NSG 5140 Advanced Pathophysiology Midterm Exam
Review – 130 Questions with Answers and Explanations for
South College Nursing Students LATEST UPATE THIS
YEAR.PDF
Q1. Explain the primary function of the sodium–potassium pump and its role in
resting membrane potential.*
Answer:* The Na⁺/K⁺-ATPase pump moves 3 Na⁺ out and 2 K⁺ into the cell using
ATP, creating a net negative intracellular charge and maintaining the resting membrane
potential essential for excitability.
Explanation: This gradient keeps the inside of the cell negative relative to the outside, which
is required for action potentials in nerve and muscle cells.
Q2. Describe how ATP depletion leads to cellular swelling in hypoxic injury.*
Answer:* ATP depletion disables the Na⁺/K⁺ pump, causing intracellular Na⁺
accumulation; water follows osmotically, leading to cellular swelling and organelle
dysfunction in hypoxic injury.
Explanation: Without ATP, ion gradients collapse, Na⁺ and water enter the cell, and
organelles such as mitochondria swell, marking early reversible injury.
Q3. Differentiate reversible from irreversible cell injury at the cellular level.*
Answer:* Reversible injury shows pump failure, cellular swelling, and fatty change with
intact membranes; irreversible injury features severe membrane damage, mitochondrial
failure, and nuclear changes (pyknosis, karyorrhexis, karyolysis).
,Explanation: Once membrane integrity and nuclear structure are lost, the cell cannot
recover and progresses to necrosis or apoptosis.
Q4. Which organelle is the primary site of ATP production, and how does hypoxia
affect it?*
Answer:* Mitochondria generate ATP via oxidative phosphorylation; hypoxia reduces
oxygen availability, impairing ATP production, forcing cells into anaerobic metabolism and
causing lactic acidosis.
Explanation: Oxygen is the final electron acceptor in the electron transport chain; without it,
ATP falls and lactate rises.
Q5. Explain the pathophysiology of metabolic acidosis in terms of pH and HCO₃⁻.*
Answer:* Metabolic acidosis is defined by decreased HCO₃⁻ (from acid gain or
bicarbonate loss), lowering pH; respiratory compensation occurs via hyperventilation to
lower PaCO₂.
Explanation: The primary disturbance is a fall in bicarbonate; the lungs compensate by
blowing off CO₂ to partially normalize pH.
Q6. Describe the role of free radicals in cellular injury.*
Answer:* Free radicals (ROS) damage lipids via peroxidation, oxidize proteins, and
cause DNA mutations; when antioxidant systems are overwhelmed, this leads to membrane
dysfunction and cell death.
,Explanation: Oxidative stress from excess ROS contributes to ischemia–reperfusion injury,
inflammation, and chronic diseases.
Q7. How does hyperkalemia affect cardiac cell excitability?*
Answer:* Hyperkalemia makes the resting membrane potential less negative, initially
increasing excitability but then inactivating Na⁺ channels, causing slowed conduction and
potentially fatal arrhythmias.
Explanation: Severe hyperkalemia can produce peaked T waves, widened QRS, and
ventricular fibrillation.
Q8. Define apoptosis and contrast it with necrosis.*
Answer:* Apoptosis is programmed, energy-dependent cell death with cell shrinkage
and no inflammation; necrosis is uncontrolled, with cell swelling, membrane rupture, and
inflammatory response.
Explanation: Apoptosis is physiologic or pathologic but tidy; necrosis is always pathologic
and messy.
Q9. What is the significance of proto-oncogenes and oncogenes in cancer?*
Answer:* Proto-oncogenes normally regulate cell growth; mutations or overexpression
convert them into oncogenes that drive unchecked proliferation and contribute to cancer
development.
Explanation: Examples include RAS and MYC; activation promotes cell cycle progression
and survival.
, Q10. Explain how tumor suppressor genes (e.g., p53) prevent cancer.*
Answer:* Tumor suppressor genes (e.g., p53) control the cell cycle, DNA repair, and
apoptosis; loss-of-function mutations allow cells with DNA damage to survive and divide,
promoting cancer.
Explanation: p53 is often called the “guardian of the genome” because it halts division or
triggers apoptosis in damaged cells.
Q11. Describe the cellular basis of edema in increased capillary hydrostatic
pressure.*
Answer:* Increased capillary hydrostatic pressure pushes more fluid out of capillaries
than is reabsorbed, causing net filtration into the interstitium and resulting in edema.
Explanation: This mechanism is seen in heart failure, venous obstruction, and fluid
overload.
Q12. How does hypoalbuminemia contribute to edema?*
Answer:* Hypoalbuminemia lowers plasma oncotic pressure, reducing fluid
reabsorption into capillaries, so more fluid remains in the interstitial space, causing edema.
Explanation: Common causes include liver disease, nephrotic syndrome, and malnutrition.
Q13. Outline the steps of cellular adaptation: hypertrophy, hyperplasia, atrophy,
metaplasia.*
Answer:* Hypertrophy = increased cell size; hyperplasia = increased cell number;
Review – 130 Questions with Answers and Explanations for
South College Nursing Students LATEST UPATE THIS
YEAR.PDF
Q1. Explain the primary function of the sodium–potassium pump and its role in
resting membrane potential.*
Answer:* The Na⁺/K⁺-ATPase pump moves 3 Na⁺ out and 2 K⁺ into the cell using
ATP, creating a net negative intracellular charge and maintaining the resting membrane
potential essential for excitability.
Explanation: This gradient keeps the inside of the cell negative relative to the outside, which
is required for action potentials in nerve and muscle cells.
Q2. Describe how ATP depletion leads to cellular swelling in hypoxic injury.*
Answer:* ATP depletion disables the Na⁺/K⁺ pump, causing intracellular Na⁺
accumulation; water follows osmotically, leading to cellular swelling and organelle
dysfunction in hypoxic injury.
Explanation: Without ATP, ion gradients collapse, Na⁺ and water enter the cell, and
organelles such as mitochondria swell, marking early reversible injury.
Q3. Differentiate reversible from irreversible cell injury at the cellular level.*
Answer:* Reversible injury shows pump failure, cellular swelling, and fatty change with
intact membranes; irreversible injury features severe membrane damage, mitochondrial
failure, and nuclear changes (pyknosis, karyorrhexis, karyolysis).
,Explanation: Once membrane integrity and nuclear structure are lost, the cell cannot
recover and progresses to necrosis or apoptosis.
Q4. Which organelle is the primary site of ATP production, and how does hypoxia
affect it?*
Answer:* Mitochondria generate ATP via oxidative phosphorylation; hypoxia reduces
oxygen availability, impairing ATP production, forcing cells into anaerobic metabolism and
causing lactic acidosis.
Explanation: Oxygen is the final electron acceptor in the electron transport chain; without it,
ATP falls and lactate rises.
Q5. Explain the pathophysiology of metabolic acidosis in terms of pH and HCO₃⁻.*
Answer:* Metabolic acidosis is defined by decreased HCO₃⁻ (from acid gain or
bicarbonate loss), lowering pH; respiratory compensation occurs via hyperventilation to
lower PaCO₂.
Explanation: The primary disturbance is a fall in bicarbonate; the lungs compensate by
blowing off CO₂ to partially normalize pH.
Q6. Describe the role of free radicals in cellular injury.*
Answer:* Free radicals (ROS) damage lipids via peroxidation, oxidize proteins, and
cause DNA mutations; when antioxidant systems are overwhelmed, this leads to membrane
dysfunction and cell death.
,Explanation: Oxidative stress from excess ROS contributes to ischemia–reperfusion injury,
inflammation, and chronic diseases.
Q7. How does hyperkalemia affect cardiac cell excitability?*
Answer:* Hyperkalemia makes the resting membrane potential less negative, initially
increasing excitability but then inactivating Na⁺ channels, causing slowed conduction and
potentially fatal arrhythmias.
Explanation: Severe hyperkalemia can produce peaked T waves, widened QRS, and
ventricular fibrillation.
Q8. Define apoptosis and contrast it with necrosis.*
Answer:* Apoptosis is programmed, energy-dependent cell death with cell shrinkage
and no inflammation; necrosis is uncontrolled, with cell swelling, membrane rupture, and
inflammatory response.
Explanation: Apoptosis is physiologic or pathologic but tidy; necrosis is always pathologic
and messy.
Q9. What is the significance of proto-oncogenes and oncogenes in cancer?*
Answer:* Proto-oncogenes normally regulate cell growth; mutations or overexpression
convert them into oncogenes that drive unchecked proliferation and contribute to cancer
development.
Explanation: Examples include RAS and MYC; activation promotes cell cycle progression
and survival.
, Q10. Explain how tumor suppressor genes (e.g., p53) prevent cancer.*
Answer:* Tumor suppressor genes (e.g., p53) control the cell cycle, DNA repair, and
apoptosis; loss-of-function mutations allow cells with DNA damage to survive and divide,
promoting cancer.
Explanation: p53 is often called the “guardian of the genome” because it halts division or
triggers apoptosis in damaged cells.
Q11. Describe the cellular basis of edema in increased capillary hydrostatic
pressure.*
Answer:* Increased capillary hydrostatic pressure pushes more fluid out of capillaries
than is reabsorbed, causing net filtration into the interstitium and resulting in edema.
Explanation: This mechanism is seen in heart failure, venous obstruction, and fluid
overload.
Q12. How does hypoalbuminemia contribute to edema?*
Answer:* Hypoalbuminemia lowers plasma oncotic pressure, reducing fluid
reabsorption into capillaries, so more fluid remains in the interstitial space, causing edema.
Explanation: Common causes include liver disease, nephrotic syndrome, and malnutrition.
Q13. Outline the steps of cellular adaptation: hypertrophy, hyperplasia, atrophy,
metaplasia.*
Answer:* Hypertrophy = increased cell size; hyperplasia = increased cell number;
