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fourth year > medicine 4 > Flashcards

medicine 4 Flashcards

1
Q

cerebrovascular incidents are

A

ischaemia or intracranial haemorrhage

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2
Q

TIA is defined as

A

symptoms of a stroke that resolve within 24 hours

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3
Q

a crescendo TIA refers too

A

two or more TIAS in a week

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4
Q

presentation of a TIA

A

Sudden weakness of limbs
Sudden facial weakness
Sudden onset dysphasia (speech disturbance)
Sudden onset visual or sensory loss

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5
Q

how to quickly identify a stroke in community

A

F – Face
A – Arm
S – Speech
T – Time (act fast and call 999)

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6
Q

ABCD2 for for patients with a TIA consists of

A

A – Age (> 60 = 1)
B – Blood pressure (> 140/90 = 1)
C – Clinical features (unilateral weakness = 2, dysphasia without weakness = 1)
D – Duration (> 60 = 2, 10 – 60 = 1, < 10 = 0)
D – Diabetes = 1

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7
Q

management of stroke

A

Admit patients to a specialist stroke centre
Exclude hypoglycaemia
Immediate CT brain to exclude primary intracerebral haemorrhage
Aspirin 300mg stat (after the CT) and continued for 2 weeks

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8
Q

with a stroke, once a CT scan has ruled out an intracranial haemorrhage what treatment can be used?

A

Thrombolysis with alteplase

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9
Q

what role does alteplase have

A

tissue plasminogen activator

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10
Q

what is the gold standard for vascular territory for stroke

A

diffusion weighted MRI

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11
Q

what investigation can assess carotid stenosis

A

carotid US

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12
Q

secondary prevention of stroke

A

Clopidogrel 75mg once daily (alternatively dipyridamole 200mg twice daily)
Atorvastatin 80mg should be started but not immediately
Carotid endarterectomy or stenting in patients with carotid artery disease
Treat modifiable risk factors such as hypertension and diabetes

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13
Q

presentation of an intracranial bleed

A

Sudden onset headache

Seizures
Weakness
Vomiting
Reduced consciousness
Other sudden onset neurological symptoms
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14
Q

glasgow coma score for eyes

A 
Spontaneous = 4
Speech = 3
Pain = 2
None = 1
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15
Q

Glasgow coma score for verbal response

A 
Orientated = 5
Confused conversation = 4
Inappropriate words = 3
Incomprehensible sounds = 2
None = 1
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16
Q

Glasgow coma score for motor response

A 
Obeys commands = 6
Localises pain = 5
Normal flexion = 4
Abnormal flexion = 3
Extends = 2
None = 1
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17
Q

subdural haemorrhage is caused by

A

rupture of bridging veins between the dura mater and arachnoid mater

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18
Q

extradural haemorrhage is caused by

A

rupture of the middle meningeal artery

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19
Q

rupture of the middle meningeal artery is associated with a fracture with

A

temporal bone

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20
Q

on Ct scan an extradural haemorrhage appears as

A

bi-convex shape

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21
Q

a cerebral aneurysm usually bleeds into

A

the subarachnoid space

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22
Q

the sub arachnoid space exists between

A

the pia mater and the arachnoid mater

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23
Q

what headache is associated with a subarachnoid haemorrhage

A

thunderclap

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24
Q

features of a thunderclap headache

A

Neck stiffness
Photophobia
Vision changes
Neurological symptoms such as speech changes, weakness, seizures and loss of consciousness

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25
Q

CSF signs of a SAH

A

red cell count and xathochromia

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26
Q

Ix of SAH

A

lumbar puncture, angiography, CT

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27
Q

surgical interventions for SAH

A

coiling the vessel or clipping

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28
Q

medical treatments for SAH

A

nimodipine is a Calcium channel blocker that can prevent vasospasms, lumbar puncture for hydrocephalus or antiepilpetics for seizures.

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29
Q

Multiple sclerosis typically only affects

A

central nervous system’s myelin sheaths (oligodrendrocytes)

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30
Q

a key expression to describe the pathology of MS lesions is

A

disseminated in time and space

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31
Q

signs/symptoms of MS eye disease

A

optic neuritis - loss of vision in one eye
double vision due to sixth cranial nerve palsy that can either be:
unilateral internuclear ophthalmoplegia
or
conjugate lateral gaze disorder (when looking laterally won’t be able to abduct)

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32
Q

general symptoms of MS

A 
focal weakness (incontinence, limb paralysis) 
focal sensory (trigeminal neuralgia, numbness, paraethesia)
Ataxia (sensory or cerebellar)
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33
Q

Lhermitte’s sign refers too

A

electric shock sensation travels down the spine and into the limbs when flexing the neck. It indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column.

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34
Q

sensory ataxia refers too

A

loss of the proprioceptive sense,

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35
Q

cerebellar ataxia refers too

A

coordination problems

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36
Q

Dx of MS

A

MRI scans can demonstrate typical lesions

Lumbar puncture can detect “oligoclonal bands” in the cerebrospinal fluid (CSF)

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37
Q

optic neuritis presentation

A

Central scotoma. This is an enlarged blind spot.
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect

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38
Q

relapse treatment for MS consists of

A

methylprednisolone:

500mg orally daily for 5 days

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39
Q

MS spasticity may be treated through

A

baclofen, gabapentin and physiotherapy

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40
Q

most common form of motor neurone disease is

A

Amylotropic lateral sclerosis (AML)

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41
Q

pathophysiology of motor neurone disease

A

progressive degeneration of both upper and lower motor neurones. The sensory neurones are spared.

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42
Q

presentation of motor neurone disease

A

insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech. The weakness is often first noticed in the upper limbs. There may be increased fatigue when exercising. They may complain of clumsiness, dropping things more often or tripping over. They can develop slurred speech (

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43
Q

lower motor neurone signs

A

Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes

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44
Q

upper motor neurone signs

A

Increased tone or spasticity
Brisk reflexes
Upgoing plantar responses

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45
Q

medication that may be used in motor neurone disease

A

Riluzole, may slow the progression

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46
Q

pathophysiology of parkinsons

A

basal ganglia are a group of structures situated in the middle of the brain. They is responsible for coordinating habitual movements. Part of the basal ganglia called the substantia nigra produces a neurotransmitter called dopamine. Dopamine is essential for the correct functioning of the basal ganglia. In Parkinson’s disease, there is a gradual but progressive fall in the production of dopamine.

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47
Q

classic triad of parkinsons is

A

Resting tremor
Rigidity
Bradykinesia

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48
Q

presentation of Parkinsons

A

unilateral tremor (pill rolling tremor)
cogwheel rigidity
bradykinesia (shuffling gait, hypomimia, difficulty initiating movement)
depression, postural instability, loss of smell, sleep disturbance and cognitive impairment

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49
Q

hypomimia refers too

A

reduced facial movements and expressions

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50
Q

Parkinson’s tremor features

A 
asymmetrical 
4-6Hz
worse at rest
improves with intentional movement
no change with alcohol
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51
Q

benign essential tremor features

A

symmetrical, 5-8Hz, improves with rest, worse with intentional movements,, improves with alcohol

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52
Q

Dementia with Lewy Bodies features

A

parkinsons, visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness.

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53
Q

levodopa is

A

synthetic dopamine

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54
Q

levodopa in parkinsons is usually given alongside

A

peripheral decarboxylase inhibitors. Examples are carbidopa and benserazide.

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55
Q

SE of dopamine Tx

A

dystonia, chorea and athetosis

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56
Q

COMT inhibitors example and pharmacology

A

entacapone. These are inhibitors of catechol-o-methyltransferase (COMT). The COMT enzyme metabolises levodopa in both the body and brain

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57
Q

examples of dopamine agonists are

A

Bromocryptine
Pergolide
Carbergoline

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58
Q

Monoamine Oxidase-B Inhibitors pharmacology

A

Monoamine oxidase enzymes break down neurotransmitters such as dopamine, serotonin and adrenaline. The monoamine oxidase-B enzyme is more specific to dopamine

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59
Q

examples of monoamine oxidase B inhibitors are

A

Selegiline

Rasagiline

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60
Q

differentials for a tremor include

A 
Parkinson’s disease
Multiple sclerosis
Huntington’s Chorea
Hyperthyroidism
Fever
Medications (e.g. antipsychotics)
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61
Q

Ix for epilepsy

A

EEG, MRI, ECG

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62
Q

generalised tonic clonic seizure description/presentation.

A

tonic (muscle tensing) and clonic (muscle jerking) episodes. Typically the tonic phase comes before the clonic phase. There may be associated tongue biting, incontinence, groaning and irregular breathing.

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63
Q

describe the post ictal phase of a generalised tonic clonic seizure

A

confused, drowsy and feels irritable or depressed.

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64
Q

Mx of generalised tonic clonic seizure is

A

First line: sodium valproate

Second line: lamotrigine or carbamazepine

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65
Q

focal seizure start in the

A

temporal lobe

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66
Q

focal seizures presentation

A

Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot

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67
Q

Tx for focal seizures include

A

First line: carbamazepine or lamotrigine

Second line: sodium valproate or levetiracetam

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68
Q

absence seizure presentation

A

children who becomes blank, stares into space and then abruptly returns to normal. During the episode they are unaware of their surroundings and won’t respond. These typically only lasts 10-20 seconds.

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69
Q

Tx of absence seizure includes

A

First line: sodium valproate or ethosuximide

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70
Q

atonic seizure presentation

A

drop attacks”. They are characterised by brief lapses in muscle tone. These don’t usually last more than 3 minutes.

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71
Q

Tx for atonic seizures are

A

First line: sodium valproate

Second line: lamotrigine

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72
Q

myoclonic seizure presentation

A

sudden brief muscle contractions, like a sudden “jump”. The patient usually remains awake during the episode.

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73
Q

Tx for myoclonic seizures

A

First line: sodium valproate

Other options: lamotrigine, levetiracetam or topiramate

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74
Q

infantile spasms are also known as

A

West syndrome

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75
Q

west syndrome Tx

A

prednisolone or vigabatrin

76
Q

sodium valproate targets

A

increasing activity of GABA

77
Q

SE of sodium valproate

A

Teratogenic so patients need careful advice about contraception
Liver damage and hepatitis
Hair loss
Tremor

78
Q

carbamazepine side effects are

A

Agranulocytosis
Aplastic anaemia
Induces the P450 system so there are many drug interactions

79
Q

phenytoin SE

A 
Folate and vitamin D deficiency
Megaloblastic anaemia (folate deficiency)
Osteomalacia (vitamin D deficiency)
80
Q

SE of ethosuximide

A

Night terrors

Rashes

81
Q

SE of lamotrigine

A

Stevens-Johnson syndrome or DRESS syndrome. These are life threatening skin rashes.
Leukopenia

82
Q

status epilepticus is defined as

A

seizure lasting more than 5 minutes

83
Q

management of status epilepticus in hospital

A

Secure the airway
Give high-concentration oxygen
Assess cardiac and respiratory function
Check blood glucose levels
Gain intravenous access (insert a cannula)
IV lorazepam 4mg, repeated after 10 minutes if the seizure continues
If seizures persist: IV phenobarbital or phenytoin

84
Q

Tx of status epilepticus in the community

A

Buccal midazolam

Rectal diazepam

85
Q

features of neuropathic pain

A 
Burning
Tingling
Pins and needles
Electric shocks
Loss of sensation to touch of the affected area
86
Q

what are the four first line treatments for neuropathic pain

A

Amitriptyline is a tricyclic antidepressant
Duloxetine is an SNRI antidepressant
Gabapentin is an anticonvulsant
Pregabalin is an anticonvulsan

87
Q

first line treatment for trigeminal neuralgia

A

carbamazepine

88
Q

facial nerve pathway

A

brainstem at the cerebellopontine angle. On its journey to the face it passes through the temporal bone and parotid gland.

89
Q

facial nerve supplies

A 
Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical
90
Q

three functions of the facial nerve

A

motor, sensory and parasympathetic.

91
Q

facial nerve motor supplies

A

muscles of facial expression, the stapedius in the inner ear and the posterior digastric, stylohyoid and platysma muscles in the neck.

92
Q

facial nerve sensory supplies

A

taste from the anterior 2/3 of the tongue.

93
Q

facial nerve parasympathetic supplies the

A

submandibular and sublingual salivary glands and the lacrimal gland

94
Q

upper motor neurone facial palsy should require

A

urgent referral with suspected stroke

95
Q

facial upper motor neurone sign is

A

forehead will be spared and the patient can move their forehead on the affected side.

96
Q

in a facial lower motor neurone lesion the sign is

A

forehead will NOT be spared and the patient cannot move their forehead on the affected side.

97
Q

bilateral upper motor neurone lesions can occur in

A

Pseudobulbar palsies

Motor neurone disease

98
Q

bells palsy is

A

idiopathic lower motor neurone facial nerve palsy

99
Q

Tx for bell’s palsy

A

prednisolone as treatment, either:

50mg for 10 days
60mg for 5 days followed by a 5 day reducing regime of 10mg a day
Patients also require lubricating eye drops

100
Q

Ramsay-Hunt syndrome is caused by the

A

herpes zoster virus

101
Q

Ramsay-Hunt syndrome presents as

A

unilateral lower motor neurone facial nerve palsy with stereotypically have a painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side. This rash can extend to the anterior 2/3 of the tongue and hard palate.

102
Q

Tx for ramsay hunt syndrome

A

Prednisolone
Aciclovir
Patients also require lubricating eye drops.

103
Q

initial presentation of a brain tumour may be

A

raised intracranial pressure or focal neuro symptoms

104
Q

a patient that has had an unusual change in personality and behaviour. This indicates a tumour

A

frontal lobe

105
Q

key fundoscopy finding for raised intracranial pressure

A

papilloedema

106
Q

presentation of raised intracranial pressure

A 
Constant
Nocturnal
Worse on waking
Worse on coughing, straining or bending forward
Vomiting
107
Q

other features of raised intracranial pressure includes

A 
Altered mental state
Visual field defects
Seizures (particularly focal)
Unilateral ptosis
Third and sixth nerve palsies
Papilloedema (on fundoscopy)
108
Q

papilloedema specifically refers too

A

CSF under high pressure to flow into the optic nerve sheath as the sheath is connected with the subarachnoid space.

109
Q

common sites of metastases for brain tumours

A

Lung
Breast
Colorectal
Prostate

110
Q

gliomas are tumours of the

A

glial cells

111
Q

most common glioma is

A

astrocytoma (glioblastoma multiforme)

112
Q

pituitary tumours cause what visual defect

A

bitemporal hemianopia

113
Q

Acoustic neuromas are tumours of the

A

Schwann cells surrounding the auditory nerve

114
Q

acoustic tumours occur at the

A

cerebellopontine angle

115
Q

unilateral acoustic neuromas are associated with

A

neurofibromatosis type 2.

116
Q

symptoms of acoustic neuroma are

A

Hearing loss
Tinnitus
Balance problems
They can also be associated with a facial nerve palsy.

117
Q

huntington’s chorea inheritance

A

autosomal dominant

118
Q

what disorder is huntington’s chorea specifically (mutation)

A

“trinucleotide repeat disorder” that involves a genetic mutation in the HTT gene on chromosome 4.

119
Q

huntington’s chorea displays what genetic characteristic

A

nticipation is a feature of trinucleotide repeat disorders. This is where successive generations have more repeats in the gene, resulting in:

Earlier age of onset
Increased severity of disease

120
Q

presentation of huntington’s chorea is

A

insidious, progressive worsening of symptoms. It typically begins with cognitive, psychiatric or mood problems. These are followed by the development of movement disorders.

Chorea (involuntary, abnormal movements)
Eye movement disorders
Speech difficulties (dysarthria)
Swallowing difficulties (dysphagia)

121
Q

medications that can be used to supress disordered movement

A

Antipsychotics (e.g. olanzapine)
Benzodiazepines (e.g. diazepam)
Dopamine-depleting agents (e.g. tetrabenazine)

122
Q

myasthenia gravis is an

A

autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.

123
Q

myasthenia gravis has a strong link with

A

thymoma, tumours of the thymus

124
Q

what neurotransmitter is sued at neuromuscular junctions?

A

acetylcholine

125
Q

myasthenia gravis pathology

A

acetylcholine receptor antibodies bind to post synaptic receptors preventing stimulation leading to less effective stimulation with increased activity.

126
Q

what other complications are there of acetylcholine receptor antibodies inappropriately binding

A

activation of the complement system damaging the post synaptic membrane

127
Q

are there any other autoantibodies implicated in myasthenia gravis

A

antibodies against muscle-specific kinase (MuSK) and antibodies against low-density lipoprotein receptor-related protein 4 (LRP4). MuSK and LRP4 and important proteins for the creation and organisation of the acetylcholine receptor

128
Q

presentation of myasthenia gravis is

A

affects the proximal muscles and small muscles of the head and neck. It leads to:

Extraocular muscle weakness causing double vision (diplopia)
Eyelid weakness causing drooping of the eyelids (ptosis)
Weakness in facial movements
Difficulty with swallowing
Fatigue in the jaw when chewing
Slurred speech
Progressive weakness with repetitive movements

129
Q

examination for myasthenia gravis points

A

Repeated blinking will exacerbate ptosis
Prolonged upward gazing will exacerbate diplopia on further eye movement testing
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
Check for a thymectomy scar.

Test the forced vital capacity (FVC).

130
Q

diagnosis of myasthenia gravis is with

A

autoantibodies (ACh-R), CT/MRI or edophonium test

131
Q

edrophonium test involves

A

IV dose of edrophonium chloride (or neostigmine). Normally, cholinesterase enzymes in the neuromuscular junction break down acetylcholine. Edrophonium block these enzymes and stop the breakdown of acetylcholine. As a result the level of acetylcholine at the neuromuscular junction increases. It briefly and temporarily relieves the weakness.

132
Q

Tx for myasthenia gravis

A

Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine), immunosuppression with prednisolone or azathioprine
thymectomy
rituximab or eculizumab

133
Q

myasthenic crisis can lead too

A

respiratory failure as a result of weakness in the muscle of respiration.

134
Q

myasthenic crisis requires

A

non-invasive ventilation, BiPAP, intubation and ventilation as well as immunomodulatory therapies such as IV immunoglobulins and plasma exchange.

135
Q

Lambert-Eaton syndrome typically occurs in patients with

A

small cell lung cancer

136
Q

the autoantibodies in lambert eaton syndrome target

A

voltage-gated calcium channels present in small cell lung cancer and presynaptic terminals of the NMJ

137
Q

presentation of lambert Eaton syndrome is

A

proximal muscle weakness. It most notably presents with proximal leg muscle weakness. It can also affect the intraocular muscles causing double vision (diplopia), the levator muscles in the eyelid causing eyelid drooping (ptosis) and the oropharyngeal muscles causing slurred speech and swallowing problems (dysphagia). Patients may also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

138
Q

what key sign may be elicited in lambert eaton syndrome

A

patient can maximally contract the quadriceps muscle for a period, then have their reflexes tested immediately afterwards, and display an improvement in the response. This is called post-tetanic potentiation.

139
Q

Tx for lambert eaton syndrome

A

amifampridine, Immunosuppressants (e.g. prednisolone or azathioprine)
IV immunoglobulins
Plasmapheresis

140
Q

amifampridine mechanism

A

blocking voltage-gated potassium channels in the presynaptic cells, which in turn prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action.

141
Q

Charcot-Marie-Tooth disease effects

A

the peripheral motor and sensory nerves.

142
Q

Charcot-Marie-Tooth inheritance is

A

autosomal dominant

143
Q

classical features of charcot marie tooth

A

High foot arches (pes cavus)
Distal muscle wasting causing “inverted champagne bottle legs”
Weakness in the lower legs, particularly loss of ankle dorsiflexion
Weakness in the hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

144
Q

causes of peripheral neuropathy

A 
A – Alcohol
B – B12 deficiency
C – Cancer and Chronic Kidney Disease
D – Diabetes and Drugs (e.g. isoniazid, amiodarone and cisplatin)
E – Every vasculitis
145
Q

guillain barre syndrome is an

A

“acute paralytic polyneuropathy”

146
Q

pathophysiology of guillain barre is with

A

molecular mimicry. The B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection. These antibodies also match proteins on the nerve cells. They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon.

147
Q

presentation of guillain barre is

A

Symmetrical ascending weakness (starting at the feet and moving up body)
Reduced reflexes
There may be peripheral loss of sensation or neuropathic pain
It may progress to the cranial nerves and cause facial nerve weakness

148
Q

diagnosis of guillain barre is through

A

Nerve conduction studies (reduced signal through the nerves)

Lumbar puncture for CSF (raised protein with a normal cell count and glucose)

149
Q

guillain barre syndrome Tx

A

IV immunoglobulins
Plasma exchange
Supportive care
VTE prophylaxis (pulmonary embolism is a leading cause of death)
In severe cases with respiratory failure patients may need intubation, ventilation and admission to the intensive care unit.

150
Q

neurofibromatosis causes

A

nerve tumours (neuromas) to develop throughout the nervous system. These tumours are benign,

151
Q

NF1 gene is found on chromosome

A

17

152
Q

NF1 codes for

A

neurofibromin, which is a tumour suppressor protein

153
Q

NF1 inheritance is through

A

autosomal dominant

154
Q

criteria for NF1

A

C – Café-au-lait spots (6 or more) measuring ≥ 5mm in children or ≥ 15mm in adults
R – Relative with NF1
A – Axillary or inguinal freckles
BB – Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules) (2 or more) are yellow brown spots on the iris
N – Neurofibromas (2 or more) or 1 plexiform neurofibroma
G – Glioma of the optic nerve

155
Q

Dx of NF1

A

genetic testing, x-rays, CT/MRI

156
Q

complications of NF1

A

Migraines
Epilepsy
Renal artery stenosis causing hypertension
Malignant peripheral nerve sheath tumours
Gastrointestinal stromal tumour
leukaemia

157
Q

NF2 is found on chromosome

A

22

158
Q

NF2 codes for

A

merlin protein, a tumour suppressor

159
Q

NF2 inheritance is

A

autosomal dominant

160
Q

NF2 leads particularly too

A

schwannoma

161
Q

Bilateral acoustic neuromas almost certainly indicate

A

neurofibromatosis type 2.

162
Q

tuberous sclerosis characteristically leads to the development of

A

hamartomas

163
Q

tuberous sclerosis is caused by mutations in on of two genes

A

TSC1 gene on chromosome 9, which codes for hamartin

TSC2 gene on chromosome 16, which codes for tuberin

164
Q

how does hamartin and tuberin interact

A

to control the size and growth of cells.

165
Q

skin signs of tuberous sclerosis

A

ash leaf spots, shagreen patches, angiofibromas, subungual fibromata, cafe au lait spots and poliosis

166
Q

Ash leaf spots are

A

depigmented areas of skin shaped like an ash leaf

167
Q

Shagreen patches are

A

thickened, dimpled, pigmented patches of skin

168
Q

Angiofibromas

A

small skin coloured or pigmented papules that occur over the nose and cheeks

169
Q

Subungual fibromata are fibromas growing from

A

the nail bed. They are usually circular painless lumps that grow slowly and displace the nail

170
Q

Cafe-au-lait spots are

A

light brown “coffee and milk” coloured flat pigmented lesions on the skin

171
Q

Poliosis is an

A

isolated patch of white hair on the head, eyebrows, eyelashes or beard

172
Q

neuro features of tuberous sclerosis

A

Epilepsy

Learning disability and developmental delay

173
Q

other features of tuberous sclerosis is

A

Rhabdomyomas in the heart
Gliomas (tumours of the brain and spinal cord)
Polycystic kidneys
Lymphangioleimyomatosis (abnormal growth in smooth muscle cells, often affecting the lungs)
Retinal hamartomas

174
Q

Trigeminal Neuralgia presents with

A

intense facial pain that comes on spontaneously and last anywhere between a few seconds to hours. It is often described as an electricity-like shooting pain. Attacks often worsen over time.

175
Q

Tx for trigeminal neuralgia is with

A

carbamazepine, followed by surgery to decompress if unsuccessful

176
Q

typical migraine features

A 
Moderate to severe intensity
Pounding or throbbing in nature
Usually unilateral but can be bilateral
Discomfort with lights (photophobia)
Discomfort with loud noises (phonophobia)
With or without aura
Nausea and vomiting
177
Q

aura in migraine refers too

A

Sparks in vision
Blurring vision
Lines across vision
Loss of different visual fields

178
Q

Hemiplegic migraines can mimic

A

stroke

179
Q

features of hemiplegic stroke

A 
Typical migraine symptoms
Sudden or gradual onset
Hemiplegia (unilateral weakness of the limbs)
Ataxia
Changes in consciousness
180
Q

5 stages of migraine include

A

Premonitory or prodromal stage (can begin 3 days before the headache)
Aura (lasting up to 60 minutes)
Headache stage (lasts 4-72 hours)
Resolution stage (the headache can fade away or be relieved completely by vomiting or sleeping)
Postdromal or recovery phase

181
Q

acute management of a migraine is with

A

Paracetamol
Triptans (e.g. sumatriptan 50mg as the migraine starts)
NSAIDs (e.g ibuprofen or naproxen)
Antiemetics if vomiting occurs (e.g. metoclopramide)

182
Q

triptan mechanism is

A

5HT receptors agonists (serotonin receptor agonists).

183
Q

migraine prophylaxis is with

A

Propranolol
Topiramate (this is teratogenic and can cause a cleft lip/palate so patients should not get pregnant)
Amitriptyline

184
Q

symptoms of a cluster headache is

A

Symptoms are typically all unilateral:

Red, swollen and watering eye
Pupil constriction (miosis)
Eyelid drooping (ptosis)
Nasal discharge
Facial sweating
185
Q

acute management of a cluster headache is with

A

Triptans (e.g. sumatriptan 6mg injected subcutaneously)

High flow 100% oxygen for 15-20 minutes (can be given at home)

186
Q

prophylaxis with cluster headaches is with

A

Verapamil
Lithium
Prednisolone (a short course for 2-3 weeks to break the cycle during clusters)

187
Q

30-50 year old male smoker. Attacks can be triggered by things like alcohol, strong smells and exercise. suffer 3 – 4 attacks a day for weeks or months followed by a pain free period lasting 1-2 years. Attacks last between 15 minutes and 3 hours. what is the diagnosis?

A

cluster headache

fourth year (12 decks)

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