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Reserve Step I Cards > Neuro > Flashcards

Neuro Flashcards

1
Q

Pancoast tumors and Horner’s syndrome

A

Among other symptoms, Pancoast tumors can lead to Horner’s syndrome due to involvement of the cervical sympathetic ganglia.

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2
Q

Neural Tube Defects

  1. Pathophysiology
  2. Presentation
  3. Dx
A
  1. NTDs occur due to failure of fusion of the neural tube during the 4th week of development. This leaves an opening between the neurotube and the amniotic cavity.
  2. Can present with encephalocele (herniation), anencephaly (no brain), or the spina bifadas
  3. Leakage of alpha-fetpoprotein and AchE occurs, allowing for prenatal diagnosis
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3
Q

Name the microscopic and macroscopic changes associated with Ischemic Brain Injury, during the following times after injury:

  • 12-24 hours
  • 24-72 hours
  • 3-7 days
  • 1-2 weeks
  • >2 weeks
A
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4
Q

What does the radial nerve do? Damage to it may result in what?

A
  1. Innervation to the skin of the posterior arm, forearm, and dorsal lateral hand
  2. Motor innervation to all of the extensors of the upper limb (below the shoulder)

Damage leads to wrist drop

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5
Q

What artery is responsible for supplying the occipital lobe?

A

Posterior Cerebral Artery

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6
Q

What is Vernet syndrome?

A

It is when you have lesions of the jugular foramen, thus leading to CN Ix, X, and XI dysfunction

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7
Q

Meningiomas

  1. Pathophysiology?
  2. Who is usually affected?
  3. Where do these tumors occur?
  4. Presentation?
A
  1. Common, slow-growing (benign), intracranial tumors
  2. Typically adults
  3. Arise in regions of dural reflection (falx cerenri, tentorium cerebelli, etc.)
  4. Patients are often asymptomatic but may present w/ HA, seizure or focal neurologic deficits depending on size/ location of tumor
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8
Q

Role of the musculocutaneous nerve (2)

A
  1. Innervates the major forearm flexors and the coracobrachialis
  2. Provides sensory innervation to the lateral forearm
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9
Q

What are the (3) main dopaminergic systems? What are their functions? What diseases are they associated with?

A
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10
Q

How can severe chronic rheumatoid arthritis lead to spinal cord injury?

A

It can cause joint destruction with verterbal malalignment (subluxation), particularly at C1. Extension of neck (particularly during ET placement), can worsen the subluxation, leading to acute compression of the spinal cord and/or vertebral arteries

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11
Q

Intraventricular Hemorrhage

  1. Most frequent occurance is in what population?
  2. Pathology?
  3. Presentation?
A
  1. Usually in infants born before 32 weeks gestation or with a low birth weight
  2. IVH in premies usually originates in germinal matrix, where neurons and glial cells migrate out during brain development
  3. Clinically silent or present with altered level of conciousness, hypotonia, and decreased movement. Symptoms of catstrophic bleeding are the same as those of increased ICP.
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12
Q

What is Kinesin and what does it do?

A

A microtubule-associated, ATP-powered motor protein that facilitates the anterograde transport of neurotranmsitter-containing secretory vesicles down axons to synaptic terminals.

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13
Q

IV Benzodiazepines

  1. Main one
  2. Indication
  3. MOA
A
  1. Lorazepam
  2. Intitial drug of choice for status epilepticus
  3. They work by enhancing the effect of GABA at GABA -A receptor, leading to increased chloride influx and suppression of AP firing
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14
Q

Why doesn’t Wallerian degeneration occur in the CNS?

A

Due to the persistence of myelin debris, secretion of neuronal inhibitory factors, and development of dense glial scarring.

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15
Q

Germinoma

  1. What type of mass is it?
  2. Classical manifestations (2) and the Sx associated with each (3)
  3. Dx
A
  1. Pineal gland mass
  2. (1) Obstructive hydrocephalus due to aqueductal stenosis - Sx: papilledema, HA, vomiting (2) Dorsal midbrain (Parinaud) syndrome due to direct compression of the pretectal region of the midbrain- Sx: paralysis of upward gaze, ptosis, pupillary abnormalities
  3. Dx via MRI
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16
Q

“Red ragged” muscle fibers on Gomori trichome are seen in what kinds of disease…?

A

Mitochondrial diseases

The mitochondria accumulate under sarcolemma

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17
Q

Diabetic Mononeuropathy

  1. Usually involves which CN?
  2. Pathology
  3. Sx (3)
A
  1. CN III is most commonly involved
  2. Caused predominantly by central ischemia
  3. Sx: ptosis, “down and out” gaze, normal light/accomodation reflexes
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18
Q

POMC, a polypeptide precursor, goes through enzymatic cleavage and modification to produce what (3) proteins?

A
  1. Beta-endorphins (endogenous opioid peptide)
  2. ACTH
  3. MSH
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19
Q

Length constant

(How is it affected by myelination?)

A

A measure of how far along an axon an electrical impulse can propagate. Myelination increases this constant.

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20
Q

Lesch-Nyhan Syndrome

  1. Inheritance?
  2. Presentation?
  3. Pathology?
  4. The [] of what enzyme increases as a result?
A
  1. X-linked recessive
  2. Presentation: self-mutilation, hyperuricemia, dystonia, and choreoathetosis in the first few years of life
  3. Pathology: HGPRT deficiency (used in purine salvage pathway). Leads to degradation of hypoxanthine bases into uric acid.
  4. Increased demand for de novo purine synthesis leads to increased PRPP activity
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21
Q

Tabes Dorsalis

  1. Epidemiology?
  2. Pathogenesis?
  3. Clinical findings?
A
  1. Epidemiology: Increased incidence of syphilis in MSM/ HIV-infected patients
  2. Pathology: Treponema pallidum spirochetes directly damage the dorsal sensory roots
  3. Clinical findings: sensory ataxia, lancinating pains, neurogenic urinary incontinence, Argyll Robertson pupils
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22
Q

Maple Syrup Urine Disease (MSUD)

  1. Pathology
  2. Presentation
  3. Treatment
    4.
A
  1. Path: defect in a-keto dehydrogenase, leading to inability to degrade branched chain amino acids (leucine, isoleucine, valine) beyond deaminated a-keto acid state
  2. Sx: Dystonia; poor feeding; maple syrup scent urine in first few days of life
  3. Tx: Dietary restriction of branched-chain AA’s
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23
Q

Causes of oral thrush (3 main)

A
  1. Candida albicans
  2. Albuterol inhaler
  3. HIV
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24
Q

Vitamin A toxicity

  1. Acute affects (3)
  2. Chronic affects (5)
  3. Teratogenic affects (3)
A
  1. Acute: N/V, vertigo, blurred vision
  2. Chronic: alopecia, dry skin, hyperlipidemia, hepatotoxicity/ hepatosplenomegaly, and visual difficulties
  3. Teratogenic: Microcephaly, cardiac anomalies, fetal death
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25
Q

What time interval is the key difference between PTSD and Acute Stress Disorder?

A

Acute stress disorder

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26
Q

What are the main effects of a glossopharyngeal nerve lesion?

A
  1. Loss of gag reflex
  2. Loss of general sensation of the upper pharynx, posterior tongue, tonsils and middle ear cavity
  3. Loss of taste on posterior third of tongue
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27
Q

Which neural structure is most affected by the thiamine deficiency associated with Wernicke encephalopathy?

A

Mamillary bodies

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28
Q

First generation anti-histamines

  1. Name them
  2. In addition to blocking histamine receptors, what other affects?
  3. How can the eye be affected?
A
  1. Ex. Chlorpheniramine, diphenhydramine
  2. Also have antimuscarinic, anti-alpha adrenergic, and anti-serotonergic properties
  3. Anticholinergic effects on occular ciliary muscles impair accomdation and cause blurring of vision for close obects
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29
Q

The anterior cerebral arteries supply which portions of the brain? (2)

What is the affect that occlusion can have?

A
  1. They supply the medial portions of the 2 hemispheres (frontal and parietal)
  2. Occlusion can cause contralateral motor and sensory deficits of the lower extremities, behavorial changes, and urinary incontinence
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30
Q
  1. Peroxisomes are responsible for metabolizing what?
  2. What does Peroxisomal disease commonly lead to?
A
  1. Metabolizes very long chain fatty acids or fatty acids with branch points at odd-numbered carbons since they cannot undergo mitochondrial beta-oxidation
  2. Can lead to neurologic defects from improper CNS myelination
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31
Q

Injury to the lower trunk of the brachial plexus

  1. What mechanism of injury which causes this?
  2. Consequence of this injury?
A
  1. Result of sudden upward jerking of the arm at the shoulder
  2. May causes paralysis of all intrinsic hand muscles (Klumpke’s palsy) w/ sparing to the extensors, leading to total claw hand deformity. Can also see sensory loss and weakness.
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32
Q

When providing a nerve block of the brachial plexus between scalene muscles, what must you be weary of?

A

Transient ipsilateral diaphragmatic paralysis due to involvement of the phrenic nerve roots as they pass through the interscalene sheath.

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33
Q

Serotonin syndrome

  1. How do we get this syndrome?
  2. Sx (3)
  3. What is the antidote?
  4. What is the precursor to serotonin?
A
  1. The result of either serotonin overdose or co-prescription with an MAOI or triptan
  2. (1) neuromuscular excitation, (2) autonomic stimulation, (3) altered mental status
  3. Antidote- Cyproheptadine ( a first generation histamine antagonist)
  4. Tryptophan is the precursor to serotonin
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34
Q

Sx of trapezius weakness vs deltoid weakness

A

Trapezius- drooping of shoulder, impaired abduction above horizontal, winging of the scapula

Deltoid- impaired abduction at angles below the horizontal plane

35
Q

Diazepam

  1. Indications (4)
  2. SEs (1 most common)
  3. Contraindications
A
  1. Indications: (1) anxiolytic, (2) sedative-hypnotic, (3) anticonvulsant, (4) muscle relaxant
  2. SE: Sedation
  3. Contraindications: Don’t give to patients on other CNS depressants (ex. chlorpheniramine)
36
Q

Huntington disease

  1. Describe the genetic/cellular level cause of this disease.
  2. How are histones involved?
A
  1. Increased CAG trinucleotide repeats in the gene that codes for the huntingtin protein, leading to gain-of-fxn mutation.
  2. Transcriptinal repression (silencing), via histone deacetylation, is thought to be one of the main mechanisms in which this mutation causes disease
37
Q

Migraine

  1. Sx
  2. Abortive therapy (1)
  3. Prophylactic therapy (3)
A
  1. Unilateral HAs, with pulsating/throbbing quality, associated with photophobia, phonophobia, and nausea
  2. Abortive: Triptans (serotonin agonists)
  3. Prophylactic: Beta-blockers, antidepressantts, and anti-convulsants
38
Q

Amyotrophic Lateral Sclerosis

  1. Sx
  2. Gross anatomy
  3. Histo/ microscopic
  4. Genetics
  5. Tx
A
  1. Sx: LMN- muscle weakness, atrophy, fasiculations; UMN- spasticity, hypereflexia, pathologic reflexes
  2. Gross: (1)Thin anterior roots; (2) mild atrophy of precentral gyrus
  3. Histo/micro: loss of anterior horn neurons, lateral CSTs, motor nuclei neurons, and denervation atrophy of muscles
  4. Genetics: mutation of gene for superoxide dismutatse (SOD1) may be implicated
  5. Tx: Riluzole (decreases glutamate release)
39
Q

Subthalamic nucleus

  1. What pathology can cause damage to this structure?
  2. What is the consequence of this damage?
A
  1. Lacunar stroke can cause damage
  2. Damage may result in contralateral hemiballism, characterized by wild, involuntary, large-amplitude, flinging movements of proximal limbs on one side of the body
40
Q

Ramelteon

  1. MOA
  2. Indications
  3. SEs
A
  1. MOA: melatonin agonist
  2. Initial insomnia treatment that demonstrates high safety and efficacy in older adults
  3. Very few SEs and no dosage adjustment needed
41
Q

Subarachnoid Hemorrhage (SAH)

  1. Presentation
  2. Pathology and associated diseases (3)
  3. Dx
A
  1. Sx: “Worst headache of my life” + fever/nuchal rigidity
  2. Path: Saccular (berry) aneurysms are most common cause. Associated with Ehlers-Danlos syndrome, ADPKD, and AV malformations
  3. Dx: Non-contrast CT showing hyperdensity in cisterns/sulci; LP showing gross blood or xanthochromia (yellow discoloration of the CSF)
42
Q

Lambort-Eaton syndrome

  1. Sx
  2. Disease associated with
  3. Pathogenesis
  4. Tensilin test result
  5. Nerve stimulation studies
A
  1. Sx: weakness improves during the day and with excercise. Weakness of proximal muscles
  2. Assc. with pre-existing malignancy
  3. Path: antibodies against pre-synaptic calcium channels
  4. No improvement from tensilon test
  5. Incremental response from nerve stim. test
43
Q

Myasthenia Gravis

  1. Sx
  2. Disease associated with
  3. Pathogenesis
  4. Tensilin test result
  5. Nerve stimulation studies
A
  1. Sx: Weakenss that is worse at the end of the day/ with exertion; extraocular muscles are affected first (ptosis/diplopia)
  2. Assc. with risk of thymoma
  3. Path: antibodies against Ach receptors
  4. Improvement/ resolution w/ tensilon test
  5. Decremental response to nerve stim. test
44
Q
  1. Inhibition of uterine contractons is a result of stimulation of which adrenergic receptor?
  2. Pupillary dilation is the result of stimulation of which adrenergic receptor?
A
  1. B2 (inhibits uterus)
  2. a2 (dilates pupils)
45
Q

Neurofibromatosis Type 1 (NF-1)

  1. Sx (4)
  2. Inheritance
  3. What type of cells are the main compent of cutaneous neurofibromas?
A
  1. (1) Cafe-au-lait spots, (2) Neurofibromas (short, sessile or pedunculated lesions), (3) Lisch nodules (pigmentated hamartomas of the iris), (4) pseudoarthritis
  2. Autosomal-dominate inheritance
  3. Schwann cells are the main component
46
Q

Ataxia-telangiectasia

  1. Inheritance
  2. Path
  3. Sx/Presentation (4)
A
  1. Autosomal-recessive
  2. Result of a defect in DNA-repair genes, making the genes hypersensitive to ionizing radiation
  3. Presents as child w/ (1) cerebellar ataxia, (2) oculocutanoeous telangiectasias, (3) repeasted sinopulmonary infxn, (4) inc. incidence of malignancy
47
Q

Ariginase

  1. Fxn
  2. Sx of Arginase deficiency
  3. Tx of Arginase deficiency
A
  1. Fxn: urea cycle enzyme that produces urea and ornithine from arginine
  2. Sx: (1) Progressive spastic diplegia, (2) growth delay, (3) abnormal movements
  3. Tx: Arginine-free, low protein diet
48
Q

Wilson Dz

  1. Sx (3)
  2. Dx
  3. Tx
A
  1. Sx: Liver injury (sometimes asymptomatic), psych sx’s, Basal ganglia injury (leading to parkinsonism)
  2. Dx: Kayser-Fleischer rings; labs show increased transaminases (liver injury) and low serum ceruloplasmin
  3. Tx: D-penicillamine
49
Q

Wilson Disease

  1. Inheritance
  2. Path
A
  1. Autosomal recessive mutation of the ATP7B gene
  2. Path: Mutation leads to a decrease in copper incorporation into ceruloplasmin and reduced biliary copper excretion leading to copper accumulation in liver, brain, and eye
50
Q

Zolpidem

  1. Indication
  2. SImilar to what drug? How does it differ?
A
  1. Short-acting hypnotic used for short-term insomnia
  2. Same MOA as benzos but a much lower risk of tolerance and dependence
51
Q

Tetrodotoxin

  1. Where does it come from?
  2. What effect does it have?
A
  1. Comes from pufferfish
  2. Binds to voltage-gated sodium channels in nerve and cardiac tissue, preventing sodium influx and depolarization – leads to paralysis
52
Q

Treacher-Collins syndrome

  1. Path?
  2. What is the effect?
A
  1. Genetic disorder resulting in abnormal development of the first and second pharyngeal arches
  2. Result: (1) Craniofacial abnormalities which often compromise airway and feeding; (2) absent or abnormal ossicles leading to profound conductive hearing loss
53
Q

What is responsible for the clinical variability of mitochondrial diseases?

A

HETEROPLASMY

The mixture of (2) types of genetic material

54
Q

Propionyl CoA is derived from which amino acids? (4)

A

Val, Ile, Met, and Thr

55
Q

After invading the nasopharnyx, how does N. meningitidis gain access to the brain?

A

Bloodstream followed by choroid plexus

56
Q

Clostridium tetani blocks the release of what?

A

The inhibitors Glycine and GABA

57
Q

What are the cutaneous neurofibromas assc. with NF1, derived from? What is its embryological derivation?

A

They are comprised mostly of Schwann cells, which are embryologically derived from the neural crest

58
Q
A
59
Q

Key AE associated with lamotrigine

A

SJS (30% of body surface)

60
Q

Capsaicin causes depletion of what neurotransmitter? What does this lead to?

A

Substance P

An intitial burning/stinging sensation, but chronic exposure leads to reduced pain transmission

61
Q

Length constant

A

A measure of how far along an axon an electrical impulse can propagate

This is increased by myelination

62
Q

What is the most common location for acoustic schwannomas?

A

Cerebellopontine angle

63
Q

If a patient with HIV has rin-enhancing lesions, and treated for toxoplasmosis is negative, what dz should you suspect?

What cell typically compose this dz?

A

Suspect Primary Central Nervous System Lymphom__a

It is typically composed of B-lymphocytes, and is associated with EBV.

64
Q

Oligodendrocytes Vs Schwann Cells

A

Oligodendrocytes- CNS myelin (oligarchy means central power)

Schwann- Peripheral Myelin

65
Q

Carbamazepine

  1. Indication
  2. MOA
  3. Adverse Effects
A
  1. Seizure tx
  2. Blockage of voltage-gated sodium channels in neuronal membranes
  3. Can cause bone marrow suppression
66
Q

Function of the suprachiasmatic nucleus (of the hypothalamus)

A

Circadian rhythm regulation and pineal gland function

67
Q

Conversion disorder

A

Neurological symptoms that are incompatible with a neurological disease. Often stressed associated.

68
Q

Describe themost important biochemical abnormality in Alzheimer dz

Where is this decline most notable?

A

A dec. in Ach level due to the deficiency of choline acetyltransferase, needed to synthesize Ach.

Most notable in the basal nucleus of Meynert or the hippocampus

69
Q

What drugs are/can be given with L-DOPA to reduce their peripheral metabolism?

A

Carbidopa- a DOPA decarboxylase inhibitor

Entacapone- a COMT inhibitor

These both increase levadopa bioavailability to the brain

70
Q

Name the (2) classes of dopamine agonists (and examples).

What dz are they most often used for?

A
  1. Ergot compounds- Bromocriptine
  2. Nonergot compounds- Pramipexole, ropinirole
71
Q

What drug is used as abortive therapy during an acute migraine?

What is its MOA?

A

Triptans

They are serotonin 5-HT1B/5-HT1D agonists, and thus inhibit the release of vasoactive peptides, promoting vasoconstriction, and blocking pain pathways in the brainstem.

72
Q

What is the affect of occluson of the anterior cerebral artery?

A

Disruption of sensory and motor function of the contralateral leg and foot, while sparing the contralateral arm/face

73
Q

What is the (4) step route that N. meningitidis uses to cause meningitis?

A

Pharynx –> blood –> choroid plexus –> meninges

74
Q

Cauda Equina Syndrome

Presentation?

Specific areas damaged?

A

Saddle anesthesia and loss of the anocutaneous reflex, assc. with damage to the S2 through S4 nerve roots

75
Q

What is responsible for the clinical variability of mitochondrial dz?

A

The mixture of two types of genetic material, known as heteroplasmy. In other words, during mitosis there is a random distribution of mitochondria, some containing lots of damaged mitochondria, others containing very few.

76
Q

What are the effects of occlusion of the MCA?

A
  1. Contralateral hemiplegia of the face/ upper limb
  2. Relative preservation of the lower limb
  3. Aphasia (if occlusion is in dominant hemisphere – usually left)
77
Q

Ethosuximide MOA

A

Blocks T-type Ca2+ channels in thalamic neurons

(used to treat absence seizures)

78
Q

Ataxia Telangiectasia

  1. Classic triad
  2. Specific defect
A
  1. Cerebellar ataxia + telangiectasias + inc. risk of sinopulmonary infections
  2. Defect in the gene that encodes for the ATM gene, which plays a role in DNA break repair
79
Q

What is the cause of Myotonic Dystrophy?

A

An autosomal dominant disorder, leading to increased number of trinucleotide repeats on the myotonia-protein kinase gene

80
Q

Myotonic dystrophy presentation (5)

A

Sustained muscle contraction (can’t release doorknob) + weakness/atrophy

(often also see cataracts, frontal balding and gonadal atrophy)

81
Q

What cell type composes the wall of the cyst in the years after a stroke?

A

Astrocytic processes (glial scar)

82
Q

What is the most common cause of bacterial meningitis in adults of all ages?

A

Strep Pneumo

83
Q

What is the neurological effect of vitamin B12 deficiency?

A

Subacute combined degeneration!!!

demyelination of dorsal columns, lateral CST, and spinocerebellar tracts, leading to: ataxic gait, paresthesia, and impaired position/vibration sense

Reserve Step I Cards (10 decks)

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