AGACNP Neuro Questions and Answers.

AGACNP Neuro Questions and Answers. What is the strongest indicator of functional impairment at discharge? Cognitive impairment Cranial nerve III EOMs Cranial nerves associated with eye movement CN III, IV, VI Cranial nerve associated with shoulder shrug CN XI Most important aspect in assessing mental status orientation TIA acute cerebral insufficiency less 24 hrs without residual defects sign of impending CVA TIA causes Atherosclerosis ICH embolism/thrombus atrial fibrillation MI CAD TIA s/s Ipsilateral monocular blindness Parasthesias of contralateral arm, leg, face transient aphasia vertigo TIA hallmark sign ipsilateral monocular blindness contralateral paresthesias arm, leg, face Vertebrobasilar TIA Inadequate blood flow from vertebral arteries Vertebrobasilar TIA s/s vertigo ataxia visual field deficits dizzy confusion Carotid TIA Carotid stenosis Carotid TIA s/s aphasia altered LOC dysarthria Gold standard diagnostic for TIA non-contrast head CT TIA diagnostics non-contrast head CT MRI Echo Carotid doppler cerebral angiography Patient is asymptomatic but a carotid bruit is present on physical examination. What is the next step in the plan of care? Order carotid doppler/ultrasound TIA management ASA clopidogrel (Plavix) 75 mg/day PO assess for HTN carotid endarterectomy Indication for carotid endarterectomy 70-80% stenosis of carotid vessels for symptomatic patient Patient presents with L hand tingling and carotid Doppler revealed 90% occlusion of both carotids. What is the next step in the plan of care? Carotid endarectomy of the right carotid first What is the number one cause of heart failure HTN When do most TIAs resolve around 3 hours CVA Rapid onset of neurological deficits lasting longer than 24 hrs CVA causes Atherosclerosis HTN AVM Aneurysm Tumor Trauma CVA Infarct subtle, progressive or sudden neurological deficits 80% CVA are ischemic Ischemic CVA s/s Changes LOC weakness paralysis visual changes Hemorrhagic CVA acute onset of focal neurological deficits 15-20% CVA Hemorrhagic CVA s/s Sudden increase ICP altered mental status vomiting headache L/dominant hemisphere R hemiparesis, aphasia, dysarthria, difficulty reading/writing R/nondominant hemisphere left hemiparesis, right visual changes, spatial disorientation What s/s do you see with an MCA infarct? hemiplegia deviation of eyes towards the lesion L hemisphere hemorrhagic CVA R hemiparesis aphasia dysarthria difficulty reading/writing R hemisphere hemorrhagic CVA L hemiparesis spatial disorientation right visual field changes In which hemisphere would a CVA be occurring if patient presented with right visual changes, left hemiparesis and spatial disorientation? R/nondominant hemisphere In a L hemisphere CVA, is aphasia and expected finding? What else? yes r hemiparesis dysarthria difficulty reading/writing A 54 yo. F suddenly falls out at church. What CVA do you expect? hemorrhagic Gold standard for diagnosing CVA non-contrast head CT CVA diagnostics non-contrast head CT cerebral angiogram LP What must be obtained before a lumbar puncture non-contrast head CT contraindication for lumbar puncture and why large cerebral bleed due to ARF herniation CVA management fibrinolytics less than 3-4.5 hrs of onset of symptoms lower BP avoid hypotension decrease ICP MAP 110-130 intravascular volume replacement hypertensive therapy nimodipine (Nimotop) goal MAP in CVA management MAP 110-130 mmHg to treat cerebral vasospasm Cerebral vasospasm management in CVA MAP 110-130 mmHg nimodipine (Nimotop) calcium channel blocker methods for increasing cerebral perfusion pressure in CVA management intravascular volume replacement hypertensive therapy window for tPA in CVA management less than 3-4.5 hrs since onset of symptoms What increases ICP in CVA? hypotension hypoxemia hypercapnia 45 yo. M s/p CVA is intubated on the ventilator. Most recent ABGs read: pH 7.48/pCO2 35/pO2 60 with FiO2 40%. What is your next step? leave pCO2 at 35 What is the function of the lateral rectus muscle? Moves eyes sideways and back Cranial nerves that are entirely sensory in function CN I, II, VIII MOA of nimodipine (Nimotop) prevent calcium from entering smooth muscles cells and causing contraction Seizure paroxysmal event that results from abnormal electrical activity in cerebral neurons Simple partial seizure common with cerebral lesions no LOC parasthesia flashing lights motor symptoms start in one place and spread to entire side of body Complex partial seizure progression of simple partial seizure LOC automatisms aura staring into space Absence generalized seizure sudden arrest of motor activity blank stare Tonic-Clonic generalized seizure tonic contractions of repeated involuntary muscle contraction clonic sustained involuntary muscle contraction 2-5 minutes incontinence LOC postictal phase Status Epilepticus tonic clonic generalized seizure lasting 10 minutes or more than 2 seizures without return to baseline between patient does not regain consciousness between attacks Seizure diagnostics - most important questions loss of consciousness duration neurological changes after seizure Seizure diagnostics seizure description EEG CT head Most important diagnostic in seizure classification EEG What four new onset signs and symptoms indicate non-contrast head CT scan stat? new onset seizure HA vertigo change in personality What do you order if a patient complains of any of the four following and what are you ruling out? New onset headache, seizure, vertigo, or personality changes. non-contrast head CT to rule out brain tumor Initial Seizure management maintain open airway benzodiazepines phenytoin (Dilantin) 20 mg/kg at 50 mg/min loading dose; continuous infusion barbiturate coma with NM blockade drug indicated in seizure management if unresponsive to phenytoin (Dilantin) phenobarbital (Luminal) DOC for status epilepticus diazepam (Valium) 5-10 mg IV DOC for immediate seizure control diazepam (Valium) 5-10 mg IV lorazepam (Ativan) 1-2 mg/minute IV Patient education in long-term seizure control must taper down drugs due to risk for withdrawal seizures What is the most commonly prescribed long-term anticonvulsant? carbamazepine (Tegretol) Top differential for new onset seizure brain tumor 35 yo. M s/p aneurysmal clipping. What is the initial action in the plan of care? Place patient in a quiet room Which serum abnormality increases the risk for pheyntoin (Dilantin) toxicity? hypoalbuminemia 60 yo. M on Norvasc for HTN management. You find out he likely had an ischemic CVA four hours ago. What about this patient excludes the use of tPA? time of onset of symptoms (3 hrs) 29 yo. F admitted to MSICU for ETOH abuse. You notice tremors during the physical exam. What is the next intervention? administer vitamin B1 for tremors in ETOH Myasthenia Gravis autoimmune disorder reduction of ACH receptor sites at the neuromuscular junction Disease caused by autoimmune destruction of the ACH receptor sites at the neuromuscular junction Myasthenia gravis Function of acetylcholine neurotransmitter released to activate muscle motor movement Myasthenia Gravis s/s bilateral extremity weakness ptosis diplopia respiratory difficulty weakness increases with activity and resolves with rest Myasthenia Gravis diagnostics antibodies to ACH receptors Tensilon test Myasthenia Gravis management refer to neurology pyridostigmine bromide (Prostigmin) antiacetycholinesterase drugs immunosuppresents plasmapheresis mechanical ventilation in MG crisis DOC for Myasthenia Gravis and MOA anticholinesterase drugs block hydrolysis of ACH pyridostigmine bromide (Prostigmin) Multiple Sclerosis Autoimmune disease caused by attack of myelin Multiple Sclerosis characteristics numbness weakness loss of muscle coordination vision problems speech bladder control What is the function of myelin? nerve insulator and helps in transmission of nerve signals Multiple Sclerosis s/s unilateral in a limb weakness numbness tingling disequilibrium diplopia Multiple Sclerosis diagnostics MRI of brain LP CSF elevated protein Elevated CSF IgG What is abnormal in the CSF with a patient diagnosed with Multiple Sclerosis? elevated CSF protein elevated CSF IgG Multiple Sclerosis management no cure refer to neurology exacerbations - steroids antispasmodics plasmapheresis immunosuppresants The most common site of intracranial thrombosis is: middle cerebral artery Differentials for syncope anxiety aortic stenosis hypoglycemia What is the most common sign of vertebrobasilar insufficiency? Vertigo 75 yo. F is diagnosed with a SAH after falling down a flight of steps. She has developed obstructive hydrocephalus. What would be the first sign of increased ICP? altered LOC 50 yo. F is in the neuro ICU POD #1 s/p craniotomy. She develops Cushing's Response. What is the criteria for Cushing's Response and what is it a sign of? bradycardia hypertension irregular RR late sign of increased ICP Guillan-Barre Syndrome Acute, rapidly progressing inflammatory polyneuropathy demyelination of peripheral nerves causing progressive symmetrical ascending paralysis Guillan-Barre Syndrome characteristics acute bilateral symmetrical ascending paralysis viral infection with fever 1-3 weeks before symptoms flaccid paralysis in 48-72 hrs Guillan-Barre Syndrome s/s rapidly progressing symmetrical ascending paralysis Difficulty speech swallowing mastication Guillan-Barre Syndrome diagnostics elevated CSF protein leukocytosis with left shift Guillan-Barre Syndrome management supportive while myelin regenerates symptoms improve around 2 weeks and full recovery around 2 years Meningitis infection of the pia mater and arachnoid mater membranes of brain and spinal cord Any patient presenting with a fever and neurological symptoms should be a concern for what? Acute bacterial meningitis In 80-90% of cases, meningitis is caused by: streptococcus pneumoniae Hemophilius influenzae Neisseria meningitidis Meningitis s/s Fever nuchal rigidity positive kernigs positive brudzinski photophobia seizures