Summary Flashcards

1
Q

which psychiatric illnesses have the highest mortality?

A

eating disorders- due to physical state and suicidal behaviours

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2
Q

main symptoms of delirium?

A

impairment of consciousness: from clouding of consciousness to coma
global disturbance of cognition: hallucinations (visual common) and delusions
psychomotor disturbance-hypoactive or hyperactive and agitated
disturbance of sleep-wake cycle-symptoms tend to be worse at night, more sleep during day
emotional disturbance-tearful or sad, or may be overly happy.

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3
Q

drugs that may cause delirium?

A
corticosteroids
lithium
TCAs
parkinsons disease medication
opioids
BZDs
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4
Q

mechanisms involved in developing delirium symptoms?

A
Inflammation responses passing the blood brain barrier and are maintained by cell with immunological properties in the brain.
Disturbance of the electrolyte balance
Hypoxia
Low availability of essential nutrients
Dehydration
Continuous high cortisol levels
Afferents of the vagal nerve
Low BDNF (Brain Derived Neurotrophic Factor)
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5
Q

complications of ECT?

A
angina
MI
stroke
arrhythmias
PE
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6
Q

skin changes during ECT?

A

goosepimple appearance of skin with SNS activation following PNS activation, increasing BP and HR

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7
Q

how can sentence structure be affected in patients with schizophrenia?

A

formal thought disorder: knights move thinking/loosening of associations
patients never quite getting to the end of a sentence or what you think the patient is going to say, seem to dodge round what you think they’re going to say.

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8
Q

A pt believes without a doubt that their neighbours are trying to harm them as they are keeping a close eye on the pt via special cameras in their house that connect with the patient’s house. There is no evidence for this. what term describes these symptoms?

A

a persecutory delusion

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9
Q

if an elderly pt was to become acutely agitated in a care home, what might your 1st management step be?

A

monitor them by recording their behaviour on a behavioural chart-ABC chart-antecedents, behaviour, consequences chart.

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10
Q

if a pt presents to A and E late on a Fri night, following violence, and appears irritable, loud, overfamiliar and has a raised HR and BP, what differential must always be considered?

A

drug intoxication e.g. amphetamines e.g. methamphetamine, cocaine

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11
Q

what tment has no proven benefit to psychotic patients?

A

family therapy

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12
Q

if a pt is deemed at risk to others, what must always be considered in terms of their social management?

A

safeguarding-espec. children

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13
Q

what is the difference between somatisation disorder and hypochondriacal disorder?

A

somatisation=multiple, recurrent and frequently changing physical symptoms which are psychological in nature rather than due to a physical disease.
hypochondriacal=persistent preoccupation with having 1 or more seriously progressive physical disorders, but pt doesn’t necessarily have any symptoms of the physical disorder they are worried about having.

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14
Q

what is factitious disorder?

A

The patient feigns symptoms repeatedly for no obvious reason and may even inflict self-harm in order to produce symptoms or signs. The motivation is obscure and presumably internal with the aim of adopting the sick role. The disorder is often combined with marked disorders of personality and relationships.

*different from malingering in that a malingerer feigns illness with obvious motivation, rather than just adopting the sick role.

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15
Q

specific early symptoms associated with fronto-temporal dementia?

A

disinhibited and/or ritualised behaviour
unusually rude, selfish or unkind behaviour
language problems especially in younger people

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16
Q

give 4 reasons as to why it is important to be able to make a diagnosis of dementia?

A

offer relief to an individual, help them make sense of what they have been experiencing
implement treatments that can help with short term control of symptoms
help patients and their families plan for the future and know what to expect
eliminate other possible causes that may present similarly to dementia but are treatable

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17
Q

ADRs of AChesterase inhibitors used in the treatment of mild to moderate alzheimer’s disease dementia?

A
nausea and vomiting
headaches
muscle cramps
insomnia
anorexia
diarrhoea
fatigue
bradycardia and syncope

main aim of drugs are to improve cognition-help prevent memory, disorientation and language problems from deteriorating, but have no effect on disease progression.

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18
Q

caution patients in use of AChesterase inhibitors in treatment of alzheimer’s disease dementia?

A
SVT
asthma
COPD
susceptibility to peptic ulcers
hx of convulsions
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19
Q

ADRs of memantine-an NMDA glutamate receptor antagonist used in moderate to severe alzheimer’s disease dementia treatment?

A
constipation
drowsiness
dizziness
dyspnoea
headache

caution if hx of convulsions

drug also has a licence for behavioural problems in severe dementia

20
Q

typical dosing of haloperidol IF was to be used in treatment of delirium

A

0.5mg OD or BD

21
Q

how do psychotic symptoms differ between dementia and delirium if present?

A

dementia: often consistent delusions if present, hallucinations infrequent, visual and auditory
delirium: often fleeting delusions if present, hallucinations common often visual.

22
Q

differences between alzheimer’s disease dementia and vascular dementia?

A

onset: insidious in AD, abrupt in vascular
progression: gradual in AD, stepwise in vascular
F more than M in AD, M more than F in vascular
focal neurological signs and symptoms often present in vascular e.g. +ve Babinski sign.
often hx of HTN in vascular.
often hx of CVA in vascular.
affective symptoms like emotionality and depression relatively common in vascular.
genetic factors important in some cases of AD but no clear genetic causes in vascular.

23
Q

classic features of lewy body dementia?

A

fluctuating cognitive symptoms
repeated unexplained falls
visual hallucinations often very vivid
parkinsonian symptoms

24
Q

how does dementia in parkinson’s disease differ from lewy body dementia?

A

in dementia in parkinson’s disease, the classical motor symptoms, resting tremor, cog wheel rigidity and bradykinesia appear BEFORE the pscychiatric symptoms of cogntive impairment and visual hallucinations.

25
Q

what pathology plays a role in all cases of frontal lobe dementias?

A

Tau proteins-this is also seen in neurofibrillary tangles in alzheimer’s disease dementia

26
Q

pathology in huntington’s chorea- an irreversible cause of dementia?

A

caudate nucleus atrophy (caudate nucleus along with the putamen forms the striatum where D1 and D2 receptors are present and form part of the direct and indirect pathways controlling voluntary movements in the basal ganglia)
frontal lobe pyramidal neurone loss

pt develops incapacitating choreiform movements, also psychiatric symptoms e.g. persecutory delusions and depression. cognitive impairment often develops later in the disease.

27
Q

pathology in wernicke-korsakoff syndrome?

A

micro bleeds to several parts of the brain, especially the mamillary bodies-form part of the hypothalamus.

thiamine deficiency in alcoholic patients

28
Q

presentation of wernicke’s encephalopathy?

A
opthalmoplegia
nystagmus
truncal ataxia
delirium
peripheral neuropathy
pupillary abnormalities
29
Q

main reasons for performing CT/MRI in querying dementia?

A

exclude reversible causes of dementia e.g. frontal lobe tumour, normal pressure hydrocephalus-disruption to CSF drainage

30
Q

define apathy

A

loss of interest, enthusiasm or concern
seen in dementia, anxiety, schizophrenia, emotionally unstable PD

there is lack of emotion
contrast this to reduced affect- where emotional expression is reduced regardless of if emotion is reduced. blunted affect-significantly reduced intensity of emotional expression, flat effect-no or nearly no emotional expression.

31
Q

investigating a patient with depression?

A

ECG-baseline as antidepressants can prolong QTc e.g. citalopram and escitalopram SSRIs, and amitriptyline TCA, QTc prolongation can lead to torsades-a broad complex irregular tachycardia, which can go into VF and cardiac arrest
bloods: FBC-anaemia-fatigue, appetite loss
Us and Es-?hyponatraemia, ?addison’s-dizziness, postural hypotension, pigmented buccal mucosa and palmar creases
Ca2+-hypercalcaemia? e.g. primary hyperparathyroidism, multiple myeloma, sarcoidosis, bone metastases, amyloidosis
TFTs-hypothyroid can present with depression, LFTs-rule out hepatitis, drug abuse
glucose-?DM
vit B12-?deficiency e.g. crohns, coeliac disease, small bowel bacterial overgrowth, antibodies against intrinsic factor-AI atrophic gastritis (pernicious anaemia)
urine drug screen-?drug abuse

if psychotic features e.g. delusions e.g. persecutory, poverty, hallucinations-often 2nd person auditory, disorder of thought control, then do CT to rule out organic cause e.g. tumour SOL

32
Q

bio-psycho-social response to depression management?

A

conservative measures-smoking cessation, reduce alcohol consumption, healthy diet, establish healthy sleep regime, increase exercise
social-encourage support from friends and family
psychological-self-help based on CBT principles, counselling-on presentation to GP can complete patient health questionnaire (PHQ-9), score can be used in wellbeing team referral who can arrange counselling, group and individual CBT, family therapy
biological-SSRIs e.g. sertraline-advise about feeling about drowsy 1st few days, advise ADRs e.g. insomnia, appetite loss, headaches, loss of libido, r/v in a week to see if helping, continue for at least 6 mnths if 1st presentation and 2 years if 2 or more presentations in last 5 years. TCAs e.g. amitriptyline can help with sleep, mirtazapine-increases appetite and causes weight gain.
antipsychotics
anxiolytics
ECT for severe and refractory depression

RISK ASSESSMENT

33
Q

how can neuroleptic malignant syndrome be differentiated clinically from serotonin syndrome?

A

neuroleptic-slow-onset idiopathic reaction to dopamine antagonists, causing lead-pipe muscular rigidity and bradykinesia
serotonin-symptoms usually within 6 hrs of taking the drug, with tremor, akathisia, autonomic hyperactivity and mental status changes e.g. delirium.

34
Q

Drug monitoring for carbamazepine? *

A

Anti-epileptic drug that may be considered as a mood stabiliser in LT prophylactic treatment of bipolar
Risk of agranulocytosis-also occurs with carbimazole, phenytoin, clozapine….
So need FBC monitoring, also LFTs?

35
Q

considerations in advice giving to bipolar patients?

A

self-monitoring
stress reduction
exercise
balance activities
build relationships
need to inform the DVLA of bipolar diagnosis
should not drive if manic episode
if on lithium for treatment or prophylaxis, must warn of need to remain well hydrated-so eat regularly, be careful with caffeine, drink plenty after exercising and in hot weather, be wary of signs of toxicity e.g. coarse tremor, bad diarrhoea or vomiting, feeling very thirsty, obvious shaking of hands and legs, feeling confused.
other advice on their medications-rpt blood tests, mood stabiliser continue at least 2 yrs after 1 episode or up to 5 if frequent previous relapses, substance misuse, prev. psychotic episodes, continuing stress at home or work.
psychological tment can be helpful in between manic or depressive episodes, and should involve psychoeducation, mood monitoring, general coping skills and CBT.
discuss pregnancy plans with psychiatrist-valproate CI in women of childbearing age, lithium safe after 26th week but risk greatest in 1st 3 mnths, and also shouldn’t breastfeed if taking lithium.
GP will give annual health check-weight, BP, lipid levels-for all over 40, blood glucose, smoking and alcohol.

36
Q

what should patients with GAD be warned about happening over the 1st few weeks of starting an SSRI e.g. sertraline?

A

will initially make them feel more anxious!

37
Q

worry with prescribing multiple QT interval prolonging drugs in psychiatry e.g. SSRIs and TCAs?

A

increase risk of sudden cardiac death

38
Q

problem with BZD dependence?

A

associated with night time deaths

39
Q

what medications should alcoholics be prescribed in order to reduce their risk of alcohol associated complications?

A
thiamine
vit B co-strong
PPI-GORD, PUD
laxative e.g. lactulose
folic acid
40
Q

how are beta blockers useful in the treatment of GAD?

A

they reduce the effects of the SNS which produce symptoms of anxiety e.g. sweating, tremor, fast HR, and although not tackling the root cause of the patient’s symptoms, this helps to control their anxiety as they don’t worry about these symptoms and what other people think of them which stops increasing anxiety further.

41
Q

complications of neuroleptic malignant syndrome?

A
AKI
PE
DIC
rhabdomyolysis
respiratory failure
liver failure
cardiac arrest
seizures
aspiration pneumonitis
42
Q

features of body dysmorphic disorder?

A

DSM-IV:
preoccupation (recurrent thoughts can be put out of mind by effort of will) with an imagined defect in appearance, excessive concern if slight physical anomaly present
preoccupation causes person clinically significant distress or impairment in social, occupational or other important areas of functioning
preoccupation is not better accounted for by another mental disorder e.g. anorexia nervosa.

43
Q

SSRI most associated with SSRI discontinuation syndrome?

A

paroxetine (short acting)

44
Q

what consideration should be made with regards to ongoing medication in a OA patient whom you are thinking about starting an SSRI for depression for?

A

is the patient on an NSAID?
if so, should co-prescribe a PPI with the SSRI as SSRIs have an increased risk of GI bleeding.

*avoid SSRIs if pt on warfarin or heparin

45
Q

give 4 features of PTSD?

A

re-experiencing-flashbacks
avoidance
hyperarousal-hypervigilence for threat, exaggerated startle response, irritability, sleep problems
emotional numbing-detached, inability to experience feelings

46
Q

specific warnings issued by MHRA for use of antipsychotics in elderly patients?

A

increased risk of stroke and VTE

47
Q

what is delirium tremens, when does it occur?

A

peak incidence at 72hrs post alcohol withdrawal

loss of GABA mediated inhibition of the CNS, and increased NMDA glutamate transmission.