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Years 1+2 > S3C6 (2.0) > Flashcards

S3C6 (2.0) Flashcards

1
Q

What are the 5 key principles of the mental capacity act?

A

A personis assumed to have capacity unless it is established otherwise
A person is not to be treated as unable to make a decision unless all practicable steps to help him to do so have been taken without success.
A person is not to be treated as unable to make a decision merely because he makes an unwise decision.
An act done, or decision made, under this Act for or on behalf of a person who lacks capacity must be done, or made, in his best interests.
Before the act is done, or the decision is made, regard must be had to whether the purpose for which it is needed can be as effectively achieved in a way that is less restrictive of the person’s rights and freedom of action.

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2
Q

What is the role of afferent neurones?

A

Neurites in sensory surfaces of body
Detect changes in environment
Transmit information to brain or spinal cord

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3
Q

What is the role of association neurones?

A

Lie between sensory and motor pathways
Connect only with other neurones
Process, store and retrieve information

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4
Q

What is the most abundant neurone type?

A

Interneurons

90% of neurons

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5
Q

What is the role of efferent neurones?

A

Axons form synapses with muscles

Command movements

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6
Q

Where are bipolar neurons found?

A

Olfactory, retina and ear

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7
Q

What are multipolar neurones?

A

Many dendrites to one axon

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8
Q

What is the role of unipolar neurones?

A

Sensory from skin and organs to spinal cord

Long myelinated fibre bypassing soma

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9
Q

How do neurons communicate?

A

Axon terminals form synapses with dendrites or soma (cell body) of other neurones
Nerve impulse arrives in axon terminal and releases neurotransmitter
Neurotransmitter binds to specific receptors
Generation of electrical signal in postsynaptic cell
Triggers action potential
Messaged gets passed on

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10
Q

What is the major excitatory neurotransmitter?

A

Glutamate

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11
Q

What is spatial summation?

A

Adding of EPSPs generated simultaneously on multiple presynaptic inputs

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12
Q

What is temporal summation?

A

Adding of EPSPs generated in quick succession at same synapse

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13
Q

What are glia?

A

non-neuronal cells in the central nervous system. They maintain homeostasis, form myelin and provide support and protection for neurons

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14
Q

What is the role of glia on neurones?

A

Synapse formation
Synaptic strength
Co-ordination of activity

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15
Q

What is the role of neurones on glia?

A

Proliferation
Differentiation
Myelination

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16
Q

What are the two types of potential?

A

Electronic potential

Action potantial

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17
Q

What is an electrotonic potential?

A

Non-propagated local potential, resulting from a local change in ionic conductance (e.g. synaptic or sensory that produces a local current). When this spreads along a stretch of the neuronal membrane, it becomes exponentially smaller

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18
Q

Where can you find cells using electrotonic potentials?

A

Amacrine cells in retina

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19
Q

What is an action potential?

A

A propagated impulse.
Longer neurons utilise electrotonic potentials to trigger the action potential.
Initially, there is always an electrotonic potential in a neuron – when this propagates, it becomes an action potential.

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20
Q

What is the resting potential of neurons?

A

-70mV

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21
Q

Where is the concentration of K+ higher?

A

Inside neurons

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22
Q

What are the two gates on sodium channels?

A

the activation gate (m gate)

the inactivation gate (h gate).

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23
Q

What gate on the Na+ channels are closed during resting state?

A

The activation gate is closed, which prevents any entry of sodium ions to the interior of the fibre through these sodium channels.

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24
Q

When does the absolute refractory period occur?

A

Na+ channel inactivation.
It is impossible to recruit a sufficient number of Na+ channels to generate a second spike unless previously activated Na+ channels have recovered from inactivation.

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25
Q

What are the 3 categories of neurotransmitter?

A

Amino acids
Amines
Peptides

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26
Q

What neurotransmitters are amino acids?

A

Glutamate
GABA
Glycine

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27
Q

What neurotransmitters are amines?

A 
Acetylcholine
Noradrenaline
Dopamine
Serotonin
Histamine
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28
Q

What neurotransmitters are peptides?

A

Substance P
Opioids (encephalin and dynorphin)
NPY

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29
Q

What are the two types of receptors?

A

Ionotropic

Metabotropic

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30
Q

How do ionotropic receptors work?

A

Glutamate is released at the pre-synapse terminal, binds to channels on the post synaptic cleft, causing influx/efflux of ions, thereby causing an action potential

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31
Q

How do metabotropic receptors work?

A

Binding of transmitter leads to activation of G-proteins.
G-proteins activate effector proteins:
Ion channels
Enzymes that generate 2nd messengers
Slower and longer lasting effects than ionotropic receptors

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32
Q

What is the epidemiology of depression?

A

Woman > Men

Peak onset is 20s

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33
Q

What are factors for depression?

A

Genetic, neurobiological, sociopsychological and environmental factors

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34
Q

What are the biological factors of depression?

A

Lack of monoamines
Genetic vulnerability
Increased levels of stress hormones and dysfunction of the hypothalamus-pituitary axis

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35
Q

What are the psychological factors of depression?

A

Traumatic and stressful experience

Personality factors - learned helplessness

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36
Q

What is the concordance rate in identical twins for depression?

A

50%

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37
Q

What are the clinical features of depression?

A

Depressed mood, present most of the day, every day
Sleep disturbance (insomnia or hypersomnia)
Loss of interest or anhedonia
Feelings of worthlessness or guilt Fatigue
Diminished concentration, ability to think or make decisions-Pseudodementia
Weight change due to appetite changes
Psychomotor changes
Suicidal ideation

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38
Q

What is the diagnostic criteria for depression?

A

5 or more symptoms for at least 2 weeks, one of them being depressed mood or anhedonia

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39
Q

What is adhedonia?

A

An inability to enjoy acts or experiences that are normally pleasurable

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40
Q

What are the positives of Buproprion?

A

lowers seizure threshold, less sexual dysfunction compared to SSRIs, and can also treat tobacco dependence

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41
Q

What is the role of glia?

A

Insulate and support and nourish neurons

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42
Q

What are microglia?

A

the resident macrophages of the brain and spinal cord, and thus acts as the first and main form of active immune defence in the CNS

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43
Q

What % of glial cell population in the brain are microglia?

A

10-15%

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44
Q

What is the role of oligodendrocytes?

A

Involved in myelin formation around axons in the CNS

These provide layers of membrane that insulate axons forming a sheath

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45
Q

What are the subtypes of astrocytes?

A

Fibrous - found primarily in white matter

Protoplasmic - found primarily in grey matter

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46
Q

What is the role of astrocytes?

A

Send processes to blood vessels where they induce capillaries to form the tight junctions making up the BBB
They also send processes that envelop the synapses and the surface of the nerve cells

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47
Q

What is the role of protoplasmic astrocytes?

A

Protoplasmic astrocytes have a membrane potential that varies with the external K+ concentration but do not generate propagated potentials
They produce substances that are tropic to neurons, and they help maintain the appropriate concentration of ions and neurotransmitters by taking up the K+, glutamate and GABA

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48
Q

What is the epidemiology of MS?

A

Incidence 2:1 W:M
onset between 20-40 y/o
Prevalence rates increase at higher latitudes

49
Q

What is the latitude effect theory on MS?

A

There is a protective effect of sun exposure. Low levels of vitamin D are common at high latitudes where sun exposure may be low, particularly during winter months.
Vitamin D deficiency is associated with an increase in MS risk.

50
Q

What is the incidence of MS in the UK?

A

1 in 800

85000 cases

51
Q

What gene has been linked with MS?

A

Human Leukocyte Antigen (HLA) – group of genes on chromosome 6 that serves as MHC.
HLA changes account for 20-60% of genetic predisposition.

52
Q

What viral exposure increases MS risk?

A

Previous exposure to Human Herpes virus and Epstein-Barr virus

53
Q

What are the types of MS?

A

Relapsing-remitting
Secondary Progressive
Primary progressive
Progressive-relapsing

54
Q

What is relapsing-remitting MS?

A

Relapses followed by a complete or partial recovery, alternate with remissions

55
Q

What is secondary progressive MS?

A

Follows on from relapsing-remitting, begins with relapses alternating with remissions, followed by a gradual progression of the disease

56
Q

What is primary progressive MS?

A

progresses gradually from onset with no remissions or obvious relapses, although there may be temporary plateaus

57
Q

What is progressive-relapsing MS?

A

progresses gradually, but progression is interrupted by sudden relapses

58
Q

What % of MS patients are progressive-relapsing?

A

<5%

59
Q

What % of MS patients are primary progressive?

A

10-15%

60
Q

What % of MS patients are relapsing-remitting?

A

85-90%

61
Q

What is optic neuritis?

A

Impaired vision and colour blindness

62
Q

What is Lhermitte’s sign?

A

A shooting electric sensation that travels down the spine when the patient flexes their neck

63
Q

What is Uhthoff’s phenomenon?

A

A reversible exacerbation of neurological symptoms following physical exertion, a warm bath or fever
Impulse conduction is dependent on temperature. An increase in body temperature presumably worsens impulse conduction in demyelinated nerves.

64
Q

What is the pathophysiology of MS?

A

Immune mediated damage characterised by inflammation, demyelination and axonal degeneration

65
Q

What is the process of dymyelination?

A

Autoreactive T-lymphocytes are activated by an unknown factor. Once activated, they migrate to the CNS, where they interact with autoantigens and initiate an inflammatory response.
Causes inflammatory process
Focal demyelination with partial preservation of axons (acute plaques)
Loss of axons and atrophy of oligodendrocytes (chronic plaques)
Inadequate remyelination

66
Q

What are the most common sites of demyelination?

A

Periventricular areas
Brainstem
Cerebellum
Spinal Cord

67
Q

What is the BBB?

A

Blood-Brain Barrier (BBB) - part of capillary system that prevents entry of T cells into the nervous system.

68
Q

How can the BBB become permeable to T cells?

A

Damage to BBB by virus or bacteria

After repair, T-cells remain trapped.

69
Q

What is the structure of the BBB?

A

Endothelial cells which line blood vessel walls of CNS.

ECs are connected by occludin and claudin which forms tight junctions in order to create a barrier.

70
Q

What happens to the BBB during inflammation?

A

Chemokine release allows activation of adhesion molecules on the lymphocytes and monocytes resulting in interaction with ECs of BBB which then activate the expression of MMP to degrade the barrier.
Disruption of BBB occurs = swelling + activation and infiltration of macrophages and lymphocytes that directly attack myelin sheaths within CNS.

71
Q

What happens to the BBB during MS?

A

BBB is disrupted and this enables entering of T-cells that attack the myelin.
Attack starts an inflammatory process whereby cytokines and antibodies are recruited.
This causes swelling, macrophage activation and further recruitment of cytokines etc.

72
Q

What is the result of inflammation of the BBB?

A

Stop neurotransmission by unaffected neurons.
Enhanced loss of myelin.
Cause axon to break down completely.

73
Q

What causes the inflammation of MS?

A

Over-production of IL-12 is what causes the inflammation
IL-12 is responsible for the differentiation of naive Th cells into inflammatory T cells. T–Lymphocytes are involved; mostly Th-1 and Th-17.

74
Q

What happens during remission phase of MS?

A

Oligodendrocytes cannot completely remyelinate or repair a destroyed myelin sheath.
CNS thus recruits oligodendrocytes stem cells capable of proliferation and migration plus differentiation into mature myelinating oligodendrocytes.
Newly formed myelin are however thinner and not as effective.
Repeated attacks (“multiple”) make this worse until a scar-like plaque (“sclerosis”) is built up around the damaged axons.
Inability of stem cells to myelinate properly can also be due to the astrocytes and prevailing inflammatory conditions.

75
Q

Where are the most common sites for lesions in MS?

A 
Optic nerve
Corpus callosum
Cerebellum
Brainstem
Basal ganglia 
Spinal cord.
76
Q

What is the pathogenesis of demyelination?

A

Initiated by CD4+ TH1 and TH17 T cells that react against self-myelin antigens and secrete cytokines.
TH1 cells secrete IFNγ, which activates macrophages.
TH17 cells promote the recruitment of leukocytes.
The demyelination is caused by these activated leukocytes and their injurious products.
The infiltrate in plaques and surrounding regions of the brain consists of T cells (mainly CD4+, some CD8+) and macrophages.

77
Q

What is the diagnosis criteria for MS?

A

Two or more episodes of symptoms
Two or more signs that reflect pathology in anatomically non-contiguous white matter tracts of the CNS
Symptoms must last for 24 hours or more and occur as distinct episodes that are separated by a month or more

78
Q

What can an MRI show in MS?

A

An increase in vascular permeability from a breakdown of the BBB is detected by leakage of IV gadolinium into the parenchyma. -Enhancement of active lesions during and up to 6 weeks after the exacerbation
Such leakage occurs early in the development of an MS lesion and serves as a useful marker of inflammation.

79
Q

What does evoked potentials test measure?

A

The electrical activity of the brain in response to stimulation of specific sensory pathways.
EP tests are able to detect the slowing of electrical conduction caused by damage (demyelination) along these pathways.

80
Q

What is the method for evoked potentials test?

A

Wires placed on scalp, overlying areas of brain being stimulated.
Sensory input provided (light, sound and sensation).
Record response of brain activity

81
Q

What is the prognosis or MS?

A

The effect of MS and its progression varies unpredictably
Remissions can last months or years
75% MS never need a wheelchair
40% MS patients normal activities aren’t disrupted

82
Q

What is a clinical relapse of MS described as?

A

Patient reported symptoms or objectively observed signs typical of an acute inflammatory demyelinating event in the CNS, current or historical, with duration of at least 24 hours, in the absence of fever or infection

83
Q

How do you treat an MS relapse?

A

High dose corticosteroids either orally or intravenously
i.e. Methylprednisolone (1g/day for 3 days)
Accelerates recovery by reducing inflam ation

84
Q

What is the MOA of methylprednisolone?

A

Bind to glucocorticoid receptor
Inhibit pro-inflam signals
Decreased leukocyte migration

85
Q

What are the side effects of steroids?

A

Gastritis, osteoporosis, hypertension, low mood, avascular necrosis of the femoral head, infection

86
Q

What are α4-integrins?

A

Found on the surface of lymphocytes and monocytes
Required for WBC to move into organs
α4-integrins (particularly α4β1) interact with vascular cell adhesion molecule 1 on vascular endothelial cells to mediate adhesion and migration of immune cells across BBB

87
Q

What is the MOA of beta interferon?

A

Inhibiting T cell activation
Preventing T cell proliferation
Blocking T cell migration across BBB

88
Q

What is the MOA of glatiramer acetate?

A

Bind to MHC class 2 molecules
Competing with myelin basic protein for binding to T-cell receptor
Inhibiting activation of MBP-reactive T-cells shifts population of T-cells from pro-inflammatory Th1 cells to regulatory Th2 cells that suppress the inflammatory response

89
Q

What is the role of myelin basic protein?

A

Protein believed to be important in myelination of nerves by maintaining structure of myelin

90
Q

What is the MOA of natalizumab?

A

A monoclonal antibody which inhibits migration of leucocytes into the CNS
Prevents binding of lymphocytes to vascular endothelium via α4β1 ligands

91
Q

What is the MOA of teriflunomide?

A

□ Blocks pyrimidine synthesis by inhibiting the mitochondrial enzyme dihydroorotate dehydrogenase and T cell function
Vital salvage pathways are preserved allowing generalised immune surveillance
Antiproliferative agent

92
Q

What is the MOA of fingolimod?

A

A sphingossine 1-phosphate receptor modulator
Binds with high affinity to S1P1 receptor
This blocks the capacity of autoreactive lymphocytes to egress from lymph nodes, reducing the number of lymphocytes in peripheral blood
Reducing lymphocyte migration into CNS

93
Q

What is the MOA of dimethyl fumerate?

A

Proinflammatory cytokine inhibitor

94
Q

What is the MOA of alemtuzumab?

A

Monoclonal targets B and T cells resulting in cell lysis

95
Q

What is the MOA of cladrabine?

A

Nucleoside analogue of deoxyadenosine depleting B and T cells

96
Q

How do glucocorticoids block the arachidonic pathway?

A

Enter cells
Bind to intracellular receptors in cytoplasm – GRα and GRβ
Receptor complex move to nucleus
Binds to DNA in nucleus
Alters gene transcription (transactivation or transsupression)

97
Q

What are the side effects of glucocorticoids?

A 
Hyperglycaemia
Decreased resistance to infection
Swelling of face
Weight gain
Congestive cardia insuffiency
Fluid and sodium retention
Oedema
Hypertension
98
Q

What is coping?

A

The process of managing stressors that have been appraised as taxing or exceeding a person’s resources.
Coping has a dynamic nature which involves appraisal and reappraisal, evaluation and re-evaluation.

99
Q

What are the goals of coping?

A

To reduce stressful environmental conditions and maximize the chance of recovery.
To adjust or tolerate negative events.
To maintain a positive self-image.
To maintain emotional equilibrium.
To continue satisfying relationships with others.

100
Q

What are the two ways of coping in Leventhals self-regulatory model?

A

Approach coping

Avoidance coping

101
Q

What are the two was of coping not in Leventhals self-regulatory model?

A

Problem Focused

Emotion Focused

102
Q

What is approach coping?

A

Confronting the problem, gathering information and taking direct action.

103
Q

What is avoidance coping?

A

Minimising the importance of the event

104
Q

What is problem-focused coping?

A

Involves attempts to take action to either reduce the demands of the stressor or to increase the resources available to manage it.

105
Q

What is emotion-focused coping?

A

Involves attempts to manage the emotions evoked by the stressful event.

106
Q

What are the two types of monoamines?

A

Catecholamines – dopamine, noradrenaline, adrenaline

Indoleamines – serotonin (5-HT)

107
Q

What amino acid makes up noradrenaline?

A

Tyrosine

108
Q

What amino acid makes up serotonin?

A

Tryptophan

109
Q

How are catecholamines produced?

A

Tyrosine is hydroxilated into L-DOPA.
L-DOPA is decarboxylated into Dopamine (in brain).
Dopamine is hydroxilated into Noradrenaline.
Noradrenaline is converted into Adrenaline.

110
Q

Where is tyrosine converted into noradrenaline?

A

Neuronal cell bodies in pons, particularly locus ceruleus.

111
Q

How is serotonin produced?

A

Tryptophan is hydroxilated into 5-Hydroxytryptophan.

5-Hydroxytryptophan is decarboxylated into 5-Hydroxytryptamine (Serotonin)

112
Q

Where is tryptophan converted into 5-HT?

A

Neuronal cell bodies in a chain of brainstem nuclei (raphe nuclei), particularly the dorsal and medial raphe.

113
Q

How are noradrenaline and 5-HT taken up from the synapse?

A

Reuptake and enzymatic degradation

114
Q

What breaks down 5-HT?

A

Monoamine oxidase (MAO-A) into 5-Hydroxyindole acetic acid (5-HIAA)

115
Q

What breaks down noradrenaline?

A

MAO-A and Catechol-O-methyl transferase (COMT) into vanillylmandelic (VMA)

116
Q

What are the two main classes of noradrenergic receptors?

A 
Alpha receptors (α) – α1 (stimulatory effect), α2 (inhibitory effect)
Beta receptors (β) – β1, β2, β3 (all stimulatory effects)
117
Q

What is the MOA of TCAs?

A

These block the reuptake of noradrenaline, 5-HT and dopamine.
Examples include: amitriptyline, clomipramine.

118
Q

What is the MOA of SNRIs?

A

Found to reversibly block 5-HT reuptake transporter (SERT) AND the noradrenaline reuptake transporter (NET) proteins on the presynaptic membrane.
Examples include imipramine, venlafaxine.

119
Q

What is the MOA of SSRIs?

A

Found to reversibly block 5-HT reuptake transporter (SERT) ONLY.
These result in sustained increase in extracellular 5-HT in a range of brain areas.
Examples include fluoxetine, sertraline, paroxetine, fluvoxamine, escitalopram, citalopram.

Years 1+2 (21 decks)

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