Exam IV-Neuro Flashcards
CNS vs PNS
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)
SNS vs ANS
Somatic nervous system: voluntary movement (sensory/afferent, motor/efferent)
Autonomic nervous system: internal regulation–involuntary. Sympathetic/parasympathetic response
Describe the structure and function of an axon
-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
Where is myelin produced in the CNS vs PNS?
CNS: oligodendrocytes
PNS: Schwann cells
Oligodendrocytes location and function
In CNS, myelination
Astrocytes location and function
In CNS, regulate ICF ion contents
Microglia location, function
In CNS, phagocytize debris–immune function
Schwann cells function, location
In PNS, myelination
Satellite cells location, function
In PNS: separate nervous cells from supporting tissue, structural support
Motor/efferent neurons are cells in the ____ and that allow us to:
-CNS
-move, speak, swallow, breath–they send commands from the brain to the body
The (CNS/PNS) has some capability for axonal regeneration.
PNS
Name the cranial nerves and how you’d test them
- olfactory–smell test
- optic–Snellan chart
- oculomotor–PERRLA w/ pen light
- trochlear–move eyes down, laterally
- trigeminal–touch face
- abducens–move eyes diagonally, laterally
- facial–frown, smile, puff cheeks, taste
- vestibulocochlear–assess gait, hearing
- glossopharyngeal–say AHHH
- vagus–gag/swallow
- spinal–shrug shoulders/turn head
- hypoglossal–stick out tongue
A __________ is an area on your
body that relies on a specific
cranial nerve.
dermatome
Compare and contrast types of stroke/ brain infarctions, give or hold thrombolytics?
Ischemic: atherosclerosis, blood clot –> blood flow to brain blocked (give thrombolytic therapy)
Hemorrhagic: artery ruptures in brain –> brain bleed (exacerbated by thrombolytic therapy)
Pathophysiology of seizures (how they occur, how it leads to brain damage)
-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
Pathophysiology and clinical manifestations of dementia, 4 main types
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
Pathophysiology + clinical manifestations of Alzheimer’s disease
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
Pathophysiology and clinical manifestations of Huntington’s disease (CAB)
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
Pathophysiology and clinical manifestations of Parkinson’s disease
P: idiopathically low levels of dopamine –> basal ganglia degeneration
S/S: Parkinsonian (resting) tremor, rigidity, bradykinesia, shuffling movement, dementia
Pathophysiology and clinical manifestations of ALS
P: unknown etiology–degeneration of upper/lower motor neurons
S/S: muscle weakness –> muscle atrophy, spasticity/hyporeflexia –> respiratory failure/death
Pathophysiology and clinical manifestations of MS
P: acquired autoimmune (IgG) lymphocyte destruction of CNS myelin –> CNS myelin loss,
S/S: progressive paresthesia, fatigue, weakness, visual issues, impaired gait, incontinence
Pathophysiology and clinical manifestations of myasthenia gravis
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
Risk factors for and clinical manifestations of CVA
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
Clinical manifestations of Traumatic Brain Injury (TBI)–mild, moderate, and severe
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)
- Pathophysiology and clinical manifestations of neural tube defects
-during 1st month of development
-supplement w/ 400 mcgs of folic acid/day
Spina bifida/ myelomeningocele:
-occulta: vertebrae missing,
- Pathophysiology of encephalopathy (Cerebral Palsy)
- Pathophysiology and clinical manifestations of retinoblastoma
- Congenital hydrocephalus
Spinal cord injury pathophysiology, clinical manifestations
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)
