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Neurology > Exam 2 > Flashcards

Exam 2 Flashcards

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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
What percentage of PD patients get dementia?
80%
26
Lewy Body Dementia vs. PD?
Psychotic symptoms (hallucinations, confusion)
27
Atrophy in Huntington's
Caudate
28
White matter dementias (2)
Biswanger's Disease and Normal Pressure Hydrocephalus
29
Which dementia is reversible?
Normal Pressure Hydrocephalus
30
Normal Pressure Hydrocephalus Symptoms
Incontinence, high ICP at night
31
Treatment for NPH?
Ventriculostomy
32
2 Fundamentals of Neurodegenerative Disorders
Progressive loss of select neuron populations Protein conformation and metabolism are usually involved
33
Prion misfolding involves
Alpha helix to beta sheet (insoluble)
34
Incorrect ways to classify NDDs?
Physical symptoms: movement, dementia, neuromuscular disorders Inherited vs. sporadic
35
Can determination of abnormal protein diagnose the NDD?
Not always, many proteins are shared among diseases.
36
Where in the brain are the changes associated w/ AD?
Cortex and Hippocampus
37
Where do pediatric tumors occur?
2/3 infratentorial
38
How do brain tumors kill patients?
No metastasis, but vital tissue destruction or mass effect are deadly
39
Do all tumors progress I to IV?
No. Some don't progress (Pilocytic Astrocytoma) and others are de novo higher grade
40
Most common tumor in children?
Pilocytic Astrocytoma, infratentorial
41
Mutations common in astrocytic pilocytomas?
BRAF fusions, favorable
42
Gangliomas usually occur where?
Temporal lobe in young adults
43
Ganglioma Appearance
Cystic, likely calcified
44
Mutations in gangliomas
BRAF point mutations
45
Choroid plexus papilloma locations
Lateral ventricles in kids, 4th ventricle in adults
46
Astrocytoma Genetic Signature
IDH mutated, ATRX/P53 mutated, no LOH1p,19q
47
Oliogodendroglioma Genetic Signature
IDH mutated, no ATRX/P53 mutation, have LOH1p,19q
48
What good is genetic information?
Prognostic information, eventually treatment
49
Diffuse Astrocytoma age and location
30s-50s, in cerebral hemispheres
50
Surgery for Diffuse Astros? Necrosis in Diffuse Astros?
Yes, only for debulking | No
51
Diffuse Astrocytoma or Oligodendroglioma better prognosis?
Oligodendroglioma
52
Ependyoma age and location
by 20 years, usually in 4th ventricle but lateral ventricles have better prognosis
53
Is anaplastic astro or oligo enhancing on MRI?
Anaplastic Oligo
54
Diffuse vs. Anaplastic distinctions
Mitotic Activity and MIB-1 labeling intensity
55
Are glioblastomas usually de novo or progressive?
De novo
56
Peak incidence of Medulloblastoma and location
3-8 years, cerebellum
57
Where do medulloblastomas come from?
External Granule Layer, SHH abnormality
58
3 types of MS
``` Relapsing Remitting (85%) Primary Progressive Secondary Progressive (50% of RRs around 45 years) ```
59
MS Epidemiology
2/3 Women 75% present 15-45 1/500 Coloradans, Wyoming Residents
60
Genetics of MS?
100 linked genes, HLADR2, IL2/7 have some connection
61
MS Lesion progression
Inflammatory then scar-like on scans
62
MS Pathogenesis
T cell activation, MMP activation to make BBB leaky, Immune cells enter CNS, Cytokines increase BBB damage, myelin damage occurs
63
Most important prognostic factor in MS?
Atrophy
64
Can you see axonal injury on scans?
No, look for small hemorrhagic lesions or stain for hemosiderin
65
Treatments for concussion | Recovery Time
Rest the brain! | Typically 7-10 days
66
Methanol Toxicity
Putamen Necrosis
67
Ethanol Acute and Chronic CNS effects
Acute: cerebral edema Chronic: cerebellar atrophy (superior vermis) with gliosis, cerebral atrophy initially in white matter
68
Wernicke's Encephalopathy/B1 Thiamine Deficinecy
Alcoholics and Hyperemesis Ataxia, Ophthalmoplegia, Confusion Mamillary body degeneration! Also hypothalamus, thalamus (confusion), PAG (occulomotor), 4th ventricle (ataxia)
69
Central Pontine Myelinosis
Sustained hyponatremia w/ rapid replacement Degeneration in Pons but also grey-white admixture areas
70
Afferent Sensory Fiber Types
``` A-alpha = muscle proprioception A-beta = skin enteroception A-delta = sharp pain, cold temp C = burning pain, warm temp ```
71
Pressure Effects on Sensory Afferents
Largest first (most metabolically active), leaving C fibers for last
72
Electrical Stimulation Effects on Sensory Afferents
Same as pressure, smallest fibers are last to activate as shock is increased.
73
Which fibers have polymodal receptors?
C fibers
74
4 Nociceptor Activators
Bradykinin, Acid, Serotonin, POtassium
75
5 Nociceptor Sensitizers
Prostaglandins, Substance P, Serotonin, ATP, Acetylcholine
76
Substance P
Released with persistent C fiber firing, binds neurokinin1 receptor which closes K channels which second order pain afferents
77
Tripartite Structure of Local Anesthetics
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
Amide v Ester
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
LA potency determined by
Lipid Solubility
80
LA Duration determined by
protein binding capacity
81
LA Speed of Onset determined by
inversely to pKa
82
Allergic Reaction to LAs caused by
metabolite PABA, very very rare
83
Paresthesia
Abnormal sensation (burning, pricking, tingling, numbness)
84
Dyesthesia
Impairment of sensation short of analgesia
85
Paresis
muscle weakness caused by nerve damage, short of paralysis
86
Dermatome
Cutaneous area innervated by an individual sensory root
87
Myotome
muscles innervated by an individual motor root
88
Radiculopathy
sensory and/or motor dysfunction due to nerve root injury
89
Myelopathy
spinal cord dysfunction disorder

Neurology (5 decks)

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