PSYCHIATRY Flashcards
define dementia
irreversible, progressive decline and impairment of more than one aspect of higher brain function (conc, memory, language, personality, emotion)
epidemiology of dementia (4)
- rare <65
- alzheimer’s most common, vasc second most
- alzheimer’s more common in F, vasc and mixed more common in M
- fronto-temporal most common in <65s
what are the 4 causes/classifications of dementia?
- Alzheimer’s
- Frontotemporal
- Lewy body
- Vascular
outline the pathophysiology of Alzheimer’s (5)
- extracellular deposition of beta-amyloid plaques
- intracellular deposition of neurofibrillary tangles (NFT)
- leads to reduction in info transmission and brain cell death
- cerebral cortex degeneration with cortical atrophy
- also loss of ACh
outline the pathophysiology of the non-Alzheimer’s dementia causes
- frontotemporal - atrophy of frontal and temporal lobes
- lewy body - deposition of lewy bodies (abnormal protein) in brain stem and neocortex, deficit of ACh and dopamine (parkinsonism)
- vascular - brain damage due to cerebrovasc infarcts e.g. major stroke/multiple small strokes. most affected = white matter of cerebral hemispheres, grey nuclei, thalamus and striatum
risk factors for dementia
AD - old age, Fhx, down’s syndrome
vasc - old age, obesity, HTN, smoking
frontotemporal - genetic mutation
signs and symptoms of AD
- GRADUAL
- most common = short term memory loss (facts, general knowledge, language use, nominal dysphagia)
- disorientation
- getting lost
- decline in ADLs
what is nominal dysphagia and who does it commonly present in?
the inability to recall names of people/objects. seen in AD
signs and symptoms of vascular dementia
- STEPWISE PROGRESSION (stable sx then sudden severity increase)
- vascular pathology hx e.g. stroke, raised BP, focal CNS signs
- cognitive impairment subacutely/acutely following vasc event
- mood disturbance e.g. psychosis, delusions, hallucinations (later stages)
signs and symptoms of lewy body dementia
- GRADUAL
- probs with complex cog actions/multitasking
- visual hallucinations
- Parkinson-like sx
- sleep disorder
signs and symptoms of frontotemporal dementia
- RAPID progression
- peak in 50s-60s
- behavioural/personality change
- loss of language fluency/comprehension
how is dementia investigated in primary and secondary care?
primary - blood screen (exclude reversible causes)
secondary - neuroimaging/structural imaging
what are some neuroimaging techniques that can be used to diagnose dementia? what are they helpful for?
1) CT - rule out lesions/other pathology
2) MRI - shows atrophy/lesions
3) DaTSCAN - dopamine imaging
neuroimaging findings in Alzheimer’s
CT - may exclude space-occupying lesions etc
MRI - generalised atrophy
neuroimaging findings in vascular dementia
CT/MRI - cerebrovascular lesion/s
neuroimaging findings in lewy body dementia
CT - abnormal
MRI - general cortical atrophy
DaTSCAN - reduced dopamine
neuroimaging findings in frontotemporal dementia
what is it often chracterised by?
MRI/CT - focal atrophy in frontal and/or anterior temporal lobes. often characterised by left-right symmetry
ddx for dementia
- delirium
- HIV-related cog impairment
- Creutzfedlt-Jakob disease
- hydrocephalus
- depression
- mild cog impairment (MCI)
how do you manage AD?
EARLY - anticholinesterase inhibitors e.g. donepezil, rivastigmine
LATER - NMDA inhibitors e.g. memantine
how do acetylcholinesterase inhibitors e.g. donepezil help manage AD?
block breakdown of ACh > increase ACh in synapse > increases synaptic transmission of ACh where it’s reduced
how do NMDA inhibitors (e.g. memantine) help manage AD?
glutamate excitotoxicity is associated with delayed evolving neurodegeneration… NDMA inhibitors blocks NMDA receptors when too active > stops excessive glutamate production > slows disease progression
how is vascular dementia managed?
- treat atherosclerosis
- lifestyle modifications e.g. smoking, diet
- antiplatelets (aspirin)
- statins (atorvastatin)
- antihypertensives
how is lewy body dementia managed?
- donepezil/rivastigmine (increase ACh)
- psychotic sx - antipsychotics e.g. risperidone
- sleep probs - SSRIs
- motor sx - carbidopa/levodopa
how is frontotemporal dementia managed?
no specific tx :( can use SSRIs for behavioural sx
what is the difference between acute stress disorder and PTSD?
acute stress disorder is a reaction in the FIRST 4 weeks after trauma, PTSD is diagnosed AFTER 4 weeks
what is akathisia? give a classic presenting history
= a sense of inner restlessness and inability to keep still
common with long hx of antipsychotic use
which anti-depressant is known to stimulate appetite?
mirtazapine
how long after starting an SSRI should patients be reviewed if they are:
a) 25 and under
b) >25
a) 1 week
b) 2 weeks
which food should be avoided when on an MAOI (e.g. tranylcypromine) and why?
cheese - has lots of tyramine in which can cause hypertensive crisis when on an MAOI
what happens when you combine an SSRI and NSAID/aspirin? how do you manage this?
= GI bleeding risk
prescribe a PPI e.g. omeprazole
what is cotard syndrome? what condition is it most commonly associated with?
a rare subtype of nihilistic delusion, where the pt believes a part of them is dead/does not exist.
commonly seen in severe depression (but also associated with schizophrenia)
antipsychotics increase the risk of what adverse effects in elderly patients?
stroke and VTE
what is the general definition of non-pathological anxiety?
a constellation of psychological and physiological responses to a potential/uncertain threat.
= an essential function of the CNS
define:
a) generalised anxiety disorder
b) phobic anxiety disorder
c) panic disorder
a) persistent anxiety not restricted to/predominant in any specific circumstances
b) abnormal state anxiety evoked only by a specific external situation/object
c) recurrent unpredictable episodes of severe acute anxiety, not restricted to particular stimuli/situations
how common are each of the anxiety disorders?
generalised - most common (5-12%)
phobic - second most (up to 12%)
panic - least (4.7%)
risk factors for anxiety disorders
- threats in development e.g. bullying, trauma, neglect, parental loss
- early attachment relationships
- family hx of anxiety/another condition
- female sex
- hx/current other psychiatric condition e.g. depression
secondary causes of anxiety (4)
- substance use e.g. caffeine, stimulants, bronchodilators, cocaine
- substance withdrawal e.g. alcohol, benzo withdrawal
- hyperthyroidism
- cushing’s
DSM-5 criteria for GAD
- excessive anxiety/worry about varying events/activities for >6 months
- worry is difficult to control
- symptoms cause significant distress/impede ability to function in important areas of their life
- excessive worry/anxiety are accompanied by 3 or more of the following symptoms…
- restlessness
- fatigue
- muscle tension
- trouble concentrating
- irritability
- sleep disturbance
signs and symptoms of phobic anxiety disorder
- avoidance of certain situation/stimuli
- anticipatory anxiety
- somatic sx e.g. palpitations, sweating, trembling, dyspnoea, chest pain, dizziness, chills, hot flushes
signs and symptoms of panic anxiety disorder
- crescendo of anxiety, usually resulting in exit from situation
- somatic sx e.g. palpitations, sweating, trembling, dyspnoea, chest pain, dizziness, chills, hot flushes
- secondary fear of dying/losing control
stepwise approach to managing GAD
- education about GAD and active monitoring
- low-intensity psych interventions e.g. individual self-help, guided self-help, psychoeducational groups
- high-intensity psych interventions (CBT or applied relaxation) or drug tx
- highly specialist input e.g. multi-agency teams
what is the 1st line drug treatment for GAD?
what if this is:
a) ineffective
b) not tolerated
1st line = sertraline
a) offer alternative SSRI (e.g. citalopram, fluoxetine) or SNRI (e.g. duloxetine, venlafaxine)
b) if cannot tolerate SSRI or SNRI, consider pregabalin
what questionnaire can help assess the severity of GAD? what are the different severity scores?
the generalised anxiety disorder questionnaire (GAD-7)
5-9 = mild
10-14 = moderate
15-21 = severe
what is erotomania (De Clerambault’s syndrome)?
a delusion where the person believes someone famous is in love with them, with the absence of other psychotic sx
what is there an increased risk of to the baby if the mother is taking sertraline in the:
a) first trimester
b) third trimester
a) congenital heart defects
b) persistent pulmonary hypertension of the newborn
what is conversion disorder?
a condition presenting with a loss of motor and sensory function, typically occurring during times of stress
what is delirium tremens? when and what does it present with?
- a severe complication of alcohol withdrawal
- reaches peak incidence 72 hrs following alcohol cessation
- presents with sx of visual and auditory hallucinations, tremors and agitation
how long after alcohol cessation would you expect these symptoms to manifest:
a) anxiety and nausea
b) seizures
c) delirium tremens
a) 6-12h
b) 36h
c) 72h
what is the difference between hypomania and mania?
both present with symptoms of elevated mood BUT mania has a prolonged time course (hypomania being <7 days) and presents with psychotic symptoms
what should be monitored in all patients at initiation and dose titration of venlafaxine?
blood pressure (venlafaxine and other SNRIs are associated with developing hypertension)
a 75-year-old lady presenting with new onset confusion has just had an increase in sertraline dose. what is probably the cause of her confusion? what does the BNF suggests should be monitored when high risk patients begin SSRIs?
hyponatremia - measure U&Es in high risk patients to assess serum sodium
depression severity classification: what PHQ-9 score indicates:
a) less severe depression
b) more severe depression
a) <16
b) 16 or over
what is a key difference between pseudodementia (depression) and dementia?
pseudodementia involves global memory loss e.g. forgetting the rules of card games, dementia predominantly involves short-term memory loss (in the early stages)
which is associated with a poorer prognosis in a schizophrenia history?
a) acute onset
b) insidious onset of sx developing gradually
b
treatments for the side-effects of long-term antipsychotics:
a) tardive dyskinesia (repetitive involuntary movements e.g. lip smacking)
b) acute dystonia (abnormal postures/movements)
c) akathisia (restlessness)
a) tetrabenazine
b) procyclidine/benztropine
c) propanolol
what is ADHD?
a persistent pattern >6 months of inattention and/or hyperactivity-impulsivity that has a direct negative impact on academic, occupational or social functioning
when do ADHD symptoms typically present?
before 12yo, typically early-mid childhood
aetiology of ADHD
Unknown - combo of environmental and genetic factors…
1. neuro chemical
2. genetics
3. CNS insults e.g. prematurity, foetal alcohol syndrome, NF
4. environmental factors
RFs for ADHD (5)
- prematurity
- low birth weight
- low paternal education
- prenatal smoking
- maternal depression
pathophysiology of ADHD - which part of the brain is implicated and which NTs?
- deficits in PREFRONTAL CORTEX (regulates attention, behaviour and emotion)
- deficit in this area leads to poor impulse control, weak attention and heightened distractibility
- norepinephrine and dopamine are key for prefrontal functioning: deficits of these
DSM-5 diagnostic criteria for ADHD (3) - <16 and 17 or over
- children up to 16: six or more symptoms of inattention and six or more symptoms of hyperactivity and impulsivity
- if 17 or over: five or more symptoms from each category
- must occur in multiple settings (e..g home and school), have been present for at least six months and are not better explained by another disorder
symptoms must have been present before ___ years old for a diagnosis of ADHD
12
investigation options for ADHD (4)
- questionnaires
- clinical interview
- ADHD nurse classroom observation
- QB test (computer test)
which questionnaire can be used to assess ADHD in adults?
the Diagnostic Interview for ADHD Adults (DIVA) questionnaire
non pharmacological management options for ADHD (3)
- education
- ADHD parenting programme
- school support and liaison
pharmacological management options for ADHD (stimulants and non stimulants)
STIMULANTS - methylphenidate (e.g. ritelin) most common
NON STIMULANTS - atomoxetine, intuniv
SEs of methylphenidate in the tx of ADHD (4)
- stunted groth
- abdo pain
- headaches
- insomnia
what is the most important side effect to monitor during tx with a child with methylphenidate (for ADHD)?
stunted growth
mechanism of action of stimulants e.g. methylphenidate in the tx of ADHD
- blocks dopamine and noradrenaline transporters > increased availability in synaptic space > increased prefrontal cortex activity
- stimulation of prefrontal cortex increases concentration, attention span and decreases impulsivity
suggest some complications of ADHD persisting into adulthood
- lower educational/employment attainments
- poor self esteem
- criminal behaviour
- relationship issues
- sleep disturbance
- substance abuse
- RTC
- self harm
what is the first-line SSRI for patients with a hx of cardiovascular disease?
sertraline
antidepressants should be continued for at least ___ months after remission of symptoms to decrease the risk of relapse
6 months
how would schizotypal personality disorder present?
- “magical thinking” focussing on paranormal phenomena
- odd speech e.g. high-pitched voice
- problems socially/with relationships
substance dependence requires at least two of the following…
- impaired control over substance use
- increasing priority over other aspects of life/responsibility
- psych features suggestive of tolerance/withdrawal
define alcohol dependence
craving and tolerance of alcohol consumption despite negative complications experienced
pathophysiology of alcoholism - what NTs are involved? what happens in withdrawal?
- consuming alcohol affects basal ganglia
- releases dopamine > reward system > positively reinforces behaviour > operant conditioning
- alcohol also causes increase in inhibitory NT GABA (sedative)
- chronic use = brain upregulates natural stimulants to achieve equilibrium with inhibitory stimulants
withdrawal = sudden drop in GABA, disrupted homeostasis as there’s now an excess of natural stimulants
symptoms of alcohol dependence (3)
- tolerance
- craving
- “eye-opener”
CAGE questions for alcoholism
- have you ever felt you should Cut down on your drinking?
- have people Annoyed you by criticising your drinking?
- have you ever felt bad or Guilty about your drinking?
- have you ever had a drink first thing in the morning to steady nerves/get rid of a hangover? (Eye-opener)
symptoms of alcohol withdrawal
6-12 hours = tremors, sweating, tachycardia, fever
12-48 hours = alcohol hallucinosis, seizures
72+ hours = delirium tremens (altered mental status, agitation, hallucinations)
investigations for alcoholism
- AUDIT-c questionnaire (screening)
- labs - FBC, LFTs, B12/folate, TFTs
what blood results may be found in a patient with alcoholism? (FBC, LFTs, folate/b12)
FBC - raised MCV, raised platelets, anaemia
LFTs - increased GGT, AST:ALT > 2:1
B12/folate - deficient
medications to help with alcohol detox symptoms (4)
- chlordiazepoxide (sedative)
- high dose benzos e.g. diazepam
- naltrexone (opiate blocker, blocks feeling/buzz of alcohol)
- prophylactic oral thiamine
psychological complications of alcoholism
alcoholic hallucinosis, delirium tremens, Wernicke-Korsakoff syndrome
what is bipolar disorder?
a mood disorder where mood switches between major depression and mania/hypomania
mood swings tend to last DAYS at a time
how long does a manic episode tend to last in bipolar disorder?
at least 7 days
signs and symptoms of
a) depression
b) mania
in a person with bipolar disorder
a) low mood, suicidal, difficulty getting out of bed, sleeping more, worthlessness
b) elevated mood, increased activity, grandiose ideas, distractibility, loss of normal social inhibitions, impulsivity, hallucinations and delusions
pharmacological treatment of bipolar disorder:
a) acute mania
b) acute depression
c) long term
a) stop ssris, oral antipsychotics e.g. haloperidol, olanzapine, quetiapine, risperidone
b) oral antidepressant + antipsychotic e.g. fluoxetine + olanzapine
consider CBT
c) mood stabilisers e.g. lithium, sodium valproate
non pharm tx of longterm bipolar disorder
psycho - CBT, family focussed therapy
social - support groups, job support
define delirium
an acute, transient and reversable state of confusion
aetiology of delirium (there’s a mnemonic!)
CHIMPS PHONED
C - constipation
H - hypoxia
I - infection
M - metabolic disturbance
P - pain
S - sleepiness
P - prescriptions e.g. opiates, benzos
H - hypothermia
O - organ dysfunction (hepatic/renal)
N - nutrition
E - environmental change
D - drugs (OTC, illicit, alcohol, smoking)
what are the two types of delirium? how do they present?
hyperactive:
- agitation
- delusions
- hallucinations
- wandering
- aggression
hypoactive
- lethargy
- slowness with everyday tasks
- excessive sleeping
- inattention
can fluctuate between the two!
what timespan of presentation helps differentiate between delirium and dementia?
delirium often in v short space of time (unlike dementia)
what cognitive assessments can be done when investigating delirium? (2)
- MMSE
- confusion assessment method (CAM)
what screening is done for patients with suspected delirium?
confusion screen - rules out common causes of confusion
outline the investigations included in a confusion screen and the underlying causes that may be found
- BLOODS
- FBC: infection, anaemia, malignancy
- U&Es: hypo/hypernatraemia
- LFTs: liver failure w secondary encephalopathy
- coag/INR: intracranial bleed
- TFTs: hypothyroid
- serum calcium: hypercalcemia
- B12 + folate: deficiency
- glucose: hypo/hyper
- blood cultures: sepsis - URINALYSIS - UTI
- IMAGING
- CT head: ischaemic stroke, bleed, abscess
- CXR: pneumonia, pul oedema
first line medical management for delirium
haloperidol (oral, IV or IM)
non-pharm management for delirium
- identify and treat underlying cause
- general support e.g. ensure access to aids
- environment - access to clock, familiar objects, involve fam and friends, control noise, ambient lighting/temperature
first-line tx for acute stress disorder
CBT
define drug overdose
excessive drug consumption leading to toxicity
what antioxidant in the body is used up in paracetemol overdose? what does it normally do?
- glutathione
- metabolise harmful NAPQI into non harmful substances
RFs for opioid overdose
a) recreational
b) intentional
c) unintentional
a) IV drug user
b) hx of self-harm/suicide
c) chronic pain/palliative pts, elderly, new/changing dose, hepatic or renal impairment, children
pathophysiology of opioid overdose - what receptors are involved and where?
- binds opioid receptors: Mu, Kappa and Delta in CNS
- activation of all three produces analgesic effects
presentation of paracetemol overdose
- N&V
- anorexia
- RUQ abdo pain
- hx of self harm
- jaundice
- may have hx of alcohol use
presentation of opioid overdose - what is the classic triad?
opioid toxidrome triad = decreased consciousness, pinpoint pupils + respiratory depression
other = N&V, confusion
investigations for paracetemol overdose (3)
- bloods - serum paracetemol, LFTs, blood glucose (hypo), ABV/VBG (lactic acidosis)
- glasgow coma scale
- full overdose hx
investigations for opioid overdose
ABCDE approach
tx of parecetemol overdose
- activated charcoal (if within 1 hour)
- IV N-acetyl cysteine
tx of opioid overdose
ABCDE
naloxone
treatments of other overdoses:
a) beta-blockers
b) calcium channel blockers
c) cocaine
d) methanol e.g. solvent/fuels
e) carbon monoxide
a) glucagon (for heart failure/shock), atropine (for bradycardia)
b) calcium chloride/gluconate
c) diazepam
d) fomepizole or ethanol
e) 100% O2
define personality disorders
an umbrella term…
- maladaptive personality traits that cause significant psychosocial distress and interfere with everyday functioning
- characterised by patterns of thought/behaviour/emotions that differ from social norm
- leads to difficult relationships, reduced QOL and poor physical health
what are the 4 key features of a personality disorder according to ICD-11?
- persistent pattern - patterns of cognition, emotional experience and behaviour deviate from cultural expectations
- impairment - e.g. relationships, work, social
- duration - stable over time, beginning in adolescence/early adulthood and are not transient
- distress/dysfunction - either to the individual or others
what are the 3 main categories of personality disorder types?
- anxious
- emotional/impulsive
- suspicious
outline the 3 anxious personality disorders and their features
- anxious avoidant - severe anxiety about rejection or disapproval, avoidance of social situations/relationships
- dependent - heavy reliance on others to make decisions and take responsibility for their lives
- obsessive-compulsive - unrealistic expectations of how things should be done by themselves/others, catastrophising what will happen if these aren’t met
outline the 3 emotional/impulsive personality disorders and their features
- emotionally unstable - fluctuating strong emotions and difficulties with identity and maintaining healthy relationships, self-destructive
- antisocial - frequently putting own needs, pleasure and personal gain before others, often associated with criminal behaviour, aggression and lack of guilt/empathy
- narcissistic - feelings that they are special, others need to recognise this or they get upset. put themselves first
outline the 3 suspicious personality disorders and their features
- paranoid - difficulty trusting/revealing personal information to others. feels everyone is against them
- schizoid - a lack of interest or desire to form relationships with others, feels this is no benefit to them, indifference to praise/criticism
- schizotypal - unusual beliefs, thoughts and behaviours, ideas of reference, magical thinking as well as social anxiety
management options for personality disorders
- dialectical behaviour therapy (DBT)
- family/relationship therapy
- therapeutic community housing
what are the 4 main groups of symptoms in EUPD?
- emotional instability/dysregulation (intense negative emotions, severe mood swings, from suicidal to feeling fine a few hours later)
- cognitive and perceptual distortions (hallucinations, dissociation)
- impulsive behaviour (self-harm, binge drinking etc)
- intense/unstable relationships with others (intensely anxious/attached or rejection/abusive)
which act enables pts to be sectioned and treated without their agreement?
when is it used?
Mental Health Act 1983
if pt needs urgent tx and are either at immediate risk to themselves or others
section 135 vs 136 warrant
what happens after?
135 - allows police to enter a patient’s HOME and take them to place of safety
136 - when police find patient in PUBLIC SPACE and take them to place of safety
can be kept up to 25h in place of safety for assessment
section 5(4) - who does it give power to? to do what? for how long?
- in hosp, gives nurse power to stop pt leaving until doctor comes
- can detain for up to 6 hours
section 5(2) - who does it give power to? to do what? for how long?
- in hosp, gives doctors ability to detain pt in hosp for up to 72 hours
- during which assessed to see if they need further detention under section 2/3
section types
a) 2
b) 3
c) 4
purpose, how long, which staff are needed
a) pt can be detained up to 28 days, purpose = assessment, needs 2 doctors (one S12 approved) and an AMHP
b) pt can be detained up to 6 months (can be renewed), purpose = treatment, allows pts to be treated against will
c) emergency order, up to 72h, purpose = urgent necessity, only needs 1 doctor and 1 AMHP
what is a community treatment order (CTO)/Section 17a? who makes them? how long do they last?
- for pts being discharged/allowed short-term leave
- set of conditions which if are broken allow pt to be recalled to hosp
- only made by pts responsible clinician
- lasts 6 months (can be renewed)
how may a pt appeal a CTO?
through a mental health tribunal
who is on the panel of a mental health tribunal? (3)
- tribunal judge
- psychiatrist
- specialist member with mental health expertise
nobody is connected to pt/hospital
diagnostic criteria for length of depression sx
> 2 weeks
presentation of depression (SIGECAPS)
Sleep probs
loss of Interest
Guilt
Energy loss
Concentration probs
Activity less
Psychomotor complications
Suicidal thoughts
what score is used to assess depression sensitivity? which score indicates less severe and which indicates more severe?
PHQ-9
<16 - less severe
> 16 - more severe
screening for suicide - what tool can be used?
SAD PERSONS
Sex (male)
Age (<19 or >45)
Depressive sx
Previous attempt
Excess alcohol/substance use
Rational thinking loss
Social support lacking
Organised plan
No spouse
Sickness
1st line med for depression if under 18?
fluoxetine
1st line med for depression in >18 yo
SSRIs
medications for depression
a) who can’t have citalopram?
b) what can SSRIs not interact with?
a) ppl with long QT
b) triptans (migraine) or MAOIs
what is:
a) tangentiality
b) circumstantiality
c) clang associations
d) flight of ideas
e) Knight’s move thinking
a) veer off topic without returning to original question
b) overly detailed responses that eventually return to the original point
c) speech driven by sounds of words, often involving rhyming or wordplay
d) rapid, disjointed shifts between topics with a frenzied pace. thinking faster than limitations of speech will allow.
e) abrupt, random shifts in thoughts, no structure
management of hypomania in primary care
routine referral to community mental health team
how to switch from fluoxetine to alternative SSRI
fluoxetine has long half-life SO…
stop fluoxetine, wait 4-7 days and then start low dose other SSRI
symptoms of SSRI discontinuation syndrome (3)
- dizziness
- electric shock sensations
- anxiety
factors associated with poor prognosis in schizophrenia:
- strong fmhx
- gradual onset
- low IQ
- prodromal phase of social withdrawal
- lack of obvious precipitant
list 5 SSRIs
- sertraline
- citalopram
- escitalopram
- fluoxetine
- paroxetine
sertraline
a) safest in which patients?
b) highest rate of which SE?
a) heart problems
b) diarrhoea
which SSRIs are considered least safe in patients with heart disease/arrythmia?
citalopram and escitalopram
which SSRI leads to QT prolongation and Torsades de pointes?
citalopram and escitalopram
which SSRI has a v long half life?
fluoxetine
which SSRI may cause weight gain and is more likely to cause discontinuation sx?
paroxetine
key SEs of SSRIs (7)
- GI upset
- headaches
- sexual dysfunction
- hyponatremia
- anxiety/agitation (1st week)
- suicidal thought/risk
- BLEEDING - GI, intracranial, PPH
examples of SNRIs
duloxetine and venlafaxine
when are SNRIs (duloxetine/venlafaxine) contraindicated?
if uncontrolled HTN
when is venlafaxine used?
if inadequate response to other antidepressants
examples of TCAs (3)
amitriptyline
nortriptyline
clomipramine
in which patients are TCAs very uncommonly used in?
- heart disease
- RFs for suicide
key side effects of TCAs (4)
- arrythmias e.g. tachycardia, BBB
- anticholinergic sx e.g. dry mouth, constipation, urinary retention, blurred vision, cog impairment
- weight gain
- sedation (so typically taken at night)
when is mirtazapine commonly used as an antidepressant?
- patients with loss of appetite/weight loss/are struggling with sleep
- older patients
key SEs of mirtazapine (3)
which SE is it less likely to cause?
- sedation
- increased appetite
- weight gain
less likely to cause sexual dysfunction!
when does changing an antidepressant require cross-tapering?
between an SSRI and mirtazapine
when does changing antidepressants just require a direct switch?
between SSRIs and SNRIs (apart from fluoxetine)
episodes of what can be triggered when antidepressants are used alone? which class of antidepressants is more at risk of this, and which specific drug is risk high in?
- acute mania/hypomania
- SSRIs/TCAs
- especially venlafaxine
management of acute mania/hypomania induced by an antidepressant
stop antidepressant, start antipsychotic therapy e.g. risperidone, haloperidol
management of serotonin syndrome
- supportive: sedation with benzos
- withdrawal of causative meds
which vitamin is low in Wernicke’s?
vitamin B1 (thiamine)
Wernicke’s triad and other possible signs
- altered mental status
- nystagmus
- ataxia
other - alcohol dependence, delirium, acute psychosis
ddx for Wernicke’s
- hyperammonemia
- meningitiis
- encephalitis
- SAH
- Wernicke-Korsakoff syndrome
acute management of Wernicke’s encephalopathy (3)
- IV thiamine 250-500mg every 8h
- IV magnesium 2-4g/day
- multivitamins
management of ongoing alcohol dependence
dietary thiamine supplementation
presentation of Wernicke-Korsakoff’s syndrome
PRECEDED by nystagmus, altered mental status, ataxia…
- amnesia
- inability to make new memories
- confabulation (filling in memory gaps with different events)
physical features of anorexia nervosa (5)
- failure of secondary sexual characteristics
- bradycardia
- cold-intolerance
- yellow tinge skin (hypercarotenaemia)
- lanugo hair (fine downy hair)
what is the commonest electrolyte abnormality in anorexia nervosa?
hypokalaemia
lithium bloods
a) when starting
b) when changing dose
c) until stable
d) once stable
a) one week after starting tx
b) one week after dose change
c) weekly until stable
d) every 3 months, 12 hours post-dose
Charles-Bonnet syndrome
persistent/recurrent complex hallucinations
pt knows they are not real
background of visual impairment (e.g. age-related macular degeneration)
first rank schizophrenic sx
- 3rd person auditory hallucinations
- delusional perceptions e.g. persecutory
- somatic passivity (external forces control actions)
- thought alienation e.g. insertion, withdrawal, broadcast
are visual hallucinations a first or second rank sx of schizophrenia?
second
example of
a) typical antipsychotics (1st gen)
b) atypical antipsychotics (2nd gen)
a) haloperidol, chlorpromazine
b) olanzapine, quetiapine, clozapine, risperidone
mechanism of action of
a) typical antipsychotics
b) atypical antipsychotics
a) dopamine D2 receptor antagonist - blocks dopaminergic transmission in mesolimbic pathways
b) same as above but acts on a variety of receptors - D2, D3, D4, 5-HT
main adverse effects of typical antipsychotics
- extra-pyramidal effects - parkinsonism, acute dystonia, akathisia, tardive dyskinesia
- hyperprolactinaemia
which typical antipsychotic is associated with prolonged QT intervals?
haloperidol
main adverse effects of atypical antipsychotics
METABOLIC
- hyperlipidaemia
- hypercholesterolaemia
- hyperglycaemia
how to remember the extra-pyramidal SEs (EPSEs) of typical antipsychotics
ADAPT
Acute Dystonia
Akathisia
Parkinsonism
Tardive dyskinesia
general adverse effects of antipsychotics
- anti-muscarinic - dry mouth, blurred vision, urinary retention, constipation
- sedation and weight gain
- raised prolactin
- impaired glucose tolerance
- reduced seizure threshold (more with atypicals)
indication for clozapine use
what needs monitoring?
resistant schizophrenia
monitor WBCs and absolute neutrophil count
specific SEs of
a) olanzapine
b) clozapine
a) weight gain, increased appetite, sedation
b) agranulocytosis, leukopenia, hypersalivation, hypotension, constipation
mechanism of action of benzodiazepines
facilitate and enhance binding of GABA to GABA receptors > hyperpolarisation > decreases neuron excitability
what med is used to reduce the sedative effects of benzos?
flumazenil
how long should benzos be prescribed for? what is the withdrawal protocol?
- 2-4 weeks
- dose withdrawn in steps of 1/8 of daily dose every fortnight
features of benzo withdrawal syndrome
similar to alcohol withdrawal
up to 3 weeks after stopping drug…
1. insomnia
2. irritability
3. anxiety
4. tremor
5. loss of appetite
6. tinnitus
7. sweating
8. perceptual disturbance
9. seizures
adverse effects of lithium (7)
- hyperparathyroidism > hypercalcemia
- fine tremor
- N&V, diarrhoea
- nephrotoxicity e.g. polyuria
- thyroid enlargement > hypo
- weight gain
- leucocytosis (benign high WCC)
features of lithium toxicity (7)
- coarse tremor
- hyperreflexia
- acute confusion
- polyuria
- seizure
- coma
- ataxia
what 3 tests should be performed prior to starting a pt on lithium
- urea & electrolytes
- thyroid function tests
- ECG
what must be considered before starting a pt on lithium
suicidal ideations and a history of self-harm
define anorexia nervosa
an eating disorder characterised by abnormally low BW, an intense fear of gaining weight and a distorted perception of weight
DSM-5 criteria for anorexia nervosa (3)
- restriction of energy intake relative to requirements > sig low body weight
- intense fear of gaining weight/becoming fat
- disturbed by one’s body weight/shape, self-worth influenced by body weight/shape or lack of recognition of condition
subtypes of anorexia nervosa (2)
- binge/purge
- restrictive eating
blood findings in anorexia nervosa
a) FBC
b) U&Es
c) TFTs
d) LFTs
e) FH and LSH, estradiol
f) Gs and Cs raised
a) normocytic normochromic anaemia, thrombocytopenia
b) hypokalaemia
c) may be normal/lowT3
d) elevated cholesterol
e) low
Gs and Cs raised - Growth hormone, Glucose, salivary Glands, Cortisol, Cholesterol, Carotenemia
characteristic clinical signs of anorexia nervosa (4)
- bradycardia
- hypotension
- enlarged salivary glands
- lanugo (soft hair)
1st and 2nd line tx for anorexia nervosa in children/young people
1st = anorexia focussed family therapy
2nd = CBT
management options for anorexia nervosa in adults
- eating-disorder-focused CBT (CBT-ED)
- maudsley anorexia nervosa treatment for adults (MANTRA)
long-term complications of anorexia nervosa (4)
- severe dehydration > kidney failure
- cardiac abnormalities
- infertility
- osteoporosis
DSM-5 criteria for bulimia nervosa (4)
- recurrent episodes of binge eating (eating within 2 hours amount that isn’t normal, feeling that one cannot stop)
- recurrent compensatory behaviours e.g. vomiting, laxative/diuretic abuse, fasting, excessive exercise
- behaviours occur at least once a week for 3 months
- self-evaluation unjustifiably influenced by body shape/weight
signs of bulimia including metabolic (7)
- metabolic alkalosis (losing Hcl)
- hypokalaemia
- teeth erosion
- swollen salivary glands
- mouth ulcers
- Russel’s sign (calluses on knuckles)
- may be normal/fluctuating weight
blood and results in bulimia nervosa
- FBC - anaemia
- LFTs - may be abnormal
- U&Es - hypokalaemia, raised creatinine, elevated HCO3
1st line management for children with bulimia nervosa
bulimia-nervosa-focused family therapy (FT-BN)
management of bulimia in adults - 1st and 2nd line
1st line = guided self help
if contraindicated/ineffective after 4 weeks…
2nd line = CBT-ED
long term complications of bulimia
- fertility problems
- gastric ulcers
- osteoporosis
- heart - arrhythmias, heart attack/failure, cardiomyopathy
hypokalaemia on ECG (e.g. in EDs)
U waves
small/absent T waves
prolonged PR interval
ST depression
long QT
tx of TCA overdose e.g. amitriptyline
- activated charcoal if within 1 hour
- IV sodium bicarbonate
definition of addictive behaviours
repeated behaviours
that dominate the patient’s life to the detriment of social, occupational,
material and family values and commitments
2 medications to help with alcohol addiction and how they work
- naltrexone
- decreases pleasure when drinking alcohol - acamprosate - decreases cravings
define alcoholism
when somebody’s drinking habits interferes with there work/social lives
