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FNP boards > Neurologic disorders > Flashcards

Neurologic disorders Flashcards

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Family Nurse Practitioner (FNP) flashcards
1
Q

What are the twelve CNs?

A
  • CN I - olfactory
  • CN II - optic
  • CN III - oculomotor
  • CN IV - trochlear
  • CN V - trigeminal
  • CN VI - abducens
  • CN VII - facial
  • CN VIII - auditory
  • CN IX - glossopharyngeal
  • CN X - vagus
  • CN XI - accessory
  • CN XII - hypoglossal
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2
Q

What are the functions of CNs I-III?

A
  • CN I - smell
  • CN II - vision
  • CN III - eyelid and eyeball movement
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3
Q

What are the functions of CNs IV-VI

A
  • CN IV - innervates superior oblique, turns eye downward and laterally
  • CN V - chewing, face and mouth, touch and pain
  • CN VI - turns eye laterally
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4
Q

What are the functions of CNs VII-IX?

A
  • CN VII - controls most facial expressions, secretion of tears and saliva, taste
  • CN VIII - hearing, equilibrium, sensation
  • CN IX - taste, senses carotid blood pressure
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5
Q

What are the functions of CNs X-XII?

A
  • CN X - senses aortic blood pressure, slows heart rate, stimulates digestive organs, taste
  • CN XI - controls trapezius and sternocleidomastoid, controls swallowing movements
  • CN XII - controls tongue movements
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6
Q

What is Bell’s palsy?

A

AKA idiopathic facial paralysis

  • Acute paralysis of CN VII (facial) that is seen without other s/s
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7
Q

Bell’s palsy clinical presentation

A
  • Sudden onset unilateral facial paralysis
  • Inability to raise eyebrow or smile on affected side
  • Decreased lacrimation
  • Difficulty closing eyelid
  • Biting on side of cheek
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8
Q

What is the prognosis of Bell’s palsy?

A

Bell’s palsy is temporary

Symptoms improve within a few weeks with complete recovery by 6 months

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9
Q

How would you differentiate Bell’s palsy from other differentials (e.g. stroke, facial tumor, brain tumor)?

A

Remaining neurological examination is normal including visual fields, EOM, sense of smell, etc.

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10
Q

Bell’s palsy diagnostic testing

A

Diagnosis made based on HPI and physical exam findings

  • Can order EMG or imaging to rule out tumor/head injury
  • Consider Lyme disease in NE states
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11
Q

Bell’s palsy treatment

A
  • Systemic oral corticosteroids (prednisone) within 72 hours of onset to improve facial function
  • Eye patch and tear substitute/lubricant
  • Facial PT
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12
Q

What are primary headaches? What are the three types?

A

Not associated with other diseases (likely complex interplay of genetic, developmental, and environmental factors)

Examples: migraine, tension-type, cluster

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13
Q

What are secondary headaches? What are examples?

A

Associated with other conditions

Examples: brain tumor, intracranial bleeding, inflammation, etc.

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14
Q

What are the two most common types of primary headaches seen in primary care?

A

Associated with a family history of headaches

  • Migraine with or without aura
  • Tension-type headache
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15
Q

Tension-type headache clinical presentation and diagnosis

A

Lasts 30 minutes to 7 days with 2+ of the following:

  • Pressing, nonpulsatile pain
  • Mild to moderate in intensity
  • Bilateral
  • One of the following: nausea, photophobia, phonophobia
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16
Q

Migraine without aura clinical presentation and diagnosis

A

Lasts 4-72 hours with 2+ of the following:

  • Unilateral (can be bilateral)
  • Pulsating quality, moderate to severe in intensity
  • Aggravation by normal activity such as walking (or causes avoidance of these activities)
  • 1+ of the following: N/V, photophobia, phonophobia
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17
Q

Migraine with aura clinical presentation and diagnosis

A

Focal dysfunction of cerebral cortex or brainstem causes aura symptoms to develop over 4 minutes, or 2+ symptoms occur in succession (no aura should last longer than 1 hour)

Symptoms:

  • Feeling of dread or anxiety
  • Unusual fatigue
  • Nervousness or excitement
  • GI upset
  • Visual or olfactory alteration
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18
Q

When is neuroimaging with head CT or MRI indicated for patient’s presenting with primary headaches?

A

If they present with headache “red flags”

SSNOOPPP mnemonic

  • Systemic symptoms - fever, unintended weight loss
  • Secondary headache risk factors - HIV, malignancy, pregnancy, anticoagulation, marked BP elevation
  • Neurological signs - confusion, impaired alertness, nuchal rigidity, etc.
  • Onset - sudden, split second (“thunderclap”), onset with exertion (sexual activity, coughing, sneezing = increased ICP)
  • Onset (age) - >50 years, <5 years
  • Prior headache history - change in quality/frequency
  • Positional
  • Papilledema - visual problems
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19
Q

Lifestyle modifications to treatment primary headaches

A
  • Consider menses, ovulation, or pregnancy
  • Birth control/HRT
  • Illness of virtually any kind
  • Intense or strenuous activity/exercise
  • Sleeping too much/too little/jet lag
  • Fasting/missing meals
  • Bright or flickering lights
  • Excessive or repetitive noises
  • Odors/fragrances/tobacco smoke
  • Weather/seasonal changes
  • High altitudes
  • Medications
  • Stress/stress letdown
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20
Q

Example of a selective serotonin receptor agonist that is used for abortive/acute migraine headache therapy

A

Triptans

  • Can be used in conjunction with NSAIDs for full relief of pain
  • Helps with photophobia, phonophobia
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21
Q

Triptan contraindications

A

Contraindications:

  • History of prinzmetal angina
  • CAD
  • Uncontrolled HTN
  • Pregnant women
  • Recent ergot use
  • Concurrent use with MAOIs, high dose SSRIs/SNRIs
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22
Q

What should the provider look out for if prescribing long term use of NSAIDs for primary headache therapy?

A

Rebound headaches

  • Lower risk with ibuprofen and naproxen; higher risk with ASA, acetaminophen, OTC products that contain caffeine, aspirin, acetaminophen (Excedrin migraine)
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23
Q

If triptans are contraindicated for headache therapy, what other medication can be prescribed? What warnings should also be mentioned?

A

Fioricet - combination of caffeine, butalbital (barbiturate), acetaminophen

  • Frequent of excessive use should be discouraged because of potential for barbiturate dependence
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24
Q

When is the onset of action if headache therapy is taken PO?

A

Takes 30 minutes to 1 hour before relief of pain

  • Best for patients with headache and no GI distress
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25
Q

What are examples of injectable headache therapy? What is its onset of action?

A

Best for patients with rapidly progressing headache accompanied by significant GI upset

  • Examples: sumatriptan, DHE, ketorolac
  • Rapid onset of action (15-30 minutes)
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26
Q

What is considered prophylactic/prevention therapy for primary headaches (migraines, tension-type)?

A

Considered if abortive or acute headache is used frequently or if inadequate symptom relief is obtained from appropriate use of these therapies

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27
Q

What is the goal of prophylactic/preventative therapy for headaches?

A

Minimum of 50% reduction in number of headaches, easier to control headaches that respond more rapidly to standard therapies, require less medication

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28
Q

What are important considerations before initiating prophylactic/preventative therapy for headaches?

A
  • Discontinue headache provoking medications (e.g. estrogen, progestin/progesterone, vasodilators)
  • Implement lifestyle changes to avoid headache triggers
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29
Q

True/false: Patients, while working with the provider, can consider tapering prophylaxis once headaches are better controlled and lifestyle modifications are in place to minimize headache risk

A

True

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30
Q

What medications can be used for prophylaxis/prevention therapy for headaches?

A
  • Beta blockers
  • Antiepileptic drugs → divalproex sodium, sodium valproate, topiramate
  • Antidepressants → TCAs (amitriptyline), SNRIs (venlafaxine)
  • Calcitonin gene related peptide (CGRP)
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31
Q

What class of medication is first line for prophylaxis/prevention against tension-type headaches?

A

TCAs

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32
Q

What are cluster headaches?

A

Primary headache - AKA migrainous neuralgia

  • Common in middle aged men, especially with heavy alcohol and tobacco use
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33
Q

Cluster headache clinical presentation and diagnosis

A
  • Tendency to occur daily in groups or clusters
  • Clusters last several weeks to months then disappear for months to years
  • Occurs at characteristic time of year at the same time of day (typically when sleeping, “alarm clock” headache)
  • Located behind one eye with steady, intense severe pain
    • Unilateral pain that lasts 15-180 minutes, once to eight times/day
34
Q

Cluster headache treatment

A
  • Reduction of triggers (e.g. tobacco, alcohol)
  • Start prophylactic and abortive therapy
    • Abortive treatment can include high low oxygen, triptans, ergot alkaloids, local anesthetics
    • Preventive treatment includes CCBs, mood stabilizers, anticonvulsants
35
Q

True/false: Cluster headaches are often called the “suicide headache” because of the severity of the pain

A

True

36
Q

Secondary headache clinical presentation

A
  • Abnormal neurological examination
  • Increased ICP - worse upon wakening and gets better as the day goes on
    • In tension headaches, pain worsens as the day goes on
37
Q

What is meningitis?

A

Infection of the meninges, CSF, and ventricles

  • Can be bacterial, viral, fungal, or other
38
Q

What vaccine has helped to reduce the incidence of meningitis in adults?

A

Hib

39
Q

Meningitis mode of transmission and risk factors

A

Direct contact or respiratory droplets from infected people

Risk factors:

  • People living in closed environments (e.g. military, college students, prison)
  • Younger than 20 years
  • Pregnancy
  • Immunocompromised
40
Q

Meningitis clinical presentation

A
  • Classic triad: fever, headache, nuchal rigidity
  • N/V, photophobia, change in MS (drowsiness, confusion, delirium, coma)
  • Purpura or petechial rash if n. meningitidis
  • Positive brudzinski and kernig signs
41
Q

What are the brudzinski and kernig sign?

A

Suggestive of nuchal rigidity and meningeal irritation seen in meningitis

  • Brudzinski → passive neck flexion in supine patient results in flexion of knees and hips
  • Kernig → patient lying supine and hip flexed at 90, positive when extension of knee elicits resistance or pain in lower back/posterior thigh
42
Q

Meningitis diagnostic testing

A

LP with CSF evaluation in febrile patients with an abnormal neuro exam

  • Pleocytosis (WBC >5 cells/mm3)
  • Elevated CSF opening pressure
  • Reduced CSF glucose
  • Elevated CSF protein
43
Q

Meningitis treatment

A
  • Pneumococcal vaccines (PCV13 and/or PPSV23)
  • Hib for children under 2 years old
44
Q

When should the MCV4 and MenB vaccines be administered in pediatrics?

A

MCV4 at 11 or 12 years then booster at 16 years

  • Students should receive MCV4 five years before starting college

MenB at 16 to 18 years

  • Priority given between 16 to 23 years old
45
Q

What is multiple sclerosis (MS)?

A

Recurrent, chronic demyelinating disorder of the CNS characterized by episodes of focal neurologic dysfunction

Symptoms occurring acutely, worsening over a few days, lasting weeks, followed by period of partial to full resolution

46
Q

Multiple sclerosis risk factors

A
  • Ages 20-40 years
  • Female
  • Family history
  • Northern European ancestry
  • Previous viral infection (e.g. EBV)
  • Presence of autoimmune disorder
47
Q

What are the two types of multiple sclerosis?

  • RRMS
A

Relapsing, remitting MS (RRMS) → episodes resolve with improvement of neurological function between exacerbations and minimal to no cumulative defects

48
Q

What are the two types of multiple sclerosis?

  • PPMS
A

Primary progressive MS (PPMS) → episodes do not fully resolve, there are cumulative defects

49
Q

Multiple sclerosis clinical presentation

A

Symptoms vary and depend on location of affected nerve fibers

  • Weakness or numbness of a limb
  • Monocular visual loss
  • Diplopia
  • Vertigo
  • Facial weakness or numbness
  • Sphincter disturbances
  • Ataxia
  • Nystagmus
50
Q

Multiple sclerosis diagnostic testing

A
  • Head MRI → demyelinated plaques, can monitor disease progression in brain and spinal cord
  • LP → pleocytosis (increased WBCs), abnormal proteins, increased monocytes
51
Q

Multiple sclerosis treatment

  • What are the three categories of treatment?
A
  • Therapy for relapses
  • Long term disease-modifying medications
  • Symptomatic management
52
Q

Multiple sclerosis treatment

  • Exacerbations
A
  • Treat underlying precipitating illness (e.g. UTI) and
  • Systemic high dose corticosteroid (can shorten course of exacerbation)
53
Q

What medications can be prescribed for long term control of multiple sclerosis?

A

Immunomodulatory therapy

  • Interferon beta-1b (betaseron, extavia)
  • Interferon beta-1a (avonex, rebif)
  • Peginterferon beta-1a (plegridy)

Immunosuppressive therapy

  • Mitoxantrone (novantrone)
54
Q

What is Parkinson’s disease and its cause?

A

Slowly progressive movement disorder that is caused by loss of pigmented dopaminergic neurons in substantia nigra pars compacta

55
Q

Parkinson’s disease clinical presentation

  • Common initial sign
  • Four cardinal features
A
  • Most common initial sign → resting tremor of upper limb
  • Four cardinal features: tremor at rest, rigidity, bradykinesia, postural instability
  • Shuffling gait, reduced arm swing
  • Hyposmia (reduced sense of smell)
  • Mask-like facies
56
Q

Parkinson’s disease treatment

A
  • Dopamine agonists → ropinirole (requip), pramipexole (mirapex)
  • Levodopa-carbidopa (sinemet)
  • Exercise and PT
57
Q

Considerations before prescribing levodopa-carbidopa (sinemet)

A
  • Long term use (5-10+ years) can lead to dyskinesia
  • “Wearing off” phenomenon
    • Can add MAO-B inhibitor or COMT can prolong effect of levodopa
58
Q

Important questions to ask patients with a history of seizure disorder

A
  • Was a warning event present?
  • What actually happened during the seizure?
  • Did the patient relate to the environment?
  • Does the patient have any recollection of the seizure?
  • How did the patient feel after the seizure?
  • How long was the recovery following the seizure?
  • what is the frequency and duration?
  • Is there a known trigger?
59
Q

Characteristics of absence (petit mal) seizure

A
  • Blank staring lasting 3-50 seconds accompanied by impaired LOC
  • Age of onset: 3-15 years
60
Q

Characteristics of myoclonic seizures

A
  • Awake state or momentary LOC with abnormal motor behavior lasting seconds to minutes
  • 1+ muscle groups causing brief jerking contractions of limbs and trunk
  • Age of onset: 2-7 years
61
Q

Characteristics of tonic clonic (grand mal) seizures

A
  • Rigid extension of arms and legs followed by sudden jerking movements with LOC
  • Bowel and bladder incontinence with postictal confusion
  • Age of onset: any age
    • Adult onset with brain tumor, head injury, alcohol withdrawal
62
Q

Characteristics of simple partial or focal seizure

A
  • Awake state with abnormal motor, sensory, autonomic, or psychic behavior
  • Movement of any part of the body (localized or generalized)
  • Age of onset: 3-15 years
63
Q

Characteristics of complex partial seizures

A
  • Aura characterized by unusual sense of smell/taste, visual/auditory hallucination, stomach upset
  • Followed by vague stare and facial movements, muscle contraction and relaxation, autonomic signs
  • Age of onset: any
64
Q

Seizure disorder diagnostic testing

A
  • Prolactin level within 20 minutes of seizure (elevated following generalized tonic clonic or complex partial seizure)
  • Video EEG (especially for unprovoked seizures)
65
Q

Examples of anti-epileptic drugs

A
  • Older products → phenytoin, carbamazepine, clonazepam, ethosuximide, valproic acid
  • New products → gabapentin, lamotrigine, topiramate
66
Q

What two AEDs have a narrow therapeutic index?

A
  • Phenytoin
  • Carbamazepine
67
Q

If used concurrently, phenytoin use increase ___ clearance by increased CYP 450 enzyme activity leading to levels of both drugs decreasing by 40%

A

Theophylline

68
Q

True/false: Carbamazepine induces estrogen metabolism

A

True - If taking birth control pills with carbamazepine, can lead to contraceptive failure

69
Q

How can you differentiate a TIA from a stroke based on presentation?

A

TIA is an acute neurological event that resolves within minutes to 24 hours

If neurologic changes persist beyond 24 hours, consider stroke

70
Q

TIA and stroke clinical presentation

A
  • Unilateral weakness
  • Numbness
  • Paralysis of face or limb
  • Slurred or garbled speech
  • Blindness or diplopia in one or both eyes
  • Dizziness and loss of balance
  • Sudden onset severe headache
71
Q

TIA and stroke diagnostic testing

A
  • Labs: BG, CBC, electrolytes, coagulation studies, 12 lead ECG
  • Head CT or MRI within 24 hours
  • Vascular imaging → doppler US, CT angiography, MRA
72
Q

TIA management and treatment

A
  • Long term antiplatelet therapy (ASA, clopidogrel)
  • If high risk for stroke or TIA associated with cardio embolism from afib or valvular disease, start anticoagulation therapy
    • DOAC or warfarin
73
Q

Symptoms that help differentiate ischemic from hemorrhagic stroke

A

Hemorrhagic strokes can present with N/V, headache, sudden change in consciousness

74
Q

Acute stroke clinical presentation

A
  • Alteration in consciousness (confusion, memory loss, agitation)
  • Headache
  • Unusual or severe neck or facial pain
  • Aphasia, facial weakness or asymmetry
  • Altered coordination, ataxia
  • Visual loss
75
Q

Stroke diagnostic testing

A
  • Head CT to identify acute hemorrhage
  • MRI to identify acute phase of ischemic stroke
76
Q

How soon after an ischemic stroke should fibrinolytic (alteplase, tPA) be used?

A

Within 3 to 4.5 hours of stroke onset

77
Q

Medications for secondary prevention against ischemic strokes

A
  • Antiplatelet therapy with ASA or clopidogrel (plavix)
  • If cardiac embolus d/t afib, DOAC therapy or warfarin
  • Antihypertensive therapy
    • Goal BP 130/80
78
Q

What is giant cell arteritis?

A

Autoimmune vasculitis involving medium and large vessels with resulting arterial inflammation that affects parts of an artery with sections of normal artery in between

79
Q

Giant cell arteritis clinical presentation

A
  • Severe unilateral headache (stabbing, located in frontal, vertex, or occipital area)
  • History of recent respiratory symptoms (cough, sore throat, hoarseness)
  • Jaw claudication
  • Acute reduction or change in vision
80
Q

Giant cell arteritis diagnostic testing

A
  • Confirmatory arterial biopsy (multiple site d/t skips in vessel)
  • Color duplex US of temporal arteries
  • Elevated ESR and CRP
81
Q

Giant cell arteritis treatment

A

As soon as diagnosis is made, start on high dose systemic corticosteroid to prevent risk of blindness

  • Add misoprostol, PPI, bisphosphonate, calcium/vitamin D supplement to minimize steroid AEs
  • Can add tocilzumab (actemra) with tapering of corticosteroid

FNP boards (20 decks)

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