NR 507 FINAL EXAM Questions with Verified Answers (Correct
Update)
Question 1: body's process for adapting to high hormone level
Answer: To adapt to high levels of hormones, some cells have the capacity to decrease the number of
receptors for that hormone through the process of down-regulation.
Question 2: Cushing's Syndrome
Answer: excessive ACTH (Adrenocorticotropic hormone) production most commonly caused by an
adrenal adenoma or a non-pituitary adenoma as is often seen with lung cancer. Clinical signs and
symptoms: weight gain and hyperpigmentation of skin.
Question 3: Lab results that point to PRIMARY hypothyroidism
Answer: Low levels of thyroid hormone (T3 and T4) and high levels of thyroid-stimulating hormone
(TSH), most commonly caused by autoimmune thyroiditis.
Question 4: Common causes of hypoparathyroidism
Answer: parathyroid gland injury or removal
Question 5: pathophysiology of thyroid storm
Answer: High levels of thyroid hormone in conjunction with high levels of stress hormones lead to
fever, tachycardia, and eventually high-output heart failure if the condition is not treated.
Question 6: signs of thyrotoxicosis
Answer: Weight loss and enlarged thyroid gland are common signs of hyperthyroidism in
thyrotoxicosis.
Question 7: diet and the prevention of prostate cancer
Answer: some evidence suggests a low fat diet, low dairy intake and increased fruit and veggie intake
prevents prostate cancer
Question 8: Impact of Benign Prostatic Hypertrophy (BPH) on the urinary system
Answer: enlarged prostate can block urine flow through the urethra. Can cause urinary retention, which
can lead to UTI, kidney infections.
Page 1
,Question 9: Dermatomes
Answer: an area of skin in which sensory nerves derive from a single spinal nerve root. Each spinal
nerve and their many processes are distributed to a specific area of the body. Specific areas of cutaneous
(skin) innervation at these spinal cord segments are called dermatomes. The dermatomes of various
spinal nerves are distributed in a fairly regular pattern, although adjacent regions between dermatomes
can be innervated by more than one spinal nerve.
Question 10: substance release at the synapse
Answer: neurons form points of contact with other neurons through synapse. Impulses transmitted
through electric and chemical conduction. Vesicles containing neurotransmitters release their contents
into the synaptic cleft and neurotransmitters diffuse across the cleft and bind to specific receptors on
postsynaptic neuron and trigger an action potential. Common neurotransmitters include norepinephrine,
acetylcholine, dopamine, histamine, serotonin, glycine, endorphins.
Question 11: 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).
Question 12: 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
areasensory speech area; responsible for reception and interpretation of speech, can result in receptive
aphasia or dysphasia when damaged.
Page 2
, Question 13: 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.
Question 14: 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.
Question 15: 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 produces neck pain and increased rigidity
Page 3
Update)
Question 1: body's process for adapting to high hormone level
Answer: To adapt to high levels of hormones, some cells have the capacity to decrease the number of
receptors for that hormone through the process of down-regulation.
Question 2: Cushing's Syndrome
Answer: excessive ACTH (Adrenocorticotropic hormone) production most commonly caused by an
adrenal adenoma or a non-pituitary adenoma as is often seen with lung cancer. Clinical signs and
symptoms: weight gain and hyperpigmentation of skin.
Question 3: Lab results that point to PRIMARY hypothyroidism
Answer: Low levels of thyroid hormone (T3 and T4) and high levels of thyroid-stimulating hormone
(TSH), most commonly caused by autoimmune thyroiditis.
Question 4: Common causes of hypoparathyroidism
Answer: parathyroid gland injury or removal
Question 5: pathophysiology of thyroid storm
Answer: High levels of thyroid hormone in conjunction with high levels of stress hormones lead to
fever, tachycardia, and eventually high-output heart failure if the condition is not treated.
Question 6: signs of thyrotoxicosis
Answer: Weight loss and enlarged thyroid gland are common signs of hyperthyroidism in
thyrotoxicosis.
Question 7: diet and the prevention of prostate cancer
Answer: some evidence suggests a low fat diet, low dairy intake and increased fruit and veggie intake
prevents prostate cancer
Question 8: Impact of Benign Prostatic Hypertrophy (BPH) on the urinary system
Answer: enlarged prostate can block urine flow through the urethra. Can cause urinary retention, which
can lead to UTI, kidney infections.
Page 1
,Question 9: Dermatomes
Answer: an area of skin in which sensory nerves derive from a single spinal nerve root. Each spinal
nerve and their many processes are distributed to a specific area of the body. Specific areas of cutaneous
(skin) innervation at these spinal cord segments are called dermatomes. The dermatomes of various
spinal nerves are distributed in a fairly regular pattern, although adjacent regions between dermatomes
can be innervated by more than one spinal nerve.
Question 10: substance release at the synapse
Answer: neurons form points of contact with other neurons through synapse. Impulses transmitted
through electric and chemical conduction. Vesicles containing neurotransmitters release their contents
into the synaptic cleft and neurotransmitters diffuse across the cleft and bind to specific receptors on
postsynaptic neuron and trigger an action potential. Common neurotransmitters include norepinephrine,
acetylcholine, dopamine, histamine, serotonin, glycine, endorphins.
Question 11: 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).
Question 12: 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
areasensory speech area; responsible for reception and interpretation of speech, can result in receptive
aphasia or dysphasia when damaged.
Page 2
, Question 13: 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.
Question 14: 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.
Question 15: 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 produces neck pain and increased rigidity
Page 3
