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JP lectures Flashcards

1
Q

What do dendrites do?

A

Receive info and convey signals to soma (increases cell surface area)

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2
Q

Which part is the metabolic part of a neuron?

A

Soma (perikaryon)

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3
Q

Where is the site of initiation of the AP?

A

Axon hillock & initial segment

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4
Q

How do glia cells affect APs?

A

Insulate axons to allow signals to travel further

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5
Q

What is saltatory conduction?

A

When AP ‘jumps’ from oneNode of Ranvier to the next

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6
Q

What is the most frequent excitatory transmitter in the CNS?

A

Glutamate

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7
Q

What are the 2 most frequent inhibitory transmitters in the CNS?

A

GABA & glycine

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8
Q

What are glutamate, GABA and glycine made of?

A

Amino acids

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9
Q

Opening of what channels allows receptor activation?

A

Voltage-activated Ca channels

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10
Q

Which 2 ions are responsible for excitatory depolarisation & flow inward?

A

Na & Ca

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11
Q

Which 2 ions ae responsible forinhibitory hyperpolarisation?

A

K & Cl

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12
Q

How do local anaesthetics work?

A

Na antagonist - stop N flow leading to inhibition

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13
Q

How do benzodiazepines work?

A

modulate GABA receptor so enhance Cl entry and enhance inhibitioninthepresence ofGABA

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14
Q

What does glutamate do?

A

Acts on ionotropic receptors to allow Na & Ca in and K out of cell = EPSP, depolarisationandexcitation

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15
Q

What does GABA do?

A

Acts on ionotropic receptors to allow Cl into the cell leading to inhibition

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16
Q

What senses does the somatosensory system mediate?

A

All sensations that are not the special senses

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17
Q

What is the receptive field of an afferent neurone?

A

Theregion that when stimulatedcauses aresponsein that neurone

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18
Q

What do pacinian corpuscles sense?

A

Vibration

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19
Q

How many sets of spinal nerves are there?

A

31

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20
Q

Which roots areresponsible for sensory function?

A

Dorsalroots

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21
Q

Which roots are responsible for motorf unction?

A

Ventral roots

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22
Q

What is grey matter?

A

Cell bodies andsensry afferent terminals

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23
Q

In which pathway do all fibres decussate together?

A

DCML pathway

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24
Q

Where i the first synapse in the DCML pathway?

A

The brain stem

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25
Q

Where do fibres decussate in DCMLpathway?

A

All decussate together at the level of the brain stem

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26
Q

if the DCML was severed will the effects be on the same side or opposite?

A

Same side

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27
Q

How does the primary afferent travel to the brain stem in the DCML pathway?

A

Via gracile & cuneate tracts

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28
Q

What is stereogenesis?

A

The ability to recognise and object by feeling it

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29
Q

Where do neurones synapse in the A

STT?

A

shortlyafter enteringspinalcord

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30
Q

Where do sensory fibres cross over in the STT?

A

All along the length of the spinal cord

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31
Q

If the STT is severed will sensation be lost on the same or opposite side?

A

Opposite side

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32
Q

How does general somatic info from the anterior head reach the brain?

A

Via trigeminal system

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33
Q

What are the 3 divisions of the trigeminal nerve?

A

V1 = ophthalmic
V2 = maxillary
V3 =mandibular

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34
Q

Where are the soma of sensory neurones of the face located?

A

Trigeminalsensory ganglion

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35
Q

Where does sensory input to T6 and above travel?

A

In the cuneate tract

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36
Q

Where does sensory info from below T6 travel?

A

In the gracile tract

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37
Q

Where is the somatosensory cortex located?

A

Post central gyrus of the parietal corte

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38
Q

What is the posterior parietal cortex responsible for?

A

Deciphering the deeper meaning of info in somatosensory cortex

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39
Q

What is the relationship between UMNs & LMNs?

A

UMNs supply input to LMNs to modulate their activity

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40
Q

What to LMNs recieve input from?

A

UMNs, proprioceptors & interneurons

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41
Q

Where are UMNs found?

A

The brain

42
Q

How do axons of LMNs exit the spinal cord?

A

In the ventral roots or via cranial nerves

43
Q

Which ype of skeletal muscle fibre has the largest a-MN?

A

Slow-oxidative (Type I) fibres

44
Q

Why are Type-1 skeletal muscle fires red?

A

High myoglobin content

45
Q

What is the myotatic reflex?

A

When skeletalmuscle ispulled itpullsback

46
Q

What spinal levels are assessed by the knee jerk reflex?

A

L3-L4

47
Q

What spinal level is assessed by the triceps reflex?

A

C7

48
Q

Which spinal levels are assessed by the biceps reflex?

A

C5-C6

49
Q

Which spinal levels are assessed by the supinator reflex?

A

C5-C6

50
Q

Which spinal level is assessed by the gastrocenemius (ankle) reflex?

A

S1

51
Q

Where are y-MN cell bodies located?

A

Ventral horn of the spinal cord

52
Q

Where are golgi tendonorganslocated?

A

thejunctionofmuscleandtendon

53
Q

What is thepurposeofgolgitendonorgans?

A

Protect muscle from overload

Regulate muscle tension to optimal range

54
Q

Where do descending spinal tracts originate?

A

Cerebral cortex & brain stem

55
Q

Which pathways are under control from the cerebral cortex?

A

Lateral pathways

56
Q

Which pathways are under control from the brainstem?

A

Ventromedialpathways

57
Q

What is the major lateral pathway?

A

Corticospinal (pyramidal) tract

58
Q

which hemisphere controls RIGHTmusculature?

A

LEFT hemisphere

59
Q

Where do most fibres in the corticospinal tract decussate?

A

The pyramidal decussation at the base of the medulla

60
Q

What des the rubrospinal tract control?

A

Limb flexor muscles

61
Q

How could lesions of the lateralcolumnspresent?

A

Loss of ‘fractionated’ movements
Slowing and impairmentofaccuracy of voluntary movements
Little effect on normal posture

62
Q

What is the function of the vestibulospinal tract?

A

Helps to hold upright and balanced posture by facilitating extensor MNs of anti-gravity muscles

63
Q

Where do cell bodies from the tectospinal tract reside?

A

Superior colliculus

64
Q

What muscles does the tectospinal tract influence?

A

Muscles of the neck, upper trunk and shoulders

65
Q

Which is more medial the medullary or pontine reticulospinal tract?

A

Pontine

66
Q

Where do both reticulospinal tracts arise from?

A

Reticular formation (mesh of neurones located along the length and core of the brainstem)

67
Q

Which reticulospinal tract descends bilaterally?

A

Medullary

68
Q

What is the function of the pontine reticulospinal tract?

A

Helps to maintain standing posture by facilitating contraction of the extensors of the lower limbs

69
Q

What is the function of the medullary reticulospinal tract?

A

Releases antigravity muscles from reflex control

70
Q

Where are cell bodies of nociceptors located?

A

Dorsal root ganglia

71
Q

What is the character of visceral pain?

A

Poorly localised, dull, aching, throbbing

72
Q

Why do patient get referred pain?

A

A some visceral & skin afferents converge on the same spinothalamic neurones

73
Q

What is viscerosomatic pain?

A

When inflammatory exudate from a diseased organ contacts a somatic structure

74
Q

Which of the nociceptive tracts is fast & which is slow?

A

STT = fast SRT = slow

75
Q

How do STT & SRT differ?

A 
STT = fast = warns exact location andseverity of pain 
SRT = slow = registers the emotional/motivationalcomponent ofpain
76
Q

What are the 3 mechanisms of actions of analgesic drugs?

A 
Direct presynaptic inhibitions (stop Ca influx) 
Direct postsynaptic inhibition (reduce excitability by opening K channels)
Indirect inhibition (activate inhibitory interneurones)
77
Q

How do opiods work?

A

Couple to GPCOR to inhibit presynaptically by opening Ca chnnels and upress excitation postsynaptically by opening K channels

78
Q

What are the 3 types of opioid receptor?

A

u
delta
Kappa

79
Q

Which opioid receptor is responsible ofrmost of the analgesic actionsofopioids?

A

u receptor

80
Q

What are the adverse effects of activating the u opioid receptr?

A 
Respiratory depression
Cnstiation
Euphoria
Sedation
Dependence
81
Q

What is the adverse effect of delta opioid receptors?

A

Proconvulsant

82
Q

What is the difference between morphine & diamorphine?

A

Diamorphine ismore lipophillic

83
Q

Which opioidagonist is given IV to provide analgesia in maintenance anaesthesia?

A

Fentanyl

84
Q

Which opioid agonist is used in acute pain,particularly labour?

A

Pethidine

85
Q

What should pethidine not beused in conjunction with? Why?

A

MAO inhibitors (excitement, convulsions, hyperthermia)

86
Q

In which patients should tramadol be avoided?

A

Epilepsy

87
Q

What is naloxone?

A

Competitive agonist of u -receptors used to reverse opioid toxicity

88
Q

Which should care be taken when prescribing naloxone?

A

SHort half-life (opioids may have longer duration)

89
Q

Why is naltrexone better than naloxone?

A

Much longer half-life

90
Q

What should be given to a newborn displaying opioid toxicity as a result of pethidine given to the mother during labour?

A

Naloxone

91
Q

How does paracetamol have analgesic effects?

A

Due toit’smetabolites

92
Q

What is a adverse effect of selective COX-2 inhibitors?

A

They are prothrombotic

93
Q

What damage can be caused by long term NSAID use

A

GI damage

94
Q

Examples of drugs usedforneuropathicpain

A

Gabapentin
Pregabalin
Amitriptlline
Carbamazepine

95
Q

How do gabapentin & pregabalin work?

A

Reduce surface area of a subunit of some voltage-gated Ca channels which are unregulated in damaged sensory neurones causing a decrease in neurotransmitters

96
Q

What can gabapentin be used as prophylaxis for?

A

Migraines

97
Q

What condition is pregabalin particularly useful in.

A

Painful diabetic neuropathy

98
Q

How do amitriptyllinr ,nortryptilline & desipramine work?

A

Act centrally decreasing the reuptake ofnoradrenaline

99
Q

How does carbamazepine work?

A

Blocks subtypes of voltage-activated Na channel that are unregulated in damaged nerve cells

100
Q

What is carbamazepine first line in?

A

To control pain intensity & frequency of attacks in trigeminal neuralgia

AY Neurology (12 decks)

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