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Neurology > ILAs 1 to 3 [03/11/20] > Flashcards

ILAs 1 to 3 [03/11/20] Flashcards

1
Q

What is the Marcus Gunn pupil, and how can it be assessed?

A

Relative afferent pupillary defect: slower response to dilate pupil in swinging light test.

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2
Q

What can a Marcus Gunn pupil be caused by?

A

Large retinal detachment, central retinal artery/vein pathology, optic nerve pathology.

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3
Q

How is visual acuity measured?

A

Snellen chart, first number viewing distance, second number is the distance an average eye can read it.
Allowed two goes per line.

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4
Q

What are the 5 main anatomical parts of vision that can have pathology?

A

Aqueous humour, vitreous humour, retina, vasculature, nerve

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5
Q

Describe the simple PP, Sx and Sx and what acute glaucoma can easily be confused by?

A

Drainage of the aqueous humour becomes blocked. Results in a rapid rise in IOP.
Sx: pain, red eye, N and V.
Confuse Sx often with migraine.

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6
Q

Sx of a vitreous haemorrhage

A

prevents light lens to retina: flashes/floaters, blurred vision

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7
Q

Sx of retinal detachment fundoscopy

A

Flashes, floaters, ‘curtain’ over part of vision [which is also seen vascular pathology].

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8
Q

Sx of anterior ischaemic optic neuropathy. What is AION? What should you think of causative?

A

Swollen optic disc, occlusion of th eposterior ciliary artery supplying had of the optic nerve.
THINK of GCA!

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9
Q

Sx of GCA

A

Jaw claudication, scalp tenderness, anorexia, anaemia, fatigue, age [over 70, though can be over], elevated ESR and CRP, no athersclerotic RFs

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10
Q

Central retinal artery occlusion on fundoscopy? Whose opinion should you ask as what could this be?

A

pale disc, cherry red spot at macula.
Occlusion of the central retinal artery [branch of the opthalmic artery] which supplies the whole retina.
Need urgent intervention.
Stroke opinion as consider a TIA.

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11
Q

Features and Sx of central retinal vein occlusion

A

Dilated of branch veins
Multiple retinal haemorrhage
Cotton wool patches [hard exudates].

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12
Q

Difference between papillitis and optic neritis?

A

Both inflammation of the optic nerve; if optic head then papillitis, if behind 2/3rds then ON

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13
Q

What does nerve damage look like fundoscopy?

A

Optic clonicity [optic enrve damage been awhile], usually more temporal. Normally paler beyond optic disc.

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14
Q

Papilloedema look like?

A

Disc margins distorted, haemorrhage lower area.
Something puhsing from the back centrally.
Swelling in this area of disc, means area is elevated.

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15
Q

Sx of optic neuritis

A

Reduced acuity over few days, pain moving eye, excerbated by heat and exercise, apparent pupillary defect, dyschromatopsia

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16
Q

Aetiology ON

A

Inflammation optic nerve, often associated with MS. can occur clinically isolated.
other causes: infection [Lyme’s, syphilis, HIV], B12 def., arteritis

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17
Q

Common course of ON

A

6w recovery vision

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18
Q

Tx of ON

A

steroids help reduce pain and hasten recovery

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19
Q

What in ON can lead to long term damage?

A

Neuromyleitis optica

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20
Q

Essential criteria for ON?

A

RAPD

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21
Q

15 year risk of developing MS if have ON?

A

40%

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22
Q

15 year risk ON is MRI normal 10y, abnormal 10y?

A

Normal then 11%, abnormal then 83%

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23
Q

Dx of MS

A

Multiple CNS lesion, whihc cause Sx that:

  • last longer 24h
  • dissminated in space
  • dissiminated in time
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24
Q

typical features MS

A
  • visual loss [ON, optic atrophy, LNO]
  • pramidal weakness, spastic paresis
  • sensory disturbances
    cerebellar Sx [nystagmus/vertigo/tremor/ataxcia etc.]
  • bladder/sexual dysfunction
    Lhermitte and Uhtoff’s phenomenon, fatigue, cognitive impairment, 3rd and 6th nerve palsy
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25
Q

Ix for MS

A

MRI scan
- T2 lesions found in four key areas [cortical/ventricular,/tenortorial/spinal cord]
LP
- unmatched oligoclonal bands

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26
Q

PP of MS

A

inflammatory, local loss myelin sheath, realtive preservation axons
neurodegenerative stage loss of axons and prgoressive fixed deficits

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27
Q

MS types

A
  • benign MS
    RRMS
    SCR
    PP [10-20%, older]
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28
Q

Tx acute episode

A

steroids [hasten recovery, thought not DMT after 6-9m]

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29
Q

DMT for chronic MS

A

sub-cut: e.g. Ib, Ga
oral e.g. figolimod
IV e.g. natalizumumab?
stem cell transplant

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30
Q

SE steroids

A

avascular necrosis, lowered blood sugar, cushings, OP, etc.

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31
Q

DDx blackouts

A

syncope, epilepsy, NEA

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32
Q

Dx syncope

A

abrupt and transient loss of consciousness associated with loss postural tone follows sudden fall cerebral perfusion

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33
Q

3 main types of syncope

A

Neurogenic, orthostatic, cardiac

34
Q

Define neurogenic syncope

A

Inappropriate activation of cardio-inhibotiry and vaso-depressor reflex leading to hypotension

35
Q

Causes of neurogenic syncope

A 
Vasovagal
Reflex:
- micturition
- cough
- carotid sinus hypersensitivity [stimulate baroreceptors e.g. when men shaving, or reaching for things]
36
Q

Types and examples of orthostatic syncope

A

Autonomic failure

  • primary [multi-system atrophy]
  • secondary [diabetes, drugs]
37
Q

Cardiac syncope causes

A

Arryhtmias [prolonged QT, bradycardias, exertional syncope]

Valvular heart disease

38
Q

Seizure definition

Compare to epilepsy

A

Clinical manifestation of distorted electrical activity of the brain [paroxysmal discharge of cerebral neurones]
Epilepsy is just tendency for recurrent seizures

39
Q

Compare triggers syncope to epilepsy

A

Syncope
- stress/fear, prolonged standing, heat, venepuncture, cough, micturition

Seizure
- sleep deprivaiton, flahsing ligths, menstruation, alcohol and alcohol withdrawal

40
Q

Describe syncopal episode [onset, duration, convulsions, colour, intontience/tongue biting]

A
  • onset = quick, but can sometimes prevent faint if lie down quickly
  • duration = short [seconds to 1 minute]
  • convulsaions = rare, but brief
  • colour = pale
  • incontience/tongue biting = rare [unless bladder full]
41
Q

Seizure description

A

onset - can have aura, tonic-clonic episodes goes rigid then clonic movement limbs
duration - 2/3 mins
convulsions - GTC seizures, focal motor fits, myoclonic jerks [on awakwning], frontal lobe motor fits
incontinence/tongue biting - yes, biting lateral side tongue

42
Q

NEA description

A

can last 30m, convulsions [non-neuroanatomically accurate], wild shaking, arms felxing and extending, may be completely still. Waxc and wane, pelvic thrusting, eyes closed. Incontinence/tongue biting can have injury to self.

43
Q

Recovery from each

A

Syncope - little or no confusion, quick recovery
Seizure - confusion or headache, may not recognise family/friends, amnseia for few miutes, first mem in ambulance, needs rest [sleep 1/2 hours]
NEA - recovery rapid, can be very upset

44
Q

Compare PMH/personal history of each

A

Syncope - previous faints, cardiac causes
[heart block, tachycardia like VT], obstructive lesions like aortic stenosis

Seizure - perinatal illness, educaitonal achievements, previous serious head injury/neurosurgery, neonatal seizures [prolonged], meningitis. If late onset [over 40], think stroke/tumours.

NEA - preivous unexplained medical Sx. PMH child abuse etc.

45
Q

Ix of blackouts

A 
Listen to heart [aortic stenosis]
12 lead ECG!!!!!
blood tests [FBC]
Brain imaging
EEG
if suspected syncope consider 24 hours tape, tilt table, autonomic function tests
46
Q

types of EEG can do

A

inter-ictal EEG
provocation [photosensitivty, hyperventilation]
sleep dewprived EEG
prolonged EEG
vidoe-telemtry: useful NEA, preo-op assess, not useful frontal seziures

47
Q

Accuracy of EEGs

A

false postiive rate 0.5-2%
false negative rate 50%
false negative rate repeat EEG 30%
false negative sleep deprived 20%

48
Q

When should/shouldn’t you do imaging? What type best?

A

If focal onset, imaging
if over 25 and new onset, imaging
if suspected idiopathic generalised epilepsy imaging less useful [rarely abnormal]
MRi best, but CT emergency can do

49
Q

Types of idiopathic generalised epilepsy

A

GTC, myoclonus, absences

50
Q

What is the interictal marker of a seizure?

A

Spike or sharp wave

51
Q

Juvenile myoclonic epilepsy on EEG

A

interictal EEG shows a normal background with frequent generalised polyspike and wave discharges

52
Q

PP of seizures

A

Normal brain, spread electrical acitvity limited
during seizure, prolonged depolairization group neurones, whihc spreads out to adjacent neurones
Failure of GABA neurotransmitter

53
Q

Type of epilepsy

A

Focal [has focus]

  • simple partial
  • complex partial
  • secondary generalised tonic-clonic

Idiopathic generalised

Epielspy [generalised from outset]

  • myoclonic jersk
  • typical absence
  • primary generalised tonic-clonic
54
Q

PP of NEA

A

often mansifestation of stress
- situations that is intolerable or unaccepetable to a peron and over whihc they have no control
- may be asssociation abuse childhoo
may occur pts epilepsy
- commonly have other medically unexplained Sx

55
Q

Early signs of a stroke

A
  • may have none
  • hyperdensw MCA
  • hloss grey white matter differntiation and sulcal effacement
  • hypodense basal ganglia
56
Q

4 main clinical syndromes with stroke

A
  • total canterior circulation infarction
  • partial anterior ciruclation infarction
  • lacunar stroke
  • posterior circulation infarct
57
Q

Complications of stroke

A
  • raised ICP: cerebral oedema, haemorrhage
  • aspiration
  • pressure sores
  • depression
  • cognitive impairment
  • other medical problems
58
Q

Raised ICP signs

A

HTN, new neurology, GCS

59
Q

High risk after a TIA?

A
  • risk of stroke in first 48 hours
60
Q

What should be done within 2 hours of stroke [NICE]?

A

Endarectomy

  • symptomatic disease [incl. stroke/TIA]
  • 50-90% stenosis
61
Q

NNT to prevent major stroke in symptomatic stenosis 70-99%

A

6%

62
Q

How to manage stroke anaphylasxis?

A

Clopidogrel

63
Q

What is ABCD2 score?

A

Risk of stroke following TIA

64
Q

ABCD2 stand for?

A

Age [over 60], BP [over 140/90], cf [unilateral weakness or speech impairment w/o weakness], duration Sx [over 60m, or 18-59 mins], diabetes

65
Q

How to Mx a TIA?

A

Antiplatelets, 72 hour tape, Dopplers

66
Q

Options for ischaemic [stress ischaemic] stroke with clear recent onset time?

A

Thrombolysis, thrombectomy

67
Q

When thrombolysis allowed?

A

4.5 hours of Sx onset

68
Q

Benefits of thrombolysis?

A

Improves chance of independance on discharge

Benefit decrease with longer Sx duration

69
Q

Risk thrombolysis

A

Risk of death the same

However, haemorrhage 1 in 20 as reaction. Reaction to rTPA.

70
Q

When thrombectomy offered?

A

mechanical retrieval of clot ig clot is seen in proximal anterior circulation and thromblysis
- offered within working hours

71
Q

Outside of time window/following care what should be offered?

A

300mg aspirin for 14d or until discharge; switch to 75mg long-term. IPCO for all pts with reduced mobility.

72
Q

Secondary prevention aftercare?

A

Cholesterol, anti-hypertensives, diet, alcohol, smoking, exercise

73
Q

Driving advice?

A

must not drive for 1m, if ongoing Sx then can drive if safe.

74
Q

Ix of haemorrhagic stroke

A

History and examination
bloods [FBC, UE, LFT, CRP, TFT, coag, lipid]
CT head
stop anticoag, antiplatelet, may drug increase risk
- reverse anticoagulation vitamin K/ Beriplex
- aggressive BP control: under 140 systolic

75
Q

How to manage AF acronym?

A

CHADS2VASc

76
Q

CHADS2VASc acronym stand for?

A

congestive HF, HTN, age [over 75], DM, stroke [TIA/systemic amoblism], vascular disease, age 65-74

If 1 then oral anticoag consiedered
If 2 and over, then oral anticoag recommended

77
Q

HASBLED for?

A
  • assess 1 year risk of major bleeding in pts taking anticoag with AF
  • HTN, abnormal liver/renal function, stroke, INR, elderly, drugs/alcohol, blacking
78
Q

Surgical Mx stroke

A

Extracranial carotid stenosis
Decompressive hemicraniotomy
PCI

79
Q

Risk if PCI

A

Risk hyrocephalus, so EVD/posterior fossa decompression

80
Q

Mx of haemorrhagic stroke

A
  1. ABCDE [monitor envinroment, regular neuro obs [GCS/pupils]
  2. BP [140-160 acutely, over 130/80 long term]
  3. Bleeding tendency [coagulation/ less platelets/ medication]
  4. Underlying malformation [?AVM]
  5. Neurosurgery [superficial clots, CSF obstruction = hydrocephalus etc.]
81
Q

Reversal of anticoagulation

A 
warfarin [beriplex, vitamin K]
heparin [protamine]
LMWH
apixiban/rivaoraixban etc.
Dabigatran

Neurology (13 decks)

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