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Year 2 BB > Overview 2 > Flashcards

Overview 2 Flashcards

1
Q

Loss of cells occurs where causing PD

A

Subsantia nigra pars compacta

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2
Q

What forms in the brain in a patient with PD?

A

Lewy bodies

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3
Q

What are Lewy bodies composed of?

A

Protein alpha-synuclein

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4
Q

What cells are lost in PD?

A

Dopaminergic cells

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5
Q

Where are dopaminergic cells lost in a patient with PD?

A

Substantia nigra pars compacta

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6
Q

What are the three main features/presentations of PD?

A

Resting tremor
Bradykinesia
Rigidity

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7
Q

Gradual development of what condition develops with PD?

A

Microphagia

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8
Q

Give five non-motor presentations of PD

A 
Olfactory dysfunction
Depression
Dementia
Sleep disturbance
Autonomic disturbance
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9
Q

Non-motor presentations of PD can occur how much earlier than the motor symptoms?

A

Up to 12-15 years

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10
Q

Loss of dopaminergic cells in PD causes an imbalance in which two pathways?

A

Direct and indirect pathways of basal ganglia

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11
Q

What is meant by a score of 100% in the Schwab and England Activities of Daily living?

A

Patient is completely independent

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12
Q

How can the brain be imaged for dopaminergic cells in PD?

A

Dopamine transporter imaging

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13
Q

PD more common in males or females?

A

Males

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14
Q

MPTP has what effect on PD?

A

Can result in very advanced PD

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15
Q

Why can MPTP cause advanced PD?

A

Transformed into MPP+ which is neurotoxic to dopaminergic neurones

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16
Q

MPTP causes dysfunction of which organelle?

A

Mitochondria

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17
Q

What is the main enzyme causing oxidative stress in PD?

A

MAOb

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18
Q

Which of the dopaminergic pathways of the CNS is involved in PD?

A

Nigrostriatal pathway

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19
Q

Which of the dopaminergic pathways of the CNS is involved in PD?

A

Nigrostriatal pathway

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20
Q

What are the two groups of dopamine receptors?

A

D1

D2

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21
Q

D1 dopamine receptor groups consists of which dopamine receptors?

A

D1 and D5

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22
Q

D2 dopamine receptor groups consists of which dopamine receptors?

A

D2, D3, D4

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23
Q

Stages of metabolism of dopamine?

A

Dopamine to DOPAC to homovanillic acid

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24
Q

What is the role of MAO in dopamine metabolism?

A

Dopamine to DOPAC via MAO

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25
Q

What is the role of COMT in dopamine metabolism?

A

DOPAC to homovanillic acid via COMT

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26
Q

What type of receptor is the dopamine receptor?

A

G-protein coupled receptors

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27
Q

L-dopa can be used to treat dopamine because?

A

Pre-cursor - will be converted into dopamine

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28
Q

L-dopa should be given to a patient along with what?

A

Peripherally acting DOPA decarboxylase inhibitor

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29
Q

Name two other drug groups used for the treatment of PD? x2

A

MAOb inhibitors
Anticholinergic compounds
COMT inhibitors

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30
Q

Why are anticholinergic compounds used to treat PD?

A

Dopamine loss leads to hyperactivity of cholinergic cells

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31
Q

What is the role of amantadine in PD treatment? x2

A

Inhibits dopamine reuptake and increases dopamine release

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32
Q

What is apomorphine?

A

Dopamien agonist used as infusion for major motor fluctuations

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33
Q

What is rotigotine?

A

Dopamine agonist - transdermal patch

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34
Q

What is carbidopa?

A

Peripherally acting DOPA decarboxylase inhibitor

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35
Q

What is ropinerole?

A

Dopaminergic agonist

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36
Q

What is rasagiline?

A

MAOb inhibitor

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37
Q

What is benserazide?

A

Peripherally acting DOPA decarboxylase inhibitor

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38
Q

What is entacapone?

A

COMT inhibitor

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39
Q

What is tolcapone?

A

COMT inhibitor

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40
Q

What is tolcapone?

A

COMT inhibitor

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41
Q

Give 5 non-motor effects of L-DOPA

A 
Nausea/vomiting
Postural hypertension
Psychosis
Impulse-control disorders
Excessive day-time sleepiness
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42
Q

Give four motor complications of L-dopa therapy

A

On-off effect
Wearing off
Dyskinesia/dystonia

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43
Q

Three types of therapy that should be offered to patients with PD?

A

Physiotherapy
Speech and language therapy
Occupational therapy

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44
Q

What is Huntington’s chorea?

A

Involuntary jerky movements

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45
Q

Cause of Huntington’s chorea?

A

Mutation on huntington protein of chromosome 4

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46
Q

Mutation involved with Huntington’s chorea is?

A

Abnormal number of repeats of glutamine (CAG)

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47
Q

Inheritance of Huntington’s chorea is?

A

Autosomal dominant

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48
Q

Four pathological changes in the brain seen in Huntington’s chorea?

A

Cortical atrophy
Striatal degneration
Loss of medium spiny neurones
Intranuclear inclusions of huntington

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49
Q

Main drug used to treat Huntington’s chorea?

A

Tetrabenazine

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50
Q

Main drug used to treat Huntington’s chorea?

A

Tetrabenazine

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51
Q

Two types of stroke are?

A

Ischaemic

Haemorrhagic

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52
Q

Main cause of intercerebral bleed is?

A

Hypertension

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53
Q

Four secondary causes of intercerberal haemorrhages?

A

Trauma
Tumour
Venous thrombosis
Drug usage

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54
Q

Four complications of ICH?

A

Local damage
Local mass effect/herniation
Raised ICP
Hydrocephalus

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55
Q

Three medical conditions that are risk factors for stroke are?

A

Hypertension
Hypercholesterolaemia
Diabetes

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56
Q

Cardiac condition that is a risk factor for stroke is?

A

AF

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57
Q

Deficit occurring from left hemisphere stroke is?

A

Reading and writing deficits

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58
Q

Prognosis for stroke?

A

1/3 - do well
1/3 - die
1/3 - poor prognosis

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59
Q

Prognosis for stroke?

A

1/3 - do well
1/3 - die
1/3 - poor prognosis

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60
Q

Three common symptom of MS?

A

Sensory/motor problems - numbness of the limbs/tingling sensation
Vision problems - blurriness/loss/diplopia
Progressive motor deficits

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61
Q

Three uncommon symptoms of MS

A

Bladder dysfunction
Heat intolerance
Dementia

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62
Q

What is MS?

A

Demyelinating, degenerative and inflammatory condition

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63
Q

What imaging is used for MS type conditions?

A

MRI

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64
Q

MRI signs of MS? x2

A

Lesion in corpus callosum

Areas of inflammation and brain atrophy

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65
Q

Non-imaging investigation used for MS?

A

Lumbar puncture

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66
Q

Three stages of MS disease progression?

A

Relapsing-remitting
Primary progressive
Secondary progressive

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67
Q

Lumbar puncture for MS - looking for what?

A

Presence of neurofilaments - oligoclonal bands

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68
Q

Four diagnostic criteria for MS?

A

Neurological deficits
Dissemination in space
Dissemination in time - damage occurred at two points in time
Exclusion of other causes

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69
Q

How many areas of the CNS must be damaged to diagnose MS?

A

At least two separate areas

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70
Q

Life expectancy of those with MS is reduced by what amount?

A

10-15 years

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71
Q

Loss of which cells occur in MS?

A

Oligodendrocytes

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72
Q

Loss of which cells occur in MS?

A

Oligodendrocytes

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73
Q

Oligodendrocytes produce what?

A

Myelin sheath

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74
Q

Four features of an MS lesion?

A

Astrocytic scar
Demyelination
Activated microglia
Oligodendrocyte loss

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75
Q

Cells involved in the demyelination of MS are?

A

Macrophages

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76
Q

Pathological hallmark of an MS lesion is?

A

Demyelinated axons

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77
Q

Infiltration of what cells occurs in MS?

A

T cells

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78
Q

T cells involved in MS are known as?

A

Autoreactive lymphocytes

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79
Q

T cells can enter brain in MS because?

A

BBB is damaged

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80
Q

Weighting of MRI for MS diagnosis?

A

T1

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81
Q

Differential diagnosis for MS? x4

A

Cerebrovascular disease
Syphilis
B12 deficiency
Lyme disease

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82
Q

Typical age of diagnosis of MS?

A

20s/30s

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83
Q

What comes first in MS - inflammation or degeneration?

A

We do not know

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84
Q

Relation of smoking to MS?

A

Smoking can cause MS

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85
Q

Four stages of MS treatment

A

Anti-inflammatory
Neuroprotection
Remyelination
Neuro-restoration

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86
Q

First line teatment for MS? x2?

A

IFNb

Natalizumab

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87
Q

Second line treatment for MS? x3

A

Fingolimod
Natalizumab
Alemtuzumab

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88
Q

Anatomical location of lumbar puncture?

A

Between L3 and L4 into subarachnoid space

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89
Q

Anatomical location of lumbar puncture?

A

Between L3 and L4 into subarachnoid space

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90
Q

Four physiological stages in the mechanism of pain?

A

Transduction
Transmission
Perception
Modulation

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91
Q

Transduction of pain involves what?

A

Noxious stimuli into electrical activity at sensory nerve endings

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92
Q

Endings of nociceptors are free or capsulated?

A

Free

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93
Q

Nociceptive channel that opens in response to heat thermal stimuli is?

A

TRPV1

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94
Q

Nociceptive channel that opens in response to cold thermal stimuli is?

A

TRPM8

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95
Q

Noxious fibres lost in diabetic neuropathy are?

A

C fibres

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96
Q

C fibres/a-delta fibres - which are myelinated?

A

A-delta

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97
Q

C fibres/a-delta fibres - which are fast conducting?

A

A-delta

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98
Q

C fibres/a-delta fibres - which is first and which is second pain?

A

A-delta - first, immediate pain

C - second, emotional pain

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99
Q

Resulting action from activation of a-delta fibres is?

A

Reflex withdrawal

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100
Q

Two classes of C fibres are?

A

Peptidergic c-fibres

Peptide-poor c fibres

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101
Q

Peptidergic C fibres release what? x2

A

Substance P

CGRP

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102
Q

Receptor of peptide poor c fibres is?

A

P2X3 - peptide poor C fibres

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103
Q

C fibre classes - which involves ATP receptors?

A

Peptide poor

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104
Q

A delta fibres project to which laminae?

A

I and V

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105
Q

C fibres project to which laminae?

A

I and II

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106
Q

What projects to lamina I?

A

All nociceptors

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107
Q

Gene responsible for the development of nociceptors is?

A

trkA

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108
Q

A-beta fibres enter/innervate which lamina?

A

V

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109
Q

What are projection neurones?

A

Second order neurones

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110
Q

What are VPL and VPM?

A

Nuclei:
Ventral posterior lateral
Ventral posterior medial

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111
Q

VPL and VPM project to where?

A

Primary somatosensory cortex

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112
Q

A-delta fibres mainly run into which spinal tract?

A

Anterior spinothalamic

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113
Q

Function of anterior spinothalamic tract is?

A

Regulates immediate need to withdraw arm from pain

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114
Q

A-delta fibres innervate which nuclei? x4

A

VPL
VPM
VPI (inferior)
CL (central lateral)

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115
Q

C-fibres mainly run into which spinal tract?

A

Lateral spinothalamic tract

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116
Q

C-fibres innervate which nucleus? x2

A

Posterior thalamus

Mediodorsal nucleus

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117
Q

Function of the lateral spinothalamic tract?

A

Regulation of punishing aspects of pain - prevent repetition

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118
Q

Lateral spinothalamic tract projects to where?

A

Anterior cingulate cortex (limbic system)

Rostral insular cortex

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119
Q

Anterior spinothalamic tract projects to where?

A

Primary and secondary somatosensory cortex

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120
Q

Lateral spinothalamic associated with which pain pathway?

A

Periaqueductal grey PAG

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121
Q

PAG pathway located where?

A

Midbrain

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122
Q

Lateral spinothalamic projects to which three specific areas?

A

PAG
Reticular formation
Parabrachial nucleus

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123
Q

Four signs of inflammation?

A

Calor - heat
Rubor - redness
Dolor - pain
Tumor - swelling

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124
Q

Inflammation results in what type of sensitisation?

A

Peripheral sensitiation

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125
Q

Three hallmarks of sensitisation?

A

Hyperalgesia
Allodynia
Spontaneous pain

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126
Q

Hyperalgesia is?

A

Abnormally heightened sensitivity to pain

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127
Q

Allodynia is?

A

Sensation of pain from non-noxious stimuli

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128
Q

Two features of peripheral sensitisation?

A

Reduced activation threshold

Increased responsiveness

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129
Q

NaV1.8 is?

A

Sodium channel

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130
Q

NaV1.9 is?

A

Sodium channel

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131
Q

Arachidonic acid released via what enzyme?

A

Phospholipase A2

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132
Q

Arachidonic acid converted to what?

A

Prostaglandins

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133
Q

Arachidonic acid converted to prostaglandins via what enzymes?

A

COX1

COX2

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134
Q

COX1 present what?

A

Normally present in all tissues at low levels

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135
Q

COX2 present when?

A

COX-2 induced during inflammation

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136
Q

Prostaglandins sensitise which pain fibres?

A

C-fibres

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137
Q

Prostaglandins are targeted by which pain relieving drug specifically?

A

NSAIDs

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138
Q

Central sensitisation caused by?

A

Prolonged nociceptive input

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139
Q

Central sensitisation results in what?

A

Modified response - low level inputs produce repsonse

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140
Q

Neurotransmitter involved in central sensitisation development?

A

Glutamate

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141
Q

Neuropathic pain is?

A

Pain due to injury/dysfunction in the PNS or CNS

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142
Q

Gate control theory of pain is?

A

Endogenous modulation e.g. acupuncture e.g. DNIC

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143
Q

Neurones responsible for pain modulation are?

A

Interneurones in lamina II

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144
Q

DNIC works how? - which fibres and pain pathway are activated?

A

Diffuse noxious inhibitory control
Activation of a-delta fibres
Stimulation of PAG pathway

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145
Q

PAG pathway involves which two neurotransmitters?

A

Serotonin

Noradrenaline

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146
Q

PAG pathway involves which other mediator, other than the neurotransmitters?

A

Opioids

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147
Q

MS lesions are located where?

A

Periventricular

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148
Q

Three types of pain are?

A

Nociceptive - acute
Inflammatory - chronic
Neuropathic - chronic maladaptive

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149
Q

What are enkephalines?

A

Endogenous opioids used in the PAG pathway

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150
Q

Transmitters from NRM to dorsal horn in the PAG pathway are? x2

A

5-HT

Enkephalines

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151
Q

Transmitter from LC to Dorsal horn in PAG pathway is?

A

Noradrenaline

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152
Q

Opioids have action at which sites of the PAG pathway? X3

A

PAG
NRPG
Dorsal horn

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153
Q

Six factors that influence pain perception are?

A 
Cognition 
Mood
Chemicals and structure
Context
Genetics
Injury
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154
Q

Enkepahline are short or long peptides?

A

Short

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155
Q

Enkephalines are derived from?

A

Proenkephalin

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156
Q

Opioid receptors are what type of receptor?

A

G protein coupled receptor

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157
Q

Three opioid/opiate receptors are?

A

Mu 1, 2, 3
Delta 1, 2
Kappa 1, 2, 3

158
Q

Mu opioid receptors are located where?

A

All over the body

159
Q

Morphine works on what channels? x2

A

Increased at K+ channel

Decreased at Ca2+ channel

160
Q

Overall effect of morphine is?

A

Decreased excitability

Increased release of neurotransmitters

161
Q

What is naloxone?

A

Opiate antagonist

162
Q

Half life of naloxone is long or short?

A

Short

163
Q

What is opioid switch?

A

Patient becomes tolerant to one particular opioid drug - switch them to another

164
Q

Strongest side effect associated with kappa opioid receptors is?

A

Dysphoria

165
Q

Three side effects associated with opioid medication?

A

Respiratory depression
Sedation
Reduced GI motility - constipation

166
Q

Three stages of analgesic ladder?

A

Non-opioids and adjuvant drugs
Moderate efficacy opioids
High efficacy opioids

167
Q

Function of paracetamol in pain management?

A

Reduces Cox-2 levels

Analgesic and antipyretic

168
Q

Function of NSAIDs in pain management?

A

Cox 1 and Cox 2 inhibitors

169
Q

Two side effects of NSAIDs?

A

Nausea

GI bleeding

170
Q

Amitriptyline is?

A

Tricyclic antidepressant

171
Q

Indication for amitriptyline in pain management is? x2

A

Neuropathic pain

Cancer

172
Q

Indication for anticonvulsant drugs in pain management is? x2

A

Neuropathic pain

Trigeminal neuralgia

173
Q

Carbamazepine is?

A

Anticonvulsant - sodium channel

174
Q

Sodium valproate is?

A

Anticonvulsant - sodium channel

175
Q

Pregabalin is?

A

Anticonvulsant - calcium channel

176
Q

Pregabalin works on which part of the calcium channel?

A

alpha 2 delta

177
Q

Anaesthetics work via what mechanism?

A

Blockage of sodium channels

178
Q

Cause of trigeminal neuralgia?

A

Compression/stretching of trigeminal nerve root

179
Q

Artery that tends to compress trigeminal nerve in trigeminal neuralgia is? x2

A

AICA or PICA

180
Q

Treatment for trigeminal neuralgia? x3

A

Carbamazepine
Baclofen
Phenytoin

181
Q

The most common site of chronic pain in the UK is?

A

Back pain

182
Q

CBT programme for management for pain lasts how long?

A

12 weeks

183
Q

Four types of pain behaviours are?

A 
Negative affect
Facial/audible expression
of distress
Distorted posture
Avoidance of activity e.g. work
184
Q

Seizures in epilepsy are described as? x2

A

Recurrent and unprovoked

185
Q

Seizures are?

A

Abnormal paroxysmal changes in electrical activity of the brain

186
Q

Epileptogenesis is?

A

Development of epilepsy in a normal brain

187
Q

Prevalence of epilepsy in the UK?

A

1%

188
Q

Status epilepticus is?

A

Form of epilepsy where seizures last more than 5 minutes/more than one seizure in the space of 5 minutes

189
Q

Is status epilepticus a medical emergency?

A

Yes

190
Q

Five stages of tonic-clonic seizure?

A 
Premonition
Pre-tonic-clonic phase
Tonic phase
Clonic phase
Postictal period
191
Q

What happens in the premonition stage?

A

Vague sense that seizure is immunent

192
Q

What happens in the pre-tonic-clonic phase?

A

Few myoclonic jerks/brief clonic seizures

193
Q

What happens in the tonic phase?

A

Contraction of axial muscles
Upward eye deviation
Epileptic cry
Respiratory muscle contraction

194
Q

What happens in the clonic phase?

A

Jerks of increasing amplitude

May have sphincter opening

195
Q

What happens in the postictal period?

A

Generalised lethargy
Decreased muscle tone
Headaches
Sore

196
Q

A person may wet themselves in which stage of a tonic clonic seizure?

A

Clonic

197
Q

You may hear a person cry out in which stage of a tonic-clonic seizure?

A

Tonic

198
Q

Someone may smell a burning smell that is not apparent to anyone else around them in which stage of a tonic-clonic seizure?

A

Premonition - this may be their aura

199
Q

Diagnostic criteria for epilepsy diagnosis?

A

Occurence of two or more seizures

Witness account essential

200
Q

Reorganisation of what particular region occurs in temporal lobe epilepsy?

A

Hippocampus

201
Q

What happens to the hippocampus in temporal lobe epilepsy?

A

Becomes sclerotic

202
Q

What may happen to fibres in the temporal lobe in temporal lobe epilepsy?

A

May have a sprouting of new fibres

203
Q

Why is a sprouting of new fibres problematic?

A

Can lead to development of aberrant circuits

204
Q

Sprouting of new fibres in temporal lobe epilepsy typically occurs from which cells?

A

Granule cells

205
Q

What cells are typically lost in epilepsy?

A

Chandelier cells

206
Q

What are chandelier cells?

A

Inhibitory GABAeric interneurones

207
Q

Chandelier cells synapse where?

A

On axon initial segment of pyramidal cells

208
Q

Chandelier cells control activity of what?

A

Cortical pyramidal cells

209
Q

Loss of chandelier cells results in what?

A

Increased risk of abnormal excitatory activity

210
Q

Three causes of secondary epilepsy?

A

Stroke
Brain tumour
CNS infection

211
Q

Three cellular mechanisms resulting in the development of epilepsy are?

A

Increased excitation - glutamate dependent
Decreased inhibition - GABA dependent
Abnormal neuronal excitability - ion channels

212
Q

What are the receptors involved in the paroxysmal depolarising shift of a seizure?

A

NMDA glutamate receptor

213
Q

Abnormalities/mutations of what cell may be involved in development of epilepsy?

A

Glial cells

214
Q

Role of glial cells with glutamate neurotransmitter?

A

Glial cells - glutamate transport and clearance

215
Q

Two pathways that may be involved in the development of epilepsy?

A

mTOR

REST

216
Q

Phenytoin has an effect on what channel?

A

Sodium

217
Q

Phenytoin should not be used in what type of seizure?

A

Absence

218
Q

Carbamazepine works on what channel?

A

Sodium

219
Q

Phenytoin has what order kinetics?

A

Zero

220
Q

Carbamazepine should not be used in what type of seizure?

A

Absence seizure

221
Q

Lamotrogine works at what two channels?

A

Sodium

Calcium

222
Q

Lamotrogine has what effect?

A

Presynaptic inhibition of glutamate release

223
Q

What drug should be used in absence seizures?

A

Ethosuxomide

224
Q

Ethosuxomide targets what channels?

A

T-type calcium channels

225
Q

Gapapentin/pregabalin targets what channels?

A

Alpha2delta subunit of calcium channels

226
Q

Tiagabine has what effect and what target?

A

Inhibits GABA uptake

GAT-1 transporter

227
Q

Vigabatrin has what effect?

A

Inhibits GABA metabolism

228
Q

Which two anti-epileptic drugs increases hepatic levels of their own enzymes?

A

Phenytoin

Carbamazepine

229
Q

Treatment for status epilepticus?

A

IV diazepam

230
Q

Three potential treatments for epilepsy? (non pharmacological)

A

DBS
Vagal nerve stimulation
Ketogenic diet

231
Q

Three types of primary headaches?

A

Tension-type
Migraine
Cluster headache

232
Q

Treatment of cluster headache?

A

Provision of 100% O2

233
Q

Pathophysiology of migraine revolves around what?

A

Cortical spreading depression

234
Q

What types of brains are subject to migraines?

A

Excitable brains

235
Q

What is heightened during a migraine?

A

Senses - smell, light, sounds, touch

236
Q

Four factors that could result in the onset of a migraine?

A

Hormones
Lack of food
Dehydration
Lack of sleep

237
Q

Migraine with/without aura - which is more common?

A

Without aura

238
Q

What part of the brain plays a major role in the onset of a migraine?

A

Hypothalamus

239
Q

A migraine aura comes from what part of the brain?

A

Visual cortex - occipital lobe

240
Q

Cortical spreading depression occurs in which region of the brain?

A

Visual cortex - occipital lobe

241
Q

Effect of cortical spreading depression on arteries?

A

Swelling of arteries - increased inflammation

242
Q

What type of inflammation occurs from cortical spreading depression?

A

Neurogenic inflammation

243
Q

Via what activation does cortical spreading depression result in the onset of pain?

A

Trigeminal ganglion activation leads to peripheral sensitisation

244
Q

Swelling of what arteries occurs during a migraine?

A

Meningeal arteres

245
Q

Trigeminal nerve conveys pain impulses to where in a migraine?

A

Trigeminal nucleus caudalis in the brainstem

246
Q

What must you never give to a patient suffering from a migraine?

A

Codeine

247
Q

Function of vestibular system? x3

A

Maintenance of balance, posture and spatial orientation

248
Q

Three receptors systems to the vestibular system are?

A

Eyes
General proprioception - muscles, joints, tendonds
Vestibular apparatus in inner ear

249
Q

Three components of the inner ear are?

A

Labyrinth
Vestibular apparatus
Cochlea

250
Q

Two parts of the vestibular apparatus?

A

Vestibular part

Auditory part

251
Q

What are the two solutions in the labyrinth?

A

Endolymph

Perilymph

252
Q

Which part of the vestibular system is the membranous part?

A

Labyrinth

253
Q

Where is the endolymph located?

A

Inner solution

254
Q

Endolymph electrolyte balance?

A

High K+ and low Na+

255
Q

Perilymph electrolyte balance

A

Low K+ and High Na+ (CSF)

256
Q

Where is the perilymph located?

A

Surrounds the labyrinth

257
Q

Components of the labyrinth are known as what?

A

Semicircular ducts

258
Q

What moves around in the semicircular ducts?

A

Endolymph

259
Q

What is on the surface of vestibular cells?

A

Cilia - hair cells

260
Q

Function of the cilia on vestibular cells?

A

These are mechanoreceptors

261
Q

Activation of cilia results in what in vestibular cells?

A

Depolarisation of the cell

262
Q

Cilia on the vestibular cells are known as what?

A

Stereocilia

263
Q

Function of the semi-circular ducts? x2

A

Provides kinetic sensitivity i.e. awareness of movement of the head

Provides information about angular acceleration

264
Q

What are utricles?

A

Cilia on hair cells are angled towards the striola

265
Q

What are saccules?

A

Cilia on hair cells are angled away from striola

266
Q

What is Meniere’s disease?

A

Mixing of the endolymph and the perilymph

267
Q

Cause of Meniere’s disease?

A

Overproduction of endolymph

268
Q

Most common symptom of Meniere’s disease?

A

Tinnitis

269
Q

What is Kinnetosis?

A

Motion sickness

270
Q

Hallpike maneuver tests for what?

A

Benign paroxysmal positional vertigo

271
Q

Mental state examination tests what?

A

Someone’s mindset

272
Q

Mini mental state examination tests what?

A

Someone’s cognition

273
Q

What is psychopathology?

A

The study of all abnormal experiences, cognition and behaviour

274
Q

What is penomenology?

A

The study of subjective psychological evetns

275
Q

Six components of the mental state examination?

A 
Appearance and behaviour
Speech and form of thought
Mood
Perceptions
Cognition
Insight
276
Q

What is classical conditioning?

A

Paring of two stimuli

Neutral stimulus elicits biological response e.g. dogs and bell

277
Q

What is operant conditioning?

A

Association between a behaviour and its consequence

278
Q

One main region of the brain where operant conditioning occurs?

A

Nucleus accumbens

279
Q

Role of nucleus accumbens in operant conditioning?

A

Release of dopamine after e.g. sex, exercise

280
Q

What is social learning?

A

People do what other people do - see them as role models

281
Q

MS is a disease of which cells in the CNS?

A

Oligodendrocytes

282
Q

Neurodegeneration of MS is most visible where?

A

Ventricles

283
Q

Three core symptoms of MS?

A

Pain
Tremor
Spasms

284
Q

Two cannabinoid receptors found in the body?

A

CB1 and CB2

285
Q

CB1 found where?

A

Abundant in adult CNS:

Brain
Adipose tissue
Muscle 
Liver
GI tract
Pancreas
286
Q

CB2 found where?

A

Restricted to the immune system

287
Q

CB1 is what type of receptor?

A

G-protein coupled receptor

288
Q

Function of cannabinoids in the body?

A

Regulation of synaptic neurotransmission

289
Q

Define addiction?

A

Chronic disease characterised by drug seeking use that is compulsive/difficult to control DESPITE harmful consequences

290
Q

What is drug abuse?

A

Drug use in amounts/methods that is directly or indirectly harmful to themselves or others

291
Q

What is drug dependence?

A

Adaptive state developing after repeated drug use - results in withdrawal symptoms upon cessation

292
Q

What is drug tolerance?

A

Diminishing effect of a drug following repeated admission at a set dose

293
Q

What is psychological dependence?

A

Dependence involving emotional-motivational symptoms e.g. depression, restlessness, anhedonia

294
Q

What is physical dependence?

A

Dependence resulting in significant physical-somatic withdrawal symptoms e.g. fatigue, nausea

295
Q

Ethanol has an action at which receptors? x2

A

GABAa

NMDA

296
Q

Hallucinogens has action at which receptor?

A

5-HT2

297
Q

Three factors that determine the development of addiction?

A

Environment
Drug-induced effects
Genes

298
Q

Where is the projection of dopamine in the brain that is most important for drug dependence? (x2 regions)

A

From ventral tegmental area to the

Nucleus accumbens

299
Q

Three stages of the addiction cycle?

A

Binge/intoxication
Withdrawal/negative affect
Preoccupation/anticipation

300
Q

What is released upon multiple uses of drug consumption?

A

GABA

301
Q

What is the effect of GABA release upon multiple drug use?

A

Attempts to dampen down the dopamine release from the drug - drug tolerance

302
Q

Drug tolerance is mediated via which neurotransmitter?

A

GABA

303
Q

Drug addicts have reduced numbers of which receptors in the brain?

A

D2 dopamine

304
Q

Lack of self-control, emotional regulation, motivation, attention, decision making, working memory etc in drug addicts is due to damage in which region of the brain?

A

Pre-frontal cortex

305
Q

Where is the ventral tegmental area/ventral tegmentum located?

A

Floor of the midbrain - near the midline

306
Q

Alcohol has an effect on which receptors?

A

NMDA - excitatory

GABAa - inhibitory

307
Q

Alcohol abuse involves drinking over how many units per day - men?

A

5

308
Q

Alcohol abuse involves drinking over how many units per day - women?

A

3

309
Q

General effect of alcohol abuse on the brain?

A

Shrinking of grey matter

310
Q

Loss of what percentage of grey matter occurs in alcohol abuse?

A

12%

311
Q

Ecstasy is also known as?

A

NMDA

312
Q

Five receptors of MDMA are?

A 
5-HT
5-HT2
Dopamine
Histamine H2
Alpha-2 adrenergic
313
Q

Loss of what innervation pathways occurs when you take NMDA?

A

5-HT

314
Q

Cannabis acts on what receptor? x2

A

CB1

CB2

315
Q

CB1 receptors are located where?

A

CNS

316
Q

CB2 receptors are located where? x2

A

Peripheral organs

Immune system

317
Q

Cannabinoids are inhibitory or excitatory?

A

Inhibitory

318
Q

What type of receptor are CB1 and CB2?

A

G protein coupled receptor

319
Q

Five methods for drug addiction management

A 
Detoxification - eliminate from the body
Psychological support - counselling
Medication 
Treatment for mental health
Long term follow up
320
Q

What is nalmefene?

A

Opioid antagonist

321
Q

Function of nalmefene in treatment drug addiction?

A

Reduction of alcohol consumption

322
Q

Use of antibiotic ceftriaxone in treatment of drug addiction?

A

Attenuate cocaine relapse after cessation

323
Q

Treatment for rhabdomyelosis?

A

Dantrolene

324
Q

Monoaminergic theory for depressions states that?

A

Reduced levels of monoamines is responsible for the development of depression

325
Q

Two monoamines outlined in the monoaminergic theory of depression?

A

Serotonin

Noradrenaline

326
Q

Patients with depression have decreased rates of metabolism where in the brain?

A

Subgenual prefrontal cortex

327
Q

Sign of depression in grey matter is?

A

Decreased cortical thickness

328
Q

What is meant by ‘default mode network’ in teh brain?

A

Network of brain regions that are active whilst the brain is at wakeful rest

329
Q

Pathway for rumination?

A

Negative stimulus activates amygdala and hippocampus
Activates subgenual cingulate cortex
Prefrontal cortex normally stops pathway here

330
Q

Effect of depression on rumination?

A

Prefrontal cortex does not have the desired effect to stop the rumination pathway

331
Q

Function of tricyclic antidepressants?

A

Inhibition of monoamine reuptake - increase levels of monomines

332
Q

SO three theories to explain development of depression?

A

Monoamine theory
Reduced dopamine level theory
Reduced grey matter theory

333
Q

Adverse effects of tricyclic antidepressants? x3

A

Dry mouth
Blurred vision
Loss of libido

334
Q

Main adverse effect of MAOb inhibitors?

A

Cheese effect

335
Q

Cheese effect involves foods containing what compound?

A

Tyramine

336
Q

Main disadvantage of TCAs?

A

Have widespread selectivity at different receptors e.g. histamine receptor

337
Q

The most selective SSRI is?

A

Citalopram

338
Q

Advantages of using SSRIs? x2

A

Similar efficacy to tricyclic antidepressants

No selectivity for other receptors

339
Q

What is moclobemide?

A

Reversible monoamine oxidase inhibitor

340
Q

Advantage of moclobemide? x3

A

Increased selectivity of MAOa
Not irreversible
No cheese effect

341
Q

Why is there a delay of action of antidepressant drugs?

A

Action of autoreceptors - these then become desensitised

342
Q

What is antidepressant drug discontinuation syndrome?

A

Symptoms occurring following sudden cessation of antidepressant medication

343
Q

Gradual decrease in antidepressant medication over how long to avoid the onset of antidepressant drug discontinuation syndrome?

A

6 months

344
Q

Drug used in treatment of bipolar disorder?

A

Lithium

345
Q

What is bipolar disorder?

A

Cycles of depression and mania

346
Q

Function of which two organs should be checked prior to lithium treatment?

A

Thyroid

Renal

347
Q

Four non-pharmacological treatments for depression?

A

Electrocompulsive therapy
CBT
Vagal nerve stimulation
DBS

348
Q

Disadvantage of ECT?

A

Long lasting cognitive effects

349
Q

Advantage of CBT in treatment of depression?

A

Can augment pharmacological effects

350
Q

Indication for use of vagal nerve stimulation for treatment fo depression?

A

Chronic depresson

351
Q

DBS in which area for treatment of depression?

A

Area 25 - subcallosal cingulate cortex

352
Q

Indication for use of ECT for treatment of depression?

A

Severe and treatment resistant depression

353
Q

Neuronal loss occurs specifically where in the brain with depression?

A

Hippocampus

354
Q

Depression - increase in levels of what in the brain? x2

A

Cortisol

IL6

355
Q

Three symptom types in schizophrenia are?

A

Positive
Negative
Cognitive

356
Q

Positive symptoms of schizophrenia are?

A

Hallucinations, delusions - things people would not normally experience

357
Q

Negative symptoms of schizophrenia are?

A

Introversion, apathy, low self-esteem - things mentally stable may experience

358
Q

Cognitive symptoms of schizophrenia are?

A

Poor memory, attention deficit

359
Q

Diagnostic criteria for schizophrenia?

A

Two or more of the outlines symptoms each present for a significant portion of time during a one month period

360
Q

Four genes associated with the development of schizophrenia?

A

BDNF
COMT
DAOA
Neuregulin 1

361
Q

Function of BDNF?

A

Neurotrophic factor that has an effect on long term memory

362
Q

Function of COMT?

A

Dopaminergic transmission

363
Q

Function of DAOA?

A

Glutaminergic transmission

364
Q

Function of neuregulin 1?

A

Neuroplasticity

365
Q

Treatment for schizophrenia are generally used for the management of which symptoms?

A

Positive symptoms

366
Q

Normally - what is seen in MRI of schizophrenia patient?

A

Normally see no change

367
Q

What might be seen in MRI of schizophrenia patient? x2

A

Larger ventricles

Smaller mesial temporal lobe structures

368
Q

Changes in cerebral perfusion in schizophrena? x3

A

Decreased perfusion in the prefrontal cortex

Increased perfusion in the thalamus and cerebellum

369
Q

Kraepelinian definition of a poor outcome for schizophrenia is?

A

Progressive deteriorating course

370
Q

Involvement of which dopaminergic pathways in schizophrenia? x2

A

Mesolimbic pathway

Mesocortical pathway

371
Q

Changes in the dopaminergic pathways in schizophrenia are?

A

Hyperactivity in the mesolimbic pathway

Hypoactivity in the mesocortical pathway

372
Q

Nigrostriatal dopaminergic pathway is involved in what condition?

A

PD

373
Q

D1 type receptors are?

A

D1, D2

374
Q

D2 type receptors are?

A

D2, D3, D4

375
Q

First medication available for treatment of schizophrenia was?

A

Chlorpromazine

376
Q

What is chlorpromazine?

A

Typical antipsychotic

377
Q

Typical vs. atypical antipsychotics?

A

Atypicals also have an effect at 5-HT receptors SO on cognitive and negative symptoms

378
Q

Typicals vs. atypicals - which is the first line treatment for schiz?

A

Atypicals

379
Q

Clozapine is?

A

Atypical antipsychotic

380
Q

Clozapine has significant action at which receptor?

A

D4

381
Q

Use of antipsychotic drugs (typicals and atypicals) restuls in an increase in which hormone?

A

Prolactin

382
Q

Usage of atypicals results in which metabolic adverse effects? x3

A

Weight gain
Dyslipidaemia
Type 2 diabetes

383
Q

Extrapyramidal effects of antypsychotic drug use? x3

A

Dystonia
Parkinsonism
Tardive dyskinesia

384
Q

Two antipsychotics that can be used as depot IM injections for slow release are?

A

Fluphenazine

Haloperidol

385
Q

Why might depot IM injection be used for treatment of schiz?

A

High levels of non-compliance

386
Q

Antipsychotic drug used in drug resistance in treatment of schiz?

A

Clozapine

387
Q

Percentage of schiz patients that do not respond to treatment is?

A

30%

388
Q

Adverse effect of clozapine?

A

Agranulocytosis

389
Q

Two non-phamacological treatments for schiz?

A

CBT

Family therapy

390
Q

Can non-pharmacological treatments replace the pharmacological treatments in schiz?

A

No

391
Q

Schiz associated with decreased levels of which neurotransmitter and receptor?

A

Glutamate NMDA

Year 2 BB (36 decks)

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