NSG 5140 Advanced Pathophysiology Final
Exam – Best Practice Questions with
Answers and Rationales – South College –
2026 Updated | pdf
INTRO:
*This comprehensive exam review is designed for students preparing for the NSG 5140 Advanced
Pathophysiology final exam at South College. The assessment evaluates mastery of graduate-level
pathophysiologic concepts, including cellular mechanisms, system-specific disease processes, and clinical
manifestations across the lifespan. Topics include cellular adaptation and injury, inflammation and
immunity, fluid/electrolyte and acid-base balance, cardiovascular and pulmonary pathophysiology, renal
and endocrine disorders, neurologic and musculoskeletal conditions, genetics, and neoplasia. This
resource includes scenario-based questions that challenge application of theoretical knowledge to real-
world patient presentations. Answers are in bold italic * with detailed rationales in italic at the end of each
question.
CORE DOMAINS COVERED
Domain Key Topics
Cellular Adaptation, Atrophy, hypertrophy, metaplasia, dysplasia, necrosis
Injury, and Death types (coagulative, liquefactive, caseous, fat),
apoptosis, ischemia-reperfusion injury, calcium
overload
Inflammation and Acute vs. chronic inflammation, cardinal signs,
Immunity neutrophils, macrophages, fever (IL-1, IL-6, TNF-α),
Type I-IV hypersensitivity, immunoglobulins
Fluid, Electrolyte, and Na⁺/K⁺-ATPase, hyponatremia, hyperkalemia, metabolic
Acid-Base Balance acidosis/alkalosis, respiratory acidosis/alkalosis, anion
gap, compensatory mechanisms
Cardiovascular HFpEF vs. HFrEF, left vs. right-sided heart failure,
Pathophysiology myocardial infarction, coronary artery occlusion,
cardiac biomarkers (troponin), hypertension, LVH,
pulmonary embolism
Pulmonary COPD, chronic bronchitis, emphysema, respiratory
Pathophysiology acidosis, pneumonia, tuberculosis, tension
pneumothorax, ARDS, V/Q mismatch
, Renal and Urinary AKI (prerenal, intrinsic, postrenal), CKD, erythropoietin,
Tract anemia, nephrotic syndrome, BUN/Cr ratio, oliguria
Pathophysiology
Endocrine and Type 1 vs. Type 2 diabetes, DKA, hyperthyroidism,
Metabolic Disorders Cushing's syndrome, Addison's disease, cortisol,
hyperparathyroidism
Neurologic Ischemic stroke, Alzheimer disease, Parkinson disease,
Pathophysiology multiple sclerosis, Wernicke encephalopathy, Bell
palsy, seizures
Gastrointestinal and Hepatic encephalopathy, cirrhosis, peptic ulcer
Hepatobiliary disease, NSAIDs, Crohn's disease, ulcerative colitis,
pancreatitis, cholecystitis, Barrett esophagus
Hematology and Iron-deficiency anemia, B12 deficiency, sickle cell
Oncology disease, polycythemia vera, Hodgkin lymphoma,
multiple myeloma, febrile neutropenia, ITP
CELLULAR ADAPTATION, INJURY, AND DEATH
1. A 62-year-old male with chronic heart failure presents with worsening dyspnea,
jugular venous distension, and peripheral edema. What cellular adaptation is most
likely occurring in his myocardium as a compensatory mechanism?
Answer: Hypertrophy
Hypertrophy is an increase in cell size due to increased workload, as seen in heart failure
where myocytes enlarge to compensate for pressure or volume overload. Hyperplasia
(increase in cell number) is not typical in terminally differentiated cardiac muscle. Metaplasia
is replacement of one cell type with another. Dysplasia is disordered cellular growth, often
preneoplastic .
2. During ischemia, the switch from aerobic to anaerobic metabolism leads to which
immediate intracellular change?
Answer: Accumulation of lactic acid
Anaerobic metabolism produces lactic acid, causing intracellular acidosis and impaired
cellular function. ATP production decreases, not increases. Intracellular pH decreases,
sodium accumulates due to Na⁺/K⁺-ATPase pump failure, and lactic acid accumulation
contributes to cell injury .
, 3. A cell adapts to a decreased workload by decreasing in size. This process is
called:
Answer: Atrophy
Atrophy is a decrease in cell size due to reduced workload, denervation, decreased blood
supply, or inadequate nutrition. It is a reversible adaptation if the stimulus is removed .
4. Chronic exposure to gastric acid in the lower esophagus causes the normal
stratified squamous epithelium to change to columnar epithelium. This change is
called:
Answer: Metaplasia
Metaplasia is the reversible replacement of one differentiated cell type with another (e.g.,
Barrett esophagus — squamous to columnar). Dysplasia is disordered growth; anaplasia is
loss of differentiation in cancer .
5. A pathologist examining a myocardial infarction under the microscope notes
preserved tissue architecture with loss of nuclei and eosinophilic cytoplasm. What
type of necrosis is this?
Answer: Coagulative necrosis
Coagulative necrosis (typical of ischemic injury in solid organs like heart, kidney, liver)
preserves tissue outline but shows nuclear loss and increased cytoplasmic eosinophilia.
Liquefactive necrosis occurs in the brain. Caseous necrosis is associated with tuberculosis .
6. Which type of necrosis is classically associated with tuberculosis and appears as
"cheesy" on gross examination?
Answer: Caseous necrosis
Caseous necrosis (e.g., TB, fungal infections) has a friable, granular, cheese-like
appearance. It is a form of coagulative necrosis with extensive destruction of tissue
architecture .
7. A patient with pancreatitis develops chalky white deposits in the peritoneum. This
represents which type of necrosis?
Answer: Fat necrosis
Fat necrosis occurs when pancreatic lipase breaks down triglycerides into free fatty acids,
which combine with calcium (saponification) forming chalky-white deposits .
8. A patient presents with a brain infarct following a stroke. What type of necrosis is
expected in the brain tissue?
Exam – Best Practice Questions with
Answers and Rationales – South College –
2026 Updated | pdf
INTRO:
*This comprehensive exam review is designed for students preparing for the NSG 5140 Advanced
Pathophysiology final exam at South College. The assessment evaluates mastery of graduate-level
pathophysiologic concepts, including cellular mechanisms, system-specific disease processes, and clinical
manifestations across the lifespan. Topics include cellular adaptation and injury, inflammation and
immunity, fluid/electrolyte and acid-base balance, cardiovascular and pulmonary pathophysiology, renal
and endocrine disorders, neurologic and musculoskeletal conditions, genetics, and neoplasia. This
resource includes scenario-based questions that challenge application of theoretical knowledge to real-
world patient presentations. Answers are in bold italic * with detailed rationales in italic at the end of each
question.
CORE DOMAINS COVERED
Domain Key Topics
Cellular Adaptation, Atrophy, hypertrophy, metaplasia, dysplasia, necrosis
Injury, and Death types (coagulative, liquefactive, caseous, fat),
apoptosis, ischemia-reperfusion injury, calcium
overload
Inflammation and Acute vs. chronic inflammation, cardinal signs,
Immunity neutrophils, macrophages, fever (IL-1, IL-6, TNF-α),
Type I-IV hypersensitivity, immunoglobulins
Fluid, Electrolyte, and Na⁺/K⁺-ATPase, hyponatremia, hyperkalemia, metabolic
Acid-Base Balance acidosis/alkalosis, respiratory acidosis/alkalosis, anion
gap, compensatory mechanisms
Cardiovascular HFpEF vs. HFrEF, left vs. right-sided heart failure,
Pathophysiology myocardial infarction, coronary artery occlusion,
cardiac biomarkers (troponin), hypertension, LVH,
pulmonary embolism
Pulmonary COPD, chronic bronchitis, emphysema, respiratory
Pathophysiology acidosis, pneumonia, tuberculosis, tension
pneumothorax, ARDS, V/Q mismatch
, Renal and Urinary AKI (prerenal, intrinsic, postrenal), CKD, erythropoietin,
Tract anemia, nephrotic syndrome, BUN/Cr ratio, oliguria
Pathophysiology
Endocrine and Type 1 vs. Type 2 diabetes, DKA, hyperthyroidism,
Metabolic Disorders Cushing's syndrome, Addison's disease, cortisol,
hyperparathyroidism
Neurologic Ischemic stroke, Alzheimer disease, Parkinson disease,
Pathophysiology multiple sclerosis, Wernicke encephalopathy, Bell
palsy, seizures
Gastrointestinal and Hepatic encephalopathy, cirrhosis, peptic ulcer
Hepatobiliary disease, NSAIDs, Crohn's disease, ulcerative colitis,
pancreatitis, cholecystitis, Barrett esophagus
Hematology and Iron-deficiency anemia, B12 deficiency, sickle cell
Oncology disease, polycythemia vera, Hodgkin lymphoma,
multiple myeloma, febrile neutropenia, ITP
CELLULAR ADAPTATION, INJURY, AND DEATH
1. A 62-year-old male with chronic heart failure presents with worsening dyspnea,
jugular venous distension, and peripheral edema. What cellular adaptation is most
likely occurring in his myocardium as a compensatory mechanism?
Answer: Hypertrophy
Hypertrophy is an increase in cell size due to increased workload, as seen in heart failure
where myocytes enlarge to compensate for pressure or volume overload. Hyperplasia
(increase in cell number) is not typical in terminally differentiated cardiac muscle. Metaplasia
is replacement of one cell type with another. Dysplasia is disordered cellular growth, often
preneoplastic .
2. During ischemia, the switch from aerobic to anaerobic metabolism leads to which
immediate intracellular change?
Answer: Accumulation of lactic acid
Anaerobic metabolism produces lactic acid, causing intracellular acidosis and impaired
cellular function. ATP production decreases, not increases. Intracellular pH decreases,
sodium accumulates due to Na⁺/K⁺-ATPase pump failure, and lactic acid accumulation
contributes to cell injury .
, 3. A cell adapts to a decreased workload by decreasing in size. This process is
called:
Answer: Atrophy
Atrophy is a decrease in cell size due to reduced workload, denervation, decreased blood
supply, or inadequate nutrition. It is a reversible adaptation if the stimulus is removed .
4. Chronic exposure to gastric acid in the lower esophagus causes the normal
stratified squamous epithelium to change to columnar epithelium. This change is
called:
Answer: Metaplasia
Metaplasia is the reversible replacement of one differentiated cell type with another (e.g.,
Barrett esophagus — squamous to columnar). Dysplasia is disordered growth; anaplasia is
loss of differentiation in cancer .
5. A pathologist examining a myocardial infarction under the microscope notes
preserved tissue architecture with loss of nuclei and eosinophilic cytoplasm. What
type of necrosis is this?
Answer: Coagulative necrosis
Coagulative necrosis (typical of ischemic injury in solid organs like heart, kidney, liver)
preserves tissue outline but shows nuclear loss and increased cytoplasmic eosinophilia.
Liquefactive necrosis occurs in the brain. Caseous necrosis is associated with tuberculosis .
6. Which type of necrosis is classically associated with tuberculosis and appears as
"cheesy" on gross examination?
Answer: Caseous necrosis
Caseous necrosis (e.g., TB, fungal infections) has a friable, granular, cheese-like
appearance. It is a form of coagulative necrosis with extensive destruction of tissue
architecture .
7. A patient with pancreatitis develops chalky white deposits in the peritoneum. This
represents which type of necrosis?
Answer: Fat necrosis
Fat necrosis occurs when pancreatic lipase breaks down triglycerides into free fatty acids,
which combine with calcium (saponification) forming chalky-white deposits .
8. A patient presents with a brain infarct following a stroke. What type of necrosis is
expected in the brain tissue?
