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NLM2 > Physiology > Flashcards

Physiology Flashcards

1
Q

What is neuropathic pain?

A

Nerve damage causing pain

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2
Q

What is spontaneous pain?

A

Pain in the absence of a stimulus

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3
Q

Two Major types of pain fibres and their properties?

A

A fibres - Fast, myelinated

C Fibres - Slow unmyelinated

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4
Q

What type of pain are C fibres involved in transmitting?

A

Aching, burning pain

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5
Q

What type of pain are A fibres involved in transmitting? the four types of fibre?

A

A alpha fibres - muscle pain
A beta fibres - mechanical
A gamma fibres - muscle and pressure
A delta - sharp pain

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6
Q

What do substance P and CGRP do at peripheral synapses?

A

Lead to flare and oedema

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7
Q

The two types of ascending pathways that transmit pain in the peripheries, their properties?

A

Spinothalamic (neospinothalamic)

  • Direct
  • immediate, exact location

Spinoreticulothalamic (Paleospinothalamic)

  • Indirect
  • Involve limbic structures (amygdala included)
  • Emotional and visceral pain
  • descending suppression of pain
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8
Q

What fibres are involved in descending suppression of pain? What do they release?

A

C Fibres release glutamate and substance P

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9
Q

How do glial cells respond to painful stimuli?

What can this lead to?

A

They release mediators to sensitise the post-synaptic receptor e.g.

IL 1 and 2
TNF
NO
Prostaglandins
Glutamate
ATP

This can lead to central sensitisation

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10
Q

Two types of sensitisation?

A

Central

Peripheral

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11
Q

What mostly leads to central sensitisation?

A

Repetitive input

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12
Q

What does repetitive input produce?

A

Wind-up

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13
Q

What is wind up?

A

Increased electrical activity that results in increased excitability of second order neurones in the spinal cord

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14
Q

What two things can central sensitisation cause?

Define them

A

Allodynia - Pain from a stimulus that is not usually painful

Hyperalgesia - increased sensitivity to painful stimuli

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15
Q

What are the three main mechanisms of central sensitisation?

A

Increase of membrane excitability

Synaptic facilitation

Disinhibition (less inhibitory neurotransmitters)

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16
Q

Where does central modulation occur?

A

The dorsal horn

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17
Q

One main example of how central modulation works?

A

The gate theory

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18
Q

What is the gate theory?

A

the theory that descending pathways inhibit pain fibres

A beta fibres inhibit pain fibres in the dorsal horn

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19
Q

Two main types of synapses in the CNS?

A

Electrical and chemical

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20
Q

What type of synapses are gap junctions?

A

Electrical

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21
Q

What type of synapses involve the SNARE complex?

A

Chemical

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22
Q

What is the SNARE complex?

A

A complex in the pre-synaptic cell that changes in the presence of high intracellular calcium.

In the presence of high calcium the SNARE complex allows a pore to be formed between the vesicles and the cell membrane which allows neurotransmittors to be released.

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23
Q

Three types of chemical synapse?

A

Axo-dendritic

Axo-somatic

Axo-axonic

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24
Q

What is the one type of chemical synapse that is excitatory as well as inhibitory, also the most common by far?

A

Axo-dendritic

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25
Q

What is the speed of ionotropic receptors compared to metabotropic receptors?

A

Ionotropic - Fast

Metabotropic - Slow

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26
Q

Two main ways neuronal transmission is modulated?

A

G-protein coupled receptors (through second messengers)

Co-transmitters - excitatory and inhibitory (neuropeptides)

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27
Q

How do neuropeptides (co-transmitters) modulate neuronal activity?

A

Through their action on G-protein coupled receptors

They are only released in high Ca concentration

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28
Q

An example of a neuropeptide involved in pain? what does it do?

A

Substance P, increases pain transmission

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29
Q

What does enkephalin do?

A

Reduces pain through reduction of substance P and Glutamate

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30
Q

As each synapse releases on average 1 vesicle each (there are 10,000+) What are the two types of synaptic integration (summation)?

A

Temporal - summation at the same synapse

Spatial - from several different synapses

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31
Q

What is the loss of both temporal fields of the eye called?

A

Bitemporal hemianopsia

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32
Q

What area is damaged to cause bitemporal hemianopsia, example of what can cause this damage?

A

Optic chiasm

Pituitary tumour

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33
Q

Where would damage have occured to cause loss of vision in one eye? examples?

A

optic nerve

MS
Glioma
Head trauma

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34
Q

What artery would be damage to give one eye full vision loss

A

Anterior cerebral artery

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35
Q

Haemorrhage of what artery would cause bitemporal hemianopsia?

A

Anterior cerebral artery (anterior communicating artery)

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36
Q

What would loss of vision to the left temporal visual field and the right nasal field be called?

A

Left homonymous hemianopsia

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37
Q

Where would damage have occurred to cause left homonymous hemianopsia? Causes?

A

Optic tract (right side) OR optic radiations

Tumour

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38
Q

What artery would be damaged to cause left homonymous hemianopsia?

A

Posterior Cerebral Artery

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39
Q

What is left superior quadrantopsia? Causes?

A

Both superior left quadrants damaged

Temporal lobe tumour

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40
Q

Where is damaged to cause left superior quadrantopsia?

A

Meyers loop (the lower radiations)

41
Q

What artery would be damaged to cause left superior quadrantopsia?

A

PCA

42
Q

What are the two pathways from V1 (primary visual area)?

What do they do?

A

The dorsal (parietal pathway) = movement

The ventral (temporal pathway) = colour and form

43
Q

4 main conditions that give rise to acute neuro-dengeneration?

A

Traumatic brain injury

Stroke

TIA

Intracranial haemorrhage

44
Q

Two types of stroke, which is more common?

A

Ischaemic (85%)

Haemorrhagic

45
Q

Causes of an ischaemic stroke?

A

Occlusion e.g. atherosclerotic arteries

Emboli

46
Q

Three main molecular mechanisms that lead to ischaemic neuro-degeneration?

A

Increased [Ca2+]

Increased Glutamate

Increased free radical levels

47
Q

What’s ischaemic depolarisation?

A

Large amounts of ATP are usually required to maintain resting potential (Na+/K+ pump)

In ischaemia there is no available ATP and depolarisation followed by normalisation of that resting potential occurs

48
Q

What free radicals are produced in ischaemic neuro-degeneration and where?

A

Superoxide formed in mitochondria (O2-)

NO formed from arginine

Bind together to form ONOO-

49
Q

How does raised calcium cause cell death in acute neuro-degeration?

A

Increased Free radical production

Oedema

activates proteases

50
Q

Two classified areas of the affected cerebrum in stroke?

A

The necrotic core

The penumbra

51
Q

Two types of cell death in the ischaemic penumbra?

A

Necrotic

Apoptotic

52
Q

Treatment for AF?

A

Warfarin

53
Q

Main types of stroke syndromes?

A

TACS - total anterior circulation syndrome

PACS - partial anterior circulation syndrome

Posterior circulation syndrome (basilar/vertebral/posterior cerebral)

Lacunar anterior circulation syndrome

54
Q

Two main arteries supplying the basal ganglia?

A

Recurrent medial striate artery

Anterior choroidal artery

55
Q

What’s a watershed infarct?

A

Infarct in the periphery of two arterial territories

56
Q

Types of haemorrhagic strokes?

A

Supratentorial

Cerebellar

Pontine

Subarachnoid haemorrhage

57
Q

Main symptom that distinguishes a haemorrhage from a stroke?

A

Sudden onset severe headache, followed by neurological signs

58
Q

Symptoms of total anterior circulation syndrome?

A

deterioration of conscious level

Contralateral homonymous hemiplegia

Contralateral hemisensory deficits

59
Q

Symptoms of partial anterior circulation syndrome, of the anterior cerebral artery?

A

Contralateral hemiparesis (leg more)

Mild/non existent sensory deficit

Apathy/disinhibition

60
Q

Symptoms of partial anterior circulation syndrome, of the middle cerebral artery?

A

Contralateral hemiplegia (arm more)

sensory deficit

hemianopia

aphasia/neglect

61
Q

Symptoms of posterior circulation syndrome, of the posterior cerebral artery?

A

Hemianopia

amnesia

occulomotor/language disturbances

62
Q

Symptoms of posterior circulation syndrome, of the vertebral artery?

A

(only supplies the posterior inferior cerebellar artery)

Laterally medullary syndrome

  • ipsilateral limb ataxia
  • ipsilateral horners
  • contralateral sensory loss to limbs
63
Q

Two types of basilar artery syndromes?

A

Complete basilar artery syndrome? (most of pons and medulla);

  • Impairment of conscious level
  • bilateral motor + sensory dysfunction
  • cranial nerve signs

‘Top of the basilar’ syndrome (midbrain/thalamic/temporal/occipital):

  • hemianopia/cortical blindness
  • amnesia
  • vertical gaze palsies
64
Q

One perhaps promising stroke treatment?

A

IL-1 receptor antagonists

65
Q

main functions of complement?

A

Lysis

Opsonization

66
Q

What’s the choroid plexus?

A

Barrier between blood and CSF

Secretes CSF

67
Q

Two categories of descending motor pathways?

A

Lateral

ventromedial

68
Q

Two tracts in the lateral descending motor pathways?

A

Rubrospinal

Corticospinal

69
Q

Where do fibres from the corticospinal tract arise?

A

The Primary motor cortex

The association motor cortex

Somatosensory areas

70
Q

lesions to both lateral tracts often cause what?

What does it not cause a deficit in?

A

Loss of fine motor control

slower and less accurate movement

Can still stand upright however

71
Q

A lesion to only the corticospinal tract cause what?

A

Intially the same deficits as a lesion to both of the tract in the lateral pathway

However the rubrospinal tract has plascticity and will take over some of the corticospinal tracts roles, apart from fine motor control.

72
Q

What are the 3 ventromedial pathways?

A

Vestibulospinal tract

Tectospinal tract

Reticulospinal tract

73
Q

What is the flexion crossed extension reflex?

A

When a cutaneous afferent causes contraction of a flexor and relaxation of an extensor, in reaction to noiceceptive input.

74
Q

What are central pattern generators?

Examples?

A

Circuits that are hardwired into the CNS that do not need to be learned.

Key components of locomotion

respiration

mastication

Swallowing

75
Q

Stages of the motor loop, involved in generating a voluntary muscle movement in the brain?

A

Feeds in from sensory cortex and prefrontal cortex will then relay to the VLN (through pons/cerebellum and basal ganglia) which will relay back to the Primary motor cortex, programme is stored in association motor cortex, which will fire if the depolarisation is above threshold

76
Q

Three areas of the cerebellum, their roles?

A

Spinocerebellum - muscle tone/coordination

Cerebrocerebellum - planning, storing of procedural memory

Vestibulocerebellum - balance, eye movement coordination

77
Q

What is the cerebellar motor loop?

A

When the cerebellum projects directly to the VLN, allowing direct movement

78
Q

3 different structures of synapses?

A

One to one

Many to one

One to many

79
Q

Mechanisms of plasticity in the CNS?

A

Presynaptic: increase or decrease transmitter release

Postsynaptic: increase or decrease in signal transduction

Recruiting silent synapses

80
Q

In simple animals how does habituation and sensitisation occur?

A

Both caused by the response of the post-synaptic cell

Habituation is caused by the desensitisation of the Voltage Dependent Calcium Channel (VDCC)

Sensitisation is caused by increased calcium influx

81
Q

In mammals what is long term potentiation? How does it occur?

A

Synapses that fire more (higher frequency) will be strengthened

Mostly through activated NMDA receptors that activate CAM kinase, which do several things to strengthen a synapse:

Phosphorylate AMPA receptors
Recruit more AMPA receptors
Cause increased neurotransmitter release

82
Q

In mammals what is long term depression? How does it occur?

A

Synapses with low frequency signals will weaken

Pre-synaptically: Decreased glutamate release due to decreased VDCC

Post-synaptically: Dephosphorylation of AMPA receptors

83
Q

How do dendritic cells present viral peptides to T-lymphocytes if they are not infected?

A

Can activate MHC class I to present a viral peptide

84
Q

How do T-cells return to the place that the APC cell was activated?

A

Through up-regulation of specific adhesion molecules

85
Q

Difference in Th1 and Th2 cells?

A

Both will stimulate the production of B-cells

Th1 is mostly involved in fighting parasites (eosinophils/basophils)

Th2 cells are mostly involved in fighting bacteria/viruses (macrophages)

86
Q

What do Tc cells use to perforate cells, two types?

A

Use cytotoxic proteins:

  • Perforin
  • Granzymes (A and B)
87
Q

How do perforin and granzymes interact to produce cell death?

A

Perforin makes pores in the cell surface membrane and granzymes will activate apoptosis in the cell, moving through pores made by perforin.

88
Q

What’s myelitis?

A

Infection of the spinal cord

89
Q

The ability to recover from a spinal cord injury is determined by what factors?

A

Age

Characteristics of the lesion

Effect of experience

Training

90
Q

Two categories of brain tumours? examples?

A

Intrinsic: glioma

Extrinsic: meningioma

91
Q

Four types of haematoma?

A

Extra-dural

Acute sub-dural

Intracerebral

Intraventricular

92
Q

Two different appearances of a scan of a subdural and an extradural haematoma?

A

Acute subdural - crescent (long and thing)

Extra dural - fatter look like a lemon

93
Q

Four types of brain herniation?

A

Subfalcine

Tentorial (uncal)

Tentorial (central)

Tonsilar

94
Q

What pathway promotes sleep?

A

VLPO (GABA) pathway

95
Q

What neurotransmitters promote wakefulness?

A

NA, Histamine, Dopamine, Ach, glutamate

96
Q

Hypnotic medications?

A

Benzodiazepines

Melatonin receptor agonists

Histamine receptor antagonists

Antidepressants

97
Q

Stages of swallowing?

A

Buccal - voluntary

Pharyngeal

Eosophageal

98
Q

What is degulation?

A

Swallowing

NLM2 (14 decks)

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