Exam IV-Neuro Flashcards

1
Q

CNS vs PNS

A

Central nervous system:
-brain and spinal cord
-contain most of the densely packed neuronal soma (nuclei)

Peripheral nervous system:
-everything else (spinal nerves, cranial nerves, ANS, SNS)
-some densely packed cell bodies (ganglia)

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2
Q

SNS vs ANS

A

Somatic nervous system: voluntary movement (sensory/afferent, motor/efferent)

Autonomic nervous system: internal regulation–involuntary. Sympathetic/parasympathetic response

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3
Q

Describe the structure and function of an axon

A

-Axons carry efferent nerve impulses
Structure:
-Axon hillock: attaches to soma, nerve impulses begin here
-Myelin: lipid segments that insulate axon
-Nodes of Ranvier: spaces in between myelin that speed up transmission
-Telodendria: attaches to dendrite/allows from impulse transmission

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4
Q

Where is myelin produced in the CNS vs PNS?

A

CNS: oligodendrocytes
PNS: Schwann cells

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5
Q

Oligodendrocytes location and function

A

In CNS, myelination

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6
Q

Astrocytes location and function

A

In CNS, regulate ICF ion contents

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7
Q

Microglia location, function

A

In CNS, phagocytize debris–immune function

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8
Q

Schwann cells function, location

A

In PNS, myelination

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9
Q

Satellite cells location, function

A

In PNS: separate nervous cells from supporting tissue, structural support

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10
Q

Motor/efferent neurons are cells in the ____ and that allow us to:

A

-CNS
-move, speak, swallow, breath–they send commands from the brain to the body

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11
Q

The (CNS/PNS) has some capability for axonal regeneration.

A

PNS

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12
Q

Name the cranial nerves and how you’d test them

A
  1. olfactory–smell test
  2. optic–Snellan chart
  3. oculomotor–PERRLA w/ pen light
  4. trochlear–move eyes down, laterally
  5. trigeminal–touch face
  6. abducens–move eyes diagonally, laterally
  7. facial–frown, smile, puff cheeks, taste
  8. vestibulocochlear–assess gait, hearing
  9. glossopharyngeal–say AHHH
  10. vagus–gag/swallow
  11. spinal–shrug shoulders/turn head
  12. hypoglossal–stick out tongue
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13
Q

A __________ is an area on your
body that relies on a specific
cranial nerve.

A

dermatome

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14
Q

Compare and contrast types of stroke/ brain infarctions, give or hold thrombolytics?

A

Ischemic: atherosclerosis, blood clot –> blood flow to brain blocked (give thrombolytic therapy)

Hemorrhagic: artery ruptures in brain –> brain bleed (exacerbated by thrombolytic therapy)

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15
Q

Pathophysiology of seizures (how they occur, how it leads to brain damage)

A

-How: metabolic/congenital issue, infection, trauma, tumor, etc. –> disruption in brain electricity –> rapid cortical neuron depolarization/AP release

-Damage is possible b/c it is highly consumed but rapidly depleted in the brain, leading to a buildup of lactic acid and glucose

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16
Q

Pathophysiology and clinical manifestations of dementia, 4 main types

A

Dementia = nerve cell degeneration (from brain trauma/compression/infection, inflammation, cerebral vessel atherosclerosis, genetics)

Symptoms r/t specific disease–Alzheimer’s, vascular, Lewy-body, frontotemporal

17
Q

Pathophysiology + clinical manifestations of Alzheimer’s disease

A

P: neurofibrillary tangles & amyloid plaques in brain –> synapse/neuron loss –> brain atrophy

S/S: memory loss, d/o to time/place, confusion, attention issues, eventual decline in cognition/abstraction/judgement

18
Q

Pathophysiology and clinical manifestations of Huntington’s disease (CAB)

A

P: rare autosomal dominant disorder –> GABA depletion –> severe degeneration of Basal ganglia and cerebral cortex

S/S: Hyperkinetic movements (CAB–Chorea, Athetosis, Ballism), some working memory loss, depression/anxiety

19
Q

Pathophysiology and clinical manifestations of Parkinson’s disease

A

P: idiopathically low levels of dopamine –> basal ganglia degeneration

S/S: Parkinsonian (resting) tremor, rigidity, bradykinesia, shuffling movement, dementia

20
Q

Pathophysiology and clinical manifestations of ALS

A

P: unknown etiology–degeneration of upper/lower motor neurons

S/S: muscle weakness –> muscle atrophy, spasticity/hyporeflexia –> respiratory failure/death

21
Q

Pathophysiology and clinical manifestations of MS

A

P: acquired autoimmune (IgG) lymphocyte destruction of CNS myelin –> CNS myelin loss,
S/S: progressive paresthesia, fatigue, weakness, visual issues, impaired gait, incontinence

22
Q

Pathophysiology and clinical manifestations of myasthenia gravis

A

P: acquired autoimmune–IgG antibodies attack Ach receptors (affects PNS and CNS)

S/S: weakness/fatigue of eyes and throat, difficult chewing/talking/swallowing. Low Ach –> botulism

23
Q

Risk factors for and clinical manifestations of CVA

A

Risks: age, sex, race, family history, hyperlipidemia, Afib, HTN, smoking, Diabetes, carotid stenosis, sickle cell anemia, alcohol use

S/S:
Ischemia/hemorrhage –>
F–facial weakness
A–arm weakness, ataxia (“drunk”)
S–speech slurred (aphasia, dysarthria)
T–time to call 911

24
Q

Clinical manifestations of Traumatic Brain Injury (TBI)–mild, moderate, and severe

A

Mild: initial confusion, LOC < 30 minutes, GCS 13-15, headache, N/V, trouble sleeping/concentrating for a few days

Moderate: LOC > 6 hrs, GCS 9-12, some decerebration/decortication, confusion, post-traumatic amnesia, permanent cognitive/mood changes

Severe: LOC > 6 hrs, GCS 3-8, signs of BS injury (pupillary, cardiac, respiratory), decerebration/decortication, profound neurologic deficit (or death/brain death)

25
Q
  • Pathophysiology and clinical manifestations of neural tube defects
A

-during 1st month of development
-supplement w/ 400 mcgs of folic acid/day
Spina bifida/ myelomeningocele:
-occulta: vertebrae missing,

26
Q
  • Pathophysiology of encephalopathy (Cerebral Palsy)
A
27
Q
  • Pathophysiology and clinical manifestations of retinoblastoma
A
28
Q
  • Congenital hydrocephalus
A
29
Q

Spinal cord injury pathophysiology, clinical manifestations

A

P: primary injury (instant mechanical trauma) vs secondary (hemorrhage, inflamm, edema, ischemia)

S/S:
-spinal shock (temporary, complete loss of function below injury)
If injury is above T6:
-neurogenic shock (parasympathetic takeover–hypotension, bradycardia)
-autonomic hyperreflexia (sympathetic takeover–headache, blurred vision, sweating, flushing, congestion, nausea, goosebumps, bradycardia)