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Neuro Flashcards

0
Q

Hypothalamic nuclei

  • Lateral vs. Ventral
  • Anterior vs. Posterior
  • SCN
A

Lateral (hunger) vs. Ventral (satiety)

Anterior (cooling “A/C” - parasymp) vs Posterior (heating- sympathetic)
SCN = circadian rhythm

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1
Q

Thalamic nuclei:
VPL, VPM
LGN, MGN
VL

A

VPL - STT (pain & temp) & dorsal column/medial lemniscus (touch, etc)
VPM - Facial sensation & taste (trigeminal, gustatory tracts)

LGN = "Light"/vision; MGN = "Music"/hearing
VL = motor (from basal ganglia to motor cortex)
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2
Q

Limbic systems structures

A

= hippocampus, amygdala, fornix, mammillary bodies, cingulate gyrus

for the “5 Fs” (Feeding, Fleeing, Fighting, Feeling, & Fornication/Sex)

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3
Q

Direct pathway in basal ganglia

A

disinhibits thalamus => STIMULATES mvmt
striatum (D1 from SNc) –l Globus Pallidus interna
=> thalamus free to transmit signal

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4
Q

INdirect pathway in basal ganglia

A

INhibits motion by inhibiting thalamus, using GABA.

striatum (D2 from SN) –l GPe => STN not inhibited -> GPi –l thalamus

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5
Q

Function of therapeutic hypOventilation

A

decrease ICP (brain pressure/edema) by decreasing cerebral perfusion

  • bc blood flow = controlled by PCO2 level
    (ie: in case of stroke or trauma)
  • Hypoxemia only influences cerebral perfusion when PO2 > 50 mmHg!
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6
Q

Brown-Sequard Syndrome

A

= hemisection of spinal cord, so mixed sensory, motor & pain Sxs
- IPsilateral: AT level of lesion - LMN & all sensation lost; below - UMN & touch/vibration/proprioception lost
- Contralateral: below lesion - pain & temp sensation lost
AND Horner’s S. if lesion above T1!

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7
Q

Horner’s syndrome

Sxs, scenario

A

Sxs: Ptosis, Miosis, Anhydrosis (all controlled by descending sympathetics from superior cervical ganglion, via IML in spinal cord)
When: lesion to spinal cord above T1

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8
Q

CNs that innervate the eye muscles

A 
CN III (occulomotor) = SR, IR, MR, IO --> "down & out" if damaged
CN IV (trochlear) = SO
CN VI (abducens) = LR
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9
Q

Uvula, tongue & jaw deviations w/ CN damage…

A
  1. Uvula deviates AWAY from lesion (CN X)
  2. Tongue deviates TOWARD lesion (CN XII)
  3. Jaw deviates TOWARD lesion (CN V)
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10
Q

muscles that move the jaw

A

Open: Lateral Pterygoid (only, “Lateral Lowers”)
Close: Medial pterygoid, Masseter, teMporalis

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11
Q

Glaucoma:

Acute angle closure vs. chronic/open

A

= optic neuropathy w/ increased IOP
Acute angle closure: painful! sudden vision loss, HARD eyeball, headache do NOT give epinephrine!!

Chronic/open: gradual, not painful

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12
Q

Case:
Infant born w/ port wine stains in V1 distribution, hemiparesis, and mental retardation…
What other risks should be checked for?

A

= Sturge Weber syndrome (sporadic)

Risks: ipsilateral leptomeningeal angiomas, pheochromocytomas, Glaucoma, and seizures.

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13
Q

Case:
Child with mental retardation, ash leaf spots, and cutaneous angiofibromas (“adenoma sebaceum”).
What other risks should be expected?

A 
= Tuberous Sclerosis (AD)
Other risks: 
- Hamartomas in CNS & skin, seizures
- mitral regurgitation & cardiac rhabdomyoma
- renal angiomyolipomas.
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14
Q

Case:

Infant born with cafe-au-lait spots. Look for what other problems?

A

= NF1, NeuroFibromatosis/”vonRecklinghausen’s disease” (AD)
Mut: NF1 gene on chrom. 17
Other risks: Lisch nodules (iris hamartomas), neurofibromas in skin (from neural crest tissue), optic gliomas, pheochromocytomas

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15
Q

Case:

Infant born w/ cavernous hemagiomas on skin. Has family Hx of neuro disorder(s).

A

= von Hippel-Lindau disease (AD), VHL mut on chrom. 3
Other problems:
- hemangioblastomas in retina, brainstem, or cerebellum
- pheochromocytomas
- bilat. renal cell carcinoma

16
Q

Case:
Young boy can’t keep up with classmates when playing. To stand up from the ground he “climbs” himself up with his arms. Muscle hypertrophy apparent in both legs.

A

Duchenne Muscular Dystrophy, X-linked recessive
= deleted dystrophin gene (muscle structural protein)
=> proximal muscle weakness (“Gower’s sign” to stand)
Histo: necrotic muscle tissue

17
Q

Case:
Young child with kyphoscoliosis, dysarthria, and ataxia.
What neural pathways are affected? What other risks?

A

= Freidrich’s ataxia (AR) trinucl. repeat in Frataxin gene
(mitochondrial impairment –> excess free radicals)
=> degeneration of spinocerebral tract, dorsal column & DRG.
Risks: hypertrophic cardiomyopathy, DM, foot deformities.

18
Q

Neural crest derivatives

A
  1. PNS
  2. Ganglion cells (of ANS & CNs)
  3. Pia mater & arachnoid (“leptomeninges”)
  4. Melanocytes
  5. Chromaffin cells (adrenal medulla)
  6. Parafollicular cells (make calcitonin)
  7. Bone & CT of pharyngeal arches
19
Q

Alar plate vs. basal plate

A

(Embryological components of spinal cord)
Alar => sensory neurons
Basal => motor neurons

20
Q

Spinal cord level for ankle jerk reflex

A

S1 (gastrocnemius m.)

21
Q

Spinal cord level for knee jerk reflex

A

L2 - L4 (quadriceps m.)

22
Q

Spinal cord level for biceps jerk reflex AND forearm jerk reflex

A

C5, C6

23
Q

Spinal cord level for triceps jerk reflex

A

C7, C8

24
Q

Cranial nerves with Parasympathetic fibers (4)

A

III - ciliary ganglion of occult motor n.
VII - pterygopalatine & submandibular ganglia of facial n.
IX - otic ganglion of glossopharyngeal n.
X - terminal/intramural ganglion of vagus n.

25
Q

Spinal cord levels w/ sympathetic ganglia

A

T1 - L3,

Superior cervical ganglion for head-C8

26
Q

Succinylcholine:

  • pattern of f(x)
  • SEs/Complications
A

= ACh R antagonist => muscle relaxant (ie: for intubation)
2 parts to f(x):
1. phase I = prolonged depolarization, No antidote. *constant train of 4
2. phase II = desensitized ACh Rs, CAN reverse w/ neostigmine
*fading train of 4
SEs: hyperK+, hyperCa2+, malignant hyperthermia

27
Q

Antidote to organophosphate poisoning

A

Atropine AND pralidoxime (regenerates active AChE)
Sxs of organophosphate poisoning:
DUMBELSS (or SLUD) bc organophosphates irreversibly –l AChE!

28
Q

General function of each of the 3 types of Parasympathetic Rs
(muscarinic - M1, M2, M3)

A

M1: gastric & CNS
M2: heart
M3: smooth muscle (peristalsis, bronchoconstriction, vascular endothelial release of NO)

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