NR 507 Final Exam: Advanced P athophysiology
body’s process for adapting to high hormone level
(ANS- 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
(ANS- 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
(ANS- Low levels of thyroid hormone (T3 and T4) and high levels of thyroidstimulating hormone (TSH), most commonly caused by autoimmune thyroiditis.
Common causes of hypoparathyroidism
(ANS- parathyroid gland injury or removal
pathophysiology of thyroid storm
(ANS- 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
(ANS- Weight loss and enlarged thyroid gland are common signs of
hyperthyroidism in thyrotoxicosis.
diet and the prevention of prostate cancer
(ANS- 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
(ANS- enlarged prostate can block urine flow through the urethra. Can cause
urinary retention, which can lead to UTI, kidney infections.<\/p>\n\n\n\n
Dermatomes
(ANS- 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
(ANS- 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
(ANS- 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
(ANS- 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.<\/p>\n\n\n\n
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
(ANS- occurs when area of brain loses blood flow due to vascular occlusion. Exemboli 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
(ANS- 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<\/p>\n","protected":false},"excerpt":{"rendered":"
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