Pasmedicine/Pastest Flashcards
most common complication of meningitis
sensorineural hearing loss
what is hoovers sign
Hoover’s sign of leg paresis is a specific manoeuvre used to distinguish between an organic and non-organic paresis of a particular leg. This is based on the concept of synergistic contraction. If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.
causes of restless leg syndrome
there is a positive family history in 50% of patients with idiopathic RLS iron deficiency anaemia uraemia diabetes mellitus pregnancy
treatment of restless leg syndrome
simple measures: walking, stretching, massaging affected limbs
treat any iron deficiency
dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole)
benzodiazepines
gabapentin
blood test used to differentiate between seizures and peudoseizures
prolactin
features of temporal lobe seizure
“HEAD”
Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing), Deja vu/Dysphasia post-ictal)
frontal lobe seizure
Head/leg movements , posturing, post-ictal weakness
parietal lobe seizurw
parasthesia
occipital lobe seizures
flashers/floaters
vein commonly used for a venous cut down
long saphenous vein
who needs CT head immediately after injury
GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture.
any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
post-traumatic seizure.
focal neurological deficit.
more than 1 episode of vomiting
who needs a CT head within 8 hours of injury
- for adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury:
age 65 years or older
any history of bleeding or clotting disorders
dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
more than 30 minutes’ retrograde amnesia of events immediately before the head injury
also .- warfarin regardless of other risk factors
what should be given in a SAH to reduce risk of cerebral vasospasm
nimodepine
suspected SAH but CT normal - what is next investigation
LP at 12 hours
best investigation from diffuse axonal injury
MRI brain
who needs urgent neurosurgical review even before CT
patients with a GCS or 8 or less
penetrating injury e.g. gunshot wound
investigation of choice to clear the C spine in trauma
CT spine
where is brocas area and what type of aphasia do you get
frontal lobe - expressive aphasia
where is wernickes and what type of aphasia do you get
temporal lobe - receptive aphasia
exmaination signs in meningitis
kernigs sign - cannot straighten leg when hip flexed at 90 dgreesb
brudinskis sign - when neck flexed knees and hips will flex
treatment of generalised tonic clonic
1st line sodium valproate/lamotrogine
2nd carbamazepine
absence seizures
1st ethosuxemide or sodium valproate
myoclonic seizures
sodium valproate
2nd line - lamotrigine
focal seizures
carbamazepine or lamotrigine
second line: levetiracetam, oxcarbazepine or sodium valproat
what type of seizure can carbamazepine make worse
absence
sodium valproate adverse affecrs
increased appetite and weight gain alopecia: regrowth may be curly P450 enzyme inhibitor ataxia tremor hepatitis pancreatitis thrombocytopaenia teratogenic (neural tube defects)
carbemazepine adverse effects
P450 enzyme inducer dizziness and ataxia drowsiness leucopenia and agranulocytosis syndrome of inappropriate ADH secretion visual disturbances (especially diplopia)
lamotrigine adverse effects
Steven johnson syndrome
phenytoin adverse effects
P450 enzyme inducer dizziness and ataxia drowsiness gingival hyperplasia, hirsutism, coarsening of facial features megaloblastic anaemia peripheral neuropathy enhanced vitamin D metabolism causing osteomalacia lymphadenopathy
Brief spasms beginning in first few months of life
1. Flexion of head, trunk, limbs → extension of arms (Salaam attack); last 1-2 secs, repeat up to 50 times
2. Progressive mental handicap
3. EEG: hypsarrhythmia
usually 2nd to serious neurological abnormality (e.g. TS, encephalitis, birth asphyxia) or may be cryptogenic
poor prognosis
infantile spasms (West syndrome)
May be extension of infantile spasms (50% have hx) onset 1-5 yrs atypical absences, falls, jerks 90% moderate-severe mental handicap EEG: slow spike ketogenic diet may help
Lennox-Gastaut syndrome
paraesthesia (e.g. unilateral face), usually on waking up
benign rolandic epilepsy
Typical onset in the teens, more common in girls
1. Infrequent generalized seizures, often in morning
2. Daytime absences
3. Sudden, shock like myoclonic seizure
usually good response to sodium valproate
juvenile myoclonic epilepsy
antibody which may be seen in GBS
Anti GM 1 (25 percent)
antibody which may be seen in Miller fisher
ant GQ1b
management of GBS
plasmapheresis and IV Ig
treatment of chronic inflammatory demyelinating polyneuropathy
steroids and immunosuppression
acute treatment of myaesthenia
plasmaphereses and iV IG
long term treatment of myaesthnia gravis
anti cholinersterase inhibitors - pyrdostymine
thymectomy
steroids
investigation of myaesthenia gravis
EMG
CT thorax
CK normal
autoantibodies: around 85-90% of patients have antibodies to acetylcholine receptors. In the remaining patients, about about 40% are positive for anti-muscle-specific tyrosine kinase antibodies
Tensilon test: IV edrophonium reduces muscle weakness temporarily - not commonly used anymore due to the risk of cardiac arrhythmia
drugs which may exacerbate myaesthenia
penicillamine quinidine, procainamide beta-blockers lithium phenytoin antibiotics: gentamicin, macrolides, quinolones, tetracyclines
what is lambert eaton syndrome
seen in association with small cell lung cancer, and to a lesser extent breast and ovarian cancer. It may also occur independently as an autoimmune disorder. Lambert-Eaton myasthenic syndrome is caused by an antibody directed against pre-synaptic voltage gated calcium channel in the peripheral nervous system
features of lambert eaton
repeated muscle contractions lead to increased muscle strength* (in contrast to myasthenia gravis)
limb girdle weakness (affects lower limbs first)
hyporeflexia
autonomic symptoms: dry mouth, impotence, difficultly micturating
ophthalmoplegia and ptosis not commonly a feature (unlike in myasthenia gravis)
treatment of lambert eaton
treat underlying cancer
immunisupressionw ith steroids or azothiaprine
intravenous immunoglobulin therapy and plasma exchange may be beneficial
what artery is affected in a POCS
vertebrobasilar
what artery is affected in lateral medullary syndrome ie Wallenburg
posterior inferior cerebellar artery
how long can you not drive for after a TIA
a month
how long can you not drive after multiple TIAs
3 months
What is glabella tap
tap on forhead - myerson sign is when blinking fails to cease with tapping
its an extrapyramidal sign
what is cogwheel rigidity
tremor superimposed in increased resting tone
what is multi system atrophy
parkinsonism
autonomic disturbance (atonic bladder, postural hypotension, erectile dysfunction)
cerebellar signs
what is progressive supranuclear palsy
parkinsonism supranuclear ophthalmoplegia Neck dystonia Parkinsonism Pseudobulbar palsy - swallowing difficulties Behavioral and cognitive impairment Imbalance and walking difficulty Frequent falls
what is corticobasilar degeneration
Parkinsonism
Alien hand syndrome
Apraxia (ideomotor apraxia and limb-kinetic apraxia)
Aphasia
what investigation can you do for parkisnons
clinical diagnosis
but if doubt then SPECT
first line treatment of parkinson’s
if the motor symptoms are affecting the patient’s quality of life: levodopa
if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor
what is the risks with dopamine agonists/levodopa
psychosis/hallucinations - more likely with dopamine agonists
neuroleptic malignant syndrome if drug abruptly stopped
impulsively
postural hypotension
excessive daytime somolence (dopamine agonists)
name a comt inhibitor
carbidopa
what is given if levodopa alone does not control motor symptoms
addition of a dopamine agonist, MAO‑B inhibitor or catechol‑O‑methyl transferase (COMT) inhibitor as an adjunct
what is the specific downside to levodopa
decreased efficacy with time
dyskinesia
what do antimuscarinics help with in parkinsons
tremor and rigidity
used to treat drug induced parkinsons
what anticonvulsant cause hyperammonaemia
sodium valproate
what anticonvulsant causes a visual field defect
vigabatrin
what fluid should be avoided in patients with a head injury
dextrose
where does herpes simplex encephalitis tend to affect
temporal lobes
small vs large sensory fibre neuropathy
small- only burnign sensation
large - glove and stocking sensation loss and loss of reflexes
what type of visual field defect occurs most commonly in MS
central scotoma
what type of visual field defect occurs most commonly in papilloedema
increased blind spot
drowsiness, bradycardia and slowrelaxing refexes + hypothermia indicates
hypothyroid coma
nerve at risk in carotid endartectomy
hypoglossal
pupils in brainstem death
unreative dilated pupils