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Internal Medicine > Deja - Internal - Neurology > Flashcards

Deja - Internal - Neurology Flashcards

1
Q

What is RIND?

A

Neurologic deficits that lasts >24h and <3wks.

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2
Q

2 greatest risk factors for a stroke?

A
  1. HTN

2. Smoking

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3
Q

2 MC etiologies for ischemia:

A
  1. Thrombotic etiology 2o to atherosclerosis.

2. Embolic etiology which is usually either cardiac in origin or from carotid arteries.

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4
Q

MC etiology of a CVA:

A

Ischemia.

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5
Q

Infarct in the deep gray matter associated with HTN and atherosclerosis:

A

Lacunar infarct.

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6
Q

MC source of emboli that leads to stroke:

A

Carotid atheroma.

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7
Q

Thalamus, internal capsule, and cerebral white matter deficit causing FLEXION of the upper extremities:

A

Decorticate posturing.

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8
Q

Upper brainstem deficit causing EXTENSION of the upper extremities:

A

Decerebrate rigidity.

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9
Q

Occlusion of MCA supplying the DOMINANT hemisphere:

A
  1. Contralateral hemiparesis.
  2. Hemisensory deficit.
  3. Aphasia.
  4. Homonymous hemianopsia.
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10
Q

Occlusion of MCA supplying the nondominant hemisphere:

A
  1. Contralateral hemiparesis.
  2. Hemisensory deficit.
  3. Homonymous hemianopsia.
  4. Confusion.
  5. Apraxia.
  6. Body neglect on contralateral side.
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11
Q

Occlusion of ACA:

A
  1. Broca aphasia.
  2. Contralateral weakness of lower extremity.
  3. Incontinence.
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12
Q

Occlusion of PCA:

A
  1. Homonymous hemianopsia with MACULAR SPARING.
  2. CN III palsy.
  3. Aphasia + Alexia if DOMINANT hemisphere is affected.
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13
Q

Occlusion of PICA:

A
  1. Vertigo.
  2. Ataxia.
  3. Contralateral pain and temperature disturbance.
  4. Dysphagia.
  5. Dysarthria.
  6. Ipsilateral Horner syndrome.
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14
Q

Occlusion of AICA:

A
  1. Deafness.
  2. Tinnitus.
  3. Ipsilateral facial weakness.
  4. Gaze palsy.
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15
Q

Occlusion of ophthalmic artery:

A

Amaurosis fugax (transient monocular blindness).

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16
Q

1st study to order if you suspect a stroke in a patient?

A

CT of head WITHOUT contrast to rule out active bleeding.

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17
Q

What other studies can be done to further assess the stroke patient?

A
  1. MRI to evaluate for subacute infarction.
  2. Carotid Doppler US to rule out carotid artery stenosis.
  3. Echocardiogram to rule out embolic sources.
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18
Q

TIA treatment:

A

Start with aspirin. If fail, give plavix (clopidogrel).

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19
Q

When would you consider a carotid endarterectomy?

A

If the patient had carotid artery stenosis >70%.

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20
Q

Cardioembolic stroke treatment:

A

Anticoagulation with heparin or Coumadin.

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21
Q

Treatment that improves outcome in a patient who present with an EMBOLIC stroke with symptoms beginning <3hr ago?

A

tPA.

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22
Q

Single most useful test to evaluate seizures?

A

EEG.

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23
Q

What tests should be done on a patient suspected to have had a seizure?

A
  1. Complete neurologic examination.
  2. Check for incontinence, tongue lacerations, other injuries to the body to distinguish from syncope.
  3. Lab: CBC, electrolytes, Ca, glucose, O2, LFTs, BUN, Cr, RPR, ESR, Urine tox screen.
  4. MRI/CT can also be done to rule out a mass.
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24
Q

Factors that increase the risk of having a seizure?

A
  1. History of having a seizure in the past.
  2. CNS tumor.
  3. CNS infection.
  4. Trauma.
  5. Stroke.
  6. High fever in children.
  7. Drugs.
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25
Q

Todd paralysis:

A

Postictal state in which there are focal neurological deficits that lasts 24-48hs.
Usually associated with focal seizures.

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26
Q

2 types of generalized seizures:

A
  1. Tonic-clonic seizures.

2. Absence seizures.

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27
Q

Phenytoin - Side effects:

A
  1. Agranulocytosis.
  2. Gingival hyperplasia.
  3. Hirsutism.
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28
Q

Valproic acid - Side effects:

A
  1. Hepatotoxic.
  2. Thrombocytopenia.
  3. Neutropenia.
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29
Q

Carbamazepine - Side effect:

A

Aplastic anemia.

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30
Q

What test is used to diagnose meningitis?

A

Lumbar puncture with CSF analysis including Gram stain, cultures.

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31
Q

How is a brain tumor diagnosed?

A

CT with contrast/MRI with gadolinium localizes the lesion and a biopsy is used to get the histologic class of the tumor.

32
Q

What is the MC mesodermal tumor?

A

Meningioma.

33
Q

How are most brain tumors treated?

A
  1. Surgical excision and radiation.

2. Medulloblastomas also require chemotherapy and schwannomas are treated with surgery alone.

34
Q

Who is at higher risk for developing MS?

A
  1. Those with a family history of MS.
  2. Those who lived up until puberty in northern latitudes or temperate climates.
  3. Females. (2:1)
35
Q

What is the typical course of MS?

A

Multiple progressive neurologic alterations that wax and wane and cannot be explained by a single lesion.

36
Q

Signs and symptoms of MS:

A
  1. Limb weakness.
  2. Paresthesias.
  3. Optic neuritis.
  4. Nystagmus.
  5. Scanning speech.
  6. Intranuclear ophthalmoplegia.
  7. Vertigo.
  8. Diplopia.
37
Q

Lhermitte sign:

A

Shock-like sensation down the spine when patient flexes their neck.
Also known as the “barber chair phenomenon”.

38
Q

What can be seen on MRI on a patient with MS?

A

MRI shows multiple, asymmetric, periventricular plaques with multiple areas of demyelination.

39
Q

What does the CSF show in an MS patient?

A

Oligoclonal bands - Elevated IgG.

40
Q

MS treatment:

A

Steroids during acute episodes and IFN-β to prolong remission.

41
Q

What is the underlying pathology in ALS?

A

Slow progressive loss of upper and lower motor neurons in CNS.

42
Q

What are the clinical signs and symptoms of ALS?

A
  1. Asymmetric, progressive muscle weakness initially with fasciculations which present clinically as difficulty swallowing.
  2. Upper + Lower motor neuron signs on physical exam.
  3. NO bowel or bladder involvement.
43
Q

How is ALS diagnosed?

A

Clinically –> Combination of UPPER + LOWER motor symptoms in 3 or more extremities.
An EMG will show widespread denervation and fibrillation potentials in at least 3 limbs.

44
Q

What is the main treatment for ALS?

A

Supportive care.

45
Q

What do ALS patients ultimately die from?

A

Respiratory failure.

46
Q

What is Guillain-Barre?

A

Autoimmune, demyelinating disorder affecting the peripheral nerves (particularly motor fibers).

47
Q

Bacterial infection associated with Guillain-Barre?

A

C.jejuni

48
Q

What often precedes Guillain-Barre?

A

Bacterial infection causing diarrhea, specifically with Campylobacter, viral infection, or vaccination.

49
Q

Clinically, how does Guillain-Barre present?

A

SYMMETRIC ASCENDING PARALYSIS.

Eventually progress to paralysis of the diaphragm, leading to respiratory failure.

50
Q

What tests would you do to diagnose Guillain-Barre syndrome?

A

Lumbar puncture and EMG.

51
Q

What would you see in the CSF after a lumbar puncture in Guillain-Barre?

A

Incr. Protein; Normal cell count –> Known as albuminocytologic dissociation.

52
Q

What interventions should be undertaken in a patient with Guillain-Barre syndrome?

A

Monitor respiratory function very closely and intubate if needed.
–> Plasmapheresis and IVIG.

53
Q

Prognosis of Guillain-Barre?

A

Good.

54
Q

MC type of headache:

A

Tension headache.

55
Q

Signs and symptoms of a tension headache?

A

Bilateral, band-like, dull, most intense at neck/occiput, worsened with stress.

56
Q

What psychiatric disorder is it most commonly associated with headache?

A

Depression.

57
Q

What is the MC age group with tension headache?

A

Between 20-50.

58
Q

Headache with rhinorrhoea, unilateral, stabbing, retro-orbital, ipsilateral lacrimation, ptosis, and nasal congestion.

A

Cluster headache.

59
Q

Headache with photophobia, nausea, aura, and being unilateral?

A

Migraine.

60
Q

Common triggers for migraines:

A
  1. Menstruation.
  2. Stress.
  3. Foods.
  4. Alcohol.
61
Q

Risks of temporal arteritis - Associated with?

A

Polumyalgia rheumatica.

62
Q

How is it diagnosed?

A

Must do a temporal artery biopsy.

Elevated ESR is just a screening test.

63
Q

MCC of SAH?

A

Trauma.

64
Q

MC underlying cause of a spontaneous SAH?

A

Aneurysm rupture.

65
Q

MC heritable disorder associated with SAH?

A

AD PKD.

66
Q

How is an SAH diagnosed?

A
  1. CT shows subarachnoid blood (dark).
  2. LP shows bloody CSF with xanthocromia.
  3. Cerebral angiography to find berry aneurysms.
67
Q

Symptom of berry aneurysm rupture?

A

CN III palsy.

68
Q

MC location for a berry aneurysm?

A

Anterior communicating artery (30%), followed by posterior communicating artery. Then MCA.

69
Q

Sequence of events in an epidural hematoma?

A

Patient has a lucid interval lasting from minutes to hrs followed by a loss of consciousness and hemiparesis.

70
Q

What can cause a “blown” pupil in a patient with an epidural hematoma?

A

Uncal herniation.

71
Q

What is seen on CT in a patient with an epidural hematoma?

A

Convex (lens shaped) hyperdensity that does NOT cross the midline.

72
Q

What vessels are involved in a subdural hemorrhage?

A

Bridging veins.

73
Q

In what population are subdural hematomas most common?

A

Elderly + Alcoholics.

74
Q

Course of events in a subdural hematoma?

A

Patient can have symptoms similar to dementia since mental status changes and hemiparesis can present subacutely.

75
Q

What is seen on CT in a patient with a subdural hematoma?

A

Crescent-shaped, concave hyperdensity that may cross the midline.

76
Q

What does RIND stand for?

A

Reversible ischemic neurologic deficit.

Internal Medicine (107 decks)

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