NR 507 FINAL EXAM QUESTIONS AND
ANSWERS
Spondylolysis - Answer-Structural defect (degeneration, fracture, or developmental
defect) in the pars interarticularis of the vertebral arch (the joining of the vertebral body
to the posterior structures). Most affected at L5 of lumbar spine. Mechanical pressure
often causes anterior displacement of the deficient vertebra (spondylolisthesis). Often
hereditary; associated with increased incidence of other congenital spine defects.
Microfractures occur at site, symptoms include lower back pain and lower limb pain.
Cervical spondylolysis is hypertrophy and disc degeneration with narrowing of cervical
spine at c5-c6 and c6-c7. Signs/symptoms include neck or occipital pain, pain in
shoulder, scapula, or arms. Sensory symptoms of numbness or tingling follow a
dermatomal pattern; weakness follows the pattern of innervation of the affected nerve
root. Occipital or suboccipital headache is another symptom. Can also cause difficulty
walking, altered sensation in feet, and sphincter disturbances (late sign).
location of the motor and sensory areas of the brain - Answer-frontal lobe-goal oriented
behavior, short term memory, elaboration of thought, and inhibition on the limbic
(emotional) areas of CNS
premotor area-programming motor movements
primary motor area in frontal lobe- forms primary voluntary motor area- electrical
stimulation of specific areas of this cortex causes specific muscles to move. Contains
corticobulbar tract that synapses in brainstems and provides voluntary control of neck
and head muscles. Corticospinal tracts descend into spinal cord and control muscles in
the body. Cerebral impulses control function on opposite sides of body-contralateral
control.
Broca area- inferior frontal lobe; is for speech and language processing. Expressive
aphasia or dysphasia occurs when area is damaged.
Parietal lobe- major area for somatic sensory input, located along the postcentral gyrus,
which is adjacent to the primary motor area in the precentral gyrus. Communication
between the two areas is through association fibers. Involved in sensory association.
Occipital lobe- behind parietal lobe and above cerebellum. Primary visual cortex,
receives input from retinas
Temporal lobe- primary auditory cortex, also in memory consolidation and smell.
Wenicke area-sensory speech area; responsible for reception and interpretation of
speech, can result in receptive aphasia or dysphasia when damaged.
pathophysiology of cerebral infarction and excitotoxins - Answer-occurs when area of
brain loses blood flow due to vascular occlusion. Ex-emboli or thrombi, gradual vessel
occlusion (atheroma), and stenosed vessels. Strokes are often cause of infarction
related to occlusions or hemorrhages, disrupting blood flow to parts of the brain.
Cerebral thrombi and cerebral emboli most often produce occlusions, but
atherosclerosis and hypotension are underlying process.
,Can be either ischemic or hemorrhagic in nature. Ischemic causes affected area to
become pale and soft within 6-12 hours after occlusion. Necrosis, swelling and mushy
degeneration after 48 to 72 hours. Then area is infiltrated with macrophages and
phagocytosis of necrotic tissue, leaving a cavity behind.
If occlusion of cerebral artery occurs, there is some vascular remodeling to maintain
some blood flow.
Hemorrhagic infarcts are bleeding into infarcted area through leaking vessels when
embolic fragments resolve, and reperfusion begins to occur. Can be exacerbated by
thrombotic therapy.
Excitotoxins- Ischemia damages the brain by triggering a cascade of biochemical
events that lead to neuronal and glial dysfunction and cell death. One major segment of
this cascade involves release of excitatory neurotransmitter amino acid, glutamate,
which can over excite and kill neurons in the vicinity.
agnosia - Answer-failure to recognize form and nature of objects. Can be visual, tactile,
or auditory. Example-person may not be able to identify a safety pin by touching it with a
hand but can name it when looking at it. Produced by dysfunction in the primary sensory
area or interpretive areas of cerebral cortex (temporo-occipital area). Most often occurs
with Cerebrovascular accidents but can occur with pathologic processes that injures
specific areas: parietal lobe, temporo-occipital area, inferior occipital cortex in left
hemisphere, right parietal lobe, left parietotemporal region, superior temporal area, right
superior temporal area.
accumulation of blood in a subarachnoid hemorrhage - Answer-the escape of blood
from a defective or injured vasculature into subarachnoid space (bleeding into the space
between the brain and tissue covering brain). At risk people are intracranial aneurysm,
intracranial arteriovenous malformation, hypertension, family history of SAH, and those
with head injuries. Can reoccur, especially from a ruptured intracranial aneurysm. Also,
heavy alcohol use, tobacco use, anticoagulation use, and contraceptive use can cause
SAH. Mortality is about 50%, one third of survivors require dependent care.
Caused by blood into subarachnoid space and blood increases intracranial volume,
irritates the meningeal and other neural tissues, and causes an inflammatory reaction.
Also blood coats nerve roots, clogs arachnoid granulations (impairing CSF
reabsorption), and clogs foramina within ventricular system (impairing CSF circulation).
Intracranial pressure increases. Expanding hematoma acts like a space-occupying
lesion, compressing and displacing brain tissue with increased ICP, decreased cerebral
perfusion pressures, decreased cerebral blood flow, blood-brain barrier breakdown,
brain edema, inflammation, and cell death.
s/s severe headache, changes in mental status or level of consciousness, nausea or
vomiting, neuro deficits. Meningeal irritation and inflammation occur and cause neck
stiffness (nuchal rigidity), photophobia, blurred vision, irritability, restlessness, positive
Kernig sign and Brudzinski signs.
Kernig sign- straightening the knee with the hip and knee in a flexed position produces
pain in back and neck regions.
Brudzinski sign- passive flexion of the neck produces neck pain and increased rigidity
, most common cause of meningitis - Answer-an inflammation of the brain or spinal cord.
Can be caused by bacteria, viruses, fungi, parasites, or toxins.
Bacterial- infection of pia mater and arachnoid villi, the subarachnoid space, ventricular
system, and CSF. Affects about 5 to 10 per 100,000 people annually. Meningococcus
and pneumococcus are most common pathogens. Common in college campuses,
military bases, young children or adolescents. Kissing disease. Most common type
Viral-aseptic meningitis- limited to meninges and an identifiable bacterium or specific
pathogen cannot be found in CSF. Most at risk populations and times of year are
dependent on the virus and immune system of patients.
Fungal- chronic condition and is much less common than bacterial or viral. Common
types: histoplasmosis, cryptococcosis, coccidioidomycosis, mucormycosis, candidiasis,
and aspergillosis.
Tubercular-common and serious form of CNS tuberculosis, common in
immunocompromised patients. Caused by mycobacteria.
conditions that result in pure water deficit (hypertonic volume depletion) - Answer-a
result of pure water losses, hyperventilation, arid climates and an increase in renal
clearance
osmoreceptors that stimulate thirst and the release of ADH - Answer-Increased
osmolality stimulates hypothalamic osmoreceptors causing thirst and signals the
posterior pituitary to release ADH
causes of hypernatremia - Answer-Caused by an acute increase sodium level or loss of
water
Hypovolemic hypernatremia: loss of body sodium accompanied by a relatively greater
loss of body water
Causes: loop diuretics, osmotic diuresis, GI losses and kidneys failing to concentrate
urine
Hypervolemic hypernatremia: increase in total body water and greater increase in total
body sodium
Causes: hypertonic saline solutions, over secretion of ACTH, near salt water drowning
Euvolemic: (most common) loss of free water with near normal total body sodium
Causes: inadequate water intake, excessive sweating, fever with hyperventilation and
water loss from lungs, burns, nausea/vomiting and Diabetes Insipidus
effects of increased aldosterone - Answer-Myocardial changes associated with heart
failure, increased sodium and water reabsorption by nephron collecting duct
dependent edema - Answer-Fluid accumulates in gravity-dependent areas. May appear
in feet and legs when standing and when pressing with fingers a pit will remain after you
remove your fingers.
definition of isotonic - Answer-Solution or fluid having same osmotic pressure as the
other solution or fluid
ANSWERS
Spondylolysis - Answer-Structural defect (degeneration, fracture, or developmental
defect) in the pars interarticularis of the vertebral arch (the joining of the vertebral body
to the posterior structures). Most affected at L5 of lumbar spine. Mechanical pressure
often causes anterior displacement of the deficient vertebra (spondylolisthesis). Often
hereditary; associated with increased incidence of other congenital spine defects.
Microfractures occur at site, symptoms include lower back pain and lower limb pain.
Cervical spondylolysis is hypertrophy and disc degeneration with narrowing of cervical
spine at c5-c6 and c6-c7. Signs/symptoms include neck or occipital pain, pain in
shoulder, scapula, or arms. Sensory symptoms of numbness or tingling follow a
dermatomal pattern; weakness follows the pattern of innervation of the affected nerve
root. Occipital or suboccipital headache is another symptom. Can also cause difficulty
walking, altered sensation in feet, and sphincter disturbances (late sign).
location of the motor and sensory areas of the brain - Answer-frontal lobe-goal oriented
behavior, short term memory, elaboration of thought, and inhibition on the limbic
(emotional) areas of CNS
premotor area-programming motor movements
primary motor area in frontal lobe- forms primary voluntary motor area- electrical
stimulation of specific areas of this cortex causes specific muscles to move. Contains
corticobulbar tract that synapses in brainstems and provides voluntary control of neck
and head muscles. Corticospinal tracts descend into spinal cord and control muscles in
the body. Cerebral impulses control function on opposite sides of body-contralateral
control.
Broca area- inferior frontal lobe; is for speech and language processing. Expressive
aphasia or dysphasia occurs when area is damaged.
Parietal lobe- major area for somatic sensory input, located along the postcentral gyrus,
which is adjacent to the primary motor area in the precentral gyrus. Communication
between the two areas is through association fibers. Involved in sensory association.
Occipital lobe- behind parietal lobe and above cerebellum. Primary visual cortex,
receives input from retinas
Temporal lobe- primary auditory cortex, also in memory consolidation and smell.
Wenicke area-sensory speech area; responsible for reception and interpretation of
speech, can result in receptive aphasia or dysphasia when damaged.
pathophysiology of cerebral infarction and excitotoxins - Answer-occurs when area of
brain loses blood flow due to vascular occlusion. Ex-emboli or thrombi, gradual vessel
occlusion (atheroma), and stenosed vessels. Strokes are often cause of infarction
related to occlusions or hemorrhages, disrupting blood flow to parts of the brain.
Cerebral thrombi and cerebral emboli most often produce occlusions, but
atherosclerosis and hypotension are underlying process.
,Can be either ischemic or hemorrhagic in nature. Ischemic causes affected area to
become pale and soft within 6-12 hours after occlusion. Necrosis, swelling and mushy
degeneration after 48 to 72 hours. Then area is infiltrated with macrophages and
phagocytosis of necrotic tissue, leaving a cavity behind.
If occlusion of cerebral artery occurs, there is some vascular remodeling to maintain
some blood flow.
Hemorrhagic infarcts are bleeding into infarcted area through leaking vessels when
embolic fragments resolve, and reperfusion begins to occur. Can be exacerbated by
thrombotic therapy.
Excitotoxins- Ischemia damages the brain by triggering a cascade of biochemical
events that lead to neuronal and glial dysfunction and cell death. One major segment of
this cascade involves release of excitatory neurotransmitter amino acid, glutamate,
which can over excite and kill neurons in the vicinity.
agnosia - Answer-failure to recognize form and nature of objects. Can be visual, tactile,
or auditory. Example-person may not be able to identify a safety pin by touching it with a
hand but can name it when looking at it. Produced by dysfunction in the primary sensory
area or interpretive areas of cerebral cortex (temporo-occipital area). Most often occurs
with Cerebrovascular accidents but can occur with pathologic processes that injures
specific areas: parietal lobe, temporo-occipital area, inferior occipital cortex in left
hemisphere, right parietal lobe, left parietotemporal region, superior temporal area, right
superior temporal area.
accumulation of blood in a subarachnoid hemorrhage - Answer-the escape of blood
from a defective or injured vasculature into subarachnoid space (bleeding into the space
between the brain and tissue covering brain). At risk people are intracranial aneurysm,
intracranial arteriovenous malformation, hypertension, family history of SAH, and those
with head injuries. Can reoccur, especially from a ruptured intracranial aneurysm. Also,
heavy alcohol use, tobacco use, anticoagulation use, and contraceptive use can cause
SAH. Mortality is about 50%, one third of survivors require dependent care.
Caused by blood into subarachnoid space and blood increases intracranial volume,
irritates the meningeal and other neural tissues, and causes an inflammatory reaction.
Also blood coats nerve roots, clogs arachnoid granulations (impairing CSF
reabsorption), and clogs foramina within ventricular system (impairing CSF circulation).
Intracranial pressure increases. Expanding hematoma acts like a space-occupying
lesion, compressing and displacing brain tissue with increased ICP, decreased cerebral
perfusion pressures, decreased cerebral blood flow, blood-brain barrier breakdown,
brain edema, inflammation, and cell death.
s/s severe headache, changes in mental status or level of consciousness, nausea or
vomiting, neuro deficits. Meningeal irritation and inflammation occur and cause neck
stiffness (nuchal rigidity), photophobia, blurred vision, irritability, restlessness, positive
Kernig sign and Brudzinski signs.
Kernig sign- straightening the knee with the hip and knee in a flexed position produces
pain in back and neck regions.
Brudzinski sign- passive flexion of the neck produces neck pain and increased rigidity
, most common cause of meningitis - Answer-an inflammation of the brain or spinal cord.
Can be caused by bacteria, viruses, fungi, parasites, or toxins.
Bacterial- infection of pia mater and arachnoid villi, the subarachnoid space, ventricular
system, and CSF. Affects about 5 to 10 per 100,000 people annually. Meningococcus
and pneumococcus are most common pathogens. Common in college campuses,
military bases, young children or adolescents. Kissing disease. Most common type
Viral-aseptic meningitis- limited to meninges and an identifiable bacterium or specific
pathogen cannot be found in CSF. Most at risk populations and times of year are
dependent on the virus and immune system of patients.
Fungal- chronic condition and is much less common than bacterial or viral. Common
types: histoplasmosis, cryptococcosis, coccidioidomycosis, mucormycosis, candidiasis,
and aspergillosis.
Tubercular-common and serious form of CNS tuberculosis, common in
immunocompromised patients. Caused by mycobacteria.
conditions that result in pure water deficit (hypertonic volume depletion) - Answer-a
result of pure water losses, hyperventilation, arid climates and an increase in renal
clearance
osmoreceptors that stimulate thirst and the release of ADH - Answer-Increased
osmolality stimulates hypothalamic osmoreceptors causing thirst and signals the
posterior pituitary to release ADH
causes of hypernatremia - Answer-Caused by an acute increase sodium level or loss of
water
Hypovolemic hypernatremia: loss of body sodium accompanied by a relatively greater
loss of body water
Causes: loop diuretics, osmotic diuresis, GI losses and kidneys failing to concentrate
urine
Hypervolemic hypernatremia: increase in total body water and greater increase in total
body sodium
Causes: hypertonic saline solutions, over secretion of ACTH, near salt water drowning
Euvolemic: (most common) loss of free water with near normal total body sodium
Causes: inadequate water intake, excessive sweating, fever with hyperventilation and
water loss from lungs, burns, nausea/vomiting and Diabetes Insipidus
effects of increased aldosterone - Answer-Myocardial changes associated with heart
failure, increased sodium and water reabsorption by nephron collecting duct
dependent edema - Answer-Fluid accumulates in gravity-dependent areas. May appear
in feet and legs when standing and when pressing with fingers a pit will remain after you
remove your fingers.
definition of isotonic - Answer-Solution or fluid having same osmotic pressure as the
other solution or fluid