Week 1 Block 8: BSPN Flashcards

Test taken 4/10/2014 Test reviewed 4/23/2014

1
Q

Morphine tolerance: (1) Possible mechanism (2) Neurotransmitter pathway involved in tolerance (3) Drug that modulates that neurotransmitter

A

(1) May involve increased phosphorylation of opioid receptors, increased adenylyl cyclase activity or increased nitric oxide levels; (2) Activation of NDMD receptors by glutamate is believed to enhance morphine tolerance by increasing phosphorylation of opioid receptors and increasing nitric oxide levels (3) NMDA receptor blocks, like ketamine, block actions of glutamate and effectively decrease morphine tolerance

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2
Q

(1) Most likely Dx/Cause: long standing diabetes with poor glycemic control, right sided ptosis with right eye looking down and out, pupils equal and reactive to light (2) Relevant neuroanatomy to recall

A

(1) diabetic CN III neuropathy, ischemic nerve damage (2) Diabetic mononeuropathy often involves CN III; Only somatic nerve fibers affected, parasympathetic fibers retain function

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3
Q

Valproate: (1) general clinical use (2) mechanism (3) congenital defect

A

(1) epilepsy (2) inhibits intestinal folic acid absorption (3) neural tube defects

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4
Q

Subdural hematoma: (1) Cause (2) Patients at risk/exposures (3) Presentation (4) CT

A

(1) Rupture of cortical bridging veins (2) Fall or MVA (3) Gradual onset of headache and confusion (4) crescent shaped, crosses suture lines, not cross falx/tentorium

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5
Q

Subarachnoid hemorrhage: (1) Cause (2) Presentation (3) Assoc. condition

A

(1) Rupture of saccular (berry) aneurysms or ateriovenous malformations (2) Generalized, excruciating headache, “worst headache of my life” (3) Bery aneurysms of Circle of Willis assoc. with ADPKD

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6
Q

1st arch syndrome: (1) Anatomic Abnormalities (2) Nerve involved

A

(1) Mandible, maxilla, malleus, incus, zygoma, vomer, palate, and temporal bone (2) Trigeminal nerve

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7
Q

(1) Most common extracranial neoplasm in children (2) Genetic association (3) Paraneoplastic syndrome

A

(1) Neuroblastoma (2) Increased number of copies of N-myc gene (3) Opsoclonus-myoclonus

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8
Q

(1) Dx: unilateral headahce, eye pain, diplopia, dilated nonreactive pupil, and ptosis with ipsilateral eye in a down and out position (2) Involved nerve contents and relevant arteries

A

(1) Aneurysm of either PCA or superior cerebellar artery, leading to non-pupil-sparing CNIII nerve palsy (2) CN III (oculomotor) carrying general somatic efferent fiber and general visceral efferent parasympathetic fiber exits the midbrain and courses between the posterior cerebral and superior cerebellar arteries

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9
Q

Dx: Contralateral homonymous hemianopia and a relative afferent pupillary defect (Marcus Gunn pupil) in the contralateral eye

A

Lesion in optic tract

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10
Q

(1) Dx: Confusion, ataxia, ophthalmoplegia (2) Classic iatrogenic cause (3) Characteristic damage

A

(1) Triad of Wernicke encephalopathy (2) Precipitation by infusion of glucose without thiamine in patient with chronic thiamine deficiency (3) Hemorrhage into mamilary bodies

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11
Q

(1) Dx: patient understands language but cannot properly formulate motor commands to form words or write, slow fragmented speech with short agrammatic phrases (2) Area of brain affected (3) Patient response to disorder

A

(1) Broca’s (motor) aphasia (2) Inferior frontal gyrus of dominant hemisphere (3) Patients have insight into their aphasia & are often frustrated by it

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12
Q

Dx: fixed segmental loss of upper extremity pain and temperature sensation, upper extremity lower motor neuron signs, and/or lower extremity upper motor neuron signs in setting of scoliosis

A

Syringomyelia

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13
Q

(1) 3 gene mutations assoc. with early-onset familial Alzheimer disease (2) Genotype assoc. with late-onset familial Alzheimer disease

A

(1) APP (chromosome 21), presenilin 1 and presenilin 2 (all above mutations thought to promote production of A Beta-amyloid) (2) Apolipoprotein E4

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14
Q

(1) Global cerebral ischemia AKA (2) Caused by (3) Cells most susceptible to ischemia (4) First area damaged during global cerebral ischemia

A

(1) Hypoxic-ischemic encephalopathy (2) Result of systemic hypoperfusion (3) Pyramidal cells of hippocampus & Neocortex and Purkinje cells of Cerebellum (4) Hippocampus

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15
Q

(1) Dx: Tinnitus, vertigo, sensorineural hearing loss (2) Pathogenesis

A

(1) Meniere’s disease (2) Related to increased volume and pressure of endolymph in vestibular apparatus

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16
Q

Syringomyelia: (1) Pathogenesis (2) Spinal cord damage & resulting deficit(s)

A

(1) Formation of cavity (syrinx) in cervical region of spinal cord (2) Damages ventral white commissure, leading to bilateral loss of pain and temperature sensation that is limited to affected levels (typically arms and hands); Distal sensation is preserved. Destruction of motor neurons in ventral horns (due to extension of syrinx) causes flaccid paralysis and atrophy of intrinsic muscles of hand

17
Q

Stains for identifying neoplastic cells: (1) Synaptophysins (2) Glial fibrillary acidic protein.

A

(1) Protein found in presynaptic vesicles of neurons, neuroendocrine and neuroectodermal cells (2) Neoplasms of glial origin (astrocystomas, ependymomas, and oligodendrogliomas)

18
Q

UMN lesions: (1) Sx’s (2) Specific lesions in brain causing UMN lesions

A

(1) spastic, rigidity, hyperreflexia, paresis (2) Corticospinal tract, internal capsule (posterior limb), and primary motor cortex lesions

19
Q

Dx: cerebellar ataxia, loss of position and vibration sensation, kyphoscoliosis, foot abnormalities, history of DM, and hypertrophic cardiomyopathy

A

Friedreich ataxia

20
Q

3 general features for localizing a transverse spinal cord section

A

(1) More proximal levels have increasing amounts of white matter and more ovoid sections (2) Lower cervical and lumbosacral regions have large ventral horns (3) Thoracic and early lumbar sections (T1 to L2) contain lateral grey matter horns

21
Q

Neonatal intraventricular hemorrhage (IVH): (1) location in which it usually occurs (2) risk factors (3) common complication of what

A

(1) Fragile germinal matrix and (2) increases in frequency with decreasing age and birth weight (3) common complication of prematurity that can lead to long-term neurodevelopment impairment

22
Q

Chemoreceptor trigger zone (CTZ): (1) location (2) effects in clinical setting

A

(1) Lies in area postrema of the dorsal medulla near fourth ventricle (2) Acute nausea following administration of systemic chemotherapy

23
Q

Neurological deficits assoc. with Vitamin B12 deficiency

A

Subacute combined degeneration - “Combined” refers to degeneration of both ascending (dorsal columns) and descending (corticospinal tract) pathways. Loss of position and vibration sensation, ataxia, and spastic paresis are common manifestations

24
Q

Beta-endorphin: (1) what is it (2) from where is it derived (3) what other substances are also derived from same (4) what implications may this shared precursor have

A

(1) endogenous opioid peptide (2) derived from propiomelanocortin (POMC), polypeptide goes through enzymatic cleavage and modification to produce not only beta-endorphins, but also (3) ACTH and MSH (4) ACTH and beta-endorphins being from same precursor suggests close physiological relationship between stress axis and opioid system

25
Q

(1) Most likely dx: 29 yo Caucasian female complains of decreased vision and pain around her eye, aggravated by eye movement, & an intention tremor of her left arm (2) why

A

(1) Autoimmune disease - Multiple sclerosis: (2) optic neuritis & intention tremor (cerebellar dysfunction) commonly seen. Also, waxing and waning neuro deficits in a 20-30 year old patient suggestive of this disorder

26
Q

Lacunar infarcts: (1) definition (2) usually involve what parts of brain (3) most common cause

A

(1) small ischemic infarcts (< 15 mm in diameter) (2) basal ganglia, pons, internal capsule, or deep white matter of brain (3) hypertensive arteriolosclerosis of small, penetrating arterioles

27
Q

Dx: difficulty rising from chair, recently dx with lung cancer, hip girdle weakness, increase on repetitive nerve stimulation

A

Lambert-Eaton syndrome

28
Q

MS: (1) imaging finding (2) 4 histological changes seen acutely

A

(1) Plaques detected on brain MRI, which is necessary for definitive dx (2) Inside acute (active) plaques: 1. Demyelination with relative preservation of axons 2. Accumulation of lipid-laden macrophages (containing products of myelin breakdown) 3. Astrocytosis (prolifeation in response to injury) 4. Infiltration by lymphocytes and mononuclear cells

29
Q

Dx: social disinhibition, speech abnormalities, emotional flattening, pronounced atrophy of frontotemporal regions

A

Pick’s disease (rare cause of dementia)

30
Q

Pancoast tumors: (1) definition (2) 3 major clinical presentation(s)

A

(1) Tumors in superior sulcus (groover produced by subclavian artery), in apex of lung (2) a. Tumor invasion with subsequent compression of brachial plexus causes ipsilateral shoulder pain, atrophy of hand muscles, and absent reflexes. b. Involvement of cervical sympathetic ganglia leads to Horner’s syndrome. c. Compression of subclavian vessels results in upper extremity edema.

31
Q

Dx & Explain: contralateral hemianopia with macular sparing, contralateral paresthesias and numbness

A

PCA stroke; PCA supplies occipital/visual cortex, but often with macular sparing due to collateral circulation from MCA; Involvement of thalamus frequently results in contralateral paresthesias and numbness affecting face, trunk, and limbs.