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2a SB-CS > Neuro 2 > Flashcards

Neuro 2 Flashcards

1
Q

explain the pathophysiology of myasthenia gravis

A

an autoimmune disease, producing antibodies to nicotinic ACh receptors, which interfere with neuromuscular transmission by depleting receptor sites.
immune complexes of anti-ACh receptor IgG and complement are deposited at the post-synaptic membranes.

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2
Q

what drug can cause a transient form of myasthenia gravis?

A

penicillamine

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3
Q

what is the main clinical feature of myasthenia gravis?

A

increasing muscular fatigue - weakness on sustained/repeated activity, that improves after rest

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4
Q

which muscle groups are affected by mysathenia gravis, in order of most affected

A

extra-ocular, bulbar (swallowing, chewing), face, neck, limb girdle, trunk

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5
Q

give some examples of things you can look for to assess mysathenia gravis

A

ptosis (eyelid droop), diplopia, mysathenic snarl on smiling.
voice fades when asked to count to 50.

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6
Q

what specific test would you carry out to investigate myasthenia gravis?

A

tensilon test - IV edrophonium given, shows improvement in weakness for about 5 minutes

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7
Q

what might you seen on serology of a patient with myasthenia gravis?

A

anti-AChR and anti-MUSK antibodies

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8
Q

what eye test might you perform to confirm a diagnosis of myasthenia gravis?

A

see if ptosis improves by >2mm after ice applied to affected lid for >2 mins

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9
Q

how would you treat myasthenia gravis?

A

symptom control - anticholinesterase (pyridostigmine).
immunosuppression - prednisolone for relapses ± azathioprine/methotrexate.

thymectomy may be considered.

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10
Q

how does pyridostigmine help treat symptoms of myasthenia gravis? name a possible side effect and how you would treat it.

A

inhibits acetylcholinesterase enzyme from breaking down ACh - thereby increasing level and duration of action of ACh.
colic, diarrhoea - atropine.

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11
Q

name a gene that causes MND. is this the usual cause?

A

SOD1.

causes rare familiar MND - most cases are sporadic.

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12
Q

what distinguishes motor neurone disease from MS/polyneuropathies?

A

NO sensory loss or sphincter disturbance in MND.

affects upper and motor neurones.

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13
Q

what happens to the nervous system in MND? what is the prognosis?

A

selective loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells.
relentless and unexplained destruction of these neurones.

most die in 3yrs from respiratory failure due to bulbar palsy and pneumonia.

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14
Q

how could you distinguish MND from myasthenia gravis?

A

MND never affects eye movement, myasthenia gravis will.

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15
Q

name the 4 clinical patterns of MND

A

ALS (amyotrophic lateral sclerosis).
progressive bulbar palsy.
progressive muscular atrophy.
primary lateral sclerosis.

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16
Q

describe the features of ALS MND and what part of the CNS it affects.

A

disease of lateral cortiospinal tracts.
causes weakness with UMN signs and LMN wasting.
progressive spastic tetraparesis with LMN signs and fasciculation.

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17
Q

who should you suspect MND in?

A

> 40yrs.
stumbling spastic gait, foot drop ± proximal myopathy.
weak grip and shoulder abduction.

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18
Q

give some UMN and LMN signs that may feature in MND

A

UMN - spasticity, brisk reflexes, upgoing plantars.

LMN - wasting, fasciculation of tongue, abdomen, back, thigh

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19
Q

how would you treat a patient with MND?

A

antiglutamatergic drugs - riluzole - only drug that slows progression.
for drooling - amitriptyline.
muscle spasticity - beclofen.

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20
Q

give 3 organisms that can trigger Guillain-Barre syndrome

A

Campylobacter jejuni, CMV, mycoplasma zoster, HIV, EBV

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21
Q

describe the pattern of disease progression seen in Guillain-Barre syndrome

A

a few weeks after infection, symmetrical ascending muscle weakness starts.
advances quickly - affects all limbs, can lead to paralysis.
progressive phase of up to 4 weeks, followed by recovery

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22
Q

describe the clinical features seen in Guillain-Barre

A

symmetrical ascending muscle weakness.
proximal muscles more affected e.g. trunk, respiratory, cranial nerves.
pain common (e.g. back limb), but no sensory signs.
autonomic dysfunction - sweating, raised pulse, BP changes, arrhythmias.

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23
Q

if you were to perform lumbar puncture on a patient with Guillain-Barre syndrome, what might you see?

A

increased protein

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24
Q

how would you treat a patient with Guillain-Barre syndrome?

A

IV immunoglobulin/plasmapharesis.

heparin to prevent DVT.

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25
Q

give 3 possible clinical features of dementia besides memory loss

A

agitation, aggression, apathy, depression, wandering, hallucination, slow repetitive speech, mood disturbance

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26
Q

list some possible causes of dementia

A

alzheimer’s.
vascular dementia.
Lewy body dementia.
Fronto-temporal dementia.

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27
Q

explain how vascular dementia arises

A

cumulative effects of many small strokes.

sudden onset, with stepwise deterioration.

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28
Q

what are the features of Lewy body dementia?

A

fluctuating cognitive impairment, detailed visual hallucinations, Parkinsonism.
histology = Lewy bodies in brainstem and neocortex.

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29
Q

what are the features of fronto-temporal (Pick’s) dementia and what causes it?

A

frontal and temporal atrophy without Alzheimer’s histology.
genes on chromosome 9.

executive impairment, behavioural/personality change, preservation of episodic memory, disinhibition, hyperorality, stereotyped behaviour, emotional unconcern

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30
Q

how would you diagnose dementia?

A

clinical history + timeline of progression - ask relatives/spouse!
cognitive testing - AMTS/TYM (dementia screens), mental state examinations.
CT/MRI.

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31
Q

how would you manage dementia?

A

develop routines early on - retained until later, prolongs independence.
trazodone, lorazepam.
watch for depression - SSRIs (citalopram).

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32
Q

what genetic disorder is associated with Alzheimer’s disease?

A

Down’s syndrome - will inevitably progress to Alzheimer’s

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33
Q

describe the pathology behind Alzheimer’s disease

A

accumulation of beta-amyloid peptide (a degradation product of amyloid precursor protein) results in progressive neuronal damage, neurofibrillary tangles, raised numbers of amyloid plaques and loss of ACh.
neuronal loss is selective - hippocampus, amygdala, temporal neocortex and subcortical nuclei.

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34
Q

give 3 risk factors for Alzheimers disease

A

1st degree relative with AD.
Down’s syndrome.
homozygous for apolipoprotein e (ApoE) 4 allele, vascular risk factors, decreased physical/cognitive activity, depression, loneliness

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35
Q

give some clinical features of Alzheimers disease

A

general dementia features.
plus - enduring, progressive and global cognitive impairment, loss of visuo-spatial skill.
memory, verbal abilities and executive function affected.
late features - irritability, mood changes, behavioural change, psychosis, agnosia.
anosognosia - lack of understanding of the problems caused by the disease.

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36
Q

how might you treat Alzheimer’s disease dementia?

A 
acetylcholinesterase inhibitors (rivastagmine, donezepil, galantamine).
antiglutamatergic treatment (memantine).
folic acid and B vits.
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37
Q

give 2 mechanisms by which you can develop neuropathy

A

demyelination - Schwann cell damage.
Axonal degeneration - axon damage, conduction remain intact.
Wallerian degeneration - follows nerve section.
Compression - disruption of myelin sheath.
Infarction - microinfarction of vasa nervorum.
Infiltration - by inflammatory cells, granulomas and neoplastic cells.

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38
Q

what are Tinel’s sign and Phalen’s test and what are they used for?

A

Tinel’s - lightly tap over a nerve to induce irritation in it e.g. over the wrist.
Phalen’s - ask patient to hold wrists in full flexion (reverse prayer position) for 30-60s, press on wrist if needed, should get tingling sensation/pain.

they are diagnostic for carpal tunnel.

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39
Q

give 3 diseases carpal tunnel is associated with

A

diabetes mellitus, acromegaly, hypothyroidism, amyloidosis, rheumatoid disease.

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40
Q

what is otherwise known as ‘Saturday night palsy’?

A

radial nerve compression - causes wrist drop and weakness of brachioradialis and finger extension, sensory loss in anatomical snuff box

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41
Q

what nerve controls the ankle jerk reflex?

A

S1

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42
Q

a slim female yoga instructor comes to see her doctor complaining that her left foot keeps dragging on the floor, what do you think could be causing her problem?

A

common peroneal palsy - her symptoms are due to weakness of ankle eversion and extension, she probably also has numbness over anterolateral border of dorsum of foot and lower shin

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43
Q

a patient comes in having had an accident on the rugby pitch with a suspect elbow fracture, he’s now complaining of sensory loss over his little finger and medial side of his hand, what do you think could be causing his symptoms and if left untreated, what could he go on to develop?

A

ulnar nerve compression, could go on to develop weakness/wasting of medial wrist flexors, interossei, medial 2 lumbricals and hypothenar eminence

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44
Q

what changes in the spine could there be in cervical/lumbar degeneration?

A

osteophytes, thickening of spinal ligaments, narrowing of spinal canal, disc degeneration and protrusion, vertebral collapse, ischaemic changes

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45
Q

what would be felt in the myotome and dermatome affected by a spinal nerve root lesion?

A

myotome - pain of root compression.

dermatome - tingling discomfort.

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46
Q

give 2 causes of nerve root lesions

A

spondylosis, herpes zoster, tumours, meningeal inflammation.

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47
Q

give 2 causes of anosmia caused by an olfactory nerve palsy

A

respiratory tract infection, olfactory groove tumour, meningitis

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48
Q

if someone is referred to you with suspected Horner’s syndrome, what do you expect to find on examination?

A

unilateral pupillary constriction with slight ptosis and enophthalmos, loss of sweating on same side

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49
Q

a patient comes to see you complaining of visual loss at the ‘sides of his eyes’ on both sides and has some vague endocrine symptoms, what are you thinking is the cause, what kind of visual loss does he have and where is the lesion?

A

pituitary neoplasm pressing on the optic chiasm causing bitemporal hemianopia.

50
Q

you are performing a cranial nerve examination on a patient who has an oculomotor nerve lesion (CN3), what would you see?

A

ptosis, large pupil, eye down and out.

51
Q

what kind of visual symptoms would you get with a trochlear nerve lesion?

A

diplopia on looking down and in

52
Q

complete external opthalmoplegia is due to palsy of which nerves and what does it cause?

A

palsy of the oculomotor, trochlear and abducens (III, IV and VI) nerves causing complete paralysis of the eye

53
Q

what is the corneal reflex and what nerve controls it?

A

trigeminal nerve.

involuntary blinking of eye when the cornea is stimulated by something such as cotton wool.

54
Q

a small child presents to you with a vesicular rash on the side of their face, their mother says they’ve been struggling to eat recently as well - what do you suspect is the cause and how would you treat it?

A

Ramsay Hunt syndrome caused by herpes zoster/shingles, treat with fanciclovir

55
Q

name a drug that can cause sensorineural deafness?

A

gentamicin, furosemide

56
Q

what symptoms are caused by vestibular nerve palsy?

A

vertigo, loss of balance and nystagmus

57
Q

why do lesions of the glossopharyngeal and vagus appear together?

A

they both leave the skull through the jugular foramen

58
Q

a patient is struggling to turn their head to the right - they think the’ve slept on it in a weird position. what nerve could have been damaged?

A

left hand side acessory nerve

59
Q

you ask a patient to stick their tongue out and it immediately deviates to the right and is very stiff to move, what do you suspect?

A

UMN lesion affecting the right hypoglossal nerve

60
Q

what is mononeuritis multiplex? give 3 examples of causes

A 
2+ peripheral nerves affected, causes tend to be systemic - WARDS PLC:
Wegener's
AIDs/Amyloid
Rheumatoid 
Diabetes mellitus
Sarcoidosis
PAN
Leprosy
Carcinomatosis
61
Q

list the muscles involved in precision grip. what nerve controls us, and what are its spinal roots?

A 
median nerve - C6-T1.
LOAD:
2 Lumbricals
Opponens pollicis.
Abductor pollicis brevis
Flexor pollicis brevis
62
Q

describe the patterns of sensory loss seen in the hand

A

median nerve damage - loss of radial 3.5 fingers and palm.

ulnar - medial/ulnar 1.5 fingers.

63
Q

give a sign of radial nerve damage and an example of how this may occur

A

wrist and finger drop - compression against humerus

64
Q

give a sign of ulnar nerve damage and how it may occur

A

weakness/wasting of ulnar side wrist flexors, interossei (can’t cross fingers) and medial two lumbricals (claw hand).
hypothenar eminence wasting.

65
Q

how would brachial plexus damage present?

A

pain/paraesthesiae and weakness in affected arm.

66
Q

how would phrenic nerve (C3-5) damage present?

A

orthopnoea with raised hemidiaphragm on CXR.

67
Q

how might damage to the lateral cutaneous nerve of the thigh present (L2-L3)?

A

meralgia paraesthetica - anterolateral burning thigh pain from entrapment under inguinal ligament

68
Q

how would sciatic nerve damage present (L4-L5)?

A

affects hamstrings and all muscles below the knee - foot drop.
loss of sensation below the knee laterally.
pelvic tumours/fractures.

69
Q

give 2 signs of damage to the common peroneal nerve (L4-S1)

A

foot drop, weak ankle dorsiflexion/eversion, sensory loss over dorsum of foot

70
Q

how would tibial nerve damage present (L4-S3)?

A

unable to stand on tiptoe, invert foot or flex toes.

originates from sciatic nerve just above the knee.

71
Q

describe the clinical features of carpal tunnel syndrome

A

aching pain in hand and arm, esp at night.
paraesthesiae in thumb, index and middle fingers.
relieved by dangling hand over edge of bed and shaking it - wake and shake.

72
Q

list 3 causes of carpal tunnel syndrome

A 
MEDIAN TRAPS:
Myxoedema.
Enforced flexion (Colles' splint).
Diabetic neuropathy.
Idiopathic.
Acromegaly.
Neoplasms e.g. myeloma.
benign Tumours.
Rheumatoid arthritis.
Amyloidosis.
Pregnancy/premenstrual oedema.
Sarcoidosis.
73
Q

how might you manage carpal tunnel syndrome?

A

splinting, local steroid injection, decompression surgery.

74
Q

describe the features of a UMN lesion

A 
pyramidal weakness - arm extensors, small muscles of hand and lower limb flexors.
no muscle wasting. 
spasticity in stronger muscles.
hyperreflexia.
upgoing plantars.
75
Q

describe the features of a LMN lesion

A

damage to anterior horn cells, nerve roots, plexi or peripheral nerves.
distribution of weakness corresponds to those muscles supplied by the involved cord segment etc.
muscles show wasting ± fasciculation.
hypotonia/flaccidity - limb feels soft and floppy.
reduced/absent reflexes.
plantars remain flexors.

76
Q

give the 2 subtypes of gliomas

A

astrocytoma and oligodendroglioma

77
Q

name 3 types of primary malignant brain tumour

A

glioma, embryonal tumours, lymphoma

78
Q

name 2 types of benign brain tumour

A

meningioma, neurofibroma (e.g. from Schann cells)

79
Q

what is the most common cause of brain tumours?

A

metastases:

bronchus, breast, stomach, prostate, thyroid, kidney.

80
Q

what are the common sites of meningiomas?

A

parasagittal region, sphenoidal region, subfrontal region, pituitary fossa and skull base

81
Q

what are the 4 main classes of symptoms you can get from a brain tumours?

A

raised ICP, seizures, focal neurology, personality change

82
Q

what investigation would you use to stage a brain tumour?

A

CT/MRI + CXR etc to look for primary

83
Q

how would you manage a brain tumour?

A

surgical removal if possible.
IV/PO dexamethasone to reduce cerebral oedema.
phenytoin to treat epileptic seizures.
radiotherapy.

84
Q

name 3 organisms that commonly cause meningitis

A

Neisseria meningitides, Streptococcus pneumoniae, H influenzae, Listeria monocytogenes.

immunocompromised - CMV, cryptococcus, TB.

85
Q

list some clinical features of meningitis

A

neck stiffness (Brudzinski’s neck sign), headache, fever.
cold hands and feet.
photophobia, Kernig’s sign (pain + resistance on passive knee extension when hip fully flexed).
non-blanching petechial rash.

vomiting, rigors, irritability, papilloedema.

86
Q

give 3 differential diagnoses of meningitis

A

malaria, encephalitis, septicaemia, subarachnoid haemorrhage, dengue, tetanus

87
Q

what antibiotics would you give to a patient presenting with meningitis?

A

cefotaxime - 3rd gen cephalosporin

88
Q

what would you need to do, apart from treat them, if you were presented with a patient with meningitis?

A

contact tracing for prophylaxis.

inform local officer/PHE.

89
Q

what drugs would you give for meningitis prophylaxis?

A

rifampicin or ciprofloxacin.

90
Q

give 2 viral causes of encephalitis

A

(viral is more common than bacterial)

herpes simplex, coxsackie, EBV, mumps, CMV, VZV, measles, rabies

91
Q

give 2 non-viral causes of encephalitis

A

bacterial meningitis, TB, malaria, listeria, lyme disease, Legionella, leptospirosis, aspergillosis, typhus

92
Q

what is encephalitis?

A

inflammation of brain parenchyma

93
Q

what clinical features would make you suspect encephalitis?

A

(can be mild, self-limiting - fever/headache/drowsiness)

odd behaviour, decreasing consciousness, seizures, focal neurology, headache, fever, history of travel/animal bite

94
Q

if you performed a lumbar puncture on a patient with encephalitis, would would you expect to see?

A

increased WCC, increased protein

95
Q

how would you treat a patient with viral encephalitis?

A

IV acyclovir, phenytoin for seizures

96
Q

what is the primary infection in shingles?

A

chicken pox - reactivation of herpes zoster/varicella zoster virus

97
Q

what are the clinical features of shingles?

A

dermatome distribution of rash (papules and vesicles), pain and tingling.
most common in lower thoracic dermatomes and ophthlamic division of trigeminal nerve.

98
Q

how would you treat shingles?

A

oral acyclovir or valaciclovir as early as possible

99
Q

what is the main complication of shingles and how would you treat it? how is it prevented?

A

post-herpetic neuraligia - pain in distribution of affected nerves.
treat with carbamazepine or phenytoin.

prevented by prompt antiviral treatment.

100
Q

how do anti-epileptic drugs work?

A

they work on sodium channels to inhibit action potentials to stop continuous firing of neurones

101
Q

pyridostigmine is used in a neurotransmitter disease, which one and how does it relieve symptoms?

A

myasthenia gravis - acetylcholinesterase inhibitor, which means ACh is around longer to attach to the post-synaptic membranes

102
Q

baclofen is used for muscle spasticity in what disease, and how does it work?

A

Huntington’s chorea - GABA agonist.

103
Q

what type of drug do you prescribe in trigeminal neuralgia?

A

anti-epileptic, carbamazepine

104
Q

ceftriaxone is prescribed in bacterial meningitis, what class of antibiotic is it?

A

3rd generation cephalosporin

105
Q

give 2 examples of benzodiazepines. what are they used for?

A

diazepam, lorazepam, chlordiazepam - first line management of seziures and status epilepticus, management of alcohol withdrawal rections.

106
Q

how do benzodiazepines work?

A

target the gamma-aminobutyric acid type A (GABA-a) receptor, which is a chloride channel that opens in response to binding by GABA (main inhibitory neurotransmitter) - opening the channel makes the cell more resistant to depolarization.

benzodiazepines facilitate and enhance binding of GABA to GABA-a receptors and have a widespread depressant effect on synaptic transmission - cause reduced anxiety, sleepiness, sedation, anti-convulsion.

107
Q

what is carbamazepine used to treat?

A

epilepsy - focal seizures ± secondary generalisation and for primary generalised.
trigeminal neuralgia.

108
Q

how does carbamazepine work?

A

inhibits neuronal sodium channels, stabilising resting membrane potentials and reducing neuronal excitability.

this may inhibit spread of seizure activity, and control spread of neuralgic pain by blocking synaptic transmission.

109
Q

what are valproates used for? name one.

A

epilepsy - 1st choice for generalised/absence seizures and focal seizure treatment.
sodium valproate, valproic acid.

110
Q

what are gabapentin/pregabalin used to treat?

A

focal epilepsies as an addition to carbamazepine.

also for neuropathic pain and migraine prophylaxis.

111
Q

how does gabapentin work?

A

closely related to GABA - binds to voltage sensitive calcium channels, preventing inflow of calcium and thus inhibiting neurotransmitter release, interfering with synaptic transmission and reducing neuronal excitability.

112
Q

give some examples of dopaminergic drugs

A

levodopa (as co-careldopa, co-beneldopa), ropinirole, pramipexol

113
Q

how do dopaminergic drugs work to treat Parkinson’s?

A

there’s a dopamine deficiency in Parkinson’s - treatment increases dopaminergic stimulation to the basal ganglia.
levodopa = dopamine precursor that is able to cross the BBB.
ropinirole and pramexipol = selective agonists for the D2 receptor, which predominates in the basal ganglia - used to delay starting levodopa.

114
Q

what is levodopa always given with? why?

A

a peripheral dopa-decarboxylase inhibitor e.g. carbidopa - combined preparations (co-careldopa, co-beneldopa).
this is to reduce conversion to dopamine outside the brain, reducing SE of nausea, and lowering the dose.

115
Q

what are triptans used to treat?

A

migraines and cluster headaches - not preventative/curing though.
e.g. sumatriptan, rizatripan.

116
Q

how do triptans work?

A

agonist effects on serotonin 5-HT-1b and d receptors in cranial blood vessels - causes their constriction, and subsequent inhibition of pro inflammatory neuropeptide release.
may also work on serotonin receptors in nerve endings to relieve pain through decrease in levels of substance P.

117
Q

what class of drug do rivastigmine and neostigmine belong to? what are they used to treat?

A

acetylcholinesterase inhibitors.

Alzheimer’s disease, Lewy body dementia and Parkinson’s disease. also myasthenia gravis.

118
Q

how do acetylcholinesterase inhibitors work as neurological drugs?

A

inhibit ACh break down. in neurodegenerative disorders they are used to treat memory and learning deficit symptoms - improve due to role of ACh in cognition.
in myasthenia gravis there are too few ACh receptors, so with greater ACh availability, symptoms improve.

119
Q

list 3 things that can worsen the weakness of myasthenia gravis

A

pregnancy, hypokalaemia, infection, over-treatment, change of climate, emotion, exercise

120
Q

what would you see in a patient with an abducens nerve (CNVI) lesion?

A

horizontal diplopia on looking out

121
Q

what might patients complain of in mysathenia gravis?

A

“stairs, chairs and hair”

can’t get up out of chairs, can’t walk up the full flight of stairs, can’t brush their hair.

2a SB-CS (18 decks)

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