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Neurology > Revision 2 > Flashcards

Revision 2 Flashcards

1
Q

what area is affected early in alzheimers

A

nucleus basalis of meynert (group of CHOLINERGIC neurones)

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2
Q

what is the treatments for alzheimers

A

acetylcholinesterase inhibitors- donzepezil, galantamine, rivastigime (monotherapies) for milf to mod
memantine (NMDA receptor antagonist) for severe/ AChEi CI

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3
Q

what mutation= 100% penetrance of huntingtons

A

40 or more CAG repeats

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4
Q

what types of inheritance does huntingtons have

A

genetic anticipation

autosomal dominant

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5
Q

what are parkinson plus syndromes

A

diseases that cause parkinsonism + other symptoms:

  • multi system atrophy
  • dementia with lewey bodies
  • progressive supranuclear palsy
  • corticobasal degeneration
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6
Q

what is multi system atrophy

A

group of disorders that progressively affect the central and autonomic nervous by system damaged oligodentrocytes (myelination) by accumulation of alpha synuclein

two types- MSA-P: characterised by parkinsons motor symptoms, deteriorates faster. MSA-C: cerebellar, lack of coordination and balance, intention tremor, slurred speech and difficulty swallowing (dysphasia)

both types characterised by autonomic symptoms- orthostatic hypotension, constipation, increased sweating, sleep apnoea, sexual dysfunction

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7
Q

what protein is found in dementia with lewey bodies

A

alpha synuclein

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8
Q

what are the symptoms of DLB

A

cognitive impairments, visual hallucinations, inability to focus, inflexible thinking and paranoia. DLB patients initially have these cognitive symptoms but also develop motor symptoms similar to PD such as bradykinesia, tremor, rigidity, and shuffling walk. Similar to PD, DLB patients also have REM sleep behavior disorder in which they act out their dreams.

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9
Q

what is progressive supranuclear palsy

A

chronic neurodegenerative syndrome which affects cognition, eye movements and posture

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10
Q

what are the symptoms of progressive supranuclear palsy

A

supranuclear (primarily vertical) gaze palsy
extrapyramidal - akinesia
cognitive dysfunction
postural instability

vague fatigue, HAs, arthralgia, dizziness, depression, modd changes, progressive dementia

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11
Q

what is a supranuclear palsy

A

the inability to look in a particular direction as a result of cerebral impairment:

  • frontal lobe (frontal eye field)-> pontine horizontal gaze centre (PPRF) -> abducens nucleus-> lateral rectus
  • occipital cortex-> oculomotor nucleus -> CN3 and medial longitudinal fasciulus -> pontine horizontal gaze centre

loss of voluntary movements of eye
as brainstem intact, all reflex conjugate eye movements normal

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12
Q

how do you distinguish a vertical gaze palsy from a cranial nerve palsy

A

both eyes affected
pupils unequal but fixed
no diplopia
reflexes intact

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13
Q

what is corticobasal degeneration

A

where multiple areas of the brain atrophy
begins around 60
start unilateral then go to other side
- poor coordination, rigidity, impaired balance, dysphagia
-personality changes, inappropriate behaviours, compulsive behaviours

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14
Q

what causes most postural tremors

A

essential- autosomal dominant inheritance, gets better when you drink alcohol

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15
Q

what is a treatment for an essential tremor

A

propanolol

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16
Q

what does an intention tremor suggest

A

cerebellar diseases

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17
Q

how does huntingtons usually present

A

strange movements and behavioural changes

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18
Q

what is sydenham chorea

A

form of chorea that is more common in females adolescents and linked to rheumatic fever (group A beta haemolytic strep infection)

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19
Q

what does myoclonus look like

A

brief electric shock like movements

e.g. 20 y/o guy gets milk but drops it= juveline myoclonic epilepsy

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20
Q

why is alzheimers linked to downs syndrome

A

alzheimers cause by beta amyloid precursor protein (insoluble, forms plaques which disrupt neuronal signalling) and the gene that codes for this is on chromosome 21 (trisomy 21= more production of amyloid= build up of plaques)

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21
Q

loss of dopaminergic neurones in the substantia nigra =?

A

parkinsons disease

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22
Q

what does the globus paladus alway inhibit

A

the thalamus - main job of direct pathway is to reduce this inhibition

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23
Q

what is the tremor like in parkinsons

A

resting
4-6 Hz
pill rolling
starts on one side then becomes bilateral

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24
Q

sudden onset bilateral parkisons with resting tremor= ?

A

drug induces parkinsonism

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25
Q

name two drugs that can cause drug induced parkinsons

A

dopamine antagonists: haloperidol, metoclopramide

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26
Q

what is hemiballism

A

wild movements of one arm/leg caused by an infarct of the subthalamic nucleus (part of the indirect pathway)

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27
Q

how is hemiballism treated

A

self limiting

treated over a few months with antipsychotics

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28
Q

parkinsonism with orthostatic hypotension and has a poor response to levodopa =?

A

multi system atrophy

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29
Q

where is the lesion in vascular parkinsons

A

infarcts in basal ganglia

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30
Q

how do the symptoms of vascular parkinsons differ from normal parkinsons

A

vascular is more prominent in the lower limbs, resting tremor in legs

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31
Q

what causes syndenhams

A

infection with group A beta haemolytic strep causes rheumatic fever- when infected antibodies from against basal ganglia and cause syndehams

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32
Q

clear CSF with normal opening pressure

oligoclonal bands present

A

MS

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33
Q

clear csf with normal opening pressure
lymphocytes present
high protein
normal glucose

A

viral

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34
Q

what are the signs of IIH

A 
high CSF opening pressure 
bilateral papilloedema (can progress to blindness)
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35
Q

what is the management for IIH

A

1st line weight loss
2nd line acetalozamide
3rd line shunt

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36
Q

is there CSF in the subarachonoid space

A

yes

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37
Q

yellow tinge in CSF 12 hours after haemorrhage = what type of haemorrhage

A

SAH

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38
Q

can SAH be spontaneous or traumatic

A

both

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39
Q

is viral meningitis more/less intense than bacterial/ TB meningitis

A

less intense

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40
Q

what are all meningitis’ treated as until proven otherwise

A

bacterial

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41
Q

what is the Tx for viral meningitis

A

supportive

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42
Q 
cloudy CSF
elevated opening pressure 
neutrophils (aka polymorphs/ polymorph pleocytosis) present 
high protein 
low glucose
A

bacterial meningitis

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43
Q 
opaque CSF 
if left to settle forms a fibrin web 
elevated opening pressure 
lymphocytes present
high protein 
low glucose
A

TB meningitis

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44
Q

best initial test to diagnose:

alzheimers

A

MMSE

  • will have impaired recall
  • lose short term memory
  • retain long term memory
  • eventually become disorientated to time, place and person
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45
Q

best initial test to diagnose:

frontotemporal dementia

A

MRI

-will show focal atrophy in frontal and superior temporal lobes

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46
Q

what is picks disease

A

FTD

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47
Q

how will FTD present

A

behavioural symptoms, self neglect, language (lose vocab)

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48
Q

what is FTD associated with

A

MND

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49
Q

how is FTD different from huntingtons

A

not inherited

has no chorea

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50
Q

best initial test to diagnose:

-vascular dementia

A

MRI

-shows long term damage from infarcts

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51
Q

what is the classic presentation of vascular dementia

A

step wise cognitive deterioration - result of multiple infarcts

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52
Q

which anti-epileptic drug:
used in pregnancy
SEs: rash, SJS

A

lamotrigine

least teratogenic, given with folic acid

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53
Q

which anti-epileptic drug:

used for treatment of absence seizures, blocks the thalamic T type Ca2+ channels

A

ethosuximide

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54
Q

what are absence seizures

A

usually happen in children
go completely blank
wont move/ remember it then snap out of it

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55
Q

which anti-epileptic drug:
Na+ channel activation
increase GABA concentration
should be avoided in women of childbearing age
used for majority of generalised seizures
SE: weight gain, alopecia
is a P450 enzyme inhibitor

A

sodium valoprate

highly teratogenic

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56
Q

what is a simple partial seizure

A

mini electrical disturbance in part of the brain
will have awareness of what is happening
can be motor (frontal lobe), visual (occipital lobe), sensory (parietal)

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57
Q

what is a complex partial seizure

A

involves a bigger bit if the brain
may have aura- hear/ see feel something abnormal/ will have de ja ve (with itself can be seizure)
then loss of awareness
confusion/ drowsiness after seizure = the post ecter phase

(aura, loss of awareness, post ecter ohase)

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58
Q

what type of seizures is an absence seizure

A

generalised

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59
Q

what is the tonic phase of a seizure

A

stiffening of whole body, stiff, rolling eyes back

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60
Q

what is the clonic phase of seizure

A

jerky movements

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61
Q

what does loss of awarness in a seizure mean

A

it cannot be a simple partial

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62
Q

what is a generalised seizure

A

seizure type characterised by loss of consciousness, widespread motor manifestations of tonic contractions followed by clonic jerking movements, and a suppressed level of arousal following the event (post ecter phase)

May either reflect an underlying generalised-onset epilepsy or focal epilepsy that has secondarily generalised.

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63
Q

what are non epileptic seizures

A

not caused by abnormal electrical activity in brain
can be psychogenic
will not have post ecter phase
movement is not coordinated

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64
Q

what treatment for non generalised seizures

A

(simple and complex partial seizures)

carbamazepine

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65
Q

what is the first line Tx for absence seizures

A

sodium valporate/ ethosuximide

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66
Q

1st line for generalised tonic clonic seizure

A

sodium valporate

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67
Q

what is status epilepticus

A

seizure lasting more than 30 mins

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68
Q

what is the Tx for status epilepticus

A

at 5 mins give IV lorazepam

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69
Q

best long term management:

uncontrolled hypertensive who develops a stroke

A

antihypertensives

BP control

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70
Q

best long term management:

patient who has a seizure due to a CVA

A

carbamazepine

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71
Q

best long term management:

patient with an ischaemic stroke is found to have AF

A

warfarin

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72
Q

best long term management:

ischaemic stroke

A

(acute treatment is aspirin in first 2 weeks)

lifelong clopidogrel

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73
Q

most useful Ix to order:
65 y/o male patient presents to the clinic with double vision and ptosis
he has weakness that gets worse during the day

A 
anti AChR (acetylchonine receptor) antibodies 
(diagnosis here is myasthenia gravis- antibodies against post synaptic channels, affects the eyes)
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74
Q

what are the features of lambert eaton syndrome

A

auto immune condition against pre synaptic channels
weakness of limb muscles
associated with small cell lung cancer

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75
Q

what antibodies for lambert eaton

A

anti musk

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76
Q

which medication:

20 y/o female with tonic clonic seizures which wants to conceive soon

A

lamotrigine

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77
Q

which medication:
patient with epilepsy on medication presents with these SEs- blurred vision, vertigo and blood results reveal a hyponatremia

A

carbamazepine

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78
Q

which medication:
a mother has noticed her 8 y/o daughter has been day dreaming and not paying attention
after discussing with GP an EEG was organised which revealed a 3Hz spike wave

A

ethosuxomide

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79
Q

best management:
58 year pld man with ischaemic heart disease requires treatment for an acute migraine attack that has not responded to paracetamol

A

high dose NSAIDs with antiemetic

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80
Q

best management:
25 year old male who presents with right sided supraorbital pain and ipsilateral ptosis and miosis
pain lasts 30 mins and usually occurs at same time every night

A

high flow oxygen with SC sumatriptan
(diagnosis is a cluster HA)

long term management for cluster HAs is verapamil

81
Q

what are the features of a cluster HA

A

Stabbing pain around orbit or in temporal lobe. Have circadian rhythm, last 30 mins to 3 hours.

82
Q

how long do migraines last

A

5-72 hours if untreated

83
Q

what part of head to migraines affect

A

are hemicranial

84
Q

best management:
55 year old female patient presents with left sided supraorbital pain with ipsilateral nasal congestion. This occurs about 20 times a day and lasts about 10 minutes

A

indomethacin

diagnosis is paroxysmal hemicrania

85
Q

how is paroxysmal hemicrania different from cluster HAs

A

occurs more frequently

lasts shorter amount of time

86
Q

how do you control vomiting in a patient with parkinsons

A

domperidone (is a dopamine antagonist but doesnt cross BBB)

87
Q

what medication:

Patient on therapy for parkinsons develops acute psychosis

A

quetiapine

pick secondary generation antipsychotics as first gen will worsen parkinsons

88
Q

what medication:

dyskinesia is a SE of this drug used in the treatment of parkinsons

A

levodopa

acts as dopamine for the brain but over time can cause excessive unwanted movement (dyskensia)

89
Q

how is dyskensia prevented when levodopa is given

A

not given on its own, given with dopadecarboxylase inhibitor which prevents peripheral conversion of the drug to dopamine

90
Q

what medication:

1st line for parkinsons

A

levodopa

91
Q

causative organism:
pregnant lady presents with signs of meningism
culture reveals gram +ve flagellate rods

A

listeria

tends to affect young babies, elderly and pregnancy women

92
Q

how is listeria meningitis treated

A

amoxicillin

93
Q

Causative organism:
18 y/o uni student presents with stiff neck, photophobia and fever
cultures reveal a gram -ve diplococcus

A

neisseria meningitidis

94
Q

what is the excitatory neurotransmitter

A

glutamate

95
Q

what is the inhibitory neurotransmitter

A

gaba/glycine

96
Q

name two opioid antagonists

A

naloxone and naltrexone

97
Q

what are alpha and delta nerve fibres

A

mechanical/ thermal nociceptors that are thinly myelinated (first response- sharp pain)

98
Q

what are C fibres

A

unmyelinated

are second response- throbbing pain

99
Q

what is the role of astrocytes

A

maintain BBB

100
Q

what is the role of oligodendrocytes

A

myelination of CNS

101
Q

what is the role of schwann cells

A

myelination of PNS

102
Q

what is the role of ependymal cells

A

CSF regulation

103
Q

what is the role of microglia

A

phagocytes

104
Q

what is the role of the inf and sup articular processes on vertebrae

A

mobilise with adjacent vertebrae via synovial facet joints

105
Q

where on a vertebrae does the rib articulate

A

transverse processes

106
Q

where do the anterior and posterior rami supply

A

anterior- anterolateral body wall

posterior- posterior body wall

107
Q

is the anterior or posterior rami bigger

A

anterior

108
Q

which part of the grey matter butterfly gives of anterior roots

A

top wings

109
Q

name the ascending tracts

A

dorsal column- fasiculus gracilis and cuneatus
dorsal and ventral spinocerebellar tract
fasciculus proprius
spinothalamic and spinoreticular tract

110
Q

name the descending tracts

A 
medial longitudinal fasciculus 
lissauers tract 
lateral and ventral corticospinal tracts 
rubrospinal tract 
pontine reticulospinal tract 
meduallry reticulospinal tract 
lateral vestibulospinal tract 
tectospinal tract
111
Q

summaries the DCML

A

fine touch
conscious proprioception
fibres cross in the medulla

112
Q

summarise the spinothalamic tract

A

pain, temperature, deep pressure

fibres cross segmentally

113
Q

summarise the corticospinal tract

A

fine precise movement, particularly of distal limb muscles
forms on the medulla - pyramidal tract
85% of fibres cross in the caudal medulla at the decussation of the pyramids

114
Q

where is the primary somatosensory cortex

A

post central gyrus in the temporal lobe

115
Q

where is the primary motor cortex

A

pre central gyrus, frontal lobe

116
Q

where is the lesion in decoricate posturing

A

(flexor)
cervical spinal tract/ cerebral hemisphere
rubrospinal tract dominant
(decorate things red at christmas)

117
Q

where is the lesion in decerebrate posturing

A

(extensor)
midbrain/ pons
vestibulospinal tract prominant

118
Q

from medial to laterla in the primary motor cortex, list the parts of body controlled by each bit of brain

A 
foot
hip 
trunk
arm
hand
face
tongue
larynx
119
Q

what is the role of the basal ganglia

A

modulates motor control

120
Q

what makes up the basal gamglia

A 
caudate 
putamen 
globus pallidus 
subthalamic nucleus 
substantia nigra
121
Q

what are the functions of the frontal lobe

A 
voluntary movement 
reasoning
executive function
personality 
inhibition 
initiative 
expressive language 
habit learning 
emotional control
122
Q

what are the functions of the parietal lobe

A 
knowing left from right 
reading 
writing
body orientation 
calculation 
two point discrimination 
graphaethesia
123
Q

what do lesions in the DOMINANT parietal lesion cause

A

dysphasia
dyscalculia
dyslexia (difficuly learning to read. interpret words, letters and symbols)
apraxia
agnosia
gerstmann syndrome (acalculia, agraphia, finger anomia, difficulty in differentiation of right and left)

124
Q

what is apraxia

A

inability to perform complex movements in the presence of normal motor, sensory and cerebellar function

125
Q

what is agnosia

A

tactile- inability to recognise or discriminate objects through touch

126
Q

what is agraphia

A

inability to write

127
Q

what is finger anomia

A

cant recognise own or other peoples fingers

128
Q

what does a lesion in the NON DOMINANT parietal lobe cause

A

spatial disorientation
constructional apraxia
dressing apraxia
anosognosia (lack of self awareness of own medical illness)

129
Q

what are the functions of the temporal lobe

A 
understanding speech 
memory 
hearing 
emotions 
sense of identity 
recognising faces
130
Q

what do strokes in the dominant half of brain often have

A

language affected which has major implications for rehab

131
Q

what is the acute treatment for an ischaemic stroke

A

Alteplase clot buster 0.9 mg/kg (max 90mg)
10% over 60 mins
Rest over 8 hours
MUST be given within 4.5 hours of symptom onset

132
Q

what is a TACS

A

total anterior circulation stroke
all three of:
-unilateral weakness and/or sensory weakness of face, arm and leg
-homonymous hemianopia
-higher cerebral dysfunction (dysphasia, visuospatial disorder)

133
Q

what is a PACS

A

partial anterior circulation syndrome
two of:
-unilateral weakness and/or sensory weakness of face, arm and leg
-homonymous hemianopia
-higher cerebral dysfunction (dysphasia, visuospatial disorder)

134
Q

what is a POCS

A 
posterior circulation syndrome 
one of: 
-cerebellar/ brainstem syndrome 
-loss of consciousness 
-isolated homonymous hemianopia
135
Q

what is a LACS

A

lacunar syndrome (subcortical stroke due to small vessel disease)
one of:
-unilateral weakness and/or sensory deficit of face and arm, arm and leg or all three
-pure sensory stroke
-ataxic hemiparesis

136
Q

what do subdural haematomas look like on MRI

A

banana

137
Q

explain the slow onset of symptoms in a subepidural haematoma

A

bridging veins rupture

these are low pressure so blood spreads around brain before displacing it, gradual increase in symptoms

138
Q

what vessel is classically ruptured in an extradural haemorrhage

A

middle meningeal artery (runs under pterion)

139
Q

what is the formula for cerebral perfusion pressure

A

CPP= MAP - ICP

140
Q

how do you remember how much each segment of the GCS scores

A

eyes (four letters)
speak (five letters)
motor (M6 motorway)

141
Q

what is the minimum GSC score

A

3

142
Q

what GCS score= coma

A

<8

143
Q

what are the headache red flags

A 
new onset headache >55 
known/ previous malignancy 
immunosuppressed 
early morning HA
excerbation by valsalva 
significant trauma in Hx
coagulopathy with trauma
144
Q

what is the management for migraines

A

Diary to find triggers – then exclude triggers
NSAIDS eg 900mg Aspirin
Triptans (oral first) - must be at start of headache and repeated only once.
More than 3 attacks in a month – prophylaxis:
-Propranolol
-Topiramate (loads of side effects, start slow)

Remember contraception issues in women

145
Q

what are the symptoms of trigeminal neuralgia

A

severe stabbing unilateral pain, v severe
Duration: 1sec to 90 secs
Frequency: 10 to 100 day
Bouts pain may last from a few weeks to months before remission
more common in females
any frequency
cutaneous trigger

146
Q

what is the main drug used to treat trigeminal neuralgia

A

P450 inducer

147
Q

what can trigger cluster HAs

A

alcohol

148
Q

what are the features of a cluster HA

A 
more common in males
boring pain 
V. severe 
orbital 
15-180 mins
1-8 per day 
autonmic features
149
Q

what are the features of paroxsymal hemicrania

A 
more common in females 
boring pain 
v severe
orbital 
lasts 2-45 mins 
1-40 per day 
autonomic features 
responds to endomethicin 
mechanical trigger
150
Q

what are the features of SUNCT

A 
(short lasting unilateral neuralgiform HA with conjunctival injection and tearing) 
more common in women 
stabbing pain 
severe 
orbital 
15-120 seconds 
1 a day- every 30 hours 
autonomic features 
cutaneous trigger
151
Q

what are the features of a stabbing/ icepick headache

A 
more common in females 
stabbing pain 
severe 
anywhere in head 
lasts <30 secs 
any prequency 
autonomic features 
no trigger 
responds to indomethicin
152
Q

summarise brown sequard syndrome

A

hemicord lesion

  • lateral corticospinal tract damage = ipsilateral UMN weakness
  • posterior column= ipsilateral vibration and proprioception loss
  • anterolateral system= contralateral pain and temperature loss
153
Q

describe the symptoms seen in central cord syndrome

A

centre part of spinal cord affected
in small lesions- spinothalamic tract fibres that cross the anterior white matter commisure are interrupted = bilateral pain and temp loss at affected levels, below this cord function intact = cape like distribution

large lesions- corticospinal, spinothalamic and dorsal column may be affected aswell= upper motor neurone pattern of deficit below the level of injury (interrupted corticospinal), with spastic paralysis and urinary retention, and a LMN deficit pattern at level of injury (damage to ant horn cells)
upper extremities more affected than lower as fibres more central

154
Q

which nerve is at risk of injury:

colles fracture

A

median

155
Q

which nerve is at risk of injury:

ant shoulder dislocation

A

axillary

156
Q

which nerve is at risk of injury:

humeral shaft #

A

radial (in spiral groove)

157
Q

which nerve is at risk of injury:

posterior dislocations of hip

A

sciatic

158
Q

which nerve is at risk of injury:

supracondylar # of the elbow

A

median (anterior interosseous branch)

159
Q

which nerve is at risk of injury:

bumper injury to the lateral knee

A

peroneal nerve (fibular)

160
Q

what differentiates back ache from sciatica

A

back ache can radiate to buttock and thigh but not below the knee like sciatica can

161
Q

what are the symptoms of an L3/4 prolapse

A

> L4 root entrapment > pain down to medial ankle (L4), loss of quadriceps power, reduced knee jerk

162
Q

what are the symptoms of an L4/5 prolapse

A

L5 root entrapment > pain down dorsum of foot, reduced power Extensor Hallucis Longus and tibialis anterior

163
Q

what are the symptoms of an L5/S1 prolapse

A

S1 root entrapment > pain to sole of foot, reduced power planarflexion, reduced ankle jerks

164
Q

what is the role of broca and wernickes areas

A

brocas- speech production

wernickes- speech comprehension

165
Q

what are the SEs of sodium valporate

A 
increased appetite= massive weight gain 
alopecia 
teratogenic (neural tube defects, cleft lip and palate, cardiovascular abnormalities, genitourinary defects, developmental delay, endocrinological disorders, limb defects, and autism)
166
Q

what is lamotrigine first line for

A 
focal seizures (carbamazepine is 2nd line) 
women with generalised seizures
167
Q

what are the SEs of lamotrigine

A

rash
HA
dry mouth

168
Q

what is levetiracetam

A

epilepsy management
2nd line in women of childbearing age
Good 3rd line alternative after sodium valproate and lamotrigine
Quite well tolerated – tiredness apathy weight gain

169
Q

what are the key symptoms of MS

A

Optic neuritis, Sensory symptoms, Lr urinary tract dysfunction, Pyramidal dysfunction (Tone+, spastcicity, F of UL, E of LL)
At least 2 episodes suggestive of demyelination + Dissemination in time and place

170
Q

what will be seen on blood tests for MS

A

nothing

171
Q

what for acute Tx for MS flare

A

steroids

172
Q

what are the treatment options for parkinsons

A

levodopa (with dopadecarboxylase inhibitor)
monoamine oxidase B inhibitor
dopamine agonist

can add on
catechol-o-methyl transferase inhibitor (prolongs actions of levodopa)

173
Q

what are the symptoms of parkinsons

A

Gait - shuffling, slow turning with multiple steps, trouble with doorways, stooped over, reduced arm swinging, fenestration

Also non-motor features: EARLY - Hyposmia (reduced smell),
Constipation,
REM sleep disturbance (can act out dreams)
depression – V V common and pronounced generally

LATE - Dementia (it is Lewy body dementia if within the first 2 years, otherwise is parkinsons disease dementia)
Everyone gets some form of cognitive decline over time with parkinsons disease.

cog wheel rigidity
resting tremour)
positive froment’s maneuver (rigidity increases in examined body segment by voluntary movement of other parts),
micrographia,
bradykinesia,
hypomimia (decreased facial expression),
hypophonia (quieter voice)

174
Q

which generation of antipsychotic is clozapine

A

2nd - is an atypical

175
Q

name extrapyramidal drugs

A

(dopamine antagonists)
all antipsychotics- typicals (haloperidol) worse than atypicals (clozapine)

metoclopramide
domperidone

176
Q

what is the main down fall of atypical antipsychotics

A

weight gain and metabolic syndrome

177
Q

what causes meningitis in neonates

A

listeria, group B streptococci, E. coli

178
Q

what causes meningitis in children

A

H influenza

179
Q

what causes meningitis in ages 10-21

A

meningococcal

180
Q

what causes meningitis in >21s

A

pneumococcal > meningococcal

181
Q

what causes meningitis in the elderly

A

pneumococcal > listeria

182
Q

what causes meningitis in immunocompromised

A

S. pneumoniae, N. meningitidis, Listeria, aerobic GNR (including Ps.aeruginosa)

183
Q

what causes meningitis in patients who have had neurosurgery/ open head trauma

A

staphylococcus, gram -ve rods

S. aureus, S. epidermidis, aerobic GNR

184
Q

what causes meningitis in patients with a # of the cribiform plate

A

pneumococcal

S. pneumoniae, H. influenzae, beta-hemolytic strep group A

185
Q

what causes meningitis in patients who have a CSF shunt

A

S. epidermidis, S. aureus, aerobic GNR, Propionibacterium acnes

186
Q

what is the management for meningitis

A

Ceftriaxone I.V 1.2mg bd +/- amoxicillin if over 60 (listeria cover)

Penicillin allergy:
Chloramphenicol + Vancomycin +/- co-trimoxazole (listeria cover)

If it is meningococcal - additional steroids are not required but everyone gets it until its established

187
Q

what is the treatment for status epilectus

A

1st stage (0−10 minutes):

  • Secure airway and resuscitate
  • Administer oxygen
  • Assess cardiorespiratory function
  • Establish intravenous access – get help to hold site still
  • Glucose (50 ml of 50% solution) and/or intravenous thiamine if appropriate

Pre-hospital - Diazepam 10−20 mg per rectum
1mg Midazolam buccally

In hospital - Lorazepam IV 0.1mg/kg with 4mg bolus (don’t worry about dose)
if unable to get IV access, go to rectal diazepam
This stage call MUST call senior/ICU

Established (20mins or more despite therapy) – IV phenytoin or fosphenytoin
MUST CALL ICU!!!

188
Q

what is the mnemonic for things that can cause cerebellar symptoms

A 
DAISIES
Demyelination 
Alcohol 
Infarction 
SOL- schwannoma 
Inherited (wilsons, fredricks ataxia) 
Epilepsy medication 
(multiple) System atrophy
189
Q

what is rhombergs testing

A

proprioception and sensory ataxia

wont be able to stay balanced with eyes shut

190
Q

what type of nystagmus in cerebellar disease

A

horizontal

191
Q

what is speech like in cerebellar disease

A

slurred staccato

192
Q

what is the fast phase of nystagmus going towards

A

the side of the lesion

193
Q

what happens to the tremor in parkinsons when counting back from 100

A

gets worse- gets worse on concentration

194
Q

what type of tremor might a dopamine agonist cause

A

bilateral

195
Q

can patients with parkinsons draw a neat circle

A

yes- have RESTING tremor

196
Q

what does a babinski +ve test mean

A

claw out

UMN lesion

197
Q

what is a bovine cough seen in

A

vagus nerve lesions

198
Q

what disease are tongue fasciculations seen in

A

MND

Neurology (35 decks)

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