NSG530 Advanced Pathophysiology
Exam 1 – 300 Questions (2026/2027)
Latest 2026/2027 Edition – Wilkes University – 100% Correct Answers
300 real exam-style questions · Full rationales · Why wrong explanations · 2026/2027 updated
Abstract: This comprehensive NSG530 Advanced Pathophysiology Exam 1 review contains 300
practice questions that mirror the actual Wilkes University exam in content, difficulty, and
structure. Each question is paired with a verified correct answer, a detailed rationale, and a "Why
Wrong" breakdown for every incorrect option. Updated for the 2026/2027 academic year, this
guide is designed to help graduate nursing students achieve a high score and pass the NSG530
Exam 1 with confidence. The questions cover all major content areas tested on the exam,
including cellular adaptation and injury, inflammation and immunity, genetics and genetic
disorders, fluid and electrolyte imbalances, acid-base disorders, cardiovascular pathophysiology,
respiratory pathophysiology, renal pathophysiology, endocrine pathophysiology, and
neurological pathophysiology.
Written by GradPathoExpert, DNP, APRN – 15 years Graduate Nursing Educator
Wilkes NSG530 Exam 1: 100% | Verified: 2026/2027 Academic Year
Section Questions Weight
Cellular Adaptation, Injury & Death 40 13%
Inflammation & Immunity 40 13%
Genetics & Congenital Disorders 30 10%
Fluid, Electrolyte & Acid-Base Balance 40 13%
Cardiovascular Pathophysiology 40 13%
Respiratory Pathophysiology 30 10%
Renal Pathophysiology 25 8%
,Section Questions Weight
Endocrine Pathophysiology 25 8%
Neurological Pathophysiology 20 7%
Hematologic & Neoplastic Pathophysiology 10 3%
Content Overview
Cellular Adaptation, Injury & Death (40 Qs - 13%): Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia,
necrosis types (coagulative, liquefactive, caseous, fat, gangrenous), apoptosis, ischemia, hypoxia, cellular swelling,
fatty change, free radical injury, amyloidosis, calcification.
Inflammation & Immunity (40 Qs - 13%): Acute vs chronic inflammation, vascular and cellular phases, chemical
mediators (histamine, prostaglandins, leukotrienes, cytokines), hypersensitivity reactions Type I-IV, autoimmune
disorders (SLE, RA, MS, T1DM), immunodeficiencies (HIV/AIDS), transplant rejection, tumor immunity.
Genetics & Congenital Disorders (30 Qs - 10%): Autosomal dominant/recessive inheritance, X-linked disorders,
chromosomal abnormalities (Down syndrome, Turner, Klinefelter), multifactorial inheritance, single-gene disorders
(cystic fibrosis, Huntington's, hemophilia, Marfan syndrome, BRCA mutations), mitochondrial inheritance.
Fluid, Electrolyte & Acid-Base Balance (40 Qs - 13%): Dehydration, overhydration, edema, Starling's forces,
hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypomagnesemia,
hypermagnesemia, metabolic acidosis/alkalosis, respiratory acidosis/alkalosis, compensation mechanisms, anion
gap, osmolality.
Cardiovascular Pathophysiology (40 Qs - 13%): Hypertension (primary/secondary), atherosclerosis, coronary
artery disease, angina (stable/unstable/variant), myocardial infarction, heart failure (systolic/diastolic, left/right),
arrhythmias (atrial fibrillation, ventricular tachycardia, heart blocks), valvular disorders (stenosis/regurgitation),
endocarditis, pericarditis, shock (hypovolemic, cardiogenic, septic, anaphylactic, neurogenic).
Respiratory Pathophysiology (30 Qs - 10%): COPD (emphysema, chronic bronchitis), asthma (allergic/non-
allergic), pneumonia (bacterial/viral/aspiration), pulmonary embolism, pulmonary hypertension, ARDS,
tuberculosis, cystic fibrosis, lung cancer (SCLC, NSCLC), pleural effusion, pneumothorax.
Renal Pathophysiology (25 Qs - 8%): Acute kidney injury (prerenal, intrarenal, postrenal), chronic kidney disease
(stages 1-5), glomerulonephritis (acute, chronic), nephrotic syndrome, pyelonephritis, nephrolithiasis, urinary tract
obstruction, renal tubular acidosis, polycystic kidney disease.
Endocrine Pathophysiology (25 Qs - 8%): Diabetes mellitus Type 1 vs Type 2, diabetic ketoacidosis (DKA),
hyperosmolar hyperglycemic state (HHS), hypoglycemia, thyroid disorders (Graves' disease, Hashimoto's
thyroiditis, goiter, myxedema), adrenal disorders (Addison's disease, Cushing syndrome, pheochromocytoma),
pituitary disorders (diabetes insipidus, SIADH, acromegaly).
Neurological Pathophysiology (20 Qs - 7%): Stroke (ischemic vs hemorrhagic), transient ischemic attack (TIA),
seizures and epilepsy, Alzheimer's disease, Parkinson's disease, multiple sclerosis, meningitis, encephalitis,
traumatic brain injury, spinal cord injury, Guillain-Barré syndrome.
Hematologic & Neoplastic Pathophysiology (10 Qs - 3%): Anemias (iron deficiency, B12/folate deficiency,
pernicious, aplastic, hemolytic, sickle cell, thalassemia), leukemias (ALL, AML, CLL, CML), lymphomas (Hodgkin's,
non-Hodgkin's), coagulopathies (hemophilia, DIC, von Willebrand disease), carcinogenesis (oncogenes, tumor
suppressor genes, metastasis, angiogenesis).
,Cellular Adaptation, Injury & Death (40 questions)
Q1. A patient with chronic alcohol abuse develops liver damage characterized by
accumulation of fat within hepatocytes. This cellular adaptation is best described as:
A Hypertrophy
B Hyperplasia
C Metaplasia
D Fatty change (steatosis)
E Dysplasia
Correct answer: D. Fatty change (steatosis)
Rationale: Fatty change (steatosis) is the accumulation of triglycerides within parenchymal
cells, often due to chronic alcohol abuse, diabetes, or obesity. Alcohol metabolism produces
NADH, which promotes lipogenesis and inhibits fatty acid oxidation. This is a reversible
cellular adaptation.
Why wrong:
A: Hypertrophy is an increase in cell size.
B: Hyperplasia is an increase in cell number.
C: Metaplasia is a replacement of one cell type with another.
E: Dysplasia is disordered cell growth.
Reference: McCance & Huether's Pathophysiology · Porth's Pathophysiology · Wilkes NSG530
Course Materials
, Q2. Which type of necrosis is most commonly associated with tuberculosis and is
characterized by a cheese-like appearance?
A Coagulative necrosis
B Liquefactive necrosis
C Caseous necrosis
D Fat necrosis
E Gangrenous necrosis
Correct answer: C. Caseous necrosis
Rationale: Caseous necrosis is a form of necrosis associated with tuberculosis and some
fungal infections. The tissue has a cheese-like (caseous) appearance and is surrounded by
granulomatous inflammation. It represents a combination of coagulative and liquefactive
necrosis.
Why wrong:
A: Coagulative necrosis is associated with ischemia (e.g., MI).
B: Liquefactive necrosis is associated with brain infarcts and abscesses.
D: Fat necrosis is associated with pancreatitis and breast trauma.
E: Gangrenous necrosis is associated with ischemia of extremities.
Reference: McCance & Huether's Pathophysiology · Porth's Pathophysiology · Wilkes NSG530
Course Materials
Exam 1 – 300 Questions (2026/2027)
Latest 2026/2027 Edition – Wilkes University – 100% Correct Answers
300 real exam-style questions · Full rationales · Why wrong explanations · 2026/2027 updated
Abstract: This comprehensive NSG530 Advanced Pathophysiology Exam 1 review contains 300
practice questions that mirror the actual Wilkes University exam in content, difficulty, and
structure. Each question is paired with a verified correct answer, a detailed rationale, and a "Why
Wrong" breakdown for every incorrect option. Updated for the 2026/2027 academic year, this
guide is designed to help graduate nursing students achieve a high score and pass the NSG530
Exam 1 with confidence. The questions cover all major content areas tested on the exam,
including cellular adaptation and injury, inflammation and immunity, genetics and genetic
disorders, fluid and electrolyte imbalances, acid-base disorders, cardiovascular pathophysiology,
respiratory pathophysiology, renal pathophysiology, endocrine pathophysiology, and
neurological pathophysiology.
Written by GradPathoExpert, DNP, APRN – 15 years Graduate Nursing Educator
Wilkes NSG530 Exam 1: 100% | Verified: 2026/2027 Academic Year
Section Questions Weight
Cellular Adaptation, Injury & Death 40 13%
Inflammation & Immunity 40 13%
Genetics & Congenital Disorders 30 10%
Fluid, Electrolyte & Acid-Base Balance 40 13%
Cardiovascular Pathophysiology 40 13%
Respiratory Pathophysiology 30 10%
Renal Pathophysiology 25 8%
,Section Questions Weight
Endocrine Pathophysiology 25 8%
Neurological Pathophysiology 20 7%
Hematologic & Neoplastic Pathophysiology 10 3%
Content Overview
Cellular Adaptation, Injury & Death (40 Qs - 13%): Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia,
necrosis types (coagulative, liquefactive, caseous, fat, gangrenous), apoptosis, ischemia, hypoxia, cellular swelling,
fatty change, free radical injury, amyloidosis, calcification.
Inflammation & Immunity (40 Qs - 13%): Acute vs chronic inflammation, vascular and cellular phases, chemical
mediators (histamine, prostaglandins, leukotrienes, cytokines), hypersensitivity reactions Type I-IV, autoimmune
disorders (SLE, RA, MS, T1DM), immunodeficiencies (HIV/AIDS), transplant rejection, tumor immunity.
Genetics & Congenital Disorders (30 Qs - 10%): Autosomal dominant/recessive inheritance, X-linked disorders,
chromosomal abnormalities (Down syndrome, Turner, Klinefelter), multifactorial inheritance, single-gene disorders
(cystic fibrosis, Huntington's, hemophilia, Marfan syndrome, BRCA mutations), mitochondrial inheritance.
Fluid, Electrolyte & Acid-Base Balance (40 Qs - 13%): Dehydration, overhydration, edema, Starling's forces,
hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypomagnesemia,
hypermagnesemia, metabolic acidosis/alkalosis, respiratory acidosis/alkalosis, compensation mechanisms, anion
gap, osmolality.
Cardiovascular Pathophysiology (40 Qs - 13%): Hypertension (primary/secondary), atherosclerosis, coronary
artery disease, angina (stable/unstable/variant), myocardial infarction, heart failure (systolic/diastolic, left/right),
arrhythmias (atrial fibrillation, ventricular tachycardia, heart blocks), valvular disorders (stenosis/regurgitation),
endocarditis, pericarditis, shock (hypovolemic, cardiogenic, septic, anaphylactic, neurogenic).
Respiratory Pathophysiology (30 Qs - 10%): COPD (emphysema, chronic bronchitis), asthma (allergic/non-
allergic), pneumonia (bacterial/viral/aspiration), pulmonary embolism, pulmonary hypertension, ARDS,
tuberculosis, cystic fibrosis, lung cancer (SCLC, NSCLC), pleural effusion, pneumothorax.
Renal Pathophysiology (25 Qs - 8%): Acute kidney injury (prerenal, intrarenal, postrenal), chronic kidney disease
(stages 1-5), glomerulonephritis (acute, chronic), nephrotic syndrome, pyelonephritis, nephrolithiasis, urinary tract
obstruction, renal tubular acidosis, polycystic kidney disease.
Endocrine Pathophysiology (25 Qs - 8%): Diabetes mellitus Type 1 vs Type 2, diabetic ketoacidosis (DKA),
hyperosmolar hyperglycemic state (HHS), hypoglycemia, thyroid disorders (Graves' disease, Hashimoto's
thyroiditis, goiter, myxedema), adrenal disorders (Addison's disease, Cushing syndrome, pheochromocytoma),
pituitary disorders (diabetes insipidus, SIADH, acromegaly).
Neurological Pathophysiology (20 Qs - 7%): Stroke (ischemic vs hemorrhagic), transient ischemic attack (TIA),
seizures and epilepsy, Alzheimer's disease, Parkinson's disease, multiple sclerosis, meningitis, encephalitis,
traumatic brain injury, spinal cord injury, Guillain-Barré syndrome.
Hematologic & Neoplastic Pathophysiology (10 Qs - 3%): Anemias (iron deficiency, B12/folate deficiency,
pernicious, aplastic, hemolytic, sickle cell, thalassemia), leukemias (ALL, AML, CLL, CML), lymphomas (Hodgkin's,
non-Hodgkin's), coagulopathies (hemophilia, DIC, von Willebrand disease), carcinogenesis (oncogenes, tumor
suppressor genes, metastasis, angiogenesis).
,Cellular Adaptation, Injury & Death (40 questions)
Q1. A patient with chronic alcohol abuse develops liver damage characterized by
accumulation of fat within hepatocytes. This cellular adaptation is best described as:
A Hypertrophy
B Hyperplasia
C Metaplasia
D Fatty change (steatosis)
E Dysplasia
Correct answer: D. Fatty change (steatosis)
Rationale: Fatty change (steatosis) is the accumulation of triglycerides within parenchymal
cells, often due to chronic alcohol abuse, diabetes, or obesity. Alcohol metabolism produces
NADH, which promotes lipogenesis and inhibits fatty acid oxidation. This is a reversible
cellular adaptation.
Why wrong:
A: Hypertrophy is an increase in cell size.
B: Hyperplasia is an increase in cell number.
C: Metaplasia is a replacement of one cell type with another.
E: Dysplasia is disordered cell growth.
Reference: McCance & Huether's Pathophysiology · Porth's Pathophysiology · Wilkes NSG530
Course Materials
, Q2. Which type of necrosis is most commonly associated with tuberculosis and is
characterized by a cheese-like appearance?
A Coagulative necrosis
B Liquefactive necrosis
C Caseous necrosis
D Fat necrosis
E Gangrenous necrosis
Correct answer: C. Caseous necrosis
Rationale: Caseous necrosis is a form of necrosis associated with tuberculosis and some
fungal infections. The tissue has a cheese-like (caseous) appearance and is surrounded by
granulomatous inflammation. It represents a combination of coagulative and liquefactive
necrosis.
Why wrong:
A: Coagulative necrosis is associated with ischemia (e.g., MI).
B: Liquefactive necrosis is associated with brain infarcts and abscesses.
D: Fat necrosis is associated with pancreatitis and breast trauma.
E: Gangrenous necrosis is associated with ischemia of extremities.
Reference: McCance & Huether's Pathophysiology · Porth's Pathophysiology · Wilkes NSG530
Course Materials
