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MRCP 2 > Neuro > Flashcards

Neuro Flashcards

1
Q

Alzheimers pathophysiology

A

neurofibrillary triangles and amyloid plaque deposits in hippocampus and temporal cortex
reduced acetylcholine production
global progressive impairment of brain function and intellect

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2
Q

Alzheimers genetics

A

risk factor- epsilon 4 of apolipoprotein E gene
early onset- APP, PSEN1, PSEN2

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3
Q

normal pressure hydrocephalus

A

apathy, inattention
urinary incontinence
gait apraxia
reversible dementia
50-70y/o

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4
Q

prion disease presentation

A

myoclonic jerks, seizures
cerebellar ataxia
starts < 50y
rapid onset and progression

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5
Q

alzheimer’s management

A

cholinesterase inhibitors for mild-mod disease to improve behaviour and cognition- donepezil, rivastigmine, galantamine

NMDA antagonist memantine for mod-severe

avoid TCAs and anticholinergics

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6
Q

types of amyloidosis

A

AL- most common, associated with myeloma
AA- assoc w/ inflammatory arthropathies and IBD
ATTR- auto dom

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7
Q

amyloidosis treatment

A

AL- chemo melphalan then stem cell
AA- control underlying condition

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8
Q

amyloidosis presentation

A

bruising, SOB, oedema, peripheral neuropathy, autonomic symptoms

AA- kidney, liver, spleen deposits. nephrotic syndrome or renal dysfunction
AL- SOB, weakness, proteinuria, nephrotic syndrome, renal dysfunction, cardiomyopathy, HF

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9
Q

amyloidosis poor prognostic factors

A

heart involvement
requirement of dialysis

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10
Q

amyloidosis investigation

A

serum immunofixation monoclonal protein
urine immunofixation
Ig free light chain assay raised kappa lambda
bone marrow clonal plasma cells
beta 2 microglobulin
congo red staining

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11
Q

kernig sign

A

pain and resistance on passive knee extension with hips flexed

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12
Q

brudzinski sign

A

hip flex on bending head forward

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13
Q

meningitis predisposing factors

A

influenza A
asplenia
complement deficiencies

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14
Q

meningitis most common organisms

A

children > 3 months:
neisseria meningitidis
strep pneumoniae
hib

neonates < 1 month:
strep agalactiae
ecoli
strep pneumoniae
listeria

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15
Q

cushings reflex

A

bradycardia
hypertension
irregular respiration
assoc w/ cerebral herniation in meningitis

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16
Q

LP results in bacterial meningitis

A

opening pressure > 180
WBC 10-10 000 mostly neutrophils
glucose < 0.4
protein > 0.45

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17
Q

abx for meningitis

A

non blanching rash:
benpen ASAP (300/600/1200mg) (<1y/1-9y/>9y)

without non blanching rash:
ceftriaxone or benpen or cefotaxime or chloramphenicol
vanc if foreign travel

ciproflox for prophylaxis for contacts

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18
Q

behcet’s presentation

A

recurrent oral ulcers
and at least two of:
genital ulcers
erythema nodosum, acne lesions
uveitis, hypopyon
positive pathergy test (papule/pustule after skin prick)
GI symptoms
DVT, thrombophlebitis
seizures, CN palsies, dizziness, memory problems

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19
Q

behcets treatment

A

ulcers:
topical steroids
colchicine, oral steroids, azathioprine
TNF alpha inhibitors

eyes:
pred + azathio
pred + monoclonal ab

GI/CNS:
pred + monoclonal ab

major vasc:
pred + ciclosporin

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20
Q

ischaemic stroke cerebral infarction pathophysiology

A

necrotic pathway w/ rapid cytoskeletal breakdown
apoptotic pathway
reduced cerebral blood flow results in death of brain tissue within 4-10 mins

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21
Q

left vs right hemisphere stroke symptoms

A

left:
aphasia, R sensory and motor loss, R visual field defects, dysarthria, dyscalculia, dysgraphia

right:
L sensory and motor loss, left gaze disturbance, dysarthria, aphasia, spatial disorientation

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22
Q

stroke management

A

thrombolysis with alteplase if presenting within 4.5 hours
aspirin 24h after thrombolysis
thrombectomy if presenting within 6h
load with aspirin if not thrombolysed

2 week follow up:
start clopi or aspirin + dipyrimidole

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23
Q

haemorrhagic stroke BP targets

A

rapidly lower BP if within 6h onset and SBP 150-220
rapidly lower BP if beyond 6h onset but SBP > 220

target SBP 130-140

do not offer rapid BP lowering therapy for pt with structural cause, GCS < 6 or planning early neurosurgery

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24
Q

when to admit TIA?

A

more than one in a week
ongoing neuro symptoms
severe cardiac stenosis
suspected cardio embolic cause
bleeding disorder or on anticoag
no one at home in case of further symptoms

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25
Q

TIA management

A

300mg aspirin 2/52
stroke doctor within 24h
switch aspirin to clopi 75mg after 2/52
add statin 40mg

stroke clinic within 7 days if TIA happened over a week ago

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26
Q

decompressive hemicraniotomy criteria

A

within 48h ischaemic stroke
clinical deficits suggest MCA territory
reduced consciousness
infarct of at least 50% of MCA territory
infarct volume > 145cm

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27
Q

NIHSS scoring

A

1a level of consciousness (/3)
1b level of consciousness questions (/2)
1c commands (/2)
2 best gaze (/2)
3 visual defects (/3)
4 facial palsy (/3)
5a,b motor arm (/4)
6a,b motor leg (/4)
7 limb ataxia /2
8 sensory /2
9 aphasia
10 dysarthria
11 extinction and inattention

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28
Q

ABCD2 score stroke

A

total score /7

age > 60y
BP > 140/90
diabetes
uni weakness (2)
speech impairment
> 60 mins (2)
10-15 mins (1)

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29
Q

botulism toxins

A

7 neurotoxins
A, B, E cause disease in humans

metalloproteinase
cleaves SNARE proteins at NMJ

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30
Q

botulism presentation

A

symmetrical descending flaccid paralysis
absent deep tendon reflexes
urinary retention, constipation, postural hypotension, dry mouth
normal sensory nerve studies
reduced muscle action potentials

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31
Q

botulin antitoxin

A

human for infants
horse derived heptavalent antitoxin for adults

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32
Q

chronic vs episodic cluster headache

A

clusters > 1y or remission < 1 month

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33
Q

cluster prophylaxis

A

verapamil
topiramate, valproate, lithium second line

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34
Q

cerebral mets- most common source

A

lung
breast
bowel
melanoma
renal cell

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35
Q

glioblastoma multiforme

A

regional heterogeneity within single lesion
highly anaplastic glial cells
vascular proliferation and thrombosis
necrosis

greyish ill defined mass with areas of necrosis and haemorrhage

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36
Q

anaplastic astrocytoma

A

nuclear atypia, diffusely infiltrating astrocytes
no microvascular proliferation or necrosis
round rubbery lobulated mass
firmly attached to dura

white ill defined mass
calcification not uncommon
sometimes whorls and lobules or sheets of spindles

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37
Q

presentation of function pituitary tumours

A

GH excess- acromegaly
ACTH excess- cushings
PRL excess- galactorrhoea
TSH excess (rare)- hyperthyroidism

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38
Q

micro vs macroadenoma

A

micro < 10mm
macro > 10mm

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39
Q

commonly used MRI sequences for brain tumours

A

T1 weighted- CSF low signal (dark)
T2 weighted- CSF high signal (white)
FLAIR for periventricular lesions
STIR

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40
Q

stereotactic RTX indications

A

small target < 3cm
AVM lesions not amenable to clipping or coiling
vestibular schwannoma/acoustic neuroma
mets

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41
Q

curative resection is not possible for what types of primary brain tumour?

A

glioblastoma
anaplastic astrocytoma

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42
Q

indications for surgery for pituitary tymours

A

non functional w/ mass effect
cushings
acromegaly
acute visual deterioration
pituitary apoplexy

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43
Q

dementia w/ Lewy bodies

A

alpha synuclein aggregates in brainstem and cortex
neurotransmitter deficiencies, predominantly cholinergic and dopaminergic
fluctuating levels of arousal
REM sleep disorder

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44
Q

treating dementia w/ lewy bodies

A

cholinesterase inhibitors for cognitive symptoms
dopaminergics for parkinsonism
dopaminergics can worsen confusion and hallucinations

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45
Q

parkinsonism

A

bradykinesia and at least one of:
tremor/rigidity/gait disturbance

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46
Q

encephalitis most common causative organism in UK

A

HSV 1

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47
Q

causes of encephalitis (infectious)

A

HSV, VZV, enterovirus, adenovirus, parechovirus, HIV

TB, listeria, strep pneumoniae, neisseria meningitidis, syphilis

crypto neoformans, toxoplasma, rickettsiae, fungal

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48
Q

causes of antibody associated encephalitis

A

paraneoplastic
non paraneoplastic
hashimotos

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49
Q

CSF findings in CNS infections

A

normal:
opening pressure 10-20
0.45g protein
50-66% glucose

bacterial:
raised opening pressure
100-50000 cells (neutrophils)
1g protein
40% glucose (low)

viral:
normal opening pressure
5-1000 cells (lymphocytes)
0.5-1.0g protein
50-66% glucose (normal)

TB:
high or v high pressure
5-500 cells (lymphocytes)
1-5g protein
glucose 33% (v low)

fungal:
v high opening pressure
0-1000 cells (lymphocytes)
0.5-2g protein
30-50% glucose

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50
Q

encephalitis management

A

IV aciclovir
also IV ben pen to cover for meningitis
add broad spec abx if bacterial encephalitis is suspected

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51
Q

neuological manifestations of eosinophilic granulomatosis w/ polyangiitis (churg strauss)

A

peripheral neuropathy/mononeuritis multiplex
stroke

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52
Q

management of epilepsy in pregnancy

A

5mg folic acid preconception and first 3/12 pregnancy
fetal anomaly scan 19-20 weeks
if on phenytoin, give vit K from 36 weeks (to counteract coagulopathy)
increased clearance of antiepileptics in pregnancy

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53
Q

epilepsy predisposing factors

A

premature birth
head injury
complicated febrile seizures
genetic conditions
FHx
structural abnormalities incl stroke and trauma
infections (TB, malaria, HIV, zika)
metabolic e.g. uraemia
immune mediated (anti NMDA encephalitis, anti LG1 encephalitis)
dementia and neurodegenerative conditions

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54
Q

seizure pathophysiology

A

influx of extracellular calcium and depolarisation neural membrane
> Na channels open
> influx of Na
> repetitive action potential
> hyperpolarisation of GABA receptors/K channels (spike on EEG)

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55
Q

eliptogenesis

A

transformation of normal neuronal network into one that is chronically hyper excitable

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56
Q

focal impaired awareness seizure anatomy

A

medial temporal (mostly hippocampal) focus

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57
Q

focal impaired awareness seizure features

A

impaired or loss of consciousness
aura
automatism
post ictal confusion

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58
Q

DVLA and seizures

A

inform after first episode
stop for 6 months after first seizure with normal EEG
stop for 12 months if abnormal report
can drive if seizure free (and aura free) for one year or if nocturnal only for the past 3 years
for vocational group 1 or group 2 license, needs to be seizure free, not on antiepileptics and no continuing liability for 10 years

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59
Q

epilepsy referral to tertiary services

A

poor control w/ medication within 2y or 2 drugs

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60
Q

resolution of epilepsy is defined as?

A

seizure free for 10 years
no antiepileptic drugs for at least 5y

61
Q

tonic clonic treatment

A

sodium valproate
carbamazepine
lamotrigine

62
Q

focal seizure treatment

A

carbamazepine
lamotrigine

63
Q

absence seizure treatment

A

ethosuxamide

64
Q

management of status epilepticus

A

pre hospital: 10-20mg PR diazepam or PO midaz and repeat every 15 mins

0-10 mins: IV loraz 0.1mg/kg and repeat once after 10-20 mins
0-160 mins: phenytoin infusion 15-18mg/kg or phosphenytoin infusion or phenobarbital bolus
refractory: GA (propofol/midaz/thiopental) continued for 12-24h after last seizure, then taper

65
Q

management of status in children

A

5 min: PO 0.5mg/kg midaz or 0.1mg/kg loraz
15 min: 0.1 mg/kg loraz
25 min: phenytoin 20mg/kg infusion or phenobarbital if on regular phenytoin
45 min: RSI thiopental 4mg/kg

66
Q

postural tremor

A

occurs when limb is raised against gravity

essential tremor
anxiety
alcohol
wilsons disease

67
Q

essential tremor management

A

propranolol or primidone
deep brain stimulation, radiofrequency thalamotomy

68
Q

friedreich’s ataxia

A

auto rec
GAA repeat expansion of frataxin
most common cause of death is congestive HF and arrhthymias
life expectancy 40-50y
symptoms begin 5-20y

affected areas:
spinocerebellar tracts and dorsal columns in spinal cord
pyramidal tracts in cerebellum and medulla

69
Q

friedreich’s ataxia presentation

A

typically more slowly progressive than other dementias

progressive ataxia
absence of deep tendon reflexes
spasticity
peripheral sensory neuropathy
dysarthria, dysphagia
muscle weakness, progressive kyphoscoliosis
pes cavus, hammer toes
HOCM, fibrosis, CCF, arrhythmias
DM, optic atrophy, hearing loss

70
Q

frontotemporal dementia pathophysiology

A

1/2: tau (Pick’s bodies)
1/2: TDP 43 transactive response DNA binding protein 43

genes: C9orf72, MAPT, GRN
associated w/ progressive supranuclear palsy PSP, corticobasal degeneration CBD, familial MND

71
Q

types/syndromes of frontotemporal dementia

A

behavioural variant
primary progressive aphasia
semantic

72
Q

semantic dementia

A

syndrome of frontotemporal dementia
loss of vocabulary and loss of recognition of familiar faces or objects
fluency of speech maintained

73
Q

histoplasmosis risk factor

A

caving (bat dropping)

74
Q

guillain barre

A

most have preceding URTI or UTI
campylobacter is most common organism
ascending paralysis
flaccid tone, hypo/areflexia
raised protein in CSF
delayed conduction velocities

> IVIG and plasma exchange
most make full recovery
20% have long term weakness/paraesthesia/fatigue

75
Q

headache urgent referral criteria

A

new/sudden/severe/unexpected
progressive/persistent
fever
neck pain/stiffness
photophobia
papilloedema
atypical or new onset aura and on COCP
visual disturbance or vomiting unless clearly migraine
contacts with similar symptoms
head trauma within last 3/12
worse on standing or lying down
pregnancy
malignancy history
HIV or immunosuppression

76
Q

Holmes Adie syndrome

A

holmes adie pupil and absent deep tendon reflexes
absent/slow response to light but normal accommodation
80% unilateral

77
Q

holmes adie syndrome pathophysiology

A

mostly idiopathic, assoc w/ syphilis, tumours, trauma, post op
damage to ciliary ganglion > interrupted parasympathetic supply to ciliary body and iris
damage to dorsal root ganglion > loss of deep tendon reflexes

78
Q

Ross syndrome

A

variant of holmes adie
holmes adie pupil, loss of tendon reflexes and hypohidrosis

79
Q

horner syndrome

A

ptosis + miosis + anhidrosis
interruption of sympathetic pupillomotor fibres

80
Q

causes of horner syndrome

A

central: anhidrosis of face, arm and trunk
- syringomyelia, MS, encephalitis, brain tumours, lateral medullary syndrome

preganglionic: anhidrosis of face
- cervical rib, thyroid cancer or removal, bronchogenic pancoast tumour, trauma, thoracic aortic aneurysm

post ganglionic: no anhidrosis
- cluster headache, carotid artery dissection or aneurysm, carvenous sinus thrombosis, middle ear infection

81
Q

pupilloconstrictor and pupillodilator pathway

A

constrictor:
Edinger Westphal nucleus in midbrain > orbit on CNIII

dilator:
1st order from posterior hypothalamus through brainstem to ciliospinal centre of Budge C8-T2
2nd order preganglionic neurones from cord to paravertebral sympathetic chain to superior cervical ganglion
3rd order postganglionic fibres traverse with internal carotid into skull to orbit

82
Q

ptosis is caused by paralysis of…

A

superior tarsal muscle

83
Q

testing for Horners syndrome

A

cocaine eye drops > lack of dilatation
apraclonidine hydrochloride beta adrenergic receptor agonist eye drops > affected eye more dilated

hydroxyamphetamine test to differentiate between 1st/2nd/3rd order (dilation occurs in 1st and 2nd order)

84
Q

huntingtons genetics

A

CAG repeat expansion chromo 4

85
Q

pharmacalogical management of chorea for huntingtons

A

anti dopaminergics e.g. tetrabenazine

86
Q

medications associated w/ IIH

A

lithium
cimetidine
tetracycline
tamoxifen
vit A
nitrofurantoin

87
Q

IIH diagnostic criteria

A

neuro exam normal except cranial nerves (may have 6th nerve palsy horizontal diplopia)
papilloedema
normal neuroimaging CT/MRI
normal CSF composition
opening pressure > 25

87
Q

conditions associated w/ IIH

A

thyroid, cushings
IDA
chronic renal conditions
lyme

88
Q

management of IIH

A

weight reduction
acetazolamide
topiramate
steroids for acute severe headache and papilloedema
series of LPs
ventriculoperitoneal shunt for recurrent disease
optic nerve sheath fenestration

89
Q

lambert eaton myaesthenic syndrome

A

presynaptic autoantibodies to P/Q calcium channels
treat with 3,4 diaminopyridine and/or pyridostigmine, steroids, plasma exchange, IVIG
assoc w/ small cell lung, ovarian, breast, lymphoproliferative ca, T1DM, thyroid disorders

90
Q

migraine prophylaxis

A

propranolol 80-160mg
topiramate 50-100mg
amitriptyline
botulinum or CGRP agent if refractory to 2 or more prophylactic drugs

91
Q

managing mitochondrial disorders

A

coenzyme Q
amino acids and vitamins
physical exercise

92
Q

lebers hereditary optic neuropathy

A

mito disorder
defective complex 1 NADH coQ oxidoreductase
> optic nerve degeneration

93
Q

kearns sayre

A

mito disorder
degeneration of retinal pigments
> ophthalmoplegia, painful eyes, cardiac conduction defects
defects in ragged red fibres

94
Q

MELAS syndrome

A

mitochondrial encephalopathy lactic acidosis stroke syndrome
energy deficiency, angiopathy, nitric oxide deficiency

95
Q

MERF

A

myoclonic epilepsy w/ ragged red fibres
mito disorder

96
Q

maternally inherited deafness and diabetes MIDD

A

mito disorder
3242 tRNA mutation
defective insulin secretion and cochlear hearing loss age 30-40y

97
Q

pearson syndrome

A

mito disorder
DNA deletions
sideroblastic anaemia, pancreatic dysfunction

98
Q

leigh syndrome

A

mito disorder
bilateral symmetric necrotising lesions
spongy changes and microcysts in basal ganlia, thalamus, brainstem, cord

99
Q

mitochondrial neurogastrointestinal encephalopathy MNGIE

A

pseudo obstruction
TYMP mutation

100
Q

causes of mononeuritis multiplex

A

diabetes
B12 deficiency
sarcoidosis
vasculitis
RA, SLE
HNPP
lyme, leprosy

101
Q

MND features

A

asymmetrical UMN and LMN
muscle weakness, wasting , fasciculation brisk reflexes, spasticity
ALS- bulbar, arm and leg UMN and LMN signs. upper limb > lower limb.
PBP- facial weakness, dysphagia, progressive dysarthria, upper and lower limb weakness, emotional lability
PMA- LMN only, poor prognosis
PLS- progressive spastic weakness arms and legs, spastic dysarthria, sensation intact. aggressive course

102
Q

causes of MND

A

infections (polio, tetanus, lyme)
lead
paraneoplastic
plasma cell dyscrasia
metabolic conditions
hyperlipidaemia
genetic

103
Q

MND treatment

A

positive pressure ventilation
riluzole (bone marrow suppression and deranged LFTs)

104
Q

Kennedy disease

A

X linked spinobulbar muscular atrophy
CAG expansion
LMN
progressive weakness and wasting, no spasticity
slight sensory neuropathy
assoc w/ gynaecomastia and reduced fertility

105
Q

MS risk factors

A

HLA DRB1
EBV
vit D deficiency
smoking
relapses- stress, post partum, infection

106
Q

MS 4 key areas of demyelination

A

periventricular
cortical/juxtacortical
infratentorial
spinal cord

107
Q

Kurtzke Disability Status Score

A

used to monitor MS disease status
0- no signs/symptoms
10- death

108
Q

primary and secondary progressive MS treatment

A

primary- ocrelizumab
secondary- siponimod

109
Q

MS drugs safe in pregnancy

A

interferon
glatiramer acetate
natalizumab
glucocorticoids or plasma exchange for acute episodes during pregnancy

110
Q

muscular dystrophy genetics

A

auto rec- some limb girdle
auto dom- myotonic dystrophy, fascioscapulohumeral, oculopharyngeal, some limb girdle
X linked- duchenne, becker, emery dreifuss

111
Q

emery dreifuss MD

A

uncommon x linked muscular dystrophy
presents in teenage years
contractures and cardiomyopathy
death from first degree AV block

112
Q

muscular dystrophy pathophysiology

A

Duchenne and Becker- dystrophin gene mutation (Xp21) > leakage of creatine phosphokinase CPK

other types- mutation of dystrophin associated glycoprotein complexed

113
Q

muscular dystrophy medication

A

steroids, creatine
ataluren for DMD above 5y who can still walk
ACEi, beta blockers

114
Q

myaesthenia gravis pathophysiology

A

90% cases nicotinic acetylcholine receptor
10% cases muscle specific tyrosine kinase MuSK

75% associated w/ thymus abnormalities

HLA B8, HLA DR3
HLA DR1 (ocular)

115
Q

myaesthenia gravid presentation

A

ophthalmoplegia (ptosis, diplopia, weakness of eyelid closure)
muscle weakness (esp shoulder)
myaesthenic snarl
dysarthria, dysphagia, dysphonia (fatiguable)
breathing difficulty

116
Q

most common CNS infections in advanced HIV

A

toxoplasmosis
cryptococcal meningitis, TB meningitis
PML (JC virus)
CMV encephalitis
neurosyphilis
CMV retinitis

117
Q

features of cryptococcal and TB meningitis

A

cryptococcal- subacute over 1-2 weeks, often also disorientation and confusion
TB- subacute over several weeks, also constitutional symptoms

118
Q

secondary causes of normal pressure hydrocephalus

A

intraventricular or subarach haemorrhage
meningitis
Paget
achondroplasia

119
Q

features of normal pressure hydrocephalus

A

gait disturbance
urinary frequency/urgency/incontinence
cognitive impairment
UMN in lower extremities

120
Q

predictors of improvement after shunting for normal pressure hydrocephalus

A

good- gait disorder as most prominent symptom, shorter duration of symptoms, clinical response from CSF removal

unfavourable- dementia early appearance, no gait disorder or appearing after dementia, alcoholism, marked white matter disease on MRI

121
Q

features of parkinsons plus syndromes

A

reduced response to Ldopa
dysarthria
autonomic dysfunction
supranuclear gaze palsy

122
Q

parkinsons plus syndromes

A

multiple system dystrophy
dementia w/ lewy bodies
progressive supranuclear palsy
corticobasal degeneration

123
Q

medications causing parkinsonism

A

antipsychotics
metoclopramide
prochlorperazine
tetrabenazine
sodium valproate
lithium

124
Q

adverse effects of ergot derived dopamine agonists e.g. cabergoline, pergolide

A

cardiac fibrosis

125
Q

parkinsons drug treatment

A
  • Ldopa + decarboxylase inhibitor
  • dopamine agonist (pramipexole, ropinirole, rotigotine)

adjuvants:
- MAOBi
- COMTi- for people who have developed dyskinesia or motor fluctuations
- amantadine (dyskinesia)
- SC apomorphine- advanced disease

126
Q

features of corticobasal degeneration

A

starts on one side of body then becomes bilateral
parkinsons symptoms + behavioural and cognitive changes

127
Q

phenytoin toxicity

A

ataxia, nystagmus, dysarthria, confusion, impaired coordination, seizures, hypoglycaemia
hypotension, bradycardia, asystole
can > DRESS, TEN, SJS
no antidote

128
Q

drugs causing polyneuropathies

A

isoniazid- subacute
pyridoxine- sensory
chemo- may start after stopping CTx
lead- may be acute, motor

129
Q

CJD histopathology findings

A

vacuolar degeneration

130
Q

CJD investigations

A

EEG: periodic sharp wave complexes in sporadic CJD
LP: high levels of proteins 14-3-3 and S100B
MRI: hyperintense signal change in basal ganglia and cortex
tissue diagnosis: gold standard but high morbidity and mortality
EEG and LP less sensitive in variant CJD (mad cow)

131
Q

SAH ECG changes

A

QT prolongation
Q waves
dysrhthymias
ST elevation

132
Q

SAH management

A

0.9% NaCl to prevent hyponatraemia
3L or more per day to keep intravascular compartment filled
inotropes or vasopressors to prevent vasospasm and ischaemia
antihypertensives to keep SBP < 180

surgery- clipping, coiling, clot evacuation
LP or ventricular drainage of hydrocephalus

133
Q

SAH most common cause

A

trauma then aneurysm

134
Q

ct within 1h head inury

A

GCS <13
GCS < 15 at 2h
suspected open/depressed skull #
signs of basal skull #
focal neuro deficit
post trauma seizure
> 1 vomit

children:
LOC > 5 mins
drowsiness
3 or more vomits
dangerous mechanism
amnesia > 5 mins
children < 1y w/ bruising, swelling or lacerations > 5cm on head

CT within 8 hours if no risk factors but on anticoagulants

135
Q

subdural haematoma on imagine

A

acute and chronic will be seen on non contrast CT
subacute need MRI or CT with contrast

136
Q

early vs late syphilis

A

early:
< 2y post infection
primary, secondary, early latent

late:
> 2y post infection
late latent (confirmed infection in absence of current clinical features), tertiary

137
Q

syphilis treatment

A

early:
- procaine penicillin 750mg IM OD for 10 days
- ben penicillin 2.4mg IM for 1-2 doses 1 week apart
- PO azithromycin if pen allergic or doxy 14/7

late:
- ben pen IM 3 doses week apart
- amox PO + probenecid 500mg QDS 28 days
- doxy if pen allergic

138
Q

causes of trigeminal neuralgia

A

90% caused by vascular compression of trigeminal n
MS
AV malformations
tumours
skill base abnormalities

139
Q

coma anatomy

A

interruption of ascending reticular activating system in midbrain and pons projecting to thalamus and cortex

causes:
- damage to reticular activating system at level of midbrain
- destruction to large surface of both cerebral hemispheres
- suppression of reticulocerebral functions by drugs/toxins/metabolic disturbances

140
Q

brainstem reflexes and localising lesions

A

pupils normal- above thalamus and below pons
pupils pinpoint- opioid or pontine lesion
fixed midpoint pupils- midbrain
dilated pupils- CN3 or midbrain, sympathomimetics

141
Q

ocular movements and localising causes of coma

A

roving eye/conjugate lateral nystagmus- intact brainstem. metabolic or bilateral hemisphere damage
skew deviaion- posterior fossa
oculocephalic dolls eye reflex- cerebral hemisphere
corneal reflex- eyelids will close if pons is intact. upward movement and eyelid closure if pons and midbrain are intact

142
Q

breathing patterns and localising coma

A

cheyne stoke- most common
deep breathing- acidosis
yawning or hiccups- brainstem
regular shallow- OD

143
Q

brain death

A

brainstem reflexes, motor responses, resp drive are absent
irreversible widespread brain lesion of known cause with satisfactory oxygenation, temp, no hypercapnia or sedation

144
Q

causes of central and peripheral visual field loss

A

central:
ARMD, macular holes
optic neuropathy
lebers optic atrophy
retinal a occlusion

peripheral:
glaucoma
retinal detachment
retinitis pigmentosa
chorioretinitis
branch of retinal a occlusion

145
Q

optic chiasm lesions

A

before chiasm:
ipsilateral defect
central, asymmetrical, unilateral
e.g. optic neuritis, optic atrophy, glaucoma, trauma
can also cause small defect in upper temporal field of other eye

at chiasm:
bitemporal hemianopia
pituitary tumour worse in upper field
craniopharyngioma worse in lower field

after chiasm:
homonymous defect
main optic radiation > complete homo hemi w/ macular sparing (e.g. stroke, MCA)
temporal radiation > upper quad homo hemi
parietal radiation > inferior quad homo hemi
anterior visual cortex- contra homo hemi w/ macula sparing (e.g. posterior cerebral a)
macular cortex > homo macular defect

146
Q

wernickes pathophysiology

A

petechial haemorrhages in mammillary bodies

147
Q

Wilsons disease

A

auto rec
ATP7B mutation
high levels of free copper (impaired binding and impaired excretion into bile)
reduced caeruloplasmin, increased urine copper
> fibrosis

children present more with liver disease
adults present more with neuro and eye signs

148
Q
A

MRCP 2 (12 decks)

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