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PHASE 3A > PSYCHIATRY > Flashcards

PSYCHIATRY Flashcards

1
Q

define dementia

A

irreversible, progressive decline and impairment of more than one aspect of higher brain function (conc, memory, language, personality, emotion)

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2
Q

epidemiology of dementia (4)

A
  1. rare <65
  2. alzheimer’s most common, vasc second most
  3. alzheimer’s more common in F, vasc and mixed more common in M
  4. fronto-temporal most common in <65s
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3
Q

what are the 4 causes/classifications of dementia?

A
  1. Alzheimer’s
  2. Frontotemporal
  3. Lewy body
  4. Vascular
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4
Q

outline the pathophysiology of Alzheimer’s (5)

A
  1. extracellular deposition of beta-amyloid plaques
  2. intracellular deposition of neurofibrillary tangles (NFT)
  3. leads to reduction in info transmission and brain cell death
  4. cerebral cortex degeneration with cortical atrophy
  5. also loss of ACh
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5
Q

outline the pathophysiology of the non-Alzheimer’s dementia causes

A
  1. frontotemporal - atrophy of frontal and temporal lobes
  2. lewy body - deposition of lewy bodies (abnormal protein) in brain stem and neocortex, deficit of ACh and dopamine (parkinsonism)
  3. 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
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6
Q

risk factors for dementia

A

AD - old age, Fhx, down’s syndrome
vasc - old age, obesity, HTN, smoking
frontotemporal - genetic mutation

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7
Q

signs and symptoms of AD

A
  • GRADUAL
  • most common = short term memory loss (facts, general knowledge, language use, nominal dysphagia)
  • disorientation
  • getting lost
  • decline in ADLs
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8
Q

what is nominal dysphagia and who does it commonly present in?

A

the inability to recall names of people/objects. seen in AD

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9
Q

signs and symptoms of vascular dementia

A
  • 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)
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10
Q

signs and symptoms of lewy body dementia

A
  • GRADUAL
  • probs with complex cog actions/multitasking
  • visual hallucinations
  • Parkinson-like sx
  • sleep disorder
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11
Q

signs and symptoms of frontotemporal dementia

A
  • RAPID progression
  • peak in 50s-60s
  • behavioural/personality change
  • loss of language fluency/comprehension
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12
Q

how is dementia investigated in primary and secondary care?

A

primary - blood screen (exclude reversible causes)
secondary - neuroimaging/structural imaging

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13
Q

what are some neuroimaging techniques that can be used to diagnose dementia? what are they helpful for?

A

1) CT - rule out lesions/other pathology
2) MRI - shows atrophy/lesions
3) DaTSCAN - dopamine imaging

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14
Q

neuroimaging findings in Alzheimer’s

A

CT - may exclude space-occupying lesions etc
MRI - generalised atrophy

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15
Q

neuroimaging findings in vascular dementia

A

CT/MRI - cerebrovascular lesion/s

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16
Q

neuroimaging findings in lewy body dementia

A

CT - abnormal
MRI - general cortical atrophy
DaTSCAN - reduced dopamine

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17
Q

neuroimaging findings in frontotemporal dementia
what is it often chracterised by?

A

MRI/CT - focal atrophy in frontal and/or anterior temporal lobes. often characterised by left-right symmetry

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18
Q

ddx for dementia

A
  1. delirium
  2. HIV-related cog impairment
  3. Creutzfedlt-Jakob disease
  4. hydrocephalus
  5. depression
  6. mild cog impairment (MCI)
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19
Q

how do you manage AD?

A

EARLY - anticholinesterase inhibitors e.g. donepezil, rivastigmine
LATER - NMDA inhibitors e.g. memantine

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20
Q

how do acetylcholinesterase inhibitors e.g. donepezil help manage AD?

A

block breakdown of ACh > increase ACh in synapse > increases synaptic transmission of ACh where it’s reduced

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21
Q

how do NMDA inhibitors help manage AD?

A

glutamate excitotoxicity is associated with delayed evolving neurodegeneration… NDMA inhibitors blocks NMDA receptors when too active > stops excessive glutamate production > slows disease progression

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22
Q

how is vascular dementia managed?

A
  1. treat atherosclerosis
  2. lifestyle modifications e.g. smoking, diet
  3. antiplatelets (aspirin)
  4. statins (atorvastatin)
  5. antihypertensives
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23
Q

how is lewy body dementia managed?

A
  1. donepezil/rivastigmine (increase ACh)
  2. psychotic sx - antipsychotics e.g. risperidone
  3. sleep probs - SSRIs
  4. motor sx - carbidopa/levodopa
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24
Q

how is frontotemporal dementia managed?

A

no specific tx :( can use SSRIs for behavioural sx

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25
Q

what is the difference between acute stress disorder and PTSD?

A

acute stress disorder is a reaction in the FIRST 4 weeks after trauma, PTSD is diagnosed AFTER 4 weeks

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26
Q

what is akathisia? give a classic presenting history

A

= a sense of inner restlessness and inability to keep still

common with long hx of antipsychotic use

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27
Q

which anti-depressant is known to stimulate appetite?

A

mirtazapine

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28
Q

how long after starting an SSRI should patients be reviewed if they are:
a) 25 and under
b) >25

A

a) 1 week
b) 2 weeks

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29
Q

which food should be avoided when on an MAOI (e.g. tranylcypromine) and why?

A

cheese - has lots of tyramine in which can cause hypertensive crisis when on an MAOI

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30
Q

what happens when you combine an SSRI and NSAID/aspirin? how do you manage this?

A

= GI bleeding risk
prescribe a PPI e.g. omeprazole

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31
Q

what is cotard syndrome? what condition is it most commonly associated with?

A

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)

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32
Q

which adverse effects to antipsychotics increase the risk of in elderly patients?

A

stroke and VTE

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33
Q

what is the general definition of non-pathological anxiety?

A

a constellation of psychological and physiological responses to a potential/uncertain threat.
= an essential function of the CNS

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34
Q

define:
a) generalised anxiety disorder
b) phobic anxiety disorder
c) panic disorder

A

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

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35
Q

how common are each of the anxiety disorders?

A

generalised - most common (5-12%)

phobic - second most (up to 12%)

panic - least (4.7%)

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36
Q

risk factors for anxiety disorders

A
  • 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
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37
Q

secondary causes of anxiety (4)

A
  1. substance use e.g. caffeine, stimulants, bronchodilators, cocaine
  2. substance withdrawal e.g. alcohol, benzo withdrawal
  3. hyperthyroidism
  4. cushing’s
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38
Q

DSM-5 criteria for GAD

A
  1. excessive anxiety/worry about varying events/activities for >6 months
  2. worry is difficult to control
  3. symptoms cause significant distress/impede ability to function in important areas of their life
  4. excessive worry/anxiety are accompanied by 3 or more of the following symptoms…
    - restlessness
    - fatigue
    - muscle tension
    - trouble concentrating
    - irritability
    - sleep disturbance
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39
Q

signs and symptoms of phobic anxiety disorder

A
  • avoidance of certain situation/stimuli
  • anticipatory anxiety
  • somatic sx e.g. palpitations, sweating, trembling, dyspnoea, chest pain, dizziness, chills, hot flushes
40
Q

signs and symptoms of panic anxiety disorder

A
  • 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
41
Q

stepwise approach to managing GAD

A
  1. education about GAD and active monitoring
  2. low-intensity psych interventions e.g. individual self-help, guided self-help, psychoeducational groups
  3. high-intensity psych interventions (CBT or applied relaxation) or drug tx
  4. highly specialist input e.g. multi-agency teams
42
Q

what is the 1st line drug treatment for GAD?
what if this is:
a) ineffective
b) not tolerated

A

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

43
Q

what questionnaire can help assess the severity of GAD? what are the different severity scores?

A

the generalised anxiety disorder questionnaire (GAD-7)

5-9 = mild
10-14 = moderate
15-21 = severe

44
Q

what is erotomania (De Clerambault’s syndrome)?

A

a delusion where the person believes someone famous is in love with them, with the absence of other psychotic sx

45
Q

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

a) congenital heart defects
b) persistent pulmonary hypertension of the newborn

46
Q

what is conversion disorder?

A

a condition presenting with a loss of motor and sensory function, typically occurring during times of stress

47
Q

what is delirium tremens? when and what does it present with?

A
  • 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
48
Q

how long after alcohol cessation would you expect these symptoms to manifest:
a) anxiety and nausea
b) seizures
c) delirium tremens

A

a) 6-12h
b) 36h
c) 72h

49
Q

what is the difference between hypomania and mania?

A

both present with symptoms of elevated mood BUT mania has a prolonged time course (hypomania being <7-10 days) and presents with psychotic symptoms

50
Q

what should be monitored in all patients at initiation and dose titration of venlafaxine?

A

blood pressure (venlafaxine and other SNRIs are associated with developing hypertension)

51
Q

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?

A

hyponatremia - measure U&Es in high risk patients to assess serum sodium

52
Q

depression severity classification: what PHQ-9 score indicates:
a) less severe depression
b) more severe depression

A

a) <16
b) 16 or over

53
Q

what is a key difference between pseudodementia (depression) and depression?

A

pseudodementia involves global memory loss e.g. forgetting the rules of card games, dementia predominantly involves short-term memory loss (in the early stages)

54
Q

which is associated with a poorer prognosis in a schizophrenia history?
a) acute onset
b) insidious onset of sx developing gradually

A

b

55
Q

treatments for the side-effects of long-term antipsychotics:

a) tardive dyskinesia (repetitive involuntary movements)
b) acute dystonia (abnormal postures/movements)
c) akathisia (restlessness)

A

a) tetrabenazine
b) procyclidine/benztropine
c) propanolol

56
Q

what is ADHD?

A

a persistent pattern >6 months of inattention and/or hyperactivity-impulsivity that has a direct negative impact on academic, occupational or social functioning

57
Q

when do ADHD symptoms typically present?

A

before 12yo, typically early-mid childhood

58
Q

aetiology of ADHD

A

Unknown - combo of environmental and generic factors…
1. neuro chemical
2. genetics
3. CNS insults e.g. prematurity, foetal alcohol syndrome, NF
4. environmental factors

59
Q

RFs for ADHD (5)

A
  1. prematurity
  2. low birth weight
  3. low paternal education
  4. prenatal smoking
  5. maternal depression
60
Q

pathophysiology of ADHD - which part of the brain is implicated and which NTs?

A
  • 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
61
Q

DSM-5 diagnostic criteria for ADHD (3) - <16 and 17 or over

A
  1. children up to 16: six or more symptoms of inattention and six or more symptoms of hyperactivity and impulsivity
  2. if 17 or over: five or more symptoms from each category
  3. 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
62
Q

symptoms must have been present before ___ years old for a diagnosis of ADHD

A

12

63
Q

investigation options for ADHD (4)

A
  1. questionnaires
  2. clinical interview
  3. ADHD nurse classroom observation
  4. QB test (computer test)
64
Q

which questionnaire can be used to assess ADHD in adults?

A

the Diagnostic Interview for ADHD Adults (DIVA) questionnaire

65
Q

non pharmacological management options for ADHD (3)

A
  1. education
  2. ADHD parenting programme
  3. school support and liaison
66
Q

pharmacological management options for ADHD (stimulants and non stimulants)

A

STIMULANTS - methylphenidate (e.g. ritelin) most common

NON STIMULANTS - atomoxetine, intuniv

67
Q

mechanism of action of stimulants e.g. methylphenidate in the tx of ADHD

A
  • 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
68
Q

suggest some complications of ADHD persisting into adulthood

A
  • lower educational/employment attainments
  • poor self esteem
  • criminal behaviour
  • relationship issues
  • sleep disturbance
  • substance abuse
  • RTC
  • self harm
69
Q

what is the first-line SSRI for patients with a hx of cardiovascular disease?

A

sertraline

70
Q

antidepressants should be continued for at least ___ months after remission of symptoms to decrease the risk of relapse

A

6 months

71
Q

how would schizotypal personality disorder present?

A
  • “magical thinking” focussing on paranormal phenomena
  • odd speech e.g. high-pitched voice
  • problems socially/with relationships
72
Q

substance dependence requires at least two of the following…

A
  1. impaired control over substance use
  2. increasing priority over other aspects of life/responsibility
  3. psych features suggestive of tolerance/withdrawal
73
Q

define alcohol dependence

A

craving and tolerance of alcohol consumption despite negative complications experienced

74
Q

pathophysiology of alcoholism - what NTs are involved? what happens in withdrawal?

A
  1. consuming alcohol affects basal ganglia
  2. releases dopamine > reward system > positively reinforces behaviour > operant conditioning
  3. alcohol also causes increase in inhibitory NT GABA (sedative)
  4. 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

75
Q

symptoms of alcohol dependence (3)

A
  1. tolerance
  2. craving
  3. “eye-opener”
76
Q

CAGE questions for alcoholism

A
  1. have you ever felt you should Cut down on your drinking?
  2. have people Annoyed you by criticising your drinking?
  3. have you ever felt bad or Guilty about your drinking?
  4. have you ever had a drink first thing in the morning to steady nerves/get rid of a hangover? (Eye-opener)
77
Q

symptoms of alcohol withdrawal

A

6-12 hours = tremors, sweating, tachycardia, fever
12-48 hours = alcohol hallucinosis, seizures
72+ hours = delirium tremens (altered mental status, agitation, hallucinations)

78
Q

investigations for alcoholism

A
  1. AUDIT-c questionnaire (screening)
  2. labs - FBC, LFTs, B12/folate, TFTs
79
Q

what blood results may be found in a patient with alcoholism? (FBC, LFTs, folate/b12)

A

FBC - raised MCV, raised platelets, anaemia
LFTs - increased GGT, AST:ALT > 2:1
B12/folate - deficient

80
Q

medications to help with alcohol detox symptoms (4)

A
  1. chlordiazepoxide (sedative)
  2. high dose benzos e.g. diazepam
  3. naltrexone (opiate blocker, blocks feeling/buzz of alcohol)
  4. prophylactic oral thiamine
81
Q

psychological complications of alcoholism

A

alcoholic hallucinosis, delirium tremens, Wernicke-Korsakoff syndrome

82
Q

what is bipolar disorder?

A

a mood disorder where mood switches between major depression and mania/hypomania

mood swings tend to last DAYS at a time

83
Q

how long does a manic episode tend to last in bipolar disorder?

A

at least 7 days

84
Q

signs and symptoms of
a) depression
b) mania

in a person with bipolar disorder

A

a) low mood, suicidal, difficulty getting out of bed, sleeping more, worthlessness

b) elevated mood, increased activity, grandiose ideas, distractibility, loss of normal social inhibitions, impulsivity

85
Q

pharmacological treatment of bipolar disorder:
a) acute mania
b) acute depression
c) long term

A

a) oral antipsychotics e.g. haloperidol, olanzapine, quetiapine, risperidone

b) oral antidepressant + antipsychotic e.g. fluoxetine + olanzapine
consider CBT

c) mood stabilisers e.g. lithium, sodium valproate

86
Q

non pharm tx of longterm bipolar disorder

A

psycho - CBT, family focussed therapy
social - support groups, job support

87
Q

define delirium

A

an acute, transient and reversable state of confusion

88
Q

aetiology of delirium (there’s a mnemonic!)

A

CHIMPS PHONED
C - constipation
H - hypoxia
I - infection
M - metabolic disturbance
P - pain
S - sleepiness

P - prescriptions e.g. opiates, benzos
H - hypothermia
O - organ dysfunction (hepatic/renal)
N - nutrition
E - environmental change
D - drugs (OTC, illicit, alcohol, smoking)

89
Q

what are the two types of delirium? how do they present?

A

hyperactive:
- agitation
- delusions
- hallucinations
- wandering
- aggression

hypoactive
- lethargy
- slowness with everyday tasks
- excessive sleeping
- inattention

can fluctuate between the two!

90
Q

what timespan of presentation helps differentiate between delirium and dementia?

A

delirium often in v short space of time (unlike dementia)

91
Q

what cognitive assessment can be done when investigating delirium?

A

MMSE

92
Q

what screening is done for patients with suspected delirium?

A

confusion screen - rules out common causes of confusion

93
Q

outline the investigations included in a confusion screen and the underlying causes that may be found

A
  1. BLOODS
    - FBC: infection, anaemia, malignancy
    - U&Es: hypo/hypernatraemia
    - LFTs: liver failure w secondary encephalopathy
    - coag/INR: intracranial bleed
    - TFTs: hypothyroid
    - serum calcium: hypercalcemia
    - B12 + folate: deficiency
    - glucose: hypo/hyper
    - blood cultures: sepsis
  2. URINALYSIS - UTI
  3. IMAGING
    - CT head: ischaemic stroke, bleed, abscess
    - CXR: pneumonia, pul oedema
94
Q

first line medical management for delirium

A

haloperidol (oral, IV or IM)

95
Q

non-pharm management for delirium

A
  1. identify and treat underlying cause
  2. general support e.g. ensure access to aids
  3. environment - access to clock, familiar objects, involve fam and friends, control noise, ambient lighting/temperature
96
Q

first-line tx for acute stress disorder

A

CBT

PHASE 3A (11 decks)

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