Pasmedicine/Pastest Flashcards by Jennifer Steen

most common complication of meningitis

sensorineural hearing loss

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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’.

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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

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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

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blood test used to differentiate between seizures and peudoseizures

prolactin

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features of temporal lobe seizure

“HEAD”

Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing), Deja vu/Dysphasia post-ictal)

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frontal lobe seizure

Head/leg movements , posturing, post-ictal weakness

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parietal lobe seizurw

parasthesia

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occipital lobe seizures

flashers/floaters

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vein commonly used for a venous cut down

long saphenous vein

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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

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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

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what should be given in a SAH to reduce risk of cerebral vasospasm

nimodepine

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suspected SAH but CT normal - what is next investigation

LP at 12 hours

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best investigation from diffuse axonal injury

MRI brain

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who needs urgent neurosurgical review even before CT

patients with a GCS or 8 or less

penetrating injury e.g. gunshot wound

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investigation of choice to clear the C spine in trauma

CT spine

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where is brocas area and what type of aphasia do you get

frontal lobe - expressive aphasia

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where is wernickes and what type of aphasia do you get

temporal lobe - receptive aphasia

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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

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treatment of generalised tonic clonic

1st line sodium valproate/lamotrogine

2nd carbamazepine

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absence seizures

1st ethosuxemide or sodium valproate

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myoclonic seizures

sodium valproate

2nd line - lamotrigine

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focal seizures

carbamazepine or lamotrigine

second line: levetiracetam, oxcarbazepine or sodium valproat

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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