NURS 5315: Advanced
Pathophysiology 2025 UTA Exam 1
UPDATED
1. Atrophy
ANS: E. Cells decrease in size
P. Still functional; imbalance between protein synthesis and degradation. Essentially
there is an increase in the catabolism of intracellular organelles, reducing structural
components of cell
Physiologic: thymus gland in early childhood
Pathological: disuse (muscle atrophy d/ decrease workload, pressure, use, blood
supply, nutrition, hormonal stimulation, or nervous stimulation)
2. Hyperplasia
ANS: E: cells increase in number, mitosis (cell division) must occur, size of cell
does not change
Phys: increased rate of division, increase in tissue mass after damage or partial
resection; may be compensatory, hormonal, or pathologic
Patho: abnormal proliferation of normal cells usually caused by increased hormonal
stimulation (endometrial). increase of production of local growth factors
Ex: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or
mammary gland enlargement during pregnancy
,3. Dysplasia
ANS: E. Not true adaptation; Cells abnormal change in size, shape, organi- zation
(classified as mild, moderate, severe)
P. caused by cell injury/irritation, characterized by disordered cell growth. aka atyp-
ical hyperplasia or pre-cancer, a disorderly proliferation
Physiologic: N/A
Pathologic: squamous dysplasia of cervix from HPV shows up on pap smear, breast
cancer development; pap smears often show dysplastic cells of the cervix that must
undergo laser/surgical tx
4. Metaplasia
ANS: E: reversible change, one type of cell changes to another type for survival
P: reversible; results from exposure of the cells to chronic stressors, injury, or
irritation; Cancer can arise from this area, stimulus induces a reprogramming of stem
cells under the influence of cytokines and growth factors
Ex: Patho: Columnar cells change to squamous cells in lungs of smoker or normal
ciliated epithelial cells of the bronchial linings are replaced by stratified squamous
epithelial cells.; Phys: Barrett Esophagus- normal squamous cells change to colum-
nar epithelial cells in response to reflux, aka intestinal metaplasia
5. Hypoxia injury
ANS: E. inadequate oxygenation of tissues
P. decrease in mitochondrial function, decreased production of ATP increases anaer-
obic metabolism. eventual cell death.
C.M. hypoxia, cyanosis, cognitive impairment, lethargy
6. Free radical and ROS
ANS: E. normal byproduct of ATP production, will overwhelm the mitochondria-
,exhaust intracellular antioxidants
P. lipid peroxidation, damage proteins, fragment DNA
, C.M. development in Alzheimer's, heart disease, Parkinson's disease, Amyotrophic
Lateral Sclerosis
7. Ethanol
ANS: E. mood altering drug, long term effects on liver and nutritional status
P. metabolized by liver, generates free radicals
C.M. CNS depression, nutrient deficiencies-Mag, Vit B6, thiamine, PO4, inflamma-
tion and fatty infiltration of liver, hepatomegaly, leads to liver failure irreversible
8. Oncosis
ANS: Na and H2O enter cell and cause swelling. Organ increases in weight,
becomes distended and pale. Associated with high fever, hypocalcemia, certain
infections
9. Fatty Infiltration
ANS: intracellular accumulation of lipids in the liver
liver fails to metabolize lipids. usually from ETOH or high fat diet. can lead to cirrhosis
10. dystrophic calcification
ANS: accumulation of Ca in dead or dying tissues calcium salt clump and
harden- interfere with cellular structure and function r/t pulmonary TB,
atherosclerosis, injured heart valves, chronic pancreatitis
11. metastatic calcification
ANS: accumulation of Ca in normal tissue
result of hypercalcemia r/t hyperparathyroidism, hyperthyroidism, toxic levels of Vit
D. Can also r/t hyperphosphatemia in renal failure
Pathophysiology 2025 UTA Exam 1
UPDATED
1. Atrophy
ANS: E. Cells decrease in size
P. Still functional; imbalance between protein synthesis and degradation. Essentially
there is an increase in the catabolism of intracellular organelles, reducing structural
components of cell
Physiologic: thymus gland in early childhood
Pathological: disuse (muscle atrophy d/ decrease workload, pressure, use, blood
supply, nutrition, hormonal stimulation, or nervous stimulation)
2. Hyperplasia
ANS: E: cells increase in number, mitosis (cell division) must occur, size of cell
does not change
Phys: increased rate of division, increase in tissue mass after damage or partial
resection; may be compensatory, hormonal, or pathologic
Patho: abnormal proliferation of normal cells usually caused by increased hormonal
stimulation (endometrial). increase of production of local growth factors
Ex: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or
mammary gland enlargement during pregnancy
,3. Dysplasia
ANS: E. Not true adaptation; Cells abnormal change in size, shape, organi- zation
(classified as mild, moderate, severe)
P. caused by cell injury/irritation, characterized by disordered cell growth. aka atyp-
ical hyperplasia or pre-cancer, a disorderly proliferation
Physiologic: N/A
Pathologic: squamous dysplasia of cervix from HPV shows up on pap smear, breast
cancer development; pap smears often show dysplastic cells of the cervix that must
undergo laser/surgical tx
4. Metaplasia
ANS: E: reversible change, one type of cell changes to another type for survival
P: reversible; results from exposure of the cells to chronic stressors, injury, or
irritation; Cancer can arise from this area, stimulus induces a reprogramming of stem
cells under the influence of cytokines and growth factors
Ex: Patho: Columnar cells change to squamous cells in lungs of smoker or normal
ciliated epithelial cells of the bronchial linings are replaced by stratified squamous
epithelial cells.; Phys: Barrett Esophagus- normal squamous cells change to colum-
nar epithelial cells in response to reflux, aka intestinal metaplasia
5. Hypoxia injury
ANS: E. inadequate oxygenation of tissues
P. decrease in mitochondrial function, decreased production of ATP increases anaer-
obic metabolism. eventual cell death.
C.M. hypoxia, cyanosis, cognitive impairment, lethargy
6. Free radical and ROS
ANS: E. normal byproduct of ATP production, will overwhelm the mitochondria-
,exhaust intracellular antioxidants
P. lipid peroxidation, damage proteins, fragment DNA
, C.M. development in Alzheimer's, heart disease, Parkinson's disease, Amyotrophic
Lateral Sclerosis
7. Ethanol
ANS: E. mood altering drug, long term effects on liver and nutritional status
P. metabolized by liver, generates free radicals
C.M. CNS depression, nutrient deficiencies-Mag, Vit B6, thiamine, PO4, inflamma-
tion and fatty infiltration of liver, hepatomegaly, leads to liver failure irreversible
8. Oncosis
ANS: Na and H2O enter cell and cause swelling. Organ increases in weight,
becomes distended and pale. Associated with high fever, hypocalcemia, certain
infections
9. Fatty Infiltration
ANS: intracellular accumulation of lipids in the liver
liver fails to metabolize lipids. usually from ETOH or high fat diet. can lead to cirrhosis
10. dystrophic calcification
ANS: accumulation of Ca in dead or dying tissues calcium salt clump and
harden- interfere with cellular structure and function r/t pulmonary TB,
atherosclerosis, injured heart valves, chronic pancreatitis
11. metastatic calcification
ANS: accumulation of Ca in normal tissue
result of hypercalcemia r/t hyperparathyroidism, hyperthyroidism, toxic levels of Vit
D. Can also r/t hyperphosphatemia in renal failure
