Psychiatry Flashcards
where is post stroke psychosis commonly seen
right side middle cerebral artery lesions
affect frontal and temporal region
what is the most common psychotic symptom
delusion
definition of delusion
false fixed belief not understandable within the person’s sociocultural setting
what are the most common perceptual abnormalities of post stroke psychosis
auditory hallucination followed by visual
what are the risk of antipsychotic use with those with dementia
increased risk of stroke
what long term medical conditions are risk factors for development of mental disorders
CVD
MSK disorders
diabetes
COPD
how is delirium classified
hyperactive
hypoactive
mixed
Risk factors of delirium (5)
advancing age
cognitive impairment
poor nutrition
polypharmacy/alcohol misuse
frailty
common causes/ precipitating factors of delirium
physical illness
injury
infection
constipation
… (multi factorial)
management of delirium
anticipate and address modifiable risk factors
optimise treatment of underlying comorbidities
treat underlying causes
re-orientation strategies
normalise sleep-wake cycles
avoid falls
in extremis, short term pharmacological interventions
what is psychosis
difficulty perceiving and interpreting reality (failure of reality testing)
what are positive symptoms of psychosis
hallucinations
delusions
what are negative symptoms of psychosis
alogia (poverty of speech, slow to respond to questioning)
anhedonia
avolition/apathy (lack motivation and poor self care)
affective flattening (unchanged facial expressions, poor eye contact, limited emotional range and lack focal intonations)
what are disorgansation symptoms of psychosis
Bizarre behavior (inappropriate social behavior, aggression, repetitive stereotyped behavior)
formal thought disorder (lack of logical connection between thoughts)
onset of psychosis
can occur at any age
peak in adolescence /early 20s
peak later in women
is schizophrenia inheritable
yes, ~46% concordance in MZ twins
what are environmental risk factors of psychosis
drug use (esp cannabis)
prenatal / birth complications
maternal infections
migrant status
childhood trauma
socioeconomic deprivation
what to look for when someone with psychosis
bizarre or inappropriate clothing
psychomotor retardation/agitation
abnormal movements
self neglect
self harm injuries
echophenomena
stupor and mutism
difficulties with treating someone with poor insight into their psychosis
concordance with treatment
attendance to follow up
willingness to be admitted to hospital
impact on ability to have capacity to consent treatmentw
which NT system is most implicated in antipsychotics mechanisms
dopamine
but antipsychotics act on diff NT eg serotonin, Ach, hhistamine
which drug actions on dopamine receptors would most likely improve psychotic symptoms
antagonist/ partial agonist/agonist
antagonist
most antipsychotics are what
Dopamine antagonsits
newer agents are partial agonists
what are side effects of antipsychotics
EPSEs (extrapyramidal side effects) (eg parkinsonism acute
dystonic reactions
tardive dyskinesia
akathisia)
increased appetite, weight gain, diabetes, dysrhthymia, increase prolactin, constipation, agranulocytosis, sedation, neutropenia
what is DSM-5 criteria
2 weeks or more of depressed mood and presence of 4/8 symptoms
sleep alterations
appetite alteratios
anhedonia
decreased concentration
low energy
guilt
psychomotor changes
suicidal thoughts
subtypes of DSM-5 for MDD (3)
atypical features (increase slp n appetite with heightened modo reactivity)
melancholic features (no mood reactivity with retardation and anhedonia)
psychotic features (delusions or hallucination)
maniac criteria
irritable mood/euphoric with 3/7
decreased need for sleep with increased energy
distractibility
grandiosity or inflated self esteem
fight of ideas or racing thoughts
increased talkativeness or pressured speech
increased goal directed activities or agitation
impulsive behaviour
how to diagnose type 1 bipolar
symptoms present for minimum 1 week with notable functional impairment
how to diagnose hypomanic episode
symptoms present for min 4 days without notable functional impairment
how to diagnose type 2 nipolar
no single manic episode occurr, only hypomanic episodes present with at least on MDD episode
how to diagnose uispecified bipolar
manic symptoms less than 4 days and other thredsholds not met
what happens if patient hospitalised, irresepctive of duration of manic symptoms
manic episode diagnosed
what happens if psychotic features present
hypomanic cannot be diagnosed
what happens in majority first episodes in bipolar 1
majority of first episodes are depressive
what are some scans that measure receptors and transmitters in human brain
PET imaging (positron emission tomography)
what are the components of mental state examination (MSE)
appearance and behaviour
speech
mood/affect
thought (content and form)
perceptions
cognition
insight
what are some organic or iatrogenic causes of mood disorder
endocrine (thyroid related, hypoglycaemia, cushing’s syndrome, addison’s)
systemic (viral bacterial infection)
deficiencies (V B12, folic acid)
neurological (MS, AD, parkinson’s)
medications (B blockers, steroids, AB)
what are vascular depressions associated with
white matter hyperintensities
can impact cognitive function causing pt more vulnerable to stressors
what is the main symptom of poststroke depression
retardation in thinking and behaviour
poststroke depression pathology
lesions in left frontal lobe or basal ganglia
differentials between BPAD and BPD
BPAD: episodic, inheritable, mood less affect by environment
BPD: mood changes over hrs or days rather than days/weeks
poor self image, fear of abandonment, feel empty, Hx of self harm and trauma
similarities in BPAD and BPD
rapid mood change
unstable interpersonal relationships
impulsive sexual behavior
suicidality
differentials between BPAD and Schizoaffective disorder
BPAD: episodic, hallucinations (rarely chronic)
Schizoaffective disorder : episodic delusion / hallucinations (residual symptoms more likely)
more prominent disorganisation of thought, paranoid delusional beliefs and auditory hallucinations
similarities in BPAD and Schizoaffective disorder
both can present with psychosis and mood symptoms (depression and mania)
differentials between BPAD and ADHD
BPAD: not necessarily present in childhood, episodic, fam hx, amphetamines worsen mania, recurrent depressive episodes
similarities in BPAD and ADHD
hyperactivity
impulsivity
impaired cognition
impaired executive function
abnormal working and short term memory
what are examples of positive reinforcement in substance use
to gain positive state
escapism
get high
stay awake
like it
what are examples of negative reinforcement in substance use
to overcome adverse state
boredom
to get to sleep
reduce anxiety
feel better
what are the ICD-10 criteria for dependence syndrome of substance use
- a strong desire or sense of compulsion to take
- difficulties in controlling in terms of its onset, termination and level of use
- physiological withdrawal state when substance use has stopped or reduced
- evidence of tolerance (take more to get same effect)
- progressive neglect of alternative interests
- persisting with substance use despite clear evidence of overtly harmful consequences
difference between addiction and dependence
addiction – compulsive drug use despite harmful consequences; inability to stop using
dependence: physical adaptation to a substance
* can be dependent but not addicted
is glutamate system excitatory or inhibitory
excitatory
is GABA system excitatory or inhibitory
inhibitory
what is NMDA receptor
ligand-gated ion channels that mediate a Ca2+-permeable component of excitatory neurotransmission in the central nervous system (CNS)
how acute drinking of alcohol affect CNS
blocks excitatory system and impaired memory
boots inhibitory system (anxiolysis and sedation)
how chronic alcohol exposure affect CNS
results in neuroadaptation, cause GABA and glutamate remain in balance in presence of alcohol
upregulate excitatory system and reduce function in inhibitory system – tolerance
GABA-A receptor switch in subunits to make it less sensitive to alcohol
how to treat chronic alcohol exposure
treat with benzodiazepines to boost GABA function
what happens when there is upregulation fo excitatory system (NMDA receptor)
increase in Ca2+, toxic leading to hyperexcitability, seizures and cell death (atrophy)
what happens to chronic alcohol consumers in absence of alcohol
imablance in inhibitory and excitatory system (increase excitatory and reduce inhibitory)
increase in Ca2+, toxic leading to hyperexcitability, seizures and cell death (atrophy)
what is the dopamine pathway referred as
pleasure reward motivation system
which part of brain is for natural rewards
ventral striatum
which system is key modulator pf reward
opioid system
what is function of amphetamine
enhance release of dopamine and block reuptake of dopamine
increase dopamine in synapse
cocaine effect to dopamine
block reuptake
more in synapse
effect of alcohol and nicotine to dopamine
increase dopamine neuron firing in ventral tegmental area
increase firing by reduce inhibition of release
what are the effects of opioid
analgesic effect
create sense of euphoria in high dose
regulate pain and mood
what are the types of treatment in psych medicine (4)
- chemical (drugs/meds)
- electrical stimulation (ECT for depression)
- structural rearrangement (surgery)
- talking therapies
what is the first drug for schizophrenia
chlorpromazine
pros and cons for classifying pscyhiatric drugs base on chemical structure
pro: each drug has unique structure, easy to allocate
cons: no use in clinical decision making
pros and cons for classifying pscyhiatric drugs base on illness
pros: easy to choose a drug
cons: many meds work in several diagnosis, most pyschiatric disorders hv multiple symptoms and a single med cannot treat them all
what are the 2 different sorts of GABA receptors
GABA - A and GABA - B receptors
difference between GABA A and GABA B receptors
GABA A receptor: ligand-gated chloride channel which mediates fast inhibitory signals through rapid postsynaptic membrane hyperpolarization,
GABA B receptor produces slow and prolonged inhibitory signals via G proteins and second messengers
mechanism of Alprazolam
GABA A receptor agonist
function of Alprazolam
treatment for anxiety, panic disorder
mechanism of Baclofen
GABA B receptor agonist
function of Baclofen
decrease alcohol craving in alcohol dependent pt
what are the 4 targets for chemical treatments medicines used in psychiatry
- receptors
- enzymes
- ion channel
- NT reuptake sites
what are MAOIs for and mechanism
block enzyme activity
treat anxiety and depression
what are acetylcholinesterase inhibitors for and mechanism
treat dementia
block enzyme activity
what are lithium for and mechanism
treat mood stability
block glycogen synthase kinase
what are receptor targeting meds
antagonists and agonists
mechanism for ion channel target meds
blk channels to reduce neuronal excitability
mechanism for sodium valporate and carbamazepine and use for what
block sodium channel
treat epilepsy and mood stabilisation
mechanism for gabapentin and pregabalin
block calcium channels
treat epilepsy and anxiety
what are fast acting NT for excitatory and inhibitory
excitatory: glutamate
inhibitory: GABA
what are fast acting NT for
on-off switch
memory
movement
vision
what are slow acting NT examples
dopamine, serotonin, NA, Ach
endorphins and other peptides
what are slow acting NT for
modulators
emotions, drives, valence of memory
usually what happens with glutamate in psychiatric disorder
excess in glutamate
what happens when XS glutamate
epilepsy
alcoholism
treatment for XS glutamate
perampanel – blocker
acamprosate – blocker
ketamine – blocker
usually what happens with GABA in psychiatric disorder
deficeiency
what happens when GABA deficiency
anxiety
treatment for GABA deficiency
benzodiazepines – GABA enhancer
usually what happens with serotonin in psychiatric disorder
deficiency
what happens when serotonin deficiency
anxiety
depression
treatment for serotonin deficiency
SRIs
MAOIs
usually what happens with dopamine in psychiatric disorder
XS
what happens when dopamine XS
psychosis
treatment for XS dopamine
dopamine receptor blocker
usually what happens with NA in psychiatric disorder
XS
what happen when XS NA
nightmares
treatment for XS NA
prazosin – blocker
usually what happens with Ach in psychiatric disorder
deficiency
what happen when Ach deficiency
impaired memory
dementia
treatment for Ach deficiency
Acetylcholineeterase enzyme blockers
benefits of using partial agonist
improved safety
in states of high NT or XS agonist meds can act as an antagonist
but lower max efficacy
what are inverse agonists
opposite effects as agonists
what kind of drug is Amitriptyline
serotonin NA uptake blocker
antidepressant
non selective
adverse effect from histamine and Ach receptor blockade
what kind of drug is citalopram
selective serotonin reuptake inhibitor
adverse effects driven solely by increased serotonin
which part of the brain matures later than other cortical areas
prefrontal cortex
what are the core features of ADHD
persistent pattern of inattention and/or hyperactivity-impulsivity
present for at least 6 months
inappropirate for their developmental level
interferes with functioning or development
several symptoms present before 12
several symptoms present in 2 or more settings
symptoms are not better explained by another mental disorder
what are behavioral and psychological symptoms in dementia (BPSD)
common in late stage dementia
apathy, mood disturbances, hallucinations, delusions, irritability, agitation, aggression, sleep changes
often precipitating symptoms which lead to pt with dementia being detained
