NURS 5433: Advanced Pathophysiology Study Guide (Updated
2026/2027)
Instructions: This guide contains 100+ key questions and model answers structured in
the requested format. Use these to test your understanding of cellular, systemic, and
disease-specific pathophysiology.
Section 1: Cellular & Genetic Foundations of Disease
1. What is the primary difference between apoptosis and necrosis in terms of
cellular death, inflammation, and disease implication?
ANSWER ✓ Apoptosis is programmed, energy-dependent cell death that is non-
inflammatory, involving cell shrinkage, membrane blebbing, and phagocytosis by
neighboring cells. It is crucial for normal development and homeostasis. Necrosis is
premature, pathological cell death due to injury (e.g., ischemia, toxins) that
is inflammatory, involving cell swelling, membrane rupture, and spillage of contents,
leading to tissue damage and potential systemic effects.
2. How does the concept of "cellular adaptation" manifest in myocardial tissue in
response to chronic hypertension?
ANSWER ✓ In response to the increased workload and wall tension of chronic
hypertension, myocardial cells undergo hypertrophy. This is an adaptive increase in
individual cell size (without cell division), leading to thickening of the left ventricular wall
(left ventricular hypertrophy). While initially compensatory, it can become maladaptive,
leading to diastolic dysfunction, increased oxygen demand, and risk of heart failure.
3. Describe the role of oncogenes and tumor suppressor genes in the development
of cancer, using a specific example.
ANSWER ✓ Oncogenes are mutated versions of normal proto-oncogenes that promote
uncontrolled cell growth and division (like a stuck accelerator). Tumor suppressor
genes normally inhibit cell division and promote apoptosis; their loss or inactivation
removes this brake. For example, in many colorectal cancers, an oncogene like KRAS is
, mutated to be constantly active, while the tumor suppressor gene APC is inactivated,
followed by loss of p53, allowing for unchecked proliferation and genomic instability.
4. Explain how a mutation in the CFTR gene leads to the systemic manifestations
of cystic fibrosis.
ANSWER ✓ A mutation in the CFTR (Cystic Fibrosis Transmembrane Conductance
Regulator) gene results in a defective chloride channel on epithelial cell surfaces. This
leads to impaired chloride secretion and excessive sodium and water reabsorption,
causing thick, viscous secretions. In the lungs, this results in chronic airway obstruction,
infection, and bronchiectasis. In the pancreas, it causes duct obstruction, leading to
exocrine pancreatic insufficiency and malnutrition.
5. What is the pathophysiologic mechanism behind the symptoms of lactose
intolerance?
ANSWER ✓ Lactose intolerance is due to a deficiency of the enzyme lactase on the
brush border of small intestinal enterocytes. Without sufficient lactase, the disaccharide
lactose cannot be hydrolyzed into absorbable monosaccharides (glucose and galactose).
The unabsorbed lactose osmotically draws water into the intestinal lumen (causing
osmotic diarrhea) and is fermented by colonic bacteria, producing gas (bloating,
flatulence) and organic acids (cramping).
Section 2: Neuropathophysiology
6. Differentiate between the primary injury and secondary injury phases following
an ischemic stroke.
ANSWER ✓ Primary injury is the immediate cessation of cerebral blood flow, causing
energy (ATP) depletion, failure of ion pumps (Na+/K+ ATPase), neuronal depolarization,
and cytotoxic edema. Secondary injury evolves over hours to days and involves a
cascade including excitotoxicity (glutamate release), inflammation, free radical
formation, blood-brain barrier disruption, vasogenic edema, and ultimately, apoptosis
and infarction.
7. How does the pathophysiology of Parkinson's disease explain its cardinal motor
symptoms?
2026/2027)
Instructions: This guide contains 100+ key questions and model answers structured in
the requested format. Use these to test your understanding of cellular, systemic, and
disease-specific pathophysiology.
Section 1: Cellular & Genetic Foundations of Disease
1. What is the primary difference between apoptosis and necrosis in terms of
cellular death, inflammation, and disease implication?
ANSWER ✓ Apoptosis is programmed, energy-dependent cell death that is non-
inflammatory, involving cell shrinkage, membrane blebbing, and phagocytosis by
neighboring cells. It is crucial for normal development and homeostasis. Necrosis is
premature, pathological cell death due to injury (e.g., ischemia, toxins) that
is inflammatory, involving cell swelling, membrane rupture, and spillage of contents,
leading to tissue damage and potential systemic effects.
2. How does the concept of "cellular adaptation" manifest in myocardial tissue in
response to chronic hypertension?
ANSWER ✓ In response to the increased workload and wall tension of chronic
hypertension, myocardial cells undergo hypertrophy. This is an adaptive increase in
individual cell size (without cell division), leading to thickening of the left ventricular wall
(left ventricular hypertrophy). While initially compensatory, it can become maladaptive,
leading to diastolic dysfunction, increased oxygen demand, and risk of heart failure.
3. Describe the role of oncogenes and tumor suppressor genes in the development
of cancer, using a specific example.
ANSWER ✓ Oncogenes are mutated versions of normal proto-oncogenes that promote
uncontrolled cell growth and division (like a stuck accelerator). Tumor suppressor
genes normally inhibit cell division and promote apoptosis; their loss or inactivation
removes this brake. For example, in many colorectal cancers, an oncogene like KRAS is
, mutated to be constantly active, while the tumor suppressor gene APC is inactivated,
followed by loss of p53, allowing for unchecked proliferation and genomic instability.
4. Explain how a mutation in the CFTR gene leads to the systemic manifestations
of cystic fibrosis.
ANSWER ✓ A mutation in the CFTR (Cystic Fibrosis Transmembrane Conductance
Regulator) gene results in a defective chloride channel on epithelial cell surfaces. This
leads to impaired chloride secretion and excessive sodium and water reabsorption,
causing thick, viscous secretions. In the lungs, this results in chronic airway obstruction,
infection, and bronchiectasis. In the pancreas, it causes duct obstruction, leading to
exocrine pancreatic insufficiency and malnutrition.
5. What is the pathophysiologic mechanism behind the symptoms of lactose
intolerance?
ANSWER ✓ Lactose intolerance is due to a deficiency of the enzyme lactase on the
brush border of small intestinal enterocytes. Without sufficient lactase, the disaccharide
lactose cannot be hydrolyzed into absorbable monosaccharides (glucose and galactose).
The unabsorbed lactose osmotically draws water into the intestinal lumen (causing
osmotic diarrhea) and is fermented by colonic bacteria, producing gas (bloating,
flatulence) and organic acids (cramping).
Section 2: Neuropathophysiology
6. Differentiate between the primary injury and secondary injury phases following
an ischemic stroke.
ANSWER ✓ Primary injury is the immediate cessation of cerebral blood flow, causing
energy (ATP) depletion, failure of ion pumps (Na+/K+ ATPase), neuronal depolarization,
and cytotoxic edema. Secondary injury evolves over hours to days and involves a
cascade including excitotoxicity (glutamate release), inflammation, free radical
formation, blood-brain barrier disruption, vasogenic edema, and ultimately, apoptosis
and infarction.
7. How does the pathophysiology of Parkinson's disease explain its cardinal motor
symptoms?
