PSYCHIATRY Flashcards
define dementia
irreversible, progressive decline and impairment of more than one aspect of higher brain function (conc, memory, language, personality, emotion)
epidemiology of dementia (4)
- rare <65
- alzheimer’s most common, vasc second most
- alzheimer’s more common in F, vasc and mixed more common in M
- fronto-temporal most common in <65s
what are the 4 causes/classifications of dementia?
- Alzheimer’s
- Frontotemporal
- Lewy body
- Vascular
outline the pathophysiology of Alzheimer’s (5)
- extracellular deposition of beta-amyloid plaques
- intracellular deposition of neurofibrillary tangles (NFT)
- leads to reduction in info transmission and brain cell death
- cerebral cortex degeneration with cortical atrophy
- also loss of ACh
outline the pathophysiology of the non-Alzheimer’s dementia causes
- frontotemporal - atrophy of frontal and temporal lobes
- lewy body - deposition of lewy bodies (abnormal protein) in brain stem and neocortex, deficit of ACh and dopamine (parkinsonism)
- vascular - brain damage due to cerebrovasc infarcts e.g. major stroke/multiple small strokes. most affected = white matter of cerebral hemispheres, grey nuclei, thalamus and striatum
risk factors for dementia
AD - old age, Fhx, down’s syndrome
vasc - old age, obesity, HTN, smoking
frontotemporal - genetic mutation
signs and symptoms of AD
- GRADUAL
- most common = short term memory loss (facts, general knowledge, language use, nominal dysphagia)
- disorientation
- getting lost
- decline in ADLs
what is nominal dysphagia and who does it commonly present in?
the inability to recall names of people/objects. seen in AD
signs and symptoms of vascular dementia
- STEPWISE PROGRESSION (stable sx then sudden severity increase)
- vascular pathology hx e.g. stroke, raised BP, focal CNS signs
- cognitive impairment subacutely/acutely following vasc event
- mood disturbance e.g. psychosis, delusions, hallucinations (later stages)
signs and symptoms of lewy body dementia
- GRADUAL
- probs with complex cog actions/multitasking
- visual hallucinations
- Parkinson-like sx
- sleep disorder
signs and symptoms of frontotemporal dementia
- RAPID progression
- peak in 50s-60s
- behavioural/personality change
- loss of language fluency/comprehension
how is dementia investigated in primary and secondary care?
primary - blood screen (exclude reversible causes)
secondary - neuroimaging/structural imaging
what are some neuroimaging techniques that can be used to diagnose dementia? what are they helpful for?
1) CT - rule out lesions/other pathology
2) MRI - shows atrophy/lesions
3) DaTSCAN - dopamine imaging
neuroimaging findings in Alzheimer’s
CT - may exclude space-occupying lesions etc
MRI - generalised atrophy
neuroimaging findings in vascular dementia
CT/MRI - cerebrovascular lesion/s
neuroimaging findings in lewy body dementia
CT - abnormal
MRI - general cortical atrophy
DaTSCAN - reduced dopamine
neuroimaging findings in frontotemporal dementia
what is it often chracterised by?
MRI/CT - focal atrophy in frontal and/or anterior temporal lobes. often characterised by left-right symmetry
ddx for dementia
- delirium
- HIV-related cog impairment
- Creutzfedlt-Jakob disease
- hydrocephalus
- depression
- mild cog impairment (MCI)
how do you manage AD?
EARLY - anticholinesterase inhibitors e.g. donepezil, rivastigmine
LATER - NMDA inhibitors e.g. memantine
how do acetylcholinesterase inhibitors e.g. donepezil help manage AD?
block breakdown of ACh > increase ACh in synapse > increases synaptic transmission of ACh where it’s reduced
how do NMDA inhibitors (e.g. memantine) help manage AD?
glutamate excitotoxicity is associated with delayed evolving neurodegeneration… NDMA inhibitors blocks NMDA receptors when too active > stops excessive glutamate production > slows disease progression
how is vascular dementia managed?
- treat atherosclerosis
- lifestyle modifications e.g. smoking, diet
- antiplatelets (aspirin)
- statins (atorvastatin)
- antihypertensives
how is lewy body dementia managed?
- donepezil/rivastigmine (increase ACh)
- psychotic sx - antipsychotics e.g. risperidone
- sleep probs - SSRIs
- motor sx - carbidopa/levodopa
how is frontotemporal dementia managed?
no specific tx :( can use SSRIs for behavioural sx
what is the difference between acute stress disorder and PTSD?
acute stress disorder is a reaction in the FIRST 4 weeks after trauma, PTSD is diagnosed AFTER 4 weeks
what is akathisia? give a classic presenting history
= a sense of inner restlessness and inability to keep still
common with long hx of antipsychotic use
which anti-depressant is known to stimulate appetite?
mirtazapine
how long after starting an SSRI should patients be reviewed if they are:
a) 25 and under
b) >25
a) 1 week
b) 2 weeks
which food should be avoided when on an MAOI (e.g. tranylcypromine) and why?
cheese - has lots of tyramine in which can cause hypertensive crisis when on an MAOI
what happens when you combine an SSRI and NSAID/aspirin? how do you manage this?
= GI bleeding risk
prescribe a PPI e.g. omeprazole
what is cotard syndrome? what condition is it most commonly associated with?
a rare subtype of nihilistic delusion, where the pt believes a part of them is dead/does not exist.
commonly seen in severe depression (but also associated with schizophrenia)
antipsychotics increase the risk of what adverse effects in elderly patients?
stroke and VTE
what is the general definition of non-pathological anxiety?
a constellation of psychological and physiological responses to a potential/uncertain threat.
= an essential function of the CNS
define:
a) generalised anxiety disorder
b) phobic anxiety disorder
c) panic disorder
a) persistent anxiety not restricted to/predominant in any specific circumstances
b) abnormal state anxiety evoked only by a specific external situation/object
c) recurrent unpredictable episodes of severe acute anxiety, not restricted to particular stimuli/situations
how common are each of the anxiety disorders?
generalised - most common (5-12%)
phobic - second most (up to 12%)
panic - least (4.7%)
risk factors for anxiety disorders
- threats in development e.g. bullying, trauma, neglect, parental loss
- early attachment relationships
- family hx of anxiety/another condition
- female sex
- hx/current other psychiatric condition e.g. depression
secondary causes of anxiety (4)
- substance use e.g. caffeine, stimulants, bronchodilators, cocaine
- substance withdrawal e.g. alcohol, benzo withdrawal
- hyperthyroidism
- cushing’s
DSM-5 criteria for GAD
- excessive anxiety/worry about varying events/activities for >6 months
- worry is difficult to control
- symptoms cause significant distress/impede ability to function in important areas of their life
- excessive worry/anxiety are accompanied by 3 or more of the following symptoms…
- restlessness
- fatigue
- muscle tension
- trouble concentrating
- irritability
- sleep disturbance
signs and symptoms of phobic anxiety disorder
- avoidance of certain situation/stimuli
- anticipatory anxiety
- somatic sx e.g. palpitations, sweating, trembling, dyspnoea, chest pain, dizziness, chills, hot flushes
signs and symptoms of panic anxiety disorder
- crescendo of anxiety, usually resulting in exit from situation
- somatic sx e.g. palpitations, sweating, trembling, dyspnoea, chest pain, dizziness, chills, hot flushes
- secondary fear of dying/losing control
stepwise approach to managing GAD
- education about GAD and active monitoring
- low-intensity psych interventions e.g. individual self-help, guided self-help, psychoeducational groups
- high-intensity psych interventions (CBT or applied relaxation) or drug tx
- highly specialist input e.g. multi-agency teams
what is the 1st line drug treatment for GAD?
what if this is:
a) ineffective
b) not tolerated
1st line = sertraline
a) offer alternative SSRI (e.g. citalopram, fluoxetine) or SNRI (e.g. duloxetine, venlafaxine)
b) if cannot tolerate SSRI or SNRI, consider pregabalin
what questionnaire can help assess the severity of GAD? what are the different severity scores?
the generalised anxiety disorder questionnaire (GAD-7)
5-9 = mild
10-14 = moderate
15-21 = severe
what is erotomania (De Clerambault’s syndrome)?
a delusion where the person believes someone famous is in love with them, with the absence of other psychotic sx
what is there an increased risk of to the baby if the mother is taking sertraline in the:
a) first trimester
b) third trimester
a) congenital heart defects
b) persistent pulmonary hypertension of the newborn
what is conversion disorder?
a condition presenting with a loss of motor and sensory function, typically occurring during times of stress
what is delirium tremens? when and what does it present with?
- a severe complication of alcohol withdrawal
- reaches peak incidence 72 hrs following alcohol cessation
- presents with sx of visual and auditory hallucinations, tremors and agitation
how long after alcohol cessation would you expect these symptoms to manifest:
a) anxiety and nausea
b) seizures
c) delirium tremens
a) 6-12h
b) 36h
c) 72h
what is the difference between hypomania and mania?
both present with symptoms of elevated mood BUT mania has a prolonged time course (hypomania being <7 days) and presents with psychotic symptoms
what should be monitored in all patients at initiation and dose titration of venlafaxine?
blood pressure (venlafaxine and other SNRIs are associated with developing hypertension)
a 75-year-old lady presenting with new onset confusion has just had an increase in sertraline dose. what is probably the cause of her confusion? what does the BNF suggests should be monitored when high risk patients begin SSRIs?
hyponatremia - measure U&Es in high risk patients to assess serum sodium
depression severity classification: what PHQ-9 score indicates:
a) less severe depression
b) more severe depression
a) <16
b) 16 or over
what is a key difference between pseudodementia (depression) and dementia?
pseudodementia involves global memory loss e.g. forgetting the rules of card games, dementia predominantly involves short-term memory loss (in the early stages)
which is associated with a poorer prognosis in a schizophrenia history?
a) acute onset
b) insidious onset of sx developing gradually
b
treatments for the side-effects of long-term antipsychotics:
a) tardive dyskinesia (repetitive involuntary movements e.g. lip smacking)
b) acute dystonia (abnormal postures/movements)
c) akathisia (restlessness)
a) tetrabenazine
b) procyclidine/benztropine
c) propanolol
what is ADHD?
a persistent pattern >6 months of inattention and/or hyperactivity-impulsivity that has a direct negative impact on academic, occupational or social functioning
when do ADHD symptoms typically present?
before 12yo, typically early-mid childhood
aetiology of ADHD
Unknown - combo of environmental and genetic factors…
1. neuro chemical
2. genetics
3. CNS insults e.g. prematurity, foetal alcohol syndrome, NF
4. environmental factors
RFs for ADHD (5)
- prematurity
- low birth weight
- low paternal education
- prenatal smoking
- maternal depression
pathophysiology of ADHD - which part of the brain is implicated and which NTs?
- deficits in PREFRONTAL CORTEX (regulates attention, behaviour and emotion)
- deficit in this area leads to poor impulse control, weak attention and heightened distractibility
- norepinephrine and dopamine are key for prefrontal functioning: deficits of these
DSM-5 diagnostic criteria for ADHD (3) - <16 and 17 or over
- children up to 16: six or more symptoms of inattention and six or more symptoms of hyperactivity and impulsivity
- if 17 or over: five or more symptoms from each category
- must occur in multiple settings (e..g home and school), have been present for at least six months and are not better explained by another disorder
symptoms must have been present before ___ years old for a diagnosis of ADHD
12
investigation options for ADHD (4)
- questionnaires
- clinical interview
- ADHD nurse classroom observation
- QB test (computer test)
which questionnaire can be used to assess ADHD in adults?
the Diagnostic Interview for ADHD Adults (DIVA) questionnaire
non pharmacological management options for ADHD (3)
- education
- ADHD parenting programme
- school support and liaison
pharmacological management options for ADHD (stimulants and non stimulants)
STIMULANTS - methylphenidate (e.g. ritelin) most common
NON STIMULANTS - atomoxetine, intuniv
SEs of methylphenidate in the tx of ADHD (4)
- stunted groth
- abdo pain
- headaches
- insomnia
what is the most important side effect to monitor during tx with a child with methylphenidate (for ADHD)?
stunted growth
mechanism of action of stimulants e.g. methylphenidate in the tx of ADHD
- blocks dopamine and noradrenaline transporters > increased availability in synaptic space > increased prefrontal cortex activity
- stimulation of prefrontal cortex increases concentration, attention span and decreases impulsivity
suggest some complications of ADHD persisting into adulthood
- lower educational/employment attainments
- poor self esteem
- criminal behaviour
- relationship issues
- sleep disturbance
- substance abuse
- RTC
- self harm
what is the first-line SSRI for patients with a hx of cardiovascular disease?
sertraline
antidepressants should be continued for at least ___ months after remission of symptoms to decrease the risk of relapse
6 months
how would schizotypal personality disorder present?
- “magical thinking” focussing on paranormal phenomena
- odd speech e.g. high-pitched voice
- problems socially/with relationships
substance dependence requires at least two of the following…
- impaired control over substance use
- increasing priority over other aspects of life/responsibility
- psych features suggestive of tolerance/withdrawal
define alcohol dependence
craving and tolerance of alcohol consumption despite negative complications experienced
pathophysiology of alcoholism - what NTs are involved? what happens in withdrawal?
- consuming alcohol affects basal ganglia
- releases dopamine > reward system > positively reinforces behaviour > operant conditioning
- alcohol also causes increase in inhibitory NT GABA (sedative)
- chronic use = brain upregulates natural stimulants to achieve equilibrium with inhibitory stimulants
withdrawal = sudden drop in GABA, disrupted homeostasis as there’s now an excess of natural stimulants
symptoms of alcohol dependence (3)
- tolerance
- craving
- “eye-opener”
CAGE questions for alcoholism
- have you ever felt you should Cut down on your drinking?
- have people Annoyed you by criticising your drinking?
- have you ever felt bad or Guilty about your drinking?
- have you ever had a drink first thing in the morning to steady nerves/get rid of a hangover? (Eye-opener)
symptoms of alcohol withdrawal
6-12 hours = tremors, sweating, tachycardia, fever
12-48 hours = alcohol hallucinosis, seizures
72+ hours = delirium tremens (altered mental status, agitation, hallucinations)
investigations for alcoholism
- AUDIT-c questionnaire (screening)
- labs - FBC, LFTs, B12/folate, TFTs
what blood results may be found in a patient with alcoholism? (FBC, LFTs, folate/b12)
FBC - raised MCV, raised platelets, anaemia
LFTs - increased GGT, AST:ALT > 2:1
B12/folate - deficient
medications to help with alcohol detox symptoms (4)
- chlordiazepoxide (sedative)
- high dose benzos e.g. diazepam
- naltrexone (opiate blocker, blocks feeling/buzz of alcohol)
- prophylactic oral thiamine