocognitive impairment - memory attention and executive function
what conditions can psychotic symptoms occur in?
schizophrenia - MC
depression
bipolar
puerperal psychosis
brief psychotic disorder - sx last less than 1 month
neuro: parkinsons, huntingtons
prescribed drugs: corticosteroids
certain ilicit drugs: cannabis phencyclidine
what is the peak age for first episode psychosis?
15-30
Typical Antipsychotics
MoA
Adverse Effects
Examples
moa : dopamine d2 receptor antagonists - block dopaminergic transmission in mesolimbic pathways.
effects: extrapyramidal and hyperprolactinaemia common
eg: haloperidol , chlorpromazine
atypical antipsychotics
moa
adverse effects
examples
moa: act on variety of receptors - d2,d3,d4,5-ht
effects: extrapyramidal and hyperprolactinaemia less common.
metabolic effects
eg: clozapine
risperidone
olanzapine
what are the extrapyramidal side effects (antipsychotics)
parkinsonisms
acute dystonia: sustained muscle contraction (torticollis, oculogyric crisis). can manage with procyclidine
akathisia - severe restlessness
tardive dyskinesia - late onset choreoathetoid movements, abnormal, involuntary, 40% pts, irreversible, mc is chewing and pouting jaw. excessive blinking
in elderly pts what are the risks for antipsychotics - normal and atypical
increased risk of
stroke
vte
what general side effects can you get from antipsychotics?
raised prolactin - galactorrhoea, due to inhibition of dopaminergic tuberoinfundibular pathway.
impaired glucose tolerance
sedation, weight gain
antimuscarinic: dry mouth blurred vision urinary retention constipation
neuroleptic malignant syndrome: pyrexia, muscle stiffness
reduced seizure threshold - greater with atypicals
prolonged QT interval - particularly haloperidol
what atypical antipsychotic is associated with agranulocytosis?
and tell me some other side effects of this drug
clozapine - very low neutrophil count.
myocarditis/cardiomyopathy - fatal
constipation
seizures
excessive salivation
general adverse effects of atypical antipsychotics
examples
weight gain and hyperprolactinaemia
clozapine - agranulocytosis
clozapine
olanzapine - higher risk of dyslipidemia and obesity.
risperidone
quetiapine
amisulpride
aripiprazole : good side effect profile, esp for prolactin elevation
what tests would you have to do on a pt you have given antipsychotics to?
fbc,u+e, lft - start of therapy, annually, clozapine do weekly initially
lipids, weight - start, 3 months, annually
fasting bg, prolactin - start , at 6 months, annually
bp - baseline - frequent during dose titration
electrocardiogram - baseline
cv risk assessment - annually
Risk factors for schizophrenia
fhx. - parents has relative risk of 7.5
risk of gettin git:
monozygotic twin has it = 50%
parent has it = 10-15%
sibling has it = 10%
no relatives = 1%
black carribean ethnicity - RR 5.4
Migration - RR 2.9
Urban Environment RR 2.4
Cannabis Use RR 1.4
environmental
poor prognostic factors of schizophrenia
strong fhx
gradual onset
low iq
prodomal phase of social withdrawal
lack of obvious precipitant
how do you manage schizophrenia?
oral atypical antipsychotics - 1st line
cbt
crisis resolution
early intervention
acute hospital admission
comm mental health team
check for cv risk factor modification due to high rates of cv disease in schizophrenic pts - linked to antipsychotic medication and high smoking rates
features of schizophrenia
auditory hallucination
thought disorder
passivity phenomena
delusional perceptions
others
PRODOME PHASE : BEFORE FULL SX : poor memory, reduced conc, mood swings, suspicion of others, loss of apetite, difficulty sleeping, social withdrawal and decreased motivation.
Psychosis:
auditory hallucinations:
- 2 or more voices discussing pt in 3rd person
-thought echo
-voices commenting on pt behaviour
thought disorder
- thought insertion
-thought withdrawal
-thought broadcasting
passivity phenomena
- bodily sensations being controlled by external influence
- actions/impulses/feelings - experiences imposed on individual or influenced by others
delusional perceptions
- 2 stage - 1st normal object percieved , 2nd sudden intense delusional insight into objects for pt: traffic light is green therefore im king
impaired insight
catatonia - abnormal movements
neologisms - made up words
persecutory delusions
negative sx:
- alogia - poverty of speech
-avolition - poor motivation
-social withdrawal
-anhedonia - inability to derive pleasure
-incongruity - blunting of affect to emotive subjects or events
what is schizophrenia?
how long sx present before diagnosis?
severe long term psychosis.
between 15-30 . earlier in men than women.
at least 6 months
what is schizoaffective disorder?
schizophrenia + bipolar.
psychosis and sx of depression and mania
what is schizophreniform disorder
same features as schizophrenia but lasts less than 6 months.
patterns of behaviour in schizophrenia
active sx can be:
continuos
episodic - relapsing and rmeitting
single episode only
how would you make a diagnosis of schizophrenia?
DSM-5
sx including prodome phase must be present min 6 months with sx of active phase (delusions, hallucinations, thought disorder) at least 1 month (or less if tx successful)
key features of neuroleptic malignant syndrome (complication of antipsychotics)
blood findings
treatment
muscle rigidity
hyperthermia
altered conciousness
autonomic dysfunction - fluctuating bp and tachy
blood findings:
raised creatine kinase
raised wcc - leukocytosis
AKI 2 to rhabdomyolysis
stop causative meds and supportive care - iv fluids and sedation with benzodiazepines.
severe may need bromocriptine - dopamine agonist or dantrolene - muscle relaxant
as an antipsychotic when would you give clozapine?
when other tx dont control sx.
if adherence was an issue for antipsychotics what would you do?
give depot antipsychotics im injection every 2 weeks-3 months.
eg:
aripiprazole
flupentixol
paliperidone
risperidone
what is somatisation disorder?
tx
also known as briquets syndrome
multiple recurrent clinically significant somatic complaints that cant be fully explained by any underlying medical conditions.
pt get wide range of physical sx - cause distress and impairement in daily function
tx: cbt
tell me about the mental health act
law for hospital pts against wish inside hospital.
if pt has capacity, its voluntary/informal admission. - doesnt involve MHA ./
section 131 of mha - pts can be admitting without MHA.
how would be involved with MHA? - mental health act
approved mental health professional - organise mha assessments
section 12 doc - does mha assessments
responsible clinician - overall responsibility of pt care.
nearest relative - pts interests relative.
independent mha advocate - independent. - support persion help understand situation
a mha admission needs to be recommended by which 2 ppl?
section 12 doc
another doc - like their gp
tell me about the different sections in mha
section 2 - compulsory admission for assessment - max 28 days. cant be renewed. ends in discharge or further detention under section 3
section 3 - compulsory admission for tx. max 6 months. requires MHA. if mental health service under section 3 straight from community. otherwise following section 2 .
section 4 - detain pts upto 72 hrs in urgent scenarios where other procedures cant be arranged in time. need AMHP+ doc.
section 5(2) - emergency to detain pt already voluntarily in hospital. upto 72 hrs. 1 doc . after mha assessment
section 5 (4) - emergency detain and voluntary. 6 hours max. requires 1 nurse.
section 17 a - supervised community treatment. can recall a pt to hospital for tx if they dont comply with conditions of order in community ie medication adherence.
section 135 - court order to allow police to break into property to remove a person to place of safety
section 136 - police to remove someone which mental health disorder from public place and take to place of safety to be assessed. last up to 24 hours.
what is self harm?
cycle of self harm?
self injury without suicidal intent. cutting mainly. more in females under 25. pt under emotional distress and try to copy.
- emotional suffering
- emotional overload
- panic
- self harm
- temporary relief
- shame and guilt
epidemiology of suicide
3 times more in men than women.
mc age around 50.
presenting features increasing risk of suicide?
previous attempts
impulsiveness
hopelessness
making plans
feelings of being a burden
writing a suicidal note
escalating self harm
what background factors increase risk of suicide?
mental health issues
physical health issue
fhx of suicide
financial difficulty
criminal issues
lack of social support
alcohol and drug use
access to means - firearms
hx of abuse/trauma
name some protective factors that might help reduce suicide risk?
social support and community
sense of responsibility
resilience coping and problem solving skills
access to mental health support
How would you manage selfharm/suicidal thoughts etc?
safety netting/safety plan and follow up.
if suicidal attempt, a+E for physical injury,overdoses, safety concern.
mental health team
CBT
treat underlying mental health condition
provide details for support services in crisis - mental health services
separating means of self harm
how would you treat overdose of suicidal attempts?
Paracetamol
Opioids
Benzodiazepine
Bb
Ccb
Cocaine
Cyanide
Methanol
Carbon monoxide
check toxbase
activated charcoal within 1 hour if aspirin ssri’s TCA, antipsychotics, benzodiazepines, quinine.
paracetamol - acetylcysteine
opoids - naloxone
benzodiazepines - flumazenil
beta blockers - glucagon for hf or cardiogenic shock . atropine for symptomatic brady
calcium channel blocks - calcium chloride or calcium gluconate
cocaine - diazepam
cyanide - dicobalt edetate
methanol - fomepizole or ethanol
carbon monoxide - 100% oxygen
what is cognitive impairement?
clinical manifestations
assesment
mx
significant reduction in pt cognitive ability, interference in ADLs .
memory loss
difficulty in executive functions
language disturbances
perceptual difficulties.
MMSE
history
cognitive testing.
bloods, neuroimagine, LP.
supportive unless specific condition.
common causes of cognitive impairement
infrequent causes of cognitive impairement
rare causes of cognitive impairement
alzheimers
depression
vascular dementia
lewy body dementia
fibromyalgia
chronic fatigue syndrome
normal pressure hydrocephalus
frontotemporal lobar degeneration
huntingtons
creutzfeld-jakob disease
duchenne muscular dystrophy
wilsons
what is wenickes encephalopathy and what are its causes?
neuropsychiatric disorder
caused by thiamine deficiency.
seen in alcoholics.
rarer causes: persistent vomiting, stomach cancer, dietary deficiency.
classic triad of sx for wernickes encephalopathy
opthalmoplegia/nystagmus (mc)
ataxia
encephalopathy
where do petechial haemorrhages commonly occur in wernickes encephalopathy
in brain in areas like mamillary bodies and ventricle walls
features of wernickes encephalopathy
oculomotor dysfunction - nystagmus (mc) and opthalmoplegia : lateral rectus palsy, conjugate gaze palsy
gait ataxia
encephalopathy: confusion,disorientation, indifference, inattentiveness
peripheral sensory neuropathy
how would you investigate wernickes encephalopathy?
how do you treat?
decreased red cell transketolase
MRI
urgent replacement of thiamine
what is the relationship between wernickes and korsakoff?
if you dont treat wernickes youll get korsakoff.
you get antero and retrograde amnesia and confabulation .
how might a drug overdose pt present?
what lab tests could you do?
how would you treat
respiratory depression
cv instability
neuro complications
blood gas analysis
FBC
toxicology screen
airway mx
iv fluids
antidote administration
how much is the limit for drinking in units?
what is binge drinking
14 units 1 week
spread evenly over 3 or more days
not more than 5 units in 1 day
6 or more units for women and 8 or more for men in 1 single session
sx of alcoholism
palmar erythema
gynaecomastia
spider naevi
dupuytrens contractures
testicular atrophy
small shrunker liver
enlarged liver
telangiectasia
tremor
blood shot eyes
hepatic flap - severe liver disease
polyneuropathy , sensory ataxia and cerebellar signs
sometimes: ataxia, opthalmoplegia (lateral gaze palsy) and confusion(wernickes).
with increased levels of acute alcohol:
slurred speech and delayed reaction
increased confidence and chattiness with decreased inhibitions
poor judgement and memory. reduced balance visual disturbance and drowsiness
confusion
incontinence, uncontrolled vomiting, reduced breathing and gag reflexes.
blue-tinged skin and seizures
coma
death
how would you diagnose alcoholism
icd-10 3 or more:
compulsion to drink
difficulty controlling alcohol consumption
physiological withdrawal
alcohol tolerance
neglect of alternative activities to drinking
persistent use of alcohol despite evidence of harm
AUDIT questionaire - 10 qus - assess for sx alcohol related problems. more than 3 in last 12 months is positive:
tolerance
withdrawal sx.
craving
loss of control
salience
continued use despite harm.
how would you investigate for alcoholism?
audit - 1st point of ix.
gamma-gt - 50% of pts so not good screen.
lfts.
neurological exam
routine bloods - vit deficiencies.
how would you manage alcoholism?
nutrition: thiamine
drug:
benzodiazepine (chlordiazepoxide) - acute withdrawal . give orally as a reducing regime. reduce dose over 5-7 days. use CIWA-Ar tool to score pt on withdrawal
high dose b vitamins (pabrinex) - IM or IV. then follow with thiamine oral.
disulfram: promote abstinence ci : IHD, psychosis
acamprosate: reduce craving - weak nmda receptor antagonist
there are 3 screening questionaires for alcoholism. name and explain them
FAST
CAGE
AUDIT - SEE ABOVE. min 0 max 40. 8 or more men or 7 or more women. 15/13 = dependence.
FAST - 4 ITEMS - MIN=0 MAX=16 - 3 OR MORE POSITIVE. 1.HOW OFTEN 8 ORE MORE/6 OR MORE (FE) DRINKS IN 1 GO 2. FORGET NIGHT BEFORE. 3. LAST YR FAILED TO DO WHAT U SHOULD BECAUSE OF DRINK. 4. ANYONE BEEN CONCERNED ABOUT YOUR DRINKING
CAGE - FEEL TO CUT, ANNOYED BY CRITISING, GUILTY, EYE OPENER
MoA of alcohol dependence
depressant.
stimulants gaba receptors - relax brain.
inhibits glutamate receptors (nmda) - relax electrical activity of brain.
long term alcohol use :
gaba system becomes down regulated
glutamate upregulated.
pt must continue drinking or will get withdrawal.
how do you calculate alcohol units
vol ml * alcohol content (%) /1000 = units of alcohol
quickest way times vol in litres by percentage
pregnancy complications of alcohol
in early pregnancy:
miscarriage
small for dates
preterm delivery
fetal alcohol syndrome
complications of alcohol excess
wernicke-korsakoff
alcoholic liver disease
cirrhosis and its comps - oesophageal varices, ascites, HCC
pancreatitis
alcoholic cardiomyopathy, myopathy with muscle wasting
cv disease risk - stroke or mi
cancer , breast mouth and throat
bloods in alcoholic
raised mcv
raised alt and ast
ast: alt above 1.5
ggt raised
a patient arrives with withdrawal symptoms from alcohol. can you tell me the times associated with which symptoms?
6-12 hrs - tremors sweating headache craving anxiety
12-24 - hallucinations
24-48 - seizures
24-72 - delirium tremens
what is delirium tremens?
emergency
associated with alcohol withdrawal. if untreated mortality 35%
long term alcohol means gaba system downregulated and glutamate upregulated. when alcohol removed, gaba system underfunctions and glutamate system over functions
extreme excitability
excessive adrenergic activity.
presentation of delirium tremens
acute confusion
severe agitation
delusions and hallucinations
tachycardia tremor htn hyperthermia
ataxia
arrhythmias
substance misuse -
opoids sedative hypotics can cause what ?
stimulants like cocaine can cause what
hallucinogens can lead to what
how would you treat?
opoids - respiratory depression
cocaine - cv comps
hallucinogens - perceptual distortions
mx: methodone for opoid dependence.
cbt
briefly explain substance use disorder
screening tool
pathophysiology
management
DSM-5
HARMFUL CONSUMPTION OF PSYCHOACTIVE SUBSTANCES.
ALTERATION IN BRAIN CIRCUITS THAT MEDIATE REWARD,STRESS AND EXECUTIVE FUNCTIONS.
WITHDRAWAL PHARMA TX.
CBT
key features of personality disorder - ICD 11
persistent pattern - cognition, emotional, behaviour, interpersonal function different from cultural expectations. - stable over time. range across personal and social situations.
impairment: problems/dysfunction in persons life relationship work and social.
duration: stable over time from adolescence. not transient
distress/dysfunction- not explained by anything else.
severity classification of personality disorder - icd-11
mild:
- some functioning impairement - limited to some part of life. sx might be noticeable to others by not causing pervasive distress.
- pt can keep stable relationships and occupational roles
moderate:
- more significant impairement in multiple areas
- struggle keeping relationships
- more distressing sx. - can manage ADL with some effort.
severe:
- profound impairement in every aspect of life.
-pervasive difficulty in interpersonal relationships, self identity.
- significant distress,dysfunction, reduced qol.
- intensive and long term therapeutic intervention needed.
personality disorder trait domains - icd-11
negative affectivity - negative emotions. mood swings etc.
detachment. - limited pleasure from relationships.
dissociality - disregard for rights/empathy. impulsivity and manipulative behaviours.
disinhibition - impulsiveness
anankastia: preoccupation with control orderliness. rigid
borderline pattern - emotional instability, intense and unstable interpersonal relationships, identity crisis, impulsivity.
icd-10 and dsm-5 recognised borderline personality disorder
previous classification of personality disorders
cluster a - explain
cluster b
cluster c
cluster a - odd or eccentric
paranoid
schizoid - indifference to praise.solitary pasand. lack of interest in sex, no desire for companion. emotionally cold.
schizotypal - odd beliefs/magical thinking. paranoid and suspicious. lack of close friends. inapproprate affect. odd speech
previous classification of personality disorders
cluster a
cluster b - explain
cluster c
dramatic emotional erratic
antisocial:
cant conform to social norms
deception
impulsive
irritable
reckless disregard for safety of others/self
irresponsible
lack of remorse
borderline (emotionally unstable)
- suicidal
-emptiness
-psychotic
-unstable self imag and interpersonal relationships
-avoid real/imagined abandonment
-impulsive
-
histrionic
- inappropriate sexual seductiveness
-centre of attention
-suggestibility
-attention seeking - physical appearance
-self dramatization
narcissistic -
- grandiose self importance
-entitlement
-chronic envy
-arrogant
-preoccupation with fantasies of unlimited success, power or beauty
-take advantage of others to achieve own needs
previous classification of personality disorders
cluster a
cluster b
cluster c- explain
anxious and fearful
obsessive compulsive
avoidant
dependent
how would you manage personality disorder?
psychological therapies: dialectical behaviour therapy
what is schizoid personality disorder?
lack of itnerest or desire to form relationships with others and feeling that its of no benefit to them
what is shizotypal personality disorder?
unusual beliefs
thoughts
behaviours
social anxiety
makes forming relationships difficult
what is functional neurological disorder?
sx
sensory and motor sx cant be explained.
weakness
gait disturbance
seizures
sensory loss
vision disturbance
what is body integrity dysphoria?
apotemnophilia
part of their body dont belong to them.
healthy body part causes distress they wanna remove it.
poss desire to be paralysed.
what is koro syndrome?
delusion that sex organs - mostly penis are retracting or shrinking and might disspaear.
pt thinks theyll die .
anxiety and panic attacks.
what is alice in wonderland syndrome?
causes
todd syndrome
incorrectly percieve the size of body parts.
changes to perception of time
sx intermitten.
causes :
migraine
epilepsy
brain tumours
what is de clerambaults syndrome?
erotomania
delusion that famous person is in love with them.
might lead to inappropraite harassment of person by pt.
usually young single woman.
what is capgras syndrome?
delusion that duplicate has replaced someone close to them.
might be suspicious/aggressive towards imposter.
seen in schizophrenia. can occur with dementia.
what is cotard delusion?
delusion that they are dead or actively dying.
walking corpse syndrome.
caused by:
depression
schizophrenia
brian tumours
migraines
what is alien hand syndrome?
pt losing control of one of their hands.
usually do to brain lesion ie tumour,injury, aneurysm or after brain surgery
what is catatonia?
abnormal movement, commmunication and behaviour.
pt awake but not acting normal.
unusual posture, odd actions, repeat sounds/words, remain blank/unresponsive.
causes:
severe depression
bipolar
psychosis - ie schizophrenia.
what is dissociative identity disorder?
multiple personality disorder.
what is dissociative amnesia?
forgetting autobiographical info about themselves and events that happened to them.
Side effects of antipsychotics
Weight gain
Diabetes
Prolonged QT
Raised prolactin
Extrapyramidal
- Akathisia (psychomotor restlessness)
- Dystonia (abnormal muscle tone and postures)
- Pseudo-parkinsonism
- Tardive dyskinesia (abnormal movements)
What are typical antipsychotics
Dopamine D2 receptor antagonists, block dopaminergic transmission in mesolimbic pathways
- Haloperidol
- Chlorpromazine
Side effects of typical antipsychotics
Hyperprolactinaemia and Extrapyramidal symptoms
Akathisia (psychomotor restlessness)
Dystonia (abnormal muscle tone and postures)
Pseudo-parkinsonism
Tardive dyskinesia (abnormal, involuntary movements “chewing and pouting of jaw”, excessive blinking)
What are atypical antipsychotics
Atypical (Second gen) created due to extrapyramidal and prolactin side effects.
Act on variety of receptors (D2, D3, D4, 5-HT)
E.g.
- Clozapine (most effective - only indicated after all else tried)
- Risperidone
- Olanzapine
What antipsychotic is most likely result in long QT
haloperidol
Some other side effects of antipsychotics
Antimuscarinic - Dry mouth, blurred vision, urinary retention, constipation
- Sedation and weight gain
- Impaired glucose tolerance
- Reduced seizure threshold
- Neuroleptic malignant syndrome
Atypical antipsychotics and some side effects
Clozapine
Olanzapine (obesity and dyslipidaemia)
Risperidone
Aripiprazole (good side effect profile)
Weight gain
hyperprolactinaemia
Clozapine associated with agranulocytosis
Metabolic Syndrome!
how to monitor lithium taking pts
Sample taken 12 hours post dose
Lithium levels weekly and after each dose change until stable
Once on stable dose, check every 3 months
If dose change, check after 1 week, and weekly again until levels stable
Thyroid and renal function every 6 months
What is lithium toxicity and how is it normally precipitated?
Lithium has narrow therapeutic range (0.4-1 mmol/L) and long plasma half-life, primarily excreted by kidneys. Toxicity normally occurs >1.5mmol/L
Dehydration
Renal failure
Diuretics(thiazides), ACEi/ARB, NSAID, metronidazole
How does lithium toxicity present?
Coarse tremor (whatever the fuck that is)
Hyperreflexia
Confusion
Polyuria
Seizure
Coma
how is lithium toxicity managed?
Mild-Moderate: Fluid resuscitation with saline
Haemodialysis if severe
Sodium bicarbonate sometimes used, alkalinity of urine promotes lithium excretion
Give me the definitions of these thought disorders:
- Circumstantiality
- Tangentiality
- Neologisms
- Clang associations
- Word salad
- Knights move thinking
- Flight of ideas
- Perserveration
- Echolalia
Circumstantiality: Inability to answer without excessive, unnecessary detail. Go on massive tangent BUT do return to original point.
Tangentiality: Wander from topic without ever returning to point.
Neologisms: New word formations, maybe combining 2 words
Clang associations: Ideas related to each other only because they sound the same or rhyme
Word salad: Completely incoherent speech made up of real words that make no sense together
Knights move thinking: Severe loosening of associations. Unexpected and illogical leaps from one idea to another.
Flight of ideas: Feature of mania, leaps from one idea to another, but with discernable links between the 2. Super fast.
Perseveration: repetition of ideas or words, despite attempting to change subject
Echolalia: repeating someone else’s speech, including asked question
What do benzodiazepines do and what are their side effects
Enhance inhibitory GABA by increasing frequency of chloride channels. Range of effects:
- Sedation, hypnosis, anxiolytic, anticonvulsant, muscle relaxant
Side effects:
- Tolerance/dependance - only prescribe for short time (2-4 weeks)
- Withdrawals, up to 3 weeks after stopping, if they come off abruptly.
- Withdrawal symptoms: insomnia, irritability, anxiety, tremors, tinnitus, perceptual disturbance, seizures
How are beta blockers used in anxiety
non selective beta blocker reduces sympathetic nervous system effects, treating physical symptoms. (Tremors, palpitations, sweating etc). Contraindication is asthma (bronchoconstriction/bronchospasms)
2 considerations when prescribing ssri in ocd
Requires longer than depression (at least 12 weeks) for initial response
If effective, continue for at least 12 months to prevent relapse
What is mirtazapine , its moa and use case and side effects
An antidepressant that works to block alpha2-adrenergic receptors, increasing release of neurotransmitters.
Fewer side effects and interactions, so good in old people, who may be on lots of meds
Two main side effects: Sedation and increased appetite, good for old people who are skinny and cant sleep.
Take in evening to sleep
withdrawal sx from benzodiazepines
anxiety
tremor
insomnia
seizure
what is malingering
fraudulent simulation or exaggeration of sx for financial or other gain
what is delusional parasitosis
delusional belief of parasitic infeciton (bugs, worms, parasites, mites, bacteria, fungi)
What is refeeding syndrome?
Occurs when someone with an extended severe nutritional deficit resumes eating. The lower the BMI, and the longer the period of malnutrition, the higher the risk.
Pathophs of refeeding syndrome
During starvation, intracellular potassium, phosphate, magnesium depleted. These electrolytes move from inside cells to blood to maintain serum levels
Cell metabolism reduces to conserve energy, causing a loss of intracellular electrolytes.
During refeeding, potassium, phosphate and sodium shift into blood. Carbs cause increase in insulin which drives glucose, potassium, phosphate into cells.
Na+/K+ pump pumps K+ into cells and Na+ out. Insulin causes sodium reabsorption from kidneys.
overall metabolic effects of refeeding syndrome on bloods
Hypomagnesaemia
Hypokalaemia
Hypophosphataemia
Fluid overload
clinical features of refeeding syndrome
Hypophosphataemia
- Main cause of symptoms
- Muscle weakness (including cardiac and diaphragm) -> heart and respiratory failure
Hypomagnesaemia may cause torsades de pointes
Clinical consequences of hypophosphataemia (as in refeeding)
Cardiac dysfunction
Respiratory failure
Confusion, seizures, coma
Tissue hypoxia and haemolysis
Rhabdomyolysis
How is refeeding syndrome prevented?
If patient hasnt eaten, or high risk, for more than 5 days, aim to refeed at no more than 50% of requirements for first 2 days.
High risk if
- BMI <16
- Unintentional weight loss >15% over 3-6 months
- Little nutritional intake 10+ days
- Derranged electrolytes prior to feeding
If 2 or more of:
- BMI <18.5
- Weight loss >10%
- Little intake >5days
- History of alcohol abuse, drugs, chemotherapy, diuretics, antacids, insulin
What is metabolic syndrome?
Hypercholesterolaemia
Hypertension
Impaired glucose tolerance
Central obesity
Caused more often by atypical antipsychotics (aripiprazole less so, has less side effects)
When can u use ect
Severe, medication resistant or psychotic depression. Course of treatments.
Involves triggering a short generalised seizure under anaesthaesia.
Side effects: Headache, muscle ache, short term memory loss
How do SSRIs, SNRIs and TCAs work
SSRI - Block reuptake of serotonin by presynaptic membrane on axon terminal. Hence, more serotonin in synapses throughout CNS, boosting communication between neurones
SNRI - Blocks reuptake of serotonin and noradrenaline by presynaptic membrane
TCA - Block serotonin reuptake and noradrenaline by presynaptic membrane. Also block ACh and histamine receptors, giving them anticholinergic and sedative effects
What are anticholinergic side effects
Anticholinergics block Ach, which is involved in bodily secretions, having a drying effect around the body.
Results in:
- Dry mouth
- Constipation
- Blurred vision
- Dizziness
- Cognitive impairment
“cant see pee or climb a tree”
Blurred vision, urinary retention and muscle pain/impaired coordination and balance
Side effects of SSRIs
Sertraline - usually safe but associated with diarrhoea
Citalopram - Can prolong QT, which can lead to torsades de pointes. Least safe SSRI in patients with heart disease
Fluoxetine - Long half life (4-7 days) first line in children
Paroxetine causes weight gain
Other side effects:
- GI symptoms
- Headaches
- Sexual dysfunction (loss of libido, ED, orgasm difficulty)
- Increased risk of bleeding (esp when taken with NSAID, anticoagulant)
- SIADH causing hyponatraemia!
SNRI side effects
Similar to SSRIs. Can increase BP so contraindicated in uncontrolled HTN.
Venlafaxine - more likely to cause discontinuation symptoms when stopped. Increased risk of death by OD
Duloxetine - Treats neuropathic pain, especially diabetic neuropathy
TCA SE
Amitriptyline - used at low dose to treat neuropathic pain
TCA - cardiotoxic!! Cause arrhythmia -> tachycardia, long QT, Bundle branch block. Dose dependent. Very dangerous in overdose, so not used in depression
Also have anticholinergic side effects.
Vortioxetine. Tell me about it
Serotonin reuptake inhibitor. 3rd line after inadequate response from 2 others.
Stimulates and blocks other serotonin receptors. Good for anti-anxiety. Not many side effects, safe in heart disease.
Causes nausea for first few weeks
Considerations when prescribing antidepressants
Can be initial period of agitation, anxiety, suicidal ideation, acts of suicide.
Review all patients within 2 weeks of starting (1 week in 18-25 due to high suicide risk)
Noticable response 2-4 weeks after starting.
Some can be directly switched, others need to be crosstapered. Most SSRI and SNRI are safe to switch between except fluoxetine due to long half life
advice for stopping antidepressants
continue for at least 6 months (2 years in recurrent) before stopping
Reduce slowly over 4 weeks to prevent discontinuation symptoms
Discontinuation symtpoms
- Flu like
- Electric shock sensations
- Insomnia
- Irritability
- Vivid dreams
what drugs interact with ssris
NSAIDs (prescribe with PPI)
Warfarin/heparin (consider mirtazapine instead)
Aspirin
Triptans and MAOIs - increased risk of serotonin syndrome!
SSRI risks in pregnancy
1st trimester - Small risk of congenital heart defects
3rd trimester - persistent pulmonary HTN of the baby
Paroxetine has risk of congenital malformations!
Clozapine side effects
One of the earliest atypical agents, carries risk of agranulocytosis. FBC monitoring ESSENTIAL!
Agranulocytosis, neutropenia
Constipation
Myocarditis
Arrhythmias
Hypersalivation
Dose adjustment if start/stop smoking
what food cant you eat with a MAOI
Cheese because it contains tyramine whatever the fuck that is
What is serotonin syndrome
Serotonin syndrome is a potentially life threatening drug reaction. Typically results from the use of serotonergic drugs.
Caused by:
- MOAI
- SSRIs (St John’s Wort and tramadol interact with SSRIs to cause serotonin syndrome)
- Ecstasy
- Amphetamines (ADHD Meds - Lisdex)
- Triptans
Usually due to interactions, doses that are too high, or a new drug is added without sufficient time to affect levels.
features of serotonin syndrome
Neuromuscular excitation
- Hyperreflexia
- Myoclonus
- Rigidity
Autonomic Nervous System excitation
- Hyperthermia
- Sweating
Altered mental state
- Confusion
mx of serotonin syndrome
How is serotonin syndrome managed
- IV fluids
- Benzodiazepines
- Serotonin antagonists, cyproheptadine, chlorpromazine if severe
How do MAOIs work, give an example or 2
Serotonin and noradrenaline are metabolised by monoamine oxidase in the presynaptic cell
MAOI = Monoamine oxidase inhibitor
Tranylcypromine, phenelzine
Adverse effects of MOAIs
Hypertensive reactions with tyramine containing foods (cheese, pickled herring, Bovril, Oxo, Marmite, broad beans)
Anticholinergic effects
- Dry mouth
- Blurred vision
- Constipation
- Urinary retention
- Confusion
- Tachycardia
How should SSRIs be stopped, what can happen if not done right
Stop gradually over 4 weeks
If fluoxetine continue at least 6 months
Discontinuation symptoms (especially with Paroxetine, Fluoxetine can be stopped whenever)
- Increased mood change
- Restlessness
- Difficulty sleeping
- Electric shock sensations
- Unsteadiness/dizziness
- GI sx - pain, cramping, diarrhoea, vomiting
- Paraesthesia
What is treatment resistant psychosis and how is it treated. What are some considerations of treatment
Uncontrolled psychosis following 2 antipsychotic drugs (right dose and timeframe)
Treated with clozapine.
48 hr rule: if missed for 48 hrs, must be retitrated.
Side effects:
- Myocarditis
- Constipation (cholinergic receptor block)
- Smoking cessation increases levels (smoking increases cytochromic b450 levels in liver)
- Increased salivation
Drugs that can cause hyponatremia
SSRI
TCA
LITHIUM
Tramadol
Ecstasy
Haloperidol
vincristine
Desmopressin
Fluphenazine
Chlorpropramkde
Carbamazepine
Alcohol withdrawal sx timings
Sx 6-12 hrs
Seizures 36 hrs
Delirium tenements 72 hrs
What is serotonin syndrome
Serotonin syndrome is a potentially life threatening drug reaction. Typically results from the use of serotonergic drugs.
Caused by:
- MOAI
- SSRIs (St John’s Wort and tramadol interact with SSRIs to cause serotonin syndrome)
- Ecstasy
- Amphetamines (ADHD Meds - Lisdex)
- Triptans
Usually due to interactions, doses that are too high, or a new drug is added without sufficient time to affect levels.
Features of serotonin syndrome
Neuromuscular excitation
- Hyperreflexia
- Myoclonus
- Rigidity
Autonomic Nervous System excitation
- Hyperthermia
- Sweating
Altered mental state
- Confusion
Management of serotonin syndrome
How is serotonin syndrome managed
- IV fluids
- Benzodiazepines
- Serotonin antagonists, cyproheptadine, chlorpromazine if severe
What is hypochondriasis
Persistent belief in the presence of a serious underlying disease, with no accepting reassurance or negative results
What is Factitious disorder
AKA Munchausen’s. Intentional production of physical or psychological symptoms
What is malingering
Fraudulent simulation or exaggeration of symptoms for financial or other gain
What is delusional parasitosis
Delusional belief of parasitic infection (bugs, worms, parasites, mites, bacteria, fungi)
What is cotard delusion?
Delusion that they are dead or dying. Most often caused by psychiatric conditions (schizophrenia, depression) but can be due to neurological conditions, such as tumours or migraines.
what is capgras syndrome?
False belief that a duplicate has replaced someone close to them, possibly causing suspicion or aggression towards them
AKA Delusional misidentification syndrome
Whats De Clerambaults
AKA Erotomania
Delusion that high status or famous person is in love with them. Can lead to harassment or stalking. Usually has little/no contact with person
Whats Todd Disorder
AKA Alice in Wonderland syndrome
Incorrectly perceiving size of body parts (too big/small). Also associated with changes to perception of time and symptoms of migraine (e.g. aura and headache).
Caused by migraine epilepsy brain tumours
What is Koro syndrome
Belief that sex organs are retracting or shrinking and will disappear, killing the patient. Causes anxiety and panic attacks.
Mostly seen in asia, especially china and india
What is body integrity dysphoria
Apotemnophilia involves a strong feeling that a body part doesn’t belong to them, causing them distress, and wanting to remove it. May have desire to be disabled.
No associations
What is Binge eating disorder
Episodes where patient overeats often as an expression of distress. Typically feels a loss of control, not restrictive like anorexia or bullimia, patients likely to be overweight
Planned binge involving binge foods, eating quickly, unrelated to hunger, becoming uncomfortably full and eating in dazed state
How do bloods present in Binge Eating Disorder
Anaemia
Leucopenia
Thrombocytopenia
Hypokalaemia
(low Hb, WCC, platelets, potassium)
Reduced bone marrow activity causes normocytic normochromic anaemia, leukopenia and thrombocytopenia
