Revision Flashcards
what is the difference between mania and hypomania
can generally function in hypomania
in mania cant usually function properly, can get psychotic symptoms
when does depression become treatment resistant
after 2 adequate trails of antidepressants with no response
how does ECT work
causes release of neurotransmitters - serotonin, dopamine, noradrenaline (why in can improve symptoms of parkinsons)
also causes growth in pathway between amygalada and prefrontal cortex (pathway involved in anxiety)
what is the drug of choice for generalised anxiety
SSRIs
is tremor a side effect of lithium
yes
what is formulation
how the patient gor ill considering genetics, psychological factors, precipitating factors
what are predisposing factors
genetics, early childhood, medical conditions, FMHx, things that happened in life before the illness started
what are precipitating factors
what caused the illness to start (stressor or other events that are related to the current symptoms- trauma, how you coped during change, personality development)
what are perpetuating factors
any conditions in the patient, family, community or larger system that exacerbate rather than solve the problem (relationship conflict, lack of education, financial stress, lack of employment)
what PD is DSH common in
emotionally unstable, bordline subtype
a MMSE below what suggests a cognitive problems
<24
what does MMSE test for
cognitive function (confusion)
what SE should you be cautious of with fluoxetine in young people
increased suicidal thoughts
what is clozapine and when is it used
an atypical antipsychotic- should only be given for treatment resistant schizophrenia after 2 antipsychotics have been tried (haloperidol, Prochlorperazine)
what are the side effets of clozapine
Can cause agranulocytosis (lower white blood cells to a level where they cant fight infection), need to be monitored with regular FBCs. Can cause weight gain, diabetes, drowsiness, dizziness, hypersalivation, myocarditis
what is the opposite of psychomotor retardation
psychomotor agitation
what is the inheritance of huntingtons
autosomal dominant
what are the psychiatric symptoms of huntingtons disease
depression compulsions suicidality aggression blunted affect (lack of affect/ no reactivity) psychosis anxiety
what are the cognitive symptoms of huntingons disease
decline in executive function
short and long term memory deficits
dementia- progressive decline in global cognition
what is included in executive function
planning, abstract thinking, cognitive flexibility, being able to use rules, initiation of actions, social communication
what are the motor symptoms of huntingtons disease
choreiform movements rigidity writhing movements gait disturbance problems chewing/ swallowing/ speaking
what is the genetics of huntingtons
CAG repeat encoding polyglutamine
genetic anticipation
toxic effect of glutamine on neuronal cells
40 repeats = 100% penetrance
is genetic anticipation worse via female or male transmission
CAG repeats multiply by more during male transmission
what is dementia
progressive decline in global cognitive function
what is implicit memory
eg carrying out tasks that are well practised
what inheritance of alzheimers
multifactoral
what suggests a familial form of dementia
more relatives affected
relatives affected at earlier age
unusual or atypical features
what is the lifetime risk of dementia
10%
25% if first degree relative affected
what percentage of UK population have BPAD
1%
what is the inheritance of BPAD
multifactorial
higher in monozygotic twins than in dizygotic
what delusions are common in psychotic depression
that you/ your organs are rotten
what drug is the primary treatment for schizophrenia
atypical antipsychotics- risperidone
when are atypical antipsychotics not used
lack of response, obesity/ FNHx of obesity - causes metabolic syndrome, parkinsons, heart disease
what is the primary mechanism of antipsychotics
block dopamine receptors
what are the two types of antipsychotic
typical and atypical
what symptoms are typical antipsychotics more likely to cause
extrapyramidal
what atypical antipsychotics are most likely to cause metabolic syndrome
olanzapine, risperidone, quetiapine, aripiprazole
what atypical antipsychotic should you use if you are worried about metabolic syndrome
aripiprazole
what is the treatment for schizophrenia
atypical antipsycotic, try two if first one has no effect
clozapine after trial of first if still no effect
what is clozapined used for
3rd line for treatment resistant schizophrenia
what do you need to monitor in clozapine
blood tests for agranulocytosis
cradiac function
bowel paralysis
what is the pharmacological treatment for acute agitation in psychosis
benzodiazepine (-epams)
then typical antipsychotic (haloperidol)
name two typical antipsychotics
haloperidol
chlorpromazine
what are depot antipsychotics
IM injection with extended release- helps in compliance issues
what is the treatment or OCD
CBT, exposure therapy, SSRI (setraline), 3rd line= tricylic
what is the mechanism of action of benzodiazepines
GABA agonist (main inhbitory neurotransmitter)
what are the risks of benzos
tolerance and addiction - dont get tolerance for SEs (resp depression, loose gag reflex - aspiration)
what are the withdrawal symptoms from benodiazepines
irritability, insomnia, dizziness, panic, nausea, sweating
which benzodiazepine has the ‘best’ half life
lorazepam- 12-20 hours, good for taking once a day
what are the treatments for GAD
1st line for GAD= CBT
2nd= SSRI (sertraline)
what is the treatment for panic disorder
exposure therapy
what can be done to reduce the risk of dependence of benzodiazepines
foe acute treatment only (1-2 weeks), slowly reduce dose
are the negative/ positive symptoms of schizophrenia harder to treat
negative harder
do people with psychosis have insight
generally no- can be restricted
is hallucinations with insight psychosis
no
what can you get command hallucinations in
depressive psychosis (2nd person, in context of mood)
mania with psychosis (grandiosity, irritability, flamboyant, elated mood)
schizophrenia (ideas of reference, 3rd person hallucinations, can go against mood that day)
what conditions do you get visual hallucinations in
organic problems- delirium, injury, intoxication, trauma, autoimmune conditions
(very uncommon in schizophrenia)
which conditions are tactile hallucinations more common in
organic conditions (injury, infection, trauma, intoxication)
give a example of a pseudohallucination
hearing a voice originating from within your own head (a thought)
what are the three first rank symptoms of schizophrenia
thought disorder
delusions of control/ passivity
3rd person auditory hallucinations
what are the positive symptoms of schizophrenia
delusions of reference, thought disorders (insertion, broadcasting, withdrawal, echo), delusions that are persistently held, neologisms, misuse of vocabulary
what are the negative symptoms of schizophrenia
apathy, blunting of affect, poverty of speech/ thought, catatonia (waxy flexibility, posturing, may echo your speech, may not eat/ speak, can become agitated very quickly)
where is brocas area
posterior inferior frontal gyrus
where is wernickes area
superior temporal gyrus
what is wernickes dysphagia
receptive, fluent aphasia
speech comprehension is poor but actual speech fine, confabulation
what type of dysphagia when brocas area damaged
expressive, non fluent dysphagia
understands but cant speak fluently
what is brodmanns area 4
primary motor cortex
what are the types of memory
short term- recall for seconds/ minutes without rehearsal
long term: episodic (things that happened), facts
what part of brain puts memories from short term into long term
hippocampus
where are long term memories stores
via permanent changes throughout cortex within individual neurones
what is dementia
global decline in cognitive function, progressive, irreversible
where is brain does alzheimers affect first
medial temporal lobe - nucleus basalis of meynert
what is agnosia
difficulty in comprehending sensory information- (visual agnosia cant recognise objects)
what is the most common cause of dementia
alzheimers
what is prospagnosia
difficulty in recognising faces
what is the pathology of alzheimers
amyloid plaques (insoluble folded proteins) formed outwith cells Tau proteins are hyper-phosphorylation and create tangles
what does the nucleus basalis of meynert do
attention/ arousal
what does the medial septal nucleus do
learning and memory
what happens to cholinergic projections in dementia
acetylcholine is very important for memory- gets reduces due to other changes in brain
what drug is used to treat dementia
acetylcholinesterase inhibitors - boost cholinergic transmission:
- slows progression
- doesnt affect underlying disease process
(reduces uptake of acetylcholine so more in synapse)
name three acetylcholinesterase inhibitors
donepezil
galatamine
rivastigmine
what is memantine
NMDA receptor agonist
licensed to treat alzheimers
what does NMDA respond to
glutamate (excitatory NT)
what is seen on imaging in vascular dementia
mild white matter hyperintensities
periventricular then spread through white matter
step wise cognitive decline= ?
vascular dementia
what is the pathology of lewy body dementia
clumps of alpha synuclein around the brain
loss of dopamine producing neurones in the substantia nigra - causes parkinsonism
neuronal changes in the nucleus of basalis of meynert
what is the treatment for lewy body dementia
cholinesterase inhibitors- rivastigmine
what are the features of lewy body dementia
visual spatial problems early fluctuating cognition and consciousness visual hallucination autonomic dysfunction - hypotension REM sleep behaviour disorder
name the dementia: 55-65 age of onset loss of neurones gliosis abnormal proteins in neurones atrophy in temporal and frontal lobes
frontotemporal
what are the symptoms of frontotemporal dementia
behavioural and personality changes progressive non fluent aphasia semantic dementia (language) lack of interest in other people disinhibition
what are the symptoms of wernickes encephalopathy
ophthalmoplegia
ataxia
confusion
visual and hearing impairment reduced conscious level hypothermia lactic acidosis circulatory changes
what causes wernickes encephalopathy
thiamine deficiency (thiamine needed for glucose metabolism- when deficient get mitochondrial injury and cell death)
- alcoholism
- malnutrition
- hyperemesis graviderum
what is used to treat thiamine deficiency
pabrinex
atropy of mamillary bodies due to thiamine deficiency= ?
korsakofs syndrome
what are features of korsakoffs
anterograde amnesia (cant form new memories)
confabulation
telescoping of events (think things happened more recently than then actually did)
what are the types of alcohol relates brain damage
wernickes korsakoffs myelin sheath degredation neuroinflammation fall -/ subdural haematoma
does the mental state exam include information form a 3rd party
no only from patient themselves
other info recorded in collateral history
what is the bets predictor for suicide
hopelessness
what conditions can you get loss of interest in food
disordered eating (NOT AN or BN) depression
in younger people what weight meets criteria for ICD-10 for anorexia nervosa
weight to height of less than 85%
adults use BMI
what is the difference between a learning difficulty and disability
difficulty= involves only one area of cognition
disability- affects global cognitive function and ability to learn
what are the learning disability IQ parameters
70-120 normal 50-69 mild 35-49 moderate 20-34 severe <20 profound
what are non epileptic attack disorders highly associated with
childhood sexual abuse
are patients conscious during non epileptic attack disorders
no, will have amnesia and are not aware what happened
how are non epileptic attack disorders differnt from epileptic seziures
NEAD are functional disorders
tend to last longer, remain continent, lack injuries associated with epileptic attacks
what is illness belief
functional conditions arise as patients view that a physical illness is more acceptable than a mental illness
what does a deficit of vit B1 cause
wernickes encephalopathy
what is the difference between lewey body and frontotemporal dementia
lewey body is a type of FTD
what causes all FTD, lewey body and alzeheimers
overproduction and tangle of TAU protein which blocks transmiassion in brain
FTD and lewey body is in frontotemporal lobes
Alzheimers is in hippocampus
what happens to cortisol in depression
is raised, loose negative feedback control, will fail to be suppressed by dexamethasone, increased expression in urine
what does chronically raised cortisol in depression result in
reduced brain volume
what is first line Tx for depression
SSRI
what is the first line x for OCD
SSRI
psychotherapy also useful
what is mild depression always treated with
CBT alone
what is (almost) pathognomonic of schizphrenia
formal thought disorders
is paranoid delusions of reference always caused by schizophrenia
no- is a psychotic symptom
what is the first line treatment for schizophrenia
atypical antipsychotic
- ripseridone (first line for most psychotic disorders)
- olanzapine (risk of metabolic syndrome)
- clozapine (only for treatment resistant)
what is an obsession
a type of thought that is invasive, irrational (patient knows it doesnt make sense but can help thinking about it), is difficult to get rid of, is ego dystonic
what is a mental compulsion
a thought which forces a patient to do an act to make it go away
how long is a standard course of ECT
6-12 sessions
what is mixed affective state
presentation of BPAD- when episodes of mania/ hypomania and depression are not discrete and can mix
eg someone with mania/ hypomania develops symptoms of low mood or preoccupation with physical health
what are the features of PSTD
flashbacks, avoidance of where it happened, bad dreams, low mood
needs to have symptoms for at least 6 months to allow acute stress reaction and adjustment disorders (1-2 weeks) to resolve
what is adult with incapacity act good for
emergency detainment- quicker than mental health act, don’t need psychiatrist, can treat
can you treat under the mental health act
only under short term detention
how long does an emergency detention last (MHA)
3 days
how long does a short term detention last (MHA)
28 days (four weeks)
how long does a compulsive treatment order last
6 months
what is the treatment for emotionally unstable personality disorder
DBT
lasts 6-12 months
