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2. Psych Flashcards

1
Q

Outline the difference between type I and type II bipolar disorder:

A
  1. Manic / mixed episodes + depression
  2. Hypomanic episodes + depression
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2
Q

Define bipolar type I disorder:

A

An episodic mood disorder defined by the occurrence of one or more manic or mixed episode PLUS one depressive episode.

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3
Q

Define a manic episode:

A

An extreme mood state lasting at least one week (unless shortened by treatment intervention).

Euphoria
Distractibility
Mood lability
Irritability
Increased energy
Reckless behaviour

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4
Q

Define a mixed episode (bipolar disorder):

A

Characterised by the presence of several prominent manic and depressive episode symptoms.
They will occur simultaneously or change rapidly i.e. day to day or within a day.
Symptoms must be present most of the day, nearly every day for 2 weeks.

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5
Q

Define bipolar type II disorder:

A

At least one or more episodes of hypomania and one episode of depressive symptoms.

No history of mania or mixed episodes.

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6
Q

Define a hypomanic episode:

A

A persistent mood state lasting for at least several days, characterised by persistent elevation of mood or irritability. Other manic symptoms may be seen but are not severe enough to cause marked impairment in functioning.

Represents a change from normal mood, energy level and behaviour.

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7
Q

Define a depressive episode:

A

A period of depressed mood and disinterest in activities lasting most of the day, nearly every day for 2 weeks.

+ other symptoms:
Changes in appetite and sleep
Psychomotor agitation or retardation
Feelings of worthlessness / guilt
Fatigue
Difficulty concentrating
Suicidality

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8
Q

What is a key differentiation between mania and hypomania?

A

Psychotic symptoms e.g. delusions of grandeur and auditory hallucinations are more likely to be mania.

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9
Q

Brief management of bipolar disorder:

A

Psychological intervention.
Lithium (mood stabilizer) 1st line, valproate 2nd.

Management of mania: antipsychotic e.g. olanzapine, haloperidol. Consider stopping antidepressant.

Management of depression: talking therapies + fluoxetine 1st line

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10
Q

Classical triad of Wernicke’s encephalopathy:

A

Opthalmoplegia
Ataxia
Altered / fluctuant mental status

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11
Q

What is the biochemical cause of Wernicke’s encephalopathy?

A

Acute thiamine / B1 deficiency

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12
Q

Causes of Wernicke’s encephalopathy:

A

Chronic alcohol abuse
(High carb load leads to high thiamine requirement + poor/restricted diet)

Secondary to other causes of malnutrition e.g. hyperemesis, diarrhoea, fasting, bariatric surgery

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13
Q

Neurological symptoms associated with Wernicke’s encephalopathy (3):

A

Nystagmus
Ataxia
Opthalmoplegia

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14
Q

Cognitive / psychiatric symptoms associated with Wernicke’s encephalopathy:

A

Confusion
Memory deficit
Apathy or agitation

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15
Q

Other clinical features that can be present in WE:

A

Hypothermia
Altered consciousness
GI symptoms
Tachycardia

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16
Q

How is Wernicke’s encephalopathy usually diagnosed?

A

Usually clinically based on presence of one or more of the classical triad.
Profound risk of harm through delayed treatment and low risk of thiamine infusion means there should be a low threshold of diagnosis.

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17
Q

Differential diagnoses for WE (4), causing relatively rapid changes in neurological function:

A

Delirium tremens
Hepatic encephalopathy
Stroke
Normal pressure encephalopathy

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18
Q

Management of Wernicke’s encephalopathy:

A

Urgent parenteral thiamine for a minimum of 5 days.

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19
Q

Describe the relationship between glucose and thiamine, including their concurrent therapeutic use:

A

Thiamine is required for the metabolism of glucose due to its role as a coenzyme in the Krebs cycle.

Administering glucose to those suspected of WE requires thiamine, and metabolisis of this extra glucose will further deplete thiamine levels.

THIAMINE MUST BE GIVEN BEFORE OR CONCURRENTLY WITH GLUCOSE.

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20
Q

Describe the prognosis of WE in the absence of treatment:

A

Mortality rate up to 20%.
Majority of survivors develop Korsakoff psychosis and progress to Wernicke-Korsakoff syndrome.

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21
Q

What is Briquet’s Syndrome also known as?

A

Somatisation Disorder

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22
Q

What is Somatisation disorder characterised by?

A

Presence of multiple, recurrent and clinically significant somatic complaints that cannot be fully explained by any underlying medical conditions.

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23
Q

What is one of the most common clinical features in somatisation disorder, and how may it manifest?

A

PAIN

Migraine-like or tension-type headaches.
Abdominal pain, often described as diffuse and poorly localized.

+ Pelvic pain, MSK pain, various GI symptoms, urogenital and menstrual symptoms

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24
Q

Poor prognostic factors for schizophrenia (5):

A

Strong family history
Gradual onset
Low IQ
Premorbid social withdrawal
Lack of precipitating event

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25
Q

Environmental factors linked to increased risk of developing schizophrenia (4):

A

Maternal infection
Maternal malnutrition
Obstetric complications
ACEs

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26
Q

ICD-1O diagnostic criteria outlines some symptoms of which only ONE present warrants a diagnosis of schizophrenia. What symptoms are these?

A

Thought echo, insertion, withdrawal or broadcasting.

Delusions of control, influence or passivity.

Hallucinations, especially auditory.

Culturally inappropriate or implausible delusions.

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27
Q

How long must schizophrenic symptoms be ongoing for to be diagnosed?

A

> 1 month

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28
Q

How are schizophrenic symptoms categorized?

A

Positive and negative symptoms.

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29
Q

Outline some positive schizophrenic symptoms (3):

A

Delusions

Hallucinations (usually auditory)

Formal thought disorder
(loss of flow, usually apparent in speech or writing)

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30
Q

Outline some negative schizophrenic symptoms (4):

A

Impairment of volition, motivation and spontaneous behaviour.

Loss of awareness of socially appropriate behaviour.

Social withdrawal.

Flattening of mood, blunting of affect, anhedonia.

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31
Q

Exclusions for a schizophrenic diagnosis (3):

A

Schizoaffective disorder, depressive or bipolar disorder with psychotic symptoms must be ruled out.

Presentation not attributable to the effects of drugs of abuse, medications or a medical condition.

Diagnosis of ASD or childhood communication disorder requires prominent delusions or hallucinations to be present, in addition to other required symptoms.

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32
Q

What is the heritability estimate for schizophrenia?

A

80%

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33
Q

What age does schizophrenia usually present?

A

Late adolescence and early adulthood.

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34
Q

Describe a panic attack.

A

Episode of intense fear or discomfort.

Peaks within minutes.

Physical symptoms such as palpitations, sweating, trembling and SOB.

Chest pain, nausea, dizziness and chills or hot flushes can also be present.

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35
Q

Discuss the diagnosis of panic disorder:

A

Panic disorder is diagnosed when panic attacks are followed by at least one month of persistent fear of having another panic attack.

OR significant changes in behaviour related to the attacks, such as avoiding certain places or activities.

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36
Q

What class of drugs are first line for panic disorder?

A

SSRIs

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37
Q

A patient has been diagnosed with panic disorder. They are commenced on an SSRI.
12 weeks later, there is no improvement. What drug should be considered next?

A

Imipramine or clomipramine

(Tricyclic antidepressants)

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38
Q

What management options are available for people with panic disorder?

A

CBT
Antidepressant medication

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39
Q

Genetic diagnoses commonly associated with ASD:

A

Fragile X
Down Syndrome
Rett’s Syndrome
Tuberous sclerosis complex
Angelman syndrome

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40
Q

The aetiology of ASD is complex and multifactorial. Discuss the genetic and environmental risk factors / associations for ASD (4).

A

Genetic causes (gene defects, chromosomal abnormalities).

Family history (sibling = 10%, monozygotic twin = 36-60%)

Advanced parental age

Toxin exposure / prenatal infections

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41
Q

How is the diagnosis of ASD qualified / assessed?

A

3 levels of severity, rated separately for social communication and restricted / repetitive behaviours.

Level 1 - requiring support
Level 2 - requiring substantial support
Level 3 - requiring very substantial support

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42
Q

Common differential diagnoses of ASD:

A

ADHD
Social communication disorder

Global developmental delay / Intellectual disability

Developmental language disorder

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43
Q

Clinical features of ASD:

A

Impaired social communication and interaction.

Repetitive behaviours, interests and activities.

Can be a/w intellectual and language impairment.

Concurrent diagnoses of ADHD (35%) and epilepsy (18%).

Typically evident 2-3 years old, but can manifest later on.

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44
Q

Which receptors does alcohol work on?

A

GABA

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45
Q

3 mechanisms by which alcoholics become thiamine / B12 deficient:

A

Malnutrition

Alcohol blocks absorption of thiamine

Overactive liver breaks thiamine down more quickly

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46
Q

Describe the timeline of symptoms of alcohol withdrawal:

A

6-12 hours: sweating, tremor, tachycardia, anxiety

36 hours: peak incidence of seizures

48-72 hours: peak incidence of delirium tremens; coarse tremor, confusion, delusion, auditory and visual hallucination

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47
Q

3 drugs sometimes used to maintain abstinence in alcoholism:

A

Antabuse (disulfiram); bad reaction when taken with alcohol

Naltrexone; reduces pleasure experience of alcohol, causes reduction in dopamine release
*stops opioid-based painkillers from working

Acamprosate; reduces cravings

48
Q

Give the 3 different drugs that are used as opiate replacement therapy:

A

Methadone
Buprenorphine
Buvidal

49
Q

Describe the administration of Buvidal:

A

Long acting buprenorphine given as injection.
Weekly administration for 3/52, then monthly.

50
Q

Describe the differences in experience for the patient between methadone and buprenorphine.

A

Methadone provides more of a cloudy-headed effect (more similar to heroin).

Buprenorphine has a ceiling effect, less cloudy head so less effective in people who were using high doses of opiates.

51
Q

Prescribing notes for methadone:

A

Tolerance is developed over time.

If 3 days are missed, must retitrate and start gradually.

52
Q

Prescribing notes for buprenorphine:

A

Must have stopped opiates 24 hours before, as is a strong binder for opiate receptors.

53
Q

Management of acute alcohol withdrawal:

A

Benzos e.g. diazepam
Pabrinex
Inpatient / community detox

54
Q

7 components of a Mental State Examination:

A
  1. Appearance and behaviour
  2. Speech
  3. Mood and affect
  4. Thought
  5. Perception
  6. Cognition
  7. Insight
55
Q

Define ‘delusion’:

A

A fixed, false belief outwith a person’s social, cultural and religious background.

56
Q

Define ‘hallucination’:

A

False sensory perception in the absence of an external stimulus.

Can be organic, drug-induced or associated with a psychiatric disorder.

57
Q

Possible causes of hallucinations (5):

A

Schizophrenia

Substance-induced psychotic disorder

Bipolar Disorder

Delirium

Dementia

58
Q

Describe the difference between internal and externally experienced auditory hallucinations. Which one carries a worse prognosis?

A

Internal = voice coming from inside the patient, usually their head.

External = coming from the external environment.
External are usually worse, indicating e.g. schizophrenia.

59
Q

4 domains of cognition:

A

Attention
Memory
Orientation
Intellect

60
Q

Describe ‘flight of ideas’ and what is it usually indicative of?

A

Onto a new subject instantly, but there is some vague connection e.g. connecting word / idea / rhyme.
Flow doesn’t make sense but you can follow it.

Indicative of mania.

61
Q

What is thought insertion?

A

When a patient believes someone else is putting thoughts into their head.

62
Q

What is thought broadcasting?

A

When a person believes their thoughts are available to everyone else.

63
Q

Indications for ECT:

A
  1. Treatment resistant depression

+ severely suicidal
+ acutely unwell / not eating and drinking
+ catatonia
+ intractable mania

64
Q

Absolute contraindications to ECT:

A

Increased ICP
Phaeochromocytoma

65
Q

Relative contraindications to ECT:

A

Recent MI
Recent stroke
Uncontrolled hypertension
Arrhythmias
Glaucoma
History of cerebral or aortic aneurysm
High risk pregnancies

These conditions are likely to increase associated risks.

66
Q

Short term side effects of ECT (5):

A

Headache
Nausea
Short term memory impairment
Memory loss of events prior to ECT
Cardiac arrhythmia

67
Q

Long term side effect of ECT:

A

some patients report impaired memory

68
Q

Name 3 SSRIs and briefly describe the MOA:

A

Fluoxetine
Sertraline
Citalopram

Selective presynaptic blockade of serotonin reuptake pumps.

69
Q

Name 2 SNRIs and briefly describe the MOA:

A

Venlafaxine
Duloxetine

Presynaptic blockade of noradrenaline and serotonin, and also dopamine in high doses.

70
Q

Name 3 TCAs and briefly describe the MOA:

A

Amitriptyline
Imipramine
Clomipramine

Presynaptic blockade of noradrenaline and serotonin, also with blockade of muscarinic, histaminergic and alpha-adrenergic receptors.

71
Q

Outline indications for mirtazapine and MOA.

A

Blocks alpha2-adrenergic receptors, which increases the release of neurotransmitters.

Indicated in depression.

72
Q

Side effects of mirtazapine:

A

Sedation
Increased appetite

Can be beneficial in older people who are suffering from insomnia and poor appetite.

73
Q

Compare the side effect profile of SSRIs and SNRIs:

A

Similar side effects, but SNRIs tend to be more severe.

74
Q

Contraindications to SSRIs:

A

Mania
Poorly controlled epilepsy
Prolonged QTc (citalopram and escitalopram)

75
Q

Side effects of SSRIs:
(GALISS)

A

GI disturbance
Anxiety
Loss of appetite and weight loss
Insomnia
Sweating
Sexual dysfunction

76
Q

Anticholinergic side effects of e.g. TCAs:

A

Dry mouth
Constipation
Urinary retention
Blurred vision

77
Q

Cardiotoxic effects of TCAs:

A

QTc prolongation
ST elevation
Heart block
Arrhythmias

78
Q

Contraindications for TCAs:

A

Recent MI
Arrhythmias
Acute porphyria
Mania
High risk for overdose (due to cardiotoxic effects)

79
Q

Which TCAs have less prominent sedative side effects (histaminergic receptors)?

A

Imipramine and lofipramine

80
Q

What side effects does alpha-adrenergic receptor blockade cause?

A

Postural hypotension
Dizziness
Syncope

81
Q

Which drugs are typically included in the ‘mood stabilizer’ class of drugs?

A

Lithium
Sodium Valproate
Carbamazepine
Lamotrigine
(Last 3 are anticonvulsants)

82
Q

Indications for lithium:

A

Prophylaxis of BPAD
Acute mania
Treatment-resistant depression

83
Q

Discuss the pharmacological features of lithium and how they relate to patient prescribing:

A

Very narrow therapeutic window between non-therapeutic and toxic blood levels.
Lower levels can be toxic in older patients.

Oral administration.
Excreted via kidneys; clearance decreased with renal impairment.

84
Q

Adverse effects of lithium:

A

Diabetes insipidus
Hypothyroidism
Hyperparathyroidism leading to hypercalcaemia
T wave flattening / inversion
Leucocytosis (benign)
Teratogenic
N+V
Fine tremor
Weight gain

85
Q

Outline the recommended monitoring of patients on lithium:

A

Samples should be taken 12 hours post dose.
Levels taken weekly after starting / dose change until concs are stable.
Once stable for 2/52, check every 3 months.
Monitor thyroid and renal function every 6 months.

Patients should be given a record book, info booklet and alert card.

86
Q

Which investigations are required prior to starting lithium therapy?

A

Pregnancy test (teratogenic)
TFTs
FBC
U+Es
Calcium (hyperparathyroidism)
ECG if cardiac disease or RFs

87
Q

Which drugs can increase lithium levels if coprescribed?

A

Thiazide diuretics
NSAIDs
ACEi

88
Q

What class of drug that is commonly coprescribed with lithium can increase risk of neurotoxicity?

A

Antipsychotics (coprescribed in acute mania)

89
Q

Signs of lithium toxicity in conjunction with blood levels a) 1.5-2mmol/L and b) >2mmol/L:

A

1.5-2 = n+v, apathy, coarse tremor, ataxia, muscle weakness

> 2 = nystagmus, dysarthria, reduced LOC, hyperactive tendon reflexes, oliguria, hypotension, convulsions, coma

90
Q

Outline some EPSEs, commonly associated with first generation antipsychotics.

A

Parkinsonism
Acute dystonia (sustained muscle contraction)
Akathisia
Tardive dyskinesia (chewing, pouting of jaw)

91
Q

Name two typical antipsychotics and outline their MOA.

A

Haloperidol
Chlorpromazine

D2 receptor antagonist, blocking dopamine transmission in mesolimbic pathways.

92
Q

Apart from EPSEs, what is the next most common side effect of typical antipsychotics?

A

Hyperprolactinaemia (can cause galactorrhoea)

93
Q

Name 3 atypical antipsychotics.

A

Clozapine
Quetiapine
Risperidone

94
Q

How is clozapine different to most antipsychotics in terms of MOA?

A

Clozapine is a weak D2 antagonist (unlike the rest), but has high affinity for 5-HT2A receptors

95
Q

What triad characterises both serotonin syndrome and neuroleptic malignant syndrome?

A

Neuromuscular abnormalities

Altered consciousness

Autonomic dysfunction

96
Q

Which drugs should be avoided in patients who are taking an SSRI, and why?

A

Triptans; risk of serotonin syndrome.

NSAIDs; SSRIs increase the risk of GI bleeding too. If must be prescribed, coprescribe a PPI.

Warfarin / heparin; avoid SSRIs, use mirtazapine.

97
Q

Short term side effects of ECT;

A

Headache
Nausea
Short term memory impairment
Cardiac arrhythmia
Memory loss of events prior to ECT

98
Q

Absolute contraindication for ECT?

A

Raised ICP

99
Q

What is the most dangerous side effect of clozapine? + symptoms

A

Agranulocytosis (severe, dangerously low levels of white blood cells.)

Malaise, fever, chills, infections (ulcers, oral necrotizing lesions), ?sepsis.
FBC, neutrophil count LOW

100
Q

Discuss the clinical presentation of Korsakoff’s syndrome.

A

Wernicke’s encephalopathy (opthalmoplegia, ataxia, confusion) +

Confabulation

Anterograde amnesia (cannot form new memories)

Retrograde amnesia

101
Q

Features of delirium tremens:

A

Coarse tremor
Confusion
Delusions
Auditory and visual hallucinations
Fever
Tachycardia
Peaks 48-72 hrs post last drink

102
Q

Differences in memory loss between dementia and severe depression:

A

Dementia causes recent memory loss

Depression / pseudodementia causes global memory loss

103
Q

What treatment options are available in severe cases of PTSD?

A

CBT
EMDR therapy
Venlafaxine / SSRI / ?risperidone

104
Q

When should lithium monitoring be performed?

A

Weekly after initiation and dose change.

Should be 12 hours after dose has been taken.

Once stable, then checked every 3 months for the first year.

105
Q

What other blood test should be checked every 6 months for patients on lithium and why?

A

Thyroid function tests

Can lead to hypothyroidism, and also transient hyperthyroidism

106
Q

When should antipsychotic medications be changed in schizophrenia?

A

Trial 2 different antipsychotics e.g. risperidone, quetiapine.

If 2 have been tried, then switch to clozapine.

107
Q

What is the strongest risk factor for psychotic disorders?

A

Family history of psychotic disorders.

108
Q

Management of mania / hypomania in patients taking antidepressants:

A

Consider stopping the antidepressant

Start antipsychotic therapy e.g. risperidone

109
Q

In anorexia nervosa, most biochemical tests are low. G’s and C’s are the exception and are raised. 3 Gs, 3 Cs:

A

Growth hormone
Glucose
salivary Glands

Cortisol
Cholesterol
Carotinaemia

110
Q

What is the next line option for patients with more severe OCD if they are unresponsive to CBT / exposure therapy?

A

Add SSRI e.g. sertraline

111
Q

Which electrolyte disturbance is associated with SSRIs?

A

Hyponatraemia

112
Q

Pharmacological therapy for generalised anxiety disorder:

A
  1. Sertraline / SSRI
  2. Different SSRI or SNRI
  3. Pregabalin
113
Q

What is the belief in a Capgras delusion?

A

That family members etc are imposters.

E.g. if you were in disguise, you’d wear a CAP

114
Q

What is the belief in a Cotard delusion?

A

Dead / rotting on the inside / part of the body is dead

115
Q

What is formication?

A

A rare type of paraesthesia where it feels like insects are crawling on the skin

116
Q

What is the belief is delusional parasitosis?

A

The belief that ones skin is infested with e.g. bugs. Patient often takes radical steps to try and kill the apparent infestation.

117
Q
A

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