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Control Symposium > C Symposium > Flashcards

C Symposium Flashcards

1
Q

What are the unique signs of an anterior circulation stroke?

A

Amaurosis fugax (vision loss)
Dysphagia
Apraxia (can’t perform purposeful actions)
Inattention

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2
Q

What are the unique signs of a posterior circulation stroke?

A

Ataxia (loss of control of full body movements)
Diplopia
Vertigo
Bilateral Symptoms

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3
Q

What is the ABCD2 score used for?

A

TIA

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4
Q

What is the polypill?

A 
Combination of:
Statin
Aspirin
Antihypertensive
Folic acid
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5
Q

Name a secondary vascular prevention of stroke?

A

Carotid Endarterectomy

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6
Q

What is negative and positive phenomena?

A

Decreased and increased sensation respectively

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7
Q

What type of stroke has feature known as neglect (not eating half a plate of food)?

A

Right hemisphere stroke

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8
Q

What is visual agnosia?

A

Inability to access semantic knowledge of an object

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9
Q

What is dyspraxia?

A

Loss of ability to plan, conceptualise and execute complex sequence of motor actions

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10
Q

What is spasticity?

A

Hyper excitability of the stretch reflex

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11
Q

Different pain onsets of headache?

A

Acute - seconds to minutes
Evolving - hours to days
Chronic - weeks to months

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12
Q

What are the causes of raised intracranial pressure?

A 
Mass effect
Brain swelling - hypertensive encephalopathy
Increased venous pressure
CSF outflow obstruction - hydrocephalus
Increased CSF production - meningitis
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13
Q

Who is temporal arteritis likely to affect and what is the treatment?

A

Older female patient

High dose steroids - prednisolone

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14
Q

Preventative migraine treatments?

A

Propanolol

Valproate

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15
Q

What are trigeminal autonomic cephalgias?

A 
Pain one side of head in trigeminal area
Activation of trigeminal parasympathetic  system
- cluster headache
- paroxysmal hemicranias
- SUNCT headache
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16
Q

What is the pain relief for trigeminal autonomic cephalgias and what is the prevention?

A

Pain relief - sumatriptan

Prevention - prednisolone, verapamil

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17
Q

What is the presentation of intracranial tumours?

A 
Raised intracranial pressure
Epilepsy
Neurological Deficit
Endocrine dysfunction
Incidental
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18
Q

What is the management of intracranial tumours?

A

Medical: steroids, anti-convulsants, hormonal replacement
Surgical
Adjuvant Therapy

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19
Q

What intracranial tumour are males and females most likely to get?

A

Males - Gliomas

Females - Meningiomas

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20
Q

What are the different types of astrocytoma and what are their grades?

A 
Astrocytic tumours - grade 1
Diffuse astrocytoma - grade 2
Anaplastic astrocytoma - grade 3
Glioblastoma - grade 4
Pilocytic astrocytoma - grade 1 - children and cerebellum
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21
Q

What is classic histological appearance of nuclei and capillaries in Oligodendroglioma?

A

Fried egg nuclei

Arborising Capillaries - chicken wire

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22
Q

What are the features of a meningioma?

A

Grade 1
Whorls
Psamomma bodies

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23
Q

What are the features of a medulloblastoma?

A

In children in the cerebellum
Grade 4
Anaplastic hyperchromatic cells
Rosette formation

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24
Q

Name nerve sheath tumours and nerves affected?

A

Schwannoma - vestibulocochlear nerve
Neurofibroma - spinal nerves - collagen rich
Spindle cell tumours - no specifics

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25
Q

Name some of the causes of dementia?

A 
Alzheimer's
Lewy Body
Vascular
Fronto-temporal
Huntington's
Prion disease
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26
Q

What are the mutated proteins in dementia?

A

Amyloid proteins - inappropriate folded versions - form insoluble fibrils
Tau proteins - no longer stabilise microtubules
Ubiquitin - no longer direct proteins to compartments in cells

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27
Q

What are the neurodegenerative dementias?

A

Alzheimer’s
Lewy Body
Fronto-temporal

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28
Q

What are neurogenerative movment disorders?

A

Parkinson’s
Huntingtons
MND

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29
Q

What is the triad of effects caused by normal pressure hydrocephalus?

A

Dementia
Gait disturbance
Urinary incontinence

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30
Q

Classification of seizures?

A

Generalised - both hemispheres
Partial - one hemisphere
Secondary generalised - one and then the second

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31
Q

What is status epilepticus?

A

When the brain is in a permanent state of persistent seizure - medical emergency

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32
Q

Mutations in which receptors can cause epilepsies?

A

GABA receptor

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33
Q

What is dravet syndrome?

A

Rare genetic epileptic encephalopathy - nonsense mutation

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34
Q

What do antiepileptic drugs do?

A

Decrease frequency and severity of seizures

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35
Q

How to antiepileptic drugs work?

A

Suppress action potential
Enhance GABA transmission
Suppression of excitatory transmission

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36
Q

What can be used as an alternative to valproate?

A

Clonazepam

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37
Q

What enhances the action of GABAA receptors?

A

Barbiturates

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38
Q

What decreases GABA uptake

A

Tiagabine

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39
Q

What increases the action of GABA?

A

Benzodiazepines

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40
Q

How do benzodiazepines work?

A

Increase affinity of GABA to receptor

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41
Q

What inhibits sodium channels?

A

Carbamazepine

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42
Q

What is valproate effective against and how does it work?

A

Good against tonic-clonic seizures and absences

Decreased GABA turnover

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43
Q

What is foetal hydantoin syndrome

A

Mother takes phenytoin/carbamazepine during pregnancy
Intrauterine growth restriction
Microcephaly
Growth problems

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44
Q

What is epilepsia partialis continua

A

Motor epileptic seizures

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45
Q

How can tetanus help suppress seizures?

A

Toxin injected into mother cortex - decrease neurotransmitter release
Therefore affects GABAergic synapses
Seizure activity controlled by light (certain lights can hyperpolarise neurons)
- Halorhodopsin

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46
Q

What is optic neuritis and its link to MS?

A

Inflammation of optic nerve
Pain and loss of vision
Can return to normal visual acuity
50% develop MS

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47
Q

What is transverse myelitis, a feature it causes and its link to MS?

A

Inflammation inside the spinal chord
Lhermittes phenomenon (resembles electric shock passing down neck)
50% develop MS

48
Q

MS definite diagnosis?

A

When transverse myelitis and optic neuritis occur at different times

49
Q

What is multiple sclerosis (MS)?

A

Disease of the CNS

Inflammatory reaction - loss of myelin - slow nerve conduction

50
Q

What is used in the treatment of MS and how does it work?

A

Natalizumab - prevents migration of immune cells across blood-brain barrier
Fingolimod - oral treatment - takes lymphocytes away from blood and susceptible target organs e.g. CNS

51
Q

Disease progression of MS?

A

Relapsing - remitting MS
Primary progressive MS
Secondary progressive MS
Progressive relapsing MS

52
Q

What type of lesion leads to tetraplegia and what is it?

A

Cervical lesion

Partial/total loss of four limbs

53
Q

What type of lesion leads to paraplegia and what is it?

A

Thoracic lesion

Impairment of lower extremities - legs

54
Q

What is Brown-Sequard Syndrome?

A

Incomplete spinal cord lesion (one side)

Ipsilateral paralysis

55
Q

Excessive vagal stimulation?

A

Lesion is above T6

Loss of parasympathetic control - overwhelming vagal output

56
Q

What are the classes of somatosensory disorders and which receptors are involved?

A

Tactile - think skin receptors
Proprioception - Golgi tendon and muscle spindles
Thermal sensation - thermoreceptors
Nociceptine sensations - nociceptors

57
Q

Features and location of Meissner’s corpuscles?

A

Looping axonal terminals that inter-twine supporting cells
Below epidermis
Rapidly adapting small receptor
Feels flutter motion

58
Q

Features and location of Merkel’s?

A

Dome structure atop axon terminals
Epidermal-dermal border
Slow adapting small receptor
Pressure, form, texture

59
Q

Features and location of Pacinian’s?

A

Onion shaped appearance
Deep dermis
Rapid acting large receptor
Vibration

60
Q

Features and location of Ruffini?

A

Terminals interwined with collagen
Deep dermis
Slow acting large receptor
Skin stretch

61
Q

What receptor feels Braille?

A

Merkel

62
Q

Where does the Herpes Zoster virus live in the infected?

A

Primary sensory neurons

63
Q

What does damage to the posterior parietal cortex cause?

A

Astereognosia - inability to identify objects based on touch alone

64
Q

How can a pure sensory stroke occur?

A

Thalamic infarct

65
Q

What is the distribution of sensation in peripheral neuropathy?

A

Glove + stocking distribution - no sensation here

66
Q

What are nociceptors?

A

Pain receptors - simple free nerve endings

67
Q

What substances released in inflammation and tissue damage sensitise peripheral nociception?

A

Prostaglandins
Bradykinin
Histamine

68
Q

Where are the nociceptive cell bodies?

A

Dorsal root ganglion

69
Q

Where does referred pain from each of the following go:

a) oesophagus
b) heart
c) bladder
d) ureter
e) prostate

A 
Oesophagus - chest wall
Heart - chest and arm
Bladder - perineum
Ureter - lower abdomen and back
Prostate - lower trunk and legs
70
Q

What is the neurotransmitter and neuropeptide for pain?

A

Glutamate and substance P respectively

71
Q

What is phantom pain?

A

Sensation without input

72
Q

In which instance will hyperalgesia occur?

A

When already damaged tissue is present - as it is unusually sensitive

73
Q

Analgesia Ladder (increasing)

A

Non-Opiod - NSAIDs
Weak Opiod
Strong Opiod
Epidural/spinal/nerve block

74
Q

What is neuropathic pain and in what instances can you get it?

A

Spontaneous pain and hypersensitivity to pain
Painful diabetic neuropathy
Post herpetic neuropathy - site of a previous attack of shingles
Trigeminal neuralgia

75
Q

What is allodynia?

A

Pain in response to non painful stimuli

76
Q

What are dysanthesias?

A

Unpleasant abnormal sensations e.g. ants crawling on skin

77
Q

Which antidepressant can be used for neuropathic pain?

A

Tricyclic agents

78
Q

Which anticonvulsants reduce pain and how do they work?

A

Gabapentin - blocks voltage gated calcium channels
Pregablin - blocks Calcium N type
Carbamazepine - blocks sodium and calcium channels

79
Q

What is the problem with the eye when there is blurred vision?

A

Refractive problem - cornea, lens, shape of eye

Macular problem

80
Q

What is the problem with the eye when there is difficulty seeing in bright light?

A

Corneal or lens problem - cataract usually

81
Q

What is the problem with the eye when there is distorted vision and what is the distortment?

A

Things look wavy and lines aren’t straight

Retina problem - wet macular degeneration or retina detachment

82
Q

What is the problem with the eye when things look pale?

A

Optic nerve disease

83
Q

What is a floater and its causes?

A

Deposit of various sizes in the vitreous humour of the eye

Posterior vitreous detachment or vitreous haemorrhage

84
Q

What is a cataract?

A

Opacity of the lens

Common aging change

85
Q

What is the treatment of cataracts?

A

Surgery - phacoextraction and then lens implant

86
Q

How can giant cell arteritis cause visual loss?

A

Anterior ischaemic optic neuropathy

Central retinal artery occlusion

87
Q

What is wet ARMD and what is it’s pathology?

A

Blurred vision or loss in visual field
Fluid entering macula (on retina)
Choroidal neovascular membrane
Rapid loss of vision

88
Q

Treatment of wet ARMD?

A

Anti VEGF

89
Q

What keeps the eye spherical?

A

Vitreous Humour

90
Q

How does the lens change to accommodate a near and a far point?

A

Fat lens is near point

Flat lens is far point

91
Q

What is hyperopia and how is it corrected?

A

Far sightedness - eyeball is too short

Place a convex lens in front of the eye

92
Q

What is myopia and how is it corrected?

A

Near sightedness - eyeball is too long

Place a concave lens in front of eye

93
Q

Where is the origin of the blood vessels in the eye?

A

Optic disk

94
Q

What is scotopic and what photoreceptors are used?

A

Night time and only rods are used

95
Q

What is mesopic and what photoreceptors are used?

A

Twilight time and both cones and rods

96
Q

What is photopic and what photoreceptors are used?

A

Day time and only cones

97
Q

What is colour blindness known as?

A

Dichromat

98
Q

What are the different types of retinal ganglion cells and how do they differ?

A

M type - large
P type - small - most common
K type - medium

99
Q

Locked in syndrome vs persistent vegetative state?

A

Awake and aware but unable to move
vs
Eyes open - chronic wakefulness

100
Q

What does the basal ganglia consist of?

A

Corpus Striatum
Amygdala
Claustram

101
Q

Corpus Striatum consists of?

A

Paleostriatum which is the globus pallidus

Neostriatum which is caudate nucleus and putamen

102
Q

What is the main function of the substantia nigra?

A

Initiate movement

103
Q

What gets disrupted in Parkinson’s?

A

Nigrostriatial input

104
Q

What happens in a patellar tap? - which fibre as well

A

Myostatic stretch reflex
Muscle spindle activated
1a

105
Q

Golgi tendon reflex? - which fibre

A

Inverse myostatic reflex
1b
Indirect inhibition via inhibitory neuron

106
Q

Stepping on a pin? - which fibre for sensory afferent

A

Flexor withdrawal

A-delta, C, Group 3 sensory afferent

107
Q

Likely cause if weakness is non-specific?

A

Illness

108
Q

Likely causes of UMN weakness?

A

Stroke, tumour

109
Q

Likely causes of LMN weakness?

A

`MND
Peripheral neuropathy
Single nerve damage

110
Q

Where is the lesion when half the body is affected?

A

Cerebral hemisphere

111
Q

Where is the lesion when all four limbs are affected?

A

High cervical cord

112
Q

If there is a lower spinal cord lesion what is affected?

A

`Lower limbs

113
Q

Where is the lesion when one limb is affected?

A

Spinal root/peripheral nerve

114
Q

Where is the lesion when there is generalised proximal weakness?

A

Myopathy

115
Q

In myopathy how does an EMG differ from normal?

A

Smaller waves

116
Q

In denervation how does an EMG differ from normal?

A

Lower frequency

117
Q

In neuropathic pain how does an EMG differ from normal?

A

Bigger waves

Control Symposium (1 decks)

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