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Phase 3a > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

What is an illusion?

A

A misperception of real external stimuli eg hearing the wind as someone crying

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2
Q

What is a hallucination?

A

Perceptions occurring in the absence of an external physical stimulus (can be auditory, visual or olfactory)
Often seen in schizophrenia

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3
Q

What is an overvalued idea?

A

False/exaggerated belief sustained beyond logic or reason eg I am the cleverest person in the world

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4
Q

What is a delusion?

A

A false, unshakable idea which is out of keeping with the patient’s educational, cultural and social background, held with extraordinary conviction and certainty
It is a belief that is clearly false eg believing they’re being spied on

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5
Q

What is a delusional perception?

A

A true perception to which a patient attributes a false meaning. Eg traffic lights turning red indicates martians are about to land

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6
Q

What is thought alienation? What 4 thought disorders does it include?

A

The feeling that their own thoughts are no longer within their control
Includes thought insertion, withdrawal, broadcast, echo

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7
Q

What is thought insertion?

A

The experience that certain thoughts are being placed in one’s mind by others

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8
Q

What is thought withdrawal?

A

The experience that one’s thoughts are being removed by an outside person or force

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9
Q

What is thought broadcast?

A

The experience that one’s thoughts are accessible (can hear or are aware of) by others so that others know what one is thinking

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10
Q

What is thought echo?

A

The experience/hallucination of hearing aloud one’s thoughts just after one has thought them

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11
Q

What is thought block?

A

Flow of thoughts suddenly interrupted > complete blank/total emptying of mind, speech suddenly stops
Can happen in the absence of a condition or in schizophrenia

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12
Q

What is concrete thinking?

A

Literal thinking that is based on what one can see, hear, feel and experience here and now - actual objects and events and not concepts or generalisations

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13
Q

What is loosening of association?

A

A lack of logical association between succeeding thoughts, often leads to incoherent speech. It is impossible to follow the patient’s train of thought

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14
Q

What is circumstantiality?

A

Too much unnecessary detail before reaching the point, manifests in speech or writing
Often seen in anxiety

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15
Q

What is perserveration?

A

Certain thought very prominent in thinking space despite not having any relevance > leading to persistent repetition of words/themes/actions
Slows progression of thinking

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16
Q

What is confabulation? Seen in what patients?

A

Genuine gaps in the memory are filled with fabricated information without the conscious intent to do this
Seen in dementia patients/organic conditions

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17
Q

What is somatic passivity? What condition might it be seen in?

A

The delusional belief that one is a passive recipient of bodily sensations from an outside force
e.g. cause pain to them
= can have risk implications

Seen in schizophrenia

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18
Q

What is delirium?

A

An acute confusional state often with changes in consciousness.
It is a medical emergency but is often reversible.

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19
Q

What is catatonia/stupor? Give some examples.

A

Excited/inhibited motor activity in the absence of a mood disorder or neurological disease
Eg mutism, posturing, grimacing, catalepsy

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20
Q

What is psychomotor retardation? Seen commonly in which diseases?

A

Slowing of thoughts and movements.
In depression, Parkinson’s disease

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21
Q

What is flight of ideas?

A

Nearly continuous flow of thoughts with rapid changes in topic, often based on understandable associations, distracting stimuli or plays on words. Usually manifested in speech.

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22
Q

What is poverty of speech? Commonly seen in?

A

Lack of content and elaboration in speech due to poverty of thought
-ve symptoms of schizophrenia

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23
Q

What is poverty of thought?

A

Reduced spontaneity/productivity of thought, evidence by vague/simple speech full of meaningless repetitions or stereotyped phrases

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24
Q

What is pressure of speech?

A

Speech in which one feels undue pressure to get out. Usually rapid, loud, emphatic, difficult to interrupt. May talk without social stimulation and continue even though no one is listening.

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25
Q

What is anhedonia?

A

Inability to experience pleasure from normally pleasurable activities/experience emotion

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26
Q

What is affective expression?

A

Outward expression of feelings/emotions/mood eg facial expression, tone of voice, body language

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27
Q

What is flattening of affect?

A

Reduction/absence of affective expression eg subdued/detached reactions to situations

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28
Q

What is incongruity of affect?

A

Mismatch between experienced emotion and its affected expression leading to an inappropriate response eg having happy thoughts/looking happy when talking about a sad event

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29
Q

What is blunting of affect?

A

A severe reduction in the expressive range and intensity of affect, but less than is observed in Flat affect eg diminished facial expression or gestures in reaction to emotion provoking stimuli

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30
Q

What is belle indifference?

A

Absence of psychological distress despite having a serious illness/set of symptoms
Associated with conversion disorder

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31
Q

What is depersonalisation?

A

Experiencing the self as strange/unreal or feeling detached from one’s thoughts, feelings, sensations, body or actions, as if one were an outside observer

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32
Q

What is derealisation?

A

Experiencing other people/objects/the world as strange/unreal eg dreamy, distant, foggy or detached from one’s surroundings

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33
Q

What is dissociation?

A

Disconnection from thoughts, feeling, memories, sense of identity

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34
Q

What is stereotypy/mannerism? For example?

A

Persistent repetition of a movement/sounds, for no obvious reason eg rocking, crossing legs

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35
Q

What is obsession? Associated with?

A

Repetitive, persistent and irrational thoughts, images and urges that are experienced as intrusive/unwanted
Associated with anxiety

Responsible for these thoughts - know they are irrational but can’t stop them

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36
Q

What is compulsion?

A

Repetitive behaviours/rituals/mental acts that the individual feel driven to perform in response to an obsession/according to rigid rules/to achieve sense of completeness

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37
Q

What is the difference between mood and affect?

A

mood = subjective, how the pt describes their current mood

affect = objective, what the dr observes e.g. how they convey emotion/non-verbal cues

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38
Q

What is the term for a good/normal mood?

A

euthymic

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39
Q

Give 2 examples of incongruent affect and what they are indicative of

A

Flat affect = eg talks about something enjoyable whilst remaining subdued/flat, indicative of depression
Elevated affect - indicative of mania

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40
Q

What is thought stream? What thought streams should be looked out for in the MSE? What are they indicative of?

A

abnormality of amount and speed of thought

e.g. pressure/poverty of speech, thought block

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41
Q

What is thought form? What thought forms should be looked out for in the MSE? What are they indicative of?

A

description of the organisation of someone’s thinking

e.g. flight of ideas, perseveration, loosening of associations

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42
Q

What is normal thought form referred to as?

A

no formal thought disorder = NFTD

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43
Q

Give some examples of different delusions?

A

grandiose - exaggerated self importance, power or influence

delusions of reference - objects, events or people have special significance eg comment on the TV is directed at them

persecutory delusion - belief that they are being watched and organisations/people are trying to harm them

delusions of control - beliefs that actions, impulses and thoughts are controlled by an outside agency

infidelity, love (convinced someone they’ve never met is in love with them), guilt (believes they are bad/evil person), nihilistic (pt denies existence of their body e.g. heart is missing), poverty (believes they are poor)
> often mood congruent/environmental

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44
Q

What is perception?

A

awareness of external sensory stimuli via the senses

hallucinations, dissociative sx, illusions

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45
Q

What does a 2nd person hallucination indicate compared to a 3rd person?

A

2nd > affective psychosis, personality disorder
3rd > paranoid schizophrenia

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46
Q

What can visual hallucinations be indicative of?

A

more common in acute organic psych disorders with clouding of consciousness e.g. brain dysfunction, epilepsy, migraine, tumour, delirium, dementia
= MUST rule out organic

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47
Q

What is a functional hallucination?

A

auditory stimulus causes a hallucination

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48
Q

What is a reflex hallucination?

A

stimulus in one sensory modality produces sensory experience in another

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49
Q

What is an extracampine hallucination?

A

outside the limits of the sensory field e.g. hears voices talking in Paris when in Sydney

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50
Q

What is a hypnagogic/hypnapompic hallucination?

A

occurs when subject is falling asleep/waking up respectively

= usually a normal experience, not always mental illness

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51
Q

What is the difference between a primary and secondary delusions?

A

primary: appears suddenly without any mental events leading up to it, very indicative of schizophrenia

secondary: arises from previous abnormal idea/experience eg persecutory delusions

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52
Q

What is dissociative amnesia?

A

sudden amnesia occurring during periods of extreme trauma, can last for hrs/days

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53
Q

What is apathy?

A

lack of interest, enthusiasm, concern etc

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54
Q

What is conversion disorder?

A

Physical sx without physical cause
eg paralysis, blindness that cannot be explained by medical evaluation

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55
Q

Define this type of catatonia:
waxy flexibility

A

pt’s limbs feel like wax/lead pipe when moved, remain in the position they are left in (rare in schizophrenia/structural brain disease)

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56
Q

Define this type of catatonia:
echolalia

A

automatic repetition of words heard

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57
Q

Define this type of catatonia:
echopraxia

A

automatic repetition by the pt of movements made by examiner

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58
Q

Define this type of catatonia:
logoclonia

A

repetition of last syllable of a word

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59
Q

Define this type of catatonia:
negativism

A

motiveless resistance to movement

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60
Q

Define this type of catatonia:
palilalia

A

repetition of a word over and again with increasing frequency

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61
Q

Define this type of catatonia:
verbigeration

A

repetition of one/several sentences/strings/strings of fragmented words, often in a monotonous tone

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62
Q

What are the 3 core sx of depression?

A

low mood
loss of energy (anergia)
loss of pleasure/interest in doing things (anhedonia)

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63
Q

What are the other sx of depression?

A

Ask about a CHANGE in these sx
BIOLOGICAL:
change in sleep (EMW at least 2hrs before normal time = characteristic)
change in appetite (none/low)
change in libido
diurnal mood variation
agitation/edgy/anxious

COGNITIVE:
loss of concentration
guilt (past)
loss of confidence (present)
hopelessness (future)
suicidal ideation

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64
Q

How many core/other sx do you need for a diagnosis of depression?

A

at least 2 core sx
and a combo of other sx

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65
Q

How many core/other sx do you need for a diagnosis of mild depression?

A

core sx + 2-3 others

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66
Q

How many core/other sx do you need for a diagnosis of moderate depression?

A

core + 4 others + functioning affected

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67
Q

How many core/other sx do you need for a diagnosis of severe depression?

A

majority of core + other sx
suicidal ideation
marked loss of functioning
+/- psychotic sx e.g. nihilistic or guilty delusions, derogatory voices

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68
Q

What is the difference between bipolar I and II?

A

I: both mania and depression, usually equally, sometimes only mania
II: more episodes of depression, only mild hypo mania = easily missed

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69
Q

What question is important to ask to distinguish between depression and bipolar II?

A

previous manic episodes in past psych hx

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70
Q

What is cyclothymia?

A

bi-polar like
numerous periods of depression + hypomania but not severe enough to be bipolar

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71
Q

How long does a hypomanic and manic episode need to be, to be diagnostic?

A

hypomania: <1wk
mania: > 1wk

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72
Q

What are the first rank sx of schizophrenia?

A

thought alienation
passivity phenomena
3rd person auditory hallucinations
delusional perception

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73
Q

What are the secondary sx of schizophrenia?

A

delusions
2nd person auditory hallucinations
hallucinations in any other modality
thought disorder
catatonic behaviour
negative sx

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74
Q

What are the +ve sc of schizophrenia? What are +ve sx?

A

extra to the normal experience

hallucinations
delusions
passivity phenomena
thought alienation
lack of insight
disturbance in mood

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75
Q

What are the -ve sc of schizophrenia? What are -ve sx?

A

taking away from them as a person

blunting of affect
amotivation
poverty of speech/thought
poor non-verbal communication
clear deterioration in functioning
self neglect
lack of insight

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76
Q

When are +ve vs -ve likely to present in the course of a pt’s schizophrenia?

A

tend to start off in teens/20s with +ve sx
progress into a more -ve state with more episodes
elderly usually present with much more -ve picture

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77
Q

What is generalised anxiety disorder?

A

feeling anxious all the time
constant, >6mo

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78
Q

Describe some sx of GAD?

A

disturbed sleep (initial insomnia rather than EMW like in depression)
muscle tension
irritability
poor concentration, tired

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79
Q

What is panic disorder?

A

acute episodes of anxiety

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80
Q

Describe the physical sx of panic disorder?

A

Palpitations
Chest pain
Tachypnoea
Dry mouth
Urgency of micturition
Dizziness
Blurred visions
Paresthesia

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81
Q

Describe the psychological sx of panic disorder?

A

Feeling of impending doom
Fear of dying - often present to GP/A&E, convinced it is physical eg heart attack
Fear of losing control
Depersonalisation
Derealisation

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82
Q

Define OCD?

A

repetitive and irrational obsessive thoughts/images (often unpleasant e.g. death/sexual/blasphemous) + compulsive acts

can have one or the other but most have both

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83
Q

What is the difference between an obsessive thought in OCD and a delusion?

A

Pts with obsessive thoughts recognise that they are their own thoughts - know they are wrong/irrational but can’t stop them

Whereas a delusion - pt’s don’t know it’s their own thoughts/that it’s not real

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84
Q

What conditions are not including as a reason to be detained in the MHA?

A

alcohol/drug misuse

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85
Q

What is the purpose of section 2 of the MHA?

A

ASSESSMENT - treatment can be given without consent if part of assessment

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86
Q

What doctors are needed to issue a section 2 and 3?

A

2 drs (1 S12 approved, one any registered medical practitioner) + 1 AMHP

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87
Q

What is the duration of a section 2 of the MHA?

A

28 days max, can be stopped before then but not renewed

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88
Q

What is the purpose of section 3 of the MHA?

A

Treatment

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89
Q

What is the duration of a section 3 of the MHA?

A

6 months
can be renewed indefinitely but usually 6mo-1yr

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90
Q

What evidence is required for a section 3?

A

(a)The patient is suffering from mental disorder of a nature (clear diagnosis usually) or degree which makes it appropriate for the patient to receive medical treatment in a hospital

b) The treatment is in the interests of his or her health and safety and the protection of others; and

c) Appropriate treatment must be available for the patient (at the hospital they are going to)

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91
Q

What evidence is required for a section 2?

A

a) The patient is suffering from a mental disorder (doesn’t need to be a diagnosis, just evidence of sx) that warrants detention in hospital for assessment; AND -

b) The patient ought to be detained for his or her own health or safety, or the protection of others

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92
Q

What is the purpose of section 4 of the MHA?

A

Emergency order - only an urgent necessity when waiting for a 2nd dr would lead to undesirable delay
(to temporarily hold someone)

Cannot be coercively treated

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93
Q

What is the duration of a section 4 of the MHA?

A

72 hrs

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94
Q

Who is needed to issue a section 4?

A

1 dr + 1 AMHP

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95
Q

What evidence is required for a section 4?

A

a) The patient is suffering from a mental disorder (not a diagnosis) of a nature or degree that warrants detention in hospital for assessment; and

b) The patient ought to be detained for his or her own health or safety, or the protection of others

c) There is not enough time for 2nd doctor to attend - there is immediate risk

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96
Q

What is a section 5(4)? Where can they happen?
Who can issue them? How long can they last?

A

for a pt already admitted but wanting to leave (not including a&e = community)

nurses’s holding power until dr can attend > for up to 6hrs
cannot be coercively treated

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97
Q

What is a section 5(2)? Where can they happen?
Who can issue them? How long can they last?

A

For a pt already admitted but wanting to leave (not a&e)

Dr’s holding power > up to 72hrs
Allows time for S2/S3 assessment/discharge
Cannot be coercively treated

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98
Q

What is the difference between a section 135 and 136? What evidence is needed? Where do they happen?

A

police sections
needs evidence of a mental disorder + needs to be considered a danger to themselves/others
often required in A&E

S136 - person suspected of having mental disorder in a public place e.g. bridge
S135 - needs court order to access pt’s home and remove them to a place of safety (psych unit/police cell) > further assessment needs an S2/3

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99
Q

Describe dementia?

A

chronic decline in higher cortical function for at least 6m

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100
Q

Describe the cognitive sx of Alzheimer’s? What is their onset like?

A

4A’s:
Amnesia (short-term memory loss, disorientation around time, long-term usually in tact)
Aphasia/dysphasia (later, receptive and expressive loss)
Apraxia/dyspraxia (button clothes, cutlery etc)
Agnosia (unable to recognise body parts/objects)

Executive function e.g. finance, cooking
Dyslexia, dysgraphia, acalculia
Insidious onset

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101
Q

Describe the non-cognitive sx of Alzheimer’s?

A

psychosis e.g. delusions, hallucinations
mood - anxiety, depression
behavioural - apathy, agitation, wandering, aggression
misidentification - can’t recognise loved ones

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102
Q

What are the key risk factors for Alzheimer’s?

A

old age
female (live longer)

linked to gene defect e.g. APO E4
FHx
CVD risk factors - HTN, diabetes, smoking, hypercholesterolaemia
Downs syndrome (present much earlier, 30/40s, most develop it by 50)

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103
Q

What are some protective factors for Alzheimer’s?

A

APO E2
high intelligence/education
oestrogen/anti-inflammatory medication possibly

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104
Q

What are the key sx of Lewy body dementia? How does it progress?

A

REM sleep disorder - commonly 1st sx

visual hallucinations
fluctuating cognition/consciousness
parkinsonian sx (motor sx) eg tremor, stooped gait
autonomic dysfunction
frequent falls

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105
Q

How can lewy body dementia and Parkinson’s be distinguished?

A
  • parkinson’s = motor sx 1st, memory problems once disease is established
  • LBD = memory sx first/at same time, more sensitive to neuroleptic medication (antipsychotics)

essentially the same pathology

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106
Q

How does frontotemporal dementia present?

A

insidious onset, poor insight
amnesia not as bad as Alzheimer’s, comes later

Frontal sx:
personality change/social and interpersonal conduct/behavioural sx e.g. aggression
euphoria/disinhibition
emotional blunting

Temporal sx:
speech disturbances
expressive dysphasia

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107
Q

What is the onset of FTD, usually? What is the prognosis like?

A

early onset
poor prognosis

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108
Q

How does vascular dementia present?

A

patchier cognitive impairment than Alzheimer’s > slowed thinking, reasoning and info processing
focal neurological signs if caused by CVA
emotional lability
can have psychotic sx e.g. delusions
memory problems

stepwise deterioration
hx of stroke/microbleed/TIA

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109
Q

In what pattern does vascular dementia progress?

A

stepwise - period of stability before acute decline

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110
Q

How is cognitive decline investigated?

A

clinical + collateral history

check for reversible causes, incl full physical exam -(anaemia, thyroid, B12, hyponatraemia, alcohol)

memory screening tool e.g. 6CIT/DiADeM in care homes
then Addenbrookes for more detail (<82 is abnormal, in at least 2 domains)

CT scan > rule out bleeds, strokes, tumours, NPH, see shrinkage (FTD)/blood vessel damage (vascular)

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111
Q

How does normal pressure hydrocephalus (NPH) present? Causes?

A

Triad: ataxia + dementia + urinary incontinence
abnormal gait

but is a key REVERSIBLE cause of dementia

causes: idiopathic, SAH, head trauma, meningitis
treat: ventriculoperitoneal shunt

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112
Q

How is Alzheimer’s dementia managed pharmacologically?

A

AChE inhibitors (increase level of ACh) e.g. donepezil = 1st line, rivastigmine, galantamine
Memantine (glutamate/NMDA antagonist ) > when pt presents in mod-severe stages/if AChE not tolerated

Treat underlying cause/comorbidities
SSRIs, antipsychotics, sleeping tablets, short acting benzos e.g. lorazepam where needed

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113
Q

What is the only antipsychotic licensed to treat dementia? Why?

A

risperidone
risk of stroke

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114
Q

How is dementia managed non-pharmacologically?

A

risk/needs assessment > care plan
carers assessment - things needed to support carer
OT assessment > environmental adaptation e.g. alarms on doors/tracking device, physio if necessary
social activity
other therapies e.g. music, snoezelen (sensory stimulation room), art, CST

consider capacity/advance care planning

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115
Q

What type of anaemia can present with memory loss?

A

Any anaemia can present with low mood/poor concentration which may manifest like dementia

B12 deficiency > memory loss = rule out

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116
Q

How does delirium present?

A

acute confusional state, quick onset
abrupt global impairment of cognitive processes > confusion, disorientation, agitation
attention difficulties
fluctuating consciousness
hallucinations
disinhibition
labile mood
worse at night (sundowning)
evidence it may be related to a physical cause

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117
Q

Describe the 4 features of confusion assessment method (CAM)? Which ones are needed for a diagnosis of delirium?

A

1 and 2 + either 3 or 4

  1. acute and fluctuating course
  2. inattention
  3. disorganised thinking
  4. altered level of consciousness
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118
Q

What are the important differentials for delirium?

A

delirium tremens in an alcohol dependants pt, especially post-op

others are: anaphylactic reactions, dementia, head injury

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119
Q

What medications can cause delirium?

A

anticholinergics
Parkinson’s medication
benzos
steroids

drug accumulation (elderly, poor kidney/liver function)
polypharmacy
post-surgery - anaesthetics, analgesics, blood loss

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120
Q

What is the management for delirium?

A

identify cause + treat
nutrition and hydration
support + behavioural management first

medications: haloperidol (1st line), benzos (avoid if possible)
long acting benzos if withdrawing from alcohol/drugs

may lack capacity - can treat under MCA

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121
Q

Delirium vs dementia:
deterioration time
course
consciousness
thought content
hallucinations

A

DELIRIUM:
rapid + usually reversible if underlying cause treated
fluctuating course
clouded consciousness/attention disorganised
vivid/complex thought content
hallucinations common, usually visual

DEMENTIA:
slow + irreversible deterioration
slowly progressive course
alert/attention often intact
impoverished thought content
hallucinations only in a 1/3rd, can be auditory/visual

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122
Q

When does mild cognitive impairment become dementia?

A

Dementia diagnosis requires - 6mo hx of cognitive decline with associated loss of functioning
often complex tasks get lost first e.g. finances, navigation

MCI little/no functional decline alongside memory loss

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123
Q

When can vascular dementia present like Alzheimer’s?

A

if there is an infarct in the temporal lobe

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124
Q

Why can donepezil sometimes be difficult to give to dementia pts? What can be given instead?

A

oral tablet - sometimes difficult to take
rivastigmine comes as a patch

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125
Q

What are the side effects of AChEs? What pts should we be careful of giving donepezil to?

What other medication might need to be reduced if a pt is put on donepezil?

A

bradycardia
postural drop
> risk of falls
GI upset

Careful with pts with a hx of falls/cardiac problems
If on beta blockers, reduce if possible

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126
Q

What is the DMS IV/V description of emotionally unstable personality disorder (EUPD)?

A

enduring pattern of inner experience and behaviour
deviates from cultural expectations
pervasive and inflexible (struggle to change the way they behave)
onset adolescence/early adult
stable over time
leads to distress
impairments in self and interpersonal functioning

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127
Q

What are the cluster A personality disorders?

A

‘odd/eccentric’ = MAD
schizoid
paranoid
schizotypal

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128
Q

What are the cluster B personality disorders?

A

‘dramatic/erratic’ = BAD
EUPD
histrionic
narcissistic
dissocial/antisocial

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129
Q

What are the cluster C personality disorders?

A

‘anxious/fearful’ = SAD
Anankastic (obsessive compulsive)
dependant
avoidant

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130
Q

What are the clinical features of EUPD?

A
  • unstable mood - fluctuates/intense/overwhelmed by emotions they can’t tolerate (RISK)
  • impulsivity (RISK - disordered eating, substance misuse, sexual behaviours etc)
  • intense unstable relationships
  • fear of/attempts to avoid abandonment
  • chronic feelings of emptiness
  • thoughts of self harm/suicide (can be habitual)
  • uncertainty of self image/identity/aims/preferences, lack of sense of who they are
  • may experience psychotic sx e.g. paranoia, derogatory/commands hallucinations
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131
Q

What are the risk factors for EUPD ?

A

attachment theory: unresponsive parenting/adverse childhood
childhood trauma e.g. sexual abuse
adverse events during pregnancy/birth/neonatal period

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132
Q

What are the differential diagnoses for EUPD?

A

bipolar affective disorder (more episodic mood changes with stability in between, presence of bio sx e.g. appetite/sleep change)

neurodevelopmental disorders (autism, ADHD - emotional fluctuation, poor attention)

psychosis (hallucinations more likely to be 3rd person/running commentary, in EUPD > internal dialogue about themselves, identify with the criticism + lack of other psychotic features e.g. delusions)

complex PTSD > overlap with hx of trauma, flashbacks, autonomic arousal with emotional dysregulation, poor impulse control, self harm/suicidal feelings

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133
Q

What comorbidities are likely to occur with EUPD?

A

psychosis
affective/anxiety disorders
alcohol/substance dependance
eating disorders
functional disorders e.g. chronic pain, non-epileptic seizures

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134
Q

Name some infectious causes of delirium?

A

UTI - very common in elderly
pneumonia
septicaemia

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135
Q

Name some toxic causes of delirium?

A

substance misuse
intoxication withdrawal e.g. delirium tremens
opioids

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136
Q

Name some vascular causes of delirium?

A

CVA (stroke)
haemorrhage
head trauma

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137
Q

Name some metabolic causes of delirium?

A

hyper/hypothyroidism
hyper/hypoglycaemia
hypoxia
hypercortisolaemia

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138
Q

Name some nutritional causes for delirium?

A

thiamine (b1) deficiency
B12/folate deficiency
dehydration

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139
Q

What people are at high risk and there should be screened for delirium on hospital admission?

A

> 65 yrs
have diffuse brain disease e.g. dementia, PD
hip fracture pts
severely ill
post-op

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140
Q

What tool is used to screen for delirium?

A

4 AT assessment

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141
Q

What are the 2 subtypes of delirium?

A
  1. hypoactive - withdrawn, sleepy, less likely to be recognised
  2. hypERactive - restless, agitated, aggressive
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142
Q

How is delirium investigated?

A

look for underlying cause:
bloods
urinalysis
full physical exam e.g. hip exam for fracture
CXR if indicated
CT head if worried about CVA/head trauma

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143
Q

Which dementia presents a lot like delirium and can be easy to miss?

A

LBD
> visual hallucinations, confusion, course can fluctuate

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144
Q

What is the difference between cortical and subcortical dementia? Name some examples of each.

A

cortical dementias - affect the cerebral cortex
e.g. Alzheimer’s, LBD, frontotemporal dementia

subcortical dementias - affect the basal ganglia and the thalamus
e.g. PD dementia, Huntington’s disease dementia, LBD, alcohol related dementia, AIDS dementia

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145
Q

What are the typical symptoms of cortical dementia?

A

Memory impairment
Dysphasia – language deficit
Visuospatial impairment (apraxia)
Problem solving and reasoning deficit

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146
Q

What are the typical symptoms of subcortical dementia?

A

Pscyhomotor slowing
Impaired memory retrieval
Depression
Apathy
Execustive dysfunction
Personality change
Language preserved- unlike in cortical

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147
Q

Describe the macroscopic pathological changes that occur in Alzheimer’s, seen on CT?

A

Shrunken brain (diffuse cerebral atrophy)
Increased sulcal widening
Enlarged ventricles

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148
Q

Define Alzheimer’s?

A

insidious onset of dementia due to generalised deterioration of the brain
most common type of dementia

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149
Q

Describe the microscopic pathological changes in Alzheimer’s disease?

A

Neuronal loss
Neurofibrillary tangles
Amyloid plaques

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150
Q

Which neurotransmitters are affected in Alzheimer’s?

A

Acetylcholine
Noradrenaline
Serotonin
Somatostatin

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151
Q

When does Alzheimer’s usually present? When is it defined as early onset?

A

> 65

<65 is early onset > more rapid decline, FHx

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152
Q

What are the domains tested in the Addenbrooke’s cognitive assessment?

A

Attention/orientation
Memory
Language
Visuospatial
Fluency

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153
Q

What are the RFs for vascular dementia?

A

HTN, smoking, diabetes, hypercholesterolaemia
Hx of PVD, IHD
AF

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154
Q

What would be seen on a CT head in someone with VD?

A

At least one area of cortical infarction – shows up white on CT

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155
Q

How is vascular dementia managed?

A

Not reversible, prevent further decline by modifying RF:
statins, anti-hypertensives, aspirin
treat diabetes, smoking cessation, lifestyle changes

no role for AChEi

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156
Q

What is the pathological feature found in the brain of someone with LBD?

A

presence of Lewy bodies (protein deposits) in the basal ganglia and cerebral cortex

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157
Q

When does LBD usually present?

A

50-80yrs

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158
Q

What is the onset/progression of LBD like?

A

fluctuating onset/progression, rapid decline - more than other dementias

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159
Q

How is LBD treated?

A

1st line = rivastigmine/donepezil

supportive/palliative/emotional guidance
OT assessment
advance directives

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160
Q

What medication must be avoided in the treatment of LBD? Why?

A

AVOID antipsychotics
can make it much worse
> may lead to neuroleptic malignant syndrome

Quetiapine if no cognitive decline
Clozapine 2nd line

Delirium with LBD > PO lorazepam first

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161
Q

What are the microscopic pathological features in frontotemporal dementia?

A

ubiquitin and tau deposits

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162
Q

How is FTD treated?

A

no specific treatment
SSRIs may help behavioural sx
OT assessment
advance directives?

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163
Q

What are the behavioural and psychological sx (BPSD) of dementia?

A
  1. anxiety
  2. depression
  3. agitation
  4. psychosis
  5. disinhibition
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164
Q

What are the treatable causes of BPSD?

A

PINCH ME
Pain
Infection
Nutrition
Constipation - check stool chart
Hydration

Medication (polypharm, codeine)
Environment (noisy hospital ward)

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165
Q

What is Creutzfeltd-Jacob disease?

A

abnormal infectious protein in brain (prion) > spongiform encephalopathy
causes rapidly fatal dementia
+ death within a yr
myoclonic jerks + extra-pyramidal signs seen

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166
Q

What is attachment theory?

A

The ideas that caregivers who are responsive to an infant’s needs allow the child to develop a sense of security

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167
Q

What are the 4 types of attachment in infant’s? How might this relate to their mental health as an adult?

A

secure
ambivalent
avoidant
disorganised

secure > should develop into an adult that can cope with the world
insecure > more likely to have mental health conditions/personality disorders

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168
Q

What is anankastic personality disorder?

A

usually high functioning and only becomes a problem when they hit a hurdle

much less debilitating than OCD
perfectionist behaviour without the same compulsions as OCD

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169
Q

What can anankastic personality disorder develop into?

A

can develop anxiety, sometimes OCD

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170
Q

How do you investigate someone who you think may have a personality disorder?

A

needs to be assessed more than once
collateral hx
MSE
risk assessment
treat comorbid psych conditions before diagnosis is made

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171
Q

How are personality disorders managed?

A

medications - mood stabilisers, sedatives during crises
psychological therapies e.g. cbt/dbt/cat/mbt
continuity of care very important
engage with services, structure, help with housing/other social matters

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172
Q

What is the gold standard treatment for EUPD?

A

DBT - dialectical behavioural therapy
group therapy with individual support

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173
Q

When is medication indicated in EUPD?

A

never to treat the PD
only for comorbid sx e.g. depression

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174
Q

Define schizophrenia?

A

Splitting/dissociation of thoughts or loss of contact with reality

Affects a person’s thoughts, perceptions/senses, personality, speech, power over their will/sense of self

175
Q

What is the difference between psychosis and neurosis?

A

Psychosis = severe mental disturbance characterised by a loss of contact with external reality (e.g. schizophrenia, delusional disorders)

Neurosis = relatively mild mental illness in which there is no loss of connection with reality (e.g. depression, anxiety)

176
Q

What is thought to cause schizophrenia?

A

Thought that some pts have a susceptibility and emotional life experiences can act as a trigger

Seems to involve dopamine excess? Antipsychotics aka dopamine blockers treat it

177
Q

Describe the onset of schizophrenia?

A

diagnosed between 15-35
slightly earlier in men
smaller peak incidence in late middle age

178
Q

What are the RFs for schizophrenia?

A

FHx
drug abuse particularly cannabis in adolescence
insult to brain development in early life - trauma, epilepsy, developmental delay, perinatal infection
stressful/adverse life experiences/physical or sexual abuse/bullying
Socioeconomic deprivation

179
Q

What are the 6 types of schizophrenia? Which is the most common?

A

paranoid (most common) - paranoid delusions + auditory hallucinations

Hebephrenic - mood changes, unpredictable behaviour, shallow affect, fragmentary hallucinations (in adolescents, por outlook as -ve sx develop rapidly)

Catatonic - psychomotor features eg posturing, rigidity, stupor

Undifferentiated - sx don’t fit into another category

Residual - -ve sx, occurs when +ve sx have burnt out

Simple - -ve sx like hebephrenic + pts have NEVER experienced +ve sx

180
Q

What combination of 1st and 2ndary sx of schizophrenia are needed for a diagnosis?

A

1+ 1st rank sx
OR 2+ 2ndary sx
For at least 1 mo

with no other cause for psychosis e.g. drug intoxication/withdrawal/brain disease or extensive depressive/manic sx

181
Q

What kind of delusions are pts with schizophrenia likely to have?

A

persecutory
delusions of reference

182
Q

How is schizophrenia investigated?

A

Rule out other causes of confusion/psychosis
- Urine culture (UTI > delirium), drug screen
- CT scan if organic neuro cause suspected
- Full physical exam
- FBC, TFTs, U&Es, LFTs, CRP, fasting glucose > tumours, cysts, PD, HD, brain injury, systemic infection
HIV/syphilis if required
Check lipids before starting antipsychotics

Collateral hx if possible
MSE
Risk assessment

183
Q

How is schizophrenia treated?

A

Typical antipsychotics: D2 receptor antagonists eg haloperidol, chlorpromazine

Or an atypical antipsychotic (more selective, also block serotonin 5 HT2 receptors) eg quetiapine, olanzapine
Aripiprazole = partial dopamine agonist and less likely to cause SEs

Clozapine used if typical and atypical antipsychotics haven’t worked

CBT, family therapy

184
Q

Which outpatient psych teams are usually involved in the care of a pt with schizophrenia?

A

Early intervention team (initial referral)
Community mental health team (day to day support/treatment)
Crisis resolution team (acute psychotic episodes)

185
Q

Delirium can last up to how long after the physical cause is removed?

A

6 weeks

186
Q

What is cotard’s syndrome?

A

severe type of depression
delusional belief that they’re bodily functions aren’t working/organs are missing/they are dead

can lead to dangerous behaviours e.g. not eating

187
Q

What tests make up a confusion screen? What are they looking for?

A

FBC, U&Es, LFTs, coagulation, TFTs, Ca2+, B12 + folate, glucose, blood cultures
Alcohol/substance misuse

CT head
Urinalysis
CXR

188
Q

What effect can SSRIs have on mania?

A

can make manic sx worse > manic reaction
bipolar/mania shouldn’t be treated with ADs alone, need mood stabilisers too

189
Q

What are the key risk factors for suicide?

A

male
peaks in young men and in middle aged

unemployment/stressful job
living alone/isolation
divorcees/being single
homelessness

previous psych hx
lack of engagement or barriers to accessing MH services
previous self harm/type of self harm/regret shown
alcohol/drug misuse
fhx

190
Q

Where does shrinkage occur on a CT scan in Alzheimer’s?

A

hippocampus
atrophy in temporal lobe next to the tips of the temporal horns > widening of the temporal horns (usually under 3mm)

191
Q

How long should ADs be continued for after sx stop?

A

at least 6 months

192
Q

What are some of the disadvantages of antidepressants?

A

can take a while to work - some people stop taking them thinking it’s not wokring

can increase suicidal thoughts/make things worse initially

improves some sx of depression but not others

193
Q

What are some medical causes for depression?

A

hypothyroidism
chronic disease
post-natal
medications e.g. isotretinoin (roaccutane) for acne, beta blockers

194
Q

What are some risk factors for depression?

A

Fhx
Hx of abuse
Drug/alcohol misuse
Low socioeconomic status
Chronic disease
Traumatic life event

195
Q

What are some differentials for depression?

A

Normal sadness eg after bereavement
Schizophrenia - flat affect of schiz may present like depression, won’t have other core sx of depression
Hypothyroidism
Alcohol/drug withdrawal

196
Q

What kind of time course does depression usually follow?

A

relapsing/remitting

197
Q

How long must sx be present for a diagnosis of depression?

A

2 weeks

198
Q

What are the 3 core sx of depression?

A

low mood
loss of energy (anergia)
loss of pleasure in doing things (anhedonia)

199
Q

What are the other sx of depression? (biological and cognitive)

A

Biological:
change in sleep (EMW - at least 2 hrs before normal time or sleeping more)
change in appetite - usually eating less/losing weight
change in libido
diurnal mood variation
agitation/edgy/anxious

Cognitive:
guilt (PAST)
loss of confidence (PRESENT)
hopelessness (FUTURE)
suicidal ideation

200
Q

What signs might you see in an MSE of a depressed person?

A

Weight loss due to reduced appetite
Psychomotor retardation seen in movement/speech
Avoids eye contact
Slow and quiet speech

201
Q

How many sx are needed to diagnose mild depression?

A

core sx + 2-3 others

202
Q

How many sx are needed to diagnose moderate depression?

A

core sx + 4 others + impact on daily functioning

203
Q

How many sx are needed to diagnose severe depression?

A

several sx, suicidal, marked loss of functioning
+/- psychotic sx

204
Q

What kind of psychotic sx might you see in depression?

A

usually mood congruent - nihilistic (world has ended), persecutory or guilty (worried they’ve killed/abused someone) delusions, derogatory auditory hallucinations

can be incongruent - likely to include more 1st rank sx e.g. thought insertion

205
Q

How should depression be investigated?

A

risk assessment - self-neglect/harm, suicidal thoughts
MSE

rule out DDs:
FBC/TFTs - hypothyroidism, chronic disease
urine drug screen - substance misuse
medication review

206
Q

How is mild depression treated?

A

low-intensity psychosocial interventions e.g. computerised/individualised CBT, guided self-help, group physical activity
psychoeducation

usually no medication

207
Q

How is moderate to severe depression treated?

A

combination of antidepressant therapy
+ high intensity psychosocial treatment eg individual CBT, interpersonal therapy, behavioural activation/couples therapy

antipsychotic if they present with psychotic sx e.g. aripiprazole, risperidone

psychoeducation

208
Q

How can treatment resistant depression be treated?

A

combo of antidepressants and lithium/atypical antipsychotics/other antidepressants

209
Q

What intervention can be used in very severe cases of depression that are resistant to treatment?

A

ECT

210
Q

What is the ICD-10 definition of GAD?

A

generalised, persistent, excessive worry
about a number of everyday events
finds the worry difficult to control
for at least 3 weeks (ICD-10) or 6 months (DSM)

211
Q

What physical heath conditions can cause GAD?

A

hyperthyroidism
pheochromocytoma
lung disease (excessive use of salbutamol)
congestive heart failure (heart medications can lead to GAD)
hypoglycaemia

212
Q

What part of the population is most effected by GAD?

A

females > young adults/middle aged

213
Q

What are the risk factors for GAD?

A

alcohol use
benzodiazepine use
stimulates - esp during withdrawal
co-existing depression
FHx of anxiety disorders
childhood abuse, neglect
excessively pushy parents during childhood
life stresses/events e.g. finances, bereavement
physical health problems - anxious about their health?

214
Q

What is the difference between GAD, panic disorder and phobias?

A

GAD - constant worry without external stimulus

Panic disorder - discreet episodes of anxiety that occur unpredictably/not restricted to a certain stimulus

Phobias - discreet anxiety attacks about a specific stimulus

215
Q

What are the key sx of GAD?

A

Unpleasant/fearful emotional state
Apprehension - feeling of impending threat/death/losing control
Increased vigilance

Physical sx (sympathetic autonomic over-activity) eg palpitations, tachycardia, sweating, tremor, chest pain, nause, abdo pain, dizziness, chills/hot flushes, feeling of choking
Bodily discomfort eg restlessness, agitations, avoidance of stimuli

Sleeping difficulties - initial insomnia, fatigue on waking
Low self-worth
Difficulty concentrating
Irritability

216
Q

What are the key sx of panic disorder?

A

usually lasts a few minutes
crescendo of anxiety > usually results in exit from situation

same physical sx as GAD

secondary apprehension - feeling of impending threat/death/losing control
depersonalisation/realisation

217
Q

What are the key sx of phobias?

A

avoidance of the situation
anticipatory anxiety
same physical sx as GAD

218
Q

Give 2 examples of phobias?

A

agoraphobia - fear of crowded places/going outside/places that are difficult to escape from quickly

social phobia - fear of social situations where a individual is exposed to unfamiliar people/possible scrutiny > low self-esteem/fear of criticism

219
Q

What are signs of anxiety in an MSE?

A

restlessness
agitation
may have a tremor

220
Q

What are the 3 diagnostic criteria for GAD?

A

Excessive anxiety + worry about a number of events/activities

Difficulty controlling the worry

For at least 3 weeks

221
Q

How are anxiety disorders investigated?

A

History including social situation, interpersonal relationships

Rule out a physical causes e.g. bloods, TFTs, BP

risk assessment

222
Q

How should anxiety disorders be treated?

A
  1. psychoeducation, sleep hygiene, self-guided CBT - low intensity to start

2a. CBT - unlearning maladaptive patterns of thought/behaviour +/- exposure therapy (phobias)/applied relaxation

2b. Pharmacological - SSRIs eg sertraline (1st line), SNRIs eg duloxetine, atypical AD eg mirtazapine - choice depending on SE profile

Alternative ssri/snri if ineffective
Consider combining medication
Benzodiazepines for crisis
Beta blockers e.g. bisoprolol for physical sx

223
Q

What medications should be avoided in chronic anxiety? Max length of time they should be prescribed?

A

benzodiazepines - highly addictive
used in transient causes of anxiety e.g. flying/crisis only
max 2 weeks prescription

224
Q

What is anxiety often comorbid with?

A

depression
substance misuse

225
Q

A patient presents with a suspected eating disorder and collapses. What other causes of collapse should be ruled out?

A

dehydration
drug/alcohol use
CVS

226
Q

What are the SCHOFF screening questions?

A

S - Do you make yourself SICK because you feel uncomfortably full?
C - Do you worry you have lost CONTROL over how much you eat?
O - Have you recently lost more than ONE stone/6kgs in a 3 month period?
F - Do you believe yourself to be FAT when others say you are thin?
F - Would you say FOOD dominates your life?
(yes to 2+ > high sensitivity for anorexia/bulimia nervosa)

227
Q

What methods of reducing their weight are used by pts with eating disorders? Why is it important to find this out?

A

restricting calories
over-exercising
laxatives
vomiting
diuretics
fasting
diet pills
important due to potential complications

228
Q

What are the differential diagnoses of weight loss?

A

malabsorption e.g. celiac disease, IBD, peptic ulcer
malignancy
drug/alcohol misuse
infection e.g. TB, HIV
AI disease e.g. RA
endocrine - hypothyroid, DM< hypercortisolism, adrenal insufficiency
medications e.g. NSAIDs

229
Q

What are the key sx of anorexia nervosa?

A

low body weight

intense fear of gaining weight
- Preoccupation with food (dieting, making elaborate meals for others)
- Selective about food, not eating around others, say they have already eaten
- Repeated weighing/measuring, checking mirror

Behaviour that interferes with gaining weight e.g. purging

  • Distortion of body image, low self-esteem, drive for perfection

Hormonal disturbance
- Amenorrhea/irregular periods
- Men - loss of libido/potency

230
Q

What are the key sx of bulimia nervosa?

A

Recurrent episodes of binge eating on average at least once a week for 3 mo
= consuming excessive amount of food with a sense of loss of control over eating
In-between likely attempts to restrict eating

Recurrent inappropriate compensatory behaviour to prevent weight gain eg vomiting

Weight often within normal limits/above average - can go undetected

Psychological features
- Over-evaluation of self-worth
- Fear of fainting weight, sharpy defined weight threshold set by patient
- Mood disturbance, sx of anxiety
- Persistent preoccupation and craving for food/feelings of guilt and shame about binging
- Self-harm

231
Q

What are the key steps to a physical exam of a suspected ED?

A
  1. calculate BMI, compare to previous recordings
  2. vital signs - temp, pulse, BP, hydration, peripheral circulation
  3. look for muscle wasting, assess muscle strength (score of 2 or less on the Sit-up-Squat-Stand test)
  4. look for complications/signs suggestive of an alternative cause
232
Q

What are the signs seen on physical exam of anorexia nervosa?

A

Dry skin, hair loss/lanugo hair (peach fuzz)
Bradycardia or postural tachycardia
Orthostatic hypotension
Hypothermia
Loss of muscle strength
Oedema, cold peripheries
Constipation
Fainting, dizziness, fatigue Weight: BMI < 17.5, emaciation (state of being abnormally thin/week) - often disguised by make-up/clothes
Anaemia - angular stomatitis

Self harm scars?

233
Q

What are the signs seen on physical exam of bulimia nervosa?

A

Bloating, fullness
Lethargy
Gastro-oesophageal reflux
Abdo pain
Sore throat from vomiting

Severe: Russell’s sign > knuckle calluses from induced vomiting, dental enamel erosion, salivary gland enlargement, hypokalaemia, alkalosis

Self harm scars?

234
Q

What bloods should be carried out for a suspected ED? What are we looking for?

A

look for physical causes - find biggest risks first

FBC - anaemia from malnutrition/GI losses, mild leukopenia/thrombocytopenia, low plasma proteins
U&Es - hypokalaemia suggestive of vomiting/laxative abuse, hyponatraemia - excess water intake to cover up weight loss
ESR/CRP - raised > organic cause of weight loss, should expect low/normal
TFTs - like to see low T3/T4 - can look like hypothyroidism
LFTs - likely to be elevated from malnutrition
Blood sugar - likely hypoglycaemic

235
Q

What investigations should be carried out for a suspected ED, other than bloods?

A

ECG - look for QT prolongation, MI, arrhythmias
CVS is the biggest cause of death

Urinalysis - hypokalaemia, renal function

could do ABG/HIV/endoscopy etc if indicated

236
Q

What are the 4 domains of the MCA?

A

can’t do 1 or more? no capacity

the patient can:
1. understand the info
2. retain it long enough to make a decision
3. weigh up the information
4. communicate their decision

237
Q

What are the 5 principles of the MCA?

A
  1. assume capacity until proven otherwise
  2. do not treat people as incapable of making a decision unless all practicable steps have been tried to help them
  3. should not be treated as incapable of making a decision because their decision seems unwise
  4. always do things or take decisions for people without capacity in their best interests
  5. before doing something, consider whether the outcome could be achieved in a less restrictive way
238
Q

What extra electrolytes must be requested on the U&Es form if referring syndrome is suspected? Why?

A

phosphate and magnesium

leads to CVS + resp failure
when starved, body has to maintain balance > massive intracellular uptake of electrolytes > serum levels fall

239
Q

What is refeeding syndrome? What happens to electrolyte levels?

A

occurs when people eat after a long period of fasting

in starvation state = protein catabolism > total body phosphate/mag depletion + normal serum levels

eat = massive IC uptake of electrolytes > serum levels fall
= resp/cvs failure
hypophosphataemia > muscle weakness > diaphragmatic insufficiency

240
Q

How long after eating does refeeding syndrome usually occur?

A

3-4 days

241
Q

What are the immediate risks for a pt with an ED?

A

CVS instability - arrhythmias, heart failure
anaemia
electrolyte imbalances - especially hypokalaemia with vomiting > MI, sudden cardiac death
hypoglycaemia

look for syncope, severe abdominal pain

242
Q

What are the immediate management steps when a pt presents with an ED?

A

chase U&Es - phosphate, mg, blood glucose
fluid resuscitation
contact dietician about refeeding plan
persuade them to stay in hospital until psychiatrist can see them

243
Q

What is the long-term management of an ED?

A

drug therapy generally not effective

ED-focussed CBT/self-help/family therapy

244
Q

What are red flags seen in a history/exam of a suspected ED?

A

weight loss (malignancy, infection?), more serious if this is rapid
erosion of dental surfaces
weakness + malaise in young females > ED with hypokalaemia

245
Q

What is bipolar affective disorder?

A

recurrent episodes of altered mood + activity
depression + hypomania/mania

246
Q

What is the peak age of onset of bipolar?

A

teenage/early 20s

247
Q

What are some RFs for developing bipolar?

A

fix/genetic factors
traumatic life events/hx of abuse
sleep deprivation

thyroid disease, ADs, steroids, alcohol, cannabis can cause rapid cycling mood

248
Q

What are the key differential diagnoses of bipolar?

A

cyclothymia
schizophrenia - psychotic sx in the absence of prominent mood sx
substance misuse - cocaine, ecstasy, amphetamines
personality disorders - less episodic than bipolar
OCD
ADHD in children

organic - stroke, thyroid, MS, FTD, AIDs, epilepsy etc
iatrogenic - ADs, corticosteroids, levodopa, stimulants
metabolic - hyperthyroid, cushings, Addison’s, vit B12 deficiency

249
Q

What is the most likely cause of mania in over 45s?

A

organic cause

250
Q

What are they differences between hypomania and mania?

A

<7 days + no psychotic sx, lower severity of sx

251
Q

Are depressive sx required for diagnosis of bipolar?

A

no

252
Q

What are the MSE signs of bipolar?

A

pressured speech, restlessness, flight of ideas

253
Q

How should suspected bipolar be investigated?

A

FBC, U&Es, LFTs, TFTs, urinary drug screen to rile out physical causes
extra endocrine tests if suspicious of anything
ECG, CT scan

254
Q

How should an acute manic episode be managed?

A

refer, determine risks/urgency of referral, establish care plan
assess capacity to consent to admission/treatment > MHA assessment if not
advise to stop driving during episode

TAPER OFF SSRIs immediately if on them when mania starts

antipsychotics (if doesn’t work > try a different one > add lithium)
short acting benzos PRN for behavioural sx

255
Q

What is the long-term pharmalogical management of bipolar?

A

4 weeks after acute episode has resolved:
1st lin = lithium, 2nd line = valproate
In pregnancy - antipsychotics instead

May need treatment for depressive episodes - quetiapine alone/fluoxetine + olanzapine/lamotrigine = careful decision, try to avoid ADs, possibly used with a mood stabiliser

256
Q

What is the long-term non-pharmalogical management of bipolar?

A

Psychological therapies may be offered but usually not as affective as in depression

Continued risk management very important - look for reckless behaviors, aggression, promiscuous sexual behaviour, self-neglect
Crisis plan
Consider LPoA, advance statement

257
Q

What is the action of lithium?

A

mood stabiliser
exact mechanism unknown
interferes with NT release + 2nd messenger systems

258
Q

What is the treatment course of lithium?
how often
how to take
length of treatment
time before it works

A

how often - once/twice daily
how to take - tablet, capsule or syrup
length of treatment - usually lifelong, regular reviews by psychiatrist
time before it works - 1-2 wks

259
Q

What tests need to be done before starting and during taking lithium?

A

Before starting - FBC, U&Es, TFTs, beta-HCG (pregnant?), ECG

Check lithium level after 5 days, then every week until stable for 4 weeks, then every 3 months

Check TFTs, U&Es, Ca2+ every 6 months

260
Q

What are the important SEs of lithium? (LITHIUM acronym)

A

L - leukocytosis
I - insipidus diabetes (nephrogenic)
T - tremors (fine, if course then think toxicity)
H - hydration (very easily dehydrated, risk of toxicity in summer, need to drink a lot as renally cleared)
I - increased GI motility > abdo pain, nausea
U - underactive thyroid
M - metallic taste (warning of toxicity), mums beware - teratogenic

water sx - thirst, polyuria, impaired urinary concentration, weight gain, oedema

261
Q

What are the sx of lithium toxicity? What should be done if it is suspected?

A

act drunk!
GI - anorexia, diarrhoea, vomiting, dry mouth/extreme thirst
Neuromuscular - dysarthria, dizziness, ataxia, muscle twitching, tremor
Drowsiness, apathy, restlessness, nausea, confusion

> stop lithium and rehydrate

262
Q

What are the 3 key complications of taking lithium?

A

Renal toxicity
Nephrogenic diabetes insipidus
Hypothyroid

263
Q

When is lithium contraindicated?

A

1st trimester pregnancy, breast feeding
Cardiac disease
Significant renal impairment
Addison’s disease
Low sodium diets
Untreated hypothyroidism

264
Q

Why should we be careful prescribing lithium with diuretics?

A

dehydration

265
Q

Why should we be careful prescribing lithium with NSAIDs?

A

kidney damage

266
Q

What are obsessions vs compulsions in OCD?

A

obsession - unwanted intrusive though

compulsion - behaviours that result from obsessive though

267
Q

How is OCD managed?

A

combo of psychotherapy (often CBT - obsession relief) + meds (often SSRIs)
exposure + response prevention therapy may relieve compulsions

268
Q

What are the CAGE screening questions for alcohol abuse?

A

2+ = problematic drinking

  1. Have you ever felt you need to CUT down on your drinking?
  2. Have people ANNOYED you by criticising your drinking?
  3. Have you every felt GUILTY about drinking?
  4. Have you ever felt you needed a drink first thing in the morning to steady nerves/get rid of a hangover? (EYE-OPENER)
269
Q

What medications have SEs worsened by alcohol intake?

A

benzodiazepines

270
Q

What is the recommended weekly intake of alcohol?

A

14 units

271
Q

How is the number of alcohol units calculated?

A

volume drunk (L) * % alcohol

1 unit = 10ml of 100% alcohol

272
Q

What are some signs of alcohol dependance?

A
  • persistence in the face of harm to physical/mental health, social/work life
  • withdrawal sx - shakes/sweats/sickness
  • increased tolerance
  • primary - how important is alcohol to them, neglecting other activities
  • loss of control
  • rapid reinstatement - if hey start again will rapidly reach level they were before
  • narrowing of repertoire - range of beverages declines, often cheapest
273
Q

When does drinking become problematic?

A

consequences of alcohol cause social, physical and psychological harm

274
Q

What can cause alcohol abuse?

A

genetics
impulsive, aggressive, hyperactive behaviour as a child
anxiety
cultural factors
accessibility to alcohol

275
Q

How is alcohol abuse managed?

A

push for detox at home is possible

at home:
- baseline obs/bloods
- weaning regime of benzos over 7 days (chlordiazepoxide preferred, diazepam if not)
- thiamine - reduces wernicke risk
- consider supportive tx eg melatonin for sleep, small high protein meals, AA group

in hospital:
- IV vit B12 + thiamine
- weaning regime
- high protein, 35Kcal/kg/day
- consider steroids
- tramadol - relieve neuralgia
- laxatives - avoid constipation
- K+ sparing diuretics - weigh everyday to check losing fluid

276
Q

Can the MHA be utilised for alcohol abuse?

A

no, only for consequences of

277
Q

What are the short term complications of alcohol abuse?

A

trauma
vomiting
radial nerve palsy
risk taking behaviour
vasodilation - risk of hypothermia
hyperglycaemia

278
Q

What is the physiology of alcohol as a CNS depressant?

A

enhances effect of inhibitory neurotransmitter GABA
> depression of inhibitory neurons = relaxed, disinhibited feeling
> then inhibition of other areas of CNS (initially learned tasks areas then mechanical later)

279
Q

What are the long term cardiac implications of alcohol abuse?

A

increases BP by increasing sensitivity to catecholamines

  • increases risk of IHD, CVA, stroke
  • arrhythmias esp AF
  • alcoholic cardiomyopathy > HF
  • vasodilator > hypothermia risk
280
Q

What are the long term hepatic implications of alcohol abuse?

A
  • hypoglycaemia > seizure risk
  • fatty liver > then alcoholic hepatitis, cirrhosis
  • clotting factor reduction
  • reduced albumin production > peripheral oedema
  • asterixis
  • oesophageal varices
  • induction of drug metabolising enzymes > drugs eg warfarin less effective
281
Q

What are the long term GI implications of alcohol abuse?

A

gastritis
pancreatitis
malnourishment
poor oral hygiene > bad teeth, scurvy
reflux
mallory weiss tea
diarrhoea
risk of ulcers

282
Q

What are the long term GUM implications of alcohol abuse?

A

altered sexual function
leydig cell damage > less testosterone > loss of libido/infertility/loss of male body hair
altered steroid production > gynaecomastia

283
Q

What are the long term neuro implications of alcohol abuse?

A

vit def - B6, B1/thiamine > korsakoff’s, predisposes PAINFUL neuropathy
convulsions
poor sleep
impaired memory
risk of head injury

284
Q

What are the long term psych implications of alcohol abuse?

A

depression/anxiety
alcoholic amnesia
korsakoff’s
alcoholic dementia

285
Q

What are the long term misc implications of alcohol abuse?

A

ID/macrocytic anaemia
risk of mouth, oesophageal + liver Ca
foetal alcohol syndrome
diabetes due to cirrhosis

286
Q

What drugs does alcohol interact with? Why?

A

metronidazole
chlorpropamide

> acetaldehyde accumulation > headache/sweating/nausea

287
Q

Is binge drinking or continuous drinking more harmful? Why?

A

repeated injury to liver at levels it cannot metabolise
repeated acute irritation/inflammation of brain/pancreas/stomach/liver

288
Q

What are alcohol withdrawal symptoms in the few hours vs 24-48hrs vs 48-72hrs after stopping drinking?

A

6-12hrs: tremor, nausea, sweats, agitation, tachy, raised BP, anxiety

24-48hrs: delusions, fear/paranoia, restlessness, confusions, diarrhoea, auditory hallucinations
convulsions/seizures = biggest killer
seizures peak = 36hrs

48-72hrs: delirium tremens

289
Q

Why do withdrawal sx occur after stopping drinking alcohol?

A

autonomic overactivity due to withdrawal of inhibiting effect

290
Q

What hallucinations are most a/w alcohol withdrawal?

A

persecutory
terrifying visual/tactile hallucinations eg insects crawling over skin, little men running around

291
Q

What is the basic screening for alcohol abuse in a normal patient?

A

CAGE questions
increased MCV
increased yGT

292
Q

How often does DT happen? When does it occur?

A

in about 5% of acute alcohol withdrawal
generally after many years of drinking

presents about 3-4 days after withdrawal

293
Q

What are the sx of DT?

A

similar to other acute brain syndromes:
restlessness
fear/paranoia
confusion/clouded consciousness
terror-stricen face
ataxia/tremor
sweaty/tachy/pyrexic/flushing/pallor
terrifying visual hallucinations, may be tactile/persecutory auditory too
esp formication - feeling of insects crawling on skin

294
Q

When does DT lead to death?

A

in 10-15%
seizures, HF, self injury, infection

295
Q

How is DT treated?

A

similar to withdrawal
- benzodiazepines - continue for up to 10 days even after sx subside to avoid nightmares
- B vits (earlier = better reduction of encephalopathy)
- fluid replacement
- dextrose - avoid hypoglyc
- monitor for signs of alcohol brain damage

296
Q

How long does DT generally last?

A

3-4 days
can have continuing anxiety for months

297
Q

What is wernicke’s encephalopathy vs korsakov’s syndrome?

A

wernicke’s: acute syndrome due to thiamine deficiency
korsakov’s: chronic condition caused by thiamine deficiency

some people can have wernicke’s that continue chronically and become korsakov’s

298
Q

What are the clinical features of wernicke’s? What is the wernicke’s triad?

A
  1. eye signs - nystagmus, opthalmoplegia (paralysis of eye muscles, particularly of abducens nerve)
  2. ataxic gait
  3. confusion

nausea
memory problems
can occur in any type of thiamine def, not just alcohol

299
Q

Define Korsakov’s

A

state of impaired memory function present after wernicke’s encephalopathy has subsided

300
Q

What kind of memories are affected in Korsakov’s?

A

anterograde memory disorder > old memories can be accessed, new memories cannot be consolidated

can immediately recall facts but cannot get it into long term memory

301
Q

How do patients usually present with Korsakov’s?

A

little/distorted sense of time
often make up events, usually sound plausible = confabulation
answer qs wrong in a laid back way - ie unconcerned answers are incorrect
no clouding of consciousness
often peripheral neuropathy

302
Q

What are some differentials for Korsakov’s?

A

acute brain syndrome of misc cause > clouding of consciousness, no neuro signs

delirium tremens > more common, no neuro signs

chronic brain syndromes - long term memory likely to be affected

303
Q

Why can chronic alcohol intake chronic brain syndrome?

A

atrophy of the cerebrum

304
Q

How is wernicke’s managed?

A

lots of thiamine + other B vits (IV or IM if necessary)
sedation if needed
fluid/electrolytes

305
Q

How is korsakov’s managed?

A

life long chronic illness - not rly any treatment
many patients may eventually require care

thiamine supplements may be useful

306
Q

What is the prognosis of Korsakov’s?

A

palsies
ataxia
neuropathy - unlikely to resolve fully
amnesia - 1/2 pts will not recover

307
Q

What is alcohol dependance versus abuse?

A

chronic relapsing and remitting alcohol abuse

308
Q

How is long term alcohol dependance managed?

A

psychological + rehab therapies

+ pharmacology:
if achieved abstinence and want to maintain it:
- disulfiram (acetaldehyde dehydrogenase inhibitor) = deterrent, causes violent N&V on alcohol consumption - can be life-threatening, 1 daily
- acamprosate (anti-craving) = no SEs, can be taken with alcohol, 3 daily

pts who want to reduce alcohol intake
for about 3-6mo:
- naltrexone (suppresses euphoria experienced with alcohol)

309
Q

Why does emotional dysregulation occur?

A

limbic system overused or a memory is triggered

due to:
- disrupted attachment
- psychological trauma - PTSD
- temporary effect of trauma, life event, stress

310
Q

What are the features of PTSD?

A

intrusive recollections, nightmares and flashbacks - more vivid than a memory
avoidance behaviour of places/events that remind them of the event
hyperarousal - exaggerated startle response, irritability, anger, insomnia, hypervigilance
nightmares, sleeping problems
hypervigilant
often hx of previous mental health problems

311
Q

What is the timeline of PTSD?

A

begins within a few months of the incident

can be:
acute - <3mo
chronic - >3mo
delayed onsent - >6mo after event

312
Q

How is PTSD treated?

A

psychological intervention:
- CBT
- eye movement desensitisation and reprocessing > recalling traumatic memories whilst moving eyes in specific patterns of movements

  • SSRIs, TCAs - good for +ve sx eg flasbacks, arousal not for -ve sx eg avoidance

yay for combo therapy

313
Q

What is EMDR therapy for PTSD?

A

heightened emotions with the traumatic event > memory is not stored correctly
= when event is recalled it is re-experienced

pt moves eyes in various patterns in 15/30 sec bursts whilst trying to recall it
> dual processing helps to re-process the memory so that it is stored correctly

314
Q

Give some examples of SSRIs?

A

fluoxetine, paroxetine, sertraline, citalopram

315
Q

Which antidepressants are most effective in severe depression?

A

TCAs

SSRIs just as effective as TCAs in mild/mod but less so in severe

316
Q

What is the mechanism of action of SSRIs?

A

reduced neuronal reuptake of serotonin

block transporters that take 5-HT and NA back into presynaptic terminal > boosts MOA in synaptic cleft

v specific - only blocks serotonin reuptake inhib

317
Q

Why do SSRIs have fewer SEs than TCAs?

A

low affinity for muscarinic, histaminergic and adrenergic receptors
= fewer SEs + less dangerous in overdose

318
Q

How long does it take to see clinical benefit from SSRIs?

A

2-4 weeks

319
Q

Which conditions are SSRIs the first line tx for?

A

depression, GAD, PTSD, eating disorders, OCD

320
Q

What are the common SEs with SSRIs?

A

generally transient
nausea, headache, dizziness, GI upset
agitation, akathisia, anxiety
sexual dysfunction
insomnia
hyponatremia

increased suicidality !

321
Q

What are SNRIs? Give an example.

A

Serotonin and noradrenaline reuptake inhibitors
eg mirtazapine
v similar to SSRIs

322
Q

What are MAO inhibitors? When are they used?

A

monoamine oxidase inhibitors
rarely used - good AD but bad SEs

323
Q

What are the SEs of MAO inhibitors?

A

cheese effect: MAOi breaks down tyramine (high in cheese) > more absorbed > acts similarly to dopamine/noradrenaline > displaces them > acute life-threatening HTN

drug interactions - nasal decongestants, salbutamol, anti-psychotics, other ADs

324
Q

How to tricyclics ADs work?

A

block transporters which take 5-HT and NA back into presynaptic terminal
not v specific - act at lots of receptors in body
boost MOA

325
Q

What are the SEs of tricyclics?

A
  • anticholinergic effects (antagonists) > can’t pee, see, spit, shit
  • alpha-1-adrenergic antagonism > postural HTN > falls
  • antihistaminergic (H1) > sedation, weight gain
  • lower seizure threshold, interfere with cardiac circulation = overdoses dangerous
326
Q

What is the MOA hypothesis of depression?

A

low MOA levels cause depression
= used to be dominant theory, now controversial

327
Q

How can stress lead to depression?

A

stress = neurotoxic > high cortisol > crosses BBB > glutamate release in brain > neurotoxic: damages brain cells and makes them less neuroplastic
+ decreases neuroprotective chemicals eg BDNF

328
Q

What is the neuroplasticity hypothesis?

A

down-stream signalling in cells > changes gene transcription

ADs cause slow increase in BDNF via GPCRs
+ decrease glutamate release
= directly increase neuroplasticity in hippocampal neurons

most evidence for this theory, still controversial

329
Q

What is serotonin syndrome? How does it present?

A

serotonin poisoning - rapid onset after increased dose/new prescription

classic triad:
- neuromuscular abnormalities: myoclonus, hyperreflexia, tremors
- altered mental state
- autonomic dysfunction: BP/HR changes, high temp

330
Q

How is serotonin syndrome treated?

A

stop AD
cyproheptadine (5-HT2 antagonist) used in severe cases

331
Q

What is the dopamine hypothesis of psychosis?

A

antipsychotics = dopamine D2 receptor antagonists

schizophrenia = underactivity in the dopaminergic meso-cortical pathways + overactivity in the meso-limbic pathway

332
Q

What are the 4 pathways of the dopaminergic system and their roles? What happens when they are blocked?

A
  1. meso-limbic: reward/pleasure centre, activated by drugs of abuse
    block = reduces +ve sx of psychosis
  2. mesocortical: executive function + cognitive control of emotions
    deficiency = causes -ve sx of psychosis
    block = dysphoria
  3. nigrostriatal: dopamine signal favours direct pathway > movement
    block = reduction in movement > dystonia, akathisia, tardive dyskinesia
  4. tuberoinfundibular: DA inhibits prolactin release
    block dopamine = increases prolactin > menstrual problems, breat engorgement, lactorrhoea, reduced sex drive, increased risk of ovarian/breast ca
333
Q

What major SE can clozapine cause?

A

agranulocytosis - can be very dangerous

334
Q

When are antipsychotics indicated?

A

psychosis -
schizophrenia
delirium (elderly with dementia, intensive care)

335
Q

When are antipsychotics indicated?

A

psychosis:
schizophrenia
delirium (elderly with dementia, intensive care)
acute behavioural disturbances

adjunct in psychiatric disorders eg mania, psychotic depression

336
Q

Give some examples of atypical antipsychotics? How are they different to typical?

A

clozapine
risperidone
sertindole
aripiprazole
zotepine
olanzapine
quetiapine

337
Q

How are typical and atypical antipsychotics different?

A

typical: tend to be from one class

atypical:
fewer motor SEs
wider range of mechanisms - from different classes
?better at treating -ve sx of schiz

338
Q

How are typical and atypical antipsychotics different?

A

typical: tend to be from one class

atypical:
fewer motor SEs
wider range of mechanisms - from different classes
?better at treating -ve sx of schiz

339
Q

What receptors do antipsychotics target?

A

blocking dopamine receptors

may block other NT receptors eg 5-HT (serotonin) which has clinical efficacy and others eg acetylcholine, histamine which cause SEs

340
Q

How many dopamine receptors are there? Which do antipsychotics target?

A

D1-5

APs mainly block D2
typical = effect D1 and 2
atypical = varying

341
Q

Blockade at which regions of the brain cause antipsychotic effects?

A

mesolimbic
mesocortical

342
Q

Blockade at which regions of the brain cause antipsychotic motor SEs?

A

nigrostriatal

343
Q

Why do APs take several weeks to become effective?

A

on 1st administration: dopaminergic neuron activity increases
over next 3 weeks activity decreases

due to block, number of receptors increases > dopaminergic neuron activity decreases due to block

344
Q

What is the therapeutic range of dopamine receptor blockage? When do and what type of SEs occur?

A

65-80%

> 80% = unwanted extrapyramidal effects

345
Q

What are the general clinical effects of APs?

A

depression of emotional responses (for delusions, thought disorders, perception etc)
sedation
antiemetic
antihistamine

346
Q

How do APs cause sedation? What is their action?

A

reduce input to reticular activating system
normal spontaneous activity of the system is preserved

= external stimuli produce reduced response

347
Q

Which symptoms of psychosis do APs treat?

A

+ve sx - delusions, hallucinations etc

atypicals MAY also help -ve sx eg low mood

348
Q

Why do APs cause extrapyramidal effects happen?

A

D2 blockage in the nigrostriatal pathway
happen in 1/2 of patients

349
Q

Give examples of extrapyramidal effects caused by APs?

A

akathisia
acute dystonia eg tongue protutrusion, torticollis
parkinsonianism

many others eg weight gain, drowsiness, insomnia, galactorrhoea, antimuscarinic effects, postural hypotension etc

350
Q

Are extrapydramidal effects of APs reversible?

A

usually reverse when drug stopped
prolonged use = increases likelihood of effects becoming permanent

351
Q

What are late-onset extrapyramidal effects of APs called? Why does this happen

A

tardive dyskinesia - difficult to treat
prevention is best - low doses, titrate upwards

due to damage to GABAergic neurons

352
Q

Which AP do extrapyramidal effects not occur with?

A

clozapine

+ much less likely with atypical APs

353
Q

What is neuroleptic malignant syndrome?

A

occurs with specific genetic variant of D2 receptor = rare
> abnormal bloclage of D2 in striatum and hypothalamus

= MEDICAL EMERGENCY - risk of death

354
Q

What S&S occur with neuroleptic malignant syndrome?

A

fever
rigidity
HTN
sweating
urinary incontinence
altered consciouness, delirium
tahcycardia
EP SEs
high creatinine kinase

355
Q

How is neuroleptic malignant syndrome treated?

A

withdraw tx immediately
give dopamine agonist
aggressively treat hyperthermia - ice packs
circulatory and ventilator support if needed

sx can take >2wks to go

356
Q

What is schizoaffective disorder?

A

controversy about diagnosis

type of schizophrenia where mood sx are unusually prominent/co-existent with mood disorder - bipolar or major depression
delusions/hallucinations eed to be present for at least 2 weeks when mood sx are not

357
Q

Which SSRIs are 1st line for breastfeeding women?

A

sertraline
paroxetine

358
Q

How is postpartum depression defined?

A

depressive episode within 4 weeks of childbirth

359
Q

What are the strongest RFs for postpartum depression?

A

previous hx of MH problems
psychological disturbance during pregnancy
poor social support
poor relationship with partner
baby blues
major life events

360
Q

What is somatisation disorder?

A

tendency to report psychological stress as somatic sx or pain

often a/w with ongoing refusal of reassurance that there is no underlying physical cause for sx

361
Q

What are the common sx reported with somatisation disorder?

A
  • N&V, abdo pain
  • pelvic pain, dysmenorrhoea
  • palpitations, SOB, chest pain
  • amnesia, voice changes, dizziness, difficulty coordinating limbs, speech difficulty, swallowing difficulty
    pain
362
Q

How is somatisation disorder identified and treated?

A

exclude underlying cause
look for underlying psychological cause

careful counselling = most effective

363
Q

How does suicide risk/method differ in men and women?

A

men <35 - suicide = greatest cause of death
men > women at all ages

men more likely to use violent methods eg shooting, handing
women more likely to take drug overdoses

364
Q

What mental health illnesses are most a/w suicide?

A

most common = depression
bipolar disorder
substance abuse

365
Q

How do rates of self harm differ in men and women?

A

roughly same

women = most common cause of acute admission
peak age = 15-25
in men peak age = 25-34

366
Q

What mental health illnesses are most a/w self harm?

A

bipolar
depression
eating disorders
personality disorders

15% repeat within a yr

367
Q

How is pharmacological therapy used for anxiety?

A

not rly considered 1st line, except in severe cases
usually reserved for pts that have failed to respond to CBT/psychoeducation etc

most useful with co-existing depression who lack motivation for self-directed approach

368
Q

What is the main inhibitory NT found in anxiolytics?

A

GABA

369
Q

Are SSRIs effective intreating GAD?

A

proven benefit, but not as much as CBT

not sure which are best
duloxetine + venlafaxine commonly recommended

370
Q

Are SSRIs effective intreating panic disorder? How should they be used

A

reduce panic attacks considerably
tx for minimum of 6mo, assess at 3mo

371
Q

What pharmacological therapies may be used to treat anxiety and in which situations?

A

SSRIs

propanolol - situational anxiety to control physiological sx

benzodiazepines - short-ter/infrequent use only, useful for specific phobias. NOT useful in panic disorder as not quick enough onset
must be used with caution

quetiapine - anti-psychotic in very small doses PRN > useful for panic attacks and insomnia

372
Q

How do benzodiazepines work? Give examples of some.

A

bind to receptors and increase amount of GABA released
eg diazepam, temazepam, loreazepam

373
Q

What are the SEs of benzodiazepines?

A

risk of addiction in regular long-term use
oversedation - impaired consciousness
adverse effect on mood
interaction with alcohol
sexual dysfunction
reduced motivation

374
Q

What is cognitive behavioural therapy? When is it used?

A

1st line for depression, anxiety, OCD, PTSD, eating disorders, psychosis

4 areas model - thoughts can impact behaviour, can impact bodily sensations, can impact emotions
looks at changing/challenging those behaviours/though processes > what change does it have on body/emotions > starts to produce change in how we feel

12-20 structured sessions

375
Q

What is counselling? When is it used?

A

cope with recent events rather than to help you change as a person

short, in primary care
aims to talk, help patient be clear about problems and come up with own answers

376
Q

What is cognitive analytical therapy? When is it used?

A

for depression, personality disorders

looks at patterns from early life and see how its affected behaviours
using interpersonal relationship with therapist to recognise on learnt ways of being and focus on changing them

377
Q

What is interpersonal therapy? When is it used?

A

for mild-mod depression

helps patients understand how problems may be connected to the way their relationships work
identifies how to strengthen relationships and find better ways of coping

378
Q

What is dialectical behaviour therapy? When is it used?

A

GS for borderline personality disorder

intensive, up to 18mo
combo of individual and group sessions
often very difficult experiences, repeating self harm behaviours, difficulty coping with emotions

about accepting yourself and learning how to manage emotions + changing behaviour in a positive way

379
Q

What is family therapy? When is it used?

A

in eating disorders, psychosis

family attend together
works with family’s strengths to help family think about and try different ways of behaving with each other
establishes context of why issues are happening

380
Q

What is electroconvulsive therapy? When is it used?

A

for uncomplicated severe depression
can be for bipolar, catatonia
when other tx hasn’t worked or pts who need rapid tx response
not a cure and requires maintenance tx
repeated course if responding well

send electric current through brain, causing a seizure under GA

381
Q

How do hypnotics work?

A

potentiate inhibitory effects of GABA

382
Q

When are hypnotics used?

A

insomnia

cause of insomnia must be established + underlying factors treated

should be used as short courses in acutely distressed
tolerance develops fast rebound insomnia possible when stopped

383
Q

How should short-acting and long-acting hypnotics be used differently?

A

short-acting - sleep-onset insomnia when sedation the next day is undesirable or for elderly

long-acting - poor sleep maintenance eg early morning waking or anxiolytic effect needed during day

384
Q

Give examples of hypnotics

A

some benzos eg nitrazepam or flurazepam - prolonged action, residual effects next day, cumulative
- others act for shorter time eg loprazolam
- diazepam if daytime anxiety too

z-drugs eg zolpidem, zopiclone - short action, not for long-term use

385
Q

What are mood stabilisers used to treat? Give examples

A

mainly bipolar disorder
mania

lithium, valproate, gabapentin, carbamazepine

386
Q

Why does lithium toxicity happen?

A

quickly becomes toxic as levels increase
catatonic state > able to replace Na+ in many reactions and enter cells via voltage gated Na+ channels

does not replace Na+ in Na+/K+ pump = accumulates in cells

= very narrow therapeutic index

387
Q

What is the mechanism of lithium?

A

poorly understood - interferes with enzymes > alters signal transduction pathways

eg increases adenylate cyclase activity + inositol monophosphatase > affects PI signalling pathway > stabilising effect on aminergic and cholinergic activity > stablised IC signalling pathways = respond less strongly to stimuli

388
Q

How are mood stabilisers used in bipolar disorder?

A

as prophylaxis
usually given long-term, take 3-4 months to work

389
Q

When are mood stabilisers other than lithium used for mania?

A

prophylaxis/tx of mania when pt is unresponsive to lithium

becoming more popular as they are safer/fewer SEs - have modulating effect on GABAergic neurons

390
Q

What is acute dystonia? When does it happen?

A

bizarre unwanted muscle movements
eg tongue protrusion, torticollis (head tilt with chin lift), oculogyric crisis (abnormal rotation of eyeballs)

acute onset due to APs

391
Q

What is an externalising vs internalising disorder?

A

tendency to act out psychological problems eg substance abuse, anti-social personality

internalising eg depression, anxiety

392
Q

The release of what substance causes something to be addictive?

A

dopamine

393
Q

What are the 5 phases of addiction in the stages of change model? Why is this useful?

A

pre-contemplation - not yet thinking about drugs
contemplation - thinking about drugs
preparation - preparing to take drugs eg buying
action - takes drugs
maintenance - continues pattern of behaviour

can target tx according to phase
eg motivational interviewing much more likely in contemplation than maintenance stage

394
Q

What is the 12-step approach?

A

supplement medical/other tx
only useful for someone with dependance

encouraged to surrender themselves to a higher power - not necessarily God

395
Q

Clinical features of opiate use?

A

pinpoint pupils
low BP
venepuncture marks

396
Q

Clinical features of benzo use?

A

disinhibited speech - gives impression of being drunk

397
Q

Clinical features of psychostimulant use?

A

eg amphetamines, cocaine

rapid speech
large pupils
agitation
restlessness
high BP

398
Q

Features of opiate withdrawal?

A

dilated pupils
high BP
sweaty
rhinorrhoea
cramps

ie similar to psychostimulant use

399
Q

Features of benzo withdrawal?

A

hypersensitivity
hyper reflexia
depersonalisation

400
Q

Features of psychostimulant withdrawal?

A

agitation
restlessness

401
Q

Features of heroin withdrawal?

A

cold/shivery
flu-like sx
pain

cannot kill you - terrible feeling but addiction is psychological not physical

402
Q

Cannabis - how is it taken, what type of drug is it, what is there a risk of it causing?

A

resin, leaf, oil (strongest)

hallucinogen - not very strong

heavy regular use > anxiety + depression
likely to make a pre-existing psychological disorder worse
addictive

403
Q

Opiates - how are they taken, what is there a risk of it causing?

A

start smoking > subcut (skin popping) > inject

very addictive
not very harmful but injecting isn’t very good for you
strong a/w depression

risk of RESP DEPRESSION > reversed with naloxone

404
Q

Cocaine - what type of drug is it, what happens when you take it, what is there a risk of it causing?

A

stimulant - pure release of dopamine into brain
cocaine not as strong as crack which releases all dopamine straight away = extremely addictive

big reward after taking, lasts around an hr > very repetitive taking

cardiotoxic = very dangerous

405
Q

Amphetamine (speed) - how is it taken, what type of drug is it, how does it make someone feel?

A

injected

stimulant

excess energy, elated

crystal meth is like the ‘crack’ version

406
Q

MDMA - what type of drug is it, how is it taken, what happens when you take it?

A

stimulant

commonly cut with other drugs, lots of clones on market
relatively safe

causes serotonin release > happy, feel close to people socially
big drop in mood about 4 days after
very high tolerance effect - have to use more

407
Q

Which drugs are non-addictive?

A

LSD
ketamine

408
Q

How is an opiate overdose reversed?

A

naloxone

409
Q

How does naloxone reverse an opiate overdose?

A

competitively binds opioid receptors = blockade

1/2 life naloxone shorter than opiates - can wear off and go back into overdose

410
Q

What are the sx of benzo overdose?

A

agitation
euphoria
blurred vision
slurred speech
ataxia
slate grey cyanosis

411
Q

How can a benzo overdose be reversed? When is it not appropriate?

A

flumazenil

not always recommended
mainly to reduce sedative effect of benzos
in long-term users can induce withdrawal > seizures

412
Q

What are the sx of a paracetamol overdose?

A

often asymptomatic
N&V

acute liver failure
renal failure
oliguria
metabolic acidosis

413
Q

When may acute liver failure occur after a paracetamol overdose? How does it present?

A

24-72hrs after

hepatic necrosis causes:
- jaundice, RUQ pain
- encephalopathy
- hypoglycaemia

414
Q

How is a paracetamol overdose treated?

A

activated charcoal - most effective if within an hr

acetylcysteine - promotes conjugation of circulating paracetamol
if within 8hrs and above tx line
given in 3 infusions, 1st one over an hr

415
Q

What is Fragile X syndrome caused by?

A

mutation in FMR1 gene > no FMRP protein = needed for normal brain development

416
Q

How does Fragile X syndrome present?

A

developmental delay
social and behavioural eg eye contact, anxiety, hand flapping, concentration
intellectual disability
leading genetic cause of autism - 1 in 3

417
Q

Does Fragile X syndrome affect males and females?

A

yes
usually females have milder sx

418
Q

Define learning disability

A

reduced intellectual ability + difficulty with everyday tasks
IQ <70

419
Q

What are the types of schizophrenia?

A

Acronym:
PARANOID: just +ve sx
PSYCHOTIC - post-shiz depression
HUMANS: hebephrenic - thought disorganisation
CAN’T: catatonic - 1+ -ve sx
SUPPLY: simple - no psychotic sc, -ve sx
UNDERSTANDABLE: undifferentiated - meet dx criteria but doesn’t fit type
REASONING: residual - -ve sx lasting 1yr following psyhotic episode

420
Q

When is schizophrenia treatment-resistant? What can be used for tx?

A

sequential use of 2 APs for 6-8wks, at least 1 is atypical

clozapine

421
Q

What SEs can clozapine cause?

A

weight gain
excessive salivation
agranulocytosis
neutropenia
myocarditis
arrhythmias

422
Q

How is opioid dependance treated?

A
  1. methadone = safer opioid, prevents withdrawal sx, sedative effect

alternative: buprenorphine (mixed opioid agonist/antagonist) - sub-lingual, less sedative, can stop pain meds working

naltrexone (opioid antagonist) = relapse prevention

423
Q

What are clang associations?

A

different ideas that are only related by rhyme or similar sounds

424
Q

What are protective factors for suicide?

A

social support
religious beliefs
children at home
regret

425
Q

Which SSRI is 1st line in children/adolescents?

A

fluoxetine

426
Q

Which SSRI is 1st line post-MI?

A

sertraline

427
Q

What is a key dangerous SE of citalopram?

A

dose - dependant QT prolongation

428
Q

What are the CI with SSRIs?

A

NSAIDS (at least prescribe a PPI if necessary)
warfarin/heparin/aspirin

triptans + MAOIs > increased risk of serotonin syndrome

429
Q

How long should an SSRI be reduced for?

A

4wks (except fluoxetine)

paroxetine shorter half life and worse discontinuation sx

430
Q

Can SSRIs be used during pregnancy?

A

weight up benefits and risks

1st tri = small increased risk of congenital heart defects
3rd tri = persistent pulmonary HTN

paroxetine = increased risk of congenital malformations

431
Q

How soon sould pts be reviewed when started on an SSRI?

A

2wks
1wk if high risk of suicide/<30

432
Q

What sx can be present after high intensity

A
432
Q

What withdrawal sx can be present after high intensity cocaine use?

A

1st phase (24 hours): increased hunger, anxiety, irritability, fatigue, lack of motivation

2nd phase: up to 10wks
3rd phase: decrease in most sx, low mood may persist for up to 6m

Phase 3a (11 decks)

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