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Neurology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Peak ages for TBI?

A

24-35 is greatest with smaller peaks in infants and eldery

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2
Q

Who is at greatest risk for TBI?

A

Males (2x incidence, 4x mortality)

Disadvantaged populations in cities

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3
Q

What are the greatest causes of concussion?

A

Falls 35.2%, MVA 17.3%

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4
Q

What percentage of acute brain injury hospitalizations are concussion?

A

80%

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5
Q

Is LOC necessary for concussion?

A

NO

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6
Q

Large Vessel Stroke

A

Affects multiple systems (motor, sensory, etc.) and is still present at 24 hours

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7
Q

Small Vessel Stroke

A

Isolated defect still present at 24 hours

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8
Q

Atypical Causes of Stroke

A

Vasculopathies
Hematologic
Inflammatory

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9
Q

Vasculopathies causing stroke

A

FMD (Women, 30-40, medial hypertrophy)
Moya-Moya (Middle cerebral occlusion, EBV)
Dissection

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10
Q

Hematologic causes of stroke

A 
Genetic Deficiencies
Malignancy
Hyperviscosity 
Oral Contraceptives
Sickle Cell does NOT increase risk
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11
Q

Inflammatory causes of stroke

A

vasculitis, venous infarction, vasospasm, migraine

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12
Q

Causes of delirium (5)

A

Polypharmacy, toxins, metabolic disorders, infectious/inflammatory causes, structural lesions

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13
Q

Complete mental status exam in delirious patient?

A

No, too confused and inattentive

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14
Q

Treatment of delirium

A

Find and treat underlying cause

in the mean time, provide environmental manipulations, get good sleep, and give calming medications

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15
Q

Alzheimer’s Atrophy Location

A

Cerebral atrophy, autopsy needed for official Dx even though clinical sings are 90% sensitive

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16
Q

Genetics associated w/ late onset Alzheimer’s

A

Epsilon-4 gene of APOE

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17
Q

Do we test for AD genes?

A

No

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18
Q

Which transmitter is missing in AD?

A

Acetylcholine

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19
Q

What do we give for AD?

A

Cholinesterase inhibitors and Memantine (NMDA antagonist)

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20
Q

Cortical Dementias (2)

A

AD and FTD

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21
Q

FTD vs AD?

A

FTD is behavioral, memory is normal. Hippocampus is spared early.

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22
Q

Subcortical Dementias (2)

A

PD and Huntington’s

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23
Q

Where are Lewy bodies? What are they made of?

A

Sustantia Nigra, made of alpha-synuclein

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24
Q

Which NT is deficient in Parkinson’s?

A

Dopamine

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25
Q

What percentage of PD patients get dementia?

A

80%

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26
Q

Lewy Body Dementia vs. PD?

A

Psychotic symptoms (hallucinations, confusion)

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27
Q

Atrophy in Huntington’s

A

Caudate

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28
Q

White matter dementias (2)

A

Biswanger’s Disease and Normal Pressure Hydrocephalus

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29
Q

Which dementia is reversible?

A

Normal Pressure Hydrocephalus

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30
Q

Normal Pressure Hydrocephalus Symptoms

A

Incontinence, high ICP at night

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31
Q

Treatment for NPH?

A

Ventriculostomy

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32
Q

2 Fundamentals of Neurodegenerative Disorders

A

Progressive loss of select neuron populations

Protein conformation and metabolism are usually involved

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33
Q

Prion misfolding involves

A

Alpha helix to beta sheet (insoluble)

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34
Q

Incorrect ways to classify NDDs?

A

Physical symptoms: movement, dementia, neuromuscular disorders
Inherited vs. sporadic

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35
Q

Can determination of abnormal protein diagnose the NDD?

A

Not always, many proteins are shared among diseases.

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36
Q

Where in the brain are the changes associated w/ AD?

A

Cortex and Hippocampus

37
Q

Where do pediatric tumors occur?

A

2/3 infratentorial

38
Q

How do brain tumors kill patients?

A

No metastasis, but vital tissue destruction or mass effect are deadly

39
Q

Do all tumors progress I to IV?

A

No. Some don’t progress (Pilocytic Astrocytoma) and others are de novo higher grade

40
Q

Most common tumor in children?

A

Pilocytic Astrocytoma, infratentorial

41
Q

Mutations common in astrocytic pilocytomas?

A

BRAF fusions, favorable

42
Q

Gangliomas usually occur where?

A

Temporal lobe in young adults

43
Q

Ganglioma Appearance

A

Cystic, likely calcified

44
Q

Mutations in gangliomas

A

BRAF point mutations

45
Q

Choroid plexus papilloma locations

A

Lateral ventricles in kids, 4th ventricle in adults

46
Q

Astrocytoma Genetic Signature

A

IDH mutated, ATRX/P53 mutated, no LOH1p,19q

47
Q

Oliogodendroglioma Genetic Signature

A

IDH mutated, no ATRX/P53 mutation, have LOH1p,19q

48
Q

What good is genetic information?

A

Prognostic information, eventually treatment

49
Q

Diffuse Astrocytoma age and location

A

30s-50s, in cerebral hemispheres

50
Q

Surgery for Diffuse Astros? Necrosis in Diffuse Astros?

A

Yes, only for debulking

No

51
Q

Diffuse Astrocytoma or Oligodendroglioma better prognosis?

A

Oligodendroglioma

52
Q

Ependyoma age and location

A

by 20 years, usually in 4th ventricle but lateral ventricles have better prognosis

53
Q

Is anaplastic astro or oligo enhancing on MRI?

A

Anaplastic Oligo

54
Q

Diffuse vs. Anaplastic distinctions

A

Mitotic Activity and MIB-1 labeling intensity

55
Q

Are glioblastomas usually de novo or progressive?

A

De novo

56
Q

Peak incidence of Medulloblastoma and location

A

3-8 years, cerebellum

57
Q

Where do medulloblastomas come from?

A

External Granule Layer, SHH abnormality

58
Q

3 types of MS

A 
Relapsing Remitting (85%)
Primary Progressive
Secondary Progressive (50% of RRs around 45 years)
59
Q

MS Epidemiology

A

2/3 Women
75% present 15-45
1/500 Coloradans, Wyoming Residents

60
Q

Genetics of MS?

A

100 linked genes, HLADR2, IL2/7 have some connection

61
Q

MS Lesion progression

A

Inflammatory then scar-like on scans

62
Q

MS Pathogenesis

A

T cell activation, MMP activation to make BBB leaky, Immune cells enter CNS, Cytokines increase BBB damage, myelin damage occurs

63
Q

Most important prognostic factor in MS?

A

Atrophy

64
Q

Can you see axonal injury on scans?

A

No, look for small hemorrhagic lesions or stain for hemosiderin

65
Q

Treatments for concussion

Recovery Time

A

Rest the brain!

Typically 7-10 days

66
Q

Methanol Toxicity

A

Putamen Necrosis

67
Q

Ethanol Acute and Chronic CNS effects

A

Acute: cerebral edema
Chronic: cerebellar atrophy (superior vermis) with gliosis, cerebral atrophy initially in white matter

68
Q

Wernicke’s Encephalopathy/B1 Thiamine Deficinecy

A

Alcoholics and Hyperemesis
Ataxia, Ophthalmoplegia, Confusion
Mamillary body degeneration!
Also hypothalamus, thalamus (confusion), PAG (occulomotor), 4th ventricle (ataxia)

69
Q

Central Pontine Myelinosis

A

Sustained hyponatremia w/ rapid replacement

Degeneration in Pons but also grey-white admixture areas

70
Q

Afferent Sensory Fiber Types

A 
A-alpha = muscle proprioception
A-beta = skin enteroception
A-delta = sharp pain, cold temp
C = burning pain, warm temp
71
Q

Pressure Effects on Sensory Afferents

A

Largest first (most metabolically active), leaving C fibers for last

72
Q

Electrical Stimulation Effects on Sensory Afferents

A

Same as pressure, smallest fibers are last to activate as shock is increased.

73
Q

Which fibers have polymodal receptors?

A

C fibers

74
Q

4 Nociceptor Activators

A

Bradykinin, Acid, Serotonin, POtassium

75
Q

5 Nociceptor Sensitizers

A

Prostaglandins, Substance P, Serotonin, ATP, Acetylcholine

76
Q

Substance P

A

Released with persistent C fiber firing, binds neurokinin1 receptor which closes K channels which second order pain afferents

77
Q

Tripartite Structure of Local Anesthetics

A

Lipophilic Ring: membrane crossing
Ester/Amide Intermediate Alkyl Chain: determines onset, duration, and potency.
Tertiary Amine: protonation status determines membrane crossing and action w/in cell

78
Q

Amide v Ester

A

Ester: metabolized in plasma by esteraes, making them less potent, shorter acting, and longer time to onset

Amide: high protein binding to alpha1-acid glycoprotein increases duration, only metabolized in liver.

79
Q

LA potency determined by

A

Lipid Solubility

80
Q

LA Duration determined by

A

protein binding capacity

81
Q

LA Speed of Onset determined by

A

inversely to pKa

82
Q

Allergic Reaction to LAs caused by

A

metabolite PABA, very very rare

83
Q

Paresthesia

A

Abnormal sensation (burning, pricking, tingling, numbness)

84
Q

Dyesthesia

A

Impairment of sensation short of analgesia

85
Q

Paresis

A

muscle weakness caused by nerve damage, short of paralysis

86
Q

Dermatome

A

Cutaneous area innervated by an individual sensory root

87
Q

Myotome

A

muscles innervated by an individual motor root

88
Q

Radiculopathy

A

sensory and/or motor dysfunction due to nerve root injury

89
Q

Myelopathy

A

spinal cord dysfunction disorder

Neurology (5 decks)

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