20 cards Flashcards
Which Ab do patients with myasthenia gravis have
Acteylecholine receptor AB
What syndrome is bronchial adenoma associated with
Purulent sputum
Carcinoid syndrome - flushing, diarrhoea, dyspnea
First line radiological investigation for suspected stroke
Non contract CT head
Clin F of guillian barre
The characteristic features of Guillain-Barre syndrome is progressive, symmetrical weakness of all the limbs.
the weakness is classically ascending i.e. the legs are affected first
reflexes are reduced or absent
sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs
Other features
there may be a history of gastroenteritis
respiratory muscle weakness
cranial nerve involvement
diplopia
bilateral facial nerve palsy
oropharyngeal weakness is common
autonomic involvement
urinary retention
diarrhoea
Investigations
lumbar puncture
rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
nerve conduction studies may be performed
decreased motor nerve conduction velocity (due to demyelination)
prolonged distal motor latency
increased F wave latency
ICP precautions
Elevation of head of the bed to greater than 30 degrees
Keep the neck midline to facilitate venous drainage from the head
Hypercarbia thus hyperventilation
Osmotic agents - mannitol
3% hypertonic saline
LP to drain
First line investigation for suspected subarachnoid hemorrhage
Non contrast CT
First line management for tonic or atonic seizures in females
Lamotrigine
What is secondary brain injury
INdirect injury caused by physiological changes triggered by an acute CNS insult and/or management of the primary insult.
Secondary brain injury is preventable/ can be minimised with neuroprotective measures
Neuroprotective measures
Avoid hypoxia, hyperoxia, hypocapnia and hypercapnia - aim for normoxia or mild hyperoxia, aim for normocapnia
Avoid hypovolemia, hypervolemia
Avoid hypoglycemia, hyperglycemia
Seizure ppx is not routinely recommended but continuous EEG monitoring is recommended in comatose pts/ those on neuromuscular blockers
Provide electrolyte repletion for electrolyte deficiencies - sodium disorders and hypokalemia are the most common seen after an acute CNS insult
Aggressively treat fever as it is associated with a poor neurological outcome/ increased mortality risk
Manage ICP
Why should hyperoxia be avoided in pts with acute CNS insult?
Can cause or worsen cerebral vasoconstriction and cerebral ischemia
Measures to achieve target oxygenation in patients with acute CNS insult
Avoid hypotension
Oxygen therapy is Spo2 <94%, use lowest possible Fio2 to maintain normoxia
Airway management
Why should hypercapnia be avoided in pts with acute CNS insult?
cause cerebral vasodilation –> increase cerebral edema, increasse ICP, intracerebral steal phenomenon
Why should hypocapnia be avoided in pts with acute CNS insult?
Cerebral vasoconstriction –> decreased cerebral blood flow –> increased risk of ischemia to uninjured brain tissue
Management of hypotension in patients with acute CNS insult
IVF - isotonic saline
Vasopressors - phenylephrine preferred in TBI and vasodilatory shock
Mng of raised ICP secondary to traumatic brain injury
IV mannitol
Mng of raised ICP secondary to vasogenic edema from CNS infections or neoplasms
IV dexamethasone
What substance can trigger attacks of cluster HAs
ETOH
Dx of cluster HA
MRI with pituitary views - can be associated with structural lesions in the pituitary gland
Acute treatment for cluster HA
SC triptan or intranasal
High flow oxygen
Bridging treatment for cluster HA
Used to control HA while starting ppx/ waiting for it to reach an effective dose
- Prednisolone PO
- Greater occipital nerve block with bupivicaine or lidocaine - can provide relief up to 3mo
Prophylaxis for cluster headaches
Can be used continuously if chronic or intermittently if episodic
- Verapamil IR- do an ECG prior to r/o heart block topiramate, sodium valproate, gabapentin, melatonin
- usually titrated very rapidly
