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Phase 2a - conditions > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a transient ischaemic attack?

A

A sudden onset, focal neurological deficit lasting under 24 hours.

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2
Q

What is the pathophysiology of a TIA?

A

Ischaemia to an area of the brain but without subsequent infarction.

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3
Q

What are the possible signs of a TIA?

A

Weak limb
Aphasia
Facial droop
Amaurosis fugax

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4
Q

What is amaurosis fugax?

A

Progressive vision loss, like a curtain coming down.

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5
Q

What artery is affected in amaurosis fugax?

A

Retinal artery

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6
Q

What are the causes of a TIA?

A

Thromboembolism
Cardiac dysrhythmia
Hyperviscosity - ie. sickle cell
Vasculitis

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7
Q

What investigations should be carried out in a TIA?

A

ABCD2 risk score - determines the urgency of treatment required.
Carotid doppler
CT angiography

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8
Q

What are the differential diagnoses for a TIA?

A

Hypoglycaemia
Migraine aura
Focal epilepsy

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9
Q

What risk factors should be controlled following a TIA?

A

Blood pressure
Cholesterol
Weight - exercise
Quit smoking

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10
Q

What drugs should be given in cases of a TIA?

A

Aspirin
Clopidogrel
Warfarin

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11
Q

What is the pathophysiology of a stroke?

A

An area of brain becomes infarcted and a permanent neurological deficit follows.

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12
Q

What are the two main types of strokes?

A

Ischaemic

Haemorrhagic

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13
Q

What are the risk factors for a stroke?

A 
High blood pressure 
Smoking 
Diabetes 
Obesity 
Hyperlipidaemia 
Past TIA 
Sedentary lifestyle
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14
Q

What aspect of a stroke determines the symptoms experienced?

A

The location of the blood vessel occlusion or haemorrhage.

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15
Q

What are the likely symptoms experienced in an anterior cerebral artery stroke?

A

Hemiparesis
Sensory disturbances
Drowsiness

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16
Q

What are the likely symptoms experienced in a middle cerebral artery stroke?

A 
Motor weakness 
Sensory disturbance 
Eye deviations 
Facial droop 
Receptive or affective aphasia.
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17
Q

What is receptive aphasia and where has been affected in a stroke that causes this?

A

Can’t understand speech.

Wernicke’s area in the temporal lobe has been infarcted.

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18
Q

What is affective aphasia and where has been affected in a stroke that causes this?

A

Can’t make speech.

Broca’s are in the frontal lobe has been infarcted.

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19
Q

What are the likely symptoms experienced in a posterior cerebral artery stroke?

A

Contralateral hemianopia

Other visual disturbances.

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20
Q

What are the likely symptoms experienced in a posterior circulation stroke?

A

Large motor deficits
Vertigo, nausea, vomiting
Altered consciousness

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21
Q

What is the largest deficit stroke?

A

Middle cerebral artery.

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22
Q

What investigations are used to investigate a stroke?

A

CT head
ECG
Carotid doppler

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23
Q

Which treatment can only be given within 4.5 hours of a stroke?

A

Thrombolytic

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24
Q

What is the contraindications for thombolytic therapy?

A

Recent surgery
Malignancy
Aneurysm

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25
Q

What must be completely excluded before antiplatelet drugs are stared?

A

Haemorrhagic stroke

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26
Q

What other therapies are given post stroke to aid recovery and prevent further events?

A

Aspirin
Clopidogrel
Statins

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27
Q

What are the four types of haemorrhage?

A

Intracranial
Subarachnoid
Subdural
Extradural

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28
Q

Where does the bleed come from in a subarachnoid haemorrhage?

A

Circle of Willis

most aften a berry aneurysm

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29
Q

What are the symptoms of a subarachnoid haemorrhage?

A

Sudden onset, severe headache - ‘thunderclap’
Vomiting
Collapse
Seizures

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30
Q

What are the signs if a subarachnoid haemorrhage?

A

Neck stiffness, low consciousness due to raised ICP

Positive Kering’s sign

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31
Q

What is Kering’s sign?

A

When both hip and knee are flexed, the extension of the knee is painful. (shows inflammation of meninges)

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32
Q

What investigations confirm a subarachnoid haemorrhage?

A

CT (detects 90%)

Lumbar puncture

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33
Q

What does a lumbar puncture show in a subarachnoid haemorrhage?

A

CSF is bloody, then turns xanthochromic (yellow) after 12 hours.

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34
Q

What are the differential diagnoses of a subarachnoid haemorrhage?

A

Migraine

Acute meningitis

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35
Q

What is the management of a subarachnoid haemorrhage?

A

Neurosurgery - very poor prognosis

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36
Q

What is a subdural haemorrhage?

A

Bleeding between the dura and arachnoid layer of the meninges.

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37
Q

What is the site of bleeding for a subdural haemorrhage?

A

Bridging veins (connect the cortex and venous sinuses)

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38
Q

What are the causes of a subdural haemorrhage?

A

Trauma (can be from a long time ago)

Metastases

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39
Q

What is the risk factor for subdural haemorrhage?

A

Brain atrophy - increases the distance the bridging brains travel, making them more susceptible to rupture.

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40
Q

What are the symptoms of subdural haemorrhage?

A

Fluctuating level of consciousness
Cognitive decline
Headache
Drowsiness

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41
Q

What investigation can diagnose a subdural haemorrhage and what does it show?

A

CT

Crescent shaped collection of blood over one hemisphere.

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42
Q

What are the differential diagnoses for subdural haemorrhage?

A

Stroke

Dementia

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43
Q

What is the management of a subdural haemorrhage?

A

Neurosurgery - good prognosis

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44
Q

What is an extradural haemorrhage?

A

Bleeding between dura and bone.

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45
Q

What is the cause of an extradural haemorrhage?

A

Skull fracture - often across the path of the middle meningeal artery.

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46
Q

What are the symptoms of an extradural haemorrhage?

A

A head injury with a following lucid period
Then decreasing consciousness
Headache, vomiting and fits

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47
Q

What investigation can diagnose an extradural haemorrhage and what does it look like?

A

CT

Convex bleed on the edge of the skull.

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48
Q

What is the management for an extradural haemorrhage?

A

Neurosurgery

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49
Q

What are the two different type of epilepsy?

A

Generalised

Focal/partial

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50
Q

What is the pathophysiological cause of epileptic seizures?

A

Hyper-synchronous neuronal discharges

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51
Q

What types of seizures are generalised?

A

Absence
Tonic-clonic
Myoclonic

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52
Q

What is a tonic-clonic seizure?

A

Period of rigidity followed by rhythmic muscle jerking

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53
Q

What is often a trigger for focal seizures?

A

Structural abnormality

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54
Q

What are the non-motor symptoms of focal seizures?

A

Feeling of deja-vu
Unusual tastes or smells
Aura - awareness within the seizure
Sensation disturbances

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55
Q

What are the motor symptoms of focal seizures?

A

Lip smacking
Chewing
Fiddling

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56
Q

What type of questions should be asked when someone reports a seizure?

A

How long did it last?
Was there a feeling before the seizure began?
How did you recover from the seizure?
Did anything occur to trigger the seizure?

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57
Q

What investigations can be carried for seizures?

A

Electroencephalography

MRI - to look for focal lesions

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58
Q

What does an EEG show in a generalised seizure?

A

Stimulation simultaneously in all parts of the brain

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59
Q

What does an EEG show in a focal seizure?

A

Stimulation in only a specific area of the brain that does not spread far.

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60
Q

Is an EEG diagnostic for epilepsy?

A

No

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61
Q

What is the mainstay of treatment for epilepsy?

A

Anti-epileptic drugs

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62
Q

What is the first line medication for generalised epilepsy?

A

Sodium valporate or Iamotrigine

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63
Q

What is the first line medication for focal epilepsy?

A

Carbamazepine

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64
Q

What is the first line medication for a patient in an epileptic emergency?

A

Lorazepam

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65
Q

What is the cause of syncope?

A

Insufficient oxygen/blood to the brain.

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66
Q

What are the features of syncope?

A

Precipitants - sudden standing, pain, fear
Prodrome - dizziness, light headed, sweats, nausea
Blackout - still, limp, eyes shut, minor jerking
Recovery - very rapid

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67
Q

What is a non-epileptic seizure?

A

Seizures that are associated with psychological distress.

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68
Q

What are the features of a non-epileptic seizure?

A 
Non-synchronous movements 
Dramatic motor 
Crying and speaking 
Long duration 
Injury is rare.
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69
Q

What is the pathology of Parkinson’s disease?

A

Deposition of Lewy bodies in the cytoplasm
Degeneration of dopaminergic neurons in the substantia nigra
lack of dopamine causes failure of basal ganglia function

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70
Q

What are the hallmark symptoms of Parkinson’s?

A

Bradykinesia (slow movements)
Tremor
Rigidity

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71
Q

How may bradykinesia present itself?

A

Problems doing up buttons

Small handwriting

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72
Q

What are the changes in gait in Parkinson’s?

A

Shuffling
Reduced arm swing
Slow to ‘get going’

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73
Q

What are the non-movement features of Parkinson’s disease?

A

Depression
Dementia
Other psychiatric problems

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74
Q

What scan can be used to see dopamine in the brain and what does it show in Parkinson’s?

A

DaTSCAN

Shows reduced dopamine in the brain.

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75
Q

What is the main mechanism of most Parkinson’s drugs?

A

Compensate for loss of dopamine.

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76
Q

What are the different pharmacological options available in Parkinson’s disease?

A

L-Dopa
Dopamine agonists ie. ropinirole
Catecholamine-O-methylytansferasse inhibitors
Monoamine oxidase B inhibitors

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77
Q

What is L-Dopa?

A

The precursor for dopamine, it can cross the BBB and is then metabolised to dopamine.

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78
Q

What is the action of COMT and MAO-B inhibitors?

A

Inhibit the breakdown of dopamine.

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79
Q

What are the complications of long term therapy use in Parkinson’s disease?

A

Drugs stop working
Symptoms when drugs are first taken ie. hyperkinetic
Drugs wear-off quicker between doses.

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80
Q

What is the genetic basis of Huntington’s disease?

A

Expansion of the CAG trinucleotide on chromosome 4. >36 repeats is diagnostic.

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81
Q

What is the inheritance of Huntington’s disease?

A

Autosomal dominant

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82
Q

What is the physiological effect of Huntington’s disease?

A

Atrophy and neuronal loss of striatum and cortex. Loss off GABA-nergic neurons.

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83
Q

What are the motor symptoms of Huntington’s disease?

A

Chorea (excessive, irregular movements)

Incoordination

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84
Q

What are non-motor symptoms of Huntington’s?

A

Depression

Dementia

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85
Q

Is there a cause for Huntington’s?

A

No

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86
Q

What are the causes of secondary headaches?

A

Subarachnoid haemorrhage
Meningitis
Low-CSF volume
Raised ICP

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87
Q

What are the types of primary headache?

A

Migraine
Cluster headache
Tension-type headache
Trigeminal neuralgia

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88
Q

Why is it important to image any headache with red flag symptoms?

A

To exclude secondary causes.

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89
Q

What is the presentation of a migraine?

A

Unilateral
Throbbing/pulsatile
Aggravated by activity
Moderate-severe

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90
Q

What can a migraine be associated with?

A 
Nausea 
Vomiting 
Photophobia 
Phonophobia
Aura
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91
Q

What is an migraine associated with aura?

A

A visual disturbance - flashing/blurring

All positive symptoms.

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92
Q

What are the triggers associated with migraines?

A 
Chocolate 
Hangovers 
Cheese 
Oral contraceptive 
Sleep changes 
Alcohol
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93
Q

What are the differential diagnoses for a migraine?

A

Cluster headache

TIAs

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94
Q

What is the treatment of an active migraine?

A 
NSAIDs 
oral triptan (ie. sumatriptan) can be taken when the migraine is first felt.
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95
Q

What are the prophylactic treatments for a migraine?

A

1 - propranolol or topiramate
2 - acupuncture
3 - botox

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96
Q

What are the symptoms of a tension-type headache?

A 
Bilateral 
Tight/pressing
Lasts from minutes to days 
Mild-moderate pain
No more than one of photo/phonophobia.
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97
Q

What is the management of a tension-type headache?

A

Reassurance
Stress relief
Avoid triggers
Analgesia

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98
Q

What are the symptoms of s cluster headache?

A

Unilateral orbital/supraorbital/temporal pain
Severe or very severe
Period of months with lots of attacks then long pain free periods.

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99
Q

What is the management of an acute cluster headache attack?

A

Sumatriptan

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100
Q

What is prophylactic management of cluster headaches?

A

Verapamil
Corticosteroids
Lithium

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101
Q

What are the features of a medication overuse headache?

A

Headache on >15 days of the month
Regular pain relief for >3 months
Headache has worsened over this period.

102
Q

What is the cause of trigeminal neuralgia?

A

Compression of the trigeminal nerve by - intracranial vessels, tumour, MS, skull.

103
Q

What is the presentation of trigeminal neuralgia?

A

Unilateral pain in the trigeminal nerve distribution (face)
Electrifying/lightning/stabbing
Precipitated by stimuli to that area of the face.

104
Q

What is the pharmacological management of trigeminal neuralgia?

A

1 - carbamazepine

2 - phenytoin, gabapentin

105
Q

What is the surgical management of trigeminal neuralgia?

A

Microvascular decompression

Stereotactic radiotherapy.

106
Q

Where does the spinal cord finish?

A

L1/L2

107
Q

What does the spinal cord turn into at L1?

A

Cauda equina

108
Q

Where would a lumbar puncture be carried out?

A

L4

109
Q

What is tetraplegia?

A

Paralysis of all 4 limbs

110
Q

What is paraplegia?

A

Paralysis of both legs

111
Q

What is hemiplegia?

A

Paralysis of one half of the body

112
Q

What are the causes of spinal cord compression?

A

Osteophytes
Disc prolapse
Malignancy
Infection

113
Q

What is the presentation of spinal cord compression?

A

Leg weakness
Sensory loss or disturbance below the compression
UMN signs below the compression - increased tone, reflexes.

114
Q

What investigation can confirm spinal cord compression?

A

MRI spine

115
Q

What is the treatment for spinal cord compression?

A

Surgical decompression

116
Q

Where would a lesion be to cause cauda equina syndrome?

A

At or below L1

117
Q

What are the symptoms of cauda equina syndrome?

A

Lower back pain
Pain that radiates down the leg
Numbness of the anus
Loss of bowel or bladder control

118
Q

What is the investigation and treatment for cauda equina syndrome?

A

MRI spine

Surgical decompression

119
Q

What is multiple sclerosis?

A

Chronic autoimmune T-cell mediated demyelination of the CNS.

120
Q

What is the epidemiology of multiple sclerosis?

A

More common in women
More common further away from the equator
Usually diagnosed at 20-40 years old

121
Q

What determines the presentation of MS?

A

The locations of the lesions

122
Q

What are the possible presentations of MS?

A 
Diplopia (double vision) 
Optic neuritis 
Numbness/tingling of limbs 
Weakness 
Ataxia
123
Q

What is required for a diagnosis of MS?

A

Two + lesions of the CNS disseminated in time and space.

Exclusion of other causes.

124
Q

Describe relapsing/remitting MS.

A

Unpredictable attacks which sometimes leave permanent deficits.

125
Q

Describe primary progressive MS.

A

Steady increase in disability without attacks

126
Q

Describe secondary progressive MS.

A

Initially relapsing and remitting, followed by progressive increase in disability.

127
Q

Describe progressive-relapsing MS.

A

Steady increase in disability with superimposed attacks.

128
Q

What investigations can show the CNS lesions in MS?

A

MRI with contrast

129
Q

What is the general management for a person with MS?

A

Reduce stress
Occupational therapy
Physiotherapy
Counselling

130
Q

What treatment can be offered during a flare up of MS?

A

Steroids - IV methylprednisolone

131
Q

What drug can be offered for MS long term and what is its role?

A

Beta-interfon

Decrease the number of attacks of MS.

132
Q

What is myasthenia gravis?

A

Autoimmune disorder of neuromuscular junction transmission.

133
Q

What are the most common autoimmune antibodies present in myasthenia gravis?

A

anti-Ach receptor antibodies in (80%)

anti-MuSK antibodies

134
Q

What is the presentation of myasthenia gravis?

A

Muscle weakness - ocular, bulber, proximal limb

The weakness is fatiguable (gets worse on repeated movements)

135
Q

What are some possible signs of myasthenia gravis?

A 
Ptosis 
Diplopia
Complex ophthalmoplegia 
Dysarthria (speech problems)
Head drop 
Limb weakness
136
Q

What are two signs that suggest myasthenia gravis?

A

Ice pack test - ice pack on eye improves ptosis

Cogan’s lid twitch - lid twitches on repetitive movements

137
Q

What investigations can be carried out in myasthenia gravis?

A

Serology - serum anti-AchR antibodies or anti-MuSK antibodies.
EEG
CT thorax

138
Q

What does and EEG show in myasthenia gravis?

A

Fatiguability

139
Q

What is the CT thorax for in myasthenia gravis?

A

Check for a thymoma

140
Q

What is the most common presentation of myasthenia gravis?

A

Ocular problems

141
Q

What percentage of myasthenia gravis presents with a thymoma?

A

20%

142
Q

What is the treatment for myasthenia gravis?

A

Pyridostigmine - acetylchoniesterase inhibitor
Steroids
Immunosuppression
Thymectomy is thymoma present

143
Q

What is the physiology of myasthenia gravis?

A

anti-ACh receptor antibodies prevent the binding of Ach on the post synaptic membrane so the impulse is not spread across the neuromuscular junction.

144
Q

What can be offered in a myasthenia gravis crisis?

A

IV immunoglobulin

Plasmapheresis

145
Q

What is lambert eaton myasthenic syndrome?

A

Anti-bodies to the voltage gated calcium channels.

146
Q

What is the physiology of lambert eaton myasthenic syndrome?

A

When an impulse arrives at the the presynaptic junction, not as many calcium channels open so less calcium floods in, so not as many neurotransmitter vesicles are transported out.

147
Q

What is the early presentation of lambert eaton myasthenic syndrome?

A

Gait changes

148
Q

Why does lambert eaton myasthenic syndrome improveme with movement?

A

Each impulse stimulates more calcium channels so eventually there is enough calcium to trigger an effective response.

149
Q

What is used to treat lambert eaton myasthenic syndrome ?

A

3,4 diaminopyridine

Immunosuppression

150
Q

What is motor neuron disease?

A

Degenerative loss of neurons.

151
Q

What is the presentation of upper motor neuron lesions?

A 
Weakness 
Increased tone 
Increased reflexes 
Extensor plantar response (babinski reflex)
No fasciculations or atrophy.
152
Q

What is the presentation of lower motor neuron lesions?

A 
Weakness 
Decreased tome 
Decreased reflexes 
Flexor/absent plantar response 
Fascilations 
Atrophy
153
Q

What is the most common form of motor neuron disease?

A

Amyotrophic lateral sclerosis - AML

154
Q

What are the general features of motor neuron disease?

A 
Reduced dexterity 
Stiffness 
Wasting of intrinsic hand muscles 
Stumbling gait 
Foot drop 
Slurred speech
155
Q

MND is a mostly clinical diagnosis. What are possible investigations that could be carried out to confirm diagnosis?

A

Bloods - raised creatinine due to muscle breakdown
Nerve conduction studies
Lumbar puncture - exclude inflam.
MRI - rule out lesions

156
Q

What is the management of MND?

A

No cute so all symptomatic treatment.
Spasticity - baclofen
Pain - analgesia

157
Q

What do A-alpha sensory fibres carry?

A

Proprioception

158
Q

What do A-beta sensory fibres carry?

A

light touch, pressure, vibration

159
Q

What do A-delta fibres carry?

A

Cold and pain

160
Q

What do C-fibres carry?

A

Warm and pain

161
Q

Which fibres are large and myelinated?

A

A-alpha

A-beta

162
Q

Which fibres are small and unmyelinated?

A

A-delta

C-fibres

163
Q

What is a mononeuropathy?

A

Problem with one nerve

164
Q

What are examples of common mononeuropaties?

A

Carpel tunnel syndrome

Sciatica

165
Q

What is carpel tunnel syndrome?

A

Compression of the median nerve, causing pain and parasthesia in the median nerve distribution, causes wasting of thenar eminence.

166
Q

How do you treat carpel tunnel syndrome?

A

Conservative - pain relief snd splint
Hydrocortisone injection
Surgical decompression

167
Q

What is sciatica?

A

Compression of the L1 nerve root - sciatic nerve. Causing sensory loss and shooting pain down the legs.

168
Q

What is a polyneuropathy?

A

Problem with many nerves

169
Q

What is the pathophysiology of polyneuropathy?

A

Axonal degeneration

Demyelination

170
Q

What are the causes of polyneuropathies?

A 
Diabetes 
Vitamin deficiency 
Infection (ie. Guillain barre)
Drugs 
Genetics
171
Q

What is the most common polyneuropathy presentations?

A

Symmetrical sensorimotor.

Deficiency in a glove and stocking distribuction (ie. diabetic neuropathy)

172
Q

What are the possible sensory symptoms of a polyneuropathy?

A

Numbness

Pins and needles

173
Q

What are the possible motor symptoms of a polyneuropathy?

A

Weak
Clumsy
Wasting

174
Q

What is Guillan-Barre syndrome?

A

Acute inflammatory demyelinating polyneuropathy

175
Q

What is the cause of Guillan-Barre syndrome?

A

Infection ie. by campylobacter jejuni, CMV, EBV.

176
Q

What are the symptoms of Guillain-Barre syndrome?

A

Progressive, ascending muscle weakness
Motor and sensory losses
Loss of reflexes.

177
Q

What is the management of Guillain-Barre syndrome?

A

Depends on its severity.
Severe - may need ventilation
Immunoglobulin can reduce the duration of paralysis.

178
Q

Which spinal nerve tracts carry motor information?

A

Corticospinal tracts

179
Q

What is the path of the corticospinal tracts?

A

85% decussate in the medulla and travel down the spinal cord ipsilaterally to the area supplied.

180
Q

What information do the dorsal column medial lemnisci tracts carry?

A

Vibration, touch, proprioception.

181
Q

What is the path of the DCML tracts?

A

Travel up the spinal cord ipsilaterally to the area supplied and decussate in the medulla.

182
Q

What information do the spinothalamic tracts carry?

A

Pain and temperature

183
Q

What is Brown-Sequard syndrome?

A

A hemi-section of spinal cord resulting in specific set of symptoms.

184
Q

What are the symptoms experience in Brown-Sequard syndrome?

A

Ipsilateral motor loss
Ipsilateral vibration, touch and proprioception loss
Contralateral pain and temperature loss

185
Q

What CN I and what is an effect of a lesion here?

A

CN I - olfactory

Anosmia

186
Q

What CN II and what is an effect of a lesion here?

A

Optic

Depends where the lesion is in the optic tract.

187
Q

What CN III and what is an effect of a lesion here?

A

Occulomotor

Third nerve palsy - affected eye looks down and out.

188
Q

What CN IV and what is an effect of a lesion here?

A

Trochlear

Weakness to the superior oblique muscle, double vision when looking down.

189
Q

What CN V and what is an effect of a lesion here?

A

Trigeminal nerve

Unlateral facial sensory loss, muscles of mastication stop working.

190
Q

What CN VI and what is an effect of a lesion here?

A

Abducens

Lateral rectus stop working, eye cannot be full abducted - causes horizontal diplopia.

191
Q

What CN VII and what is an effect of a lesion here?

A

Facial
Bell’s palsy - mouth sagging, speech problems, failure of eye closure.
Often caused by swelling of nerve within petrous bone canal due to infection.

192
Q

What CN VIII and what is an effect of a lesion here?

A

Vestibulococlear

Hearing and balance deficits

193
Q

What CN IX and what is an effect of a lesion here?

A

Glossopharyngeal

Diminished pharynx sensation

194
Q

What CN X and what is an effect of a lesion here?

A

Vagus

Swallow and gag problems, uvula deviates away from lesion.

195
Q

What CN XI and what is an effect of a lesion here?

A

Accessory

Weakness of sternocleidomastoid and trapezius muscle, head turning and shoulder shrugging.

196
Q

What CN XII and what is an effect of a lesion here?

A

Hypoglossal

Tongue weakness, wasting and fasciculation.

197
Q

What is the presentation of a brain tumour?

A

Progressive focal neurological deficit
Raised ICP - headache, vomiting
Seizures
General cancer symptoms - malaise, weight loss.

198
Q

What are the two main groups of brain tumours?

A

Primary or secondary.

199
Q

What is a sign of raised ICP?

A

Papilloedema

200
Q

What investigations can be carried out for a suspected brain tumour?

A

CT/MRI

Consider biopsy

201
Q

What are the differential diagnoses for a brain tumour?

A

Stroke
Abcess
Cyst

202
Q

What is the most common primary brain tumour?

A

Gliomas

203
Q

What are three types of glioma?

A

Astrocytoma
Oligodendroglioma
Ependymal

204
Q

What classification grades gliomas?

A

WHO classification

205
Q

What does a grade I glioma mean?

A

Benign

206
Q

What does a grade II glioma mean?

A

Diffuse - but can progress to be more aggressive

207
Q

What does a grade III glioma mean?

A

Anaplastic

208
Q

What does a grade IV glioma mean?

A

Glioblastoma

209
Q

How are gliomas classified?

A

Histology

Molecular genetics

210
Q

What specific mutation can indicate a oligodendroglioma?

A

1p19q deletion

211
Q

For which grade of tumour can curative therapy be aimed?

A

Grade I

212
Q

What are the common sites for brain mets to origionate?

A

Lung
Breast
Sometimes - kidney, GI tract, melanoma.

213
Q

What is the most common causative organism of meningitis?

A

Strep pneumoniae

214
Q

What cause of meningitis has a notoriously poor prognosis?

A

Neisseria meningitides

215
Q

What is the presentation of meningitis?

A

Headache
Neck stiffness
Fever
Photophobia

216
Q

What signs can be elicited in meningitis?

A

Kering’s - when both knee and hip are flexed knee extension is painful.
Brudkinski’s sign - flexion of neck causes leg flexion.

217
Q

What is a sign of meningococcal septicaemia?

A

Non-blanching petechial rash

218
Q

What are differential diagnoses for meningitis?

A

Malaria
Subarachnoid haemorrhage
Migraine

219
Q

What would do if someone in the surgery is suspected to have meningitis?

A

Give IM benzylpenicillin

Call 999 or send to hospital

220
Q

What are the investigations that should be carried out in meningitis?

A

Lumbar puncture
Head CT
Bloods - culture, FBC

221
Q

What is the contraindication of a lumbar puncture?

A

Septicaemic - could cause a spread of infection to CSF that was not already there.

222
Q

What is seen in the CSF of a meningitis caused by bacteria?

A 
Cloudy
Neutrophils 
Gram film visible 
High protein 
Low glucose
223
Q

What is seen in the CSF of a meningitis caused by virus?

A 
Clear 
Lymphocytes 
Not visible on gram film 
High protein 
Normal glucose 
Visible by PCR
224
Q

What is seen in the CSF of a meningitis caused by TB?

A 
Fibrin web appearance
Lymphocytes 
High protein 
Low glucose 
Visible by PCR
225
Q

What is seen in the CSF of a meningitis caused by crytococcal (fungal) cause?

A 
Fibrin web appearance 
Lymphocytes 
Visible by India ink stain 
High protein 
Low glucose
226
Q

What antibiotic is given for meningitis in hospital at the first instant?

A

IV cefotaxime

+ amoxicillin if listeria suspected

227
Q

What must always be done in a case of meningitis?

A

A notification of Public Health England.

228
Q

What can PHE do when notified about a case of menigitis?

A

Trace contacts - men C vaccine

If N menigitides can give rifampicin as prophylaxis.

229
Q

What is encephalitis?

A

Inflammation of the brain paranchyma

230
Q

What are the common causes of encephalitis?

A

Viral - HSV, VZV

231
Q

What is the presentation of encephalitis?

A 
Fever
Headache 
Behavioural change 
Coma 
Seizures
232
Q

What investigations should be carried out in encephalitis?

A

MRI head

LP and CSF analysis

233
Q

What is the most common CSF finding in encephalitis?

A

Viral so lymphocytes, PCR visible.

234
Q

What can be given in a viral cause of encephalitis?

A

IV acyclovir

235
Q

What infection causes shingles?

A

Herpes voster

236
Q

The reactivation of what infection causes shingles?

A

Varicella zoster (chicken pox)

237
Q

What is the presentation of herpes zoster?

A

Rash

Pain

238
Q

What can be given to treat herpes zoster?

A

Acyclovir

239
Q

What causative organism of tetanus?

A

Clostridium tetani

240
Q

What is the effect of a tetanus infection?

A

Extreme spasm and pain

Can be localised or whole body.

241
Q

What is the management of tetanus?

A

Vaccination for prevention

242
Q

What are the four types of dementia?

A

Alzheimer’s
Vascular
Lewy body
Fronto-temporal

243
Q

What is the pathogenesis of Alzheimer’s disease?

A

Accumulation of B-amyloid plaques in the brain

Structural changes to tau protein

244
Q

What does an MRI show in Alzheimer’s disease?

A

Gross atrophy

245
Q

What is the pathogenesis of vascular dementia?

A

Multiple infarcts, stroke, small vessel disease causing a vascular deficit to the brain.

246
Q

What is the pathogenesis of lewy body dementia?

A

Deposition of lewy bodies in the brain.

247
Q

What is the pathogenesis of fronto-temporal dementia?

A

Fronto-temporal lobe atrophy

248
Q

What is the general effect of dementia?

A

Gradual onset, progressive decline in cognitive function, memory, problem solving, language and activities of daily living.

249
Q

What are specific symptoms of lewy body dementia?

A

Can be fluctuating

Can have visual hallucinations early on

250
Q

What are specific symptoms of fronto-temporal dementia?

A

Behaviour and personality changes predominate.

251
Q

What can dementia be distinguished from depression?

A

Depression onsets more rapidly, patient is aware of their memory loss, patient is distress and has variable cognitive function.

252
Q

What is the recommended management for dementia?

A

Healthy lifestyle
Develop routines
Social support and care
Treat any associated co-morbidities

Phase 2a - conditions (11 decks)

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