NUR 505 Advanced Pathophysiology Exam 3 All the 50
Questions from Actual 2026 Version With 100% Correct
Answers and Rationale
stages of dying - -answer-pallor mortis, algor mortis, rigor mortis, livor mortis, putrefaction,
decomposition, skeletonization
pallor mortis - -answer-pale and yellow skin
algo mortis - -answer-decreased body temp
rigor mortis - -answer-stiff muscles cased by lack of ATP
livor mortis - -answer-blood pooling causing blue/purple color
putrefaction - -answer-tissues and organs breakdown to gaseous and liquid
decomposition - -answer-breakdown of elemental matter
skeletonization - -answer-tissue decay, only disarticulated bones remain
Adaptive changes - -answer-atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia
atrophy - -answer-decrease in cell size
,hypertrophy - -answer-increase in cell size
hyperplasia - -answer-increase number of cells
dysplasia - -answer-abnormal changes in size, shape, and organization of mature cell.
Can be reversible
Precursor to cancer, but disorderly tissues are not cancer
Metaplasia - -answer-reversible replacement of one mature cell by another less mature that is more
likely to with stand stresses
pathologic atrophy - -answer-decrease in workload, use, pressure, or blood supply
physiologic atrophy - -answer-occurs with early development
pathologic hypertrophy - -answer-chromic hemodynamic overload, hypertension
physiologic hypertrophy - -answer-increased demand, hormones, growth factor
physiologic hyperplasia - -answer-compensatory, organ regenerate, hormonal, endocrine hormone
control
pathologic hyperplasia - -answer-hormonal, abnormal proliferation of normal cells
mechanisms of cellular injury - -answer-hypoxic injury
ischemia reperfusion injury
, free radicals and reactive oxygen species
xenbiotics
environmental toxins
hypoxic injury - -answer-most common cause of cellular injury
results from reduced oxygen and blood supply
Ischmia-reperfusion injury - -answer-injury and death caused by restoration of blood flow and oxygen
oxidative stress, increased calcium, inflammation, complement activation
Free Radicals/Reactive Oxygen Species (ROS) - -answer-cause oxidative stress
electrically uncharged atom of unpaired electron damaged DNA, lipid peroxidation, protein alteration
Xenobiotics - -answer-toxic, carcinogenic
carbon monoxide, lead, ethanol, mercury, drugs
Environmental toxins - -answer-air pollution, lead, calcium, arsenic, mercury, ethanol
causes fetal alcohol syndrome
Unintentional injuries - -answer-blunt force, asphyxial, immunologic and inflammatory injury
blunt force - -answer-tearing, crushing, contusions, lacerations, fractures
asphyxial - -answer-failure of cells to receive or use oxygen
suffocation, strangulation, chemical asphyxiants, drowning
immunologic and inflammatory injury - -answer-injury from substances generated during inflammatory
response
Questions from Actual 2026 Version With 100% Correct
Answers and Rationale
stages of dying - -answer-pallor mortis, algor mortis, rigor mortis, livor mortis, putrefaction,
decomposition, skeletonization
pallor mortis - -answer-pale and yellow skin
algo mortis - -answer-decreased body temp
rigor mortis - -answer-stiff muscles cased by lack of ATP
livor mortis - -answer-blood pooling causing blue/purple color
putrefaction - -answer-tissues and organs breakdown to gaseous and liquid
decomposition - -answer-breakdown of elemental matter
skeletonization - -answer-tissue decay, only disarticulated bones remain
Adaptive changes - -answer-atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia
atrophy - -answer-decrease in cell size
,hypertrophy - -answer-increase in cell size
hyperplasia - -answer-increase number of cells
dysplasia - -answer-abnormal changes in size, shape, and organization of mature cell.
Can be reversible
Precursor to cancer, but disorderly tissues are not cancer
Metaplasia - -answer-reversible replacement of one mature cell by another less mature that is more
likely to with stand stresses
pathologic atrophy - -answer-decrease in workload, use, pressure, or blood supply
physiologic atrophy - -answer-occurs with early development
pathologic hypertrophy - -answer-chromic hemodynamic overload, hypertension
physiologic hypertrophy - -answer-increased demand, hormones, growth factor
physiologic hyperplasia - -answer-compensatory, organ regenerate, hormonal, endocrine hormone
control
pathologic hyperplasia - -answer-hormonal, abnormal proliferation of normal cells
mechanisms of cellular injury - -answer-hypoxic injury
ischemia reperfusion injury
, free radicals and reactive oxygen species
xenbiotics
environmental toxins
hypoxic injury - -answer-most common cause of cellular injury
results from reduced oxygen and blood supply
Ischmia-reperfusion injury - -answer-injury and death caused by restoration of blood flow and oxygen
oxidative stress, increased calcium, inflammation, complement activation
Free Radicals/Reactive Oxygen Species (ROS) - -answer-cause oxidative stress
electrically uncharged atom of unpaired electron damaged DNA, lipid peroxidation, protein alteration
Xenobiotics - -answer-toxic, carcinogenic
carbon monoxide, lead, ethanol, mercury, drugs
Environmental toxins - -answer-air pollution, lead, calcium, arsenic, mercury, ethanol
causes fetal alcohol syndrome
Unintentional injuries - -answer-blunt force, asphyxial, immunologic and inflammatory injury
blunt force - -answer-tearing, crushing, contusions, lacerations, fractures
asphyxial - -answer-failure of cells to receive or use oxygen
suffocation, strangulation, chemical asphyxiants, drowning
immunologic and inflammatory injury - -answer-injury from substances generated during inflammatory
response
