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Review / Wrong Answers > DIT Review - Neurology 2 > Flashcards

DIT Review - Neurology 2 Flashcards

1
Q

Structures of 1st branchial cleft

A

external ear

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2
Q

Structures of 1st branchial arch

A
  • Cartilage:
    • Maxillary process, mandibular process
  • Muscles:
    • Muscles of mastication, mylohyoid, tensor tympani, tensor veli palatine
  • Nerves:
    • CN V2 and V3
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3
Q

Structures of 2nd branchial arch

A
  • Cartilage:
    • Stapes, styloid, stylohyoid
  • Muscles:
    • Muscles of facial expression
    • Stapedius, stylohyoid
  • Nerves:
    • CN VII
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4
Q

Structures of 3rd branchial arch

A
  • Cartilage:
    • Greater horn of hyoid
  • Muscles:
    • Stylopharyngeus
  • Nerves:
    • CN IX
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5
Q

Structures of 4th and 6th branchial arch

A
  • Cartilage
    • Arytenoids, cricoid, thyroid
  • Muscles:
    • 4th à Cricothyroid, most pharyngeal constrictors, levator veli palatini
    • 6th à All laryngeal muscles except cricothyroid
  • Nerves:
    • 4th à CN X superior laryngeal branch (swallowing)
    • 6th à CN X recurrent laryngeal branch (speaking)
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6
Q

Structures of 1st branchial pouch

A

Middle ear

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7
Q

Structures of 2nd branchial pouch

A

epithelial lining of tonsils

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8
Q

Structures of 3rd branchial pouch

A

thymus, inferior parathyroids

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9
Q

Structures of 4th branchial pouch

A

superior parathyroids

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10
Q

Describe areas of the spinal cord involved in syringomyelia

A
  • Anterior white commissure:
    • Loss of pain and temp with sparing of fine touch and position à “cape-like” distribution
  • Anterior horn involvement can occur with progression of disease
    • Lower motor neuron effects
  • Lateral horn of hypothalamospinal tract
    • Horner syndrome
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11
Q

BH4 (tetrahydrobiopterin) is a cofactor used for synthesis of what substances?

A

Tyrosine, dopamine, melanin, and serotonin

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12
Q

What is the mechanism behind fibrates causing increased risk for cholesterol stones?

A
  • Inhibition of cholesterol 7a-hydroxylase, which catalyzes the rate-limiting step in the synthesis of bile acids
    • Reduced bile acid production results in decreased cholesterol solubility in bile
    • Leads to increased formation of cholesterol stones
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13
Q

What is the enzyme that catalyzes the formation of ribose sugars in the HMP shunt?

A

Transketolase

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14
Q

What is the predominant inflammatory cell in gout?

A

neutrophils

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15
Q

What is the defect and presentation of alkaptonuria?

A

Inability to degrade tyrosine due to defect in homogentisate oxidase

Presentation:

o Blueish-black connective tissue (e.g. ear cartilage) and sclera

o Black urine upon prolonged exposure to air

o Debilitating arthralgias

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16
Q

What is the treatment for a patient with pyruvate dehydrogenase deficiency?

A

Ketogenic diet (high fat, low carb diet with moderate levels of protein)

This forces the production of ketone bodies to fuel the body in place of glucose, so less pyruvate is generated via glycolysis

Lysine and leucine are exclusively ketogenic aminao acids and cannot be metabolized to pyruvate

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17
Q

What is the function of the arcuate fasciculus

A

Connects Broca’s and Wernicke’s area

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18
Q

What structures does the anterior cerebral artery supply?

A
  • Supplies anteromedial surface
    • Motor and sensory cortex of the foot and leg area (think of homunculus)
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19
Q

What structures does the middle cerebral artery supply?

A
  • Supplies the lateral surface
    • Motor and sensory cortex of the face and upper limbs
    • Temporal lobe à Broca and Wernicke’s area
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20
Q

What structures does the posterior cerebral artery supply?

A
  • Supplies posterior and inferior surface
    • Occipital lobe
    • Visual cortex
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21
Q

Describe the defect and effect of conduction aphasia

A

Conduction aphasia - damage to arcuate fasciculus (connection between Broca’s and Wernicke’s area)

Broca’s and Wernicke’s are intact (speech and comprehension are intact), but no connection between what you hear and what you say (repitition is impaired)

22
Q

Describe the defect and effect of global aphasia

A

Global aphasia - Broca and Wernicke area affected

Influent speech and impaired comprehension

23
Q

Describe expressive dysprosody

A
  • Non-dominant Broca
    • Inability to express emotion or inflection in speech
24
Q

Describe receptive dysprosody

A
  • Non-dominant Wernicke
    • Inability to comprehend emotion or inflection in speech
25
Q

Effect of lesion to the non-dominant parietal cortex

A
  • Hemispatial neglect syndrome (ignoring contralateral half of the world)
26
Q

Effect of lesion to the reticular activating system

A
  • Reticular activating system contains:
    • Reticular formation
    • Locus ceruleus (produces NE)
    • Raphe nucleus (produces 5HT)
  • Lesion causes reduced level of arousal and wakefulness (e.g. coma)
27
Q

Effect so lesion to the dominant parietal cortex

A
  • Gerstmann syndrome
    • agraphia (inability to write), acalculia (inability to calculate), finger agnosia (inability to distinguish fingers), left-right disorientation
28
Q

Effect of lesion to the mammillary bodies

A
  • Wernicke-Korsakoff syndrome
    • confusion, ophthlamoplegia, ataxia, memory loss, confabulation, personality changes
29
Q

Effect of lesion to the basal ganglia

A
  • Resting tremor, chorea, athetosis
  • E.g. Parkinson or Huntington
30
Q

Effect of lesion to the cerebellar hemisphere

A
  • Occurs with chronic alcohol use
  • Intention tremor, limb ataxia
31
Q

Effect of lesion to the cerebellar vermis

A
  • Truncal ataxia, dysarthria
32
Q

Effect of lesion to the subthalamic nucleus

A
  • Hemiballismus (involuntary flailing of limbs)
33
Q

Effect of lesion to the hippocampus

A
  • Anterograde amnesia (inability to create new memories)
34
Q

Effect of lesion to the paramedian pontine reticular formation (PPRF)

A
  • Eyes look away from side of lesion
35
Q
A
36
Q

Presentation of serotonin syndrome

A

Hyperthermia, HTN, Hyperreflexia and clonus (vs. NMS which has rigidity and hyporeflexia)

37
Q

What are the 3 C’s to remember about toxicity of TCA’s?

A

Cardiac, coma (anti-H1), convulsions (anti-GABA)

38
Q

Describe the differences between delirium and dementia

A
  • Delirium:
    • Acute onset (hours – days)
    • Waxing and waning level of consciousness
    • Disorganized thoughts, delusions, hallucinations, sleep disturbance
    • Abnormal EEG
    • Reversible
  • Dementia:
    • Gradual onset (months – years)
    • Normal consciousness
    • Cognitive decline, with minimal psychotic symptoms
    • EEG usually normal
    • Irreversible
39
Q

Most common cause of delirium

A
  • Drugs – Benzos and Anticholinergics
  • UTI
40
Q

What are the 2 characteristic microscopic features of Alzheimers?

A
  • Extracellular beta-amyloid plaques
  • Intracellular neurofibrillary tangles
41
Q

Describe the pathogenesis behind beta-amyloid plaque

A
  • Neurons have receptors derived from amyloid precursor proteins (APP – coded on chr 21)
  • APP is normally broken down by a-secretase, which allows turnover
  • APP broken down b-secretase creates Ab-amyloid which deposits in the brain
42
Q

What is the composition of neurofibrillary tangles?

A
  • Composed of tau protein (microtubule associated protein)
43
Q

What two disease are tau proteins seen in?

A

Alzheimer - neurofibrillary tangles

Frontotemporal dementia - Pick bodies

44
Q

What proteins are risk factors/protective against Alzheimers

A
  • ApoE2 is protective
  • ApoE4 has increased risk (due to increased production of beta-form of APP)
  • Early onset associated with:
    • Presenilin-1 and Presenilin-2
    • Trisomy 21 (extra APP gene)
45
Q

Neurotransmitter level in Alzheimers?

A

Decreased ACh

46
Q

Treatment of Alzheimers

A
  • Cholinesterase inhibitors (Galantamine, Rivastigmine, Donepezil)
  • NMDA antagonist (Memantine
47
Q

Presentation of Pick disease

A
  • Early - Behavior changes (frontal lobe) and/or aphasia (temporal lobe)
  • Late - Dementia
48
Q

Compare Parkinson’s to Lewy body dementia

A
  • Lewy body:
    • Early onset dementia + Lewy bodies
      • Vs. Parkinson’s which has late onset dementia + Lewy bodies
    • Lewy bodies within the cortex (aggregates of a-synuclein)
      • Vs. Parkinson’s which affects the substantia nigra
    • Characterized by dementia and visual hallucinations, followed by Parkinsonian features
49
Q

Describe the defect that causes Creutzfeldt-Jakob disease

A
  • Degenerative disease to prions in B-pleated sheets
    • PrPc to PrPsc
    • Beta protein is resistant to proteases and converts normal protein into pathologic form
50
Q

Presentation of CJD

A
  • Rapidly progressive dementia + ataxia + startle myoclonus

Review / Wrong Answers (140 decks)

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