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NURS5315 Advanced Pathophysiology UTA Exam 1 Study Guide

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Comprehensive study guide for NURS5315 Advanced Pathophysiology Exam 1 at UTA. Covers key topics including cellular injury, free radicals, action potentials, fluid balance, genetic disorders, and cancer pathophysiology.

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NURS 5315 Advanced Pathophysiology UTA Exam 1 (Latest 2025 /
2026 Update) Real Questions and Verified Answers | 100% Correct
| Already Graded A+.



1. What can Reactive Oxygen Species cause?: Heart 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

2. What is the body's defense against ROS?: Antioxidants (Vitamin E, Vitamin C, cysteine, glutathione, albumin,
ceruloplasmin, transferrin)

3. How are free radicals produced?: 1. 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

4. action potential: Process of conducting an impulse. Activates the neuron --> the neuron depolarizes --> then
repolarizes

5. Threshold potential: Point at which depolarization must reach in order to initiate an action potential

6. Hypokalemia and action potentials: HYPERpolarized (more negative, ex.

-100). Less excitable. Decreased neuromuscular excitability: weakness, smooth muscle atony, paresthesia, cardiac

dysrhythmias

7. Hyperkalemia and action potentials: HYPOpolarized (more positive, ex: closer to 0). More excitable. Peaked T


,waves.

When resting membrane potential=threshold potential, it is BAD = cardiac standstill, paresthesia, paralysis

8. Hypocalcemia and action potentials: Increased permeability to Na+. More excitable. Tetany, hyperreflexia,
circumoral paresthesia, seizures, dysrhythmias.

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

10. Atrophy: Occurs 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.

11. Atrophy examples: Physiologic atrophy- shrinking of the thymus gland during childhood.

Disuse atrophy- someone that ends up being paralyzed

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



13. Hypertrophy examples: physiologic 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 hyper- tensive patients / *left ventricular

hypertrophy*

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

15. Hyperplasia examples: 1. Thickening of skin because of hyperplasia of epider- mal 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 endome- trial lining undergoes hyperplasia and
increased risk for endometrial cancer

16. Dysplasia: abnormal changes in the size, shape, and organization of mature cells due to persistent, severe cell
injury or irritation

17. Dysplasia examples: Pre cancer pap smears often show dysplastic cells of the cervix that must undergo treatment.

18. Metaplasia: Changed 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

19. Metaplasia examples: Most common is change from columnar cells to squa- mous cells (chronic smokers).

Less common is change from squamous to columnar cells, like in Barrett Esophagus caused by heart burn.

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

21. Hypoxic injury: 1. Decrease in oxygen in the air (high altitudes, asphyxiation, drowning)

2. Loss of hemoglobin function (hemorrhage or sickle cell anemia)

3. Decrease in production of red blood cells (anemia or leukemia)

4. Diseases of cardiopulmonary systems (ischemia, blood supply loss, arterioscle- rosis)

22. Hypoxic injury clinical manifestations: 1. Increased CK (muscle and heart)

2. Increased LDH (muscle, liver, lung, heart, RBC, brain)

3. Increased ALT and AST (liver)

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