NR 507 FINAL Study Guide Questions with
100% Verified Correct Answers
body's process for adapting to high hormone level
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.
Cushing's Syndrome
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.
Lab results that point to PRIMARY hypothyroidism
Low levels of thyroid hormone (T3 and T4) and high levels of thyroid-stimulating hormone
(TSH), most commonly caused by autoimmune thyroiditis.
Common causes of hypoparathyroidism
parathyroid gland injury or removal
pathophysiology of thyroid storm
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.
signs of thyrotoxicosis
Weight loss and enlarged thyroid gland are common signs of hyperthyroidism in
thyrotoxicosis.
diet and the prevention of prostate cancer
,some evidence suggests a low fat diet, low dairy intake and increased fruit and veggie intake
prevents prostate cancer
Impact of Benign Prostatic Hypertrophy (BPH) on the urinary system
enlarged prostate can block urine flow through the urethra. Can cause urinary retention,
which can lead to UTI, kidney infections.
Dermatomes
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.
substance release at the synapse
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.
Spondylolysis
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
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
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
100% Verified Correct Answers
body's process for adapting to high hormone level
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.
Cushing's Syndrome
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.
Lab results that point to PRIMARY hypothyroidism
Low levels of thyroid hormone (T3 and T4) and high levels of thyroid-stimulating hormone
(TSH), most commonly caused by autoimmune thyroiditis.
Common causes of hypoparathyroidism
parathyroid gland injury or removal
pathophysiology of thyroid storm
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.
signs of thyrotoxicosis
Weight loss and enlarged thyroid gland are common signs of hyperthyroidism in
thyrotoxicosis.
diet and the prevention of prostate cancer
,some evidence suggests a low fat diet, low dairy intake and increased fruit and veggie intake
prevents prostate cancer
Impact of Benign Prostatic Hypertrophy (BPH) on the urinary system
enlarged prostate can block urine flow through the urethra. Can cause urinary retention,
which can lead to UTI, kidney infections.
Dermatomes
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.
substance release at the synapse
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.
Spondylolysis
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
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
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
