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USMLE Step 3 > UWorld Neurology > Flashcards

UWorld Neurology Flashcards

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USMLE® Step 1 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
Q

Clonidine

A

alpha 2 adrenergic agonist

26
Q

Guillan Barre syndrome

A

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
Q

When should patients with GBS be treated with IVIG

A
  • nonambulatory

- within 4 weeks of symptom onset

28
Q

GBS time course

A

2 weeks of progressive motor weakness that can lead to paralysis

  • 2-4 weeks of plateaued symptoms
  • Slow spontaneous recovery over months
29
Q

How does IVIG help GBS

A

shortens time to recovery by 50%

30
Q

Cauda equina syndrome

A

severe low back pain, urinary or bowel incontinence, motor weakness or sensory loss, saddle anesthesia

31
Q

Cremastaric reflex

A
  • corresponds to L1-L2 (also hip flexion and adduction)
32
Q

Tabes dorsalis

A

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
Q

Positive Romberg test

A

Due to problem with sensation

34
Q

Vitamin B12 deficiency neurologic

A

Peripheral neuropathy and/or subacute combined degeneration

35
Q

Subacute combined degeneration

A

Posterior spinal column disease and lateral cortical spinal disease (spastic paresis and hyperreflexia)

36
Q

Clinical criteria for diagnosis of brain death

A
  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
Q

Neurologic exam findings suggesting brain death

A
  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
Q

Lewy body dementia

A

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
Q

Dopamine agonists in Lewy body dementia

A
  • Can increase visual hallucinations
40
Q

Treatment of Lewy body dementia

A

Dopamine agonsts

Cholinesterase inhibitors

41
Q

Benign essential tremor

A

Most common cause of postural tremor
Autosomal dominant inheritance pattern
Tremor worsens with action

42
Q

Treatment of benign essential tremor

A
  • Should be delayed if not immediately necessary

- Use propranolol

43
Q

Cushing’s triad

A

Manifestations of intracranial hypertension:

  • bradycardia
  • hypertension
  • respiratory depression
44
Q

Late signs of elevated intracranial pressure

A

transtentorial herniation of brain tissue, altered level of consciousness, dilation of ipsilateral pupil, third cranial nerve palsy, hemiparesis, decerebrate posturing, respiratory arrest

45
Q

Hyperventilation for elevated ICP

A

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
Q

First-line therapy in Alzheiemer’s disease

A 
acetylcholinesterase inhibitor (patients have decreased acetylcholine due to degeneration of basal nucleus of Meynert 
- Donepizil is first-choice drug
47
Q

Parkinson’s disease diagnosis

A

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
Q

Treatment of Parkinson’s disease

A

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
Q

Entacapone

A

COMT inhibitor that can increase effectiveness of levodopa

50
Q

Indirect hyperbilirubinemia in B12 deficiency

A

Megaloblastic transformation of the bone marrow with intramedullary hemolysis
- absent reticulocyte response

51
Q

Abusive head trauma clinical features

A

subdural hemorrhages
retinal hemorrhages
diffuse brain injury

52
Q

Imaging for abusive head trauma

A

emergency CT scan to determine if neurosurgical evaluation is needed
- Typically have mixed-density pattern

53
Q

Carotid artery dissection etiologies

A

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
Q

Signs and symptoms of carotid dissection

A
  • 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
Q

Diagnosis of carotid artery dissection

A

CT angiography
MRA
catheter angiography

56
Q

Treatment of carotid artery dissection

A

Antithrombotic therapy
Stroke can complicate
Tight blood pressure control is not indicated

57
Q

Focal dystonia treatment

A

Botulinum toxin injections

58
Q

Diagnosis of sleep disorders

A

Overnight polysomnography

59
Q

Diagnosis of narcolepsy

A

polysomnography, multiple sleep latency

60
Q

Carbamazepine complications

A

Fulminent hepatic failure with hyperammonemia, hepatic encephalopathy and seizure

USMLE Step 3 (2 decks)

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