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FINAL EXAM- NR507 / NR 507 Advanced Pathophysiology
Newest Guide Questions and Verified Answers- Chamberlain
1. 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.
2. Cushing's Syndrome : excessive ACTH (Adrenocorticotropic hormone) produc- tion
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.
3. 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.
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4. Common causes of hypoparathyroidism : parathyroid gland injury or removal
5. pathophysiology of thyroid storm : High levels of thyroid hormone in conjunc- tion
with high levels of stress hormones lead to fever, tachycardia, and eventually high-output
heart failure if the condition is not treated.
6. signs of thyrotoxicosis : Weight loss and enlarged thyroid gland are common signs of
hyperthyroidism in thyrotoxicosis.
7. 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
8. 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.
9. Dermatomes : an area of skin in which sensory nerves derive from a single spinal nerve
root.
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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.
10. substance release at the synapse : neurons form points of contact with oth- er
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, hist- amine,
serotonin, glycine, endorphins.
11. Spondylolysis : Structural defect (degeneration, fracture, or developmental de- fect) 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).
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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).
12. 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 con-
trol 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
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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. Commu- nication 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.
13. 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
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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 seg- ment of this cascade
involves release of excitatory neurotransmitter amino acid, glutamate, which can over excite
and kill neurons in the vicinity.
14. agnosia : 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 process- es 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.
15. accumulation of blood in a subarachnoid hemorrhage : 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
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injuries. Can reoccur, especially from a ruptured in- tracranial 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 re- action. Also blood coats
nerve roots, clogs arachnoid granulations (impairing CSF reabsorption), and clogs foramina
within ventricular system (impairing CSF circula- tion). Intracranial pressure increases.
Expanding hematoma acts like a space-occu- pying 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.
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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
16. most common cause of meningitis : 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, ven- tricular
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, candidi- asis, and
aspergillosis.
Tubercular-common and serious form of CNS tuberculosis, common in immunocom- promised
patients. Caused by mycobacteria.
17. conditions that result in pure water deficit (hypertonic volume depletion) : a result
of pure water losses, hyperventilation, arid climates and an increase in renal clearance
