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Medicine Year 2 > Scenario 25 > Flashcards

Scenario 25 Flashcards

1
Q

What is the incidence of stroke?

A

114/100,000 75% over 65

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2
Q

What is the mortality of stroke?

A

64,000 deaths per year 12% of deaths

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3
Q

What are the vascular risk factors for stroke?

A

High BP, Diabetes, Smoking, high cholesterol

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4
Q

What is left hemiplegia?

A

Arm in flexion, leg in extension

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5
Q

What should you do if suspected stroke?

A

CT to see if caused by a clot and can use thrombolytics in under 3 hours

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6
Q

How much of the cardiac output does the brain receive?

A

17%

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7
Q

What are the 2 main arterial routes to the brain?

A

ICA (carotid canal into middle cranial fossa adj to optic chasm) and Vertebral arteries (foramen transversaria entering via formamen magnum passing through cavernous sinus)

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8
Q

What does the ICA give rise to?

A

Anterior and middle cerebral arteries and opthalmic artery

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9
Q

What does the Anterior cerebral artery supply

A

Medial and superior aspects of the parietal and frontal lobes

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10
Q

What does occlusion of the ACA cause?

A

Paralysis and sensory defecits to contralateral leg and perineum, mental confusion and sometimes contralateral fact, tongue and upper limb due to IC

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11
Q

What does the MCA supply?

A

Lateral cerebral cortes, anterior temporal lobes and insular cortices

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12
Q

What does occlusion of MCA cause?

A

(most common) paralysis of contalateral face and arm and sensory loss, hemianopia of contralateral visual fields
Damage to dominant hemisphere results in aphasia (Broca/ Wernickes) and non-dominant results in contralateral neglect syndrome

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13
Q

Where does the posterior cerebral artery arise?

A

Intersection of post communicating and basilar

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14
Q

Where does the PCA supply?

A

Posterior aspect of the brain (occipital lobe) and part of temporal lobe

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15
Q

What does PCA occlusion cause?

A

Blindness in contralateral visual field, hippocampal memory may be affected but usually temp

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16
Q

What does the vertebrobasiliar system supply?

A

Brainstep, cerebellum and posterior aspect of cerebral hemispheres

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17
Q

What is the basilar artery formed from?

A

Union of the two vertebral arteries

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18
Q

What does the basilar artery give rise to?

A

Splits into posterior cerebral arteries before this giving rise to superior cerebellar arteries, before this several small pontine arteries and before this the anterior inferior cerebellar arteries

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19
Q

What do the vertebral arteries give rise to?

A

Posterior inferior cerebellar arteries, anterior and posterior spinal arteries

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20
Q

Where do the 2 systems anastamose?

A

Circle of Willis

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21
Q

What are the advantages of anastamoses?

A

Provide an alternative route if normal one is occluded

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22
Q

What are the disadvantages of anastamoses?

A

Can cause aneurysms which can leak or explode causing a sub arachnoid haemmorhage

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23
Q

What does occlusion of vertebral or basilar arteries lead to?

A

Cerebellar defects, instantly fatal due to coma and loss of resp control, cranial nerve defects, deafness, infarction of ventral pons leads to loss of all voluntary movements except eyes

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24
Q

What is the blood supply to the IC?

A

Small perforating arteries from circle of willis mostly supplied by ACA and MCA (LENTICULOSTRIATE)

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25
Q

What is the venous drainage of the brain?

A

Intracranial veins drain into dural venous sinuses then to internal jugular via jugular foramen in post cranial fossa

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26
Q

Where is the superior saggital venous sinus

A

Down midline

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27
Q

Where is falx cerebri?

A

Between superior and inferior saggital sinus

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28
Q

Where are left and right transverse sinus?

A

at the back of the head horizontally

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29
Q

Where is the sigmoid sinus and where does it exit skull?

A

At the sides of the head a continuation of transverse, exits through jugular foramen

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30
Q

Where does the middle meningeal artery enter the intracranial region?

A

Foramen spinosum

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31
Q

What does the middle meningeal artery supply?

A

The bones of the vault

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32
Q

What could a leak from the MMA cause?

A

Extradural haemmorhage- prolonged

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33
Q

What is a subdural haemmorhage?

A

Caused by leak of superior cerebral vein, low pressure slow accumulation (between dura and arachnoid) pushes on the brain

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34
Q

What is a sub-arach?

A

Between arachnoid and pia eg from ruptured aneurysm form curcle of willis very sudden and painful

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35
Q

Intracerebral haemmorhage

A

Within the brain tissue itself

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36
Q

What is the blood supply to the spinal cord?

A

Posterior and anterior spinal arteries from vertebras and radicular arteries from segmental spinal arteries

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37
Q

What does the brain consume at rest?

A

60% of glucose, 20% of oxygen (120g glucose a day)

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38
Q

How do NTs work?

A

AP arrives at the cell presynaptic cell depolarises and releases vesicles which diffuse across the synapse and cause Na to enter the next cell and K to be released, depolarising the postsynaptic cell.

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39
Q

How is NT removed?

A

Uptake into astrocytes- powered by ionic gradients (Na/K ATPase) and then glutamate is converted into glutamine (requires another ATP) and glutamine is exported and taken up pre-synaptically, converted back and packed into vesicles (another ATP)

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40
Q

Why does glutamate need to be removed?

A

Highly active at receptors, depolarises post-synaptic cells

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41
Q

What is neurovascular coupling?

A

Activity at the synapses leads to increased blood flow to deliver oxygen and glucose

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42
Q

How is glucose used for energy in the brain??

A

glucose transported from blood into glial cells where its converted into glucose-6-phosphate and then metabolised or stored as glycogen (very small store)

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43
Q

How is glucose metabolised in the presence of oxygen?

A

glucose gives 2 pyruvate, 2 ATP but uses 2 NAD and the pyruvate feeds into the next step, NAD regenerated elsewhere

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44
Q

How is glucose metabolised in the absence of oxygen?

A

Pyruvate is converted to lactate and NADH to NAD allowing glycolysis to continue using lactate

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45
Q

What happens in oxidative phosphorylation

A

In the mitochondrion pyruvate in the presence of oxygen gives CO2 and NADH which feeds into ox phos to give 34 ATP (overall 36ATP)

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46
Q

Without mitochondria how many ATP can be made?

A

2

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47
Q

What is the leptomeningeal collateral circulation made up of?

A

The A, M and P cerebral arteries

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48
Q

What happens if the MCA is occluded?

A

Blood flow initially drops but by 2 minutes the collateral circulation form the ACA takes oevr but cant reach the core of the MCA territory

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49
Q

What perfusion is below survival threshold (core)

A
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50
Q

What is the perfusion in the penumbra?

A
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51
Q

Why does the core expand?

A

The AP is potassium out sodium in as normal but the ECS is flooded with potassium and glutamate so the output is a massive release of potassium allowing the wave to propagate.All neighbouring neurons and astrocytes depolarise- massive ATP use

52
Q

In the normal brain what is the response to spreading depolarisations?

A

Hyperaemia- increase in blood flow

53
Q

Why do we need to reperfuse quickly?

A

After each wave lactate increases and glucose decreases

54
Q

Why does the brain swell when reperfused?

A

Neuronal ATPase is lost and Na is accepted into the cell causing cerebral oedema. When reperfused whole territory dilares and more capillaries open and are weak and leak causing swelling

55
Q

Where is the central sulcus

A

between frontal and parietal lobes

56
Q

How many layers is the cerebral neocortex?

A

6 layers

57
Q

What is the function of the supragranular layers?

A

Makes you you, controls cognitive function, executive for motor and sensory function and instructs the infragranular layer

58
Q

What does the forebrain contain?

A

Cerebral hemispheres and diencephalon (thalamus, hypothalamus, epithalamus and sub thalamus)

59
Q

What are the roles of the cerebral hemispheres?

A

Sensory integration, control of voluntary movement, higher intellectual functions like speech

60
Q

What is the role of the thalamus?

A

Relay centre between the medulla oblongata an cerebrum

61
Q

What is the role of the hypothalamus?

A

control centre for pain, hunger, thirst, BP, temp and produced hormones

62
Q

What is the primary somatosensory cortex reponsible for

A

Touch and proprioception (lost in somatosensory anaesthesia

63
Q

Supplementary somatosensory area injury

A

Superior parietal lobule- contralateral somatosensory agnosia- inability to recognise common objects by palpation
Inferior parietal lobule- in dominant hemisphere concerned with language, other hemisphere contralateral body neglect

64
Q

Where is the olfactory cortex found?

A

Frontal and temporal lobe

65
Q

What is the hippocampus critical for?

A

Critical for memory- large in taxi drivers, small in AD

66
Q

What areas are either side of the central sulcus?

A

Precentral (in front)- primary motor cortex

Postcentral (behind)- somatosensory cortex

67
Q

Where are the visual cortex and association area?

A

Back of the brain

68
Q

Where is Wernickes area?

A

Back of the brain

69
Q

What ascending connections are there to the cortex?

A

Somatosensory from the thalamus (inputs via VPL and trigeminal via VPM), Auditory from the thalamus (inputs from cochlea via medial geniculate nucleus), Visual from the thalamus (inputs from retina via lateral geniculate nucleus), smell (direct into olfactory cortex and taste via VPM)

70
Q

What descending connections are there from the cortex?

A

Motor to spinal cord (corticospinal)
Motor to brain stem motor nuclei (corico-bulbar tract)
To the motor control centres (targeted to the basal ganglia and cerebellum)
To the limbic system

71
Q

What are the connections between the cortex on the same side

A

Association fibres

72
Q

What are the connections between the cortex on the opposite sides

A

Corpus Callosum

73
Q

What happens if there is a lesion to the primary visual cortex or retina?

A

Blindness

74
Q

What happens if there is damage to the visual supplementary areas?

A

visual agnosia, disregard, facial recognition

75
Q

Where is spoken language processed and sent to?

A

Mid brain then to Wernicke’s rea

76
Q

Where is written language prcessed and sent to?

A

Visual are then sent to angular gyrus in L hemisphere, changed to sound and sent to Wernicke’s area

77
Q

What happens in Wernicke’s area?

A

extracts the meaning of language and sends to brocas area

78
Q

What happens in Brocas area?

A

Information refined into grammatical form and sent to motor cortex to make speech

79
Q

What happens if R hemisphere damage

A

loss of ability to interpret emotional content

80
Q

What happens if Brocas area damage?

A

Know what to say but cant do it with grammar (no fluency)

81
Q

What happens if Wernicke’s area is damaged?

A

Perfect grammar but meaningless

82
Q

What association fibres connect frontal and occipital lobes?

A

Superior longitudinal fasciculus

83
Q

What association fibres connect occipital and temporal lobes (visual recognition)?

A

Inferior longitudinal fasciculus

84
Q

What association fibres connect Wernicke and Brocas areas?

A

Arcuate fasciculus

85
Q

What does a tumour of the corpus callosum cause?

A

Alexia without agraphia (speak and write but not read)

86
Q

What happens if a focal cortical lesion?

A

Epilepsy, sensor and/or motor defects and psychological defecits

87
Q

Bilateral cortical degeneration

A

AD- temporal parietal and limbic (loss of language and memory)

88
Q

Left parietal damage

A

Anomia, acalculia, alexia and agraphia

89
Q

Right parietal damage

A

Constructional apraxia (skilled movements)

90
Q

Left temporal damage

A

Absenses, deja vu, Wernickes aphasia

91
Q

Occipital damage

A

Single- hallucinations, contralat visual field loss

Bilateral- blindness

92
Q

What is the brainstem made up of

A

Midbrain, pons, medulla

93
Q

What are surface markings on the midbrain part of the brainstem?

A

Anterior- mamillary body and crus cerebri

Posterior- sup and inf colliculi

94
Q

What are the surface markings on the pons?

A

Ant- middle cerebellar peduncle laterally

Post- sup, mid and inf peduncles and floor of 4th ventricle

95
Q

What are the surface markings on the medulla?

A

Ant- pyramid and olive (med to lat)

Post- Gracile and cuneate tubercle (med to lat) and below the fasciculus cuneatus and fasciculus gracilis

96
Q

Where does the corticospinal tract dessucate?

A

Level of the pyramids (80% of the fibres)

97
Q

Which cranial nerves join to the brainstem?

A

3-12

98
Q

Where is the occulomotor nerve attatched to the BS?

A

Motor- Edinger-Westphal nucleus and occulomotor nucleus- exit at level of crus cerebri

99
Q

Where is trochlear nerve attached to BS?

A

Trochlear nucleus then decussates controlling sup oblique exiting at level of crus cerebri

100
Q

Where is the trigeminal nerve attached to BS?

A

Trigeminal motor nucleus motor to muscles of mastication, sensort to trigeminal sensory nucleus

101
Q

Where is abducens nerve attached to BS?

A

Abducens nucleus controls lateral rectus (abducts eyeball)

102
Q

Where is the facial nerve attached to BS?

A

sensory form nucleus solitarius, motor from facial motor nucleus and superior salivatory nucleus

103
Q

Where is the vestibulococchlear nerve joined to BS?

A

Sensory from cochlear and vestibular nuclei for hearing and balance

104
Q

Where is the glossopharyngeal nerve joined to the BS?

A

Lateral to the olive. General sensation from trigeminal sensory nucleus, taste and visceral sensation from nucleus solitarus, inferior salivatory nucleus for parotid salivary gland, nucleus ambiguous and hypoglossal nucleus for pharynx and back of tongue

105
Q

Where is the vagus nerve joined to BS?

A

Trigeminal sensory nucleus, nucleus solitarus for visceral sensation, nucleus ambiguous for muscles of soft palate, pharynx, larynx and upper part of oesophagus, dorsal motor nucleus of the vagus

106
Q

Where is the accessory nerve joined to BS?

A

2 roots cranial and spinal, exits neurocranium via jugular foramen, motor nucleus ambiguus

107
Q

Where is hypoglossal nerve joined to BS?

A

motor to tongue from hypoglossal nucleus to extrinsic and intrinsic tongue muscles, rootlets emerge between pyramids and olives

108
Q

What is motor neurone disease?

A

Chronic degeneration of corticobulbar tracts

109
Q

Which nucleus’ degenerate in MND?

A

Nucleus Ambiguus and hypoglossal nucleus

110
Q

What are the signs and symptoms of MND?

A

Dysphonia, dysphagia, dysarthia, weakness, spacisity of tongue

111
Q

What happens is CN9-12 are compressed by tumours?

A

Dysphonia, unilateral weakness, wasting and fasciculation of tongue, suppression of gag reflex, unilateral wasting of sternomastoid and trapezius muscles

112
Q

What is the reticular formation?

A

Has widespread ascending and descending projections and involved in normal and pathogenic processes

113
Q

Brain stem lesion unilaterally causes

A

ipsilateral cranial nerve dysfunction, contralateral spastic hemiparesis, hyperreflexia, ipsilateral incoordination, contralateral hemisensory loss

114
Q

Brain stem bilateral lesion causes

A

coma, death

115
Q

What part of the brain initiates voluntary movement?

A

Basal ganglia

116
Q

Which part of the brain controls messages and actual position?

A

Cerebellum

117
Q

Which part puts the breaks on movement

A

Basal ganglia and cerebellum

118
Q

Which area of the brain has the idea and motivation to move

A

Prefrontal cortex

119
Q

What area of the brain controls conceptualisation of the plan

A

Premotor cortex (MCA)

120
Q

What area of the brain plans and strategises?

A

Supplementary motor area (ACA)

121
Q

What does the posterior parietal cortex do?

A

Analyses sensory information and activates the motor areas

122
Q

What does the cerebellum do?

A

Balance, co-ordination, motor memory (3 cerebellar arteries)

123
Q

What does the basal ganglia do?

A

Amplitude, timing, programming (MCA ACA)

124
Q

How are the spinal motor neurons activated?

A

Via corticospinal tracts from the primary motor cortex

125
Q

What is the process of repair after a stroke?

A

Initially contralateral flaccid paralysis but the motor cortex reorganisation and extrapyramidal pathways take control then speciosity (change in gamma motor neurone and regulatory interneurons and increase in alpha motor neurone activity)

126
Q

How can you identify the ventral side of the spinal cord?

A

Median fissure is prominent

127
Q

What is the denticulate ligament?

A

Extensions of pia matter onto arachnoid to anchor the cord

Medicine Year 2 (19 decks)

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