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NURS 5315 Advanced Pathophysiology UTA Exam 1 GUARANTEED PASS !! Questions with Correct Answers

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What can Reactive Oxygen Species cause? - ANSWERSHeart disease, Alzheimers, Parkinsons, Amyotrophic Lateral Sclerosis (ALS), CV disease, HTN, HLD, DM, ischemic heart disease, HF, OSA. Lipid perioxidation, damage proteins, fragment DNA, less *protein synthesis*, chromatin destruction, damage mitochondria What is the body's defense against ROS? - ANSWERSAntioxidants (Vitamin E, Vitamin C, cysteine, glutathione, albumin, ceruloplasmin, transferrin) How are free radicals produced? - ANSWERS1. Normal cellular respiration 2. Absorption of extreme energy sources (radiation, UV light) 3. Metabolism of exogenous chemicals, drugs, and pesticides 4. Transition of metals 5. Nitric oxide acting like a chemical mediator and a free radical action potential - ANSWERSProcess of conducting an impulse. Activates the neuron -- the neuron depolarizes -- then repolarizes Threshold potential - ANSWERSPoint at which depolarization must reach in order to initiate an action potential Hypokalemia and action potentials - ANSWERSHYPERpolarized (more negative, ex. -100). Less excitable. Decreased neuromuscular excitability: weakness, smooth muscle atony, paresthesia, cardiac dysrhythmias Hyperkalemia and action potentials - ANSWERSHYPOpolarized (more positive, ex: closer to 0). More excitable. Peaked T waves. When resting membrane potential=threshold potential, it is BAD = cardiac standstill, paresthesia, paralysis Hypocalcemia and action potentials - ANSWERSIncreased permeability to Na+. More excitable. Tetany, hyperreflexia, circumoral paresthesia, seizures, dysrhythmias. Hypercalcemia and action potentials - ANSWERSDecreased permeability to Na+. Less excitable. Weakness, hyporeflexia, fatigue, lethargy, confusion, encephalopathy, depressed T waves

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NURS 5315 Advanced
Pathophysiology UTA Exam 1
GUARANTEED PASS !! Questions with
Correct Answers
What can Reactive Oxygen Species cause? - ANSWERSHeart disease, Alzheimers,
Parkinsons, Amyotrophic Lateral Sclerosis (ALS), CV disease, HTN, HLD, DM, ischemic
heart disease, HF, OSA. Lipid perioxidation, damage proteins, fragment DNA, less
*protein synthesis*, chromatin destruction, damage mitochondria

What is the body's defense against ROS? - ANSWERSAntioxidants (Vitamin E, Vitamin
C, cysteine, glutathione, albumin, ceruloplasmin, transferrin)

How are free radicals produced? - ANSWERS1. Normal cellular respiration
2. Absorption of extreme energy sources (radiation, UV light)
3. Metabolism of exogenous chemicals, drugs, and pesticides
4. Transition of metals
5. Nitric oxide acting like a chemical mediator and a free radical

action potential - ANSWERSProcess of conducting an impulse. Activates the neuron -->
the neuron depolarizes --> then repolarizes

Threshold potential - ANSWERSPoint at which depolarization must reach in order to
initiate an action potential

Hypokalemia and action potentials - ANSWERSHYPERpolarized (more negative, ex. -
100). Less excitable. Decreased neuromuscular excitability: weakness, smooth muscle
atony, paresthesia, cardiac dysrhythmias

Hyperkalemia and action potentials - ANSWERSHYPOpolarized (more positive, ex:
closer to 0). More excitable. Peaked T waves.
When resting membrane potential=threshold potential, it is BAD = cardiac standstill,
paresthesia, paralysis

Hypocalcemia and action potentials - ANSWERSIncreased permeability to Na+. More
excitable. Tetany, hyperreflexia, circumoral paresthesia, seizures, dysrhythmias.

Hypercalcemia and action potentials - ANSWERSDecreased permeability to Na+. Less
excitable. Weakness, hyporeflexia, fatigue, lethargy, confusion, encephalopathy,
depressed T waves

, Atrophy - ANSWERSOccurs as a result of decrease in work load, pressure, use, blood
supply, nutrition, hormonal stimulation, or nervous stimulation. Once the cell has
decreased in size, it has now compensated for decreased blood supply, nerve supply,
nutrient supply, hormonal supply, and has achieved new homeostasis. Cells are alive
but have diminished function and may lead to cellular death.

Atrophy examples - ANSWERSPhysiologic atrophy- shrinking of the thymus gland
during childhood.
Disuse atrophy- someone that ends up being paralyzed

Hypertrophy - ANSWERSIncrease in SIZE of cells, which will lead to increase in size of
organ. Caused by hormonal stimulation or increased functional demand.

Hypertrophy examples - ANSWERSphysiologic hypertrophy- skeletal hypertrophy when
a person does heavy work or weight lifting / when a kidney is surgically removed, the
other kidney increases in size
pathologic hypertrophy- cardiomegaly results from an increased workload in
hypertensive patients / *left ventricular hypertrophy*

Hyperplasia - ANSWERSIncrease in NUMBER of cells. Results from increased rate of
mitosis. Can ONLY happen in cells that are capable of mitosis (cell division).

Hyperplasia examples - ANSWERS1. Thickening of skin because of hyperplasia of
epidermal cells.
2. Hormonal hyperplasia- occurs in estrogen dependent organs like uterus and breast.
3. Compensatory hyperplasia- liver regenerates, callus on skin
4. Pathologic hyperplasia- estrogen is unopposed by progesterone and the endometrial
lining undergoes hyperplasia and increased risk for endometrial cancer

Dysplasia - ANSWERSabnormal changes in the size, shape, and organization of
mature cells due to persistent, severe cell injury or irritation

Dysplasia examples - ANSWERSPre cancer pap smears often show dysplastic cells of
the cervix that must undergo treatment.

Metaplasia - ANSWERSChanged cell that is REVERSIBLE (one cell is replaced by
another cell). Exposure to chronic stressors, injury or irritation, like smoking or
hydrochloric acid from heart burn

Metaplasia examples - ANSWERSMost common is change from columnar cells to
squamous cells (chronic smokers).
Less common is change from squamous to columnar cells, like in Barrett Esophagus
caused by heart burn.

Carcinoma in situ - ANSWERSPre-invasive epithelial malignant tumors of glandular or
squamous origin. Sites including cervix, skin, oral cavity, esophagus, and bronchus

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Subido en
16 de julio de 2026
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