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Neurology > Basic Science > Flashcards

Basic Science Flashcards

1
Q

What are the 5 morphological regions of a neuron?

A 
dendrites
soma
axon hillock
axon
synapse
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2
Q

what is the function of dendrites within a neuron?

A

increase surface area of neuron cell membrane and receives inputs from other neurones

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3
Q

what is the function of the soma of a neuron?

A

integrates the input signal to generate a net depolarising or hyperpolarising signal

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4
Q

how are the input signals entering a neuron passed from the dendrites to the soma to the axon hillock?

A

passively

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5
Q

what is the function of the axon hillock?

A

site of initiation of all-or-none AP

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6
Q

what are the 2 main types of pain?

A

nociceptive pain

neuropathic pain

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7
Q

compare nociceptive and neuropathic pain?

A

nociceptive- an appropriate physiological response to painful stimuli via intact nervous system
neuropathic- an inappropriate response to caused by a dysfunction in the nervous system

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8
Q

what is allodynia?

A

pain from a non-painful stimulus

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9
Q

what is hyperalgesia?

A

more pain than expected from a painful stimulus

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10
Q

what type of pain do NSAIDs mainly act on?

A

nociceptive pain

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11
Q

what is the mode of action of NSAIDs?

A

inhibit COX

reduce prostaglandin synthesis

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12
Q

what are the 3 main side effects of NSAIDs?

A
  • GI irritation/bleeding
  • renal toxicity
  • cardiovascular side effects (COX 2)
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13
Q

what effect does paracetamol have in addition to its analgesic effects?

A

antipyretic

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14
Q

what is the mode of action of paracetamol?

A

inhibition of central prostaglandin synthesis

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15
Q

what is the main side effect of paracetamol?

A

risk of liver damage

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16
Q

what type of pain do opiods mainly act on?

A

nociceptive pain

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17
Q

what is the mode of action of opiods?

A

activate the endogenous analgesic system
modulate pain perception
reduce pain signal transmission

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18
Q

what are the 6 main side effects of opiods?

A 
nausea
vomiting
constipation
dizziness/vertigo
drowsiness
dry skin/pruritus
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19
Q

what type of pain do tricyclic antidepressants mainly act on?

A

neuropathic pain

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20
Q

what class of pain medication works best for complex regional pain syndrome?

A

tricyclic antidepressants

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21
Q

what class of pain medication works best for tension headaches?

A

tricyclic antidepressants

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22
Q

what are the 6 main side effects of tricyclic antidepressants?

A 
constipation
dry mouth
drowsiness
abnormalities in heart rate/rhythm
insomnia
increased appetite
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23
Q

what type of pain do SNRI/SSRIs mainly act on?

A

neuropathic pain

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24
Q

what is the mode of action of SNRI/SSRIs?

A

selectively inhibit reuptake of noradrenaline or serotonin

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25
Q

what are the 7 main side effects of SNRI/SSRIs?

A 
nausea
vomiting
constipation
drowsiness
dry mouth
increased sweating
loss of appetite
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26
Q

what type of pain do anticonvulsants mainly act on?

A

neuropathic pain

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27
Q

what is the mode of action of gabapentin? (anticonvulsant)

A

binds to presynaptic voltage-dependent calcium channels

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28
Q

what is the mode of action of pregabalin? (anticonvulsant)

A

interacts with N-type calcium channels

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29
Q

what is the mode of action of carbamazepine? (anticonvulsant)

A

block Na and Ca channels

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30
Q

what pain fibres do topical analgesics work on?

A

A-delta fibres

C-fibres

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31
Q

what are the main 3 side effects of topical analgesics?

A

rash
pruritus
erythema

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32
Q

what are the 6 main side effects of anti-convulsants?

A 
sedation
dizziness
ataxia
peripheral oedema
nausea
weight gain
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33
Q

what is ataxia?

A

loss of full control of body movements

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34
Q

in a neuron what is the rough ER known as?

A

nissl substance

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35
Q

what is the function of an axon with a neuron?

A

conducts APs to other neurones

mediates transport of materials between soma and presynaptic terminal

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36
Q

what are the 2 main ways of axoplasmi transport within a neuron?

A

anterograde

retrograde

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37
Q

what are the 2 rates of axoplasmic transport?

A

fast

slow

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38
Q

how does polio get into the soma of a neuron?

A

gets into presynaptic terminal and then via retrograde axoplasmic transport reaches the soma

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39
Q

what is a neurite of a neuron?

A

a process arising from the soma

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40
Q

what are the 4 main type of neuron?

A

unipolar
pseudounipolar
bipolar
multipolar

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41
Q

how many neurites does a unipolar neuron have?

A

1 neurite

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42
Q

how many neurites does a pseudounipolar neuron have?

A

1 neurite

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43
Q

how many neurites does a bipolar neuron have?

A

2 neurites

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44
Q

how many neurites does a multipolar neuron have?

A

3+ neurites

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45
Q

compare a unipolar neuron to a pseudounipolar neuron?

A

both have one neurite, but the pseudounipolar neurones neurite bifurcates into two axons

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46
Q

what is the normal resting membrane potential?

A

-70mV

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47
Q

what is the membrane potential threshold for voltage activated Na channels to open?

A

-60mV

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48
Q

in the upstroke of an AP in a neuron, what is the resting membrane potential?

A

+40mV

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49
Q

influx of what ion causes the upstroke in an AP?

A

influx of Na

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50
Q

efflux of what ion causes the dowstroke in an AP?

A

efflux of K

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51
Q

what does myelin do to the passive current spread of APs?

A

increases speed

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52
Q

what cells provide the myelin sheath in the PNS?

A

schwann cells

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53
Q

what cells provide the myelin sheath in the CNS?

A

oligodendrocytes

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54
Q

compare schwann cells and oligodendrocytes in how they insulate axons?

A

many schwann cells needed for one axon

one oligodendrocyte surrounds many axons

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55
Q

what are nodes of ranvier?

A

gaps in the myelin sheath

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56
Q

what type of conduction occurs through the nodes of ranvier?

A

saltatory conduction

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57
Q

what type of cells are schwann cells and oligodendrocytes?

A

macroglia

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58
Q

does MS cause demyelination in the CNS or PNS?

A

CNS

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59
Q

does Guillian-Barre syndrome cause demyelination in the CNS or PNS?

A

PNS

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60
Q

what are the 3 main types of synapse?

A

axodendritic
axosomatic
axoaxonic

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61
Q

what is an axodendritic synapse?

A

synapse between an axon of one neuron and the dendrite of another

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62
Q

what is an axosomatic synapse?

A

synapse between an axon of one neuron and the soma of another

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63
Q

what is an axoaxonic synapse?

A

synapse between an aon of one neuron and the axon of another

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64
Q

what is the most common type of synapse?

A

axodendritic

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65
Q

how are synapses functionally classified?

A

inhibitory or excitatory

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66
Q

is an excitatory response depolarising or hyperpolarising?

A

depolarising

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67
Q

is an inhibitory response depolarising or hyperpolarising?

A

hyperpolarising

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68
Q

what is the main transmitter used in excitatory synapses in the CNS?

A

glutamate

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69
Q

what are the main transmitters used in the inhibitory synapses in the CNS?

A

GABA or glycine

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70
Q

what receptors does glutamate activate?

A

post-synaptic cation selective, ionotropic, glutamate receptors

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71
Q

what receptors do GABA or glucine activate?

A

post-synaptic anion selective, ionotropic GABA or glycine receptors

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72
Q

what are the major amino acid neurotransmitters in the CNS?

A

glutamate, GABA and glycine

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73
Q

what charge influx occurs when glutamate activates the cation selective, ionotropic glutamate receptors on the postsynaptic neuron? what does this cause?

A

positive influx

depolarisation

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74
Q

what occurs when GABA or glycine activates the anion selective ionotropic GABA/glycine receptors on the postsynaptic neuron? what does this cause?

A

negative influx

hyperpolarisation

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75
Q

what are pre and post synaptic membranes separated by?

A

synaptic cleft

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76
Q

what is spatial summation?

A

many inputs converge upon a neuron to determine its output

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77
Q

what is temporal summation?

A

output determined by the frequency of APs of a single input

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78
Q

compare the type of vesicles amino acids, amines and peptides are released from?

A

amino acids and amines- synaptic vesicles

peptides- secretory vesicles

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79
Q

compare ionotropic ligand-gated ion channels and G-protein coupled receptors in terms of speed of neurotransmission?

A

ionotropic ligand gated ion channels- fast

GPCR- slow

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80
Q

what causes the release of neurotransmitter from vesicles into the synaptic cleft?

A

influx of Ca through voltage gated Ca channels

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81
Q

after neurotransmitters activate receptors on the post-synaptic membrane, what are the 2 things that can happen to them?

A
  1. enzyme-mediate inactivation of transmitter

2. reuptake of transmitter

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82
Q

compare glycine, glutamate, GABA and amines in terms of what cells make them?

A

glycine and glutamate- all cell

GABA, amines- neurones specifically

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83
Q

how are enzymes that are synthesised in the cell body of neuron transported to the presynaptic terminal?

A

axoplasmic transport via microtubules

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84
Q

at resting membrane potential, describe the flow of Na, Ca, Cl and K if they were to move freely?

A

Na flows inward
Ca flows inward
Cl flows inward
K flows outward

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85
Q

do drugs that are agonists of Na channels cause excitation or inhibition of neurotransmission?

A

excitation

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86
Q

do drugs that are antagonists of Na channels cause excitation or inhibition of neurotransmission?

A

inhibition

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87
Q

do drugs that are agonist of K channels cause excitation or inhibition of neurotransmission?

A

inhibition

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88
Q

do drugs that are antagonists of K channels cause excitation or inhibition of neurotransmission?

A

excitation

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89
Q

compare ionotropic and metabotropic receptors?

A

ionotropic receptors are direct signalling- fast

metanotropic receptors are indirect signalling- slow

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90
Q

what neurotransmitters signal via non-NMDA ionotropic receptors?

A

AMPA

kainate

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91
Q

compare non-NMDA and NMDA in terms of what components within an excitatory synaptic potential they mediate?

A

non-NMDA- fast component

NMDA- slow component

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92
Q

what are the 2 types of receptor GABA activates?

A

ionotropic GABAa receptor

metabotropic GABAb receptor

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93
Q

what channel does the ionotropic GABAa receptor operate?

A

Cl-

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94
Q

what channel does the metabotropic GABAb receptor operate?

A

usually K+ channel

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95
Q

what do benzodiazepines do to the GABAa receptor?

A 
positive modulator (allosterically)
therefore increase Cl- entry to enhance inhibition
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96
Q

what is a quanta?

A

amount of neurotransmitter released from a single vesicle

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97
Q

what are the 2 types of low threshold sensory units?

A
  • low threshold mechanoreceptors

- low threshold thermoreceptors

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98
Q

what are the 4 types of high threshold sensory units?

A
  • high threshold mechanoreceptors (mechanical nociceptors)
  • thermal nociceptors
  • chemical nociceptors
  • polymodal nociceptors
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99
Q

what do polymodal nociceptors respond to?

A

at least 2 of:

  • high intenity mechanical stimuli
  • extreme degrees of heat
  • substances in tissue
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100
Q

what are the 4 types of axons arising from skin/muscle?

A

Aa/I
Ab/II
Ad/III
C/IV

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101
Q

as you move from axon group I to IV, what happens to myelination and conduction velocity?

A

degree of myelination decreases

conduction velocity increases

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102
Q

what group of axons are involved in proprioception of skeletal muscles?

A

Aa/I

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103
Q

what group of axons are involved in temperature pain and itch?

A

C/IV

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104
Q

what group of axons are involved in pain and temperature?

A

Ad/III

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105
Q

what group of axons are involved in low intensity mechanical stimulation of skin?

A

Ab/II

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106
Q

how is the receptive field of a neurone measured?

A

two-point discrimination

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107
Q

what is the major difference between meissner’s corpuscles and merkel’s discs in terms of location on skin?

A

meissner’s corpuscles are not present on hairy skin

merkel’s disc are

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108
Q

what is brown-sequard syndrome?

A

ipsilateral hemiplegia with contralateral pain and temperature deficits

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109
Q

when does the dorsal column medial leminscal pathway cross the spinal cord?

A

great sensory decussation in the brainstem

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110
Q

when does the spinothalmic tract cross the spinal cord?

A

at level of output from the spinal cord

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111
Q

what are the dorsal column medial leminscal pathways formed by?

A

fasciculus gracilis

fasciculus cuneatus

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112
Q

which is more medial- fasciculus gracilis or fasciculus cuneatus?

A

fasciculus gracilis

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113
Q

compare sensory input to T6 and below with above T6

A

T6 and below- fasciculus gracilis

above- fasciculus cuneatus

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114
Q

what is the major route by which touch and proprioceptive information ascends to the cerebral cortex?

A

dorsal column medial lemniscal pathway

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115
Q

what horn within the spinal cord do the first order neurones in the dorsal column medial lemniscal pathway enter?

A

dorsal horn

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116
Q

where do the first order neurones in the dorsal column medial lemniscal synapse?

A

dorsal column gracile nucleus and cuneate nucleus

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117
Q

once the second order neurones in the dorsal column medial lemniscal pathway cross at the great sensory decussation where do they ascend?

A

medial lemniscus

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118
Q

once the second order neurones in the dorsal column medial lemniscal pathway ascend the medial lemniscus, where do they synapse?

A

ventral posteriolateral nucleus of the thalamus

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119
Q

where do the third order neurones in the dorsal column medial lemniscal pathway synapse?

A

primary somatosensory cortex (S1)

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120
Q

what replaces the dorsal column medial lemniscal pathway in conveying sensory information from the anterior head?

A

trigeminal system

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121
Q

what is stereognosis?

A

ability to recognise an object by feeling it

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122
Q

what are the 5 main capabilities of the dorsal column medial lemniscal pathway?

A 
stereognosis
vibration detection
fine touch
conscious proprioception
weight discrimination
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123
Q

what are the 3 divisions of the trigeminal nerve?

A

V1 ophthalmic
V2 maxillary
V3 mandibular

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124
Q

where do primary neurones in the trigeminal system synapse?

A

in chief sensory nucleus of spinal nucleus

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125
Q

where do secondary neurones in the trigeminal system synapse?

A

ventroposteriomedial nucleus of the thalamus

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126
Q

where do third order neurones in the trigeminal system synapse?

A

cortex

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127
Q

where is the somatosensory cortex located?

A

in the post central gyrus of the parietal cortex

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128
Q

where is the post central gyrus of the parietal cortex in relation to the central sulcus?

A

post central gyrus of the parietal cortex is immediately posterior to the parietal cortex

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129
Q

what are the 4 areas of the somatosensory cortex?

A

brodmann areas 1, 2, 3a, 3b

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130
Q

what percentages of input from the ventral posteriomedial go to the brodmann areas of the somatosensory cortex?

A

30% to BA 1 and 2

70% to BA 3a and 3b

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131
Q

where does the input for brodmann area 1 come from?

A

cutaneous input

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132
Q

where does the input for brodmann area 2 come from?

A

joint afferents, golgi tendon organs, deep tissues

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133
Q

where does the input for brodmann area 3a come from?

A

proprioreceptors (muscle spindles)

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134
Q

where does the input for brodmann area 3b come from?

A

cutaneous receptors

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135
Q

what does brodmann area 1 sense?

A

texture discrimination

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136
Q

what does brodmann area 2 sense?

A

object perception (ie sterognosis)

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137
Q

what does brodmann area 3a sense?

A

body position

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138
Q

what does brodmann area 3b sense?

A

touch

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139
Q

how many layers are within the somatosensory cortex?

A

six cell layers

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140
Q

thalamic inputs to the somatosentsory cortex terminate mainly on neurnes within which layer?

A

layer IV

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141
Q

if an area of the body is amputed, what happens to the area of somatosensory cortex representing the finger?

A

utilised by other sensoryy inputs

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142
Q

what happens to the area of somatosensory cortex representing an area of the body that has a lot of sensory activity?

A

slowly increases relatively

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143
Q

what do alpha motor neurones innervate?

A

a bulk of muscle fibres within a muscle

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144
Q

what do gamma motor neurones innervate?

A

muscle spindle fibres

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145
Q

axons of lower motor neurones leave the spinal cord from which spinal roots?

A

ventral roots

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146
Q

ventral roots join dorsal roots to form what nerves?

A

mixed spinal nerves

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147
Q

what type of nerve fibres do mixed spinal nerves consist of?

A

sensory and motor fibres

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148
Q

what are the 2 enlargements of motor neurone bundles within the spinal cord?

A

cervical enlargment

lumbar enlargement

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149
Q

what does the cervical enlargement of motor neurones supply?

A

the arm

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150
Q

what does the lumbar enlargement of motor neurones supply?

A

the leg

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151
Q

what is the smallest functional component of the motor system?

A

motor unit

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152
Q

what does a motor unit consist of?

A

alpha motor neurone and all of the skeletal muscle fibres that it innervates

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153
Q

what is the name for a collection of alpha motor neurones that innervate a single muscle?

A

motor neurone pool

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154
Q

what are the 2 principles that grades the force of muscle contraction?

A
  • frequency of APs from the alpha motor neuron

- recruitement of additional synergistic motor units

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155
Q

within the ventral horn, where are LMNs innervating axial muscles in relation to LMNs innervating distal muscles?

A

LMNs innervating axial muscles are medial to those innervating distal muscles

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156
Q

within the ventral horn, where are the LMNs innervating flexors in relation to LMNs innervating extensors?

A

LMNs innervating flexors are dorsal to those innervating extensors

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157
Q

compare unfused tetani to fused tetani?

A

unfused tetani- time for muscle relaxation between contractions
fused tetani- no time for relaxation between contractions

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158
Q

compare the soma diameters of the alpha motor neurones of small motor units compared with larger motor units?

A

the smaller the motor uni the smaller the soma of the alpha motor unit

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159
Q

what are the main 2 classes of skeletal muscle fibres?

A 
slow oxidative (type 1)
fast fibres (type 2)
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160
Q

what are the 2 types of fast skeletal muscle fibres?

A

type 2a

type 2b

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161
Q

how is ATP derived in type 1 skeletal muscle fibres?

A

oxidative phosphorylation

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162
Q

how is ATP derived in type 2a skeletal muscle fibres?

A

oxidative phosphorylation

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163
Q

how is ATP derived in type 2b skeletal muscle fibres?

A

from glycolysis

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164
Q

why are type 1 skeletal muscles red in colour?

A

high myoglobin content

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165
Q

compare speed of contraction of type 1, 2a and 2b skeletal muscles fibres?

A

1- slow

2a and 2b- fast

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166
Q

compare type 1, 2a and 2b skeletal muscles in the ability to fatigue?

A

1- fatigue resistant
2a- fatigue resistant
2b- not fatigue resistant

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167
Q

what are the 3 types of motor units?

A

slow
fatigue resistant
fast fatiguing

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168
Q

compare type 1, 2a and 2b skeletal muscles in terms of size of alpha motor neuron?

A

1- small a-MN
2a- intermediate a-MN
2b- large

169
Q

what happens to the AP threshold as the size of the alpha-motor neuron increases? (Henneman Size Principle)

A

AP threshold increases

170
Q

what is the myotatic reflex?

A

when a muscle is stretched, it contracts

171
Q

what sensory organ registers change in length of a muscle?

A

muscle spindle fibre

172
Q

compare intrafusal and extrafusal muscle fibres in terms of ability to generate muscle force?

A

intrafusal- don’t generate force

extrafusal- generate force

173
Q

what type of reflex arc is the myotatic reflex?

A

monosynaptic reflex arc

174
Q

what neurotransmitter mediates the myotatic reflex?

A

release of glutamate (excitatory)

175
Q

what spinal cord level is tested by the supinator reflex?

A

C5/6

176
Q

what spinal cord level is tested by the biceps reflex?

A

C5/6

177
Q

what spinal cord level is tested by the triceps reflex?

A

C7

178
Q

what spinal cord level is tested by the quadriceps reflex?

A

L3/4

179
Q

what spinal cord level is tested by the gastrocnemius reflex?

A

S1

180
Q

during voluntatry movement, why are a-MN and y-MN normally co-activated?

A

so that the intrafusal muscle fibres contract in parallel with the extrafusal fibres, stops spindle going slack and therefore maintains sensitivity

181
Q

where are golgi tendon organs located?

A

at junction of muscle and tendon

182
Q

what is the function of golgi tendon organs?

A

regulate muscle tension to protect from overload

183
Q

what is the inverse myotactic reflex?

A

contraction of skeletal muscle causes muscle to relax

184
Q

what are the components of the inverse myotactic reflex?

A

-Ib afferent nerve which innervates golgi tendon organ
and synapses inhibitory interneurone
which causes alpha motor neurone to relax

185
Q

where are the 3 main organs/cells/receptors that proprioceptive information arises from?

A
  • muscle spindles
  • golgi tendon organs
  • joint receptors
186
Q

what type of interneurons mediate the inverse myotatic response?

A

inhibitory interneurons

187
Q

what type of interneurones mediate reciprocal inhibition between extensor and flexor muscles?

A

inhibitory interneurons

188
Q

what type of interneurons mediate the flexor reflex?

A

excitatory interneurons and inhibitory interneurons

189
Q

what is the flexor reflex?

A

when a limb flexes in response to noxious stimuli

190
Q

what type of interneurons mediate the crossed extensor reflex?

A

excitatory interneurons and inhibitory interneurons

191
Q

what is the crossed extensor reflex?

A

during flexor reflex, the contralateral limb extends in order to maintain balance

192
Q

what are the 2 important descending spinal tracts?

A

lateral spinal tracts

ventromedial (/anteromedial) spinal tracts

193
Q

what part of the brain are the lateral descending spinal tracts under control of?

A

cerebral cortex

194
Q

what part of the brain are the venteromedial descending spinal tracts under control of?

A

brainstem

195
Q

what is the function of the lateral descending spinal tracts?

A

voluntary control of distal muscles, eg for small skilled movements

196
Q

what is the function of the ventromedial descending spinal tracts?

A

posture and locomotion

197
Q

what is the major lateral descending spinal tract?

A

the corticospinal (or pyramidal) tract

198
Q

where do the fibres from the corticospinal tract cross?

A

85% cross in the medulla

15% cross at level of exit

199
Q

for the fibres of the corticospinal tract which cross at the medulla, what is this tract now named?

A

lateral corticospinal tract

200
Q

for the fibres of the corticospinal tract which dont cross at the medulla, what is this tract now named?

A

ventral corticospinal tract

201
Q

compare how far axons from the lateral vestibular nucleus and the medial vestibular nucleus travel down the spinal cord?

A

lateral -down to lumbar spinal cord

medial - down to cervical spinal cord

202
Q

what is the function of the lateral vestibulospinal tract?

A

helps hold body upright by facilitating antigravity muscles

203
Q

what is the function of the medial vestibulospinal tract?

A

head movements

204
Q

compare skin, muscle and viscera in terms of how localised pain is?

A

skin- well localised
muscle- poorly localised
viscera- poorly localised

205
Q

what are nociceptors activated by?

A

intense noxious or damaging stimuli

206
Q

where are nociceptor cell bodies located?

A

dorsal root ganglia or trigeminal ganglia

207
Q

what order neurones are nociceptors?

A

first order neurones

208
Q

what sensory fibres do nociceptors comprise of?

A

Ad and C fibres

209
Q

what kind of noxious stimuli do Ad fibres respond to?

A

noxious mechanical and thermal stimuli

210
Q

what kind of noxious stimuli do C fibres respond to?

A

all noxious stimuli (polymodal)

211
Q

compare Ad and C fibres response time to noxious stimuli?

A

Ad- fast

C- slow

212
Q

where are soma of trigeminal sensory neurones located?

A

trigeminal sensory ganglion

213
Q

the second order neurones of the trigeminal system project to the ventroposteriomedial nucleus of the thalamus via what?

A

trigeminal lemniscus

214
Q

the third order neurones of the trigeminal system project to the cortex via what?

A

thalamocortical neurones

215
Q

what is CT contrast determined by?

A

electron density

216
Q

what artificial contrast agents can be used on CT scan?

A

injected iodine based agents

217
Q

why do iodine based agents not pass into the brain?

A

because of the blood brain barrier

218
Q

if iodine based contrast agents cannot get into the brain, why are they used in brain CT?

A

because if there is enhancement (whiteness) it shows that the blood brain barrier has been disrupted (some pathology)

219
Q

how long after a CT angiogram will the CT venogram occur?

A

30 seconds

220
Q

what is MRI contrast deterined by?

A

Proton density, T1 and T2

221
Q

what artificial contrast material can be used in T1 weighted MRI?

A

injected gadolinium compounds

222
Q

compare bone detail of CT and MRI?

A

CT has better bone detail

223
Q

which is generally more tolerated by patients- CT or MRI?

A

CT

224
Q

what is the most common cause of spontaneous subarachnoid haemorrhage?

A

ruptured aneurysm

225
Q

what investigation is needed to rule out a subarachnoid haemorrhage if CT scan is negative?

A

lumbar puncture

226
Q

what are the 2 main methods of aneurysm treatment?

A

craniotomy and clipping of aneurysm

endovascular treatment

227
Q

which form of imaging (CT or MRI) is compatible with most ICU/emergency equipment?

A

CT

228
Q

what type of inheritance is duchennes muscular dystrophy?

A

X-linked recessive

229
Q

what type of inheritance is huntingtons disease?

A

autosomal dominant

230
Q

what area of childhood development is delayed in duchennes muscular dystrophy?

A

delay in motor development

231
Q

at what age does the weakness of muscle start in duchennes muscular dystrophy?

A

3-4 years

232
Q

why do patients with duchennes muscular dystrophy die in their 20s?

A

death from involvement of respiratory and cardiac muscles

233
Q

in both duchennes and beckers muscular dystrophy, what happens to the calves?

A

calf hypertrophy

234
Q

what gene is affected in duchennes muscular dystrophy?

A

dystrophin gene

235
Q

what marker is very raised in muscular dystrophys?

A

serum creatinine kinase

236
Q

what is dystonia?

A

abnormal muscle tone

237
Q

what is the genetic defect in huntingtons disease?

A

repeated CAG codes (codes for glutamine)

238
Q

what is the most common cause of dementia?

A

alzheimers

239
Q

what are the 3 main pathologies within the brain that lead to alzheimer disease?

A
  • loss of cortical neurones
  • neurofibrillary tangles (intracellular)
  • senile plaques (Extracellular)
240
Q

what are the senile plaques in alzheimers made of?

A

amyloid B protein

241
Q

amyloid B protein is a fragment of the product of what protein?

A

amyloid precursor protein

242
Q

what chromosome is the gene for amyloid precursor protein?

A

chromosome 21

243
Q

what apolipoprotein allele predisposes to alzheimers disease?

A

apolipoprotein E4

244
Q

what are the 2 distinct processes of sensitisation of the nociceptive pathway following tissue damage?

A

peripheral sensitisation

central sensitisation

245
Q

does peripheral sensitisation after tissue damage cause primary or secondary hyperalgesia?

A

primary hyperalgesia

246
Q

does central sensitisation after tissue damage cause primary or secondary hyperalgesia?

A

secondary hyperalgesia

247
Q

which causes allodynia after tissue damage- peripheral or central sensitisation?

A

central sensitisation

248
Q

which type of pain sensitisation is the cause of persistant pain after tissue healing?

A

central sensitisation

249
Q

what are the 2 nociceptive tracts?

A

spinothalmic tract

spinoreticular tract

250
Q

where in the spinal column are the nociceptive tracts?

A

anterolateral spinal cord

251
Q

within the dorsal horn of the spinal cord, sensory primary afferent nerves terminate at what?

A

the laminae of rexed (I- V)

252
Q

what is located in the dorsal root ganglia?

A

cell bodies of primary afferent sensory neurones

253
Q

in which lamina of rexed do nociceptive C fibres terminate?

A

laminae I and II

254
Q

in which lamina of rexed do nociceptive Ae terminate?

A

laminae I, II and V

255
Q

what type of pain does the spinoreticular tract mainly transmit?

A

slow C-fibre pain

256
Q

what type of pain does the spinothalmic tract mainly transmit?

A

fast fibre pain

257
Q

where do second order neurones of the spinothalmic tract terminate?

A

posterior and ventroposterior thalamus

258
Q

where do second order neurones of the spinoreticular tract terminate?

A

reticular nuclei in the brainstem

259
Q

within the spinothalmic tract, what neurones relay the signal from the thalamus to the primary somatosensory cortex?

A

thalamocortical neurones

260
Q

within the spinoreticular tract, what neurones relay the signal from the reticular formation to the thalamus?

A

reticulothalamic tracts

261
Q

within the spinoreticular tract, what neurones relay the signal from the thalamus to the limbic areas of the forebrain?

A

thalamocortical neurones

262
Q

why does ‘rubbing it better’ actually help with pain?

A

counter-stimulation analgesia
-stimulation of non-nociceptive afferents activates inhibitory interneurones that suppress firing of the nociceptive pathway

263
Q

how do TENS machines work?

A

counter-stimulation analgesia
-stimulation of non-nociceptive afferents activate inhibitory interneurones that suppress firing of the nociceptive pain pathway

264
Q

how do NSAID reduce nociception?

A

act at site of injury to decrease nociception sensitisation in inflammation

265
Q

how do local anaesthetics reduce nociception?

A

block nerve conduction

266
Q

how do opiods reduce nociception?

A

modify transmission of nociceptive signals in the dorsal horn of the spinal cord and activating descending inhibitory controls

267
Q

what is step 1 of the WHO analgesic ladder?

A

paracetamol or NSAID

268
Q

what is step 2 of the WHO analgesic ladder?

A

NSAID + weak opiod

269
Q

what is step 3 of the WHO analgesic ladder?

A

NSAID + strong opiod

270
Q

what receptors mediate opiod action?

A

G protein coupled opiod receptors

271
Q

what 2 things occur when opiods bind to G protein coupled opiod receptors?

A
  • inhibition of voltage-activated Ca channels on presynaptic neurone (suppresses neurotransmitter release from nociceptor terminal)
  • opening of K channels on postsynaptic neurone (hyperpolarises cell so suppresses neurone excitation)
272
Q

what medical condition should you avoid tramadol in?

A

patients with epilepsy

273
Q

what drugs can be used to reverse opiod toxicity?

A 
naloxone 
naltrexone (longer half life)
274
Q

are aspirin, ibuprofen, naproxen, diclofenac and indometacin COX2-selective inhibitors or non selective inhibitors?

A

non-selective

275
Q

what does inhibiting COX 1/2 do to rate of prostaglandin synthesis?

A

decreases synthesis

276
Q

what specific prostaglandin is involed in sensitisation of nociceptive neurones?

A

PGE2

277
Q

does inhibition of COX1 or COX2 cause GI toxicity?

A

inhibition of COX 1

278
Q

what anti-convulsant drug is often used in painful diabetic neuropathy?

A

pregabalin

279
Q

what anti-convulsant drug is used in migraine prophylaxis?

A

gabapentin

280
Q

how do tricyclic antidepressants work?

A

act centrally by decreasing reuptake of noradrenaline

281
Q

what drug is first line treatment in controlling trigeminal neuralgia?

A

carbamazepine

282
Q

what is the function of the nodes of ranvier?

A

increases conduction speed

283
Q

why are neurones particularly suscpetible to hypoxia?

A

cannot generate energy through anaebolic glycolysis

284
Q

what are the 4 main neuronal responses to injury/disease?

A

acute neuronal injury
simple neuronal atrophy
sub-cellular alterations
axonal reaction

285
Q

what is an axonal reaction?

A

a reaction within the cell body that is associated with axonal injury

286
Q

why does the cell body of a neurone swell and the nucleus become peripherally displaced in response to axonal injury?

A

increased RNA and protein synthesis

287
Q

in response to axonal injury, what way does the degeneration of the axon occur?

A

anterograde degeneration of axon distal to site of injury

288
Q

what happens to the myelin sheath in response to axonal injury?

A

breakdown

289
Q

what happens to the number of astrocytes in response to neuronal injury?

A

increases

290
Q

what is gliosis?

A

proliferation of astrocytes as a reactive response to injury

291
Q

what is the most important histopathological indicator of CNS damage?

A

gliosis

292
Q

why do microglia proliferate in response to injury?

A

to phagocytose the debris of dying neurones (neuronphagia)

293
Q

what are the two organs which autoregulate their blood supply?

A

brain and kidneys

294
Q

above and below what BP, are the brain/kidneys unable to regulate their blood flow?

A

below DBP 50mmHg

above DBP 130mmHg

295
Q

within the brain, what happens to the vasculature in response to hypotension?

A

dilates to maintain blood flow

296
Q

within the brain, what happens to the vasculature in response to hypertension?

A

constricts to maintain blood flow

297
Q

what lobe is affected in an anterior cerebral artery stroke?

A

frontal lobe

298
Q

what is aphasia/dysphasia?

A

language disorder

299
Q

in a middle cerebral artery stoke, what is an important determinant of how bad the signs/symptoms will be?

A

if dominant or non-dominant side is affected

300
Q

why are brainstem infarcts life threatening?

A

because cardiorespiratory centres might be affected

301
Q

what part of the brain is affected in webers syndrome?

A

midbrain

302
Q

what part of the brain is affected in medial and lateral inferior pontine syndromes?

A

pons

303
Q

what part of the brain is affected in lateral medullary syndrome?

A

medulla

304
Q

what visual field defect can occur with an infarct causing damage to the occipital lobe?

A

homonymous hemianopia with macular sparing

305
Q

what kind of gait is acquired in a infarct affecting the cerebellum?

A

ataxic gait

306
Q

what is an intention tremor?

A

a tremor which is not present at rest but is worse as you are trying to do something

307
Q

what are watershed areas within the brain?

A

boundary areas of where the cerebral arteries meet

308
Q

when do watershed infarcts occur?

A

fall in blood pressure

309
Q

what lobe of the cerebrum is affected by a posterior cerebral artery infarct?

A

occipital

310
Q

why do haemorrhages within the brain cause ischaemia?

A
  • blood vessel goes into spasm

- can act like a SOL causing increased ICP resulting in impaired blood flow to the brain

311
Q

what is the strongest risk factor for a stroke caused by cerebral haemorrhage?

A

hypertension

312
Q

what are arteriovenous malformations?

A

failure in normal development of an artery leading to high pressures within the vein
-suscpetible to tearing

313
Q

in mild and moderate ischaemia to the brain, what cells are first to be lost?

A

neurones

314
Q

what is a stroke?

A

sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours

315
Q

what is a TIA?

A

sudden disturbance in cerebral function which lasts less than 24 hours

316
Q

which is more common- stroke due to infarction or haemorrhage?

A

infarction

317
Q

what are the 2 most common originating sites for an embolism causing stroke?

A

heart and carotid arteries

318
Q

which cerebral arteries are most likely to be affected by embolic strokes?

A

middle cerebral arteries

319
Q

what are the 2 main complications of atheroma?

A

thrombosis

aneurysm formation

320
Q

why do cystic fluid filled spaces form as a consequence of cerebral infarct?

A

as cells die, the liquid phospholipids get left behind- this leaves fluid filled cysts

321
Q

what is the most common cause of a spontaneous subarachnoid haemorrhage?

A

rupture of saccular/berry aneurysm

322
Q

where do most saccular/berry aneurysms occur?

A

arterial bifurcations at internal carotid artery

323
Q

what life saving procedure can be done for a saccular aneurysm?

A

clipping

324
Q

what is the onset like for a subarachnoid haemorrhage?

A

abrupt

325
Q

what are lacunes/lacunar infarcts?

A

small cavities found in the basal ganglia, thalamus and pons

326
Q

who are lacunes/lacunar infarcts found in?

A

elderly patients or hypertensives (mainly)

327
Q

when can hypertensive encephalopathy occur?

A

when severe hypertension exceeds the upper limit of autoregulation

328
Q

what kind of dementia is associated with hypertension?

A

multi-infarct dementia

accumulation of lacunar infarcts

329
Q

what demyelinating condition can you get post measles?

A

subacute sclerosing panencephalitis

330
Q

does MS affect white or grey matter?

A

white matter

331
Q

what can you see on a cut-section of the brain of a patient with MS?

A

plaques

areas of demyelination

332
Q

describe the plaques of acute MS?

A

yellow/brown with an ill-defined edge

333
Q

describe the plaques of chronic MS?

A

grey/brown and well demarcated

334
Q

why is there an increased incidence of dementia in Downs syndrome?

A

because the genes involved are on chromosome 21 (downs is trisomy 21)

335
Q

what lobe is generally spared of atrophy in Alzheimers?

A

occipital lobe

336
Q

what do you see when staining amyloid with congo red and then looking at it under polarised light?

A

apple green birefringence

337
Q

what protein is very commonly found in traumatic dementia especially?

A

tau protein

338
Q

what are the hallmarks of dementia with Lewy bodies?

A

hallucinations and fluctuating levels of attention

339
Q

what is the pathogenesis of dementia with lewy bodies?

A

degeneration of the substantia nigra
lewy bodies found in remaining nerve cells
cortical atrophy

340
Q

what is the age of Huntingtons disease onset?

A

35-50 years old

341
Q

what is the inheritance pattern of huntingtons disease?

A

autosomal dominant

342
Q

what gene is involved in huntingtons disease?

A

huntingtin gene

343
Q

what is the triad of clinical features for huntingtons disease?

A

emotional, cognitive and motor disturbance

344
Q

what is myoclonus?

A

jerky contraction of groups of muscles

345
Q

at what age is the onset of Pick’s disease?

A

50-60 years old

346
Q

in Picks disease, what is the frontal lobe function that has very prominent deterioration?

A

personality and social

347
Q

what lobes are mainy affected in Pick’s disease?

A

frontal and temporal lobes

348
Q

what are the histological hallmarks of Pick’s disease?

A

pick’s cells (swollen neurones)

pick’s bodies (intracytoplasmic filamentous inclusions)

349
Q

compare the progression of alzheimers and vascular dementia?

A

alzheimers is continuously progressive

vascular dementia has an abrupt onset with stepwise progression

350
Q

how do the ossicles within th emiddle ear correct for the loss of amplitude that occurs within the fluid in the cochlea?

A

impedance matching

by increasing sound pressure (to match the loss that occurs later)

351
Q

what are the 3 mechanisms by which the ossicles of the middle ear impedance match? (ie increase dBs)

A
  • ratio of tympanic membrane to stapes footplate (20:1)
  • lever action of ossicles
  • buckling of tympanic membrane
352
Q

what membrane separates the scala vestibuli from the scala media?

A

reissner’s membrane

353
Q

what membrane separates the scala media from the scala tympani?

A

basilar membrane

354
Q

where does transduction occur in the inner ear?

A

organ of corti

355
Q

where do the scala vestibuli and the scala tympani connect?

A

at helicotrema

356
Q

what window does the scala vestibuli meet?

A

oval window

357
Q

what window does the scala tympani meet?

A

round window

358
Q

as the basilar membrane goes along (and increases in width), what frequency sound waves correspond to it?

A

decreasing frequency of sound waves

359
Q

which auditory receptor hair cells are most abundant- inner or outer hair cells?

A

outer hair cells

360
Q

what separates the inner and outer hair cells?

A

rods of corti

361
Q

what are inner and outer hair cells?

A

auditory receptors with sterocilia

362
Q

which two membranes within the inner ear do the hair cells stretch between?

A

basilar membrane and tectorial membrane

363
Q

is the kinocilium directly before or after the stereocilia on a hair cell?

A

directly after

364
Q

how does hair cell transduction occur? (ie how is an AP formed?)

A

force towards the kinocilium opens cation channels
K+ enters causing depolarisation
force then goes back away from the kinocilium
cation channels close
repolarisation

365
Q

the bending of the hair cells in the cochlea causes vibration of which membrane?

A

tectorial membrane

366
Q

which cells within the cochlea release neurotransmitter?

A

hair cells

367
Q

compare inner and outer hair cells in terms of which sends afferent signals and which receives efferent signals?

A

inner hair cells- send afferent signals to auditory nerve

outer hair cells- receive efferent signals

368
Q

the efferent signals that outer hair cells receive control what?

A

stiffness

to amplify membrane vibration

369
Q

compare inner and outer hair cells in terms of the how many hair cells are innervated by a single nerve?

A

inner hair cells- one cell innervates many nerves

outer hair cells- many nerves innervate one hair cell

370
Q

what is the motor protein within the outer hair cells composed of?

A

prestin

371
Q

what is the function of the motor protein within outer hair cells?

A

changes the length of the outer hair cells

372
Q

why is it important that the outer hair cells change in length?

A

increased vibration of basilar membrane so increased bending of inner hair cells

373
Q

why can furosemide cause hearing problems?

A

inactivates the membrane motor within the outer hair cells

374
Q

does place code or temporal code operate for pitches under 5kHz?

A

temporal code for under 5kHz

375
Q

does place code or temporal code operate for pitches above 5kHz?

A

place code

376
Q

from cochlea to the auditory cortex, what the is central auditory pathway?

A

eight cranial nerve

cochlear nucleus
superior olivary complex
lateral lemniscus
inferior colliculus
medial geniculate body
377
Q

where do sound waves from both ears merge?

A

superior olivary complex

378
Q

what are the 3 cochlear nuclei?

A

dorsal cochlear nucleus
posteroventral cochlear nucleus
anteroventral cochlear nucleus

379
Q

what part of the vestibular system senses head rotation?

A

semicircular canals

380
Q

what part of the vestibular system senses translational motion and gravity?

A

saccule and utricle

381
Q

within the semicircular canals, what do the cilia project into?

A

cupula

382
Q

are the semicircular canals filled with endolymph or perilymph?

A

endolymph

383
Q

what is the name for sheets of cells where hair cells are clustered within the semicircular canals?

A

crista

384
Q

what plane does the saccule sense movement in?

A

verticle plane

385
Q

what plane does the utricle sense movement in?

A

horizontal plane

386
Q

what separates the hair cells within the otolith organs?

A

striola

387
Q

compare the direction of hair cells in semicircular canals and otolith organs?

A

semicircular canals- all in same direction

otolith organs- oriented in all directions

388
Q

what are the 3 major vestibular reflexes?

A

vestibulo-ocular reflex
vestibulo-colic reflex
vestibular-spinal reflex

389
Q

what is the vestibulo-ocular reflex?

A

keeps eyes wtill in space when head moves

390
Q

what is the vestibulo-colic reflex?

A

keeps head still in space when you walk

391
Q

what is the vestibular-spinal reflex?

A

adjusts for posture for rapid changes in position

392
Q

why does alcohol cause dizziness?

A

makes the cupula less dense meaning it floats in the endolymph more
-you think you are rotating when you are still

393
Q

what happens to the membrane potential of a photoreceptor when light enters the eye?

A

hyperpolarises

394
Q

why do photoreceptors hyperpolarise when light enters the eye?

A

Na+ channels close

395
Q

what does light do to 11-cis-retinal within rods?

A

converts it to its active form: all-trans-retinal

396
Q

why do Na+ channels within photoreceptors cose when light enters the eye?

A

the all-trans-retinal that is formed causes the Na+ channels to close (and then cell hyperpolarises)

397
Q

during phototransduction, compare light and dark in terms of how much glutamate there is?

A

light- less glutamate

dark- more glutamate

398
Q

what is visual acuity determined by?

A

photoreceptor spacing mainly

and refractive power

399
Q

what is the receptive field of a ganglion cell?

A

the part of the retina that needs to be stimulated to elicit APs from that specific ganglion cell

400
Q

are rods or cnes used for seeing in dim light?

A

rods

401
Q

do the ganglion cells of rods have high or low convergence?

A

high convergence

402
Q

ganglion cells of rods have high convergence, what does this mean in terms of sensitivity and acuity?

A

increased sensitivity

decreased acuity

403
Q

do ganglion cells of cones have high or low convergence?

A

low convergence

404
Q

ganglion cells of cones have low convergence, what does this mean in terms of sensitivity and acuity?

A

low sensitivity

high acuity

405
Q

as you move from blue to green to red light, what happens to the wavelength and the frequency?

A

wavelength increases

frequency decreases

406
Q

compare rods and cones in terms of chromaticity?

A

rods- achromatic

cones- chromatic

407
Q

compare rods and cones interms of location on the retina?

A

rods- peripheral

cones- central

408
Q

compare rods and cones in terms of light sensitivity?

A

rods- high light sensitivity

cones- low light sensitivity

409
Q

compare rods and cones in terms of visual acuity?

A

rods- low visual acuity

cones- high visual acuity

410
Q

lateral inhibition of neurones within the optic system aids with what?

A

localisation of image

411
Q

what is the name for the synapse between the motor neuron and the muscle?

A

mtor end plate

412
Q

what enzyme degrades acetylcholine?

A

acetylcholinesterase

413
Q

what does acetylcholinesterase convert acetyl choline into?

A

acetate and choline

414
Q

how does the curare (D-tubocuracine) poison kill you?

A

binds to the ACh receptor on the postysynaptic membrane and inhibits it
-no muscle contraction and so respiration stops

415
Q

what are type 1 muscle fibres?

A

slow oxidative, resist fatigue

416
Q

what are type 2a muscle fibres?

A

fast oxidative (aerobic)

417
Q

what are type 2b muscle fibres?

A

fast glycolytic, easiy fatigued

418
Q

what does a fasciculation usually indicate?

A

disease of motor neurone

Neurology (3 decks)

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