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Phase 2a Ru > Neuro > Flashcards

Neuro Flashcards

1
Q

% split between ICA and vertabral artery for TIA

A

90% ICA
10% Vertabral

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2
Q

What evaluates stroke risk in patients with af

A

CHA2DS2-VASc

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3
Q

ACA affected in TIA Sx

A

Weak numb contralateral leg

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4
Q

MCA affected in TIA Sx

A

Weak numb contralateral side of the body, face drooping with forehead spared, dysphasia

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5
Q

PCA affected in TIA Sx

A

Vision loss (contralateral homonymous hemianopia w/ macular sparing)

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6
Q

Vertebral artery affected in TIA Sx

A

Cerebellar syndrome
CN lesions 3-12
Sensory + motor ataxia

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7
Q

How can you assess someone’s proprioception

A

Romberg test

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8
Q

Wha tool is used to recognition of a stoke in emergency room

A

ROSIER

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9
Q

Treatment for TIA

A

Acutley:- Apirin 300mg
Prophylaxis long term:- Clopidogrel+ Atorvastatin

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10
Q

% split between haemorrhagic and ischemic stroke

A

85% Ischaemic
Haemorrhagic 15%

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11
Q

What is pronator drift

A

In stroke patients ask the patient to lift their arms to the ceiling, pronator take over. Arm on affected will pronate + palms face down

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12
Q

What is a crescendo TIA

A

Two or more TIA’s in a week

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13
Q

Gold standard investigation for stroke

A

Diffusion-weighted MRI
NCCT head if not possible

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14
Q

What is a lacunar stroke

A

Most common type of ischemic stroke. Blockage of lenticulostriate Arteries that supply the deep brain structures

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15
Q

Treatment for ischemic stroke

A

Presents within 4.5hours clot-buster- Alteplase IV
Aspirin 300 mg 2 weeks
Lifelong clopidogrel 75mg
Thrombectomy

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16
Q

Treatment for haemorrhagic stroke

A

Neurosurgery referral
IV mannitol for raised ICP
Atorvastatin, ramipril prophylaxis

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17
Q

Examples of primary headache

A

Migraine
Cluster
Tension
Drug overdose

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18
Q

Causes of secondary headache

A

Infection
Trauma
Cerebrovascular disease

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19
Q

What is a migrane

A

Episodes of recurrent throbbing headache +/- aura, often with vision change

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20
Q

Who is most at risk from a migrnae

A

Woman under 40

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21
Q

What can trigger a migraine

A

CHOCOLATE
Chocolate
Hangover
Orgasms
Cheese
Oral contraceptive
Lie ins
Alcohol
Tumult (loud noise)
Exercise

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22
Q

Describe build up to migrane

A

Prodrome:- days before attack, mood change

Aura:- minutes before headache, visual phenomena, zig-zag lines

Throbbing headache lasting 4-72hr

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23
Q

Sx of migraine

A

1< Unilateral pain, throbbing, motion-sickness, moderate to severe pain

1 of N+V, photophobia

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24
Q

Treatment for migraine

A

Acute:- Oral triptan or aspirin 900mg

Prophylaxis:- Beta-blocker (propanolol) or topiramte is athma

Consider antiemetics

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25
Q

What is a cluster headache

A

Unilateral preorbital pain with autonomic features

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26
Q

How long does a cluster headache last

A

15-160 minutes

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27
Q

What is the most disabling primary headache

A

Cluster

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28
Q

RF for cluster headache

A

Male, smoker, genetics

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29
Q

Sx of cluster headache (not autonomic)

A

Crescendo, unilateral preorbital excruciating pain, may affect temples, face flushing

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30
Q

Autonomic Sx of cluster headache

A

Conjunctival infection + lacrimation (watery bloodshot eyes)
Ptosis
Miosis (dilated unilateral pupil)
Rhinorrhoea (runny nose)

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31
Q

How many attacks to make diagnosis of cluster headache

A

5

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32
Q

Treatment for cluster headache

A

Acutely:- Triptans (sumatriptan)

Prophylaxis:- Veramaprill (CCB)

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33
Q

What is a tension headache

A

Bilateral generalised headache, radiates to kneck

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34
Q

What is the most common primary headache

A

Tension

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35
Q

Trigger for tension headache

A

Stress

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36
Q

Sx of tension headache

A

Rubber band tight around head, bilateral pain, feel it in the trapezius
Mild to moderate severity
No motion sickness, photophobia, aura

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37
Q

Treatment for tension headache

A

Simple analgesia:- Aspirin or paracetamol

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38
Q

What is trigeminal neuralgia

A

Unilateral shocking pain in 1 or more of trigeminal branches

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39
Q

RF for trigeminal neuralgia

A

Multiple sclerosis, old age, female

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40
Q

What can trigger trigeminal neuralgia

A

Eating, shaving, talking, brushing teeth

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41
Q

Sx of trigeminal neuralgia

A

Electrical shock pain in v1/v2/v3 for secs to 2 minuets

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42
Q

How many attacks for diagnosis of trigeminal neuralgia

A

3

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43
Q

Treatment for trigeminal neuralgia

A

Carbamazepine

Consider surgery

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44
Q

What is the classical presentation of giant cell arteritis

A

50 y/o Caucasian women presents with unilateral tender scalp, intermittent jaw claudication
Worst case amaurosis fugax

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45
Q

What is amaruosis fugax

A

Transient vision loss in one eye, curtain over the field of view

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46
Q

What is GS investigation for giant cell artritis
and what do you see

A

Temporal artery biopsy, big sample as many skip lesions
Granulomatous non-caseating inflammation of intima+ media w/ skip leasion

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47
Q

How would you describe the anaemia in GCA

A

Normocytic normochromic

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48
Q

Are ESR/ CRP affected in GCA

A

Yes both are raised

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49
Q

Treatment for GCA

A

Corticosteroids (prednisolone)
If any sign of amaurosis fugax/ vision change give high dose IV methylprednisolone STAT

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50
Q

Cuases of sezuire

A

VITAMIN DE
Vascular
Infection
Trauma
Autoimmune
Metabolic
Idiopathic (epilepsy)
Neoplasms
Dematia + Drugs
Eclampsia

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51
Q

RF for Epilepsy

A

Inherited
Dementia

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52
Q

Epileptic seizure vs non-epileptic

A

Epileptic:- Eyes open, Synchronous movements, can occur in sleep

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53
Q

Pathology of epileptic seizure

A

Imbalance between inhibitory GABA and excitatory glutamate

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54
Q

How long do epileptic seizures usually last

A

Less than 2 mins

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55
Q

Periods involved with epileptic seizure

A

Prodrome
Aura
Ictal Event
Post ictal period

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56
Q

2 types of generalised seizures

A

Tonic-clonic
Absenece

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57
Q

What happens in tonic-clonic seizure

A

No aura
Tonic phase:- rigidity, fall to floor
Clonic phase:- Jerking of limbs

Upgazing open eyes, incontinence, tongue biting

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58
Q

What occurs in absence seizure

A

Moments of staring blankly into space (secs to mins) then carrying on from where they left of

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59
Q

What size spike is seen on EEG in absence seizure

A

3Hz

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60
Q

What type of epilepsy is the aura period seen most commonly in

A

Temporal lobe epilepsy

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61
Q

What can happen in the aura period

A

Deja-vu + auto spasms
Lip smacking, rapid blinking

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62
Q

What can be seen in post ictal period

A

Headache, Confusion, Todd’s paralysis (if motor cortex affected), Dysphasia, amnesia, sore tongue (only in epileptic seizure not in syncope)

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63
Q

What are 2 types of focal seizure?

A

Simple focal (no loss of consciousness) and complex focal (loss of consciousness) +ve ictal period

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64
Q

Sx of focal temporal epilepsy

A

Aura, dysphasia, postictal

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65
Q

Sx of focal frontal epilepsy

A

Jacksonian march + todds palsy

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66
Q

Sx of focal parietal epilepsy

A

Paraesthesia (pins and needles)

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67
Q

Sx of occipital focal sezure

A

Vision change

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68
Q

Investigation to perform after seizure

A

EEG
CT HEAD + MRI (examine hippocampus)
Bloods:- rule out metabolic cause/ infection

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69
Q

Treatment for epilepsy

A

Sodium valproate (tetragonic)
Lamotrigine

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70
Q

Complication of epilepsy

A

Status epilepticus:- seizures lasting more than 5 minutes or back-to-back seizures

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71
Q

Treatment for status epileptics

A

Benzodiazepines; Lorazepam IV
If doesn’t work then lorazepam again then phenytoin

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72
Q

Pathology of Parkinson’s

A

Loss of dopaminergic neurons from substania nigra pars compacta

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73
Q

RF for parkinsons

A

fHx, male, older age,

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74
Q

Why does loss of dopmanigeric neurons cause Parkinsons

A

Do longer send signals to SN pars reticula, don’t send to thalamus to inhibit cortex.

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75
Q

Cardinal symptoms of parkinsons (parkinosonisum)

A

Bradykinesia, resting tremor, rigidity, postural instability

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76
Q

Other than cardinal symptoms, what seen in parkisons

A

Shuffling gait, pill-rolling thumb, cogwheel/ lead pipe forearm.

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77
Q

Is Pakinsons typically symmetrical or asymmetrical

A

Asymmetrical

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78
Q

Treat for Parkinsons

A

LDOPA+ decarboxylase inhibitor (beneldopa)

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79
Q

Problem with LDOPA

A

Works very well initially but body becomes resistant so dont want to give to early

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80
Q

Most common form of dementia

A

Alzhiemers

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81
Q

Pathological features of Alzheimers

A

Amyloid plaques (breakdown product of amyloid precursor protein) and tall neurofibrillary tangles in the cerebral cortex.
Cortical scarring + brain atrophy and decrease in Ach neurotransmitter)

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82
Q

RF for alzhimers

A

Downs:- inevitable APP gene mutation
ApoE4 allele

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83
Q

Sx of alzhimers

A

Agnosia (dont recognise)
Apraxia (cant do basic motor skills)
Aphasia (cant talk as well as normal)

Steady decline

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84
Q

How does disease progress in vascular dementia

A

Stepwise

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85
Q

Dx of vascular dementia

A

Hx of TIA/ Stroke, UMN signs and general decrease in cognition

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86
Q

Progression of lewy body dementia

A

Fast, death most common within 7 years post-diagnosis

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87
Q

Pathological features of Lewy body dementia

A

Spherical lewy body proteins (alpha-synuclein+ ubiquitin aggregates) are deposited in cortex

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88
Q

Name for parkinons before lewy bpdy dementia

A

Parkinson dementia
IF L.B.D. before Parkinsons:- lewy body dementia with parkinsonism

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89
Q

The inheritance pattern for frontotemporal dementia and which chromosome

A

Autosomal dominant, chromosome 17

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90
Q

RF for frontotemporal demetia

A

fHx
fHx of MND

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91
Q

Pathological features of frontotemporal dementia

A

Frontotemporal atrophy

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92
Q

Sx of frontotemporal dementia

A

Temporal affected:- speech and language
Frontal:- thinking + memory affected

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93
Q

What exam used in dementia

A

Mini-Mental Strae Exam
>25:-normal
18-25:- impaired
<17:- severely impaired

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94
Q

Management for dementia (non pharmacological)

A

Social stimulation, exercise

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95
Q

Pharmacological treatment for Alzheimer’s

A

Achase-I (Donedazil/ rivastigmine)

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96
Q

Pharmacological treatment for vascular dementia

A

Antihypertensives:- rampiprill

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97
Q

Inheritance pattern for Huntington’s disease

A

Autosomal dominant with full penetrance

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98
Q

What is gene abnormality in Huntington’s disorder

A

CAG repeats on chromosome 4 affecting HTT gene. The more trinucleotide repeats to early and more severe symptoms.

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99
Q

What does mutation in huntingtons lead to

A

Lack of GABA+ excessive nigrostantial pathwya

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100
Q

Number of trinucleotide repeats in Huntington’s chorea

A

<35:- no huntington
35-55:- huntongtons
60+ severe huntington

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101
Q

Sx of huntington

A

Chorea, dementia, psychiatric issues, depression

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102
Q

Management for huntington

A

Extensive counselling (inevitable symtpoms)
DA antagonist for chorea + etrabenzine

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103
Q

What type of hypersensitivity in MS

A

Type 4 vs myelin basic protein of oligodendrocytes

104
Q

RF for MS

A

Female, 20-40, autoimmune disease, fHx, EBV

105
Q

3 types of Multiple Sclerosis

A

Relapsing-Remitting MC:- Sx, incomplete recovery, Sx
Primary progressive:- Gradual deterioration
Secondary progressive:- Relapsing-remitting into primary progressive (75% or RR cases)

106
Q

What is the first presenting symptom in MS

A

Optic neuritis/ blurred vision

107
Q

Symptoms of MS

A

Paratheisa, blurred vision, uthoffs phenomenon (Sx exacerbated after heat e.g shower)

108
Q

Signs of MS

A

Optic neuritis (cant see red properly), Lhermite phenomenon (electric shock sensation with kneck flexion), charcots neurological triad
UMN signs

109
Q

What is charcots triad in nuerology

A

Dysarthria
Nystagmus
Intention tremour

110
Q

What criteria is used in the diagnosis of MS

A

McDonald’s criteria:- 2 or more attacks disseminated in time (separate events) and space (different parts of CNS)

111
Q

GS investigation for MS

A

MRI brain + cord

112
Q

Nerve roots that can be affected by myelopathy spinal cord compression

A

C1-L1/2

113
Q

Causes of myelopathy

A

Vertebral body neoplasms
Spinal body pathology (e.g. disc prolapse/ hernaiation)

114
Q

Most common cause of Vertabral body neoplasm

A

Mets from lung, breast, RCC, melanoma

115
Q

Sx of Myelopathy

A

Progressive leg weakness with UMN signs
Sensory loss below lesion
Sphincter involvement uncommon

116
Q

Investigations for myelopathy

A

MRI cord ASAP
CXR if malignancy suspected

117
Q

Treatment for myelopathy

A

Neurosurgery

118
Q

What is corda equina syndrome

A

Compression below conus medullaris (EMERGENCY)

119
Q

Cause of cauda equina

A

Occurs in 2% of lumbar herniation (L4/5 or L5/S1)

120
Q

Sx of cauda equina

A

Leg weakness with LMN signs
Saddle anaesthesia (perianal numbness)
Bladder/ bowel disfunction + sphincyter involvment common

121
Q

Diagnostic investigation in cauda equina

A

MRI cord + testing nerve roots

122
Q

Treatment for cauda equina

A

Neurosurgery ASAP

123
Q

What are median nerve roots

A

C6-T1

124
Q

RF for carpal tunnel syndrome

A

Female, hypothyroidism, acromegaly, pregnancy, RA, obesity

125
Q

Sx of carpal tunnel syndrome

A

Gradual onset:- weakness of grip, aching hand/ forearm, paraesthesia of hand, wasting of thenar eminence

126
Q

When is pain worst in carpal tunnel syndrome?

A

At night, relieved by hanging hand of side of the bed

127
Q

What tests for carpel tunnel syndrome

A

Phalen test:- flex wrist for 1 minute, +ve if paraesthesia + pain at wrist

Tinels test:- (tapping wrist causes tingling)

EMG diagnostic if above tests uncertain

128
Q

Managment for carpal tunnel syndrome

A

Wrist splint at night + steroid injection (acutely very painful)
Last resort:- surgical decrompression

129
Q

What nerve roots is the radial nerve

A

C5 to T1

130
Q

How does radial nerve palsy present

A

Wrist drop

131
Q

What nerve roots is ulnar nerve

A

C8 + T1

132
Q

How does ulnar nerve palsy present

A

Claw hand

133
Q

At what spinal level is a sciatica lesion

A

L5/S1

134
Q

What can cause sciatica

A

Spinal:- Disc herniation/ prolapse

Non-spinal:- piriformis syndrome, tumour pregnancy

135
Q

Sx of sciatica

A

Pain from buttock down lateral leg to pinky toe
Weak plantarflexion + absent ankle jerk

136
Q

How do you examine for sciatica

A

Can’t do straight leg raise test without pain

137
Q

How do you confirm sciatica

A

MRI

138
Q

What can cause sub-arachnoid haemorrhage

A

Berry aneurysm, circle of Willis rupture

139
Q

What can cause subdural haemorrhage

A

Briding vein rupture

140
Q

What can cause an extra dural haemorrhage

A

Middle meningeal artery, trauma

141
Q

Most common berry aneurysm rupture location

A

Anterior communicating artery/ ACA junction

142
Q

Risk factor for subarachnoid haemorrhage

A

Hypertension
Smoking
FHx
Autosomal dominant polycystic kidney disease
50+
Female

143
Q

Sx of subarachnoid haemorrhage

A

Occipital thunderclap headache
Decrease in consciousness
Nerve palsy CN3+6
Kernig sign/ Brudzinski sign

144
Q

What is Kernig sign

A

Can’t extend leg when knee is flexed

145
Q

What is Bridzinski’s sign

A

When the neck is elevated, knee unintentionally flexes

146
Q

Describe Glasgow coma score

A

Out of 15 Eyes4, Verbal5, Motor6
15:- normal
8:- Comatose
3:- Unresponsive

147
Q

GS investigation for subarachnoid haemorrhage

A

CT Head

148
Q

What do you do after CT head if +ve/-ve in Subarachnoid haemorrhage

A

+ve:- Ct angiography to show the extent of the rupture

-ve:- wait 12hr then do lumbar puncture- will see Xanthocheomia (yellowish CSF due to RBC haemolysis)

149
Q

Treatment for subarachnoid haemorrhage

A

Neurosurgery:- endovascular coiling

Also, give Nimodipine (CCB) to reduce cerebral artery spasm

150
Q

How long is time period for acute/ subacute/ chronic sub dural haemorrhage

A

<3, 3-31, >21

151
Q

What type of injury can cause a subdural haemorrhage

A

Deceleration injury and in abused children (shaken baby syndrome)

152
Q

Sx of subdural haemorrhage

A

Gradual onset with a latent period as bleeding is small
Signs of increased ICP:- Cushing’s triad (bradycardia, increased pulse pressure, irregular breathing)
Fluctuating GCS
Papilo oedema

153
Q

GS investigation for subdural haemorrhage

A

NCCT head:- Bana or crescent-shaped, not confined to suture lines, midline shift

154
Q

How to tell is SD haemorrhage is acute/ chronic on NCCT head

A

Acute:- Hyperdense (bright)
Subacute:- Isodense
Chronic:- Hyopdense (darker than brain)

155
Q

Treatment for subdural haemorrhage

A

Burr Hole + craniotomy
IV mannitol to decrease ICP

156
Q

Complications of SD haemorrhage

A

Brainstem herniation, respiratory arrest

157
Q

Who gets extra dural haemorrhage the most

A

Young adults 20-30, male

158
Q

Why does extradural haemorrhage risk decrease with age

A

Dura more firmly adhered to the skull

159
Q

Progression of extra dural haemorrhage

A

Initial event then lucid interval (hours/ days/ weeks) then rapid deterioration

160
Q

Sx of Extradural haemorrhage

A

Decrease in GCS
Cushing’s triad/ papilledema

161
Q

Why do you get rapid deterioration after lucid interval in ED haemorrhage

A

Blood clots become haemolysed and take up water. Increases volume in skull and thus ICP

162
Q

What do you see on NCCT head in extradural haemorrhage

A

Lens-shaped hyperdense bleed.
Contained to suture lines
Midline shift

163
Q

Treatment for ED haemorrhage

A

Surgery. IV mannitol to decrease ICP

164
Q

UMN lesion signs (not arm vs legs)

A

Hypertonia, rigidity, spasticity
Hyperreflexia
No fasciculation
Babinski +ve

165
Q

How does power differ in extensor/ flexor in arms/ legs

A

Arm:- Flexor> extensor
Leg:- Extensor> flexor

166
Q

LMN lesion signs

A

Hypotonia+ muscle wasting
Hypoflexia
Fasciculations
Babinski -ve
Generally decreased power

167
Q

RF for MND

A

Male, fHx, older age

168
Q

What mutation is present in motor neuron disease

A

SOD-1 mutation

169
Q

What does MND never affect

A

Eye muscle:- MS +MG do
Sensory function:- MS +polyneuropathies do
Sphincters

170
Q

Types of MND

A

Amyotrophic lateral sclerosis MC
Progressive Muscular atrophy
Primary lateral Sclerosis
Progressive Bulbar Palsy

171
Q

What cranial nerves are affected in bulbar palsy

A

CN9-12

172
Q

Which MND has the worst prognosis

A

Progressive bulbar palsy as big chance of resp failure

173
Q

What investigation can you perform in MND and what does it show

A

Electromyography:- Fibrillation potentials

174
Q

Management for MND

A

Riluzole (antiglutaminergic) :- slows progression
Non-invasive ventilation used at home to support breathing at night

175
Q

Complications of MND

A

Resp failure, aspiration pneumonia, swallowing failure

176
Q

Is meningitis a notifiable disease

A

Yes

177
Q

Most common cause of meningitis

A

Viral (Enteroviruses, HSV-2, V2V)

178
Q

Most severe cause of meningitis

A

Bacterial (S. pneumoniae + N, meningitides)

179
Q

RF for meningitis

A

Extremes of age
Immunocompromised
Crowded area
Not vaccinated

180
Q

What bacteria most common in mengingitis in neonates (+ others)

A

Group B alpha haemolytic strep (S. agalactia)

Listeria, E. Coli, S. pneumaniae

181
Q

Causes of meningitis in infants (3m to 6y)

A

S. Pneumoniae
N. Meningitidis

H. Influenza (less common due to vaccine)

182
Q

Causes of meningitis in adults (6-60)

A

S. pneumonia
N. Meningitidis

183
Q

Causes of meningitis in elderly 60+

A

S. pneumonia
N. meningitides

184
Q

Why is group B alpha haemolytic strep the most common cause of meningitis in neonates

A

Colonisies matenral vagina

185
Q

Main Sx of N. meningitidis

A

Non-blanching purpuric rash

186
Q

What type of bacteria is N. meningitidis

A

Gram -ve diplococci

187
Q

What type of bacteria is S. pneumoniae

A

Gram +ve diplococci in chains

188
Q

What type of bacteria is group B strep

A

Gram +ve cocci in chains

189
Q

What type of bacteria is Listeria monocytogenes

A

Gram +ve bacillis

190
Q

Where can Listeria be found

A

Cheese

191
Q

What does PCV vaccine protect against

A

S. pneumoniae

192
Q

Symptoms of meningitis

A

Headache, neck stiffness, photophobia

193
Q

Signs in meningitis

A

Kernig:- cant extend knee when hips flexed

Brudzinski:- When neck flexed, knees +hips automatically flex)

194
Q

What investigation do you carry out in suspected meningitis

A

Lumbar puncture from L3/4 and CSF analysis

195
Q

When is a lumbar puncture contraindicated

A

When ICP is high

196
Q

CSF analysis results on bacterial infection

A

High opening pressure
Appearance:- cloudy yellow
WCC:- Raised neutrophils
Protein:- High
Glucose vs serum levels:- low (<50%)

197
Q

CSF analysis results of viral infection

A

Normal opening pressure
Appearance:- Clear/ Normal
WCC:- Raised lymphocytes
Protein:- Normal
Glucose vs serum levels:- >60%

198
Q

CSF analysis of Fungal infection

A

Raised opening pressure
Appearance:- Cloudy
WCC:- raised lymphocytes
Protein:- Raised
Glucose vs serum levels:- low <50%

199
Q

Treatment for bacterial meningitis in hospital

A

Ceftriaxone/ cefotaxime + Steroids (dexamethasone)

Amoxicillin covers Listeria

200
Q

Treatment if a patient presents to GP with non-blanching rash + meningococcal septicemia suspected

A

IM Benzylpenicillin + immediate hospital referral

201
Q

Management of close contact of meningitis infection

A

7+ dasy
One off dose ciprofloxacin

202
Q

Why do you give steroids in meningitis

A

Reduce frequency and severity of hearing loss

203
Q

Treatment for herpes simplex virus meningitis

A

Aciclovir

204
Q

Complications of meningitis

A

Disseminated intravascular coagulation
Waterhouse friedrichsen syndrome

205
Q

What is waterhouse friedrichsen syndrome

A

Adrenal insufficiency cause by intra adrenal haemorrhage as a result of meningococcal DIC

206
Q

What is most common cause of encephalitis

A

Herpes simplex virus 1

207
Q

Other than HSV, what can cause encephalitis

A

CMV, EBV, HIV, Toxoplasmosis (close contact with cats)

208
Q

RF for encephalitis

A

Immunocompromised
Extremes of age

209
Q

Sx of encephalitis

A

Fever, headache, encephalopathy, focal neurology (temporal lobe most commonly affected)

210
Q

Investigations to perform in encephalitis

A

Lumbar puncture and send CSF for PCR
CT scan is LP contraindicated
Then MRI

211
Q

What is the treatment for Encephalitis?

A

Acyclovir (very good vs HSV)
Ganciclovir vs Cytomegalovirus

212
Q

Are primary or secondary brain tumours more common?

A

Secondary

213
Q

What are examples of primary brain tumours with the most common

A

Astrocytoma (90%)
Oligodendrocytoma
Meninggioma + Schwannoma

214
Q

Causes of secondary brain tumour with most common

A

NSCLC (MC)
Brain
Melanoma
RCC
Gastric cancer

215
Q

Sx of astrocytoma

A

Raised ICP (Cushing’s triad)
Focal neurology
Epileptic seizures
Lethargy + weight loss
CN6 Palsy
Pappilodema

216
Q

1st line investigation for astrocytoma

A

MRI to locate tumour

217
Q

After you’ve located the astrocytoma, what is the next investigation

A

Biopsy to determine grade (1-4)

218
Q

Treatment for astrocytoma

A

Surgery
Chemo (before/during/after surgery)

Steroids may help

219
Q

What are Sx in Brown Sequard

A

Ipsilateral motor weakness
Ipsilateral DCML dysfunction (proprioception, 2-point distinction)
Contralateral spinothalamic dysfunction (pain)

220
Q

What is Myasthenia Gravis

A

Autoimmune Response vs NMJ postsynaptic receptors

221
Q

What type of hypersensitivity is Myasthenia Gravis

A

Type 2

222
Q

The typical age of presentation with myasthenia gravis

A

Women under 40 (more related to autoimmune disease) or Men over 60 9more related to thymoma)

223
Q

What cancer is Myanthesia Gravis associated with

A

Thymoma

224
Q

What are 2 antibodies present in myasthenia gravis and which is more prevalent

A

Anti Ach-R 85%
Anti MuSK 15%

225
Q

How do anti-Ach-R antibodies cause Myanthesia Sx

A

Bind to postsynaptic receptor + inhibit competitively Ach binding (more binding with exertion)
Activate compliment system leading to damage to cells at the postsynaptic membrane.

226
Q

How to do Anti-MuSK antibodies cause Sx in myasthenia Gravis

A

MuSK helps synthesise Ach-R so less Ach-R expression

227
Q

Sx of Myasthenia Gravis

A

Worse later on in the day/ with exertion, starts @ head + neck and progresses to the lower body
Weak eye muscles (Diplopia)
Ptosis
Myasthenic Snarl (difficult smiling)
Jaw Fatiguability
Swallowing difficulty (bulbar weakness)
Speech Fatigubailty

228
Q

What test can you carry out to aid in diagnosis of Myasthenia Gravis

A

Tensilon/ Edrophonium test
Administer edrophonium (fast acting Ach ase inhibitor) then increase in muscle power for a few secs

229
Q

Other than serology/ edrophonium what should you do in MG

A

CT thyroid

230
Q

1st line treatment for MG

A

ACHase inhibitors; Pyradostigmine/ Neostigmine

231
Q

2nd line treatment for MG

A

Immunosuppression (steroids)

232
Q

Complication of MG

A

Myasthenic crisis; Acute Sx worsening with severe resp weakness

233
Q

How to treat a myasthenic crisis

A

Plasma exchange + IV Ig
BIPAP for resp failure

234
Q

Classic age of onset for GBS

A

Male, 15-30 or 50-70

235
Q

MC cause of GBS

A

C. Jejuni

236
Q

What is the pathophysiology of GBS

A

Molecular mimicry, organism antigens very similar to those on Schwann cells. Results in antibody production vs Schwann cell and leads to demyelination and acute polyneuropathy

237
Q

Sx of GBS

A

Post-infection presents with ascending symmetrical muscle weakness + paralysis.
Loss of deep tendon reflexes
Autonomic involvement in 50%

238
Q

Investigations to perform in GBS

A

Nerve conduction studies
LP at L3/4:- raised protein + normal WCC
(Inflammation but no infection)

239
Q

Treatment for GBS

A

IV Ig for 5 days + plasma exchange

240
Q

When is IV Ig contraindicated

A

When a patient has IgA deficiency as allergic reaction

241
Q

What is Wernicke’s Encephalopathy

A

Reversible acute emergency due to severe B1 (thiamine) deficiency

242
Q

Main cause of Wernikes Encephalopathy

A

Alcohol

243
Q

Sx of Wernikes Encephalopathy

A

Ataxia, Confusion, Opthalmoplegia

244
Q

Dx of Wernikes Encephalopathy

A

Clinically recognised and supported with Macrocytic anemia and deranged LFTs

245
Q

Acute treatment for Wernikes Encephalopathy

A

Parenteral Pabrinex (vit B1 + others) for 5 days

246
Q

Prophylaxis Management for Wernikes Encephalopathy

A

Oral Thiamine

247
Q

Complication of Wernikes Encephalopathy

A

Korsakoff Syndrome:- When WE is left too long without Tx, Severe Thiamine deficiency
Hig levels of memory loss. Irreversible damge

248
Q

Inheritance pattern for Duchenne Muscular Dystrophy

A

X linked recessive

249
Q

What happens in Duchenne Muscular Dystrophy

A

Muscel replaced with adipose tissue

250
Q

Sx of Duchene muscular Dystrophy

A

Difficulty getting up from laying down (Growers sign) and skeletal deformities (scoliosis)

251
Q

Dx of Duchenne Muscular Dysttrophy

A

Prenatal tests and DNA genetic tests

252
Q

Tx for Duchenne

A

Supportive

253
Q

What is reactivation of VZV known as

A

Shingles

254
Q

Sx of Herpes Zoster (Chicken pox/ Shingles)

A

Painful rash confined to a dermatome

255
Q

Treatment for Herpes zoster

A

Oral Aciclovir

Phase 2a Ru (10 decks)

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