DECK PT Flashcards
- Q. What is a transient ischemic attack? What makes it different from a stroke?
A. Focal, sudden onset ischemia (often due to thromboembolism from carotids)
B. Neurological deficit that lasts < 24 hours with complete clinical recovery
C. Causes: Thromboembolism from carotids, cardioembolism, hyperviscosity e.g. polycythaemia
- Q. What is amaurosis fugax?
A. When emboli passes into the retinal artery - “a curtain descending over my field of vision”
Q. What score predicts the risk of stroke after TIA?
A. ABCD2 score: Age > 60 (1), Blood pressure > 140/80 (1), Clinical features:unilateral weakness (2)
or speech impairment without weakness (1), Duration of sx > 60 mins (2), 10-59 mins (1), Diabetes
(1)
- Q. How should TIAs is managed?
A. Ix: ABCD2 score, carotid doppler (no brain changes with TIA - may MRI to look for other existing
infarcts)
B. Tx: 1st line clopidogrel (P2Y12 inhibitor), carotid endarterectomy if stenosis
- Q. What symptoms is an occlusion of the vertebral and basilar arteries likely to produce?
A. Nystagmus, vertigo, dysphagia, ataxia, vomiting, horner’s syndrome
- Q. What symptoms is an occlusion of the cerebellar arteries likely to produce?
A. Vertigo, headache, ataxia, vomiting
Q. What is the most common cause of haemorrhagic stroke?
A. HTN: Charcot-Bouchard’s aneurysms -most often in the basal ganglia due to chronic hypertension
B. Also lobar hemorrhagic strokes due to cerebral amyloid angiopathy (often in elderly)
C. Others: metastatic tumours, AV malformations, hemorrhagic transformation from infarct, anticoag
e.g. warfarin
- Q. How are ischaemic and haemorrhagic strokes differentiated clinically? Describe the treatment for both
A. CT brain (MRI, carotid doppler, cerebral angiography, ECHO, ECG - AF)
B. Ischaemic: 1. Thrombosis IV alteplase < 4.5 hours 2. Aspirin for 2 weeks then clopidogrel
C. Haemorrhagic: 1. BP control with B-blocker, Beriplex if warfarin related bleed, clot evacuation
D. + rehab: physio, OT, SALT,
E. + RF management: antihypertensives, statins
Q. What is the most common cause of subarachnoid haemorrhage? What conditions is it
associated with?
A. Subarachnoid haemorrhage: caused by berry aneurysm causing spontaneous bleed into the
subarchnoid space (or AV malformation, idiopathetic) - where is it likely to occur?
B. Associated with PKD, coarction of the aorta, Ehler’s Danos syndrome
C. Berry aneurysms at bifurcation of arteries - 40% at the anterior communicating artery, posterior
communicating (20)
Q. How is subarachnoid haemorrhage investigated? Managed?
A. CT head (white star shape)
B. LP: wait 12 hours, xanthochromia (yellow) - breakdown of HB → bilirubin
C. Neurosurgery
D. CCB: nimodipine reduces vasospasm and morbidity for cerebral ischemia
Q. Name 3 triggers of migraines, what is the treatment?
A. CHOCOLATE: chocolate, cheese, hangovers, oral contraceptive pill, caffeine, organsms, lie ins,
alcohol, travel, exercise - also by noise and lights
B. Acute: oral triptan e.g. sumatriptan and NSAID
C. Prophylaxis: BB e.g. propanolol
Q. Name 3 triggers of tension headache, what is the treatment?
A. Causes: fumes/smells, stress, noise, concentrated visual effort
B. Tx: reassurance, stress relief, short term analgesia e.g. paracetamol
Q. Name 3 features of cluster headache, what is the tx?
A. Unilateral, occurs in clusters, lasts 15-160 mins, ‘alarm clock’ headache, more common in smokers
and males
B. 100% oxygen (not in COPD), sumatriptan onset
C. Prevention: verapamil
Q. Name 3 features of giant cell arteritis, what conditions can cause it? Ix? Tx?
A. GCA: tenderness, pain in jar, loss of vision, non-pulsatile temporal arteries
B. SS: weight loss, fatigue, proximal muscle pain
C. Secondary causes: SLE, RA, HIV
D. Ix: increased ESR, temporal artery biopsy
E. Tx: high dose steroids e.g. IV methylprednisolone
- Q. Trigeminal neuralgia - Ix? Tx?
A. Ix: MRI, Tx: carbamazepine
Q. Name 4 signs/symptoms of parkinson’s disease
A. Pill-rolling Tremor
B. Cog-wheel Rigidity
C. Bradykinesia
D. Postural instability
E. Cognitive impairment
F. Gait: reduced arm swing on one side, shuffling, stooped posture, difficulty starting
Q. How does Myasthenia Gravis present?
A. Weakness and fatigability - worse at the end of the day
B. Autoimmune IgG autoantibodies attach the postsynaptic actelycholine receptors at NMJ
C. Ix: bedside count to 50, antiAch receptor antibodies, EMG - fatigability, CT/MRI thymus hyperplasia
D. Tx: pyridostigmine (acetylecholinesterase) and prednisolone (immunosuppression)
E. 2nd: methotrexate/cyclosporin, IV immunoglobulin in crisis
Q. What occurs in motor neurone disease?
A. Degeneration of motor neurons in motor cortex and spinal cord (not sensory!)
B. Amyotrophic lateral sclerosis (ALS) is the most common
C. UMN and LMN symptoms = spastic paralysis AND muscle tone loss (no eyes, no sensory, no
sphincters)
D. Ix: ECG, increased creatinine kinase due to muscle breakdown
E. Tx: Na channel blocker: riluzole - slows disease progression
F. Baclofen (spasticity), amitriptyline (Drooling), physio/ventilator etc
