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Year 2 > Case 12 > Flashcards

Case 12 Flashcards

1
Q

4 central dopamine pathways

A

Mesocortical - VTA to PFC
Mesolimbic - VTA to NAc
Nigrostriatal - Substantia Nigra to Striatum
Tuberoinfundibular - Hypothalamus to Pituitary

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2
Q

Components of limbic system

A

Hippocampus
Cingulate gyrus
Hypothalamus
Anterior thalamic nuclei

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3
Q

Function of limbic system

A

Cortical control of emotion

Storage of memory

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4
Q

Function of prefrontal cortex

A

Planning and executing actions

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5
Q

PFC and limbic system are connected by

A

Cortical-Subcortical-Cortical loops

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6
Q

Connections between PFC and Limbic system are affected by…

A

Major depressive disorder

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7
Q

Schema

A

Pattern of negative thoughts

about self, the world, and the future

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8
Q

Biased attention

A

Negative views about self

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9
Q

Biased processing

A

Negative views about the world

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10
Q

Biased memory

A

Negative views about the future

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11
Q

Areas of the brain which have increased activity in depression (increased metabolism)

A

Hippocampus
Amygdala
Thalamus

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12
Q

Areas of the brain which have decreased activity in depression (decreased metabolism)

A

Prefrontal cortex
Dorsal Anterior Cingulate Cortex
Dorsolateral prefrontal cortex

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13
Q

Dorsal Vs Ventral Anterior Cingulate Cortex

A

Dorsal - Cognitive (connected to prefrontal cortex)

Ventral - Emotional (connected to amygdala and hippocampus)

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14
Q

Function of Ventrolateral PFC

A

Mediator of pain, aggression, libido and appetite

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15
Q

Function of Lateral-Orbital PFC

A

Mediator of maladaptive, perseverative mood states

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16
Q

Function of Dorsolateral PFC

A

Maintains executive function, sustained attention/concentration and working memory

(Hypoactive in depression - appear withdrawn)

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17
Q

Dopamine binds to…

A

D1 and D2 receptors

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18
Q

Noradrenaline binds to…

A

Adrenergic receptors

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19
Q

Excitatory and inhibitory neurotransmitters are… (fast/slow)

A

Fast

Exert effects in less than 1 millisecond

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20
Q

Modulatory neurotransmitters are… (fast/slow)

A

Slow

Take up to minutes but have longer lasting effects

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21
Q

Excitatory neurotransmitters

A

Glutamate
Dopamine (D1)
Noradrenaline
Adrenaline

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22
Q

Inhibitory neurotransmitters

A

Dopamine (D2)
Serotonin
GABA

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23
Q

Tyrosine Hydroxylase

A

Converts Tyrosine to L-DOPA

Requires Fe2+, O2 and BH4

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24
Q

Conversion of L-DOPA to Dopamine requires…

A

AADC enzyme

Vitamin B6 cofactor

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25
Q

Conversion of Dopamine to Noradrenaline requires…

A

DBH enzyme
Vitamin C cofactor
Cu2+ cofactor

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26
Q

Conversion of Noradrenaline to adrenaline requires…

A

PNMT enzyme

A methyl donor

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27
Q

Where is NA converted to A?

A

Locus coeruleus

Adrenergic neurons and adrenal medulla

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28
Q

Where is dopamine converted to noradrenaline?

A

Noradrenergic neurons

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29
Q

Where is L-DOPA converted to dopamine?

A

Cytosol of dopaminergic neurons

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30
Q

Tryptophan Hydroxylase (TPH)

A

Converts Tryptophan to 5HT

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31
Q

Conversion of 5HT to 5-HT requires…

A

AADC

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32
Q

Conversion of 5HT to 5-HT causes release of…

A

CO2

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33
Q

Function of locus coeruleus

A

Alertness/Arousal

response to stress and panic

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34
Q

Locus Coeruleus contains

A

Noradrenergic neurons

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35
Q

Serotonin receptors 1A,B,D,E,F

A

Activated by triptans

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36
Q

Serotonin receptors 2A-C

A

Activated by hallucinogenic drugs

Blocked by atypical antipsychotics

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37
Q

5HT3 Receptor

A

The only ionotropic receptor

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38
Q

Serotonin receptors are usually

A

GPCR

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39
Q

Adrenergic system receptors

A

Alpha 1 = Gq
Alpha 2 = Gi
Beta = Gs

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40
Q

Dopaminergic system receptors

A 
D1 = Gs
D2 = Gi
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41
Q

Monoamine hypothesis

A

Depression caused by a functional deficit in monoamines (esp. 5-HT and NA)

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42
Q

Chemical hypothesis

A

Depression is caused by underactivity/impaired function of monoamines

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43
Q

Network hypothesis

A

Depression is caused by impaired neuronal communication and problems processing information

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44
Q

Cortisol concentration in depressed people is…

A

High

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45
Q

Brain-derived neurotrophic factor

A

Supports neuronal survival in hippocampus, cortex and basal forebrain

Low in depression

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46
Q

MOA of Imipramine/Nortryptyline/Amitriptyline

A

TCAs

Inhibit 5-HT and NA reuptake into presynaptic cleft

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47
Q

ADRs caused by TCAs blocking mACh receptors

A

Dry mouth
Constipation
Drowsiness
Blurred vision

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48
Q

ADRs caused by TCAs blocking H1 Histamine receptors

A

Drowsiness

Weight gain

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49
Q

ADRs caused by TCAs blocking alpha-1 adrenergic receptors

A

Dizziness

Hypotension

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50
Q

ADRs caused by TCAs blocking voltage-gated Na+ channels

A

Arrhythmias

Long QT syndrome (Torsade de Pointes)

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51
Q

Contraindications of Desipramine/Amitryptyline

A

TCAs:

On adrenergic vasoconstrictors - cause arrhythmias
On barbiturates (sedative hypnotics) - cause severe respiratory depression
On acetaminophen (paracetamol) - P reduces metabolism of TCA
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52
Q

Effect of TCAs with adrenergic vasoconstrictors

A

Can cause arrhythmias

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53
Q

Effects of TCAs with barbiturates

A

Severe respiratory depression

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54
Q

Effects of TCAs with acetaminophen (paracetamol)

A

Paracetamol reduces metabolism of TCA, causing toxicity

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55
Q

MOA of citalopram/sertraline

A

SSRIs

Selectively inhibit reuptake of 5-HT into presynaptic cleft

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56
Q

Common ADRs of SSRIs (paroxetine/citalopram)

A 
Anxiety
Gastric upset
Headache
Weight gain 
Nausea and vomiting (overactivation of 5HT3)
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57
Q

Effect of overactivation of 5HT3 due to SSRIs

A

Nausea and vomiting

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58
Q

Effect of overactivation of 5HT2A in spinal cord and nucleus accumbens due to SSRIs

A

Sexual dysfunction

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59
Q

Notable ADRs of SSRIs (citalopram/fluvoxamine)

A

Insomnia
SSRI dyscontinuation syndrome
Sexual dysfunction
Increased risk of bleeding

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60
Q

SSRI dyscontinuation syndrome

A

Flu-like symptoms

Changes in sleep, movement, thinking, mood, movement, senses

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61
Q

Serious ADRs of SSRIs

A

Hyponatraemia
Increased bleeding
Serotonin syndrome

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62
Q

Serotonin syndrome

A 
Increased temperature
Increased reflexes
Agitation 
Tremor 
Sweating 
Dilated pupils 
Diarrhoea
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63
Q

Drug interactions of SSRIs

A

SSRIs decrease metabolism of Codeine, benzodiazepines, Erythromycin

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64
Q

MOA of reboxetine/atomoxetine

A

NRIs

Inhibition of noradrenaline reuptake into synaptic cleft

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65
Q

ADRs of reboxetine/atomoxetine

A

NRIs:

Anorexia
Chills
Constipation
Dry mouth
Headache
Insomnia 
Urinary retention
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66
Q

MOA of SNRIs (Venlafaxine/Duloxetine/Milnacipran)

A

Inhibit 5-HT and norarenaline reuptake into presynaptic cleft

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67
Q

ADRs of Venlafaxine/Duloxetine

A

SNRIs:

Agitation - tremor, increased blood pressure and heart rate
Nausea
Diarrhoea
Anorgasmia

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68
Q

Risk in TCA overdose

A

Ventricular dysrhythmias

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69
Q

Contraindications of venlafaxine/milnacipran

A

SNRIs:
Conditions with high risk of cardiac arrhythmias
Uncontrolled hypertension

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70
Q

MOA of Moclobemide

A

Selective Monoamine Oxidase A inhibitor

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71
Q

MOA of Phenelzine/Tranylcypromine

A

Non-selective MAO inhibitor

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72
Q

ADRs of phenelzine

A 
MAOI:
Dry mouth, 
Constipation,
Drowsiness,
Hypotension, 
Insomnia
Weight gain
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73
Q

Interactions of phenelzine

A

MAOI:

Cheese Reaction with foods containing tyramine (beer, wine, aged cheese, marmite)

Rage, mania, suicidal behaviour

Tyramine = increased release of NA = increased activation of SNS

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74
Q

Contraindications of phenelzine/moclobemide

A

Phaeochromocytoma
Cerebrovascular disease
Thyrotoxicosis
Bipolar Affective Disorder

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75
Q

MOA of Buproprion

A

Atypical

Inhibits Dopamine reuptake and weakly inhibits NA reuptake

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76
Q

ADRs of buproprion

A 
Atypical antidepressant:
Headache
Dry mouth
Agitation
Insomnia
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77
Q

Contraindications of buprioprion

A 
Atypical Antidepressant:
Acute alcohol withdrawal
Acute benzodiazepine withdrawal
Hx of seizures
Hepatic cirrhosis
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78
Q

MOA of mirtazapine

A

Alpha-2 adrenergic receptor antagonist

Also antagonist of 5HT2A and 5HT3

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79
Q

ADRs of mirtazapine

A

Atypical Antidepressant:
Dry mouth
Sedation
Weight gain

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80
Q

Why does alpha-2 adrenoceptor antagonism aid in depression?

A

Presynaptic Alpha-2 receptors are the ‘brakes’ on noradrenergic neurones.
When alpha-2 receptors are blocked, there is no inhibition of NA neurons

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81
Q

Why is St John’s Wort not prescribed for depression?

A

Many interactions with conventional drugs due to induction of metabolising enzymes (If StJW is stopped, increase in concentration of interacting drug = TOXICITY)

Amount of active ingredient varies between preparations.

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82
Q

MOA of ketamine

A

NMDA receptor antagonist (the glutamate receptor)

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83
Q

How does ketamine improve mood?

A

Blocks action of glutamate.
Increased in BDNF - causing synaptogenesis
Reversal of cellular atrophy due to stress/glucocorticoids

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84
Q

Negative impact of giving exogenous cytokines (interferon-alpha and TNF)

A

Profound depressive illness

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85
Q

Immunological Hypothesis for depression

A

Raised inflammatory cytokines (The sick role)
Modulation of HPA axis
Raised cortisol
Cortisol is neurotoxic - particularly to hippocampus

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86
Q

Singular Nucleotide base Polymorphisms (SNPs)

A

Variation in a single nucleotide that occurs at a specific position in a genome

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87
Q

Copy Number Variants (CNVs)

A

Sections of genome are repeated and number of repeats in genome varies between individuals in the human population.

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88
Q

Penetrance

A

The extent to which a gene is expressed in the phenotypes of individuals carrying it

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89
Q

CNVs with relatively high risk of schizophrenia

A

VCFS deletion

3q29 deletion

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90
Q

Orexin is released from…

A

Lateral and posterior hypothalamus

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91
Q

Orexin is released in response to…

A

Low blood glucose

High ghrelin

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92
Q

Effect of orexin

A

Orexigenic

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93
Q

Leptin is released from…

A

Adipocytes

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94
Q

Leptin is released in response to…

A

Stomach distention

Insulin

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95
Q

Effect of leptin

A

Anorexigenic

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96
Q

Ghrelin is released from…

A

Gastric mucosa in stomach and small intestine

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97
Q

Ghrelin is released in response to…

A

Empty stomach

Low blood glucose

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98
Q

Effect of ghrelin

A

Orexigenic

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99
Q

PYY is released from…

A

L cells in colon/ileum

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100
Q

PYY is released in response to…

A

Calorie intake

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101
Q

Effect of PYY

A 
Anorexigenic 
Slows peristalsis (to maximise absorption)
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102
Q

CCK is released from…

A

I cells in duodenal mucosa

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103
Q

CCK is released in response to…

A

Products of protein an fat digestion in duodenum

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104
Q

Effect of CCK

A

Anorexigenic
Slows gastric emptying
Emptying of gallbladder (contraction)

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105
Q

Why do patients with PWS have increased appetite?

A

Hyperghrelinaemia (orexigenic) = failed satiety response

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106
Q

Areas of brain involved in “Wanting”

A

VTA
Amygdala
Ventral Pallidum
Nucleus Accumbens

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107
Q

Areas of brain involved in “Liking”

A

Ventral Pallidum

Nucleus Accumbens

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108
Q

How does ghrelin stimulate appetite?

A

Acts on ghrelin neurons
Ghrelin neurons send fibres to NYP and AgRP containing neurones
Stimulates release of orexigenic peptides

Ghrelin neurons also send inhibitory fibres to POMC containing neurones.
Inhibits release of anorexigenic peptides.

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109
Q

How does leptin inhibit appetite?

A

Inhibits NYP and AgRP containing neurons.

Stimulates POMC neurons

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110
Q

Effect on appetite of 5HT2c activation

A

Inhibits (activates POMC containing neurons)

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111
Q

Effect on appetite of 5HT1b activation

A

Stimulates (inhibits POMC containing neurons)

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112
Q

Somatic syndrome

A

Loss of appetite and weight loss >5% in one month

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113
Q

Symptoms of atypical depression (CRH deficient)

A

Craving foods high in CHO + weight gain

Hypersomnia

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114
Q

Effect of inflammatory cytokines on appetite

A

Decreases appetite

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115
Q

3 Key aspects of storm and stress in adolescence

A

Conflict with parents
Mood disruptions
Risk behaviour

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116
Q

Onset of adrenarche in females

A

6-9yrs

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117
Q

Onset of adrenarche in males

A

7-10yrs

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118
Q

Adrenarche

A

Activation of HPA axis
Zona reticularis to produce androgens
Results in secondary sexual characteristics and changes in sweat glands

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119
Q

Onset of gonadarche in females

A

8-14yrs (11 mean)

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120
Q

Onset of gonadarche in males

A

9-15yrs (12 mean)

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121
Q

Gonadarche

A

Reactivation of hypothalamic-pituitary-gonadal axis.
Pulsatile release of GnRH during sleep.
FSH and LH release from A. Pituitary.
Gonadal steroid release - oestrogen and testosterone.

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122
Q

3x Endocrine events during puberty

A

Adrenarche
Gonadarche
Activation of growth axis

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123
Q

Age of pubertal growth spurt in females

A

12yo

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124
Q

Age of pubertal growth spurt in males

A

14yo

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125
Q

Function of testosterone in puberty

A

Develop neural circuitry for typical male behaviour

Defeminisation

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126
Q

Behavioural effects of sex steroid hormones (Oestrogen and testosterone)

A

Reproductive behaviours
Reorganisation of sensory and association regions
Motivation and reward behaviour

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127
Q

Area of the brain responsible for reproductive behaviours

A

Hippocampus

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128
Q

Areas of brain responsible for motivation and reward behaviour

A

Nucleus Accumbens

Dopaminergic pathways to PFC

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129
Q

Effect of early life stressors on the brain

A

Neuronal atrophy due to chronically high cortisol

Leads to dysregulation of HPA system

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130
Q

Pruning

A

Elimination of rarely used neural connections in the brain to make it more efficient.
Occurs during adolescence

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131
Q

Grey matter maturation occurs in…. first, then ….

A

Motor and sensory systems first

Then frontal, parietal and temporal cortices (involved in integrating primary function)

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132
Q

Maturation of PFC during adolescence results in…

A

Greater control of thoughts and behaviour
Long term planning
Self evaluation

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133
Q

Improved connectivity between PFC and limbic system during adolescence results in…

A

Improved decision making

Better risk and reward system

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134
Q

Average age of schizophrenia onset

A

15-25 yrs

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135
Q

Circadian rhythms

A

Occurring over approximately one day

Includes changes in temperature, heart rate, respiration rate and metabolism.

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136
Q

Ultradian rhythms

A

Occur over less than one day

e.g. passing through different stages of sleep

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137
Q

Infradian Rhythm

A

Occurs over more than 1 day

e.g. menstrual cycle

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138
Q

Stage 1 of sleep

A

Alpha waves 8-12 Hz
Low amplitude, moderate frequency.

Drowsy wakefulness
(Wakes immediately if aroused)

139
Q

Stage 2 of sleep

A

High amplitude
Slower frequency
K complexes
Sleep spindles

(More difficult to arouse than stage 1)

140
Q

K complexes

A

Unique to stage 2 of sleep
Suppress cortical arousal
Aid sleep-based memory consolidation

141
Q

Sleep spindles

A

Unique to stage 2 of NREM sleep

Immediately follow muscle twitching

142
Q

Stage 3 of sleep

A

Delta waves appear (1-2Hz)
Large amplitude,
Low frequency

Decreased breathing, heart rate and body temperature)

143
Q

Stage 4 of sleep

A

Dominated by delta waves

144
Q

Bruxism

A

Jaw clenching

145
Q

Hrs of sleep for a baby

A

16

146
Q

Hrs sleep for children

A

9-16

147
Q

Hrs sleep for teenagers

A

9

148
Q

Hrs sleep for adults

A

7-8

149
Q

Why is muscle tone lost in REM sleep?

A

Alpha motor neurons inhibited

150
Q

Vital signs in REM sleep…

Because…

A

Increased blood pressure, respiration and heart rate

Because sympathetic NS is partially activated

151
Q

Blood flow to the brain during REM sleep

A

High blood flow to visual cortex - due to complex visual material in dreams.

Low blood flow to inferior frontal cortex - poor temporal organisation and bizarreness)

152
Q

What is the effect of shutting down the frontal cortex during REM sleep?

A

Limbic system no longer inhibited

Limbic system involved in emotion, motivation, long term memory and olfaction

153
Q

Effect of activity in noradrenergic neurons on REM sleep

A

Inhibits REM sleep

154
Q

Effect of activity in 5-HT neurons on REM sleep

A

Inhibits REM sleep

155
Q

Effect of activity in cholinergic neurons on REM sleep

A

Promotes REM sleep

156
Q

Seasonal Affective Disorder

A

Increased melatonin release from pineal gland during darkness.
Melatonin causes sleepiness.
Leads to severe disruption in mood.

157
Q

Preferred phase shift pattern of sleep

A

Day shift
Evening shift
Night shift

i.e. Delay > Advance

158
Q

Morning melatonin causes…

A

Delay (go to sleep later - when it is dark in the morning)

159
Q

Afternoon melatonin causes…

A

Advance (go to sleep earlier - when it is dark in the afternoon)

160
Q

Evening melatonin is…

A

Ineffective

161
Q

Zeitgebers

A

Cues in the regulation of the body’s circadian rhythm

e.g. Light

162
Q

Initiation of sleep

A

Activity in serotonergic neurones.
Decreased activity in reticular formation and cortex.
Allows sleep to be initiated.

163
Q

REM sleep is initiated by..

A

Activity in noradrenergic neurons

164
Q

Melanopsin

A

Photopigment found in light sensitive retinal ganglion cells

165
Q

SCN retains its cyclicity when maintained in vitro, therefore….

A

It can be transplanted - sets the rhythm of the donor animal in the receiving

166
Q

How does the body respond to sleep deprivation?

A

Increases slow wave, NREM sleep (stages 3 and 4)

Decreases REM sleep (satisfying sleep)

167
Q

Why is NREM sleep less satisfying?

A

Areas of the brain involved in memory consolidation and retrieval are not shut down.

168
Q

Serotypes associated with low hypocretin levels in CSF

A

HLA DR2 and DQ1

169
Q

Patient enters REM sleep almost immediately after starting a daytime nap.
This suggests…

A

Chronic sleep deprivation

170
Q

Multiple sleep latency test (MSLT)

A

Measure time elapsed from start of a daytime nap to the first signs of sleep.
Used in diagnosis of sleep disease.

171
Q

Hypocretin

A

Neuropeptide that regulates arousal, wakefulness and appetite

172
Q

Serotypes associated with Narcolepsy

A

HLA DR2 and DQ1

Cause a reduction in hypocretin in CSF

173
Q

Narcolepsy is caused by…

A

Destruction of cells that produce hypocretin

Therefore, reduction in levels of hypocretin in CSF

174
Q

Symptoms of narcolepsy

A

Excessive daytime sleepiness

Falling asleep suddenly, without warning

Sleep paralysis (unable to move or speak when waking or falling asleep)

175
Q

Treatment of narcolepsy

A

Modafinil - daytime
Sodium oxybate - at night
Education
Psychology

176
Q

MOA of Modafinil

A

Inhibits DA reuptake
Activates glutamatergic circuits
Inhibits GABA
Promotes wakefulness

Used in narcolepsy.

177
Q

Sodium Oxybate

A

A metabolite of GABA.

Taken at night by narcolepsy patients.

178
Q

Cataplexy

A

Sudden muscular weakness caused by strong emotions.

179
Q

Symptoms of cataplexy

A

Jaw drop, head slump, leg collapse, slurred speech, double vision etc.

Triggered by strong emotion e.g. laughter, anger, surprise

180
Q

Treatment of cataplexy

A

Gamma-hydroxybutyrate (CNS depressant)

Antidepressants

181
Q

Gamma-hydroxybutyrate (GBH)

A

CNS depressant used to treat cataplexy.

Active ingredient is Sodium Oxybate, a metabolite of GABA.

182
Q

Benign Rolandic Epilepsy

A

Partial epileptic seizures during sleep, causing a reduction in REM sleep.

183
Q

Sleep disorders often seen in people with epilepsy

A

Narcolepsy
Sleep apnoea
Restless leg syndrome
Night terrors

184
Q

Sleep deprivation and epilepsy

A

Sleep deprivation often causes seizures in people with epilepsy.

185
Q

Drugs which induce an unnatural sleeping pattern…

A

Morphine
Barbiturates
Benzodiazepines

186
Q

What is the effect of drugs which induce an unnatural sleeping pattern?

A

Reduction in REM sleep

Patient will appear drowsy on waking

187
Q

Drugs which induce a natural sleeping pattern..

A

Melatonin

Tryptophan

188
Q

Use of melatonin in hospitals

A

Used to promote a natural sleeping pattern.

Can be used for a maximum of 2 weeks.

189
Q

Napping rules for good sleep hygiene

A

Avoid napping during the daym particularly after 3pm.

Limit naps to 1 hour

190
Q

Role of astrocytes in blood brain barrier

A

Formation and maintenance of tight junctions between cerebral endothelial cells.

191
Q

Role of pericytes in the blood brain barrier

A

Secrete proteins to contribute to basal membrane

192
Q

Area postrema is located..

A

In medulla

193
Q

Area of brain that lacks a blood-brain barrier

A

Area Postrema

194
Q

Function of area postrema

A

Controls vomiting

Fenestrated capillaries allow small molecules to enter brain.
Chemoreceptors detect toxins in the blood and trigger vomiting.

195
Q

MOA of valproate

A

Sodium channel blocker

Increases GABA in the brain

196
Q

Indications for valproate

A

Bipolar
Epilepsy
Migraine

197
Q

SERT

A

Serotonin transporter

198
Q

Definition of clinical anxiety

A

Preparation for danger in the absence of an immediately threatening stimuli

199
Q

Cognitive component of emotional memories occurs in..

A

Hippocampus

200
Q

Emotional component of emotional memories occurs in…

A

Lateral nuclear complex of Amygdala

201
Q

Panic disorder

A

Discrete episodes of intense anxiety accompanied by somatic symptoms

202
Q

Glutamic acid Decarboxylase

A

Converts glutamate to GABA

203
Q

Structure of GABA-A receptos

A

Pentamer

B2, a1, B2, a1, G2

204
Q

GABA-A is selectively permeable to…

A

Cl-

205
Q

Function of GABA-B channels

A

Inhibit voltage gated Ca2+ channels
Inhibit Adenylyl Cyclase
Open K+ channels (hyperpolarisation)

206
Q

CRF/CRH neurons are found in the….

A

Hypothalamic periventricular nucleus

207
Q

Patients with anxiety have (high/low) GABA in the cortex

A

Low

208
Q

Treatment of acute anxiety attacks

A

Benzodiazepines with sustained action:

Diazepam, Alprazolam, Chlordiazepoxide, Clobazam

209
Q

Active metabolite in diazepam

A

Nordazapam

210
Q

ADRs of benzodiazepam

A

Drowsiness,
Confusion
Retrograde amnesia
Impaired coordination

211
Q

How does ethanol exert its anxiolytic effects?

A

Facilitates GABA-mediated GABA-A receptor Cl- channels

212
Q

Long acting benzodiazepines

A

Diazepam,

Chordiazepoxide

213
Q

Short acting benzodiazepine

A

Lorazepam

Temazepam

214
Q

Indication for propanolol in treatment of anxiety

A

When physical symptoms such as sweating, tremor and tachycardia occur

215
Q

MOA of buspirone

A

5-HT1A receptor agonist

216
Q

Indication for buspirone

A

Generalised anxiety disorder

217
Q

ADRs of buspirone

A

Nausea
Dizziness
Headache
Nervousness/Excitement

218
Q

Contraindications of buspirone

A

Epilepsy

Acute porphyria

219
Q

Paranoid schizophrenia accounts for… of all schizophrenia

A

40%

220
Q

Disorganised schizophrenia

A

Disorganised speech and behaviour

Find it hard to do every day tasks

221
Q

Catatonic schizophrenia

A

Abnormal movement or behaviour

222
Q

Undifferentiated schizophrenia

A

Mixture of different type of schizophrenia

223
Q

Residual schizophrenia

A

History of episodes

No current symptoms

224
Q

Effect of activation of D1 receptors

A

Activates Adenylyl Cyclase

225
Q

Effect of activation of D2 receptors

A

Inhibits Adenylyl Cyclase

226
Q

D1 type D1 receptors are localised to…

A

Nucleus Accumbens
Hypothalamus
Thalamus
Frontal cortex

227
Q

D1 receptors are localised to..

D2 receptors are localised to…

A

D1 - Mesolimbic pathway

D2 - Mesocortical pathway

228
Q

Dopamine Theory of Psychosis

A

Psychosis is caused by dysregulation of dopaminergic pathways.

Overactive mesolimbic pathway (D1 - Gs) causing positive symptoms

Underactive mesocortical pathway (D2 - Gi) causing negative symptoms

229
Q

Glutamate Theory of Psychosis

A

NMDA hypofunction

Causes decreased activity in mesocortical pathway (D1) causing negative symptoms

Causes increased activity in mesolimbic pathway (D2) cauing positive symptoms.

230
Q

MOA of chlorpromazine

A

Dopamine receptor antagonist (non-selective)

231
Q

MOA of Haloperidol

A

Dopamine receptor antagonist (higher affinity for D2 than D1)

232
Q

Extrapyramidal symptoms of chlorpromazine and haloperidol resulting from D2 blockade of extrapyramidal system

A

Acute dystonia
Tardive kinesia
Akathisia

233
Q

Acute Dystonia

A

Sudden and spastic contraction of muscles, often in face and neck.
Caused by blockade of D2 receptors in extrapyramidal system.

234
Q

Oculogyric Crisis

A

Prolonged, involuntary, upward movement of the eyes

A form of acute dystonia

235
Q

Tardive dyskinesia

A

Involuntary, abnormal movements
e.g. Oro-buccal-facial causing tongue movements and excessive blinking

Caused by D2 blockade in extrapyramidal motor system

236
Q

Akathisia

A

Subjective sense of anxiety and restlessness

Caused by D2 blockade in extrapyramidal motor system

237
Q

ADRs of conventional antipsychotics

A 
Sedation 
Dry mouth
Blurred vision 
Urinary retention 
Constipation

+ Acute dystonia
Tardive kinesia
Akathisia

238
Q

Main ADRs of chlorpromazine

A 
Increased prolactin (gynaecomastia)
Hypothermia 
Anticholinergic effects 
Hypersensitivity reactions 
Obstructive jaundice
239
Q

Main ADRs of haloperidol

A

Increased prolactin (gynaecomastia)
Hypothermia
Anticholinergic effects (fewer than chlopromazine)
Hypersensitivity reactions

240
Q

MOA of clozapine

A

Atypical

Antagonist of dopamine, serotonin (5-HT2) and other monoamine receptors

241
Q

ADRs of clozapine

A 
Seizures
Salivation 
ACh effects (dry mouth, constipation)
Weight gain 
Hyperlipidaemia 
Hyperglycaemia
Risk of agranulocytosis
242
Q

MOA of newer atypical antipsychotics

A

5-HT2A blockade (higher affinity for 5-HT2A than D2)

Examples: Risperidone, olanzapine and quetiapine

243
Q

ADRs of risperidone

A

Weight gain
Hypotension
Hyperprolactinaemia

244
Q

ADRs of olanzapine

A

Weight gain
Hyperlipidaemia
Hyperglycaemia

245
Q

ADRs of Quetiapine

A

Sedation/Drowsiness
Tachycardia
Weight gain
Constipation

246
Q

MOA of caffeine

A

A2 purine receptor antagonist

Partial phosphodiesterase inhibitor

247
Q

MOA of amphetamines

A

Inhibit of reuptake of monoamines into presynaptic membrane

Increases dopamine release

248
Q

Effects of amphetamines

A 
Euphoria 
Insomnia 
Increased stamina 
Anorexia 
Increased blood pressure 
Decreased GI motility
249
Q

MOA of cocaine

A

Inhibits catecholamine reuptake
Increases firing of 5-HT in mesolimbic pathway
Decreases 5-HT firing of neurons in dorsal raphe nuclei

250
Q

Physiological effects of cocaine

A

Tachycardia
Vasoconstriction
Increased blood pressure

251
Q

MOA of MDMA

A

Inhibits 5-HT reuptake

Stimulates 5-HT release

252
Q

Effects of MDMA

A

Psychostimulant

Empathogenic

253
Q

MOA of LSD

A

Mimics 5-HT

Agonist of 5-HT2A receptors

254
Q

Effects of LSD

A

Alters perception by affecting how the retina processes information and conducts it to the brain
(Psychotomimetic)

255
Q

MOA of cannabis

A

THC acts on CB1 receptors in brain and CB2 receptors in peripheral tissues.
Inhibits GABA release
Therefore, dopamine released from Nucleus Accumbens

256
Q

How do opiates cause euphoria?

A

Mu-opioid receptor agonist

Acting on receptors in the limbic system

257
Q

Side effects of opiates

A

Constipation

Respiratory depression

258
Q

Structures in brain responsible for opiate tolerance

A

Ventral Tegmental Area

Nucleus Accumbens

259
Q

Structures in brain responsible for opiate withdrawal

A

Locus coeruleus

Noradrenergic neurones in brainstem

260
Q

Pre and perinatal insults associated with schizophrenia

A

Low birth weight

Obstetric complications and infection

261
Q

Markers of neurodevelopmental disorder associated with schizophrenia

A

Cognitive impairment

Motor delay

262
Q

Brain changes at onset of schizophrenia

A

Enlarged ventricles

Reduced grey matter

263
Q

Contraindications of clozapine

A 
Cardiac disorders
Hx of neutropenia/agranulocytosis 
Bone marrow disorder 
Alcoholic and toxic psychosis 
Uncontrolled epilepsy
264
Q

Pharmacological control of ADRs of clozapine

A

Aripiprazole

Metformin can also be used to control weight gain

265
Q

Effects of Aripiprazole

A

Reduces weight, serum cholesterol and triglyceride levels.

Used in conjunction with clozapine to reduce its side effects.

266
Q

Eye Movement Desensitisation and Reprocessing (EMDR) is used for…

A

PTSD

267
Q

Exposure and Response Prevention (ERP) is used for…

A

Certain anxiety disorders e.g. OCD

268
Q

Dialectical Behavioural Therapy (DBT) is used for…

A

Personality disorders
Substance use
Self Harm

269
Q

Functional Analytic Psychotherapy (FAP) is used for…

A

An alternative to CBT,

Depression
Anxiety disorders
Bipolar

270
Q

Hallucinations can be…

A 
Auditory
Visual
Tactile
Olfactory
Gustatory
271
Q

What are delusions?

A

Abnormal thoughts
Beliefs that do not form part of the person’s culture.
Fixed, usually paranoid and persecutory in nature.

272
Q

Thought disorder/Confusion is…

A

Trouble organising thoughts logically, making up meaningless words, feeling as though thoughts are being removed (thought blocking)

273
Q

Insight (a symptoms of schizophrenia)

A

Subject of delusion is believed to be true with 100% conviction

274
Q

The 5As - Negative Symptoms of Schizophrenia

A 
Affective flattening
Alogia
Avolition/Apathy
Attention 
Anhedonia
275
Q

Alogia

A

Poverty of speech (reduction in amount of speech)

276
Q

Anhedonia

A

Loss of interest in and pleasure from previously rewarding activities

277
Q

Avolition/Apathy

A

Lack of motivation and interest in goal directed behaviour

278
Q

Affective flattening

A

Diminished range of emotional expressiveness

279
Q

When Px in clozapine are quitting smoking they must…

A

Have their daily dose of clozapine monitored by the psychiatrist.
Since nicotine is an enzyme inhibitor.
Drastic reduction in smoking could produce toxic effects.

280
Q

OCEAN (personalities)

A 
Openness
Conscientiousness
Extraversion 
Agreeableness
Neuroticism
281
Q

Temperament inventory

A

Novelty seeking
Harm avoidance
Reward dependence
Persistence

282
Q

Character inventory

A

Self-directedness
Cooperativeness
Self-transcendence

283
Q

Thought components assessed in MSE

A

Content
Process
Flow
Form of thought

284
Q

Form of thought is circumstantial…

A

Long-winded

285
Q

Form of thought is tangiential…

A

Loses goal direction

286
Q

Neologism

A

Making up new words

287
Q

Knight’s Move/Derailment

A

Discourse consisting of a sequence of unrelated or only remotely related ideas

288
Q

Distortions

A

Hyperaesthesia (excessive physical sensitivity)
Vivid sounds and colours

Seen in mania and autism

289
Q

Illusions

A

Real stimulus
False perception

e.g. “I saw a man down a dark alley”

290
Q

Hallucinations

A

No stimulus
False perception
Can be in any sensory modality

291
Q

Pseudohallucinations

A

Voices heard within mind
Involuntary
Internal
Seen in personality disorder

292
Q

Echo de la Pensee

A

Own thoughts spoken aloud

293
Q

“In external space”

A

Speaking in 2nd or 3rd person

294
Q

Depersonalisation

A

Feeling detached from your own body and sense of self

Seen in anxiety, sleep deprivation, sensory deprivation, drug intoxication

295
Q

Derealisation

A

Feeling that everything around you is not real (is plastic, or has a “movie quality”)

Seen in anxiety, sleep deprivation, sensory deprivation, drug intoxication.

296
Q

Parts of MSE (7)

A 
Appearance/Behaviour 
Speech
Mood/Affect
Perceptions 
Thoughts
Cognition
Insight
297
Q

Confabulation

A

Lying without meaning to (Wernicke-Korsakoff’s)

298
Q

Insight

A

Level of understanding exhibited in relation to symptoms.

Do they attribute symptoms to mental disorder?
Accept the need for treatment?

299
Q

Fugue

A

Loss of awareness of identity

300
Q

Dissociative Conversion Disorder

A

Patients present with numbness/blindness/paralysis with no organic cause

301
Q

Secondary delusions

A

Understandable in the context of their emotional state

e.g. low self esteem - believe they are responsible for a crime

302
Q

Secondary delusion of persecution

A

“Someone is trying to kill me”

303
Q

Secondary delusion of grandiosity

A

“I am the new messiah”

304
Q

Secondary delusion of nihilism

A

“I am already dead”

305
Q

Delusional perception

A

Perception is normal but has been interpreted delusionally

306
Q

Delusions of thought interference

A

Insertion, withdrawal, broadcasting i.e. someone is putting thoughts in their head

307
Q

Delusions of passivity

A

Affect, impulse, volition

Someone is making them do what they are doing

308
Q

Core symptoms of unipolar depression

A

Low mood
Anhedonia
Anergia

309
Q

Type 1 Bipolar Affective Disorder

A

One episode of MANIA

Other episodes of depression/hypomania/mixed affective state

310
Q

Type 2 Bipolar Affective Disorder

A

Episode of hypomania
Other episodes of depression (more depression than type 1, more suicidal acts)

NO MANIA or mixed affective state

311
Q

How does mania differ from hypomania?

A

Mania is more severe and completely disruptive in daily life.

Hypomania lasts for a few days
Mania must last for at least one week.

312
Q

Symptoms of somatic syndrome

A 
Anhedonia 
Early morning waking 
Psychomotor agitation/retardation 
Loss of appetite 
Weight loss 
Loss of libido
313
Q

Incidence

A

Number of new cases in a population over a period of time

314
Q

Prevalence

A

Proportion of people in the population with the condition

315
Q

Cotards Syndrome

A

Person believes that they are already dead

Seen in psychotic depression and dementias

316
Q

Electroconvulsive Therapy

A

Induction of Generalised Tonic Clonic Seizure by an electric current under general anaesthetic

317
Q

Risks associated with ECT

A

Short term memory impairment

Risks associated ith repeated general anaesthetic (1/5000 deaths)

318
Q

Dysthymia

A

Persistent mild depression

319
Q

Cancer with the highest risk of depression

A

Lung (13.1%)

320
Q

How doe stress cause deterioration in cancers?

A

Stress results in release in TNF-alpha
TNF-alpha inhibits activity of tyrosine phosphatase
Reduced expression of MHC II
Malignant cells escape immune surveillance

321
Q

Treatment for depression in cancer patients

A

SSRIs

SNRIs if SSRIs are ineffective

322
Q

Features of PTSD

A

Avoidance of reminders
Flashbacks/Nightmares
Negative cognitions (guilt, numbing, shame, anger)
Hyperarousal

323
Q

Brain structures affected by PTSD

A

Hyperactive amygdala and insula

Hypoactive mPFC and rACC

324
Q

Self-stigma

A

Fear or shame that an individual might have that they and their condition will be negatively viewed

325
Q

Enacted stigma

A

When a person or group is shunned, denied protection under the law or dehumanised

326
Q

MOA of Fluoxetine

A

SSRI

327
Q

ADRs of fluoxetine

A

Dose-related abdominal pain
Constipation
Nausea
GI disturbance

328
Q

Contraindications of fluoxetine

A

In manic phase of BPAD
Cardiac disease
Epilepsy

329
Q

MOA of Lorazepam

A

Benzodiazepine

Acts on GABA-A receptors causing an opening of Cl- channels

330
Q

ADRs of lorazepam

A

Amnesia
Confusion
Ataxia

331
Q

Contraindications of Lorazepam

A

If respiratory weakness
Chronic psychosis
Sleep apnoea

332
Q

Indications for fluoxetine

A

Depression and anxiety disorders

333
Q

Indications for lorazepam

A

Anxiety and sleep disorders

Status epilepticus

334
Q

MOA of moclobemide

A

Selective MAO-A inhibitor

335
Q

Indications for mocolobemide

A

Depression
Anxiety
Psychosis

336
Q

ADRs of moclobemide

A 
Confusional states (agitation)
Dizziness
Dry mouth
Drowsiness 
Weight gain
Hypotension 
Insomnia
337
Q

Contraindications of moclobemide

A

Thyrotoxicosis

Bipolar (may trigger manic episodes)

338
Q

MOA of Amitryptyline

A

TCA
Limits 5-HT and NA reuptake
Also blocks voltage gated Ca2+ channels in CNS

339
Q

ADRs of amitryptyline

A

Abdominal pain
Restlessness
Fatigue
Hypertension

340
Q

Contraindications of Amitryptyline

A

Cardiac arrhythmias
Acute porphyria
In manic phase of BPAD

341
Q

ADR which is present in all antipsychotics

A

Prolonged QT interval

342
Q

Structural stigmatisation

A

The belief that mental health services and research don’t deserve as much funding as other health problems

343
Q

Adjustment disorder

A

Temporary condition caused by stress - display some symptoms of clinical depression without as many physical/emotional symptoms e.g. sleep and appetite changes

Year 2 (17 decks)

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