Galen NSG 3280 Pathophysiology for Nurses I: Midterm Exam
(Units 1-7) - Questions with Correct Answers
100 questions
1. Asphyxial injury from strangulation causes cell injury by:
A. Increasing oxygen delivery
B. Causing hyperthermia
C. Obstructing airflow and blood flow, leading to hypoxia
D. Releasing lipases
Correct Answer: C. Obstructing airflow and blood flow, leading to hypoxia
Rationale: Strangulation compresses the airway and blood vessels, preventing oxygen delivery to the
brain. Petechiae in the eyes and face are common findings. The other mechanisms do not apply.
2. Frostbite injures tissues mainly through:
A. Protein denaturation from heat
B. Ice crystal formation and vasoconstriction causing ischemia
C. Free radical production from radiation
D. Bacterial toxin release
Correct Answer: B. Ice crystal formation and vasoconstriction causing ischemia
Rationale: Freezing forms intracellular and extracellular ice crystals and causes vasoconstriction and
increased blood viscosity, leading to ischemia; rewarming may cause reperfusion injury. Heat, radiation
and toxins are different mechanisms.
3. Hypokalemia makes nerve and muscle cells less excitable because it:
A. Makes the resting potential less negative
B. Opens sodium channels permanently
C. Increases calcium inside cells
D. Makes the resting membrane potential more negative (hyperpolarized)
Correct Answer: D. Makes the resting membrane potential more negative (hyperpolarized)
Rationale: Low extracellular potassium increases the gradient for potassium to leave, so the resting
potential moves further from threshold, causing muscle weakness. Hyperkalemia initially makes the
resting potential less negative. The other options do not describe this mechanism.
,4. An action potential in a neuron begins when:
A. Potassium rushes into the cell
B. Sodium channels open and sodium rushes into the cell, causing depolarization
C. Calcium leaves the cell
D. Chloride enters and hyperpolarizes the cell
Correct Answer: B. Sodium channels open and sodium rushes into the cell, causing
depolarization
Rationale: Depolarization occurs when voltage-gated sodium channels open and the inside becomes
positive; repolarization follows as potassium exits. Chloride influx hyperpolarizes and inhibits firing.
Potassium moving in would not trigger depolarization.
5. Carbon monoxide causes cellular hypoxia because it:
A. Blocks the sodium-potassium pump directly
B. Destroys red blood cells
C. Causes bronchospasm
D. Binds hemoglobin with much higher affinity than oxygen
Correct Answer: D. Binds hemoglobin with much higher affinity than oxygen
Rationale: CO binds hemoglobin about 200 times more tightly than oxygen, reducing oxygen delivery and
shifting the dissociation curve left; pulse oximetry can be falsely normal. It does not destroy red cells or
cause bronchospasm. Treatment is high-flow or hyperbaric oxygen.
6. The left ventricle thickens in a patient with long-standing hypertension. This change is:
A. Physiologic hyperplasia
B. Atrophy
C. Pathologic hypertrophy from increased workload
D. Dysplasia
Correct Answer: C. Pathologic hypertrophy from increased workload
Rationale: Cardiomyocytes enlarge to pump against increased afterload, but over time the thickened wall
becomes stiff, has relatively poor blood supply and predisposes to heart failure and arrhythmias.
Cardiomyocytes cannot undergo meaningful hyperplasia.
,7. Lead poisoning in children is particularly harmful because lead:
A. Only affects the skin
B. Is excreted quickly in urine
C. Strengthens bones
D. Interferes with neurodevelopment and heme synthesis
Correct Answer: D. Interferes with neurodevelopment and heme synthesis
Rationale: Lead crosses the developing blood-brain barrier, causing cognitive and behavioral problems,
and inhibits heme synthesis enzymes, causing microcytic anemia. It accumulates in bone and is excreted
slowly. Effects can occur at low levels without symptoms.
8. Increased intracellular calcium during cell injury is harmful because it:
A. Strengthens the cytoskeleton
B. Decreases mitochondrial permeability
C. Prevents apoptosis
D. Activates enzymes that damage membranes, proteins, and DNA
Correct Answer: D. Activates enzymes that damage membranes, proteins, and DNA
Rationale: Excess cytosolic calcium activates phospholipases, proteases, endonucleases and ATPases,
accelerating injury and increasing mitochondrial permeability. It promotes rather than prevents apoptosis.
It weakens rather than strengthens cell structure.
9. Dysplasia is clinically significant because it:
A. Shows abnormal cell size, shape, and organization and may progress to cancer
B. Is always irreversible and malignant
C. Represents normal tissue repair
D. Only occurs in muscle tissue
Correct Answer: A. Shows abnormal cell size, shape, and organization and may progress to
cancer
Rationale: Dysplasia is atypical hyperplasia that is not cancer but can progress to it, as in cervical
dysplasia, which is why screening detects and removes it. It may regress if the stimulus is removed, so it
is not always irreversible. It is not normal repair and occurs mostly in epithelium.
, 10. Dystrophic calcification occurs in:
A. Dead or dying tissue with normal serum calcium levels
B. Healthy tissue with high serum calcium
C. Bones only
D. Normal heart valves of young people
Correct Answer: A. Dead or dying tissue with normal serum calcium levels
Rationale: Dystrophic calcification is calcium deposition in damaged tissue such as atherosclerotic
plaques and damaged heart valves despite normal blood calcium. Metastatic calcification occurs in
normal tissue when serum calcium is high, as in hyperparathyroidism.
11. Accumulation of fat in liver cells from chronic alcohol use is called:
A. Hemosiderosis
B. Amyloidosis
C. Steatosis (fatty change)
D. Glycogen storage disease
Correct Answer: C. Steatosis (fatty change)
Rationale: Alcohol impairs fatty acid oxidation and lipoprotein export, causing triglyceride accumulation in
hepatocytes, which is reversible if drinking stops. Hemosiderosis is iron overload, amyloidosis involves
abnormal proteins, and glycogen storage disease is genetic.
12. Somatic death is followed by algor mortis, which is:
A. Stiffening of the muscles
B. Purple discoloration in dependent areas
C. Cooling of the body to environmental temperature
D. Decomposition by bacteria
Correct Answer: C. Cooling of the body to environmental temperature
Rationale: Algor mortis is post-mortem cooling. Rigor mortis is muscle stiffening from ATP depletion, livor
mortis is purple pooling of blood in dependent areas, and putrefaction is bacterial decomposition.
(Units 1-7) - Questions with Correct Answers
100 questions
1. Asphyxial injury from strangulation causes cell injury by:
A. Increasing oxygen delivery
B. Causing hyperthermia
C. Obstructing airflow and blood flow, leading to hypoxia
D. Releasing lipases
Correct Answer: C. Obstructing airflow and blood flow, leading to hypoxia
Rationale: Strangulation compresses the airway and blood vessels, preventing oxygen delivery to the
brain. Petechiae in the eyes and face are common findings. The other mechanisms do not apply.
2. Frostbite injures tissues mainly through:
A. Protein denaturation from heat
B. Ice crystal formation and vasoconstriction causing ischemia
C. Free radical production from radiation
D. Bacterial toxin release
Correct Answer: B. Ice crystal formation and vasoconstriction causing ischemia
Rationale: Freezing forms intracellular and extracellular ice crystals and causes vasoconstriction and
increased blood viscosity, leading to ischemia; rewarming may cause reperfusion injury. Heat, radiation
and toxins are different mechanisms.
3. Hypokalemia makes nerve and muscle cells less excitable because it:
A. Makes the resting potential less negative
B. Opens sodium channels permanently
C. Increases calcium inside cells
D. Makes the resting membrane potential more negative (hyperpolarized)
Correct Answer: D. Makes the resting membrane potential more negative (hyperpolarized)
Rationale: Low extracellular potassium increases the gradient for potassium to leave, so the resting
potential moves further from threshold, causing muscle weakness. Hyperkalemia initially makes the
resting potential less negative. The other options do not describe this mechanism.
,4. An action potential in a neuron begins when:
A. Potassium rushes into the cell
B. Sodium channels open and sodium rushes into the cell, causing depolarization
C. Calcium leaves the cell
D. Chloride enters and hyperpolarizes the cell
Correct Answer: B. Sodium channels open and sodium rushes into the cell, causing
depolarization
Rationale: Depolarization occurs when voltage-gated sodium channels open and the inside becomes
positive; repolarization follows as potassium exits. Chloride influx hyperpolarizes and inhibits firing.
Potassium moving in would not trigger depolarization.
5. Carbon monoxide causes cellular hypoxia because it:
A. Blocks the sodium-potassium pump directly
B. Destroys red blood cells
C. Causes bronchospasm
D. Binds hemoglobin with much higher affinity than oxygen
Correct Answer: D. Binds hemoglobin with much higher affinity than oxygen
Rationale: CO binds hemoglobin about 200 times more tightly than oxygen, reducing oxygen delivery and
shifting the dissociation curve left; pulse oximetry can be falsely normal. It does not destroy red cells or
cause bronchospasm. Treatment is high-flow or hyperbaric oxygen.
6. The left ventricle thickens in a patient with long-standing hypertension. This change is:
A. Physiologic hyperplasia
B. Atrophy
C. Pathologic hypertrophy from increased workload
D. Dysplasia
Correct Answer: C. Pathologic hypertrophy from increased workload
Rationale: Cardiomyocytes enlarge to pump against increased afterload, but over time the thickened wall
becomes stiff, has relatively poor blood supply and predisposes to heart failure and arrhythmias.
Cardiomyocytes cannot undergo meaningful hyperplasia.
,7. Lead poisoning in children is particularly harmful because lead:
A. Only affects the skin
B. Is excreted quickly in urine
C. Strengthens bones
D. Interferes with neurodevelopment and heme synthesis
Correct Answer: D. Interferes with neurodevelopment and heme synthesis
Rationale: Lead crosses the developing blood-brain barrier, causing cognitive and behavioral problems,
and inhibits heme synthesis enzymes, causing microcytic anemia. It accumulates in bone and is excreted
slowly. Effects can occur at low levels without symptoms.
8. Increased intracellular calcium during cell injury is harmful because it:
A. Strengthens the cytoskeleton
B. Decreases mitochondrial permeability
C. Prevents apoptosis
D. Activates enzymes that damage membranes, proteins, and DNA
Correct Answer: D. Activates enzymes that damage membranes, proteins, and DNA
Rationale: Excess cytosolic calcium activates phospholipases, proteases, endonucleases and ATPases,
accelerating injury and increasing mitochondrial permeability. It promotes rather than prevents apoptosis.
It weakens rather than strengthens cell structure.
9. Dysplasia is clinically significant because it:
A. Shows abnormal cell size, shape, and organization and may progress to cancer
B. Is always irreversible and malignant
C. Represents normal tissue repair
D. Only occurs in muscle tissue
Correct Answer: A. Shows abnormal cell size, shape, and organization and may progress to
cancer
Rationale: Dysplasia is atypical hyperplasia that is not cancer but can progress to it, as in cervical
dysplasia, which is why screening detects and removes it. It may regress if the stimulus is removed, so it
is not always irreversible. It is not normal repair and occurs mostly in epithelium.
, 10. Dystrophic calcification occurs in:
A. Dead or dying tissue with normal serum calcium levels
B. Healthy tissue with high serum calcium
C. Bones only
D. Normal heart valves of young people
Correct Answer: A. Dead or dying tissue with normal serum calcium levels
Rationale: Dystrophic calcification is calcium deposition in damaged tissue such as atherosclerotic
plaques and damaged heart valves despite normal blood calcium. Metastatic calcification occurs in
normal tissue when serum calcium is high, as in hyperparathyroidism.
11. Accumulation of fat in liver cells from chronic alcohol use is called:
A. Hemosiderosis
B. Amyloidosis
C. Steatosis (fatty change)
D. Glycogen storage disease
Correct Answer: C. Steatosis (fatty change)
Rationale: Alcohol impairs fatty acid oxidation and lipoprotein export, causing triglyceride accumulation in
hepatocytes, which is reversible if drinking stops. Hemosiderosis is iron overload, amyloidosis involves
abnormal proteins, and glycogen storage disease is genetic.
12. Somatic death is followed by algor mortis, which is:
A. Stiffening of the muscles
B. Purple discoloration in dependent areas
C. Cooling of the body to environmental temperature
D. Decomposition by bacteria
Correct Answer: C. Cooling of the body to environmental temperature
Rationale: Algor mortis is post-mortem cooling. Rigor mortis is muscle stiffening from ATP depletion, livor
mortis is purple pooling of blood in dependent areas, and putrefaction is bacterial decomposition.
