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Year 3 - Psychiatry > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What are the 7 components of the Mental State Exam (MSE)?

A

Appearance and Behaviour

Speech

Affect and Mood

Thoughts: control and content

Perception

Cognition

Insight

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2
Q

What might you note for a patient’s appearance and behaviour?

A

Appearance

  • age, gender, race
  • body habitus
  • grooming
  • attire
  • posture and gait
  • odd movements/tics
  • evidence of injuries or illness
  • smell

Behaviour

  • eye contact
  • ease of rapport
  • open/guarded/suspicious
  • agitation/psychomotor retardation
  • disinhibition/overfamiliarity
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3
Q

What do we note when we assess speech?

A

Rate

Amount

Variation in tone (prosody)

Speech delay

Volume

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4
Q

What is the difference between Mood and Affect?

A

Mood - how a patient describes the way they are feeling, in their own words (subjective)

Affect - your observation of how the patient appears, considering their baseline and how much they vary from this (objective)

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5
Q

What do we look for when assessing cognition in a patient?

A

Orientation in time (what is the date), place (where are we just now) and person (name, age, DOB)

Concentration

Memory

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6
Q

What do we look for when assessing insight in a patient?

A

Does the patient know they are unwell?

Do they attribute it to a mental health issue

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7
Q

What are some of the common symptoms of a mood disorder?

A

Sleep disturbance

Poor self care

Hopelessness

Suicidal thoughts

Self-contempt/feelings of guilt

Diurnal variation

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8
Q

Define the following terms…

  • Anhedonia
  • Early morning waking
  • Psychomotor retardation
  • Stupor
  • Euthymia
A
  • Anhedonia - loss of enjoyment
  • Early morning waking - waking at least 2 hours before normal waking time and being unable to fall asleep again
  • Psychomotor retardation - subjective and/or objective slowing of thoughts/movements
  • Stupor - absence of relational functions e.g. action, speech etc.
  • Euthymia - normal mood
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9
Q

How would someone with depression present, in terms of Appearance and Behaviour?

A

Reduced facial expression

Furrowed brow

Reduced eye contact

Limited gesturing

Rapport is difficult to establish

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10
Q

How would someone with depression present, in terms of speech?

A

Reduced rate

Lowered pitch

Reduced volume

Reduced intonation (monotonous)

Increased speech latencies

Limited answers

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11
Q

When diagnosing depression, what are the 3 major criteria?

A
  • Low mood
  • Fatigue
  • Loss of interest or pleasure
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12
Q

What are some of the additional symptoms that can be used to grade severity of depression?

A

Loss of confidence/self-esteem

Unreasonable feelings of guilt/self-reproach

Recurrent thoughts of death/suicide or suicidal behaviours

Inability to concentrate

Change in psychomotor activity - agitation or retardation

Sleep disturbance of any type

Change in appetite (increase or decrease) with corresponding weight change

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13
Q

How is severity of depression assessed?

What are the classifications?

A

Rating scales

  • Hamilton rating scale for depression
  • Montgomery-Asperg Depression rating scale
  • Beck depression inventory

Moderate depression - 2/3 of the core symptoms, plus enough of the additional symptoms to total 6 or more

Severe depression - 3/3 of the core symptoms, plus enough of the additional symptoms to total 8 or more

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14
Q

Name some mood disorders, as classified by the ICD

A

Manic episode

Bipolar affective disorder

Depressive episode

Recurrent Depressive Disorder

Persistent mood disorders

Unspecified mood disorders

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15
Q

How does the DSM classify Bipolar Mood Disorder?

A

Bipolar I

  • has to have met the criteria for mania, although previous episodes may have been hypomanic and/or depressive
  • represents the ‘classic’ form of manic-depressive psychosis
  • NB - not just mania, most people will have had episodes of major depression

Bipolar II

  • current or past hypomanic episodes AND current or past depressive episodes
  • has never met the criteria for a manic episode
  • likely the most common form of BPD
  • NB - not just a milder form of the illness, results in just as much disability

Bipolar III

  • hypomanic episodes only occur following the use of antidepressants for depression
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16
Q

How does the ICD classify Bipolar Mood Disorders?

A

“Disorder characterised by two or more episodes in which the patient’s mood and activity levels are significantly disturbed, this consisting of mania/hypomania in some occasions and depression in others

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17
Q

How can you tell between depression and bipolar disorder when classifying?

A

A single episode of mania/hypomania is classed as BPD, even if they haven’t had a depressive episode (yet)

Any episode of mania/hypomania in someone with a background of recurrent depression means they are classed as bipolar and no longer as depressive

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18
Q

How is a hypomanic episode classified?

A

A. mood is elevated/irritable to a degree that is definitely abnormal for the individual, and lasts for at least 4 consecutive days

B. at least 3 of the following…

  • increased activity/physical restlessness
  • increased talkativeness
  • difficulty in concentrating/distractability
  • decreased need for sleep
  • increased sexual energy
  • mild spending sprees/other types of irresponsible behaviours
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19
Q

How is a manic episode classified?

A

A. mood is elevated/irritable to a degree that is definitely abnormal for the individual, and lasts for at least 1 week (unless severe enough to require hospital admission)

B. at least 3 of the following…

  • increased activity/restlessness
  • increased talkativeness (pressure of speech), can’t be interrupted
  • flight of ideas/subjective experience of thoughts racing
  • loss of normal social inhibitions
  • decreased need for sleep
  • inflated self-esteem or grandiosity
  • distractability/constant changes in activity or plans
  • reckless/foolhardy behaviours
  • marked sexual energy/sexual indiscretions
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20
Q

How can mania be further classified?

A

With or without psychotic symptoms

Without

  • Absence of hallucinations or delusions
  • However, perceptual disorders may occur

With

  • Delusions/hallucinations are present
  • Most common example is grandiosity/self-referential/erotic/persecutory
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21
Q

What comorbidities may be seen with Bipolar Disorders?

A

Anxiety disorders

Alcohol and drug misuse

Personality disorders

Eating disorders

Schizoaffective disorder

Schizophrenia

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22
Q

How do the clinical courses for unipolar and bipolar mood disorders compare and differ?

A

Unipolar disorders go from a period of “normalcy” downwards, and back up, but never past this.

Bipolar disorders are all over the place…

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23
Q

What are the main classes of anitdepressant drug?

A

Monoamine oxidase inhibitors

Monoamine reuptake inhibitors (tricyclics, SSRIs, SNRIs)

Atypical drugs (post-synaptic receptor effects)

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24
Q

Name some monoamine oxidase inhibitors

What is the difference between these two?

What are some of the side effects of MAO inhbitors?

A

Phenelzine (non-reversible inhibitor)

Moclobemide (reversible inhibitor)

Side Effects

  • “cheese reaction”/hypertensive crisis - causes extremely bad headache and can potentially be fatal
  • potentiates effects of other drugs e.g. barbituates by decreasing their metabolism
  • insomnia
  • postural hypotension
  • peripheral oedema
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25
Q

Name some tricyclic antidepressant drugs

How do they work?

A

Imipramine

Dosulepin

Amitriptyline

Lofepramine

Tricyclics block the reuptake of monoamines into presynaptic terminals (mainly serotonin and noradrenaline), and thus increase their time in the synaptic cleft without increasing their amount

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26
Q

What are some of the side effects of tricyclic antidepressants?

A

Anticholinergic effects - blurred vision, dry mouth, constipation, urinary retention

Sedation

Weight gain

cardiovascular effects - postural hypotension, tachycardia, arrhythmias

NB - tricyclics can be fatal in overdose by causing arrhythmias (paradox of providing potentially fatal drugs to those with depression…)

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27
Q

Name some SSRIs

How do they differ in function to e.g. tricyclics?

A

Fluoxetine

Citalopram/Escitalopram

Sertraline

Paroxetine

Where tricyclics block the reuptake of numerous monoamines (mainly serotonin and noradrenaline), SSRIs exclusively block the reuptake of serotonin

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28
Q

What are some of the side effects of SSRIs?

A

Nausea

Headache (usually settles after a couple of weeks)

Sweating/vivid dreams

Worsened anxiety

Sexual dysfunction

hyponatraemia in the elderly

Discontinuation effects (esp. in paroxetine, due to short half life and rapid clearance from the body)

29
Q

Name some dual reuptake inhibitors or SNRIs

What is the benefit of this class of drug?

A

Venlafaxine

Duloxetine

Side effects are similar to those of SSRIs, however they lack major receptor-blocking actions and so have fewer side effects that tricyclics

30
Q

Name some atypical antidepressant drugs

A

Mixed receptor effects: Mitrazapine

Dopamine uptake inhibitor: Bupropion

31
Q

Describe the efficacy of antidepressant drugs

A

Most classes have a similar clinical efficacy (40-70%)

Most have a delayed onset of action (taking several weeks to take effect)

Side effect profiles differ, as does individual response, and some trial and error may be required

Caution should be taken in prescribing for young adults/teens due to transient increase in suicidal/aggressive ideas

32
Q

How is Bipolar Affective Disorder treated? What needs to be managed and what drugs are given

A

Acute treatment of symptoms

  • to reduce mood in episodes of mania
  • to raise mood in eisodes of depression

Long term treatment

  • to stabilise mood and prevent recurrence of mania and depression

Lithium (mainly given as lithium carbonate) - treatment and prophylaxis in mania and recurrent depression

Anticonvulsants as mood stabilisers - Valproic acid, Lamotrigine, Carbamazepine are used in long-term treatment

Antipsychotics as mood stabilisers - Quetiapine, Aripiprazole, Olanzapine, Lurasidone

33
Q

What are some of the side effects of Lithium? Both common side effects and toxic effects…

What has to be done when prescribing Lithium?

A

Common Side Effects

  • dry mouth/strange taste
  • polydipsia and polyuria
  • tremor
  • hypothyroidism
  • long term reduced renal function
  • nephrogenic diabetes insipidus
  • weight gain

Toxic Effects

  • vomiting
  • diarrhoea
  • ataxia/coarse tremor
  • drowsiness
  • convulsions
  • coma

Regular monitoring of patients on Lithium is required, due to the narrow therapeutic index

34
Q

What is the difference between the Appetitive/Approach Systems and the Aversive/Defensive Systems? Include function, brain regions and primary neurotransmitter

A

Appetitive/Approach Systems​

  • Function - to mediate seeking and approach behaviours (including pleasure)
  • Brain regions - mesolimbic/cortical projections, ventral and dorsal striatum, amygdala, anterior cingulate, orbitofrontal cortex
  • Main neurotransmitter - Dopamine

Aversive/Defensive Systems​

  • Function - to promote survival in the event of threat
  • Brain regions - central nucleus of amygdala, hippocampus, ventroanterior and medial hypothalamus, periaqueductal grey matter
  • Main neurotransmitter - Serotonin
35
Q

How might disordered appetitive functioning result in depression?

A

Difficulty in identifying ‘rewarding’ stimuli

Reduced contact with previously rewarding stimuli

Increased contact with aversive stimuli

Overall reduction of behaviour

Move less, eat less, lose weight etc.

Presents as impaired attention/concentration, loss of interest, avoidance and inactivity

36
Q

How might disordered appetitive functioning result in Mania/Hypomania?

A

Previously neutral stimuli become rewarding

Increased exploration/overall activity

Increased ‘appetite’ for food, activity, sex etc.

Intolerance of aversion/boredom/frustration

Presents as increased interest/distractability, overactivity/loss of need for sleep, disinhibition/risk taking, irritability, elevated/elated mood

37
Q

What hormonal changes might you see in someone with major depression?

A

HPA Axis (Cortisol)

  • increased secretion of ACTH
  • increased secretion of cortisol > elevated amounts in urine and saliva
  • increased CRH in CSF
  • blunted ACTH to CRH
  • enlarged adrenal glands
  • 50-70% fail to suppress cortisol production following DEX

HPT Axis (Thyroid T3 and T4)

  • 20-30% of those with major depression show some dysfunction
  • increased TSH in CSF
  • TSH response to TRH is blunted in 20-25%, despite normal basal TSH, T3 and T4
38
Q

What effect does Major Depression have on the hippocampus in the longer term?

A

Causes the volume to decrease

39
Q

What are the “Top 4” Antidepressant drugs, according to that one lecture?…

A

Escitalopram - probably the best all round SSRI

Sertraline - well established, has good cardiac safety profile and allows for easy dose titration

Mirtazapine - promotes sleep and appetite/weight gain

Venlafaxine - associated with a higher rate of adverse effects, but shows a dose-response relationship

40
Q

When starting a patient on antidepressants, what should be done?

A

Get ratings of depressive symptoms before and after each trial with a drug

Warn patients about the possible side effects and the probability that they will be transient

Review the patient after 1-2 weeks

Ensure the patient has an adequate dose for an adequate amount of time

41
Q

What drug type is ‘usually’ first line in treating someone with newly presenting depression?

How long do antidepressants typically take to start working, and what should the aim be?

A

SSRIs (fluoxetine, sertraline, citalopram etc.) are typically the first line choice

ADs typically take 2-6 weeks to take effect, and the aim should be complete resolution of symptoms

42
Q

What are some of the common factors that should be taken into account when considering what AD to prescribe for a patient?

A

What worked before?

Indications

Comorbidites and risk factors

Patient preference and side effect profile

Safety in pregnancy and breast feeding

Dose frequency and risk of overdose etc.

43
Q

How long should AD treatment be continued for? What should be done when a patient decides to stop?

A

Continue treatment for 6-12 months after full resolution of symptoms after first episode, 12-24 months for a recurrence, and indefinitely after a third recurrence if the patient is willing

Before stopping, a patient’s dose should be tapered

44
Q

What are the mainstays of treatment for BPDs?

A

Mood stabilisers - lithium, anticonvulsants and antipsychotics

(Lamotrigine, an anticonvulsant, is good for bipolar depression)

(Valproate, another anticonvulsant, is good for mania/hypomania)

Antidepressants should generally be avoided in BPDs, however may be useful in the short term for severe episodes - don’t give an antidepressant without a mood stabiliser however!

45
Q

SSRIs - side effects

When should SSRIs be taken?

A

GI upset

Anxiety

Agitation

Insomnia

Sexual dysfunction

Myoclonus (discontinuation symptom)

Increased risk of GI bleeding if taken with NSAIDs

Other discontinuation symptoms (worst in paroxetine)

Should be taken in the morning to reduce insomnia

46
Q

Tricyclics - side effects

When should these be taken?

A

Sedation

Confusion

Dizziness

Anticholinergic/muscarinic effects

Sexual dysfunction

Cardiac arrhythmias (rare, but important, and can be fatal in overdose)

Should be taken at night due to sedation effects

47
Q

When should MAO inhibitors be used? What are the side effects?

When should they be taken?

A

Very effective, but should be used only in treatment-resistant depression due to dietary and medication restrictions

Postural hypotension

Drowsiness

Insomnia

Nausea

Tiredness

Constipation

Hypertensive crisis/cheese response (rarely, but can be deadly) due to lack of MAO-A and, thus, elevated tyramine causing increased noradrenaline

Needs to be taken 3 times a day - causes difficulties with adherence

48
Q

What is the first line treatment for an acute manic episode?

A

Antipschotics - olanzapine, quetiapine, risperidone

Other options - Lithium, valproate, carbamazepine

Benzodiazepines can be used for symptom control e.g. agitation, insomnia etc.

49
Q

What is the first line treatment for Bipolar Depression?

A

Antipsychotic - quetiapine, olanzapine, lurasidone

Antidepressants can be used alongside an antipsychotic, lithium, or valproate

50
Q

What drug is the Gold Standard in BPD maintenance therapy?

A

Lithium

Other options are antipsychotics, Lamotrigine (if primarily depression) or Valproate (if primarily manic/hypomanic)

51
Q

What is ECT? Which form is most commonly used?

What are some of the contraindications?

A

ECT = electroconvulsive therapy

Bilateral is used more commonly than unilateral as it is quicker and more effective, however is also more likely to cause cognitive problems

Contraindications

  • Recent MI/Stroke - ABSOLUTE
  • Intracranial mass - ABSOLUTE
  • Phaeochromocytoma - ABSOLUTE
  • Angina
  • Congestive heart failure
  • Pulmonary disease
  • Osteoporosis
  • Pregnancy
52
Q

Which part of the brain (with what neurotransmitter) guides reward-seeking behaviour?

Which part of the brain allows intention to guide behaviour, allows us to set goals, make sound decisions and to focus our attention?

Why does this distinction explain teenagers?…

A

Mesolimbic system (with dopamine) guides reward-seeking behaviour, and is one of the first parts of our brain to develop.

Mesolimbic system is kept in check by the prefrontal cortex, which allows us to do all of the above and enables us to keep emotions and impulses under control in order to achieve long term goals.

In teenagers/adolescents, the mesolimbic system is fully developed but the PFC is not, meaning teenagers make stupid decisions, aim for strong stimulus reward and have minimal judgement/impulse control

53
Q

What part of the brain shows increased activity when drug addicts are presented with drug cues?

A

The Orbito-frontal cortex, a key creator of the motivation to act

Hyperactivity correlates with self-reported drug cravings following exposure to cues

These changes in OFC persist into abstinence…

54
Q

How does stress cause drug seeking behaviour?

A

Acute stress triggers the release of dopamine in the neural reward pathway

Rapid increase in dopamine can prompt drug-seeking behaviour in dependent individuals

Chronic stress also leads to a dampening of dopaminergic activity, which reduces the sensitivity to normal rewards and encourages exposure to other ‘highly rewarding’ behaviours

55
Q

What metabolised product, present in the blood, would indicate that someone is taking heroin?

A

6-mono-acetyl morphine

If morphine only is detected in the blood, the individual may have just been taking codeine

56
Q

Heroin - effects

A

Euphoria

Analgesia

Respiratory depression

Constipation

Reduced conscious level (“gouching”)

Hypotension and bradycardia

Pupillary constriction

57
Q

Heroin - withdrawal symptoms

A

Occurs typically within 6-8 hours

Dysphoria and cravings

Agitation

Tachycardia and hypertension

Piloerection

Diarrhoea, nausea and vomiting

Dilated pupils

Joint pain

Yawning

Runny nose and watery eyes

58
Q

What drug is given to treat overdose of heroin?

A

Naloxone - blocks opioid receptors

59
Q

What is seen in almost all (97%) of drug related deaths? Give some examples

A

Consumption of multiple substances - other opioids, benzodiazepines, gabapentin

60
Q

What is the most common way of treating opiate misuse?

A

Replacement of a short-acting opiate with a long-acting opiate - opiate substitution therapy

Buprenorphine or Methadone - once daily dosing, initially done under supervision and given in liquid form (buprenorphine only)

61
Q

What is the major downside of opiate detoxification?

A

Aim is complete abstinence from all opiates

This occurs ‘naturally’ sometimes e.g. prison, detox centre etc., however when people go back to using, they use the same dose they were using before…

HOWEVER - 70-80% of detox completers will relapse within a year and death rate is high, because users have become ‘re-sensitised’ to the drug and can’t handle their old dosage, resulting in overdose

62
Q

How many units are in 750ml vodka, 40%ABV?

A

1 unit = 10ml alcohol

No. of units = (% x volume)/10

= (0.4x750)/10

= 30 units

63
Q

What are some of the features of Alcohol Dependence Syndrome?

A

Strong desire/sense of compulsion

Difficulty controlling use of substance (in terms of onset, termination, level etc.)

Physiological withdrawal state

Evidence of tolerance

Progressive neglect of other pleasures/interests

peristence with use despite harmful consequences

64
Q

What identification tools are used to detect people with alcohol problems?

A

AUDIT - Alcohol User Disorder Identification Test - 10 questions which aim to detect hazardous drinking. NB - this is just a screening questionnaire

CAGE - Cut down, Annoyed, Guilty, Eye opener - 4 questions that aim to detect alcohol abuse and dependence

PAT and FAST - Paddington Alcohol Test and Fast Alcohol Screening Test - used in A and E, these are followed up with SADQ

65
Q

What are the components of the FRAMES framework for interventions?

A

Feedback - review the problems experienced

Responsibility - patient is responsible for change

Advice - advise reduction or abstinence

Menu - provide options for changing behaviour

Empathy

Self-efficacy - encourage optimism about changing behaviour

66
Q

How is alcohol withdrawal managed?

A

General support

Benzodiazepines (long-acting e.g. Diazepam, Chlordiazepoxide

Vitamin supplementation - thiamine as prophylaxis against Wernicke’s Encephalopathy. Supplementation must be parenteral, and increase the dose if Wernicke’s is suspected

67
Q

What are the triad of symptoms seen in Wernicke’s Encephalopathy?

A

Confusion

Ataxia

Ophthalmoplegia

68
Q

What drugs can be used for relapse prevention? How do they work?

Are benzodiazepines of any use?

A

Disulfiram (antabuse)

Inhibits acetaldehyde dehydrogenase, leading to accumulation of acetaldehyde which causes flushed skin, tachycardia, nausea and vomiting, hypotension and arrhythmias if alcohol is consumed

Acamprosate - acts centrally on GABA and glutamate systems to reduce cravings

Naltrexone - first line agent for relapse prevention, reduces reward from alcohol with opioid antagonistic effect

Benzos have no place beyond the detoxification period

69
Q
A

Year 3 - Psychiatry (5 decks)

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