NURS 5315 ADVANCED PATHOPHYSIOLOGY
EXAM 1 CERTIFICATION EVALUATION TEST
PAPER 2026 COMPLETE STUDY QUESTIONS
WITH CORRECT ANSWERS
◉ Oxygen and Oxygen derived free radicals. Answer: decrease
oxygen delivery to cells results in the production of activated oxygen
species (free radicals, H2O2, NO) which destroy the cell membranes
and structures.
◉ Most common cause of cellular injury. Answer: Hypoxic Injury
◉ Clinical Manifestations of Hypoxic Injury. Answer: Reduced
ischemia, loss of hemoglobin, diseases, etc. Heart attack, etc
◉ Pathophysiology of Hypoxic Injury. Answer: Ischemia - ↓
mitochondrial oxygenation, ↓ATP, Na-K & Na-Ca pumps fail -> ↑
intracellular Na & Ca -> K to diffuse out of cell -> acute cellular
swelling (from ↑ Na in cell), anaerobic glycolysis, ↑Lactate, necrosis
◉ Reperfusion Injury. Answer: Reoxygenation, Tissue
transplantation, ischemic syndromes of heart, liver, GI, kidneys, and
cerebrum.
,◉ Clinical Manifestations of Reperfusion Injury. Answer: Neutrophils
especially affected, causing neutrophil adhesion to endothelium
Serious complication in transplantation and ischemic diseases
◉ Patho of Reperfusion Injury. Answer: -Triggers the production of
highly reactive oxygen intermediates (hydroxyl radical & hydrogen
peroxide -> cell membrane damage & mitochondrial Ca overload).
-WBC function is impaired as result of injury. *
Xanthine dehydrogenase -> converts to xanthine oxidate -> creates
massive amounts of free radicals, superoxide & hydrogen peroxide -
> etc... apoptosis
◉ Free Radical. Answer: Any molecular species capable of
independent existence that contains a single unpaired electron in an
outer orbit
Highly reactive
◉ Clinical Manifestations of Free Radical. Answer: -Redox reactions
in normal metabolic processes (respiration)
-Absorption of extreme energy sources (UV light, radiation)
-Enzymatic metabolism of exogenous chemicals, drugs, and
pesticides
-Process of transition metals (iron, copper) (fenton reaction)
,-Nitric oxide (NO) acting as an important chemical mediator,
colorless gas
◉ Reactive Oxygen Species (ROS). Answer: -Chemically reactive
molecules from molecular oxygen formed as natural oxidant species
in cells during mitochondrial respiration & energy generation.
-This form of injury is called oxidative stress
◉ Cellular Effect on Necrosis. Answer: -Characterized by rapid loss
of plasma membrane structure, organelle swelling, mitochondrial
dysfunction. Leads to local cell death and autolysis. Outcome for
common injuries (ischemia, toxin exposure, infections, trauma).
Swelling, accidental cell death
Cell Size - Swelling
Nucleus - Pyknosis, karyorrhexis, Karyolysis
Plasma Membrane -Disrupted
Cellular Contents - Enzymatic digestion; may leak out of cell
Adjacent inflammation - Frequent
Physiologic or pathologic role - usually pathologic (culmination of
irreversible cell injury)
◉ Cellular Effect on Apoptosis. Answer: -Regulated/programmed
cell process, "dropping off" of cellular fragments (apoptotic bodies).
Reduced (shrinking), plasma membrane intact
, Cell Size - Shrinking
Nucleus - Fragmentation into nucleosome-size fragments
Plasma Membrane - Intact; altered structure, especially orientation
of lipids
Cellular Contents - Intact; may be released in apoptotic bodies
Adjacent inflammation - No
Physiologic or pathologic role - often physiologic, means of
eliminating unwanted cells; may be pathologic after some forms of
cell injury, especially DNA damage
◉ Autophagy. Answer: "eating of self" self-destructive process &
survival mechanism
-When cells are starved/nutrient deprived, autophagic process
institutes cannibalizations & recycles digested contents.
Maintains cellular metabolism under starvation conditions, remove
damaged organelles & misfolded proteins under stress conditions,
improves survival of cells
During times of metabolic stress, autophagy provides ATP & other
macromolecules for energy and cell survival, however as the stress
progresses autophagic cell death will occur.
When cells lack nutrition, autophagy is triggered.
If stress is excessive, autophagic programmed cell death
Can suppress & facilitate tumor development
Process decelerates
EXAM 1 CERTIFICATION EVALUATION TEST
PAPER 2026 COMPLETE STUDY QUESTIONS
WITH CORRECT ANSWERS
◉ Oxygen and Oxygen derived free radicals. Answer: decrease
oxygen delivery to cells results in the production of activated oxygen
species (free radicals, H2O2, NO) which destroy the cell membranes
and structures.
◉ Most common cause of cellular injury. Answer: Hypoxic Injury
◉ Clinical Manifestations of Hypoxic Injury. Answer: Reduced
ischemia, loss of hemoglobin, diseases, etc. Heart attack, etc
◉ Pathophysiology of Hypoxic Injury. Answer: Ischemia - ↓
mitochondrial oxygenation, ↓ATP, Na-K & Na-Ca pumps fail -> ↑
intracellular Na & Ca -> K to diffuse out of cell -> acute cellular
swelling (from ↑ Na in cell), anaerobic glycolysis, ↑Lactate, necrosis
◉ Reperfusion Injury. Answer: Reoxygenation, Tissue
transplantation, ischemic syndromes of heart, liver, GI, kidneys, and
cerebrum.
,◉ Clinical Manifestations of Reperfusion Injury. Answer: Neutrophils
especially affected, causing neutrophil adhesion to endothelium
Serious complication in transplantation and ischemic diseases
◉ Patho of Reperfusion Injury. Answer: -Triggers the production of
highly reactive oxygen intermediates (hydroxyl radical & hydrogen
peroxide -> cell membrane damage & mitochondrial Ca overload).
-WBC function is impaired as result of injury. *
Xanthine dehydrogenase -> converts to xanthine oxidate -> creates
massive amounts of free radicals, superoxide & hydrogen peroxide -
> etc... apoptosis
◉ Free Radical. Answer: Any molecular species capable of
independent existence that contains a single unpaired electron in an
outer orbit
Highly reactive
◉ Clinical Manifestations of Free Radical. Answer: -Redox reactions
in normal metabolic processes (respiration)
-Absorption of extreme energy sources (UV light, radiation)
-Enzymatic metabolism of exogenous chemicals, drugs, and
pesticides
-Process of transition metals (iron, copper) (fenton reaction)
,-Nitric oxide (NO) acting as an important chemical mediator,
colorless gas
◉ Reactive Oxygen Species (ROS). Answer: -Chemically reactive
molecules from molecular oxygen formed as natural oxidant species
in cells during mitochondrial respiration & energy generation.
-This form of injury is called oxidative stress
◉ Cellular Effect on Necrosis. Answer: -Characterized by rapid loss
of plasma membrane structure, organelle swelling, mitochondrial
dysfunction. Leads to local cell death and autolysis. Outcome for
common injuries (ischemia, toxin exposure, infections, trauma).
Swelling, accidental cell death
Cell Size - Swelling
Nucleus - Pyknosis, karyorrhexis, Karyolysis
Plasma Membrane -Disrupted
Cellular Contents - Enzymatic digestion; may leak out of cell
Adjacent inflammation - Frequent
Physiologic or pathologic role - usually pathologic (culmination of
irreversible cell injury)
◉ Cellular Effect on Apoptosis. Answer: -Regulated/programmed
cell process, "dropping off" of cellular fragments (apoptotic bodies).
Reduced (shrinking), plasma membrane intact
, Cell Size - Shrinking
Nucleus - Fragmentation into nucleosome-size fragments
Plasma Membrane - Intact; altered structure, especially orientation
of lipids
Cellular Contents - Intact; may be released in apoptotic bodies
Adjacent inflammation - No
Physiologic or pathologic role - often physiologic, means of
eliminating unwanted cells; may be pathologic after some forms of
cell injury, especially DNA damage
◉ Autophagy. Answer: "eating of self" self-destructive process &
survival mechanism
-When cells are starved/nutrient deprived, autophagic process
institutes cannibalizations & recycles digested contents.
Maintains cellular metabolism under starvation conditions, remove
damaged organelles & misfolded proteins under stress conditions,
improves survival of cells
During times of metabolic stress, autophagy provides ATP & other
macromolecules for energy and cell survival, however as the stress
progresses autophagic cell death will occur.
When cells lack nutrition, autophagy is triggered.
If stress is excessive, autophagic programmed cell death
Can suppress & facilitate tumor development
Process decelerates
