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Phase 3A > Neurology > Flashcards

Neurology Flashcards

1
Q

Define myasthenia gravis

A

A disorder of neuromuscular transmission characterised by: weakness and fatiguing of some or all muscle groups, weakness worsening on sustained or repeated exertion, or towards the end of the day, relieved by rest

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2
Q

Myasthenia Gravis pathophysiology

A

Autoimmune destruction of the nicotinic postsynaptic receptors for acetylcholine (AChR)

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3
Q

Clinical features of myasthenia gravis

A

Ptosis, muscle paresis, weakness of jaw muscles leaves mouth hanging open,, characteristic smile - myasthenic snarl, muscle wasting, hyperactive limb reflexes

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4
Q

Investigations for myasthenia gravis

A

Acetylcholine receptor antibodies (anti-AchR)
Anti-MUSK also
Anticholinesterase drugs used to confirm diagnosis - Tensilon test
CT of the thymus - thymic hyperplasia found in 70% of sufferers

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5
Q

Treatment for myasthenia gravis

A

Anticholinesterase durgs - Pyridostigmine
Muscarinic inhibitor - atropine to counter side effects
Prednisolone
Thymectomy

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6
Q

Define meningitis

A

Inflammation of the leptomeninges and underlying subarachnoid CSF

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7
Q

Risk factors for meningitis

A

Alcoholism, overcrowding, spinal procedures, diabetes mellitus, IV drug abuse, malignancy, cystic fibrosis

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8
Q

Causes of meningitis

A 
Neonates= Gram -ve bacilli: E.coli, Klebsiella, H.influenzae
Children= H.influenzae, Strep. pneumoniae, N.Meningitidis
Adults= Strep. pneumoniae, H.influenzae,
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9
Q

Symptoms of meningitis

A

Fever, headache, stiff neck, photophobia, non-blanching petechial skin rash, Kernig’s sign, Brudzinski’s sign, seizures

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10
Q

Differential diagnoses of meningitis

A

Encephalitis, subarachnoid haemorrhage, malaria, septicaemia

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11
Q

Investigations for meningitis

A

LP - Ziehl-Neelsen stain, glucose, protein, rapid antigen screen,
U&Es, FBC, LFT
X-ray
CT scan

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12
Q

Treatment for meningitis

A

Dexamethasone + Ceftriaxone (E.Coli)/Benzylpenicillin (Pneumococcus + Meningococcus)

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13
Q

Define Guillain Barre syndrome

A

A disorder causing demyelination and axonal degeneration resulting in acute, ascending and progressive neuropathy, characterised by weakness, paraesthesiae and hyporeflexia

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14
Q

Causative organisms of Guillain Barre syndrome

A 
CMV
EBV
Camplyobacter jejuni
HIV
Haemophilus influenzae
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15
Q

Risk factors for Guillain Barre syndrome

A

History of GI or respiratory infection, association with Zika virus, vaccinations, malignancies, pregnancy

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16
Q

Symptoms of Guillain Barre syndrome

A

Weakness - facial, dysphasia, dysarthria, back pain, reduced reflexes, paraesthesiae, hypotonia
Autonomic symptoms - reduced sweating, reduced heat tolerance, urinary hesitancy, tachycardia

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17
Q

Differential diagnosis for Guillain Barre

A 
Stroke
Encephalitis
Spinal cord compression
Vasculitis
Myasthenia Gravis
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18
Q

Investigations for Guillain Barre

A

Confirmed with Nerve conduction studies
Electrolytes - inappropriate ADH secretion
LP - Elevated CSF: elevated protein, low WBC
ECG - T-wave abnormalities, ST depression, QRS widening
Spirometry

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19
Q

Management of Guillain Barre

A

IV immunoglobulin
Plasma exchange
Low molecular weight heparin

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20
Q

Define Parkinson’s disease

A

A progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the pars compacta of the substantia nigra - low levels of dopamine

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21
Q

Causes of Parkinson’s

A 
Idiopathic
Drugs - Neuroleptics, Metocloparide, Prochloperazine, sodium valproate
Truma
HIV
Manganese/copper toxicity
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22
Q

Triad of symptoms of Parkinson’s

A

Bradykinesia - slowness of movement
Pill-rolling tremor
Cogwheel rigidity

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23
Q

Other symptoms of Parkinson’s

A 
Constipation
Frequency, urgency and incontinence
Hallucinations
Sweating
Dribbling of saliva
Weight loss
Sleep problems
Depression
Anxiety
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24
Q

Main treatment for Parkinson’s

A

Levodopa (converted to dopamine)
Complications: Postural hypotension
On-off effect

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25
Q

What is levodopa given with?

A

Decarboxylase inhibitor - Carbidopa

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26
Q

Other treatments for Parkinson’s

A

Dopamine agonists - Ropinirole
MAO-B inhibitors - Rasagiline
COMT inhibitors - Tolcapone

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27
Q

How is meningitis spread?

A

By respiratory droplet

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28
Q

Define meningococcal septicaemia

A

Petechial rash + signs of sepsis

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29
Q

CSF findings in bacterial meningitis

A

Raised protein

Low glucose

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30
Q

CSF findings in viral meningitis

A

Normal protein

Normal glucose

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31
Q

Prophylaxis for meningitis

A

Rifampicin

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32
Q

Define TIA

A

Transient ischaemic attack

Sudden onset of neurological dysfunction which lasts less than 24 hours

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33
Q

TIA pathophysiology

A

Cerebral ischaemia due to arterial embolism or thrombosis in an atheromatous carotid, vertebral or cerebral artery

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34
Q

Risk factors for TIA

A 
Smoking
Hypertension
Diabetes mellitus
Increasing age
Alcohol
Previous TIA
Hypercholesterolemia
Vasculitis
AF
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35
Q

Signs and symptoms of TIA

A

Hemiparesis, hemi sensory disturbance, dysphasa, amaurosis fugax

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36
Q

Define amaurosis fugax

A

Painless transient monocular visual loss - ‘a curtain coming down vertically into field of vision’
Leads to retinal hypoxia

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37
Q

Differential diagnosis for a TIA

A

Stroke
Hypoglycaemia
Migraine aura
Focal epilepsy

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38
Q

Diagnosis for TIA

A

ECG - check for AF or myocardial ischaemia
FBC, U&Es, glucose, ESR, LFTs, TSH
Echocardiogram or cardiac monitoring
Doppler ultrasound of the carotid arteries

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39
Q

How is risk of a stroke following a TIA assessed?

A

Use ABCD2 score
A - age >60
B - BP 140/90 or greater
C - Clinical features: unilateral weakness/speech disturbance without weakness
D - duration of symptoms: 60 minutes 2 points, 10-59 = 1 point
D - diabetes
High risk = 4+
Refer for specialist assessment within 24 hours. Low risk need assessment within 1 week

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40
Q

How is a TIA managed?

A 
Control cardiovascular risk factors: stop smoking, improve diet, regular exercise, cut down on alcohol, lose weight
Manage AF, diabetes, hypertension
Aspirin
Antiplatelet therapy - clopidogrel
Statin - simvastatin
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41
Q

Define stroke

A

Disruption of blood to the brain lasting for more than 24 hours

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42
Q

Pathophysiology of a stroke

A

May be due to a blockage in a cerebral blood vessel leading to ischaemic infarction (70%) or due to a intracerebral haemorrhage (30%)

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43
Q

Causes of a stroke

A 
Small vessel occlusion/thrombosis
Cardiac emboli (AF, MI, IE)
Atherothromboembolism
CNS bleeds (trauma, SAH)
Coronary artery dissecton
Vasculitis
Hyperviscosity (polycythaemia, sickle cell anaemia, myeloma)
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44
Q

Risk factors for a stroke

A 
Diabetes mellitus
Hypertension
AF
Smoker
Alcohol
Increasing age
Previous TIA
Hypercholesterolemia
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45
Q

Signs and symptoms of a stroke

A 
Total anterior circulation stroke = Unilateral weakness of face, arm and leg, homonymous hemianopia, higher cerebral dysfunction (dysphagia, visuospatial disorder)
Partial anterior circulation stroke: 2 of the 3 above
Posterior circulation syndrome = cerebellar or brainstem syndromes, loss of consciousness, isolated homonymous hemianopia
Lacunar syndrome (LACS) = unilateral weakness, pure sensory loss, ataxic hemiparesis
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46
Q

Diagnosis of a stroke

A

Urgent CT head
MRI
BP/ECG, blood glucose

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47
Q

Management of a stroke

A

ABCDE approach
Ensure hydration, keep O2 saturation >95%
Thrombolysis for ischaemic stroke = Alteplase
Antiplatelet therapy - Clopidogrel
MDT team

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48
Q

Define primary prevention

A

Risk factor control before any stroke

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49
Q

Define secondary prevention

A

Risk factor control to prevent recurrence of a stroke including lifelong antiplatelet

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50
Q

Define Subarachnoid haemorrhage

A

Bleeding into the subarachnoid space - between the arachnoid layer of the meninges and the brain parenchyma

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51
Q

Risk factors for a subarachnoid haemorrhage

A

Hypertension
Family history
Diseases which predispose to aneurysms - Polycystic kidney disease, Ehlers Danlos syndrome, coarcation of the aorta

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52
Q

Pathophysiology of a subarachnoid haemorrhage

A

Rupture of a berry aneurysm (70%), 10% are due to an ateriovenous malformation

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53
Q

Signs and symptoms of a subarachnoid haemorrhage

A

Thunder clap headache, vomiting, Kernig’s sign, neck stiffness, altered level of consciousness - drowsiness, collapse, seizures, coma, papilloedema

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54
Q

Diagnosis of a subarachnoid haemorrhage

A

CT scan

Lumbar puncture - blood xanthochromic (yellow) due to billirubin from Hb breakdown

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55
Q

Management of a subarachnoid haemorrhage

A

Dexamethasone to decrease cerebral oedema
Neurosurgery - surgical clipping or coiling of anuerysm
Nimodipine to reduce risk of vasospasm

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56
Q

Complications of subarachnoid haemorrhage

A

Rebleeding
Hydrocephalus
Hyponatraemia (SIADH)
Cerebral ischaemia due to vasospasm

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57
Q

Define subdural haematoma

A

A collection of clotting blood in the subdural space (space between the dura mater and the arachnoid mater)

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58
Q

Pathophysiology of subdural haematoma

A

Due to a rupture of a vein between the venous sinuses and the cortex, the accumulating haematoma causes raised ICP, shifting the midline structures

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59
Q

Risk factors for subdural haematoma

A

Traumatic head injury
Increasing age
Alcoholism
Anticoagulation medications

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60
Q

Signs and symptoms for subdural haematoma

A 
Raised ICP - headache, nausea, vomiting, raised BP
Confusion
Seizure
Focal neurology
Alternating level of consciousness
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61
Q

Complications of a subdural haematoma

A

Death due to herniation
Raised ICP
Cerebral oedema
Coma

62
Q

Differential diagnosis for subdural haematoma

A

EDH, SAH, meningitis, encephalitis, stroke, dementia, DKA

63
Q

Investigations for a subdural haematoma

A

CT - gold standard = crescent shaped mass
FBCs, U&E’s, LFT’s
MRI

64
Q

Management for subdural haematoma

A

Prioritise CT head
Surgery - evacuate the haematoma e.g. Craniotomy
Mannitol if raised ICP

65
Q

Define extradural haematoma

A

Collection of blood between the dura mater and the bone, usually caused by head injury

66
Q

Pathophysiology of an extradural haematoma

A

Due to fracture of the temporal or parietal bone causing laceration of the middle meningeal artery, typically after trauma to the temple

67
Q

Risk factors for extradural haematoma

A

Young adults

68
Q

Signs and symptoms for extradural haematoma

A

Loss of consciousness
Lucid interval
Headache, nausea and vomiting, confusion and seizures
Increased ICP

69
Q

Differential diagnosis for extradural haematoma

A

Subdural haematoma
SAH
Meningitis
Encephalitis

70
Q

Diagnosis for extradural haematoma

A

CT scan - gold standard = lemon shape

71
Q

Management for extradural haematoma

A

ABCDE
Mannitol if increased ICP
Surgery - Craniotomy and clot evaculation

72
Q

Define tension headache

A

Commonest primary headache. Can be episodic (<15 days/month) or chronic (>15 days for at least 3 months)

73
Q

Risk factors for tension headaches

A

Stress
Anxiety
Noise
Fumes

74
Q

Signs and symptoms of tension headaches

A

Bilateral, non-pulsatile, chronic daily headache - ‘tight band-like sensation’, pressure behind eyes, mild-moderate pain
Scalp muscle tenderness
No vomiting, no aura

75
Q

Differential diagnosis for tension headache

A

Migraine, cluster, GCA, PMR

76
Q

Diagnosis for tension headache

A

Clinical diagnosis

77
Q

Management for tension headache

A

Lifestyle advice - regular exercise, avoid triggers, massage

Aspirin, paracetamol, NSAIDs

78
Q

Define migraine

A

Recurrent throbbing headache often preceded by an aura and associated with nausea, vomiting and visual changes

79
Q

Triggers for a migraine

A

Cheese, caffeine, alcohol, menstruation, oral contraceptives, anxiety, travel, exercise

80
Q

Symptoms and signs

A

Aura - lasting 5-60 minutes, visual = flashing, jagged lines, hemianopia, sensory = paraesthesia, numbness, motor
Classic features - moderate to severe headache, unilateral pulsatile throbbing aggravated by movement, nausea + vomiting, photophobia

81
Q

Differential diagnosis for migraine

A

Tension headache, cluster headache

82
Q

Investigations for migraine

A

Clinical diagnosis
CRP, ESR,
LP

83
Q

Management for migraine

A

Reduce triggers - e.g. dietary factors

Oral triptan - sumatriptan + NSAIDs/paracetamol

84
Q

Prophylaxis for a migraine

A

Propanolol/topiramate

Consider amitriptyline

85
Q

Define cluster headache

A

‘Migraineous neuralgia’ - rapid onset, excruciating unilateral pain around one eye, typically wakes the patient from sleep
Occurs in clusters of 1-2x a day, lasting 5-12 weeks, followed by pain free periods of months-years

86
Q

Risk factors for cluster headache

A

Male: Female = 5:1

Smoking

87
Q

Signs and symptoms for cluster headache

A

Pain around one eye
Lasts 15-60 minutes
Wakes patient from sleep
Watery and bloodshot eye, lid swelling, lacrimation, facial flushing, rhinorrhoea, miosis + ptosis

88
Q

Investigations for cluster headache

A

Clinical diagnosis

89
Q

Management for cluster headache

A

100% 15 O2

Sumatriptan or Zolmitriptan

90
Q

Prophylaxis for cluster headache

A

Verapamil
Avoid alcohol
Prednisoline may help

91
Q

Define trigeminal neuralgia

A

Paroxysms of instense, debilitating pain in the distribution of the trigeminal nerve

92
Q

Pathophysiology of trigeminal neuralgia

A

Compression of trigeminal nerve causing demyelination and excitation of the trigeminal nerve

93
Q

Risk factors for trigeminal neuralgia

A

Hypertension

94
Q

Signs and symptoms of trigeminal neuralgia

A

Sudden, unilateral, paroxysms of knife-like/electric shock like pain
Starts in mandibular divison, spreading upwards to maxillary and ophthalmic divisions, lasts seconds to minutes

95
Q

Triggers for trigeminal neuralgia

A

Shaving, eating, talking, vibration, exposure to cold wind

96
Q

Differential diagnosis for trigeminal neuralgia

A

Temporal arteritis

Multipel sclerosis

97
Q

Investigations for trigeminal neuralgia

A

MRI

98
Q

Management for trigeminal neuralgia

A

Carbamazepine
Others: Gabapentin, lamotrigine, phenytoin
Percutaneous procedures: Rhizotomy
Surgical: Neurovascular decompression

99
Q

Pathophysiology of Giant Cell Arteritis

A

Inflammatory granulomatous vasculitis of large cerebral arteries

100
Q

Risk factors for giant cell arteritis

A

Male

>50 years

101
Q

Signs and symptoms for giant cell arteritis

A

Temporal pulsating headache
Scalp tenderness (when combing/washing hair)
Jaw claudication (jaw pain on eating)
Amaurosis fugax (sudden blindness)
Tender, thickened, pulseless or nodular temporal artery
Fever, fatigue, breathlessness, myalgia, morning stiffness

102
Q

Investigations for giant cell arteritis

A

ESR raised

Temporal artery biopsy

103
Q

Management for giant cell arteritis

A

Prednisolone

104
Q

Complications of giant cell arteritis

A

Polymyalgia rheumatica

105
Q

Define encephalitis

A

Infection and inflammation of the brain parenchyma

106
Q

Pathophysiology of encephalitis

A

Disease which mostly affected the frontal and temporal lobes, so causes decreased consciousness, confusion and focal signs

107
Q

Causes of encephalitis

A

Viral infection
Herpes simplex virus
Varicella zoster virus, EBV, CMV, HIV, mumps, measles
Non viral: TB, toxoplasma, malaria, listeria

108
Q

Risk factors for encephalitis

A

Extremes of age

Immunocompromised patients

109
Q

Signs and symptoms for encephalitis

A

Fever, headache, myalgia, fatigue, nausea

Decreased consciousness, confusion, seizures, coma

110
Q

Differential diagnosis for encephalitis

A

Meningitis, stroke, brain tumour

111
Q

Investigations for encephalitis

A 
Lumbar puncture + CSF studies (increase in protein level, decreased glucose)
FBC
Throat swabs, stool culture
CT/MRI scan
EEG
112
Q

Management for encephalitis

A

Viral - Acyclovir

113
Q

Define Huntington’s disease

A

An autosomal dominant, progressive neurodegenerative disorder

114
Q

Pathophysiology of Huntington’s

A

Autosomal dominant
Mutation in chromosome 4, repeated expression of CAG
Cerebral atrophy with loss of neurones in the caudate nucleus and putamen of the basal ganglia
Decreased ACh synthesis and GABA in striatum

115
Q

Signs and symptoms of Huntington’s

A

Prodrome
Chorea - jerky, explosive, figidity movements
Rigidity, writhing and abnormal posture
Dysarthria, dysphagia and abnormal eye movements
Behavioural change - aggression, addictive behaviour, depression/anxiety
Dementia
Seizures
Clonus

116
Q

Investigations for Huntington’s

A

Diagnosis is clinical
CT/MRI
Genetic testing

117
Q

Management for Huntington’s

A

No treatment to prevent progression

Management of chorea = benzodiazepines, valproic acid

118
Q

Define motor neurone disease

A

A sporadic or hereditary disease affecting upper and/or lower motor neurones - characterised by progressive degeneration of motor neurone in the spinal cord (anterior horn), cranial nerve motor nuclei and within the cortex

119
Q

Risk factors for motor neurone disease

A

Genetic

120
Q

Upper motor neurone signs

A

Weakness
Hypertonia
Upgoing plantars (positive Babinski)
Clonus

121
Q

Low motor neuron signs

A 
Weakness
Depressed/absent reflexes
Decreased tone
Wasting
Fasciculations
122
Q

Name the four types of MND

A

Amyotrophic lateral sclerosis (ALS)
Primary lateral sclerosis (PLS)
Progressive muscular atrophy (PMA)
Progressive bulbar palsy (PBP)

123
Q

Investigations for MND

A

Clinical findings

Nerve conduction studies

124
Q

Management for MND

A

Riluzole - not a cure, extends life by 3 months
MDT approach
Baclofen for spasms

125
Q

Define multiple sclerosis

A

A chronic inflammatory disorder of the central nervous system associated with progressive disability

126
Q

Risk factors for multiple sclerosis

A

EBV
MMR
Higher prevalence in the north and south hemispheres - lowest rates around the equator

127
Q

Pathophysiology of multiple sclerosis

A

Immune-mediated demyelination at multiple CNS sites occurs as discrete plaques. Thought to be T-cell mediated: T-cells activate B cells to produce auto-antibodies against myelin. Repeat demyelination leads to axonal loss and incomplete recovery between attacks

128
Q

Name the subtypes of multiple sclerosis

A

Relapsing-remitting (80%)
Secondary progressive
Primary progressive

129
Q

Symptoms and signs of multiple sclerosis

A

Unilateral optic neuritis, diplopia, ataxia, vertigo, bladder/sexual dysfunction, fatigue, UMN signs
Symptoms worsen with heat/exercise - Uhthoff’s phenomenon

130
Q

Investigations for multiple sclerosis

A

Electrophysiology - delayed nerve conduction studies suggests demyelination
MRI
Lumbar puncture - increased protein, OLIGOCLONAL bands of increased immunoglobulin concentration
>2 CNS lesions disseminated in time and space

131
Q

Management for multiple sclerosis

A

Oral methylprednisolone

Natalizumab

132
Q

Risk factors for brain tumours

A

Family history
Exposure to ionising radiation
Immunosuppression

133
Q

Types of tumours

A

High grade - Gliomas (astrocytomas or oligodendromas)
Low grade - Meningioma (benign), neurofibromas, pituitary tumour, pineal tumour
Metastases

134
Q

Where can a tumour metastasis from

A

lung, breast, prostate, colorectal, melanoma and kidney

135
Q

Signs and symptoms of tumours

A

Increased ICP
Nausea and vomiting
Seizures
Personality change, confusion, papilloedema

136
Q

Investigations for tumours

A

CT or MRI scan

137
Q

Management for tumours

A

Neurosurgery

138
Q

Where is the most common site for disc herniation

A

L4/L5

139
Q

What is spinal cord compression

A

Myelopathy with UMN signs

140
Q

What is spinal root compression

A

Radiculopathy with LMN signs

141
Q

Causes of spinal cord compression

A

Secondary malignancy
Disc herniation
Intervertebral disc prolapse

142
Q

Investigations for spinal cord compression

A

MRI - gold standard

143
Q

Management for spinal cord compression

A

Neurosurgery

Epidural steroid injection

144
Q

Signs and symptoms at L5/S1

A

SCIATICA

Sensory loss/pain - back of thigh, leg, lateral aspect of little toe

145
Q

Signs and symptoms at L4/L5

A

Sensory loss/pain - lateral thigh/lateral leg

146
Q

Pathophysiology of cauda equina syndrome

A

Nerve root compression caudal to the termination of the spinal cord
Usually large central disc herniation at L4/L5 or L5/S1 levels

147
Q

Causes of cauda equina syndrome

A

Disc herniation
Tumours/metastasis
Trauma
Congenital e.g. spinal bifida

148
Q

Signs and symptoms of cauda equina syndrome

A 
Bilateral/unilateral pain in legs
Vairable leg weakness
Saddle anaesthesia
Poor anal tone
Erectile dysfunction
Bladder/bowel dysfunction
149
Q

Investigations for cauda equina syndrome

A

MRI

150
Q

Management for cauda equina syndrome

A

Neurosurgery - MEDICAL EMERGENCY

Phase 3A (10 decks)

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