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Semester 3: Mind and Movement > PBL Topic 3 Case 6 > Flashcards

PBL Topic 3 Case 6 Flashcards

1
Q

What is a diffusion potential?

A
  • The potential difference between the inside and outside of the membrane
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2
Q

What is the Nernst potential?

A
  • The diffusion level that exactly opposes the net diffusion of a particular ion through a memrbane
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3
Q

What is the role of the sodium potassium pump?

A
  • Moves 3Na+ to the outside of the cell
  • For every 2K+ to the inside of the cell
  • In order to restore the resting membrane potential
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4
Q

What are leak channels and how do they differ in permeability to different ions?

A
  • Channels through which ions leak

- Greater leakage of potassium because it is more permeable

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5
Q

What is the value of the resting potential in large nerve fibres?

A
  • -90 millivolts

- Meaning the potential inside is 90 millivolts more negative than the potential in the extracellular fluid

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6
Q

Explain why the Nernst potential for sodium and potassium differs

A
  • Potassium Nernst potential is -94 millivolts because there is a high ratio of potassium ions inside to outside
  • Sodium Nernst potential is +61 because there is a lower ratio of sodium ions inside to outside
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7
Q

What is the resting stage of an action potential?

A
  • Membrane is polarised due to -90 millivolts generated by sodium potassium pump
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8
Q

What is the depolarisation stage of an action potential?

A
  • Membrane becomes permeable to sodium
  • Large number of sodium ions diffuse into axon
  • Overshoot caused by excess of sodium entering
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9
Q

What is the repolarisation stage of an action potential?

A
  • Sodium channels close
  • Potassium channels open
  • Rapid diffusion of potassium out
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10
Q

Identify the two types of gating

A
  • Voltage gating involving opening of a protein channel as a result of changing potential
  • Chemical ligand gating involving opening of a protein channel due to binding of a ligand e.g. ACh
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11
Q

Describe the gates of a voltage gated sodium channels

A
  • Activation M gate opens when membrane potential becomes less negative than the resting potential
  • Inactivation H gate closes as a result of same increase in voltage but it closes slower
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12
Q

What is meant by threshold for stimulation and what is its value?

A
  • Membrane potential becomes less negative than resting potential
  • To around -65 millivolts
  • Which causes explosive development of an action potential
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13
Q

Explain the process behind the propagation of an action potential

A
  • Excited portion of nerve fibre causes local circuit of current flow to adjacent resting membrane areas
  • Positive electrical charges are carried by inward diffusion sodium ions
  • Increasing threshold in adjacent areas above threshold for stimulation
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14
Q

What is meant by the all or nothing principle?

A
  • Action potential only occurs if sufficient voltage to stimulate the next area of the membrane builds up
  • Above the threshold
  • Or it does not travel at all
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15
Q

What is the importance of ATP in nerve impulse?

A
  • Sodium potassium pump re-establishes sodium and potassium concentration differences
  • Which requires ATP
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16
Q

What is the ratio of myelinated to unmyelinated nerve fibres?

A
  • 1:2
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17
Q

What is the velocity of conduction in a small unmyelinated nerve fibre compared to a large myelinated fibre?

A
  • Small unmyelinated: 0.25m/sec

- Large myelinated: 1m/sec

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18
Q

Describe the structure of a myelinated nerve fibre

A
  • Central core is the axon filled with axoplasm

- Surrounded by a myelin sheath

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19
Q

Outline the process of myelination

A
  • Membrane of Schwann cell envelops the axon
  • Schwann cell rotates around axon many times
  • Depositing many layers of sphingomyelin
  • Which is an insulator that decreases ion flow through the membrane
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20
Q

What is saltatory conduction?

A
  • Junction between Schwann cells is known as node of Ranvier
  • Nerve impulse jumps between nodes of Ranvier
  • Increasing the velocity of transmission
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21
Q

What is primary demyelination?

A
  • Myelin sheath is destroyed

- Axons remains intact

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22
Q

What is secondary demyelination?

A
  • Damage to axon

- Resulting in breakdown of of myelin

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23
Q

What happens to the debris of myelin breakdown?

A
  • Phagocytosed by macrophages

- Transformed into droplets of neutral lipids (cholesterol esters)

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24
Q

What is an acute sub-threshold potential?

A
  • Weak negative stimulus incapable of exciting a nerve fibre
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25
Q

What is an acute local potential?

A
  • Excitation takes place in response to voltage increase
  • However it is not great enough to pass the threshold level
  • Therefore an action potential does not occur
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26
Q

What is an absolute refractory period and why does it occur?

A
  • Period during a which a second action potential cannot be elicited even with a strong stimulus
  • Because sodium channels become inactivated
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27
Q

What is a relative refractory period?

A
  • Period during which nerve fibre is more difficult to excite
  • But can be excited by a very strong signal
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28
Q

What is a membrane stabilising factor. How does lidocaine act as a stabilising factor?

A
  • Factor that decreases excitability

- Lidocaine acts on activation gate of sodium channels making it more difficult for it to open

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29
Q

Explain how chemical synapses work

A
  • Presynaptic cell releases neurotransmitter

- That acts on postsynaptic receptor proteins

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30
Q

Explain how electrical synapses work

A
  • Direct open fluid channels
  • That conduct electricity from one cell to next
  • Usually through gap junctions
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31
Q

How does transmission of impulses differ between chemical and electrical synapses?

A
  • Chemical synapses: One way transmission

- Electrical synapses: Signals are transmitted in either direction

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32
Q

What is the importance of one way transmission?

A
  • Specific transmission of signals to discrete and highly focuses areas in the CNS and PNS
  • Allows the nervous system to perform its myriad functions
  • Including sensation, motor control, memory and many others.
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33
Q

Describe how neurotransmitters are stored and released from the presynaptic terminal

A
  • Stored in transmitter vesicles
  • Mitochondria provides ATP for synthesising new transmitter substance
  • Action potential spreads over presynaptic terminal
  • Depolarisation of membrane causes release of vesicles into synaptic cleft
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34
Q

What are SNARE proteins?

A
  • Proteins that dock vesicles in active zone of presynaptic terminal

-

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35
Q

Identify two types of SNARE protein

A
  • V-SNARES: Synaptobrevin, Synaptotagmins, found on vesicular membrane
  • T-SNARES: Syntax, Snap-25, found at nerve terminal membrane
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36
Q

Outline the role of calcium ions in neurotransmitter release

A
  • Binds to another vesicle protein, synaptotagmins
  • Triggering conformational change in SNARE complex
  • Leading to membrane fusion and neurotransmitter release into the cleft
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37
Q

Identify two types of postsynaptic receptors that neurotransmitters bind to

A
  • Ionotropic receptors: ion channels

- Metabotropic receptors: G-protein second messenger system

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38
Q

What are cation and anion channels?

A
  • Opened as a result of activation of ionotropic / metabotropic receptors in response to neurotransmitters
  • Cation channels allow entry of sodium, but block entry of chloride due to lining of negative charges
  • Anion channels allow entry of potassium, but block entry of sodium due to small size
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39
Q

What is an excitatory postsynaptic potential (EPSP)?

A
  • Electrical response at an excitatory cation channel
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40
Q

What is an inhibitory postsynaptic potential (IPSP)?

A
  • Hyperpolarisation at an inhibitory anion channel
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41
Q

Outline the molecular and membrane mechanisms used at excitatory receptors

A
  • Opening of sodium channels, influx of sodium ions
  • Decrease influx of chloride ions and efflux of potassium ions
  • Changes in internal metabolism to excite cell activity
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42
Q

Outline the molecular and membrane mechanisms used at inhibitory receptors

A
  • Opening of chloride channels, influx of chloride ions
  • Increased efflux of potassium ions
  • Activation of receptor enzymes that inhibit metabolic functions
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43
Q

Outline the process of presynaptic inhibition

A
  • Release of GABA by presynaptic cell
  • Which opens presynaptic anion channels
  • Allowing influx of chloride into presynaptic cell
  • Inhibiting synaptic transmission
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44
Q

What is spatial summation?

A
  • Effect of triggering an action potential in a neuron from one or more presynaptic neurons.
  • This occurs when more than one excitatory postsynaptic potential (EPSP) originates simultaneously and a different part of the neurone
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45
Q

What is temporal summation?

A
  • High frequency of action potentials in the presynaptic neuron elicits postsynaptic potentials that summate with each other
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46
Q

What is the role of small molecular neurotransmitters?

A
  • Acute responses of nervous system e.g. sensory signals to brain and motor signals to muscle
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47
Q

What is the role of neuropeptide transmitters?

A
  • More prolonged actions such as long-term changes in numbers of neuronal receptors, long term opening and closure of certain ion channels
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48
Q

How are small molecular neurotransmitters synthesised?

A
  • In cytosol of presynaptic terminal by active transport into transmitter vesicles in the terminal
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49
Q

How are neuropeptides produced?

A
  • Ribosomes as integral parts of large protein molecules
  • Which is then enzymatically split from the protein by the Golgi apparatus
  • Transported to tips of nerve fibres by axonal steaming
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50
Q

What is Multiple Sclerosis?

A
  • Autoimmune T-cell mediated inflammatory disorder
  • Formation of plaques of demyelination throughout the brain and spinal cord
  • Occurring sporadically over years (dissemination in time and space)
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51
Q

Outline the epidemiology of MS

A
  • Prevalence of 1.2/1000
  • Women outnumber men 2:1
  • Typically affects people between 20 and 40 years
  • More common in white populations with increasing distance from the equator
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52
Q

Outline 4 environmental causes of MS

A
  • Epstein-Barr Virus (EBV)
  • Human Herpes Virus 6 (HHV-6)
  • Low levels of vitamin D
  • Lack of sunlight
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53
Q

Outline the pathology of MS

A
  • T-cells cross the BBB
  • They recognised myelin derived antigens on microglia and undergo clonal proliferation
  • Resulting in inflammatory cascade and cytokine release initiating destruction of oligodendrocyte-myelin unit
  • Impaired impulse propagation
  • Progressive axonal loss
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54
Q

Outline the three types of MS

A
  • Relapsing-remitting, symptoms occurring in attacks over days, and then recovery over weeks
  • Secondary progressive, late stage symptoms with gradually worsening disability caused by axonal loss
  • Primary progressive, late stage symptoms with gradually worsening disability without relapses or remissions
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55
Q

Outline 3 clinical features of multiple sclerosis

A
  • Optic neuritis caused by demyelination of optic nerve
  • Diplopia, vertigo, facial numbness, weakness caused by brainstem demyelination
  • Paraparesis with possible Lhermitte’s sign caused by spinal cord lesions in cervical or thoracic cord
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56
Q

Outline the investigations and diagnosis of MS

A
  • Clinical history of neurological symptoms
  • MRI demonstrates demyelination
  • CSF examination shows lymphocytic pleocytosis and oligoclonal bands of IgG
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57
Q

What is the Clinically Isolated Syndrome?

A
  • Diagnosis of MS cannot be made on first episode of neurological symptoms
  • Though an abnormal brain MRI confers a high chance of developing MS
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58
Q

What is treatment for acute relapses of MS?

A
  • Methylprednisolone
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59
Q

How does B-interferon work?

A
  • Inhibits T cell activation
  • Preventing T cell proliferation
  • Blocks T-cell migration across the BBB
60
Q

How does glatiramer acetate work?

A
  • Competitive inhibitor of MHC-II

- Since it has a similar structure to myelin basic protein

61
Q

How does oral fingolimod work?

A
  • Sphingosine-1-phosphate receptor

- That prevents T cells leaving lymph nodes

62
Q

How does natalizumab work?

A
  • Alpha-4 integrin vascular adhesion molecule

- Preventing lymphocytes entering the CNS

63
Q

How does alemtuzumab work?

A
  • Anti-CD52 molecule

- Responsible for lymphocyte depletion

64
Q

What is the prognosis of MS?

A
  • Life expectancy reduced by 7 years on average
65
Q

Outline the mechanism of action of methylprednisolone

A
  • Binds to intracellular glucocorticoid receptors
  • Which dimerises then enters the nucleus
  • Which binds to glucocorticoid response element and upregulates transcription
66
Q

Outline the immunosuppressive and anti-inflammatory properties of glucocorticoids such as methylprednisolone

A
  • Reduced activation of neutrophils, macrophages, mast cells
  • Reduced activation of T-helper cells, reduced clonal proliferation of T-cells
  • Decreased production of prostanoids owing to decreased COX-2 expression
  • Decreased generation of cytokines
  • Increased synthesis of inflammatory factors such as IL-2 and annexin 1
67
Q

Outline 4 adverse effects of glucocorticoids

A
  • Poor response to infection or injury, poor wound healing
  • Oral candidiasis
  • Peptic ulceration
68
Q

Describe the biosynthesis of serotonin

A
  • Tryptophan is converted into 5-hydroxytryptophan by tryptophan hydroxylase
  • 5-hydroxytryptophan is converted to 5-hydroxytryptamine by an amino acid decarboxylase
69
Q

How is serotonin degraded?

A
  • Monoamine oxidase
  • Which converts it to 5-hydroxindole acetaldehyde
  • Which is then dehydrogenated and excreted in the urine
70
Q

Where in the body are the highest concentrations of serotonin found?

A
  • Enterochromaffin cells of the gut regulating peristalsis and motility
  • Platelets, causing platelet aggregation
  • CNS where it excites and inhibits neurons
  • In sensory nerve endings to stimulate nociceptive nerve endings
71
Q

Where are serotonergic cell bodies found and how do the nuclei project to other regions of the brain?

A
  • Raphe nuclei of the pons and upper medulla

- Via the median forebrain bundle

72
Q

What type of receptors are serotonin receptors? What is the exception?

A
  • All are G-protein coupled

- Except for 5-HT3 which is a ligand gated cationic channel

73
Q

What are 5-HT1 receptors?

A
  • Somatodendritic autoreceptors in the raphe nuclei

- Major target for drugs used to treat anxiety and depression

74
Q

Outline the four physiological functions that relate to 5-HT pathways

A
  • Hallucinatory effects
  • Sleep, wakefulness and mood
  • Feeding behaviour
  • Pain pathways
75
Q

Describe the biosynthesis of noradrenaline

A
  • L-tyrosine is converted to dopa by tyrosine hydroxylase
  • Dopa is converted to dopamine by dopa decarboxylase
  • Dopamine is converted to noradrenaline by dopamine beta-hydroxylase
76
Q

Which protein is involved with transport of noradrenaline into vesicles. What is stored in vesicles containing noradrenaline?

A
  • Reserpine-sensitive Vesicular Monoamine Transporter (VMAT)
  • ATP
  • Chromogranin
  • DBH
77
Q

Which receptor is responsible for noradrenaline reuptake?

A
  • Noradrenaline (NET) transporter
78
Q

Where are noradrenergic cell bodies found and how do the nuclei project to other regions of the brain?

A
  • Locus coeruleus located in the pons

- Via the median forebrain bundle

79
Q

What type of receptors are adrenoreceptors?

A
  • G-protein coupled receptors
80
Q

Identify 3 functions of alpha-1 receptors

A
  • Motor control
  • Condition
  • Fear
81
Q

Identify 3 functions of alpha-2 receptors

A
  • Blood pressure control
  • Sedation
  • Analgesia
82
Q

What are beta-1 receptors?

A
  • Found in cortex, striatum and hippocampus

- Involved in long-term effects of antidepressant

83
Q

What are beta-2 receptors?

A
  • Found in cerebellum

- Involved in long-term effects of antidepressant drugs

84
Q

Outline the physical features of depression

A
  • Insomnia or hypersomnia
  • Poor appetite and weight loss
  • Increased appetite and weight gain
  • Loss of libido and erectile dysfunction
85
Q

Outline the emotional features of depression

A
  • Feelings of unworthiness
  • Worrying
  • Suicidal thoughts
  • Delusions of guilt
  • Feelings of futility
  • Hypochondriacal preoccupations
86
Q

Outline the epidemiology of depression

A
  • 5% prevalence
  • More common in women
  • No increase with age, difference by ethnic group of socio-economic class
87
Q

What is dysthymia?

A
  • Mild or moderate depressive illness
  • Intermittently over 2 years
  • Characterised by tiredness and low mood
88
Q

What is seasonal affective disorder?

A
  • Recurrent episodes of depressive illness
  • Occurring in the winter months in the northern hemisphere
  • Can be treated with bright light therapy
89
Q

Identify three types of puerperal affective disorder

A
  • Maternity blues, brief episode of tearfulness that occurs in the majority of women and resolves spontaneously
  • Postnatal depressive disorders, lack of emotional bonding and poor relationship with partner
  • Postpartum psychosis, attempts to kill the child or suicide
90
Q

Outline two differential diagnoses for depression?

A
  • Alcohol misuse

- Thyroid disease

91
Q

Outline two investigations for depression

A
  • Clinical history to rule out alcohol misuse

- Less commonly used T4 or TSH measurements

92
Q

Outline the pathogenesis of depression

A
  • Deficit of noradrenaline and 5-HT and BDNF
  • Elevated levels of glutamate and action of NMDA receptors
  • Stress leads to increased cortisol release
  • All of which result in a detrimental gene transcription response and neural apoptosis
93
Q

Outline the genetic component of depression

A
  • Polygenic
  • Polymorphisms include serotonin transport genes
  • Short/short allele implicated in greatest risk. long/long allele implicated in lowest risk
94
Q

Outline environmental factors that predispose a person to depression

A
  • Physical, sexual and emotional abuse or neglect in childhood
  • Serious life events, including divorce in women and unemployment in men
95
Q

Outline two examples of SSRI

A
  • Fluoxetine, sertraline
96
Q

Outline two examples of TCAs

A
  • Amitriptyline, nortriptyline
97
Q

Outline an example of an SNRI

A
  • Venlafaxine
98
Q

Outline an example of an NRI

A
  • Bupropion
99
Q

Outline two examples irreversible, non-selective MAOIs

A
  • Phenelzine, tranylcypromine
100
Q

Outline three examples example of MRA

A
  • Mirtazapine, trazodone, mainserin
101
Q

Outline the effects of acute administration of SSRIs

A
  • Increased levels of 5-HT results in increased activation of 5-HT1a receptors
  • Which reduce 5-HT release
102
Q

Outline the effects of prologued administration of SSRIs

A
  • Elevated levels of 5-HT desensitise 5-HT1a receptors

- Which increases 5-HT release

103
Q

How can alpha-2 adrenoreceptor antagonism enhance 5-HT release?

A
  • Block of a2 autoreceptors on noradrenergic nerve terminals innervating cell bodies of 5-HT containing neurons in dorsal raphe
  • Enhanced noradrenaline release will activate excitatory postsynaptic a1 receptors on 5-HT neurons
  • Increasing firing and thus release of 5-HT
104
Q

How is sertraline administered and what is the dosage?

A
  • Taken orally 50mg daily
  • Increased in steps of 50mg weekly
  • To a maximum of 200mg
105
Q

Outline three common side effects of sertraline

A
  • Nausea
  • Anorexia
  • Insomnia
  • Loss of libido and anorgasmia
106
Q

Outline three uncommon side effects of sertraline

A
  • Serotonin syndrome when combined with MOI characterised by tremor, hyperthermia, and cardiovascular collapse
  • Risk of bleeding associated with inhibition of 5-HT reuptake by platelets
  • Discontinuity syndrome marked by shivering, anxiety and dizziness
107
Q

How is venlafaxine administered and what is the dosage?

A
  • Orally
  • Taken 75mg daily in 2 divided doses
  • To a maximum of 375mg daily
108
Q

Outline 4 side effects of venlafaxine

A
  • Antimuscarinic effects such as dry mouth, blurred vision, constipation and urinary retention
  • Cardiovascular effects such as postural hypotension
  • Weight gain
  • Sedation
109
Q

Outline two roles of monoamine oxidase

A
  • Within nerve terminals it regulates intraneuronal concentration of NA and 5-HT
  • Inactivation of endogenous amines such as tyramine
110
Q

What is the cheese reaction?

A
  • Tyramine is normally metabolised by NAO so little reaches circulation
  • MAO inhibition results in acute hypertension, severe throbbing headache and rarely intracranial haemorrhage
111
Q

What is ECT?

A
  • Used in severe life-threatening depression
  • Performed under general anaesthetic, involves passage of current over scalp to induce epileptic fit
  • Given twice a week for 3-6 weeks
  • Free of serious side effects
112
Q

What is CBT?

A
  • Identification of automatic thoughts about self, situation and future
  • Including catastrophising, overgeneralising, categorical thinking
  • Identifying links between thoughts, behaviour and mood
  • Testing logic of said thoughts e.g. Socratic questioning
113
Q

Outline the mechanism of action of nortriptyline and amitriptyline

A
  • Inhibition of noradrenaline (physical symptoms), 5-HT (emotional symptoms) and dopamine uptake (less so)
  • By competition for the binding site of the nerve terminal
114
Q

Identify 3 side effects of nortriptyline and amitriptyline

A
  • Antimuscarinic effects e.g. dry mouth, blurred vision, constipation and urinary retention
  • Cardiovascular effects e.g. postural hypotension and QT prolongation
  • Weight gain
  • Sedation
115
Q

Identify another use of TCAs aside from antidepressants and outline how they work

A
  • Neuropathic pain
  • Preventing noradrenaline reuptake
  • Which inhibits transmission of nociception
116
Q

Outline the mechanism of action of mirtazapine

A
  • Blocks a2 adrenoceptors
  • Blocks 5-HT2C receptors
  • Enhancing noradrenaline and 5-HT release
117
Q

Outline the mechanism of action of trazodone

A
  • Blocks 5-HT2A and 5-HT2C receptors

- Enhancing 5-HT release

118
Q

Outline the mechanism of action of mainserin and explain why it is no longer used

A
  • Blocks a1 adrenoreceptors
  • Blocks 5-HT2a receptors
  • Blocks H1 receptors
  • Causes bone marrow depression
119
Q

Give an example of a selective, MAO-A specific inhibitor and an advantage of this type of drug over phenelzine and tranylcypromine

A
  • Moclobemide

- Cheese reaction and drug reactions are much less severe

120
Q

What is meant by coping?

A
  • The process of managing stressors

- That have been appraised as taxing or exceeding a person’s resources

121
Q

What is meant by primary appraisal?

A
  • Assessing the potential threat of the external stressor
122
Q

What is meant by secondary appraisal?

A
  • Assessing the effectiveness of options to manage the situation and the person’s internal responses
123
Q

Identify 5 goals of coping

A
  • Reduce stressful conditions
  • Adjust or tolerate negative effects
  • Positive self image
  • Emotional equilibrium
  • Maintain relationships
124
Q

What is meant by approach coping and what type of stressor is it more suitable for?

A
  • Confronting problem and taking direct action

- Long-term stressor

125
Q

What is meant by avoidance coping?

A
  • Minimising the importance of the event

- Short term stressor

126
Q

Identify two types of approach coping

A
  • Problem focused

- Emotional focused

127
Q

Identify two examples of emotional-focused coping

A
  • Behavioural strategies e.g. talking to friends about the emotions
  • Cognitive strategies e.g. thinking about a problem in a positive way
128
Q

Which type of problem evokes problem focused coping?

A
  • Work related
129
Q

Which type of problem evokes emotional focused coping?

A
  • Health

- Relationships

130
Q

How does coping strategy differ between ages?

A
  • Children and middle-aged people use problem focused coping

- Teens and elderly people use emotional focused coping

131
Q

How does coping strategies differ between men and women?

A
  • Men tend to use problem focused

- Women tend to use emotional focused

132
Q

How does controllability affect coping strategies?

A
  • If the individual believes the condition is controllable they are more likely to use problem-focused coping
  • If the individual does not believe the condition is controllable they are more likely to use emotion-focused coping
133
Q

What does the ‘ways of coping’ checklist measure?

A
  • Different coping styles
134
Q

Identify two effects coping should have

A
  • Reduce intensity and duration of stressor

- Reduce likelihood that stress will lead to illness

135
Q

Which type of coping is associated with better outcomes?

A
  • Approach, problem-solving coping
136
Q

Outline Leventhal’s self regulatory model

A
  • Illness is dealt with in the same way as any other problem
  • Individuals try to maintain status quo in three stages
  • Interpretation of problem
  • Coping strategy
  • Appraisal
137
Q

Identify four causes of help-seeking behaviour

A
  • Interpersonal crisis
  • Interference with social and work life
  • Sanctioning (family and friends encouraging help-seeking)
  • Temporising (putting a time limit on symptoms)
138
Q

Identify two reasons for not demonstrating help-seeking behaviour

A
  • Fear of embarrassment

- Fear of the condition

139
Q

What is the purpose of the Mental Capacity Act?

A
  • Protect people who cannot make decisions for themselves or lack the capacity to do so
140
Q

Who does the Mental Capacity Act apply to?

A
  • Severe mental health condition
  • Severe learning disability
  • Brian injury
  • Stroke
  • State of unconsciousness
141
Q

Identify five key principles of the Mental Capacity Act

A
  • Person assumed to have capacity unless established otherwise
  • Person not to be treated as unable to make a decision unless all steps to help them do so are unsuccessful
  • Person not to be treated as unable to make a decision because they make an unwise decision
  • Act or decision must be in their best interests.
  • Regard must be had to whether the outcome can be as effectively achieved in a way that is less restrictive of the person’s rights and freedom of action
142
Q

What is meant by advanced decision?

A
  • A decision made by a person
  • After they have reached the age of 18 and have the capacity to do so
  • Regarding specified treatment (or lack of) when they eventually lack capacity
143
Q

When does an advanced decision have full legal force?

A
  • In writing
  • Signed by patient or by a person in patient’s presence
  • With a signature fo a witness
144
Q

When is an advanced decision invalid?

A
  • If patient does something inconsistent with advanced decision
145
Q

What is Lasting Power of Attorney?

A
  • Legal document allowing a person who is at least 21
  • To appoint a person to make decisions on their behalf should they lose capacity one day
  • Personal welfare or property and affairs matters
146
Q

Outline the NICE guidelines for depression

A
  • Mild depression: Psychological intervention e.g. CBT
  • Moderate - severe depression: Stepwise treatment:
  • (1) SSRI (sertraline)
  • (2) SNRI (venlafaxine) / MRA (mirtazapine) >
  • (3) Antipsychotic (quetiapine) / lithium
  • (4) TCA (nortriptyline)
  • (5) MAOI (phenelzine)

Semester 3: Mind and Movement (21 decks)

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