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Years 1+2 > S3C2 (2.0) > Flashcards

S3C2 (2.0) Flashcards

1
Q

What is a dermatome?

A

an area of skin that is mainly supplied by afferent nerve fibers from a single dorsal root of spinal nerve which forms a part of a spinal nerve

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2
Q

What innervates muscles?

A

Myotomes - a single ventral root

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3
Q

What are most muscles innervated by?

A

Axons from two spinal segments

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4
Q

What muscles are unsegmentally innervated?

A

Intrinsic muscles of the hand

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5
Q

When do muscles share innervation by the same spinal segment?

A

When they have a common primary action

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6
Q

What is the innervation for muscles with opposing action? Example?

A

They are supplied in sequence
i.e. C5/C6 bicep flexors
C7/C8 triceps extensors

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7
Q

What does complete sensory loss mean?

A

More than one spinal root must be damaged as there are functional overlap at boundaries between dermatomes/myotomes

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8
Q

When does the notochord appear in the medoserm?

A

3rd week

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9
Q

When are dermatomes formed?

A

3rd week - the tri-laminar disc has been established and the middle layer (mesoderm) has differentiated into its different types

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10
Q

What is directly adjacent to the neural tube?

A

Paraxial mesoderm

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11
Q

What does the paraxial mesoderm differentiate into?

A

44 somites

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12
Q

How many somites are formed? How many break down? How many are left?

A

44 formed
13 broken down
31 somites left

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13
Q

What does the ventral portion of somites contain?

A

Sclerotome, the precursor to the ribs and vertebral column.

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14
Q

What does the dorsal portion of somites contain?

A

Dermomyotome

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15
Q

How can spinal cord cells be classified?

A

Interneurons

Projection neurons

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16
Q

What % of spinal cord cells are interneurons?

A

97%

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17
Q

What is the role of interneurons?

A

Involved in modulating sensory input and motor output and make local connections with other cells in the spinal cord

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18
Q

What can interneurons be subdivided into?

A

Inhibitory and excitatory

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19
Q

What is the role of inhibitory neurones?

A

Limit receptive field size or activity of other neurones

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20
Q

What neurotransmitters do inhibitory neurones use?

A

GABA
glycine
enkephalin
{others}

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21
Q

What neurotransmitters do excitatory neurones use?

A

Glutamate

various neuropeptides

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22
Q

What is the role of excitatory neurones?

A

Their stimulation evokes action potentials in other cells

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23
Q

What % of spinal cord cells are projection neurons?

A

3%

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24
Q

What can projection neurons be subdivided into?

A 
Axons of the ascending pathways (1%)
Motor neurones (2%) - project from the spinal cord to innervate skeletal muscle and others
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25
Q

Describe A-alpha fibres

A 
Myelinated
Afferent - muscle spindles
Efferent - alpha motorneurons
 Very fast conduction (60-120 m/s)
Large (15 µm)
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26
Q

Describe A-beta fibres

A

Myelinated
Afferent - skin mechanoreceptors
Fast (30-60 m/s)
Medium sized (8 µm)

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27
Q

Describe A-gamma fibres

A

Myelinated
Efferent - muscle spindles
Slower (2-30 m/s)
Medium sized (5 µm)

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28
Q

Describe A-delta fibres

A 
Myelinated
Afferent - pain
-free nerve endings
-responsible for withdrawal reflex to pain
Slower (2-30 m/s)
Small (3 µm)
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29
Q

Describe C fibres

A

Unmyelinated
Afferent - pain
Slowest (0.24-1.5 m/s)
Small (1 µm)

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30
Q

What are low-threshold mechanoreceptors innervated by?

A

A-beta

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31
Q

What is Merkel’s disks good for?

A

highest spatial resolution, allows them to resolve tiny spatial details. Ideal for processing

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32
Q

What is the role of meisenner corpuscle?

A

40% of hand machinosensory information. Efficient in processing information about low-frequency vibration that occurs when objects move across the skin

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33
Q

What are ruffini endings essential for?

A

Internally generated stimuli

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34
Q

What is the role of pacinian corpuscle?

A

Detecting vibrations transmitted through objects that contact the hand

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35
Q

Where can muscle spindles be found?

A

Skeletal muscle

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36
Q

What do muscle spindles consist of?

A

4-8 specialised intrafusal muscle fibres surrounded by a capsule of connective tissue

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37
Q

How are intrafusal fibres distributed?

A

Distributed among the extrafusal fibres of skeletal muscle in a parallel arrangement

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38
Q

How are nuclei arranged in the largest intrafusal fibres?

A

In the largest of intrafusal fibres, the nuclei are collected in an expanded region named the nuclear bag fibres

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39
Q

How are nuclei arranged in the smaller intrafusal fibres?

A

Lined up single file - called nuclear chain fibres

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40
Q

What type of neurons are first order neurons?

A

Pseudo-unipolar neurons which have cell bodies within the dorsal root ganglion

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41
Q

Where are the cell bodies of second order neurons found?

A

In the rexed laminae of the spinal cords, or in the nuclei of the cranial nerves within the brainstem

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42
Q

Where are the cell bodies of third order neurons found?

A

Thalamus

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43
Q

Where do third order neurons project?

A

Ipsilateral postcentral gyrus

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44
Q

How are neurons in the sensory tracts arranged?

A

According to 3 anatomical principles:
Sensory modality
Somatotopic
Medial-lateral rule

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45
Q

What is the medial-lateral rule of neurons?

A

Sensory neurons that enter a low level of the spinal cord are more medial within the spinal cord
Sensory neurons that enter at a higher level are more lateral

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46
Q

What sensory information does the Dorsal column tract supply?

A

Proprioception
Fine touch
Pressure

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47
Q

What sensory information does the Spinothalamic tract supply?

A

Lateral - pain and temperature

Anterior - crude touch and pressure

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48
Q

What sensory information does the Spinocerebellar tract supply?

A

Proprioception

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49
Q

What sensory information does the Spinorecticular tract supply?

A

Arousal

Emotional aspects of pain

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50
Q

What fibres are used in the Dorsal column tract?

A

A-beta

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51
Q

Describe the first order neuron in the Dorsal column tract

A

Located in dorsal root ganglion
A-Beta fibres enter spinal column and ascend uncrossed in dorsal columns
F.gracilis up to T6
F.cuneatus after T6

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52
Q

Describe the second order neuron in the Dorsal column tract

A

Located in n.gracilis and n.cuneatus in lower medulla

Decussation: cross midline at medulla and form medial lemniscus

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53
Q

Describe the third order neuron in the Dorsal column tract

A

Ventral posterolateral nucleus in thalamus

Projects to somatosensory cortex

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54
Q

Where is the final destination of the Dorsal column tract

A

Post central gyrus in parietal lobe

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55
Q

What fibres are used in the anterior spinothalamic tract?

A

A-beta/A-delta SA fibres

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56
Q

Describe the first order neuron in the anterior spinothalamic tract

A

Located in dorsal root ganglion

Fibres enter spinal cord and project to lamina I and II

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57
Q

Describe the second order neuron in the anterior spinothalamic tract

A

Neurons in dorsal horn generate bilateral output fibres

Decussation: ascend in anterolateral fasciculus to terminate in thalamus

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58
Q

Describe the third order neuron in the anterior spinothalamic tract

A

VPL nucleus in thalamus

Projects to somatosensory cortex

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59
Q

Where is the final destination in the anterior spinothalamic tract?

A

Postcentral gyrus in parietal lobe

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60
Q

What fibres are used in the lateral spinothalamic tract?

A

A-delta SA fibres

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61
Q

Describe the first order neuron in the lateral spinothalamic tract

A

Located in dorsal root ganglion

Fibres enter spinal column and project to lamina II

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62
Q

Describe the second order neuron in the lateral spinothalamic tract

A

Lamina I and V neurons collect edited signals from lamina II

Decussation: cross midline at spinal segment, ascends in anterolateral fasciculus to terminate in thalamus

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63
Q

Describe the third order neuron in the lateral spinothalamic tract

A

VPL nucleus in thalamus

Projects to somatosensory cortex

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64
Q

Where is the final destination in the lateral spinothalamic tract?

A

Postcentral gyrus in parietal lobe

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65
Q

Define Malinering

A

The conscious fabrication of symptoms to achieve some form of benefits such as attention, to be relieved of undesirable activities, to obtain prescription medication, or to qualify for disability compensation.

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66
Q

Define pain behaviours

A

Non-conscious modes of communicating pain and distress and unlike cases of symptom magnification and malingering are not produced intentionally.

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67
Q

Define catastrophising

A

Extremely negative thoughts about one’s plight, even with minor problems being interpreted as major catastrophes. Catastrophising and consequently adaptive coping strategies are important in determining one’s reaction to pain.

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68
Q

What are important psychological predictors of chronic back pain?

A

Greater catastrophising and feeling a lower sense of control are among the most important predictors of chronic back pain.

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69
Q

What are the different types of pain?

A

Acute nociceptive
Inflammatory
Neuropathic

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70
Q

What stimuli can produce acute nociceptive pain?

A

Thermal
Mechanical
Chemical

71
Q

What evokes acute nociceptive pain?

A

High-threshold stimulus-dependent pain

evoked in a graded response by appropriate high intensity (noxious stimuli)

72
Q

What evokes inflammatory pain?

A

Active inflammation

Evoked by low (innocuous) and noxious stimuli

73
Q

What causes neuropathic pain?

A

A lesion or disease of the somatosensory nervous system

Marked neuroimmune component

74
Q

What are the features of neuropathic pain?

A 
Maladaptive
Persistent
Hyperalgesia
Allodynia
Abnormal amplification
75
Q

What is hyperalgesia?

A

Enhanced pain evoked by a noxious thermal or mechanical stimulus

76
Q

What is allodynia?

A

pained evoked by a normally innocuous stimulus

77
Q

How is neuropathic pain described?

A

Spontaneous pain: often described as a burning tightness accompanied with paresthesias, tingling, shooting or stabbing pains

78
Q

What is neuropathic pain associated with?

A

Co-morbidities such as anxiety, depression and sleep-disturbance

79
Q

What are the different causes of neuropathic pain? (with examples)

A 
Trauma - nerve entrapment
Central - spinal injury
Neurotoxic - neuropathy
Infections - post-herpatic neuralgia
Metabolic - diabetic neuropathy
Idiopathic
80
Q

What is the mechanism of neuropathic pain?

A

Increased inflammatory cells and mediators in PNS and CNS
Altered nociceptor activity (receptor/ion channel expression)
Altered spinal processing: sensitisation, synaptic reorganisation
Altered central procession, descending inhibition

81
Q

What are the four stages of acute pain?

A

Transduction
Transmission
Perception
Modulation

82
Q

What happens during transduction in acute pain?

A

Injury results in the release of inflammatory mediators which bind to nociceptors converting thermal, mechanical or chemical insult into an electrical signa

83
Q

What happens during transmission in acute pain?

A

Travels up:
Spinothalamic tract
Spinoreticular tract
Spinomesencephalic tract

84
Q

What happens during perception in acute pain?

A

Nociceptive traffic is filtered through the individuals genetics, cognition, affect, environment and previous pain experiences

85
Q

What happens during modulation in acute pain?

A

Nociceptive traffic is modulated by excitatory and inhibitory effects on the somatosensory system

86
Q

What is the mechanism of modulation in acute pain?

A

Cortical/subcortical impulses
Impulses to the periaqueductal matter
Locus coeruleus (noradrenergic inhibitory system)
Raphé nucleus (serotonergic inhibitory system)
Inhibitory synapses in the dorsal horn
Ascending spinothalamic tract
Motor neuron reflex

87
Q

What is post-herpatic neuralgia?

A

The pain that persists after shingles has cleared

88
Q

What % of patients with PHN have mechanical allodynia?

A

> 75%

89
Q

What % of patients with PHN have thermal hyperalgesia?

A

40%

90
Q

What % of patients with PHN report pain improvement with pregabalin

A

35%

91
Q

What neurotransmitter is used for pain afferents?

A

Glutamate

92
Q

What does the release of glutamate evoke?

A

Fast synaptic potentials in dorsal horn neurons by activating the AMPA-type glutamate receptors

93
Q

What is substance P required for?

A

The mediation of synaptic transmission for moderate to intense pain

94
Q

Where is substance P stored?

A

Contained within storage granules in the axon terminals

95
Q

How is substance P released?

A

Can be released by high-frequency trains of action potentials in C fibres

96
Q

What is peripheral sensitisation?

A

A reduction in threshold and an increase in responsiveness of the peripheral ends of the nociceptor (high-threshold pain receptors) results from the interaction of nociceptors with the inflammatory chemicals at the site of tissue damage of inflammation

97
Q

What effect does peripheral sensitisation have?

A

Protect the injured area - a result of painful perceptions produced by ordinary stimuli close to the site of damage
Promote healing and guard against infection - such as increased blood flow and the migration of white blood cells to the site

98
Q

What is central sensitisation?

A

An increase in the excitability of neurons within the CNS, so that normal inputs begin to produce abnormal responses

99
Q

What are the products of tissue damage substances?

A

ATP
Bradykinin
Prostaglandins
Substance P

100
Q

How does ATP assist in tissue damage?

A

Directly depolarises nociceptors

101
Q

How does bradykinin assist in tissue damage?

A

Directly depolarises nociceptors Stimulates long-lasting intracellular changes that make heat-activated ion channels more sensitive

102
Q

How do prostaglandins assist in tissue damage?

A

Generated by enzymatic breakdown of the lipid membrane of cells
Do not elicit overt pain
Increase the sensitivity of nociceptors to other stimuli

103
Q

What does substance P release cause?

A

Vasodilation and release of histamine from mast cells

Sensitisation of other nociceptors around the site of injury

104
Q

What is primary hyperalgesia?

A

Increased sensitivity to pain within the area of damaged tissue

105
Q

What is secondary hyperalgesia?

A

Increased to pain in the tissues surrounding a damaged area

106
Q

What is the gate control theory?

A

That the spinal cord may either block pain signals or allow them to pass on to the brain
Pain signals are blocked when the gate is closed
Pain signals pass from the spinal cords to the brain when the gate is open
According to the gate control theory, we can be distracted from the pain by the release of endorphins (neurotransmitters)

107
Q

How can the pain gate be closed?

A

A-beta fibre activation

108
Q

What can be done to activate A-beta fibres to close the pain gate?

A

Massage
Acupuncture
TENS

109
Q

What is cocodamol?

A

An opioid analgesic derived from morphine but less potent, less sedative and less toxic

110
Q

Why is cocodamol less likely to cause dependence?

A

Causes little to no euphoria

111
Q

What is the main side effect of cocodamol?

A

Constipation

112
Q

What is the MOA for cocodamol?

A

Selective agonist for mu opioid receptor

113
Q

What is the primary action of NSAIDs?

A

Inhibition of arachidonic acid oxidation by COX enzymes

This inhibits production of prostaglandins and thromboxanes

114
Q

What is COX-2 inhibition linked to?

A

Anti-inflammatory and analgesic actions

115
Q

What is COX-1 inhibition linked to?

A

The unwanted side effects, particularly those linking to GI tract

116
Q

What are the 3 main therapeutic effects of NSAIDs?

A

Anti-inflam
Analgesic
Antipyretic (lower temp)

117
Q

How do NSAIDs cause an anti inflammatory response?

A

Occurs as a result of decrease in prostaglandin E2 and prostacyclin
Reduces vasodilation and oedema
Accumulation of inflammatory cells is not reduced

118
Q

How do NSAIDs cause an analgesic response?

A

§ Decrease in the production of prostaglandins that sensitise nociceptors (ORL1) to inflammatory mediators such as bradykinin
NSAIDS are effective in all conditions that are associated with increased local prostaglandin synthesis

119
Q

How do NSAIDs cause an antipyretic response?

A

IL-1 releases prostaglandins in the CNS, where they elevate the hypothalamic set point for temperature control causing fever
NSAIDs prevent this

120
Q

What are the side effects of NSAIDs?

A

GI disturbance
Rash
Prolonged bleeding due to decreased thromboxanes
Increased likelihood of thrombotic events (i.e. MI) by inhibiting PG12 synthesis
Bronchospasm
Liver disorders

121
Q

What is Ibuprofen?

A

NSAID
weakly Cox-1 selective
Shortlived antiplatelet activity

122
Q

What is Paracetamol?

A

Selective weak COX-2 inhibitor

No GI side effects

123
Q

What are some examples of TCAs?

A

Imipramine, desipramine, amitriptyline, nortriptyline, clomipramine

124
Q

What can TCAs be used to treat?

A

Depression in big doses

Neuropathic pain in small

125
Q

How do TCAs treat depression?

A

Inhibit noradrenaline and 5-HT reuptake but have much less effect on dopamine reuptake
Improvement of emotional symptoms reflects an enhancement of 5-HT mediated transmission

126
Q

How do TCAs treat Neuropathic pain?

A

Inhibit noradrenaline and 5-HT reuptake but have much less effect on dopamine reuptake
Improvement of biological symptoms results from the facilitation of noradrenergic transmission

127
Q

What is the MOA of TCAs?

A

Block the reuptake of amines by nerve terminals by competition for the binding site of the amine transporter

128
Q

What are the side effects of TCAs?

A 
Antimuscarinic
Sedation
Confusion
Motor incoordination
Dry mouth
Postural hypotension
Increased risk of sudden cardiac death
129
Q

What is gabapentin used to treat?

A

Anticonvulsant drug used to treat neuropathic pain including peripheral neuropathy

130
Q

What is the MOA of gabapentin?

A

Interacts with cortical neurons at auxiliary subunits of voltage-sensitive calcium channels
It increases the synpatic concentration of GABA, enhances GABA responses at non-synaptic sites in neuronal tissues and reduces the release of mono-amine neurotransmitters (catecholamines)

131
Q

What are the side effects of gabapentin?

A

GI disturbance
Dizzy
Drowsy

132
Q

How do opioids relieve pain?

A

Raising pain mechanisms

Change in pain perception

133
Q

How do opioids change pain perception?

A

Patients still experience pain consciously but do not attach negative emotional reactions to it.
This effect is mediated primarily via the limbic system which has the highest concentration of opioid receptors in the brain.

134
Q

What in the brain has the highest concentration of opioid receptors?

A

Limbic system

135
Q

Name endogenous opioids (produced in body)

A

Beta-endorphin
Enkephalin
Dynorphin

136
Q

What are natural opioids?

A

Alkaloids derived from the opium poppy, also referred to as opiates
i.e. morphine and codeine

137
Q

Name semi-synthetic opioids

A

Diamorphine (heroin)

Buprenorphine

138
Q

Name synthetic opioids

A

Methadone

Fentanyl

139
Q

What is an opioid receptor?

A

a group of G-protein coupled receptors with opioids as ligands

140
Q

What does binding of an opioid receptor agonist cause?

A

Reduction of synaptic transmission
Closes presynaptic Ca2+ channels - hyperpolarises - reduced acetylcholine, noradrenaline, serotonin, glutamate, nitric oxide, and substance P released
Opens postsynaptic K+ channels - hyperpolarises

141
Q

What are the 3 types of opioid receptor?

A

Mu
Delta
Kappa

142
Q

What are Mu receptors responsible for?

A

Responsible for most of the analgesic effects of opioids and have some major unwanted effects
Located in the brain, spinal cord, Peripheral sensory neurons and intestinal tract
Strong analgesia

143
Q

What does activation of Mu receptor 1 cause?

A

μ1 - analgesia, physical dependence
Chronic use of opioids produce tolerance
Negative physical withdrawal symptoms result from abrupt discontinuation or reduction

144
Q

What does activation of Mu receptor 2 cause?

A

Respiratory depression, miosis, euphoria, reduced GI mobility, physical dependence

145
Q

What does activation of Mu receptor 3 cause?

A

Vasodilation

146
Q

What are delta receptors responsible for?

A

Result in analgesia
proconvulsant
Located in brain and peripheral sensory neurons

147
Q

What does activation of delta receptors 1+2 cause?

A

Analgesia, respiratory depression, tolerance, strong addictive potential

148
Q

Where are kappa receptors?

A

Located at the spinal cord, brain and peripheral sensory neurons

149
Q

What does activation of kappa receptors 1,2+3 cause?

A

Analgesia, sedation, dysphoria and constipations

Do not contribute to dependence

150
Q

What is Naloxone?

A

Opioid receptor antagonist

rapid onset, short duration (1–2 hours) → preferred for treatment of acute opioid intoxication

151
Q

What is Naltrexone?

A 
Opioid receptor antagonist
long duration (24–48 hours) → used for withdrawal treatment after acute detoxification
152
Q

What are the clinical features of opioid intoxication?

A 
Altered mental state - can range from euphoria to apathy, impaired consciousness or seemingly normal mental state
Bilateral miosis
Respiratory depression 
Haemorrhagic lung oedema
Seizures
Decreased bowel sounds
Decreased heart rate, blood pressure
Hypothermia
Rhabdomyolysis - breakdown of skeletal muscle tissue
153
Q

What is the acute management of opioid intoxication?

A

Airway management
IV naloxone
Neutralisation of opioid effects
Restoration of ventilation
Slow administration to prevent acute withdrawal
Management of complications such as seizures

154
Q

What are the clinical features of opioid withdrawal?

A

Flu-like symptoms: rhinorrhoea, chills, piloerection, myalgia, arthralgia, leg cramps
Gastrointestinal complaints: nausea, vomiting, abdominal pain, diarrhoea, hyperactive bowel sounds
Features of sympathetic hyperactivity: mydriasis, tachycardia, hypertension, hyperreflexia
Features of CNS stimulation: insomnia, yawning, irritability, anxiety, agitation, aggression

155
Q

What is the treatment for opioid withdrawal?

A

Buprenorphine/naloxone is taken sublingually
Buprenorphine has a mild opioid effect after sublingual administration, while naloxone is hardly absorbed.
Naloxone prevents drug abuse by antagonizing the effects of buprenorphine if it is injected intravenously to achieve a stronger effect.

156
Q

What is the cost of class A drug use in the UK?

A

£15.5 billion

157
Q

How many hospital admission with primary diagnosis of a drug-related mental health problem?

A

6640

158
Q

How many hospital admission with primary diagnosis of poisoning by drugs?

A

12586

159
Q

How many deaths due to class A overdose in one year?

A

1784

160
Q

Define drug abuse

A

substance used in a manner that does not conform to social norms. Can abuse drugs without being dependent or addicted

161
Q

Define drug dependence

A

Physical - individual depends on drug for normal physiological functioning. Abstinence produces physical withdrawal reactions
Psychological - acquiring and using drug are strong motivators of behaviour. Compulsive use.

162
Q

Where are the sites of rewarding brain stimulation?

A 
Dorsal pons
Septal area
Lateral hypothalamus
Medial forebrain bundle
Ventral tegmental area
163
Q

What do all drugs of abuse do?

A

Increase dopamine levels in nucleus accumbens

164
Q

What is the management of opiate detoxification?

A

Detoxification
Reverse neuroadaptation from chronic use
Promote long term changes leading to lifestyle changes
Relapse prevention
Agonist maintenance (methadone)
Partial agonist maintenance (buprenorphine)
Antagonist maintenance (naltrexone)
Lifestyle and behaviour change

165
Q

What does water and lipids show as on T1 MRI?

A

Water appears dark, fatty tissues appear bright
CSF appears dark
Grey matter is grey (higher water content)
White matter is white (higher lipid content)

166
Q

What does water and lipids show as on T2 MRI?

A

Water appears bright and lipids appear dark

167
Q

What is an issue with T2 MRI when scanning the brain?

A

Bright CSF can obscure pathology located in the parenchyma adjacent to ventricles or pia

168
Q

Describe the somatic motor pathway

A

Upper motor neuron arises in primary motor cortex
Decussates in brainstem/spinal cord
Lower motor neuron arises in spinal cord
axon projects to skeletal muscle

169
Q

What are the 3 subnuclei of the trigeminal sensory nucleus?

A

Chief - touch and pressure
Spinal - pain and temperature
Mesencephalic - proprioception

170
Q

What CN is innervated contralaterally?

A

CN XII

Hypoglossal

171
Q

What is an agonist?

A

Substance which stimulate the receptors and mimic the natural ligand

172
Q

What is an antagonist?

A

Substance which block the receptors and stop the effect of the natural ligand

173
Q

What is an ionotropic receptor?

A

Part of a ligand-gated ion channel protein and activation results in ion conduction changes
Opening by transmitter to allow Na+ (excitatory) or K+/Cl- (inhibitory) in
Involved in fast transmission

174
Q

What is a metabotropic receptor?

A

Coupled to effector mechanism via G-proteins

agonist molecule combines with receptor and causes activation of membrane-associated proteins

Years 1+2 (21 decks)

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