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USMLE Step 3 > UWorld Neurology > Flashcards

UWorld Neurology Flashcards

1
Q

Diastolic heart murmur

A

aortic insufficiency or mitral stenosis

- related to ischemic CVA

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2
Q

Systolic heart murmur

A

aortic stenosis or mitral regurgitation or tricuspid regurgitation
- related to heart failure

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3
Q

Acute retinal vein thrombosis

A

extensive hemorrhage of the retina

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4
Q

Optic disc symptoms of ischemia

A

paleness

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5
Q

Damage to the recurrent laryngeal nerve

A

change in voice quality

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6
Q

Ansa hypoglossus nerve innervation

A

strap muscles of the neck

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7
Q

Symptoms of median nerve entrapment between two heads of pronator teres

A

Pain in volar forearm

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8
Q

Radial nerve inflammatory symptoms

A

sensory findings in the dorsal aspect of the forearm and hand

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9
Q

Cannabis withdrawal

A

abdominal pain, sweating, shakiness, fever, chills, headache, irritability, anxiety, insomnia, decreased appetite, restlessness, depressed mood

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10
Q

Vasovagal syncope

A

tunnel vision, diaphoresis, nausea, and pallor

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11
Q

Amyotrophic lateral sclerosis

A

involves both lower (neurons of the anterior horns in the spinal cord and brainstem neurons innervating the bulbar muscles) - weakness and atrophy and upper motor neurons - spasticity, increased DTRs
- Ocular motility, sensory, bowel, bladder, and cognitive function are preserved

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12
Q

Binswanger’s disease

A

form of vascular dementia with white matter infarcts

Symptoms: apathy, agitation, bilateral corticospinal or bulbar signs

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13
Q

Riluzole

A

glutamate inhibitor; may prolong survival and delay tracheostomy

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14
Q

Causes of papilledema

A
  • mass lesions
  • cerebral edema
  • increased CSF production
  • decreased CSF outflow (venous thrombosis)
  • Idiopathic intracranial hypertension (pseudotumor cerbri)
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15
Q

Construction apraxia

A

Involve the nondominant (often right) parietal lobe

- Confusion, difficulty copying simple things, and difficulty dressing

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16
Q

Damage to dominant parietal lobe (especially inferior portion)

A

Gerstmann syndrome:
acalculia - difficulty performing simple arithmatic
finger agnosia - difficulty naming individual fingers
agraphia - impaired writing
right-left confusion - difficulty distinguishing left side from right side

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17
Q

Damage to nondominant temporal lobe

A

visual disorders - homonymous upper quadranopia

auditory agnosia - impaired perception of complex sounds

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18
Q

Damage to dominant temporal lobe

A

homonymous upper quadranopia

aphasia (Wernicke’s) - difficulty creating meaningful language

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19
Q

Phenytoin toxicity

A

presence of nystagmus on far lateral gaze
blurred vision, diplopia, ataxia, slurred speech, dizziness, drowsiness, lethargy, decreased mentation, progression to coma
- side effect development is very patient specific - some will develop side effects within normal drug levels

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20
Q

OCPs and phenytoin

A

OCPs do not affect phenytoin levels, but phenytoin can increase metabolism of OCPs, making them less effective

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21
Q

How to manage phenytoin toxicity

A

reduce drug levels and watch for symptom resolution

- to stop, gradually taper drug

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22
Q

Brain death

A
  • Patient must not be hypothermic when this determination is made (must be >36 C)
  • Absent respiratory drive after 8-10 mins off the ventilator
    PaCO2 >60 and pH <7.28
  • Patient can have spontaneous limb movements (peripheral nerves and spinal reflexes)
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23
Q

Myasthenia gravis

A

autoantibodies against acetylcholine receptors

- Associated with thymoma

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24
Q

Febrile seizure

A
  • Often a family history
  • Typically seen in 3 months-6 yrs
  • no previous afebrile seizure
  • abortive therapy if >5 mins
  • <5% epilepsy
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25
Clonidine
alpha 2 adrenergic agonist
26
Guillan Barre syndrome
Typically develops after a GI or respiratory illness - Antibdodies to antigens mimic peripheral nerves - Symmetric muscle weakness, dysautonomia, parasthesias, decreased DTRs - Have to monitor respiratory status with frequent measurement of vital capacity (looks at muscular function)
27
When should patients with GBS be treated with IVIG
- nonambulatory | - within 4 weeks of symptom onset
28
GBS time course
2 weeks of progressive motor weakness that can lead to paralysis - 2-4 weeks of plateaued symptoms - Slow spontaneous recovery over months
29
How does IVIG help GBS
shortens time to recovery by 50%
30
Cauda equina syndrome
severe low back pain, urinary or bowel incontinence, motor weakness or sensory loss, saddle anesthesia
31
Cremastaric reflex
- corresponds to L1-L2 (also hip flexion and adduction)
32
Tabes dorsalis
Trepenema pallidum spirochetes directly damage the dorsal sensory roots and cause secondary degeneration of the dorsal columns Symptoms: sensory ataxia, lancinating pains, neurogenic urinary incontinence, Argyll-Robertson pupils
33
Positive Romberg test
Due to problem with sensation
34
Vitamin B12 deficiency neurologic
Peripheral neuropathy and/or subacute combined degeneration
35
Subacute combined degeneration
Posterior spinal column disease and lateral cortical spinal disease (spastic paresis and hyperreflexia)
36
Clinical criteria for diagnosis of brain death
1. Clinical/brain imaging evidence of devestating known cause 2. Absence of confounding factors (sedatives, metabolic) 3. No evidence of drug intoxication or poisoning 4. Core temperature >36 C and systolic BP >100
37
Neurologic exam findings suggesting brain death
1. coma 2. absent brain-originating motor response (flexor and extensor posturing) 3. absent oculovestibular response (caloric testing) 4. absent cough with tracheal suctioning 5. absent pupillary light and corneal reflexes 6. absent rooting or sucking reflexes 7. absent gag reflex 8. Apnea test 9. Silence on EEG 10. absence of cerebral blood flow
38
Lewy body dementia
REM sleep disorder (vivid dreams) Severe neuroleptic sensitivity SPECT or PET showing low dopamine transporter uptake in basal ganglia severe autonomic dysfunction - Usually don't have tremor of Parkinson's disease
39
Dopamine agonists in Lewy body dementia
- Can increase visual hallucinations
40
Treatment of Lewy body dementia
Dopamine agonsts | Cholinesterase inhibitors
41
Benign essential tremor
Most common cause of postural tremor Autosomal dominant inheritance pattern Tremor worsens with action
42
Treatment of benign essential tremor
- Should be delayed if not immediately necessary | - Use propranolol
43
Cushing's triad
Manifestations of intracranial hypertension: - bradycardia - hypertension - respiratory depression
44
Late signs of elevated intracranial pressure
transtentorial herniation of brain tissue, altered level of consciousness, dilation of ipsilateral pupil, third cranial nerve palsy, hemiparesis, decerebrate posturing, respiratory arrest
45
Hyperventilation for elevated ICP
Increases PCO2 leading to vasoconstriction and reduced cerebral blood flow, decreasing ICP - contraindicated in patients with trauma because it can lead to further neurologic loss
46
First-line therapy in Alzheiemer's disease
``` acetylcholinesterase inhibitor (patients have decreased acetylcholine due to degeneration of basal nucleus of Meynert - Donepizil is first-choice drug ```
47
Parkinson's disease diagnosis
Clinical diagnosis - Improvement with dopaminergic medications - Unilateral onset and persistent asymmetry support the diagnosis - Striatal dopamine transporter scan - used in patients with equivocal PE, same sensitivity as exam Bradykinesia in addition to tremor or rigiditiy - MRI should be obtained to rule out other conditions
48
Treatment of Parkinson's disease
In patients under 65 yrs, dopamine agonists are usually tried first (pramipexole, bromocriptine) In patients >65 levodopa might be first, but it has more side effects (dyskinesia) - May hasten destruction of substantia nigra cells
49
Entacapone
COMT inhibitor that can increase effectiveness of levodopa
50
Indirect hyperbilirubinemia in B12 deficiency
Megaloblastic transformation of the bone marrow with intramedullary hemolysis - absent reticulocyte response
51
Abusive head trauma clinical features
subdural hemorrhages retinal hemorrhages diffuse brain injury
52
Imaging for abusive head trauma
emergency CT scan to determine if neurosurgical evaluation is needed - Typically have mixed-density pattern
53
Carotid artery dissection etiologies
Traumatic: Trauma, high-velocity chiropractic manipulation of the spine Spontaneous: severe atherosclerotic disease, poorly controlled HTN, collagen vascular disorders, fibromuscular dysplasia, autosomal polycystic kidney disease
54
Signs and symptoms of carotid dissection
- Head/neck pain with severe thunderclap headache - Partial Horner's syndrome (ptosis and miosis but no anhydrosis) - due to disruption of the sympathetic nerves, but anhydrosis is absent because sweat fibers travel along external carotid artery - TIAs, ischemic or embolic strokes - Transient visual loss due to retinal artery occlusion or ischemic optic neuropathy
55
Diagnosis of carotid artery dissection
CT angiography MRA catheter angiography
56
Treatment of carotid artery dissection
Antithrombotic therapy Stroke can complicate Tight blood pressure control is not indicated
57
Focal dystonia treatment
Botulinum toxin injections
58
Diagnosis of sleep disorders
Overnight polysomnography
59
Diagnosis of narcolepsy
polysomnography, multiple sleep latency
60
Carbamazepine complications
Fulminent hepatic failure with hyperammonemia, hepatic encephalopathy and seizure

USMLE Step 3 (2 decks)

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