DECK PT Flashcards

1
Q
  1. Q. What is a transient ischemic attack? What makes it different from a stroke?
A

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

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2
Q
  1. Q. What is amaurosis fugax?
A

A. When emboli passes into the retinal artery - “a curtain descending over my field of vision”

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3
Q

Q. What score predicts the risk of stroke after TIA?

A

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)

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4
Q
  1. Q. How should TIAs is managed?
A

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

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5
Q
  1. Q. What symptoms is an occlusion of the vertebral and basilar arteries likely to produce?
A

A. Nystagmus, vertigo, dysphagia, ataxia, vomiting, horner’s syndrome

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6
Q
  1. Q. What symptoms is an occlusion of the cerebellar arteries likely to produce?
A

A. Vertigo, headache, ataxia, vomiting

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7
Q

Q. What is the most common cause of haemorrhagic stroke?

A

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

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8
Q
  1. Q. How are ischaemic and haemorrhagic strokes differentiated clinically? Describe the treatment for both
A

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

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9
Q

Q. What is the most common cause of subarachnoid haemorrhage? What conditions is it

associated with?

A

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)

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10
Q

Q. How is subarachnoid haemorrhage investigated? Managed?

A

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

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11
Q

Q. Name 3 triggers of migraines, what is the treatment?

A

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

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12
Q

Q. Name 3 triggers of tension headache, what is the treatment?

A

A. Causes: fumes/smells, stress, noise, concentrated visual effort

B. Tx: reassurance, stress relief, short term analgesia e.g. paracetamol

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13
Q

Q. Name 3 features of cluster headache, what is the tx?

A

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

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14
Q

Q. Name 3 features of giant cell arteritis, what conditions can cause it? Ix? Tx?

A

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

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15
Q
  1. Q. Trigeminal neuralgia - Ix? Tx?
A

A. Ix: MRI, Tx: carbamazepine

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16
Q

Q. Name 4 signs/symptoms of parkinson’s disease

A

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

17
Q

Q. How does Myasthenia Gravis present?

A

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

18
Q

Q. What occurs in motor neurone disease?

A

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