Psychiatry Flashcards
What is an illusion?
A misperception of real external stimuli eg hearing the wind as someone crying
What is a hallucination?
Perceptions occurring in the absence of an external physical stimulus (can be auditory, visual or olfactory)
Often seen in schizophrenia
What is an overvalued idea?
False/exaggerated belief sustained beyond logic or reason eg I am the cleverest person in the world
What is a delusion?
A false, unshakable idea which is out of keeping with the patient’s educational, cultural and social background, held with extraordinary conviction and certainty
It is a belief that is clearly false eg believing they’re being spied on
What is a delusional perception?
A true perception to which a patient attributes a false meaning. Eg traffic lights turning red indicates martians are about to land
What is thought alienation? What 4 thought disorders does it include?
The feeling that their own thoughts are no longer within their control
Includes thought insertion, withdrawal, broadcast, echo
What is thought insertion?
The experience that certain thoughts are being placed in one’s mind by others
What is thought withdrawal?
The experience that one’s thoughts are being removed by an outside person or force
What is thought broadcast?
The experience that one’s thoughts are accessible (can hear or are aware of) by others so that others know what one is thinking
What is thought echo?
The experience/hallucination of hearing aloud one’s thoughts just after one has thought them
What is thought block?
Flow of thoughts suddenly interrupted > complete blank/total emptying of mind, speech suddenly stops
Can happen in the absence of a condition or in schizophrenia
What is concrete thinking?
Literal thinking that is based on what one can see, hear, feel and experience here and now - actual objects and events and not concepts or generalisations
What is loosening of association?
A lack of logical association between succeeding thoughts, often leads to incoherent speech. It is impossible to follow the patient’s train of thought
What is circumstantiality?
Too much unnecessary detail before reaching the point, manifests in speech or writing
Often seen in anxiety
What is perserveration?
Certain thought very prominent in thinking space despite not having any relevance > leading to persistent repetition of words/themes/actions
Slows progression of thinking
What is confabulation? Seen in what patients?
Genuine gaps in the memory are filled with fabricated information without the conscious intent to do this
Seen in dementia patients/organic conditions
What is somatic passivity? What condition might it be seen in?
The delusional belief that one is a passive recipient of bodily sensations from an outside force
e.g. cause pain to them
= can have risk implications
Seen in schizophrenia
What is delirium?
An acute confusional state often with changes in consciousness.
It is a medical emergency but is often reversible.
What is catatonia/stupor? Give some examples.
Excited/inhibited motor activity in the absence of a mood disorder or neurological disease
Eg mutism, posturing, grimacing, catalepsy
What is psychomotor retardation? Seen commonly in which diseases?
Slowing of thoughts and movements.
In depression, Parkinson’s disease
What is flight of ideas?
Nearly continuous flow of thoughts with rapid changes in topic, often based on understandable associations, distracting stimuli or plays on words. Usually manifested in speech.
What is poverty of speech? Commonly seen in?
Lack of content and elaboration in speech due to poverty of thought
-ve symptoms of schizophrenia
What is poverty of thought?
Reduced spontaneity/productivity of thought, evidence by vague/simple speech full of meaningless repetitions or stereotyped phrases
What is pressure of speech?
Speech in which one feels undue pressure to get out. Usually rapid, loud, emphatic, difficult to interrupt. May talk without social stimulation and continue even though no one is listening.
What is anhedonia?
Inability to experience pleasure from normally pleasurable activities/experience emotion
What is affective expression?
Outward expression of feelings/emotions/mood eg facial expression, tone of voice, body language
What is flattening of affect?
Reduction/absence of affective expression eg subdued/detached reactions to situations
What is incongruity of affect?
Mismatch between experienced emotion and its affected expression leading to an inappropriate response eg having happy thoughts/looking happy when talking about a sad event
What is blunting of affect?
A severe reduction in the expressive range and intensity of affect, but less than is observed in Flat affect eg diminished facial expression or gestures in reaction to emotion provoking stimuli
What is belle indifference?
Absence of psychological distress despite having a serious illness/set of symptoms
Associated with conversion disorder
What is depersonalisation?
Experiencing the self as strange/unreal or feeling detached from one’s thoughts, feelings, sensations, body or actions, as if one were an outside observer
What is derealisation?
Experiencing other people/objects/the world as strange/unreal eg dreamy, distant, foggy or detached from one’s surroundings
What is dissociation?
Disconnection from thoughts, feeling, memories, sense of identity
What is stereotypy/mannerism? For example?
Persistent repetition of a movement/sounds, for no obvious reason eg rocking, crossing legs
What is obsession? Associated with?
Repetitive, persistent and irrational thoughts, images and urges that are experienced as intrusive/unwanted
Associated with anxiety
Responsible for these thoughts - know they are irrational but can’t stop them
What is compulsion?
Repetitive behaviours/rituals/mental acts that the individual feel driven to perform in response to an obsession/according to rigid rules/to achieve sense of completeness
What is the difference between mood and affect?
mood = subjective, how the pt describes their current mood
affect = objective, what the dr observes e.g. how they convey emotion/non-verbal cues
What is the term for a good/normal mood?
euthymic
Give 2 examples of incongruent affect and what they are indicative of
Flat affect = eg talks about something enjoyable whilst remaining subdued/flat, indicative of depression
Elevated affect - indicative of mania
What is thought stream? What thought streams should be looked out for in the MSE? What are they indicative of?
abnormality of amount and speed of thought
e.g. pressure/poverty of speech, thought block
What is thought form? What thought forms should be looked out for in the MSE? What are they indicative of?
description of the organisation of someone’s thinking
e.g. flight of ideas, perseveration, loosening of associations
What is normal thought form referred to as?
no formal thought disorder = NFTD
Give some examples of different delusions?
grandiose - exaggerated self importance, power or influence
delusions of reference - objects, events or people have special significance eg comment on the TV is directed at them
persecutory delusion - belief that they are being watched and organisations/people are trying to harm them
delusions of control - beliefs that actions, impulses and thoughts are controlled by an outside agency
infidelity, love (convinced someone they’ve never met is in love with them), guilt (believes they are bad/evil person), nihilistic (pt denies existence of their body e.g. heart is missing), poverty (believes they are poor)
> often mood congruent/environmental
What is perception?
awareness of external sensory stimuli via the senses
hallucinations, dissociative sx, illusions
What does a 2nd person hallucination indicate compared to a 3rd person?
2nd > affective psychosis, personality disorder
3rd > paranoid schizophrenia
What can visual hallucinations be indicative of?
more common in acute organic psych disorders with clouding of consciousness e.g. brain dysfunction, epilepsy, migraine, tumour, delirium, dementia
= MUST rule out organic
What is a functional hallucination?
auditory stimulus causes a hallucination
What is a reflex hallucination?
stimulus in one sensory modality produces sensory experience in another
What is an extracampine hallucination?
outside the limits of the sensory field e.g. hears voices talking in Paris when in Sydney
What is a hypnagogic/hypnapompic hallucination?
occurs when subject is falling asleep/waking up respectively
= usually a normal experience, not always mental illness
What is the difference between a primary and secondary delusions?
primary: appears suddenly without any mental events leading up to it, very indicative of schizophrenia
secondary: arises from previous abnormal idea/experience eg persecutory delusions
What is dissociative amnesia?
sudden amnesia occurring during periods of extreme trauma, can last for hrs/days
What is apathy?
lack of interest, enthusiasm, concern etc
What is conversion disorder?
Physical sx without physical cause
eg paralysis, blindness that cannot be explained by medical evaluation
Define this type of catatonia:
waxy flexibility
pt’s limbs feel like wax/lead pipe when moved, remain in the position they are left in (rare in schizophrenia/structural brain disease)
Define this type of catatonia:
echolalia
automatic repetition of words heard
Define this type of catatonia:
echopraxia
automatic repetition by the pt of movements made by examiner
Define this type of catatonia:
logoclonia
repetition of last syllable of a word
Define this type of catatonia:
negativism
motiveless resistance to movement
Define this type of catatonia:
palilalia
repetition of a word over and again with increasing frequency
Define this type of catatonia:
verbigeration
repetition of one/several sentences/strings/strings of fragmented words, often in a monotonous tone
What are the 3 core sx of depression?
low mood
loss of energy (anergia)
loss of pleasure/interest in doing things (anhedonia)
What are the other sx of depression?
Ask about a CHANGE in these sx
BIOLOGICAL:
change in sleep (EMW at least 2hrs before normal time = characteristic)
change in appetite (none/low)
change in libido
diurnal mood variation
agitation/edgy/anxious
COGNITIVE:
loss of concentration
guilt (past)
loss of confidence (present)
hopelessness (future)
suicidal ideation
How many core/other sx do you need for a diagnosis of depression?
at least 2 core sx
and a combo of other sx
How many core/other sx do you need for a diagnosis of mild depression?
core sx + 2-3 others
How many core/other sx do you need for a diagnosis of moderate depression?
core + 4 others + functioning affected
How many core/other sx do you need for a diagnosis of severe depression?
majority of core + other sx
suicidal ideation
marked loss of functioning
+/- psychotic sx e.g. nihilistic or guilty delusions, derogatory voices
What is the difference between bipolar I and II?
I: both mania and depression, usually equally, sometimes only mania
II: more episodes of depression, only mild hypo mania = easily missed
What question is important to ask to distinguish between depression and bipolar II?
previous manic episodes in past psych hx
What is cyclothymia?
bi-polar like
numerous periods of depression + hypomania but not severe enough to be bipolar
How long does a hypomanic and manic episode need to be, to be diagnostic?
hypomania: <1wk
mania: > 1wk
What are the first rank sx of schizophrenia?
thought alienation
passivity phenomena
3rd person auditory hallucinations
delusional perception
What are the secondary sx of schizophrenia?
delusions
2nd person auditory hallucinations
hallucinations in any other modality
thought disorder
catatonic behaviour
negative sx
What are the +ve sc of schizophrenia? What are +ve sx?
extra to the normal experience
hallucinations
delusions
passivity phenomena
thought alienation
lack of insight
disturbance in mood
What are the -ve sc of schizophrenia? What are -ve sx?
taking away from them as a person
blunting of affect
amotivation
poverty of speech/thought
poor non-verbal communication
clear deterioration in functioning
self neglect
lack of insight
When are +ve vs -ve likely to present in the course of a pt’s schizophrenia?
tend to start off in teens/20s with +ve sx
progress into a more -ve state with more episodes
elderly usually present with much more -ve picture
What is generalised anxiety disorder?
feeling anxious all the time
constant, >6mo
Describe some sx of GAD?
disturbed sleep (initial insomnia rather than EMW like in depression)
muscle tension
irritability
poor concentration, tired
What is panic disorder?
acute episodes of anxiety
Describe the physical sx of panic disorder?
Palpitations
Chest pain
Tachypnoea
Dry mouth
Urgency of micturition
Dizziness
Blurred visions
Paresthesia
Describe the psychological sx of panic disorder?
Feeling of impending doom
Fear of dying - often present to GP/A&E, convinced it is physical eg heart attack
Fear of losing control
Depersonalisation
Derealisation
Define OCD?
repetitive and irrational obsessive thoughts/images (often unpleasant e.g. death/sexual/blasphemous) + compulsive acts
can have one or the other but most have both
What is the difference between an obsessive thought in OCD and a delusion?
Pts with obsessive thoughts recognise that they are their own thoughts - know they are wrong/irrational but can’t stop them
Whereas a delusion - pt’s don’t know it’s their own thoughts/that it’s not real
What conditions are not including as a reason to be detained in the MHA?
alcohol/drug misuse
What is the purpose of section 2 of the MHA?
ASSESSMENT - treatment can be given without consent if part of assessment
What doctors are needed to issue a section 2 and 3?
2 drs (1 S12 approved, one any registered medical practitioner) + 1 AMHP
What is the duration of a section 2 of the MHA?
28 days max, can be stopped before then but not renewed
What is the purpose of section 3 of the MHA?
Treatment
What is the duration of a section 3 of the MHA?
6 months
can be renewed indefinitely but usually 6mo-1yr
What evidence is required for a section 3?
(a)The patient is suffering from mental disorder of a nature (clear diagnosis usually) or degree which makes it appropriate for the patient to receive medical treatment in a hospital
b) The treatment is in the interests of his or her health and safety and the protection of others; and
c) Appropriate treatment must be available for the patient (at the hospital they are going to)
What evidence is required for a section 2?
a) The patient is suffering from a mental disorder (doesn’t need to be a diagnosis, just evidence of sx) that warrants detention in hospital for assessment; AND -
b) The patient ought to be detained for his or her own health or safety, or the protection of others
What is the purpose of section 4 of the MHA?
Emergency order - only an urgent necessity when waiting for a 2nd dr would lead to undesirable delay
(to temporarily hold someone)
Cannot be coercively treated
What is the duration of a section 4 of the MHA?
72 hrs
Who is needed to issue a section 4?
1 dr + 1 AMHP
What evidence is required for a section 4?
a) The patient is suffering from a mental disorder (not a diagnosis) of a nature or degree that warrants detention in hospital for assessment; and
b) The patient ought to be detained for his or her own health or safety, or the protection of others
c) There is not enough time for 2nd doctor to attend - there is immediate risk
What is a section 5(4)? Where can they happen?
Who can issue them? How long can they last?
for a pt already admitted but wanting to leave (not including a&e = community)
nurses’s holding power until dr can attend > for up to 6hrs
cannot be coercively treated
What is a section 5(2)? Where can they happen?
Who can issue them? How long can they last?
For a pt already admitted but wanting to leave (not a&e)
Dr’s holding power > up to 72hrs
Allows time for S2/S3 assessment/discharge
Cannot be coercively treated
What is the difference between a section 135 and 136? What evidence is needed? Where do they happen?
police sections
needs evidence of a mental disorder + needs to be considered a danger to themselves/others
often required in A&E
S136 - person suspected of having mental disorder in a public place e.g. bridge
S135 - needs court order to access pt’s home and remove them to a place of safety (psych unit/police cell) > further assessment needs an S2/3
Describe dementia?
chronic decline in higher cortical function for at least 6m
Describe the cognitive sx of Alzheimer’s? What is their onset like?
4A’s:
Amnesia (short-term memory loss, disorientation around time, long-term usually in tact)
Aphasia/dysphasia (later, receptive and expressive loss)
Apraxia/dyspraxia (button clothes, cutlery etc)
Agnosia (unable to recognise body parts/objects)
Executive function e.g. finance, cooking
Dyslexia, dysgraphia, acalculia
Insidious onset
Describe the non-cognitive sx of Alzheimer’s?
psychosis e.g. delusions, hallucinations
mood - anxiety, depression
behavioural - apathy, agitation, wandering, aggression
misidentification - can’t recognise loved ones
What are the key risk factors for Alzheimer’s?
old age
female (live longer)
linked to gene defect e.g. APO E4
FHx
CVD risk factors - HTN, diabetes, smoking, hypercholesterolaemia
Downs syndrome (present much earlier, 30/40s, most develop it by 50)
What are some protective factors for Alzheimer’s?
APO E2
high intelligence/education
oestrogen/anti-inflammatory medication possibly
What are the key sx of Lewy body dementia? How does it progress?
REM sleep disorder - commonly 1st sx
visual hallucinations
fluctuating cognition/consciousness
parkinsonian sx (motor sx) eg tremor, stooped gait
autonomic dysfunction
frequent falls
How can lewy body dementia and Parkinson’s be distinguished?
- parkinson’s = motor sx 1st, memory problems once disease is established
- LBD = memory sx first/at same time, more sensitive to neuroleptic medication (antipsychotics)
essentially the same pathology
How does frontotemporal dementia present?
insidious onset, poor insight
amnesia not as bad as Alzheimer’s, comes later
Frontal sx:
personality change/social and interpersonal conduct/behavioural sx e.g. aggression
euphoria/disinhibition
emotional blunting
Temporal sx:
speech disturbances
expressive dysphasia
What is the onset of FTD, usually? What is the prognosis like?
early onset
poor prognosis
How does vascular dementia present?
patchier cognitive impairment than Alzheimer’s > slowed thinking, reasoning and info processing
focal neurological signs if caused by CVA
emotional lability
can have psychotic sx e.g. delusions
memory problems
stepwise deterioration
hx of stroke/microbleed/TIA
In what pattern does vascular dementia progress?
stepwise - period of stability before acute decline
How is cognitive decline investigated?
clinical + collateral history
check for reversible causes, incl full physical exam -(anaemia, thyroid, B12, hyponatraemia, alcohol)
memory screening tool e.g. 6CIT/DiADeM in care homes
then Addenbrookes for more detail (<82 is abnormal, in at least 2 domains)
CT scan > rule out bleeds, strokes, tumours, NPH, see shrinkage (FTD)/blood vessel damage (vascular)
How does normal pressure hydrocephalus (NPH) present? Causes?
Triad: ataxia + dementia + urinary incontinence
abnormal gait
but is a key REVERSIBLE cause of dementia
causes: idiopathic, SAH, head trauma, meningitis
treat: ventriculoperitoneal shunt
How is Alzheimer’s dementia managed pharmacologically?
AChE inhibitors (increase level of ACh) e.g. donepezil = 1st line, rivastigmine, galantamine
Memantine (glutamate/NMDA antagonist ) > when pt presents in mod-severe stages/if AChE not tolerated
Treat underlying cause/comorbidities
SSRIs, antipsychotics, sleeping tablets, short acting benzos e.g. lorazepam where needed
What is the only antipsychotic licensed to treat dementia? Why?
risperidone
risk of stroke
How is dementia managed non-pharmacologically?
risk/needs assessment > care plan
carers assessment - things needed to support carer
OT assessment > environmental adaptation e.g. alarms on doors/tracking device, physio if necessary
social activity
other therapies e.g. music, snoezelen (sensory stimulation room), art, CST
consider capacity/advance care planning
What type of anaemia can present with memory loss?
Any anaemia can present with low mood/poor concentration which may manifest like dementia
B12 deficiency > memory loss = rule out
How does delirium present?
acute confusional state, quick onset
abrupt global impairment of cognitive processes > confusion, disorientation, agitation
attention difficulties
fluctuating consciousness
hallucinations
disinhibition
labile mood
worse at night (sundowning)
evidence it may be related to a physical cause
Describe the 4 features of confusion assessment method (CAM)? Which ones are needed for a diagnosis of delirium?
1 and 2 + either 3 or 4
- acute and fluctuating course
- inattention
- disorganised thinking
- altered level of consciousness
What are the important differentials for delirium?
delirium tremens in an alcohol dependants pt, especially post-op
others are: anaphylactic reactions, dementia, head injury
What medications can cause delirium?
anticholinergics
Parkinson’s medication
benzos
steroids
drug accumulation (elderly, poor kidney/liver function)
polypharmacy
post-surgery - anaesthetics, analgesics, blood loss
What is the management for delirium?
identify cause + treat
nutrition and hydration
support + behavioural management first
medications: haloperidol (1st line), benzos (avoid if possible)
long acting benzos if withdrawing from alcohol/drugs
may lack capacity - can treat under MCA
Delirium vs dementia:
deterioration time
course
consciousness
thought content
hallucinations
DELIRIUM:
rapid + usually reversible if underlying cause treated
fluctuating course
clouded consciousness/attention disorganised
vivid/complex thought content
hallucinations common, usually visual
DEMENTIA:
slow + irreversible deterioration
slowly progressive course
alert/attention often intact
impoverished thought content
hallucinations only in a 1/3rd, can be auditory/visual
When does mild cognitive impairment become dementia?
Dementia diagnosis requires - 6mo hx of cognitive decline with associated loss of functioning
often complex tasks get lost first e.g. finances, navigation
MCI little/no functional decline alongside memory loss
When can vascular dementia present like Alzheimer’s?
if there is an infarct in the temporal lobe
Why can donepezil sometimes be difficult to give to dementia pts? What can be given instead?
oral tablet - sometimes difficult to take
rivastigmine comes as a patch
What are the side effects of AChEs? What pts should we be careful of giving donepezil to?
What other medication might need to be reduced if a pt is put on donepezil?
bradycardia
postural drop
> risk of falls
GI upset
Careful with pts with a hx of falls/cardiac problems
If on beta blockers, reduce if possible
What is the DMS IV/V description of emotionally unstable personality disorder (EUPD)?
enduring pattern of inner experience and behaviour
deviates from cultural expectations
pervasive and inflexible (struggle to change the way they behave)
onset adolescence/early adult
stable over time
leads to distress
impairments in self and interpersonal functioning
What are the cluster A personality disorders?
‘odd/eccentric’ = MAD
schizoid
paranoid
schizotypal
What are the cluster B personality disorders?
‘dramatic/erratic’ = BAD
EUPD
histrionic
narcissistic
dissocial/antisocial
What are the cluster C personality disorders?
‘anxious/fearful’ = SAD
Anankastic (obsessive compulsive)
dependant
avoidant
What are the clinical features of EUPD?
- unstable mood - fluctuates/intense/overwhelmed by emotions they can’t tolerate (RISK)
- impulsivity (RISK - disordered eating, substance misuse, sexual behaviours etc)
- intense unstable relationships
- fear of/attempts to avoid abandonment
- chronic feelings of emptiness
- thoughts of self harm/suicide (can be habitual)
- uncertainty of self image/identity/aims/preferences, lack of sense of who they are
- may experience psychotic sx e.g. paranoia, derogatory/commands hallucinations
What are the risk factors for EUPD ?
attachment theory: unresponsive parenting/adverse childhood
childhood trauma e.g. sexual abuse
adverse events during pregnancy/birth/neonatal period
What are the differential diagnoses for EUPD?
bipolar affective disorder (more episodic mood changes with stability in between, presence of bio sx e.g. appetite/sleep change)
neurodevelopmental disorders (autism, ADHD - emotional fluctuation, poor attention)
psychosis (hallucinations more likely to be 3rd person/running commentary, in EUPD > internal dialogue about themselves, identify with the criticism + lack of other psychotic features e.g. delusions)
complex PTSD > overlap with hx of trauma, flashbacks, autonomic arousal with emotional dysregulation, poor impulse control, self harm/suicidal feelings
What comorbidities are likely to occur with EUPD?
psychosis
affective/anxiety disorders
alcohol/substance dependance
eating disorders
functional disorders e.g. chronic pain, non-epileptic seizures
Name some infectious causes of delirium?
UTI - very common in elderly
pneumonia
septicaemia
Name some toxic causes of delirium?
substance misuse
intoxication withdrawal e.g. delirium tremens
opioids
Name some vascular causes of delirium?
CVA (stroke)
haemorrhage
head trauma
Name some metabolic causes of delirium?
hyper/hypothyroidism
hyper/hypoglycaemia
hypoxia
hypercortisolaemia
Name some nutritional causes for delirium?
thiamine (b1) deficiency
B12/folate deficiency
dehydration
What people are at high risk and there should be screened for delirium on hospital admission?
> 65 yrs
have diffuse brain disease e.g. dementia, PD
hip fracture pts
severely ill
post-op
What tool is used to screen for delirium?
4 AT assessment
What are the 2 subtypes of delirium?
- hypoactive - withdrawn, sleepy, less likely to be recognised
- hypERactive - restless, agitated, aggressive
How is delirium investigated?
look for underlying cause:
bloods
urinalysis
full physical exam e.g. hip exam for fracture
CXR if indicated
CT head if worried about CVA/head trauma
Which dementia presents a lot like delirium and can be easy to miss?
LBD
> visual hallucinations, confusion, course can fluctuate
What is the difference between cortical and subcortical dementia? Name some examples of each.
cortical dementias - affect the cerebral cortex
e.g. Alzheimer’s, LBD, frontotemporal dementia
subcortical dementias - affect the basal ganglia and the thalamus
e.g. PD dementia, Huntington’s disease dementia, LBD, alcohol related dementia, AIDS dementia
What are the typical symptoms of cortical dementia?
Memory impairment
Dysphasia – language deficit
Visuospatial impairment (apraxia)
Problem solving and reasoning deficit
What are the typical symptoms of subcortical dementia?
Pscyhomotor slowing
Impaired memory retrieval
Depression
Apathy
Execustive dysfunction
Personality change
Language preserved- unlike in cortical
Describe the macroscopic pathological changes that occur in Alzheimer’s, seen on CT?
Shrunken brain (diffuse cerebral atrophy)
Increased sulcal widening
Enlarged ventricles
Define Alzheimer’s?
insidious onset of dementia due to generalised deterioration of the brain
most common type of dementia
Describe the microscopic pathological changes in Alzheimer’s disease?
Neuronal loss
Neurofibrillary tangles
Amyloid plaques
Which neurotransmitters are affected in Alzheimer’s?
Acetylcholine
Noradrenaline
Serotonin
Somatostatin
When does Alzheimer’s usually present? When is it defined as early onset?
> 65
<65 is early onset > more rapid decline, FHx
What are the domains tested in the Addenbrooke’s cognitive assessment?
Attention/orientation
Memory
Language
Visuospatial
Fluency
What are the RFs for vascular dementia?
HTN, smoking, diabetes, hypercholesterolaemia
Hx of PVD, IHD
AF
What would be seen on a CT head in someone with VD?
At least one area of cortical infarction – shows up white on CT
How is vascular dementia managed?
Not reversible, prevent further decline by modifying RF:
statins, anti-hypertensives, aspirin
treat diabetes, smoking cessation, lifestyle changes
no role for AChEi
What is the pathological feature found in the brain of someone with LBD?
presence of Lewy bodies (protein deposits) in the basal ganglia and cerebral cortex
When does LBD usually present?
50-80yrs
What is the onset/progression of LBD like?
fluctuating onset/progression, rapid decline - more than other dementias
How is LBD treated?
1st line = rivastigmine/donepezil
supportive/palliative/emotional guidance
OT assessment
advance directives
What medication must be avoided in the treatment of LBD? Why?
AVOID antipsychotics
can make it much worse
> may lead to neuroleptic malignant syndrome
Quetiapine if no cognitive decline
Clozapine 2nd line
Delirium with LBD > PO lorazepam first
What are the microscopic pathological features in frontotemporal dementia?
ubiquitin and tau deposits
How is FTD treated?
no specific treatment
SSRIs may help behavioural sx
OT assessment
advance directives?
What are the behavioural and psychological sx (BPSD) of dementia?
- anxiety
- depression
- agitation
- psychosis
- disinhibition
What are the treatable causes of BPSD?
PINCH ME
Pain
Infection
Nutrition
Constipation - check stool chart
Hydration
Medication (polypharm, codeine)
Environment (noisy hospital ward)
What is Creutzfeltd-Jacob disease?
abnormal infectious protein in brain (prion) > spongiform encephalopathy
causes rapidly fatal dementia
+ death within a yr
myoclonic jerks + extra-pyramidal signs seen
What is attachment theory?
The ideas that caregivers who are responsive to an infant’s needs allow the child to develop a sense of security
What are the 4 types of attachment in infant’s? How might this relate to their mental health as an adult?
secure
ambivalent
avoidant
disorganised
secure > should develop into an adult that can cope with the world
insecure > more likely to have mental health conditions/personality disorders
What is anankastic personality disorder?
usually high functioning and only becomes a problem when they hit a hurdle
much less debilitating than OCD
perfectionist behaviour without the same compulsions as OCD
What can anankastic personality disorder develop into?
can develop anxiety, sometimes OCD
How do you investigate someone who you think may have a personality disorder?
needs to be assessed more than once
collateral hx
MSE
risk assessment
treat comorbid psych conditions before diagnosis is made
How are personality disorders managed?
medications - mood stabilisers, sedatives during crises
psychological therapies e.g. cbt/dbt/cat/mbt
continuity of care very important
engage with services, structure, help with housing/other social matters
What is the gold standard treatment for EUPD?
DBT - dialectical behavioural therapy
group therapy with individual support
When is medication indicated in EUPD?
never to treat the PD
only for comorbid sx e.g. depression
Define schizophrenia?
Splitting/dissociation of thoughts or loss of contact with reality
Affects a person’s thoughts, perceptions/senses, personality, speech, power over their will/sense of self
What is the difference between psychosis and neurosis?
Psychosis = severe mental disturbance characterised by a loss of contact with external reality (e.g. schizophrenia, delusional disorders)
Neurosis = relatively mild mental illness in which there is no loss of connection with reality (e.g. depression, anxiety)
What is thought to cause schizophrenia?
Thought that some pts have a susceptibility and emotional life experiences can act as a trigger
Seems to involve dopamine excess? Antipsychotics aka dopamine blockers treat it
Describe the onset of schizophrenia?
diagnosed between 15-35
slightly earlier in men
smaller peak incidence in late middle age
What are the RFs for schizophrenia?
FHx
drug abuse particularly cannabis in adolescence
insult to brain development in early life - trauma, epilepsy, developmental delay, perinatal infection
stressful/adverse life experiences/physical or sexual abuse/bullying
Socioeconomic deprivation
What are the 6 types of schizophrenia? Which is the most common?
paranoid (most common) - paranoid delusions + auditory hallucinations
Hebephrenic - mood changes, unpredictable behaviour, shallow affect, fragmentary hallucinations (in adolescents, por outlook as -ve sx develop rapidly)
Catatonic - psychomotor features eg posturing, rigidity, stupor
Undifferentiated - sx don’t fit into another category
Residual - -ve sx, occurs when +ve sx have burnt out
Simple - -ve sx like hebephrenic + pts have NEVER experienced +ve sx
What combination of 1st and 2ndary sx of schizophrenia are needed for a diagnosis?
1+ 1st rank sx
OR 2+ 2ndary sx
For at least 1 mo
with no other cause for psychosis e.g. drug intoxication/withdrawal/brain disease or extensive depressive/manic sx
What kind of delusions are pts with schizophrenia likely to have?
persecutory
delusions of reference
How is schizophrenia investigated?
Rule out other causes of confusion/psychosis
- Urine culture (UTI > delirium), drug screen
- CT scan if organic neuro cause suspected
- Full physical exam
- FBC, TFTs, U&Es, LFTs, CRP, fasting glucose > tumours, cysts, PD, HD, brain injury, systemic infection
HIV/syphilis if required
Check lipids before starting antipsychotics
Collateral hx if possible
MSE
Risk assessment
How is schizophrenia treated?
Typical antipsychotics: D2 receptor antagonists eg haloperidol, chlorpromazine
Or an atypical antipsychotic (more selective, also block serotonin 5 HT2 receptors) eg quetiapine, olanzapine
Aripiprazole = partial dopamine agonist and less likely to cause SEs
Clozapine used if typical and atypical antipsychotics haven’t worked
CBT, family therapy
Which outpatient psych teams are usually involved in the care of a pt with schizophrenia?
Early intervention team (initial referral)
Community mental health team (day to day support/treatment)
Crisis resolution team (acute psychotic episodes)
Delirium can last up to how long after the physical cause is removed?
6 weeks
What is cotard’s syndrome?
severe type of depression
delusional belief that they’re bodily functions aren’t working/organs are missing/they are dead
can lead to dangerous behaviours e.g. not eating
What tests make up a confusion screen? What are they looking for?
FBC, U&Es, LFTs, coagulation, TFTs, Ca2+, B12 + folate, glucose, blood cultures
Alcohol/substance misuse
CT head
Urinalysis
CXR
What effect can SSRIs have on mania?
can make manic sx worse > manic reaction
bipolar/mania shouldn’t be treated with ADs alone, need mood stabilisers too
What are the key risk factors for suicide?
male
peaks in young men and in middle aged
unemployment/stressful job
living alone/isolation
divorcees/being single
homelessness
previous psych hx
lack of engagement or barriers to accessing MH services
previous self harm/type of self harm/regret shown
alcohol/drug misuse
fhx
Where does shrinkage occur on a CT scan in Alzheimer’s?
hippocampus
atrophy in temporal lobe next to the tips of the temporal horns > widening of the temporal horns (usually under 3mm)
How long should ADs be continued for after sx stop?
at least 6 months
What are some of the disadvantages of antidepressants?
can take a while to work - some people stop taking them thinking it’s not wokring
can increase suicidal thoughts/make things worse initially
improves some sx of depression but not others
What are some medical causes for depression?
hypothyroidism
chronic disease
post-natal
medications e.g. isotretinoin (roaccutane) for acne, beta blockers
What are some risk factors for depression?
Fhx
Hx of abuse
Drug/alcohol misuse
Low socioeconomic status
Chronic disease
Traumatic life event
What are some differentials for depression?
Normal sadness eg after bereavement
Schizophrenia - flat affect of schiz may present like depression, won’t have other core sx of depression
Hypothyroidism
Alcohol/drug withdrawal
What kind of time course does depression usually follow?
relapsing/remitting
How long must sx be present for a diagnosis of depression?
2 weeks
What are the 3 core sx of depression?
low mood
loss of energy (anergia)
loss of pleasure in doing things (anhedonia)
What are the other sx of depression? (biological and cognitive)
Biological:
change in sleep (EMW - at least 2 hrs before normal time or sleeping more)
change in appetite - usually eating less/losing weight
change in libido
diurnal mood variation
agitation/edgy/anxious
Cognitive:
guilt (PAST)
loss of confidence (PRESENT)
hopelessness (FUTURE)
suicidal ideation
What signs might you see in an MSE of a depressed person?
Weight loss due to reduced appetite
Psychomotor retardation seen in movement/speech
Avoids eye contact
Slow and quiet speech
How many sx are needed to diagnose mild depression?
core sx + 2-3 others
How many sx are needed to diagnose moderate depression?
core sx + 4 others + impact on daily functioning
How many sx are needed to diagnose severe depression?
several sx, suicidal, marked loss of functioning
+/- psychotic sx
What kind of psychotic sx might you see in depression?
usually mood congruent - nihilistic (world has ended), persecutory or guilty (worried they’ve killed/abused someone) delusions, derogatory auditory hallucinations
can be incongruent - likely to include more 1st rank sx e.g. thought insertion
How should depression be investigated?
risk assessment - self-neglect/harm, suicidal thoughts
MSE
rule out DDs:
FBC/TFTs - hypothyroidism, chronic disease
urine drug screen - substance misuse
medication review
How is mild depression treated?
low-intensity psychosocial interventions e.g. computerised/individualised CBT, guided self-help, group physical activity
psychoeducation
usually no medication
How is moderate to severe depression treated?
combination of antidepressant therapy
+ high intensity psychosocial treatment eg individual CBT, interpersonal therapy, behavioural activation/couples therapy
antipsychotic if they present with psychotic sx e.g. aripiprazole, risperidone
psychoeducation
How can treatment resistant depression be treated?
combo of antidepressants and lithium/atypical antipsychotics/other antidepressants
What intervention can be used in very severe cases of depression that are resistant to treatment?
ECT
What is the ICD-10 definition of GAD?
generalised, persistent, excessive worry
about a number of everyday events
finds the worry difficult to control
for at least 3 weeks (ICD-10) or 6 months (DSM)
What physical heath conditions can cause GAD?
hyperthyroidism
pheochromocytoma
lung disease (excessive use of salbutamol)
congestive heart failure (heart medications can lead to GAD)
hypoglycaemia
What part of the population is most effected by GAD?
females > young adults/middle aged
What are the risk factors for GAD?
alcohol use
benzodiazepine use
stimulates - esp during withdrawal
co-existing depression
FHx of anxiety disorders
childhood abuse, neglect
excessively pushy parents during childhood
life stresses/events e.g. finances, bereavement
physical health problems - anxious about their health?
What is the difference between GAD, panic disorder and phobias?
GAD - constant worry without external stimulus
Panic disorder - discreet episodes of anxiety that occur unpredictably/not restricted to a certain stimulus
Phobias - discreet anxiety attacks about a specific stimulus
What are the key sx of GAD?
Unpleasant/fearful emotional state
Apprehension - feeling of impending threat/death/losing control
Increased vigilance
Physical sx (sympathetic autonomic over-activity) eg palpitations, tachycardia, sweating, tremor, chest pain, nause, abdo pain, dizziness, chills/hot flushes, feeling of choking
Bodily discomfort eg restlessness, agitations, avoidance of stimuli
Sleeping difficulties - initial insomnia, fatigue on waking
Low self-worth
Difficulty concentrating
Irritability
What are the key sx of panic disorder?
usually lasts a few minutes
crescendo of anxiety > usually results in exit from situation
same physical sx as GAD
secondary apprehension - feeling of impending threat/death/losing control
depersonalisation/realisation
What are the key sx of phobias?
avoidance of the situation
anticipatory anxiety
same physical sx as GAD
Give 2 examples of phobias?
agoraphobia - fear of crowded places/going outside/places that are difficult to escape from quickly
social phobia - fear of social situations where a individual is exposed to unfamiliar people/possible scrutiny > low self-esteem/fear of criticism
What are signs of anxiety in an MSE?
restlessness
agitation
may have a tremor
What are the 3 diagnostic criteria for GAD?
Excessive anxiety + worry about a number of events/activities
Difficulty controlling the worry
For at least 3 weeks
How are anxiety disorders investigated?
History including social situation, interpersonal relationships
Rule out a physical causes e.g. bloods, TFTs, BP
risk assessment
How should anxiety disorders be treated?
- psychoeducation, sleep hygiene, self-guided CBT - low intensity to start
2a. CBT - unlearning maladaptive patterns of thought/behaviour +/- exposure therapy (phobias)/applied relaxation
2b. Pharmacological - SSRIs eg sertraline (1st line), SNRIs eg duloxetine, atypical AD eg mirtazapine - choice depending on SE profile
Alternative ssri/snri if ineffective
Consider combining medication
Benzodiazepines for crisis
Beta blockers e.g. bisoprolol for physical sx
What medications should be avoided in chronic anxiety? Max length of time they should be prescribed?
benzodiazepines - highly addictive
used in transient causes of anxiety e.g. flying/crisis only
max 2 weeks prescription
What is anxiety often comorbid with?
depression
substance misuse
A patient presents with a suspected eating disorder and collapses. What other causes of collapse should be ruled out?
dehydration
drug/alcohol use
CVS
What are the SCHOFF screening questions?
S - Do you make yourself SICK because you feel uncomfortably full?
C - Do you worry you have lost CONTROL over how much you eat?
O - Have you recently lost more than ONE stone/6kgs in a 3 month period?
F - Do you believe yourself to be FAT when others say you are thin?
F - Would you say FOOD dominates your life?
(yes to 2+ > high sensitivity for anorexia/bulimia nervosa)
What methods of reducing their weight are used by pts with eating disorders? Why is it important to find this out?
restricting calories
over-exercising
laxatives
vomiting
diuretics
fasting
diet pills
important due to potential complications
What are the differential diagnoses of weight loss?
malabsorption e.g. celiac disease, IBD, peptic ulcer
malignancy
drug/alcohol misuse
infection e.g. TB, HIV
AI disease e.g. RA
endocrine - hypothyroid, DM< hypercortisolism, adrenal insufficiency
medications e.g. NSAIDs
What are the key sx of anorexia nervosa?
low body weight
intense fear of gaining weight
- Preoccupation with food (dieting, making elaborate meals for others)
- Selective about food, not eating around others, say they have already eaten
- Repeated weighing/measuring, checking mirror
Behaviour that interferes with gaining weight e.g. purging
- Distortion of body image, low self-esteem, drive for perfection
Hormonal disturbance
- Amenorrhea/irregular periods
- Men - loss of libido/potency
What are the key sx of bulimia nervosa?
Recurrent episodes of binge eating on average at least once a week for 3 mo
= consuming excessive amount of food with a sense of loss of control over eating
In-between likely attempts to restrict eating
Recurrent inappropriate compensatory behaviour to prevent weight gain eg vomiting
Weight often within normal limits/above average - can go undetected
Psychological features
- Over-evaluation of self-worth
- Fear of fainting weight, sharpy defined weight threshold set by patient
- Mood disturbance, sx of anxiety
- Persistent preoccupation and craving for food/feelings of guilt and shame about binging
- Self-harm
What are the key steps to a physical exam of a suspected ED?
- calculate BMI, compare to previous recordings
- vital signs - temp, pulse, BP, hydration, peripheral circulation
- look for muscle wasting, assess muscle strength (score of 2 or less on the Sit-up-Squat-Stand test)
- look for complications/signs suggestive of an alternative cause
What are the signs seen on physical exam of anorexia nervosa?
Dry skin, hair loss/lanugo hair (peach fuzz)
Bradycardia or postural tachycardia
Orthostatic hypotension
Hypothermia
Loss of muscle strength
Oedema, cold peripheries
Constipation
Fainting, dizziness, fatigue Weight: BMI < 17.5, emaciation (state of being abnormally thin/week) - often disguised by make-up/clothes
Anaemia - angular stomatitis
Self harm scars?
What are the signs seen on physical exam of bulimia nervosa?
Bloating, fullness
Lethargy
Gastro-oesophageal reflux
Abdo pain
Sore throat from vomiting
Severe: Russell’s sign > knuckle calluses from induced vomiting, dental enamel erosion, salivary gland enlargement, hypokalaemia, alkalosis
Self harm scars?
What bloods should be carried out for a suspected ED? What are we looking for?
look for physical causes - find biggest risks first
FBC - anaemia from malnutrition/GI losses, mild leukopenia/thrombocytopenia, low plasma proteins
U&Es - hypokalaemia suggestive of vomiting/laxative abuse, hyponatraemia - excess water intake to cover up weight loss
ESR/CRP - raised > organic cause of weight loss, should expect low/normal
TFTs - like to see low T3/T4 - can look like hypothyroidism
LFTs - likely to be elevated from malnutrition
Blood sugar - likely hypoglycaemic
What investigations should be carried out for a suspected ED, other than bloods?
ECG - look for QT prolongation, MI, arrhythmias
CVS is the biggest cause of death
Urinalysis - hypokalaemia, renal function
could do ABG/HIV/endoscopy etc if indicated
What are the 4 domains of the MCA?
can’t do 1 or more? no capacity
the patient can:
1. understand the info
2. retain it long enough to make a decision
3. weigh up the information
4. communicate their decision
What are the 5 principles of the MCA?
- assume capacity until proven otherwise
- do not treat people as incapable of making a decision unless all practicable steps have been tried to help them
- should not be treated as incapable of making a decision because their decision seems unwise
- always do things or take decisions for people without capacity in their best interests
- before doing something, consider whether the outcome could be achieved in a less restrictive way
What extra electrolytes must be requested on the U&Es form if referring syndrome is suspected? Why?
phosphate and magnesium
leads to CVS + resp failure
when starved, body has to maintain balance > massive intracellular uptake of electrolytes > serum levels fall
What is refeeding syndrome? What happens to electrolyte levels?
occurs when people eat after a long period of fasting
in starvation state = protein catabolism > total body phosphate/mag depletion + normal serum levels
eat = massive IC uptake of electrolytes > serum levels fall
= resp/cvs failure
hypophosphataemia > muscle weakness > diaphragmatic insufficiency
How long after eating does refeeding syndrome usually occur?
3-4 days
What are the immediate risks for a pt with an ED?
CVS instability - arrhythmias, heart failure
anaemia
electrolyte imbalances - especially hypokalaemia with vomiting > MI, sudden cardiac death
hypoglycaemia
look for syncope, severe abdominal pain
What are the immediate management steps when a pt presents with an ED?
chase U&Es - phosphate, mg, blood glucose
fluid resuscitation
contact dietician about refeeding plan
persuade them to stay in hospital until psychiatrist can see them
What is the long-term management of an ED?
drug therapy generally not effective
ED-focussed CBT/self-help/family therapy
What are red flags seen in a history/exam of a suspected ED?
weight loss (malignancy, infection?), more serious if this is rapid
erosion of dental surfaces
weakness + malaise in young females > ED with hypokalaemia
What is bipolar affective disorder?
recurrent episodes of altered mood + activity
depression + hypomania/mania
What is the peak age of onset of bipolar?
teenage/early 20s
What are some RFs for developing bipolar?
fix/genetic factors
traumatic life events/hx of abuse
sleep deprivation
thyroid disease, ADs, steroids, alcohol, cannabis can cause rapid cycling mood
What are the key differential diagnoses of bipolar?
cyclothymia
schizophrenia - psychotic sx in the absence of prominent mood sx
substance misuse - cocaine, ecstasy, amphetamines
personality disorders - less episodic than bipolar
OCD
ADHD in children
organic - stroke, thyroid, MS, FTD, AIDs, epilepsy etc
iatrogenic - ADs, corticosteroids, levodopa, stimulants
metabolic - hyperthyroid, cushings, Addison’s, vit B12 deficiency
What is the most likely cause of mania in over 45s?
organic cause
What are they differences between hypomania and mania?
<7 days + no psychotic sx, lower severity of sx
Are depressive sx required for diagnosis of bipolar?
no
What are the MSE signs of bipolar?
pressured speech, restlessness, flight of ideas
How should suspected bipolar be investigated?
FBC, U&Es, LFTs, TFTs, urinary drug screen to rile out physical causes
extra endocrine tests if suspicious of anything
ECG, CT scan
How should an acute manic episode be managed?
refer, determine risks/urgency of referral, establish care plan
assess capacity to consent to admission/treatment > MHA assessment if not
advise to stop driving during episode
TAPER OFF SSRIs immediately if on them when mania starts
antipsychotics (if doesn’t work > try a different one > add lithium)
short acting benzos PRN for behavioural sx
What is the long-term pharmalogical management of bipolar?
4 weeks after acute episode has resolved:
1st lin = lithium, 2nd line = valproate
In pregnancy - antipsychotics instead
May need treatment for depressive episodes - quetiapine alone/fluoxetine + olanzapine/lamotrigine = careful decision, try to avoid ADs, possibly used with a mood stabiliser
What is the long-term non-pharmalogical management of bipolar?
Psychological therapies may be offered but usually not as affective as in depression
Continued risk management very important - look for reckless behaviors, aggression, promiscuous sexual behaviour, self-neglect
Crisis plan
Consider LPoA, advance statement
What is the action of lithium?
mood stabiliser
exact mechanism unknown
interferes with NT release + 2nd messenger systems
What is the treatment course of lithium?
how often
how to take
length of treatment
time before it works
how often - once/twice daily
how to take - tablet, capsule or syrup
length of treatment - usually lifelong, regular reviews by psychiatrist
time before it works - 1-2 wks
What tests need to be done before starting and during taking lithium?
Before starting - FBC, U&Es, TFTs, beta-HCG (pregnant?), ECG
Check lithium level after 5 days, then every week until stable for 4 weeks, then every 3 months
Check TFTs, U&Es, Ca2+ every 6 months
What are the important SEs of lithium? (LITHIUM acronym)
L - leukocytosis
I - insipidus diabetes (nephrogenic)
T - tremors (fine, if course then think toxicity)
H - hydration (very easily dehydrated, risk of toxicity in summer, need to drink a lot as renally cleared)
I - increased GI motility > abdo pain, nausea
U - underactive thyroid
M - metallic taste (warning of toxicity), mums beware - teratogenic
water sx - thirst, polyuria, impaired urinary concentration, weight gain, oedema
What are the sx of lithium toxicity? What should be done if it is suspected?
act drunk!
GI - anorexia, diarrhoea, vomiting, dry mouth/extreme thirst
Neuromuscular - dysarthria, dizziness, ataxia, muscle twitching, tremor
Drowsiness, apathy, restlessness, nausea, confusion
> stop lithium and rehydrate
What are the 3 key complications of taking lithium?
Renal toxicity
Nephrogenic diabetes insipidus
Hypothyroid
When is lithium contraindicated?
1st trimester pregnancy, breast feeding
Cardiac disease
Significant renal impairment
Addison’s disease
Low sodium diets
Untreated hypothyroidism
Why should we be careful prescribing lithium with diuretics?
dehydration
Why should we be careful prescribing lithium with NSAIDs?
kidney damage
What are obsessions vs compulsions in OCD?
obsession - unwanted intrusive though
compulsion - behaviours that result from obsessive though
How is OCD managed?
combo of psychotherapy (often CBT - obsession relief) + meds (often SSRIs)
exposure + response prevention therapy may relieve compulsions
What are the CAGE screening questions for alcohol abuse?
2+ = problematic drinking
- Have you ever felt you need to CUT down on your drinking?
- Have people ANNOYED you by criticising your drinking?
- Have you every felt GUILTY about drinking?
- Have you ever felt you needed a drink first thing in the morning to steady nerves/get rid of a hangover? (EYE-OPENER)
What medications have SEs worsened by alcohol intake?
benzodiazepines
What is the recommended weekly intake of alcohol?
14 units
How is the number of alcohol units calculated?
volume drunk (L) * % alcohol
1 unit = 10ml of 100% alcohol
What are some signs of alcohol dependance?
- persistence in the face of harm to physical/mental health, social/work life
- withdrawal sx - shakes/sweats/sickness
- increased tolerance
- primary - how important is alcohol to them, neglecting other activities
- loss of control
- rapid reinstatement - if hey start again will rapidly reach level they were before
- narrowing of repertoire - range of beverages declines, often cheapest
When does drinking become problematic?
consequences of alcohol cause social, physical and psychological harm
What can cause alcohol abuse?
genetics
impulsive, aggressive, hyperactive behaviour as a child
anxiety
cultural factors
accessibility to alcohol
How is alcohol abuse managed?
push for detox at home is possible
at home:
- baseline obs/bloods
- weaning regime of benzos over 7 days (chlordiazepoxide preferred, diazepam if not)
- thiamine - reduces wernicke risk
- consider supportive tx eg melatonin for sleep, small high protein meals, AA group
in hospital:
- IV vit B12 + thiamine
- weaning regime
- high protein, 35Kcal/kg/day
- consider steroids
- tramadol - relieve neuralgia
- laxatives - avoid constipation
- K+ sparing diuretics - weigh everyday to check losing fluid
Can the MHA be utilised for alcohol abuse?
no, only for consequences of
What are the short term complications of alcohol abuse?
trauma
vomiting
radial nerve palsy
risk taking behaviour
vasodilation - risk of hypothermia
hyperglycaemia
What is the physiology of alcohol as a CNS depressant?
enhances effect of inhibitory neurotransmitter GABA
> depression of inhibitory neurons = relaxed, disinhibited feeling
> then inhibition of other areas of CNS (initially learned tasks areas then mechanical later)
What are the long term cardiac implications of alcohol abuse?
increases BP by increasing sensitivity to catecholamines
- increases risk of IHD, CVA, stroke
- arrhythmias esp AF
- alcoholic cardiomyopathy > HF
- vasodilator > hypothermia risk
What are the long term hepatic implications of alcohol abuse?
- hypoglycaemia > seizure risk
- fatty liver > then alcoholic hepatitis, cirrhosis
- clotting factor reduction
- reduced albumin production > peripheral oedema
- asterixis
- oesophageal varices
- induction of drug metabolising enzymes > drugs eg warfarin less effective
What are the long term GI implications of alcohol abuse?
gastritis
pancreatitis
malnourishment
poor oral hygiene > bad teeth, scurvy
reflux
mallory weiss tea
diarrhoea
risk of ulcers
What are the long term GUM implications of alcohol abuse?
altered sexual function
leydig cell damage > less testosterone > loss of libido/infertility/loss of male body hair
altered steroid production > gynaecomastia
What are the long term neuro implications of alcohol abuse?
vit def - B6, B1/thiamine > korsakoff’s, predisposes PAINFUL neuropathy
convulsions
poor sleep
impaired memory
risk of head injury
What are the long term psych implications of alcohol abuse?
depression/anxiety
alcoholic amnesia
korsakoff’s
alcoholic dementia
What are the long term misc implications of alcohol abuse?
ID/macrocytic anaemia
risk of mouth, oesophageal + liver Ca
foetal alcohol syndrome
diabetes due to cirrhosis
What drugs does alcohol interact with? Why?
metronidazole
chlorpropamide
> acetaldehyde accumulation > headache/sweating/nausea
Is binge drinking or continuous drinking more harmful? Why?
repeated injury to liver at levels it cannot metabolise
repeated acute irritation/inflammation of brain/pancreas/stomach/liver
What are alcohol withdrawal symptoms in the few hours vs 24-48hrs vs 48-72hrs after stopping drinking?
6-12hrs: tremor, nausea, sweats, agitation, tachy, raised BP, anxiety
24-48hrs: delusions, fear/paranoia, restlessness, confusions, diarrhoea, auditory hallucinations
convulsions/seizures = biggest killer
seizures peak = 36hrs
48-72hrs: delirium tremens
Why do withdrawal sx occur after stopping drinking alcohol?
autonomic overactivity due to withdrawal of inhibiting effect
What hallucinations are most a/w alcohol withdrawal?
persecutory
terrifying visual/tactile hallucinations eg insects crawling over skin, little men running around
What is the basic screening for alcohol abuse in a normal patient?
CAGE questions
increased MCV
increased yGT
How often does DT happen? When does it occur?
in about 5% of acute alcohol withdrawal
generally after many years of drinking
presents about 3-4 days after withdrawal
What are the sx of DT?
similar to other acute brain syndromes:
restlessness
fear/paranoia
confusion/clouded consciousness
terror-stricen face
ataxia/tremor
sweaty/tachy/pyrexic/flushing/pallor
terrifying visual hallucinations, may be tactile/persecutory auditory too
esp formication - feeling of insects crawling on skin
When does DT lead to death?
in 10-15%
seizures, HF, self injury, infection
How is DT treated?
similar to withdrawal
- benzodiazepines - continue for up to 10 days even after sx subside to avoid nightmares
- B vits (earlier = better reduction of encephalopathy)
- fluid replacement
- dextrose - avoid hypoglyc
- monitor for signs of alcohol brain damage
How long does DT generally last?
3-4 days
can have continuing anxiety for months
What is wernicke’s encephalopathy vs korsakov’s syndrome?
wernicke’s: acute syndrome due to thiamine deficiency
korsakov’s: chronic condition caused by thiamine deficiency
some people can have wernicke’s that continue chronically and become korsakov’s
What are the clinical features of wernicke’s? What is the wernicke’s triad?
- eye signs - nystagmus, opthalmoplegia (paralysis of eye muscles, particularly of abducens nerve)
- ataxic gait
- confusion
nausea
memory problems
can occur in any type of thiamine def, not just alcohol
Define Korsakov’s
state of impaired memory function present after wernicke’s encephalopathy has subsided
What kind of memories are affected in Korsakov’s?
anterograde memory disorder > old memories can be accessed, new memories cannot be consolidated
can immediately recall facts but cannot get it into long term memory
How do patients usually present with Korsakov’s?
little/distorted sense of time
often make up events, usually sound plausible = confabulation
answer qs wrong in a laid back way - ie unconcerned answers are incorrect
no clouding of consciousness
often peripheral neuropathy
What are some differentials for Korsakov’s?
acute brain syndrome of misc cause > clouding of consciousness, no neuro signs
delirium tremens > more common, no neuro signs
chronic brain syndromes - long term memory likely to be affected
Why can chronic alcohol intake chronic brain syndrome?
atrophy of the cerebrum
How is wernicke’s managed?
lots of thiamine + other B vits (IV or IM if necessary)
sedation if needed
fluid/electrolytes
How is korsakov’s managed?
life long chronic illness - not rly any treatment
many patients may eventually require care
thiamine supplements may be useful
What is the prognosis of Korsakov’s?
palsies
ataxia
neuropathy - unlikely to resolve fully
amnesia - 1/2 pts will not recover
What is alcohol dependance versus abuse?
chronic relapsing and remitting alcohol abuse
How is long term alcohol dependance managed?
psychological + rehab therapies
+ pharmacology:
if achieved abstinence and want to maintain it:
- disulfiram (acetaldehyde dehydrogenase inhibitor) = deterrent, causes violent N&V on alcohol consumption - can be life-threatening, 1 daily
- acamprosate (anti-craving) = no SEs, can be taken with alcohol, 3 daily
pts who want to reduce alcohol intake
for about 3-6mo:
- naltrexone (suppresses euphoria experienced with alcohol)
Why does emotional dysregulation occur?
limbic system overused or a memory is triggered
due to:
- disrupted attachment
- psychological trauma - PTSD
- temporary effect of trauma, life event, stress
What are the features of PTSD?
intrusive recollections, nightmares and flashbacks - more vivid than a memory
avoidance behaviour of places/events that remind them of the event
hyperarousal - exaggerated startle response, irritability, anger, insomnia, hypervigilance
nightmares, sleeping problems
hypervigilant
often hx of previous mental health problems
What is the timeline of PTSD?
begins within a few months of the incident
can be:
acute - <3mo
chronic - >3mo
delayed onsent - >6mo after event
How is PTSD treated?
psychological intervention:
- CBT
- eye movement desensitisation and reprocessing > recalling traumatic memories whilst moving eyes in specific patterns of movements
- SSRIs, TCAs - good for +ve sx eg flasbacks, arousal not for -ve sx eg avoidance
yay for combo therapy
What is EMDR therapy for PTSD?
heightened emotions with the traumatic event > memory is not stored correctly
= when event is recalled it is re-experienced
pt moves eyes in various patterns in 15/30 sec bursts whilst trying to recall it
> dual processing helps to re-process the memory so that it is stored correctly
Give some examples of SSRIs?
fluoxetine, paroxetine, sertraline, citalopram
Which antidepressants are most effective in severe depression?
TCAs
SSRIs just as effective as TCAs in mild/mod but less so in severe
What is the mechanism of action of SSRIs?
reduced neuronal reuptake of serotonin
block transporters that take 5-HT and NA back into presynaptic terminal > boosts MOA in synaptic cleft
v specific - only blocks serotonin reuptake inhib
Why do SSRIs have fewer SEs than TCAs?
low affinity for muscarinic, histaminergic and adrenergic receptors
= fewer SEs + less dangerous in overdose
How long does it take to see clinical benefit from SSRIs?
2-4 weeks
Which conditions are SSRIs the first line tx for?
depression, GAD, PTSD, eating disorders, OCD
What are the common SEs with SSRIs?
generally transient
nausea, headache, dizziness, GI upset
agitation, akathisia, anxiety
sexual dysfunction
insomnia
hyponatremia
increased suicidality !
What are SNRIs? Give an example.
Serotonin and noradrenaline reuptake inhibitors
eg mirtazapine
v similar to SSRIs
What are MAO inhibitors? When are they used?
monoamine oxidase inhibitors
rarely used - good AD but bad SEs
What are the SEs of MAO inhibitors?
cheese effect: MAOi breaks down tyramine (high in cheese) > more absorbed > acts similarly to dopamine/noradrenaline > displaces them > acute life-threatening HTN
drug interactions - nasal decongestants, salbutamol, anti-psychotics, other ADs
How to tricyclics ADs work?
block transporters which take 5-HT and NA back into presynaptic terminal
not v specific - act at lots of receptors in body
boost MOA
What are the SEs of tricyclics?
- anticholinergic effects (antagonists) > can’t pee, see, spit, shit
- alpha-1-adrenergic antagonism > postural HTN > falls
- antihistaminergic (H1) > sedation, weight gain
- lower seizure threshold, interfere with cardiac circulation = overdoses dangerous
What is the MOA hypothesis of depression?
low MOA levels cause depression
= used to be dominant theory, now controversial
How can stress lead to depression?
stress = neurotoxic > high cortisol > crosses BBB > glutamate release in brain > neurotoxic: damages brain cells and makes them less neuroplastic
+ decreases neuroprotective chemicals eg BDNF
What is the neuroplasticity hypothesis?
down-stream signalling in cells > changes gene transcription
ADs cause slow increase in BDNF via GPCRs
+ decrease glutamate release
= directly increase neuroplasticity in hippocampal neurons
most evidence for this theory, still controversial
What is serotonin syndrome? How does it present?
serotonin poisoning - rapid onset after increased dose/new prescription
classic triad:
- neuromuscular abnormalities: myoclonus, hyperreflexia, tremors
- altered mental state
- autonomic dysfunction: BP/HR changes, high temp
How is serotonin syndrome treated?
stop AD
cyproheptadine (5-HT2 antagonist) used in severe cases
What is the dopamine hypothesis of psychosis?
antipsychotics = dopamine D2 receptor antagonists
schizophrenia = underactivity in the dopaminergic meso-cortical pathways + overactivity in the meso-limbic pathway
What are the 4 pathways of the dopaminergic system and their roles? What happens when they are blocked?
- meso-limbic: reward/pleasure centre, activated by drugs of abuse
block = reduces +ve sx of psychosis - mesocortical: executive function + cognitive control of emotions
deficiency = causes -ve sx of psychosis
block = dysphoria - nigrostriatal: dopamine signal favours direct pathway > movement
block = reduction in movement > dystonia, akathisia, tardive dyskinesia - tuberoinfundibular: DA inhibits prolactin release
block dopamine = increases prolactin > menstrual problems, breat engorgement, lactorrhoea, reduced sex drive, increased risk of ovarian/breast ca
What major SE can clozapine cause?
agranulocytosis - can be very dangerous
When are antipsychotics indicated?
psychosis -
schizophrenia
delirium (elderly with dementia, intensive care)
When are antipsychotics indicated?
psychosis:
schizophrenia
delirium (elderly with dementia, intensive care)
acute behavioural disturbances
adjunct in psychiatric disorders eg mania, psychotic depression
Give some examples of atypical antipsychotics? How are they different to typical?
clozapine
risperidone
sertindole
aripiprazole
zotepine
olanzapine
quetiapine
How are typical and atypical antipsychotics different?
typical: tend to be from one class
atypical:
fewer motor SEs
wider range of mechanisms - from different classes
?better at treating -ve sx of schiz
How are typical and atypical antipsychotics different?
typical: tend to be from one class
atypical:
fewer motor SEs
wider range of mechanisms - from different classes
?better at treating -ve sx of schiz
What receptors do antipsychotics target?
blocking dopamine receptors
may block other NT receptors eg 5-HT (serotonin) which has clinical efficacy and others eg acetylcholine, histamine which cause SEs
How many dopamine receptors are there? Which do antipsychotics target?
D1-5
APs mainly block D2
typical = effect D1 and 2
atypical = varying
Blockade at which regions of the brain cause antipsychotic effects?
mesolimbic
mesocortical
Blockade at which regions of the brain cause antipsychotic motor SEs?
nigrostriatal
Why do APs take several weeks to become effective?
on 1st administration: dopaminergic neuron activity increases
over next 3 weeks activity decreases
due to block, number of receptors increases > dopaminergic neuron activity decreases due to block
What is the therapeutic range of dopamine receptor blockage? When do and what type of SEs occur?
65-80%
> 80% = unwanted extrapyramidal effects
What are the general clinical effects of APs?
depression of emotional responses (for delusions, thought disorders, perception etc)
sedation
antiemetic
antihistamine
How do APs cause sedation? What is their action?
reduce input to reticular activating system
normal spontaneous activity of the system is preserved
= external stimuli produce reduced response
Which symptoms of psychosis do APs treat?
+ve sx - delusions, hallucinations etc
atypicals MAY also help -ve sx eg low mood
Why do APs cause extrapyramidal effects happen?
D2 blockage in the nigrostriatal pathway
happen in 1/2 of patients
Give examples of extrapyramidal effects caused by APs?
akathisia
acute dystonia eg tongue protutrusion, torticollis
parkinsonianism
many others eg weight gain, drowsiness, insomnia, galactorrhoea, antimuscarinic effects, postural hypotension etc
Are extrapydramidal effects of APs reversible?
usually reverse when drug stopped
prolonged use = increases likelihood of effects becoming permanent
What are late-onset extrapyramidal effects of APs called? Why does this happen
tardive dyskinesia - difficult to treat
prevention is best - low doses, titrate upwards
due to damage to GABAergic neurons
Which AP do extrapyramidal effects not occur with?
clozapine
+ much less likely with atypical APs
What is neuroleptic malignant syndrome?
occurs with specific genetic variant of D2 receptor = rare
> abnormal bloclage of D2 in striatum and hypothalamus
= MEDICAL EMERGENCY - risk of death
What S&S occur with neuroleptic malignant syndrome?
fever
rigidity
HTN
sweating
urinary incontinence
altered consciouness, delirium
tahcycardia
EP SEs
high creatinine kinase
How is neuroleptic malignant syndrome treated?
withdraw tx immediately
give dopamine agonist
aggressively treat hyperthermia - ice packs
circulatory and ventilator support if needed
sx can take >2wks to go
What is schizoaffective disorder?
controversy about diagnosis
type of schizophrenia where mood sx are unusually prominent/co-existent with mood disorder - bipolar or major depression
delusions/hallucinations eed to be present for at least 2 weeks when mood sx are not
Which SSRIs are 1st line for breastfeeding women?
sertraline
paroxetine
How is postpartum depression defined?
depressive episode within 4 weeks of childbirth
What are the strongest RFs for postpartum depression?
previous hx of MH problems
psychological disturbance during pregnancy
poor social support
poor relationship with partner
baby blues
major life events
What is somatisation disorder?
tendency to report psychological stress as somatic sx or pain
often a/w with ongoing refusal of reassurance that there is no underlying physical cause for sx
What are the common sx reported with somatisation disorder?
- N&V, abdo pain
- pelvic pain, dysmenorrhoea
- palpitations, SOB, chest pain
- amnesia, voice changes, dizziness, difficulty coordinating limbs, speech difficulty, swallowing difficulty
pain
How is somatisation disorder identified and treated?
exclude underlying cause
look for underlying psychological cause
careful counselling = most effective
How does suicide risk/method differ in men and women?
men <35 - suicide = greatest cause of death
men > women at all ages
men more likely to use violent methods eg shooting, handing
women more likely to take drug overdoses
What mental health illnesses are most a/w suicide?
most common = depression
bipolar disorder
substance abuse
How do rates of self harm differ in men and women?
roughly same
women = most common cause of acute admission
peak age = 15-25
in men peak age = 25-34
What mental health illnesses are most a/w self harm?
bipolar
depression
eating disorders
personality disorders
15% repeat within a yr
How is pharmacological therapy used for anxiety?
not rly considered 1st line, except in severe cases
usually reserved for pts that have failed to respond to CBT/psychoeducation etc
most useful with co-existing depression who lack motivation for self-directed approach
What is the main inhibitory NT found in anxiolytics?
GABA
Are SSRIs effective intreating GAD?
proven benefit, but not as much as CBT
not sure which are best
duloxetine + venlafaxine commonly recommended
Are SSRIs effective intreating panic disorder? How should they be used
reduce panic attacks considerably
tx for minimum of 6mo, assess at 3mo
What pharmacological therapies may be used to treat anxiety and in which situations?
SSRIs
propanolol - situational anxiety to control physiological sx
benzodiazepines - short-ter/infrequent use only, useful for specific phobias. NOT useful in panic disorder as not quick enough onset
must be used with caution
quetiapine - anti-psychotic in very small doses PRN > useful for panic attacks and insomnia
How do benzodiazepines work? Give examples of some.
bind to receptors and increase amount of GABA released
eg diazepam, temazepam, loreazepam
What are the SEs of benzodiazepines?
risk of addiction in regular long-term use
oversedation - impaired consciousness
adverse effect on mood
interaction with alcohol
sexual dysfunction
reduced motivation
What is cognitive behavioural therapy? When is it used?
1st line for depression, anxiety, OCD, PTSD, eating disorders, psychosis
4 areas model - thoughts can impact behaviour, can impact bodily sensations, can impact emotions
looks at changing/challenging those behaviours/though processes > what change does it have on body/emotions > starts to produce change in how we feel
12-20 structured sessions
What is counselling? When is it used?
cope with recent events rather than to help you change as a person
short, in primary care
aims to talk, help patient be clear about problems and come up with own answers
What is cognitive analytical therapy? When is it used?
for depression, personality disorders
looks at patterns from early life and see how its affected behaviours
using interpersonal relationship with therapist to recognise on learnt ways of being and focus on changing them
What is interpersonal therapy? When is it used?
for mild-mod depression
helps patients understand how problems may be connected to the way their relationships work
identifies how to strengthen relationships and find better ways of coping
What is dialectical behaviour therapy? When is it used?
GS for borderline personality disorder
intensive, up to 18mo
combo of individual and group sessions
often very difficult experiences, repeating self harm behaviours, difficulty coping with emotions
about accepting yourself and learning how to manage emotions + changing behaviour in a positive way
What is family therapy? When is it used?
in eating disorders, psychosis
family attend together
works with family’s strengths to help family think about and try different ways of behaving with each other
establishes context of why issues are happening
What is electroconvulsive therapy? When is it used?
for uncomplicated severe depression
can be for bipolar, catatonia
when other tx hasn’t worked or pts who need rapid tx response
not a cure and requires maintenance tx
repeated course if responding well
send electric current through brain, causing a seizure under GA
How do hypnotics work?
potentiate inhibitory effects of GABA
When are hypnotics used?
insomnia
cause of insomnia must be established + underlying factors treated
should be used as short courses in acutely distressed
tolerance develops fast rebound insomnia possible when stopped
How should short-acting and long-acting hypnotics be used differently?
short-acting - sleep-onset insomnia when sedation the next day is undesirable or for elderly
long-acting - poor sleep maintenance eg early morning waking or anxiolytic effect needed during day
Give examples of hypnotics
some benzos eg nitrazepam or flurazepam - prolonged action, residual effects next day, cumulative
- others act for shorter time eg loprazolam
- diazepam if daytime anxiety too
z-drugs eg zolpidem, zopiclone - short action, not for long-term use
What are mood stabilisers used to treat? Give examples
mainly bipolar disorder
mania
lithium, valproate, gabapentin, carbamazepine
Why does lithium toxicity happen?
quickly becomes toxic as levels increase
catatonic state > able to replace Na+ in many reactions and enter cells via voltage gated Na+ channels
does not replace Na+ in Na+/K+ pump = accumulates in cells
= very narrow therapeutic index
What is the mechanism of lithium?
poorly understood - interferes with enzymes > alters signal transduction pathways
eg increases adenylate cyclase activity + inositol monophosphatase > affects PI signalling pathway > stabilising effect on aminergic and cholinergic activity > stablised IC signalling pathways = respond less strongly to stimuli
How are mood stabilisers used in bipolar disorder?
as prophylaxis
usually given long-term, take 3-4 months to work
When are mood stabilisers other than lithium used for mania?
prophylaxis/tx of mania when pt is unresponsive to lithium
becoming more popular as they are safer/fewer SEs - have modulating effect on GABAergic neurons
What is acute dystonia? When does it happen?
bizarre unwanted muscle movements
eg tongue protrusion, torticollis (head tilt with chin lift), oculogyric crisis (abnormal rotation of eyeballs)
acute onset due to APs
What is an externalising vs internalising disorder?
tendency to act out psychological problems eg substance abuse, anti-social personality
internalising eg depression, anxiety
The release of what substance causes something to be addictive?
dopamine
What are the 5 phases of addiction in the stages of change model? Why is this useful?
pre-contemplation - not yet thinking about drugs
contemplation - thinking about drugs
preparation - preparing to take drugs eg buying
action - takes drugs
maintenance - continues pattern of behaviour
can target tx according to phase
eg motivational interviewing much more likely in contemplation than maintenance stage
What is the 12-step approach?
supplement medical/other tx
only useful for someone with dependance
encouraged to surrender themselves to a higher power - not necessarily God
Clinical features of opiate use?
pinpoint pupils
low BP
venepuncture marks
Clinical features of benzo use?
disinhibited speech - gives impression of being drunk
Clinical features of psychostimulant use?
eg amphetamines, cocaine
rapid speech
large pupils
agitation
restlessness
high BP
Features of opiate withdrawal?
dilated pupils
high BP
sweaty
rhinorrhoea
cramps
ie similar to psychostimulant use
Features of benzo withdrawal?
hypersensitivity
hyper reflexia
depersonalisation
Features of psychostimulant withdrawal?
agitation
restlessness
Features of heroin withdrawal?
cold/shivery
flu-like sx
pain
cannot kill you - terrible feeling but addiction is psychological not physical
Cannabis - how is it taken, what type of drug is it, what is there a risk of it causing?
resin, leaf, oil (strongest)
hallucinogen - not very strong
heavy regular use > anxiety + depression
likely to make a pre-existing psychological disorder worse
addictive
Opiates - how are they taken, what is there a risk of it causing?
start smoking > subcut (skin popping) > inject
very addictive
not very harmful but injecting isn’t very good for you
strong a/w depression
risk of RESP DEPRESSION > reversed with naloxone
Cocaine - what type of drug is it, what happens when you take it, what is there a risk of it causing?
stimulant - pure release of dopamine into brain
cocaine not as strong as crack which releases all dopamine straight away = extremely addictive
big reward after taking, lasts around an hr > very repetitive taking
cardiotoxic = very dangerous
Amphetamine (speed) - how is it taken, what type of drug is it, how does it make someone feel?
injected
stimulant
excess energy, elated
crystal meth is like the ‘crack’ version
MDMA - what type of drug is it, how is it taken, what happens when you take it?
stimulant
commonly cut with other drugs, lots of clones on market
relatively safe
causes serotonin release > happy, feel close to people socially
big drop in mood about 4 days after
very high tolerance effect - have to use more
Which drugs are non-addictive?
LSD
ketamine
How is an opiate overdose reversed?
naloxone
How does naloxone reverse an opiate overdose?
competitively binds opioid receptors = blockade
1/2 life naloxone shorter than opiates - can wear off and go back into overdose
What are the sx of benzo overdose?
agitation
euphoria
blurred vision
slurred speech
ataxia
slate grey cyanosis
How can a benzo overdose be reversed? When is it not appropriate?
flumazenil
not always recommended
mainly to reduce sedative effect of benzos
in long-term users can induce withdrawal > seizures
What are the sx of a paracetamol overdose?
often asymptomatic
N&V
acute liver failure
renal failure
oliguria
metabolic acidosis
When may acute liver failure occur after a paracetamol overdose? How does it present?
24-72hrs after
hepatic necrosis causes:
- jaundice, RUQ pain
- encephalopathy
- hypoglycaemia
How is a paracetamol overdose treated?
activated charcoal - most effective if within an hr
acetylcysteine - promotes conjugation of circulating paracetamol
if within 8hrs and above tx line
given in 3 infusions, 1st one over an hr
What is Fragile X syndrome caused by?
mutation in FMR1 gene > no FMRP protein = needed for normal brain development
How does Fragile X syndrome present?
developmental delay
social and behavioural eg eye contact, anxiety, hand flapping, concentration
intellectual disability
leading genetic cause of autism - 1 in 3
Does Fragile X syndrome affect males and females?
yes
usually females have milder sx
Define learning disability
reduced intellectual ability + difficulty with everyday tasks
IQ <70
What are the types of schizophrenia?
Acronym:
PARANOID: just +ve sx
PSYCHOTIC - post-shiz depression
HUMANS: hebephrenic - thought disorganisation
CAN’T: catatonic - 1+ -ve sx
SUPPLY: simple - no psychotic sc, -ve sx
UNDERSTANDABLE: undifferentiated - meet dx criteria but doesn’t fit type
REASONING: residual - -ve sx lasting 1yr following psyhotic episode
When is schizophrenia treatment-resistant? What can be used for tx?
sequential use of 2 APs for 6-8wks, at least 1 is atypical
clozapine
What SEs can clozapine cause?
weight gain
excessive salivation
agranulocytosis
neutropenia
myocarditis
arrhythmias
How is opioid dependance treated?
- methadone = safer opioid, prevents withdrawal sx, sedative effect
alternative: buprenorphine (mixed opioid agonist/antagonist) - sub-lingual, less sedative, can stop pain meds working
naltrexone (opioid antagonist) = relapse prevention
What are clang associations?
different ideas that are only related by rhyme or similar sounds
What are protective factors for suicide?
social support
religious beliefs
children at home
regret
Which SSRI is 1st line in children/adolescents?
fluoxetine
Which SSRI is 1st line post-MI?
sertraline
What is a key dangerous SE of citalopram?
dose - dependant QT prolongation
What are the CI with SSRIs?
NSAIDS (at least prescribe a PPI if necessary)
warfarin/heparin/aspirin
triptans + MAOIs > increased risk of serotonin syndrome
How long should an SSRI be reduced for?
4wks (except fluoxetine)
paroxetine shorter half life and worse discontinuation sx
Can SSRIs be used during pregnancy?
weight up benefits and risks
1st tri = small increased risk of congenital heart defects
3rd tri = persistent pulmonary HTN
paroxetine = increased risk of congenital malformations
How soon sould pts be reviewed when started on an SSRI?
2wks
1wk if high risk of suicide/<30
What sx can be present after high intensity
What withdrawal sx can be present after high intensity cocaine use?
1st phase (24 hours): increased hunger, anxiety, irritability, fatigue, lack of motivation
2nd phase: up to 10wks
3rd phase: decrease in most sx, low mood may persist for up to 6m
