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A concise overview of key concepts related to the central nervous system, including its components, functions, and common disorders. It covers topics such as neuron structure, brain lobes, reflexes, intracranial pressure, and stroke. The material is presented in a question-and-answer format, making it useful for exam preparation and quick review. It is particularly relevant for students in nursing or related healthcare fields, offering a structured approach to understanding complex neurological concepts. Designed to facilitate efficient learning and retention of essential information about the nervous system, aiding students in mastering the subject matter.
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spinal nerves subdivided into somatic and autonomic nervous system"
receptors in the skin, muscles, and joints to the central nervous system"
information from the CNS to cells, tissues and organs."
fuel source: glucose"
Function: Area of the brain responsible for all voluntary activities of the body Sign of injury/lesion/disorder: movements that are slow and uncoordinated"
myelinated axons of the CNS"
Function: directs voluntary skeletal actions; responsible for communication, emotions, intellect, reasoning, judgment and behavior. Contains Broca's area: responsible for speech Sign of injury/lesion/disorder: Head and eye movement to one side. Complete or partial unresponsiveness or difficulty speaking. Explosive screams, including profanities, or laughter."
Function: interprets tactile sensation such as touch, pain, temperature, shapes and 2-point discrimination
Sign of injury/lesion/disorder:"
membrane that helps in separating it from cerebellum function: houses the ability to read with comprehension and is the primary visual receptor center Sign of injury/lesion/disorder: vision and perception problems"
the brain, and can be considered the "middle" region of each brain hemisphere. function: interprets impulses from the ear. contains Wernicke's area: auditory stimuli Sign of injury/lesion/disorder: Disturbance of auditory sensation and perception. Disturbance of selective attention of auditory and visual input. Disorders of visual perception. Impaired organisation and categorisation of verbal material. Disturbance of language comprehension. Impaired long-term memory."
system that arouses the body, mobilizing its energy in stressful situations"
nervous system that calms the body, conserving its energy"
increase the heart's rate and strength of contraction"
arteries of the skeletal muscles cause vasodilation, reduces total peripheral resistance, bronchodilation"
vasoCONSTRICTION -> increase BP contraction of smooth muscles glucose metabolism"
CM: lose consciousness quickly, develop apnea, reactive pupils that later dilate, decorticate posturing"
Simple partial with sensory symptoms Complex partial"
correctable cause can be found"
following an epileptic seizure"
Widening pulse pressure Bradycardia Increased Systolic Cushing's Triad"
vasoconstriction and external compression - patient may be asymptomatic"
intracranial vault, brain unable to compensate; CM: confusion, restlessness, lethargy, pupil and breathing changes, decreased LOC"
patient decompensates quickly. CM: decreased LOC, widening pulse pressure, bradycardia, pupils small and sluggish, CO accumulation causes vasodilation > decreased hydrostatic pressure, and increased blood volume"
ICP > no CPP > cellular hypoxia, cell death herniation occurs when the brain tissue moves from an area of high pressure to an area of low pressure"
injury that damages the brain
Complications: post-concussion syndrome, posttraumatic seizures, chronic traumatic encephalopathy"
structures that is a direct result of impact to the head. Focal-limited to one area (closed head trauma) Diffuse-shaking force which strains the brain"
includes abnormal processes such as cerebral edema, increased intracranial pressure, cerebral ischemia and hypoxia, and infection; onset is often delayed following the primary brain injury."
occur to the underlying vessels, dura sinus, brain and cranial nerves without harming the integrity of the skull May cause immediate loss of consciousness, loss of reflexes, transient loss of respiration, bradycardia and low BP"
mass or swelling. Leads to ischemia and tissue damage."
not usually associated with loss of function"
and autonomic function immediately after injury- resolves 7-20 days s/s: flaccid, bradycardia, hypotension, paralytic ileus"
defect containing meninges and cerebral spinal fluid. Does not involve the spinal cord and it is possible that the infant will not have any neurologic deficits"
syndrome as symptoms of abrupt cessation of heavy and prolonged use"
the increased permeability of the capillary endothelium of the brain after injury to the vascular structure"
the brain causing failure of the active transport systems"
the lateral ventricles when an increase in intravascular pressure causes an abnormal flow of fluid from the intraventricular CSF across the ependymal lining to the periventricular white matter"
then back in the other direction"
presence of renal stones within the renal pelvis and/or calyces"
Caucasian, diet, HTN, atherosclerosis, metabolic syndrome, obesity and DM Type 2"
excretion and therefore to calcium stone formation"
association is not clear."
oliguria"
the baseline or ≥ 0.3mg/dL increase in creatinine"
the baseline."
the baseline or an increase in serum creatinine to ≥ 4.0 mg/dL or the initiation of renal replacement therapy or in person less than 18 years old a decrease in eGFR to < 35ml/minute per 1.732"
in a decreased GFR. Anything which decreases renal perfusion can cause a pre-renal AKI"
medications or shock states. • Hypotension • Hypovolemia • Hemorrhage • Inadequate cardiac output i.e. heart failure • NSAIDS • Renal artery stenosis"
consistent with AKI include a FeNa of < 1% and a BUN:Creatinine ratio of > 20." "What is used to evaluate an acute kidney injury and to differentiate between a pre-renal and
creatinine, urine sodium and urine creatinine. It is reported as a percentage and is a marker of renal sodium excretion."
conserving sodium and is indicative of a pre-renal AKI"
wasting sodium and is consistent with an acute tubular necrosis."
differentiating between the two disease processes"
renal acute kidney injury (AKI)"
function at the cellular level in the kidney."
metabolic acidosis, hyperkalemia, sodium and water retention and elevated BUN/creatinine. Additional symptoms include moderate HTN, hyperphosphatemia, and anemia."
experience anemia, and have an increase in creatinine and urea. They will have mild HTN."
disease, increasing plasma creatinine and urea. They may have subtle hypertension."
asymptomatic"
will also experience severe HTN, anemia and hyperphosphatemia."
hemodialysis."
disease and Obstructive problems such as renal stones"
erythropoietin levels, Fluid and electrolyte imbalances"
Hyperkalemia Fluid volume deficit and Hyponatremia-during the early stages Fluid overload and hypernatremia- occur in late stages Hyperphosphatemia Hypocalcemia Metabolic Acidosis"
sodium and fluid wasting occurs secondary to lack of the kidney's ability to concentrate urine"
patient becomes oliguric. Sodium is not excreted and accumulates as does fluid."
phosphorus."
relationship to phosphorus. A decreased production of the active form of vitamin D (calcitriol). This is needed for the absorption of calcium in the gut."
reabsorb urinary bicarb (HCO3) or excrete H+"
calcium levels which are secondary to the hyperphosphatemia"
Remember PTH causes an increase in osteoclastic activity, which causes the breakdown of bone. Osteodystrophy is defective bone formation which leads to osteoporosis. The metabolic acidosis associated with CKD also contributes to the development of osteodystrophy"
secretion of erythropoietin from the kidney"
This results in more angiotensin II and vasoconstriction"
other uremic toxins. This usually will not be seen unless the BUN is > 100"
decreases insulin sensitivity and impairs glucose tolerance. As the kidney function decreases it is not able to clear adiponectin and leptin which can contribute to the insulin resistance. Also the failing kidney is not able to degrade insulin so insulin's half life is prolonged."
triglyceride levels, low HDLs and high LDLs"
conducts sensory impulses from mouth, nose, eyes; motor fibers for muscles of mastication. Control of jaw movements -Testing procedure: pain, touch, and temperature are tested with proper stimulus; corneal reflex tested with a wisp of cotton; person is asked to move jaw through full ranges of motion"
fibers to/from lateral rectus muscle. Lateral eye movements -Testing procedure: tested in conjunction with cranial nerve III relative to moving eye laterally"
sensory fibers to taste buds and anterior 2/3 tongue; motor fibers to muscles of facial expression and to salivary glands -Testing procedure: check symmetry of face, ask person to attempt various facial expressions; sweet, salty, sour, and bitter substances are applied to tongue to test tasting ability"
senses of hearing and balance; Foramen: internal auditory canal; Consequence of Loss: loss of hearing, loss of balance and equilibrium, nausea, vertigo, vomiting"
pharynx and salivary glands; sensory fibers for pharynx and posterior tongue. Taste sensation for sweet, bitter and sour -Testing procedure: gag and swallow reflexes are checked; posterior one third of tongue is tested for taste"
and pharynx; parasympathetic motor fibers supply smooth muscles of abdominal organs; sensory impulses from viscera -Testing procedure: tested in conjunction with cranial nerve IX"
sternocleidomastoid and trapezius; Foramen: foramen magnum, jugular foramen; Consequence of Loss: difficulty elevating scapula or rotating neck"
to/from tongue. Movement of tongue -Testing procedure: ask person to stick out tongue, positional abnormalities are noted"
functions include processing sensory input and coordinating movement output and balance Sign of injury/lesion/disorder: ataxia, which may affect the limbs, trunk, or even speech"
Astrocytes, oligodendroglia, microglia, ependymal cells"
responsible for the formation of myelin."
Monoamines: histamine, serotonin, dopamine, epinephrine, norepinephrine deficiency of dopamine leads to Parkinson Disease Amino Acids: glutamate, GABA, glycine"
deep structures of the cerebral hemispheres and the cervical spinal cord Contains: midbrain, pons, medulla oblongata and reticular formation. Ten of the 12 cranial nerves arise from the brain stem. Function: It contains the respiratory and vasomotor centers, which are responsible, respectively, for breathing and the maintenance of blood pressure. Signs if injury/lesion/disorder: coma, irregular breathing, insomnia, balance issues, slurred speech, etc."
alterations in arousal and sleep-wake transitions Extreme damage can cause coma"
brainstem; it directs messages to the sensory receiving areas in the cortex and transmits replies to the cerebellum and medulla"
eating, drinking, body temperature; helps govern the endocrine system via the pituitary gland, and is linked to emotion"
and hypothalamus) located below the cerebral hemispheres; associated with emotions and drives."
Function: speech comprehension, language development
hand will grasp. appears: Birth Disappears: 6 months"
causes the toes of the feet to "grasp" appears: Birth Disappears: 10 months"
right: Right arm/leg EXTEND Left arm/leg flex appears: 2 months
weight and size, fibrosis o meninges, widening sulci and narrowing gyri, increase in ventricles cellular: decrease in neurons, myellin, dendritic and synaptic processes, increased neuroinflammation, declines in melatonin, atrophy of the epithelial cells in the choroid plexus cerebrovascular: arteriosclerosis, increased permeability of the blood-brain barrier, decreased vascular density functional changes: decreased deep tendon reflexes, skeletal muscle atrophy, progressive decrease in taste and smell, decreased vibratory sense, decrease control of gai and posture, sleep disturbances and memory impairments"
brain. 20% of cardiac output altered by the concentration of CO2 and O CBF decreases when CO2 decreases and increases when the PaO2 < 50mmHg When PaO2 = 70-90 mmHg, CBF is maintained"
to the brain CPP = MAP - ICP Normal is 70-90 mmHg Low CPP caused by hypovolemia or hypotension > brain ischemia High CPP caused by hypertension > increased in hydrostatic pressure > fluid moves into the interstitium in the brain and > increased ICP > decreased CPP"
overcome to be perfused normal ICP = 5-15 mmHg increased ICP > decreased CPP and impaired cerebral perfusion"
and external compression - patient may be asymptomatic Stage 2: increasing amount of contents inside intracranial vault, brain unable to compensate; CM: confusion, restlessness, lethargy, pupil and breathing changes, decreased LOC Stage 3: ICP appraches arterial pressure - patient decompensates quickly. CM: decreased LOC, widening pulse pressure, bradycardia, pupils small and sluggish, CO2 accumulation causes vsodilation > decreased hydrostatic pressure and increased blood volume Stage 4: equalization of arterial pressure and ICP > no CPP > cellular hypoxia, cell death"
gyrus under the falx cerebri"
through an opening in the skull"
downward movement of the cerebellum through the foramen magnum CM: stiff neck, decreased LOC, respiratory abnormalities and pulse variations"
movement out of the vessels and into the interstitium and then into the cell. in the brain, they enter the neuron causing cerebral edema associated with CNS symptoms Hypernatremia is associated with a rapid decrease in intracellular water content and brain volume caused by an osmotic shift of free water out of the cells causing dehydrated neurons"
being able to understand language) Location of dysfunction: Broca's area of the frontal lobe"
being able to hear it and produce it) Location of dysfunction: Wernicke's area of the temporal lobe"
Broca's and Wernicke's areas affected."
which most often begin in the face and hands, tend to be clonic"
made of corticospinal and corticobulbar tracts impulses are generated in the brain and sent to control voluntary movements of purpose and skill. crossover at the junction between the spinal cord and brain defects in this tract will be contralateral to the brain. Upper motor neuron deficits manifest as spastic paralysis, hyperreflexia, and Babinski reflex i.e. Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease) lower motor neuron deficits manifest as flaccid paralysis, muscular atrophy, fasciculations, fibrillations or hyporeflexia. i.e. poliomyelitis"
made of rubrospinal tract, the reticulospinal tract, tectospinal tract, and vestibulospinal tract crosses over at the junction between the brain stem and spinal cord. deficits are manifested contralaterally responsible for gross motor movements, automatic motor movements, facial expression, posture, muscle tone, speech, and swallowing. CM: spastic increase in muscle tone, abnormal postures, involuntary movements, tremors, i.e. Parkinson's Disease"
cranial vault are open to the environment Affecting a specific area of the brain tissue, Focal/localized damage. Example: Skull fracture."
type of brain injury characterized by shearing, stretching, or tearing of nerve fibers with subsequent axonal damage."
Generally occurs in about 80% of persons with mild and moderate TBI"
body"
flexed upon the abdomen and the person is sitting or lying down"
knees to flex when the neck is flexed."
partially or completely severed"
for developing autonomic dysreflexia (T-6 or above) parasympathetic nervous system is unable to send signals below the area of injury. Above injury: flushing sweating and bradycardia below injury: pale and cool skin Other CM: SBP up to 300mmHg, HA, blurred vision and nausea"
anterior spinal artery occlusion, primary spinal cord tumors or metastatic CA CM: loss of pain and temperature sensation, motor weakness"
hyperextension injuries CM: loss of pain and temperature at level of lesion with other modalities preserved"
B12 deficiency, syphilis, multiple sclerosis, primary spinal cord tumors, metastatic CA CM: loss of fine touch, loss of vibratory sensation, loss of proprioception, motor weakness"
several hours before the headache (e.g. depression, irritability, craving for foods etc.) Aura Phase - 1 in 5 people have an aura phase with: visual ( can include hallucinations), skin ( pin prick or needles) or language (expressing thoughts) difficulties HA Phase - throbbing pain and can last from several hours to days; may have fatigue, N/V or dizziness Recovery: After the Storm -patient feels extreme tiredness, weakness and or confusion, irritability, may take days to resolve"
tube that results in incomplete development of the brain and bones of the skull; the most drastic neural tube defect usually results in a stillbirth"
area"
amino acid found in most proteins)"