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3a Psych Flashcards

Psych lectures from phase 3a 2019

1
Q

What is phenomenology?

A

Phenomenology is the observation and assessment of the patient’s subjective experience.

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2
Q

Define an illusion.

A

The misperception of an actual stimulus.

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3
Q

Define a hallucination and give 3 modalities.

A

The experience of sensation in absence of stimulus. For example, auditory, visual, tactile, gustatory, olfactory.

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4
Q

What is a hypnogogic hallucination?

A

Hallucination as you are falling asleep

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5
Q

What is a hypnopompic hallucination?

A

Hallucination as you are waking up

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6
Q

What is a reflex hallucination?

A

Stimulus in one modality, hallucination in another. For example, ‘when you write, i can feel your pen pressing on my heart’.

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7
Q

What is an extracampine hallucination?

A

An illusion which is not possible - eg, hearing voices in Australia.

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8
Q

What is an overvalued idea?

A

Attachment of extra importance to something, the person is not fixed in their belief.

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9
Q

Define a delusion.

A

An unshakeable thought or belief outside cultural norms, held without insight.

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10
Q

A patient is falsely convinced that a murderer is trying to kill them. What is this?

A

Persecutory delusion

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11
Q

A person believes they have super powers. What kind of delusion is this?

A

Grandiose delusion

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12
Q

Give an example of a self-referential delusion.

A

Hearing a song on the radio and thinking that it is speaking directly to you.

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13
Q

What is it called when a person believes they are dead or rotting?

A

Nihilistic delusion

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14
Q

Give 3 examples of misidentification delusions and their definitions.

A

Capgras delusion: Someone close to them, normally a spouse, has been replaced by an imposter.
Fregoli delusion: Various people are the same person in disguise.
Intermetamorphasis: Belief that people in the environment swap identities with each other while maintaining the same appearance (freaky friday)
Subjective doubles: Belief that they have a doppelganger.

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15
Q

Define and give an example of a delusional perception.

A

A delusional belief triggered by a perception. Seeing a traffic light change and believing this means the FBI are after you.

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16
Q

Define and give the subtypes of thought alienation.

A 
Thought alienation is when a person believes their thoughts are not their own. This includes:
Thought insertion (someone putting thoughts into your head)
Thought withdrawal (someone taking thoughts out of your head)
Thought broadcast (everyone can read your thoughts)
Thought echo (thought 'bouncing around' in your head after you think it)
Thought block (sudden mind blank)
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17
Q

What is looseness of association?

A

When the person is speaking and you cannot follow their train of thought. AKA Knight’s move thinking.

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18
Q

What is it called when someone takes a very long time to get to the point?

A

Circumstantiality

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19
Q

What is perseveration?

A

Repeating a word/phrase inappropriately, or continuing to feel pain or do an action after it is unnecessary/inappropriate.

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20
Q

What is confabulation?

A

Filling in a gap in memory with fabricated, untrue accounts (not necessarily grandiose)

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21
Q

What is it called when someone believes that the sensations they are feeling are caused by an external agency?

A

Somatic passivity. Eg, my leg feels hot because the devil has possessed it.

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22
Q

A person says they were forced to move their arm by an external agency. What is this called?

A

Made act.

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23
Q

Define catatonia.

A

A state of excited or inhibited motor activity in the absence of a mood disorder or neurological disease.

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24
Q

Define waxy flexibility.

A

The patients limbs feel like wax/lead pipe when moved, and remain in the position in which they are left. Found rarely in catatonic schizophrenia and structural brain disease.

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25
Q

What is the term for automatic repetition of words heard?

A

Echolalia.

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26
Q

What is the term for repetition of the last syllable of a word?

A

Logoclonia.

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27
Q

What is echopraxia?

A

Automatic repetition by patient of movements made by the examiner.

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28
Q

What is negativism?

A

Motiveless resistance to movement.

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29
Q

What is palilalia?

A

Repetition of a word over and over with increasing frequency.

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30
Q

What is verbigeration?

A

Repetition of one or several sentences or strings of fragmented words, often in a monotonous tone.

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31
Q

What is psychomotor retardation?

A

Slowing of thoughts and movements to a variable degree. Occurs in depression, but also caused by psychotropics, parkinson’s, etc.

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32
Q

What is pressure of speech and of what is it suggestive?

A

Seen often in mania. Rapid speech delivery, unusual associations, often with rhyming and punning.

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33
Q

What is flight of ideas?

A

Rapid skipping between ideas with tenuous links using rhyming etc.

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34
Q

What is anhedonia?

A

Loss of pleasure from activities normally found enjoyable.

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35
Q

What is apathy?

A

Lack of interest/engagement/emotion.

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36
Q

Define affect.

A

The emotional state in a patient in a particular moment and in response to a particular event or situation.

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37
Q

Define mood.

A

Prevailing emotional state over a longer period of time than affect.

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38
Q

Define incongruity of affect.

A

Emotional response is out of tune with the subject being discussed. For example, laughing when things are sad.

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39
Q

Define blunting of affect and flattening of affect.

A

Blunting of affect is the objective absence of normal emotional responses without evidence of depression or psychomotor retardation. Flattening of affect is when no emotion is shown at all.

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40
Q

What is a conversion disorder?

A

Conversion of an emotional/psychological issue into a physical issue.
Passmed:
typically involves loss of motor or sensory function
the patient doesn’t consciously feign the symptoms (factitious disorder) or seek material gain (malingering)
Don’t need to be worried about it - might even have la belle indifferent.

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41
Q

What is the term for feeling indifferent about a serious medical problem?

A

La belle indifference.

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42
Q

What is the term for when a person feels detached from their body, like a spectator of their own activities?

A

Depersonalisation

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43
Q

What is derealisation?

A

A sense of one’s own surroundings lacking reality, often appearing grey, dull and lifeless.

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44
Q

What is dissociation?

A

Feeling disconnected from one’s self or surroundings.

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45
Q

Define a mannerism

A

.A sometimes bizarre but not necessarily pathological elaboration of normal activities. For example, twirling one’s hair when anxious.

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46
Q

Define stereotyped behaviour.

A

Uniform, repetitive non-goal-directed actions. This may be simple movements or utterances.

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47
Q

Define an obsession.

A

A recurrent persistent thought, recognised as one’s own, that is hard to resist.

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48
Q

Define a compulsion.

A

The feeling that you need to act on the thought. Repetitive behaviour accompanied by the subjective sense that it must be carried out despite recognition of senselessness. Recognised by individual as morbid.

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49
Q

What is the term for restlessness and discomfort sitting still?

A

Akathisia

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50
Q

Define projection

A

When someone projects onto others what is emotionally unacceptable to the self. For example, a mother claiming that her children are anxious but she is not.

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51
Q

What is the term for the redirection of emotions from an individuals childhood to a substitute, usually a therapist?

A

Transference.

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52
Q

How does Mirtazapine work? What is it used for?

A

Mirtazapine is a NaSSA: noradrenergic and specific serotonergic antidepressant. It blocks a-2 adrenergic receptors, serotonin 5HT receptors, and histamine H1 receptors. Its strongest activity is blocking H1. This causes sedative and hypnotic effects. After a period of use, these effects wear off. It is primarily used to treat mood disorders such as depression.

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53
Q

Which section allows someone to be detained for up to 28 days?

A

Section 2. Cannot be renewed, for assessment

Need: Section 12 approved doctor, doctor who knows patient, and AMHP.

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54
Q

Which section allows someone to be detained for up to 6 months?

A

Section 3.

Can be renewed, for treatment. Need Section 12 approved doctor, doctor who knows patient, and AMHP (same as section 2).

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55
Q

How long can a section 3 be renewed for?

A

A section 3 can be renewed for 6 months the first time, 6 months the second time, and 12 months all the times after that.

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56
Q

What is a section 4?

A

A section 4 is an emergency measure which allows you to detain a patient for up to 72 hours, if they have a mental disorder, it is urgently necessary for them to be admitted, and waiting for the second doctor would cause an undesirable delay. One doctor and one AMHP needed.

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57
Q

What is a section 5 (2)? When used?

A

Allows one doctor to detain an informal patient or inpatient for up to 72 hours while waiting for a second doctor and AMHP to assess for section 2/3. The doctor must be F2 and above.

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58
Q

What is a section 5 (4)? When used?

A

Allows a mental health trained nurse to detain a voluntary mental health patient for up to 6 hours or until the section 12 approved doctor arrives. Applicable if: patient needs to be kept in hospital for their own/others safety, or it is so urgent that it is not practicable for a report to be provided to the hospital managers.

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59
Q

What is a section 17?

A

Gives the clinician power to grant leave to a patient already detained under the MHA. Can involve conditions such as must stay with a particular person.

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60
Q

What is a section 135?

A

Section 135 allows police enter the premises of a patient under a warrant and take them to a place of safety, if they are being ill-treated/neglected or showing self neglect. It lasts up to 24 hours.

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61
Q

What is section 136?

A

Section 136 allows police to take the patient to, or keep them in, a place of safety for up to 24 hours. Can only do this from a public place.

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62
Q

What is the function of glutamate?

A

Glutamate is the most common excitatory neurotransmitter in the brain. It has a role in synaptic plasticity, which means it is involved with cognitive functions such as learning and memory.

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63
Q

What can happen if there is a buildup of glutamate in the brain?

A

It is neurotoxic and can lead to a loss of neuroplasticity.

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64
Q

How is stress harmful to the brain?

A

Stress causes a buildup of glutamate in the brain which is neurotoxic. It also neurotoxic via elevation of serum cortisol levels, especially in the hippocampus.

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65
Q

Which receptors do typical/first generation antipsychotics usually affect?

A

D2/3 Receptors. ML, TI, NS and cholinergic pathways.

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66
Q

What are the 4 dopamine pathways?

A

Mesolimbic - underactivity –> negative sx
Mesocortical - hyperactivity –> positive sx
Nigrostriatal- voluntary movement
Tuberoinfundibular - prolactin secretion (affect your tubes)

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67
Q

What are the pyramidal tracts?

A

Nerve fibres which run from the cerebral cortex to the brainstem (corticobulbar tract) or spinal cord (corticospinal tract), involved in controlling the voluntary motor functions of the body. They run through the medullary pyramids.

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68
Q

What are the extrapyramidal tracts?

A

Part of the motor system network causing involuntary actions. They target lower motor neurones in the spinal cord that are involved in reflexes, locomotion, complex movements and postural control.
They consist of the rubrospinal, reticulospinal, vestibulospinal and tectospinal tracts.

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69
Q

What is the important difference between pyramidal and extrapyramidal tracts?

A

Pyramidal tracts are involved in voluntary actions, extrapyramidal tracts are involved in involuntary actions.

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70
Q

What are extrapyramidal side effects?

A

Acute dystonia (muscle), akathisia (rustle) and akinesia (hustle).

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71
Q

How long after taking an antipsychotic would dystonia occur?

A

About 4 hours

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72
Q

How long after taking an antipsychotic would akathisia occur?

A

About 4 days

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73
Q

How long after taking an antipsychotic would akinesia occur?

A

About 4 weeks

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74
Q

How would you treat mild to moderate depression?

A

CBT, watchful waiting, lifestyle changes.

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75
Q

How would you treat moderate to severe depression?

A

Combination therapy with talking therapy and antidepressants.

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76
Q

What would be the first, second and third line pharmacological treatments for depression?

A
  1. SSRI eg citalopram/ sertraline/ fluoxetine
  2. Change to another SSRI/ trazadone/ mirtazapine
  3. SNRI eg venlafaxine
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77
Q

What are the issues with paroxetine?

A

Paroxetine has a short half life so needs to be taken more regularly and levels fluctuate. This increases the risk of discontinuation symptoms making it harder to come off. It also causes weight gain.

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78
Q

How long is an adequate trial of antipsychotics?

A

6 weeks

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79
Q

What are the side-effects of SSRIs?

A 
GI symptoms
Suicidal ideation
Sexual dysfunction
Insomnia
Headache
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80
Q

What are the contraindications of SSRIs?

A

Risk of serotonin syndrome - this is increased if someone is on another serotonin directed drug eg antipsychotics, or tramadol.
Risk of upper GI bleed - increased if someone is on NSAIDs or has other risk factors for gastritis/bleed.
Give gastroprotection eg omeprazole.

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81
Q

What are the side effects of SNRIs?

A

Same as SSRIs at lower doses, but at higher doses risk of hypertension, especially with venlafaxine.

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82
Q

What class is phenelzine and what are the risks?

A

MAOI.
Risk of serotonin syndrome - NEVER use with an SSRI.
Low-tyramine diet must be kept, eg no cheese, to reduce risk of hypertensive crisis.

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83
Q

What class is amitriptyline and what is it used for?

A

TCA, used for neuropathic pain at lower doses.

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84
Q

What class is clomipramine and what is it used for?

A

TCA, used for OCD

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85
Q

Which TCA is safest in overdose?

A

Lofepramine.

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86
Q

What are the effects of TCAs?

A

Increase serotonin and norepinephrine –> :-)
Anticholinergic –> dry mouth, constipation, urinary retention (therefore overflow incontinence_, blurred vision, confusion.
Antihistaminergic –> Sedation, wt gain.
Decreases Na and Ca –> Wide QRS in overdose.
More dangerous in overdose than other antidepressants, lofepromine least risk.
Manic switch

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87
Q

What are the side-effects of mirtazapine?

A

Increased sleep and weight gain - therefore good for people who struggle with these things.

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88
Q

What is trazadone?

A

Trazadone in an SARI - serotonin antagonist reuptake inhibitor. It is often used to treat depression in primary care.

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89
Q

What are the side effects of trazadone?

A

Postural hypotension, sedation.

90
Q

What is tardive dyskinesia?

A

An involuntary movement of the perioral muscles which can be irreversible. (memory aid: think chewing TAR)

91
Q

What are the functions of dopamine?

A 
DOPAMINE:
•	Drive – dopamine governs motivation and reward.
•	O – Psychosis 
•	P – Parkinson’s
•	A – attention
•	M – dopamine is strongly linked to motor function
•	I – Dopamine inhibits prolactin
•	N –narcotics.
•	Extrapyramidal
92
Q

Give a side effect of risperidone.

A

(memory aid: RIS PERidone gives RISE to a PAIR.)

93
Q

What are the symptoms and signs of neuroleptic malignant syndrome (NMS)?

A

NMS is a life threatening complication of antipsychotic medications.
Hyperthermia (feeling hot hot hot)
Muscle rigidity
Altered mental status, confusion, agitation
Autonomic dysfunction eg hypotension, incontinence
Seizures.

94
Q

How do you treat NMS?

A

Dantrolene is a muscle relaxant used to treat NMS. (think of dan and a trolley)

95
Q

What side effect can be caused by blocking ACh?

A

Memory impairment

96
Q

What side effect can be caused by blocking noradrenaline?

A

Hypotension

97
Q

What side effect can be caused by blocking histamine?

A

Sedation

98
Q

What is delirium?

A

Clinical syndrome of acute confusion, clouding of consciousness, visual illusions/hallucinations, lability of affect, and disorientation.
Aka acute confusional state.
Can be hypoactive, hyperactive and mixed.
[oxford]

99
Q

Give 5 causes of delirium (hint: Pinch me i’m delirious).

A 
Pain
Infection/intracranial
Nutrition - vitamin deficiencies
Constipation
Hydration

Medication - bdz, anticonvulsants, nsaids, lithium, diuretics, anticholinergics, antihypertensives, steroids, digoxin
Environment.

Intracranial
Metabolic - diabetes, thyroid/parathyroid, glucose

= DELIRIOUS!

100
Q

What are the principles of management of delirium?

A

Identify and treat cause and exacerbating factors, optimise patients condition.
Provide environmental and supportive measures - adequate lighting, quiet, clocks, calendars, staff continuity
Avoid sedation if possible. bdz worsen delirium so give antipyschotic 1st
Regular clinical review and follow up.
Do MMSE.

101
Q

What is dementia?

A

Brain disease causing cognitive impairment sufficient to cause impairment in daily functioning.

102
Q

What is mild cognitive impairment?

A

Cognitive impairment which is not impairing daily functioning sufficiently to be diagnosed as dementia. May or may not progress to dementia, and some get better.

103
Q

What are the causes of dementia?

A
  1. Alzheimer’s (Dementia of Alzheimers Type)
  2. Vascular
  3. Lewy body
  4. Frontotemporal/Pick’s
  5. Other
104
Q

How is Alzheimer’s disease diagnosed?

A

A) specific clinical phenotype +
B) in vivo evidence of alzheimers pathology.
MMSE <25/30, clinical dementia rating, neuropsychology, ACE
Without the pathology, you can only diagnose probable alzheimers.
Definitive diagnosis and staging is on autopsy (Braak staging).

105
Q

What is the pathophysiology of AD?

A 
Neurofibrillary tangles (NFTs, consist of p-tau) and beta-amyloid plaques in the brain causing synaptic loss and deteriorating cognition.
FHx in 40%
APP gene (Down's syndrome association), APOE4 gene.
106
Q

How does AD present?

A

Early: amnesia, recent deficit, leaving the kettle on but scores fine in language.
Mid: Personality and social changes, recognising people, word finding difficulties
Late: Motor problems, swallowing difficulty, incontinence, psych problems, paranoia, aggression etc. Fully dependent.

107
Q

Give 3 poor prognostic factors for Alzheimers dementia.

A

Male, onset <65 (young), parietal lobe damage, apraxia, depression.
Lower education?

108
Q

How is Alzheimer’s disease treated?

A

2nd generation Acetylcholinesterase inhibitors (AChEI) eg donepezil/rivastigmine.
Side effects: GI.

109
Q

What is the pathophysiology of vascular dementia?

A

VD = Cognitive deficit >2 domains, focal neurology, impaired social functioning with hx of vascular disease.
3 syndromes:
1. Cognitive deficits following a single stroke
2. Multi-infarct dementia: Multiple ‘mini strokes’ –> stepwise deterioration in cognitive function with stability between strokes.
Causes and RFs therefore same as for CVAs
3. Progressive small-vessel disease (Binswanger disease).
Spectrum of disease with mixed AD/vascular dementia.

110
Q

How does vascular dementia present?

A

Stepwise deterioration in cognitive function, more acute onset than AD.
Early: emotional/personality change, cognitive deficits, depression, affective lability
Seizures in 10%
Onset may follow CVA. Features of cortical (cortex) and subcortical (basal ganglia, limbic system, hippocampus) dementia

111
Q

How is vascular dementia diagnosed?

A

MoCA
ACE
Neuropsychology
Bloods - cholest, EST, CRP, FBC, HbA1C, APL-abs
MRI - small vessel disease, white matter pathology, hippocampal sparing

112
Q

How is vascular dementia treated?

A

Treat causes/RFs - antiplatelets, statins, antihypertensives

General dementia mx (MDT etc)

113
Q

What is the pathophysiology of dementia with lewy bodies?

A

Lewy bodies - inclusions of abnormally phosphorylated neurofilament proteins in basal ganglia, paralimbic and neocortical structures. Leads to neuronal loss and less ACh transmission. Vascular and Alzheimer-type changes often co-occur.
Braak stages:
Medulla –> pons -> midbrain -> amygdala -> cortex.

114
Q

How is DLB diagnosed?

A

Clinical - similar to alzheimers, only a probably dx can be made, based on progressive decline sufficient to interfere with normal function with >2 core features:
fluctuating cognition,
visual hallucinations,
parkinsonism.
CT/MRI - deep white matter lesions, periventricular lucency on MRI, sparing of medial temporal lobes
SPECT
Genotyping: ApoE E4.

115
Q

How is DLB managed?

A

Social care, acetylcholinesterase-inhibitors, treat Parkinsonism - levodopa/co-careldopa has fewer psych SEs than DAs (cabergoline). start low go slow
Particular caution with antipsychotics - irreversible parkinsonism, NMS-like autonomic disturbances, 2-3x mortality

116
Q

What is the pathophysiology and main types of frontotemporal dementia?

A

Bilateral atrophy of frontotemporal regions of the brain, degeneration of the striatum.
Microvacuolar type (60%) - microvacuolar (spongiform) degeneration
Pick type (25%) - loss of large cortical nerve cells, <65 years old
MND-associated (15%)
Onset younger, survival 6-8 years, FHx in 40%.
C9ORF72 gene.

117
Q

How does frontotemporal dementia present compared to other dementias?

A

Social misconduct - disinhibition, wandering, passivity
Emotional blunting
Impaired insight
Dietary changes, sweet tooth
Perseverative behaviours eg drinking from empty cup
Cognitive - poor executive function

118
Q

How is FTD diagnosed/ what are the core features?

A

Core features:
Insidious onset, gradual progression
Early decline in social interpersonal conduct
Early impairment in regulation of personal conduct, emotional blunting, loss of insight

119
Q

What is bipolar affective disorder? What are the main types?

A

Disorder of alternative high and low mood with remission periods.
Bipolar 1: mania + major depression (severe end of spectrum)
Bipolar 2: hypomania + major depression
Cyclothymia: hypomania + minor depression for 2
years.
Dysthymia = mild end of spectrum.

120
Q

What is mania and how do you differentiate it from hypomania?
(hint: I dig fast)

A 
Both:
Irritability
Distractability
Inhibition loss
Grandiosity
Flight of ideas
Activity increased
Sleep not needed
Talkative
Mania = >1 week with psychotic symptoms
Hypomania = 4+ days, no psychotic symptoms.
[passmed]
121
Q

Give 3 causes of mania/hypomania.

A 
Antidepressants - less so with SSRIs
Bdz
Antipsychotics - olanzapine, risperidone
Lithim (and when combined with TCAs)
Anti-parkinsonian meds - l-dopa, bromocriptine etc.
Cardiovascular drugs - ephedrine, salbutamol.
Anti-infection - chloroquine, tramadol
many others.
122
Q

Give 3 risk factors for bipolar affective disorder.

A 
FHx
Stressful life events
Substance misuse
Age <25y
Anxiety/depression
Obesity
CV disease
Higher SES.
123
Q

How is bipolar affective disorder managed?

A

Psychosocial - CBT, interpersonal and social rhythm training (IPSRT), psychoeducation eg signs of relapse, crisis team contact, caregiver support, support groups.
Mood stabilisers - lithium (monitor)
Depression –> antidepressants but beware Mania - antipsychotic eg olanzapine, risperidone
Valproate is also a mood stabiliser, can be used if lithium CI.
ECT

124
Q

What are the risks with lithium treatment and how are these reduced?

A 
Inhibits dopamine neurotransmission, promotes GABAergic (inhibitory) transmission, downregulates NMDA glutamate receptor (excitatory).
Narrow therapeutic window, risk of toxicity.
Leukocytosis 
Increased weight
Tremors (fine, coarse in toxicity)
Hypothyroidim/Hypercalcaemia
diabetes Insipidus
Urine output up
Mums beware (teratogenic)
Cardiac eg long QT
Oedema
Nephro/neurotoxic.

Before starting: ECG, BMI, U+E, eGFR, FBC, TFT.
After any changes, measure levels after 1 week
When stable, measure every 3 months
Plus U+Es and TFTs every 6 months for thyroid and renal function.
Always measure 12 hours post-dose.

125
Q

What is schizophrenia?

A

A type of ‘functional psychosis’ (as opposed to organic/structural), characterised by positive and negative symptoms.

126
Q

What are Schneider’s first rank symptoms of schizophrenia?

A

Auditory hallucinations
Broadcasting, insertion, withdrawal of thoughts
Controlled feelings/acts - passivity phenomena.
Delusional perceptions

127
Q

How is schizophrenia diagnosed?

A
  1. One first-rank sx (auditory hallucinations, thought broadcasting/echo/withdrawal/insertion, delusions of control/passivity, delusional perceptions.
  2. Or two of: hallucinations, catatonia, negative symptoms, grandiose delusions
  3. > 1 month
128
Q

How is schizophrenia managed?

A

Psychological: CBT, cognitive rehab, motivational interview, crisis team
Social: social worker, EIP, community psych nurse, patient education, social skills training
Acute episode: assess need to admit, antipsychotics
Maintenance regime eg:
SGA (olanzapine, quetiapine, risperidone, amisulpride); depot if non-compliance.

129
Q

What causes schizophrenia/who does it usually affect?

A

Onset in teenage-early adulthood.
RFs: FHx, increasing paternal age, obstetric complications, cannabis use, low IQ, psychological stress, birth in late winter/early spring.

130
Q

What are the symptoms of catatonia?

A

Stupor - akinetic mutism
Excitement - constant purposeless activity, agitation, hyperactivity
Posturing
Waxy flexibility
Negativism - resistant to instructions/attempts to be moved.

131
Q

What are the negative symptoms in schizophrenia?

A 
Blunting of affect
Amotivation
Poverty of speech/thought
self-neglect
lack of insight
132
Q

What are the types of schizophrenia?

A

Paranoid - main one, delusions, auditory hallucinations
Catatonic - with hyperkinesis/negativism
Hebephrenic - fluctuating affect, older people.
Residual - long term negative symptoms
Simple - negative symptoms without psychotic symptoms

133
Q

What are the indications and side effects of first generation antipsychotics?

A

1st gen/typical antipsychotics:
Chlorpromazine, haloperidol, promazine, flupentixol. –> act on all pathways, D2, D3 and ACh
inhibits ML –> Treat positive sx of schizophrenia
inhibits MC –> worsen negative and cognitive symptoms.
SEs:
Neurological eg NMS.
Movement - extrapyramidal, TD, acute dystonia (muscle then rustle then hustle)
Tuberoinfundibular pathway –> ‘tubes’ -Hyperprolactinaemia -> gynecomasia, infertility
Anticholinergic –> dry mouth, confusion, urinary retention etc
Antihistaminergic –> sedation
Long QT

134
Q

How do 2nd gen antipyschotics work and what are their indications/side effects?

A

Second gen/atypical -
Risperidone, olanzapine, quetiapine, amisulpride, clozapine
–> act on D1/2/3, 5HT3 antagonists.
Mesolimbic pathway so treats +ve symptoms, but doesnt act as much on other pathways so less other sx.
Cause metabolic sx due to 5HT - wt gain, impaired glucose tolerance, lipid abnormalities (Dyslipidemia), hypercholesterolaemia.
Hyperprolactinaemia.

135
Q

What are the effects of aripiprazole?

A

3rd gen antipsychotic.
Works on D2/3, 5HT2A,
Inhibits mesolimbic pathway to treat +ve sx of schizophrenia.
5HT2 antagonist –> wt gain, impaired GT, lipid abnormalities.
Agitation, anxiety, insomnia, withdrawal, risk taking behaviours.

136
Q

What are the effects of clozapine?

A 
D1/D4 (D2) --> treats negative sx
 5HT2a.
Mesolimbic --> treats positive sx
Clozapine --> Constipation, Convulsions, Cell count, Cholesterol --> cardiac.
Used for treatment resistant schizophrenia but with close monitoring:
FBC - agranulocytosis
Blood lipids, wt, fasting blood glu 
Prolactin
Blood clozapine concentration
137
Q

What is acute dystonic reaction?

A

Dystonia (spasms, abnormal posture) usually affecting head and neck, within days of starting an antipsychotic or increasing the dose. Could affect speech.
Discontinue the cause and treat with anticholinergic eg procyclidine IM

138
Q

Give 5 investigations and their results for NMS.

A 
Elevated CK
Raised white cell count
Deranged LFTs
Acute renal failure - abnormal U+Es 
Metabolic acidosis - low pH, low HCO3.
139
Q

How is NMS treated?

A 
ABCDE
Stop causative agent
IV benzos for agitation
Cooling devices/antipyretics
Treat rhabdomyolysis
Sometimes bromocriptine and amantadine are used as muscle relaxants
140
Q

A patient with depression is brought to ED appearing unsteady, confused, and agitated. On examination they are pyrexial, sweating with increased reflexes. What could be the diagnosis?

A

Serotonin syndrome.
Risk of coma.
ABCDE, Drug hx - remove causative agent, supportive measures
Can use bzd to control agitation
Serotonin receptor antagonists eg cyproheptadine.
! Rhabdomyolysis? - increase urine output, sodium bicarbonate
Differential: NMS, substance abuse, overdose, infection, metabolic disturbances

141
Q

What is the difference between SS and NMS, and how are they treated?

A

NMS:
normal antipsychotics
slow (onset) and low
Rigidity, hyporeflexia, bradykinesia

SS
wrong/OD dose of SSRI
fast (onset) and furious.
hyperreflexia, hyperkinesia
GI sx in SS, eg nausea, vomiting, diarrheoa

!Chlorpromazine for SS but may worsen NMS

142
Q

What is schizoaffective disorder?

A

Mood symptoms (manic or depressive) and schizophrenic symptoms present in approximately equal proportions, simultaneously. Basically treat both schizophrenia and mood disorder.

143
Q

How is first-episode psychosis treated?

A

Admit people suspected of first schizophrenic episodes to assess their psychopathology, educate patient and family, and treat where compliance can be assessed. Always admit if danger to self or others.

144
Q

How is brief psychotic disorder defined?

A

Diagnosed retrospectively after psychotic symptoms resolve.

145
Q

How is delusional disorder defined?

A

One or more non-bizarre delusion, >3 months, no other sx. No insight.
Often come into contact with health service through police/trying to persecute someone else.

146
Q

Give 3 substances that could cause substance induced psychosis.

A 
Alcohol
Stimulants
Hallucinogens
Steroids
Antihistamines
Sympathomimetics
Hx may reveal onset, persistence, and cessation of symptoms to be related to drug use or withdrawal.
147
Q

What causes organic psychosis?

A

Medical hx important here.
Brain - head injury, CNS infection, tumour, TLE, post-epileptic states, vCJD
Metabolic - High/low Na, porphyria, uraemia.
Endocrine disturbance (hyper/hypothyroidism, Cushings, Addison’s disease)
Autoimmune - ‘lupus psychosis
Drugs - steroids, L-dopa, isoniazid, anti-ACh, antihypertensives, anticonvulsants, methylphenidate, and drugs of abuse
Toxins
[oxford]

148
Q

A teenage girl has BMI 17, loss of appetite, eats large quantities of food when she is not hungry then feels guilty and disgusted. She is terrified of gaining weight and thinks she is fat. What is the diagnosis?

A

BMI <17.5, bingeing –> Anorexia nervosa-binge-purge variant.
Anorexia: low body weight, intense fear of gaining weight, and body image disturbance.

149
Q

A young woman eats excessively without control, then goes for long runs every day and uses laxatives. Her BMI is 20. What is the diagnosis?

A

BMI >18.5, binges, has compensatory behaviour –> bulimia nervosa.

150
Q

A young woman presents because she eats very quickly and often alone in her room. She says she cannot control it and feels awful afterwards. Her BMI is 24. What is the diagnosis (and what would you ask about/)

A

Binge eating disorder - ask about compensatory behaviours eg vomiting, starvation, drugs, exercise. These are not present –> BED.

151
Q

Give 3 signs on examination of bulimia nervosa.

A

Russell’s sign - callouses on knuckles due to self induced vomiting.
Dental erosion
Parotid hypertrophy
Arrhythmia.

152
Q

Give 3 signs on examination of anorexia nervosa.

A

‘Cs and Gs’ raised:
Raised GH, glucose, salivary Glands
Raised Cortisol, Cholesterol and Carotinoids (yellow!!)

Everything else low:
Lanugo hair - soft baby hair eg on face.
Low body weight
Dry skin
Cracked nails
Hair loss (telogen effluvium)
Proximal muscle weakness
GI: constipation, red inflamed throat, angular stomatitis
CVS - arrhythmia (long QT, heart block), oedema of hands, feet and face
Hypothyroidism
153
Q

What is refeeding syndrome and why does it happen?

A

Potentially fatal shifts in fluids and electrolytes which occur in malnourised patients receiving rapid refeeding.
Starvation –> insulin decreases, glucagon increases. Decreased cellular phos, Mg, K, thiamine, same serum concentration.
Refeeding –> glucose and insulin increased, basal metabolism increases, K, phos and Mg move into intracellular space. Increased thiamine use, Na retention
–> this leads to low blood phos, Mg and K (Arrhythmias), Thiamine def (nystagmus),
Salt and water retention
GI disturbance, weakness, SOB, delirium, seizures

154
Q

What are the diagnostic criteria for typical anorexia nervosa?

A

Low body weight - 15% below expected or <17.5
Self induced wt loss
Body image distortion, dread of fatness
Endocrine - amenorrhea, reduced sexual interest
Delayed puberty if onset pre-pubertal.

155
Q

How is anorexia nervosa treated?

A

Structured eating plan + vitamins, thiamine, close monitoring of electrolytes.
SSRI
Therapy - family therapy, CBT-ED, MANTRA (cognitive interpersonal therapy for anorexia).
BMI
ECG
Bloods - FBC, ESR, U+E, glu, LFTs, TFTs (anorexia can cause hypothyroidism) cholesterol
DEXA for osteoporosis

156
Q

What is personality disorder and what are the main types?

A

Acquired ingrained personality traits, causing severe maladaptive patterns of behaviour, resulting in functional impairment in relationships or society.
Usually associated with childhood trauma.

Cluster A - weird - paranoid, schizoid, schizotypal.
Cluster B - wild - narcissistic, antisocial
Cluster C - worried

157
Q

What is paranoid personality disorder and how would it present?

A

Cluster A personality disorder.
Excessive sensitivity to setbacks, unforgiving, suspicious that others are trying to harm or deceive, misconstruing actions of others as hostile, suspicious partner is cheating on them, reluctant to confide in others.

158
Q

What is schizoid personality disorder and how does it present?

A

Cluster A personality disorder.
Withdrawn from social contact, likes to be alone, unaffectionate and can’t express feelings, little fulfilment from relationships or hobbies, emotionally cold with blunted affect.

159
Q

What is schizotypal personality disorder and how might it present?

A

Cluster A personality disorder. Odd beliefs, thinking and speech; eccentric, suspicious, social anxiety/avoidance. No first rank sx of schizoprenia.

160
Q

What is narcissistic personality disorder and how does it present?

A

Cluster B personality disorder.

Grandiose self-importance, preoccupied with beauty, lacks empathy and manipulates others, requires excessive admiration.

161
Q

What is antisocial personality disorder and how might it present?

A

Cluster B personality disorder.
Unlawful behaviour, impulsivity, irresponsible, disregard for safety, lack of remorse.
If under 18 - conduct disorder.

162
Q

What is histrionic personality disorder and how might it present?

A

Cluster B personality disorder.

Shallow, labile affect, dramatic, egocentric, inappropriate behaviour, uses appearance to draw attention, suggestible.

163
Q

What is emotionally unstable personality disorder and how does it present?

A 
(EUPD) - cluster B personality disorder.
Impulsive behaviour
Prone to conflict and angry outbursts
Unstable relationships
Feelings of emptiness or depression
Fear of abandonment
Impulsive type - prominent lack of impulse control.
Borderline type - self harm or impulsive suicide.
164
Q

What is anankastic personality disorder and how does it present?

A

Cluster C personality disorder aka OCPD.
Overly concerned with details, excessively devoted to work, unable to discard worthless objects, rigid and stubborn, perfectionism interferes with task completion, reluctant to delegate.

165
Q

What is anxious avoidance personality disorder and how does it present?

A

Cluster C personality disorder.
Feelings of tension and apprehension due to fear of ridicule,
Always want to be liked + accepted,
Avoids socialising for fear of criticism or rejection
Views self as socially inept, unappealing or inferior
Inhibited by feelings of inadequacy

166
Q

What is dependent personality disorder?

A

Cluster C personality disorder.
Reliance on others to make decisions, feelings of helplessness and incompetence when alone, goes to excessive lengths to obtain support from others, difficulty expressing disagreement, urgently seeks another relationship when one ends.

167
Q

How is the diagnosis of personality disorder made?

A

Minnesota Multiphasic Personality Inventory (MMPI)

Eysenk Personality Inventory and Personality Diagnostic Questionnaire.

168
Q

How is personality disorder managed/treated?

A 
Dialectic behavioural therapy (DBT)
CBT
Interpersonal therapy
Group psychotherapy
Mentalisation-based therapy (MBT)
169
Q

What is dependence?

A

Physical dependence: adaptations to chronic, regular use (tolerance); withdrawal symptoms.
Psychological dependence: behavioural adaptation
Compulsion to take/do something. Difficulty controlling behaviour; neglecting other activities, persisting despite harm.

170
Q

Describe the stages of change model for drug addiction.

A

Pre-contemplation - not recognised problem
Contemplation - recognises problem
Decision - decides to attempt change
Action - attempts change, with or without medical help
Maintenance - and attempting to improve areas of life harmed by drug use.
Relapse at any point - return to previous behaviour

171
Q

How is alcohol addiction diagnosed?

A

> 12 months alcohol use harmful to physical and/or mental health.
Screening: CAGE, AUDIT, FAST, MSASQ

172
Q

What is the CAGE-2 questionnaire?

A

C: Have you ever felt you should Cut back on your drinking?
A: Has anyone ever Annoyed you by criticising your drinking?
G: Have you ever felt Guilty about your drinking?
E: Have you ever had a drink early in the morning as an Eye-opener?

+:

  1. What is the most alcohol you have drunk in a single day?
  2. What is the most alcohol you have drunk in a single week?
173
Q

How do you calculate alcohol units?

How many alcohol units are in a 125ml glass of 11.5% wine?

A

1 unit = 8g of alcohol.
Units = volume (L) x % alcohol.
= 0.125L x11.5% = 1.4 units.
Remember a home measure is usually more than a pub measure!

174
Q

What is FRAMES?

A

A brief intervention for risky alcohol use that can be done within typical consultations.
Feedback of personal risks - ‘you have scored 16 on the audit which indicates…’
Responsibility - ‘its up to you…’
Advice - ‘i advise you to limit your drinking…’
Menu of strategies - setting personal drinking limits, alternating alcohol drinks with soft drinks, having regular alcohol-free days etc.
Empathy - therapeutic alliance. Not authoritarian or confrontational.
Self-efficacy - ‘many people successfully control their drinking or stop drinking all together. With the right support and information i’m confident that you will too’

175
Q

How is alcohol addiction treated?

A 
FRAMES in consultations
Mutual aid: AA, UK smart recovery
Detox: long acting bzd eg chlordiazepoxide, thiamine
Maintenance:
Acamprosate
Disulfiram
Naltrexone
176
Q

What are 3 acute complications of alcohol misuse?

A

Wernicke’s encephalopathy - reversible ophthalmoplegia, ataxia and decreased consciousness due to thiamine deficiency.
Korsakoff’s - less reversible amnesia, confabulation and apathy.
Delirium tremens - withdrawal of alcohol causing decreased GABA, which is an inhibitory neurotransmitter –> tremor, anxiety, vomiting, insomnia, seizures, hallucinations, confusion.

177
Q

How is Wernicke’s encephalopathy treated?

A 
Thiamine replacement (Pabrinex), magnesium, multivitamin.
Korsakoff's rx similar.
178
Q

How is delirium tremens treated?

A

High dose bdz eg oral chlordiazepoxide; IV Pabrinex (thiamine)

179
Q

What are 3 chronic complications of alcohol misuse?

A

CVS - htn, arrhythmia, CVA
Metabolic - lactic acidosis
GI - N+V, mallory-weiss tears, malnutrition
Haem: Folate def, impaired clotting
Neuro - seizures, peripheral neuropathy
Psychiatric - dependence, withdrawal, mood disorders, dementia
Endocrine: miscarriage, impotence, gonadal atrophy
Liver: alcoholic hepatitis, pancreatitis
Cancer: hepatic, lung, colorectal, pancreatic
….. etc etc etc!

180
Q

Give 5 examples of opioids.

A

Codeine, fentanyl, morphine, methadone, tramadol, buprenorphine, heroin

181
Q

Give 3 risk factors for opioid dependence.

A

Male, young, hx psych disorder and substance misuse, long-term opioid therapy.
5% of the UK are on opiates.

182
Q

A young man presents to ED with a resp rate of 10 and GCS of 13. He is nauseous and has vomited once. On examination his pupils are constricted (miosis). How would you treat him?

A

Opioid overdose.
Ask about how much/if they have taken, as well as other substances, IVDU.
Look for needle marks, abdo pain.
Mx: Naloxone +/- ventilation.

183
Q

What would make you consider opioid dependence in a patient presenting with pain?

A 
Drug seeking behaviour
Addiction severity index
Tolerance
Intoxication - miosis, shallow breathing
Needle marks
Constipation, wt loss
184
Q

What are the symptoms of opioid withdrawal?

A 
N+V
Dilated pupils
Insomnia
Sneezing/yawning
Abdominal cramps
Diarrhoea
Muscle spasms
Hot/cold flashes
Agitation
Sweating
Rhinorrhea
cold turkey - 'sheer hell'
controlled detox 'not pleasant but achievable'
185
Q

What is the DS-9?

A 
Urine/serum drug screen 9:
Opioids
Cocaine
Marjiuana
Benzos
PCP
Amphetamines
Barbiturates
186
Q

What is the treatment for opioid dependence?

A

Detoxification using:
buprenorphine - sublingual/injection
Methadone
Naltrexone

187
Q

What is the difference between coke and crack?

A 
Coke = white powder snorted/injected.
Crack = produced by alkalinization, which produces the hydrochloride-free ion form, smoked and behaves like IV coke.
188
Q

What are the immediate effects of cocaine?

A

Blocks dopamine reuptake –> pleasure, reinforcing

20 mins - euphoria, reduced hunger, restless, tachycardia, hypertension, sweating, dilated pupils.

189
Q

What are the effects of chronic cocaine use?

A 
Formication 'cocaine bugs' - tactile hallucination of something crawling under the skin
Aggression
Severe paranoia
Restlessness
Confusion
Pregnancy - fetal damage.
Necrosis of nasal septum

Withdrawal - dysphoria, anxiety/depression, irritability, fatigue, intense cravings.

190
Q

A young man is brought into the ED by his friend because he is agitated and sweating profusely. On examination his HR is 100, BP 145/100, and his pupils are dilated. What should you consider and how would you treat?

A

Cocaine overdose.
Bdzs for agitation, propofol, cooling.
Body-packers - laxatives, monitoring +/- benzos
Chronic: drug counselling, safe injection advice

191
Q

What are the components of cannabis and which is the psychoactive component?

A

THC and CBD. THC is psychoactive.

192
Q

What are the effects of cannabis use?

A

Euphoria, reduced anxiety, alteration in perception of time/colour/space, short term memory loss, food craving
Physical effects: dry mouth and dry bloodshot eyes, tachycardia
Can cause dependence but addiction is uncommon
Increased risk of schizophrenia, depression and airway damage.

193
Q

What is pathological gambling disorder and what are the diagnostic criteria?

A

Persistent and recurrent maladaptive patterns of gambling behaviour that may lead to significant personal, family and occupational difficulties.
Diagnostic criteria:
Pre-occupation with gambling
Needing to gamble with larger amounts of money
Unsuccessful attempts to stop
Restlessness when trying to stop
Gambling to escape from problems
Chasing losses
Lying about gambling
Committing illegal acts to finance gambling
Lost or jeopardised a significant relationship, job, career etc because of gambling
Relies on family or friends for money to relieve financial problems caused by gambling
The gambling behaviour is not better accounted for by a manic episode.

194
Q

When forming a biopsychosocial formulation of a patient’s case, what factors must be included?

A

Predisposing- vulnerability
Precipitating - triggers
Perpetuating - maintaining
Protective - strength

195
Q

What are neuroses?

A

Anxiety-related disorders. Common types:
1. Anxiety/phobic disorders eg panic disorder, GAD, ‘understandable’ phobias.
2. Stress-related disorders eg adjustment disorder, acute stress reactions and PTSD
3. OCD
Unusual: somatoform, conversion, dissociative, ‘non-understandable’ phobias.
Culture-specific: CFS, eating disorders

196
Q

What is panic disorder?

A

Recurrent panic attacks not secondary to substance misuse, medical conditions or another psychiatric disorder. Worry about attacks –> avoidance behaviour.

Panic attack = period of intense fear, symptoms that develop rapidly, reach a peak in 10 mins, rarely last over 1hr. Can be spontaneous or situational, nocturnal, and rarely non-fearful.

Symptoms: autonomic arousal –> sympathetic sx, hyperventilation syndrome in 50%. Concerns of death from cardiac or resp problems often leads to ED presentation. Can be any symptoms eg medically unexplained symptoms.

ICD-10:
Recurrent panic attacks that are not consistently associated with a specific situation or object, and often occur spontaneously. The panic attacks are not associated with marked exertion or with exposure to dangerous or life-threatening situations
B.) Characterized by ALL of:
Discrete episode of intense fear or discomfort
Starts abruptly
Reaches a crescendo within a few minutes and lasts at least some minutes
At least 1 symptom of autonomic arousal
Other symptoms of anxiety

197
Q

How is panic disorder treated?

A

Psychological: CBT
Pharmacological:
NICE 1st line: citalopram, escitalopram, paroxetine, sertraline. Start low, go slow.
Acute panic attack –> calm, will resolve within 30min usually. BDZs may be used at the start for immediate relief to reassure patient (they arent dying). Exclude medical causes!

198
Q

What is agoraphobia?

A

Anxiety and panic symptoms associated with places or situations where escape may be difficult or embarrassing, eg crowds, leaving to avoidance.
ICD-10:
A) marked and consistent fear in or avoidance of at least 2 of:
crowds
public spaces
travelling alone
travelling away from home
B) symptoms of anxiety in the feared sutuation
c) significant emotional distress due to the avoidance or anxiety symptoms
d) recognised as excessive or unreasonable
e) symptoms restricted to feared situation

199
Q

How is agoraphobia treated?

A

Psycho: exposure therapy, education
Pharma: citalopram, escitalopram, paroxetine, sertraline.

200
Q

What is the definition of a phobia and what are your differential disorders?

A

Recurring excessive and unreasonable psychological or autonomic symptoms of anxiety, in the (anticipated) presence of a specific feared object or situation.
Differential:
Panic disorder - fear of further attacks
Agoraphobia
Social phobia
OCD
Psychosis - fears tend to be overly excessive.

201
Q

How does memantine work and when is it indicated?

A

An NMDA receptor antagonist. Also serotonin receptor antagonist (anti-5ht) and dopamine receptor agonist (pro-dope).

Used 2nd line for alzheimers: moderate alzheimers where AChEIs CI or intolerant,
add-on to AChEI in moderate or severe Alzheimer’s,
Monotherapy in severe Alzheimers.
(NICE 2018)

202
Q

What is OCD and how do you differentiate is from psychosis?

A

> 2 weeks
Obsessions: Unwanted intrusive thoughts.
Compulsions: Acts to try and reduce obsessions.
Insight in OCD, no insight in psychosis.

203
Q

What is the diagnostic criteria for depression? (Hint: sigecaps)

A 
2 blue weeks
SIGECAPS symptoms:
Sleep
Interest
Guilt
Energy
Concentration
Appetite
Psychomotor retardation
Suicidality
CORE sx: low mood, low energy, low interest.
Mild = 2/3 core, 2 others
Moderate = 2/3 core, 4 others
Severe = 3/3 core, 5 other. = MDD.
(Antidepressants only 1st line if moderate-severe.)
204
Q

Give 3 poor prognostic indicators of schizophrenia.

A

antisocial/withdrawal prodrome, gradual onset, strong family history, low IQ, lack of obvious precipitant.
[passmed]

205
Q

What are the important interactions of SSRIs?

A 
SSRIs increase risk of GI BLEEDING
NSAIDs - avoid SSRIs or prescribe PPI.
Warfarin/heparin - consider mirtazapine instead
Triptans and MAOIs - serotonin syndrome
Pregnancy risks
Fluoxetine and paroxetine have higher propensity for drug interactions.
Hyponatremia
Weigh up benefits and risks.
[NICE, passmed]
206
Q

How is OCD treated?

A

1st line: Low intensity psychological therapy eg exposure and response prevention.

207
Q

If someone comes to GP with manic symptoms, how is this managed?

A

Hypomania –> routine referral to CMHT

Mania –> urgent referral to CMHT

208
Q

What is frontal lobe syndrome and how does it present?

A

Damage to prefrontal cortex for any reason eg trauma, CVA, infection, Pick’s disease (FTD).
Presentation: reduced spontaneous activity, attention, apathy, perseveration, disinhibition, loss of abstract thought.

209
Q

What could cause frontal lobe syndrome and how would you diagnose the cause?

A

B12 deficiency - check B12
Hyper/hypothyroidism - TFTs
Syphilis - serology
Tumour/infarction - MRI/CT

210
Q

How does ECT work and when is it indicated?

A

Induction of a 30-second tonic-clonic seizure under sedation, to enable brain remodelling and improve perfusion. 6-12 sessions, 2-3 per week, maintenance every 1-8 weeks.
Indications: Depression especially persistent or with psychosis, life threatening sx, medication CI, schizophrenia, bipolar mania phase, NMS.
Highly effective. Better when paired with medications even in pts who were treatment resistant. Raises seizure threshold –> used for some intractable seizures.

211
Q

What are the disadvantages of ECT?

A

Relative CI: raised ICP, SOL, recent MI, pregnancy, pacemakers. None of the CIs are absolute.
SE: reversible amnesia, tension headache, nausea, transient muscle pain., needs to be repeated.

212
Q

Give 3 risk factors for suicidal acts.

A

Completed suicide more common in males but attempts more common in females, adverse event, single/widow/divorces, social isolation, hx self harm/suicide attempts, illness (any but esp HIV), substance abuse, impulsive/aggressive personality (violent method), poor support/connections, abuse, previous suicidal behaviour and persistent suicidal ideas.
[oxford]

213
Q

Benzodiazapine:

a) mechanism of action
b) what are the indications
c) and contraindications?

A

How they work: enhance binding of GABA to GABA-A receptors, causing anxiolytic effect.

Indications:
Short term relief (2-4w) of anxiety that is severe, disabling, or causes patient unacceptable distress (inappropriate to use for short-term mild anxiety).
Given for insomnia only if severe, disabling, or causes patient extreme distress

CIs/risks:
Avoid in elderly
Withdrawal syndrome - may develop any time up to 3w after stopping long-acting benzodiazepine.
‘Paradoxical reaction’ in 1% of population - increased anxiety, disinhibition, hyperactivity and aggression. Similar reactions to other depressants eg alcohol, barbuturates.

214
Q

An elderly lady with dehydration says she does not want IV fluids. The last time she was in hospital she had a UTI and her blood was taken against her will because she was deemed not to have capacity. Would you give her the fluids?

A

Autonomy vs best interests.
Capacity:
Understands the information, can retain it long enough to make the decision, weigh up the options and communicate their decision.
Capacity is assumed until proven otherwise. It is assessed on a decision-by-decision basis so the previous event does not mean she doesn’t have capacity now.
Must be supported to make her own decisions including being given information in different ways - what is she worried about? If after all this she still refuses, don’t treat her because she has the right to make unwise decisions.
If she doesn’t have capacity, treatment must be in her best interests and the least restrictive option.

215
Q

What are the risks of SSRIs in pregnancy?

A

1st tri: small increased risk of congenital heart defects
3rd tri: persistent pulmonary htn of the newborn
Paroxetine has an increased risk of congenital malformations, particularly in the first trimester.
Not an absolute CI - weigh up risks and benefits.
[passmed/bnf]

216
Q

What is Charles-Bonnet syndrome?

A

Persistent or recurrent hallucinations (usually visual or auditory, particularly faces, children and wild animals), associated with eye disease in clear consciousness.

217
Q

Give 3 risk factors for Charles-Bonnet syndrome.

A 
Increasing age
Peripheral visual impairment
Social isolation
Sensory deprivation
Early cognitive impairment
(M=F)
218
Q

What is somatisation disorder?

A

multiple physical SYMPTOMS present for at least 2 years with no organic cause
patient refuses to accept reassurance or negative test results
[passmed]

219
Q

When stopping an SSRI, what do you need to consider?

A

SSRI discontinuation syndrome - gradually reduce over a 4 week period.
Fluoxetine has longest half life so can be stopped abruptly. Paroxetine has the shortest half life and therefore highest incidence of discontinuation symptoms.
Continue SSRIs for at least 6 months even if patient feels fine, to reduce risk of relapse.
[passmed]

220
Q

Give 5 symptoms/signs of SSRI discontinuation syndrome.

A

diarrhoea, vomiting, abdominal pain, difficulty sleeping, restlessness, mood change, unsteadiness, sweating, paresthesia

221
Q

What could cause dementia with personality changes and speech difficulty in someone under 65 years of age?

A

Pick’s disease/FTD - primary progressive aphasia variant.

3a (6 decks)

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