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PACES initial prep Flashcards

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1
Q

Differential diagnosis for a systolic murmur

A

Aortic stenosis - ejection systolic, louder over aortic region, radiates to carotids

Mitral regurgitation - pansystolic, louder over mitral region and radiates to axilla

Aortic sclerosis - shorter, softer, less harsh, does not radiate

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2
Q

Most common causes for aortic stenosis

A

Elderly = degenerative calcification
Younger = congential bicuspid
Very rare = rheumatic fever

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3
Q

Signs of severe aortic stenosis

A

Murmur
Slow rising pulse
Evidence of decompensation
soft/absent S2
longer murmur

ECG - evidence of LVH
ECHO - mean gradient over 40, peak gradient over the value of 64

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4
Q

TAVI vs AVR

A

Over 75 normally get TAVI
younger population = normally surgical

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5
Q

Complications associated with untreated aortic stenosis

A

heart failure
brady and tachy-arrhythmias
anaemia/angiodysplasia - Heyde syndrome

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5
Q

Complications post-TAVI

A

10% end up requiring pacemaker
vascular access complication - stent or operation required
stroke, MI, annular rupture, perforate apex

Prognosis untreated = 50% of 1 year mortality

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6
Q

Causes of sensory polyneuropathy

A

Most common = diabetes

Metabolic causes - hypothyroidism, uraemia, vitamin b1, b6, b12

Toxic causes - chemotherapy, abx, alcohol

Inflammatory conditions - CIDP, sarcoidosis, ANCA positive vasculitis, RA

Paraneoplastic causes - organ malignancy or paraproteinaemia

Rarer causes - genetic, or infections such as HIV

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6
Q

Bedside measures to work out cause of sensory polyneuropathy

A

Ophthalmoscopy - diabetic retinopathy
urinarlysis - glucose in urine
BM measurement
HbA1c
Lying and standing BP - autonomic instability

FBC - macrocytic anaemia
U&E for urea level
LFT - transaminase derangement in alcohol use

TFT, vitamin B12
ESR - autoimmune inflammatory condition, connective tissue disease screen
Immungoglobulins and serum electrophroesis

Neurophysiological studies such as nerve conduction and electromyography
- length dependant (not length dependant tend to be inflammatory)

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7
Q

Nerve conduction studies in peripheral neuropathy

A

distinguish between demyelinating or axonal

normally axonal
demyelinating seen in GBS or CIDP

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8
Q

Points for peripheral neuropathy caused by diabetes

A

Midline gait ataxia
Romberg positive due to sensory ataxia

stocking distribution of sensory loss
hyporeflexia
ataxic gait
distal weakness

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9
Q

Diabetes peripheral neuropathy management

A

Tight glycaemic control
Physiotherapy for gait stability
Regular podiatry for foot care

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10
Q

Peripheral neuropathy - demyelinating vs axonal causes

A

Demyelinating - GBS, CIDP, Amiodarone, Hereditary sensorimotor neuropathy type 1, paraprotein neuropathy
** diabetes, vitamin B12 deficiency

Axonal pathology - alcohol, diabetes, vasculitis, vitamin B12, hereditary sensorimotor neuropathy type 2

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11
Q

Investigations for Charcot Marie Tooth disease/ HSMN

A

Neurophysiology - determine if demyelinating or axonal (type 1 is associated with demyelination)

Genetic condition - autosomal dominant - so genetic studies

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12
Q

Treatments available for Charcot Marie Tooth disease/ HSMN

A

no disease modifying treatment
important to be diagnosed
genetic - help direct family members

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13
Q

Management plan for Charcot Marie Tooth Disease

A

No disease modifying treatment
MDT approach

physio - help with mobility
orthotics - bilateral foot orthoses which help him drive
occupational therapy team - help at home
psychology team linked to chronic neurological conditions - provide support

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14
Q

What is Charcot Marie Tooth disease/ HSMN?

A

most common hereditary peripheral neuropathy
predominantly motor loss
no cure, managed on physical and occupational therapy

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15
Q

Features of Charcot Marie Tooth disease/ HSMN

A

hx of frequently sprained ankles
foot drop
high arched feet - pes cavus
hammer toes
distal muscle weakness
distal muscle atrophy
hyporeflexia
stork leg deformity

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16
Q

Asymmetric spastic paraparesis/ partial Brown Sequard syndrome differentials

A

Compressive causes - disk herniation, tumours (intramedullary/extramedullary, primary or secondary - mets), spinal stenosis

Autoimmune causes - multiple sclerosis, lupus, sarcoidosis

Infectious causes - HIV, varicella

Nutritional - B12 and copper deficiency

Rarer diseases - genetic = hereditary spastic, paraparesis

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17
Q

Signs you would find in cervical myelopathy (already examined lower limbs)

A

Completely normal cranial nerve examination

Upper limbs - increased tone, reduced power, brisk reflexes, potentially a sesnory level in the cervical region

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18
Q

Features in history to help determine aetiology of someone’s myelopathy

A

onset and progression

minutes - vascular
acute - over a day or two - trauma or disk herniation

subacute (days to weeks) - autoimmune = demyelination and lupus

more chronic time (months - years) - genetic causes

previous episodes of neurological dysfunction - caused by demyelination

full systems enquiry - autoimmune causes and malignancies

full family history

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19
Q

Summarise features for spastic paraparesis

A

increased tone
ankle clonus
brisk reflexes
mild weakness

UMN signs

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20
Q

Pale optic disc
Rapid Afferent pupillary defect
- optic neuropathy

partial myelopathy

A

multiple sclerosis

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21
Q

Left sided homonymous hemianopia likely due to R MCA infarct

other signs?

A

increased tone
reduced power
hyperreflexia
any evidence of clonus

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22
Q

Localising the lesion with left sided homonymous hemianopia

A

respected midline
no evidence of macular sparing
left sided sensory changes
= middle cerebral artery stroke

macular sparring = posterior cerebral artery stroke

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23
Left sided homonymous hemianopia secondary to likely MCA infarct what other physical signs would you want to look for?
pulse - irregularly irregular like in AF - increase risk of stroke BP - HTN associated with high risk of stroke auscultate caotirs - evidence of bruit = stenosis in that vessel auscultate heart - cardiac mumur = valvular disease = increased risk of stroke
24
Trigeminal neuropathy vs MCA infarct
check sensation on neck - would still be gone in MCA infarct no corneal reflex in trigeminal neuropathy
25
Initial tests confirm ischaemic stroke - next tests?
carotid doppler - for stenosis ECHO - cardiac thrombus or valvular disease Holter tape - for arrhythmia
26
Hyperacute management for stroke vs presenting in clinic
hyperacute - possibility of thrombolysis with CT head long term - anti-platelet therapy, statin, ACE inhibitor
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Total anterior circulation infarct
unilateral hemiparesis and/or hemisensory loss of face, arm and leg homonymous hemianopia higher cortical dysfunction - dysphasia etc. Middle and anterior cerebral arteries
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Partial anterior circulation infarcts
smaller arteries of anterior circulation (upper or lower division of MCA) 2/3 - homonymous hemianopia - unilateral hemiparesis and/or hemisensory loss of face, arm and leg higher cognitive dysfunction
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Lacunar infarct
perforating arteries around internal capsule, thalamus and basal ganglia 1 out of: - unilateral weakness and/or sensory deficit of face, arm and leg or all three - pure sensory stroke - ataxic hemiparesis
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Posterior circulation infarct
vertebrobasilar arteries 1 out of: - cerebellar or brainstem syndromes - loss of consciousness - isolated homonymous hemianopia
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Lateral medullary syndrome - Wallenberg's syndrome
posterior inferior cerebellar artery ipsilateral - ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy (Horner's) contralateral - limb sensory loss
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Weber's syndrome
ipsilateral 3rd nerve palsy contralateral weakness
33
Homonymous hemianopia - where is the lesion?
same side both eyes incongruous defect - lesion of optic tract congruous defect - lesion of optic radiation or occipital cortex macula sparing - lesion of occipital cortex
34
Homonymous quadrantanopias
Superior - lesion of inferior in temporal lobe inferior - lesion of superior in parietal lobe PITS
35
Bitemporal hemianopia - where is the lesion?
lesion of optic chiasm Upper quadrant defect > lower = inferior chiasmal compression == pituitary tumour Lower quadrant defect > upper = superior chiasmal compression == craniopharyngioma
36
Asymmetrical spastic paraparesis and signs of MS - what other eye signs would you look for?
Eyes - relative afferent pupillary defect and pale optic disc - keeping with optic neuropathy Examining eye movement - failure of one eye to adduct with nystagmus on abduction of other eye = lesion in medial longitudinal fasciculus -- internuclear ophthalmoplegia
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Investigations in MS
MRI of cervicothoracic spine MRI of brain - presnce of lesions in other places - lesions in periventricular region lumbar puncture - normal cell count, oligoclonal bands present in MS
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Acute flare of MS management
relapse of MS High dose IV corticosteroids such as methylprednisolone - need negative urine dip and no signs of infection before starting this - warn: affect sleep, personality changes, mania, gastrointestinal ulceration, rarely cause avascualr necrosis - monitor - blood glucose
39
Spasticity vs rigitidity in tone
spasticity is velocity dependant - rapid movement makes it more obvious rigidity - speed of movement makes no difference
40
Causes for cerebellar syndrome of ataxia
Acute - stroke, either infarct or haemorrhage Relapsing and remitting - multiple sclerosis which can affect cerebellum social history - alcohol intake rarer causes - genetic or paraneoplastic causes of cerebellar degeneration
41
Cerebellar ataxia - signs you would look for (did upper limb)
eyes - nystagmus and expect jerky movements when checking pursuit movements speech - repeat 42 West Register Street or baby hippopotamus
42
Investigating cerebellar ataxia syndrome
MRI is far superior to CT when imaging the posterior fossa CT plays an important role in hyper-acute presentations when haemorrhage needs to be rapidly excluded
43
Considerations when managing a patient with an ataxic syndrome
base on underlying cause - any reversible causes MDT approach - physio - help with mobility and exercises to preserve strength - occupational therapists to see what adaptations can be made at home - mobility aids to help with independance
44
Lifestyle advice for cerebellar ataxia syndrome
occupation - any risk whilst at work, any adaptations to make at work medical history - medications that could contribute or exacerbate any causes of dizziness or unsteadiness Reduce alcohol consumption as it can exacerbate symptoms
45
Ataxia - sensory or cerebellar
cerebellar = nystagmus and dysarthria - evidence of scanning or staccato speech all 4 modalities of sensation would be intact sensory = impaired sensation (joint position sense and vibration), pseudoathetosis, finger-nose with eyes open but struggle with eyes closed - caused by central or peripheral (both in B12 deficiency) central - spinal cord pathology - dorsal column damage peripheral - neuropathy with large myelinated sensory fibres most obviously affected
46
PDA murmur on auscultation - evaluate this further?
full history young - abnormalities at birth FH of congential heart disease full set of blood tests inflammatory markers 3 sets of blood cultures ECHO would be diagnostic investigation
47
Concerning features on ECHO for patent ductus arteriosus
raised pulmonary pressures dilated pulmonary arteries evidenve of right ventricular dilation and tricuspid regurgitation evidence of left ventricular dysfunction
48
PDA vs pulmonary stenosis
PDA - loudest in expiration, radiates to the back and loudest over left scapula pulmonary stenosis - loudest in inspiration, radiates to centre of the back and also to the shoulders
49
Severity of PDA based on examination findings
collapsing pulse right ventricular heave evidence of left ventricular failure left subclavicular thrill, heaving apex beat, wide pulse pressure making it to adulthood - not as severe
50
How does inspiration make right sided murmurs louder
Inspiration - human body increases its venous return more flow across the right sided heart valves more flow across pulmonary and tricuspid valves - increases the severity and character of the murmur
51
What is patent ductus arteriosus?
ductus arteriosus is a connection between proximal left pulmonary artery and descending aorta, just distal to left subclavian artery in a developing fetus fetus lungs filled with amniotic fluid so this allows a connection for blood from right ventricle to bypass the non-functioning lungs at birth, usually closes and becomes ligamentum arteriosum failure of connection = condition patent ductus arteriosus. Can be associated with other heart conditions but in adults, usually isolated finding.
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Tests for patent ductus arteriosus
ECHO - diagnosis, info on LV volume overload, estimate pulmonary artery pressure and info on pulmonary artery size and right heart dimensions cardiac MR and cardiac CT Invasive assessment when pulmonary artery pressure is estimated to be high on ECHO Cardiac catheterisation - invasive measurement of right sided pressures and calculation of pulmonary and systemic vascular resistance
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Indications for closure of PDA
signs of LV volume overload patients with pulmonary hypertension but with pulmonary artery pressure less than 2/3rds of systemic pressure or a pulmonary vascular resistance < 2/3rds of SVR
54
PDA follow up after closure
no residual shunt, normal left ventricle and normal pulmoanry artery pressure - do not require follow up beyond 6 months LV dysfunction or residual pulmonary HTN should be followed up at 1-3 year intervals depending on severity and should include evaluation in specialised grown up congenital heart disease centre
55
Mononeuritis multiplex vs ulnar nerve lesion what would you do? key signs to differentiate
full history, cranial nerves and lower limbs reflexes normal in ulnar nerve lesion inflammatory neurological condition - some degree of areflexia
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Ulnar nerve lesion vs major upper limb peripheral nerves
ulnar - radial nerve wrist extension was strong strong finger extension - good motor function at posterior interosseus nerve strong abductor pollicis brevis = good motor function of median nerve sensation will only affect ulnar distribution
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Finger extension which motor nerve?
motor - posterior interosseous nerve
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Abductor pollicis brevis
motor function - median nerve
59
Treatments for sharp, shooting pains in the hand - ulnar nerve lesion
1st line - tricyclic agent for neuropathic pain - amitriptyline SE - drowsiness and dry mouth 2nd line - anti-epileptic drug for neuropathic pain - gabapentin or pregablin 3rd line - SNRI - duloextine not tolerate tablets - topical therapy like capsicum patch
60
Investigations in ulnar nerve lesion
Neurophysiological testing nerve conduction studies - help localise lesion more thoroughly Electromyography - provide some prognosis in terms of recovery Doubt on cervical radiculopathy - MRI of neck
61
Wrist extension - which nerve?
radial nerve
62
Finger extension - which nerve?
posterior interosseous
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abductor pollicis brevis - supplied by which nerve?
median nerve on thumb
64
History taking - distinguish between MND, multifocal motor neuropathy with conduction block and Kennedy's disease
MND - asymmetrical disease process, rapid and quite aggressive behavioural or cognitive dysfunction to fit with frontotemporal dementia Multifocal motor neuropathy - pronouned distal weakness early in the disease process, complaining of clumsiness Kennedy disease - family history
65
Key management steps in MND/ALS
Specialist neurology clinic - neurologist and MND specialist nurses consider riluzole MDT apprach - supportive measures and patient centred Physio OT Regular screening - weight, appetite, swallow - consider PEG - communication aids - respiratory function - early morning blood gas - FVC T2RF - quite common - need NIV at night cough assist devices cognitive and behavioural changes that could suggest frontotemporal dementia
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Weakness, wasting and fasciculations
Motor neuron disease presence of combined UMN and LMN - changes in bulbar segment, cervical segment, thoracic and lumbosacral segments
67
How does Motor Neuron disease present in terms of signs?
Upper and Lower Motor Neuron Signs with absence of any sensory signs some also have co-morbid frontotemporal dementia
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Other differentials for Motor Neuron Disease
Spinal muscular atrophy Kennedy's disease - peri-oral fasciculations both have mainly lower motor features primary lateral sclerosis - mainly UMN features
69
Ix if thinking motor neuron disease?
Neurophysiology - looking at peripheral nerves for evidence of denervation and lack of sensory changes if thinking Kennedy disease - genetic tests
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General management of degenerative motor system disorder (like MND)
Riluzole is only drug treatment - improved prognosis Supportive measures - MDT approach - consultant neurologist, nurse specialist, OT, physio - SALT - consider PEG - Respiratory function - may benefit from NIV - improves quality of life
71
What is Kennedy's disease?
X-linked spino-bulbar muscular atrophy motor system disorder but only LMN affected perioral fasciculations = pathognomonic X linked recessive associated with androgen insensitivity very slow rate of progression which distinguishes it from sporadic amyotrophic lateral sclerosis
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1st heart sound
closing of mitral and tricuspid valves at the beginning of ventricular systole - prevent backflow into atria - heart begins to pump blood out to the lungs and body - heard best at heart's apex
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2nd heart sound
caused by the closure of aortic and pulmonary valves at the end of ventricular contraction made up of A2 and P2 - aortic valve and pulmonary valve normal splitting - A2 closes before P2 not heard in expiration
74
3rd heart sound
early diastolic sound caused by rapid ventricular filling - due to dilated, overly compliant ventricle in heart failure also seen in severe mitral or tricuspid regurgitation best heard in left lateral decubitus position
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4th heart sound
heard during atrial contraction - caused by blood being forced into a stiff or hypertrophic ventricle - left ventricular hypertrophy - caused by HTN or aortic stenosis atrial gallop heard at end of diastole do not hear S4 in AF - requires strong, synchronised atrial contraction to occur
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