WILKES | ADVANCED PATHOPHYSIOLOGY | EXAM 1 | 2026/2027 UPDATE
NSG 530 EXAM 1
ADVANCED PATHOPHYSIOLOGY
WILKES 2026/2027
Comprehensive Study Quiz 2026/2027 UPDATE | Wilkes University
EXAM 1 ADV PATHO WILKES 2026/2027 UPDATE
, EXAM COVERAGE AREAS
Advanced Pathophysiology - Exam 1 Domains | NSG 530 Wilkes | 2026/2027 Update
Cellular Biology, Genetics & Fluid Electrolytes
• Cellular injury: hypoxia, free radicals, apoptosis vs necrosis
• Genetics: Mendelian, autosomal dominant/recessive, X-linked, epigenetics
• Fluid & electrolytes: Na, K, Ca, Mg, Phos - regulation & imbalances
• Acid-base: metabolic acidosis/alkalosis, respiratory, ABG interpretation
Inflammation, Immunity & Infection
• Acute vs chronic inflammation: mediators, cardinal signs, healing
• Innate vs adaptive immunity: B cells, T cells, antibodies, complement
• Hypersensitivity: Type I-IV, autoimmunity, immunodeficiency
• Infection: bacterial, viral mechanisms, sepsis pathophysiology
Cardiovascular & Hematologic Pathophysiology
• HTN, atherosclerosis, CAD, MI: plaque rupture, ischemia-reperfusion
• Heart failure: systolic vs diastolic, left vs right, compensation
• Shock: cardiogenic, hypovolemic, distributive, obstructive - stages
• Anemia, coagulation disorders, leukemia basics
Pulmonary & Renal Pathophysiology
• Ventilation/perfusion mismatch, hypoxemia mechanisms
• Obstructive vs restrictive lung diseases: asthma, COPD, pulmonary edema
• AKI vs CKD: prerenal, intrinsic, postrenal, GFR, azotemia
• Glomerular disorders, nephrotic vs nephritic
Neurologic & Endocrine Pathophysiology
• Intracranial pressure, cerebral edema, herniation
• Stroke: ischemic vs hemorrhagic, seizure pathophysiology
• Diabetes: Type 1 vs Type 2, DKA vs HHS, metabolic syndrome
• Thyroid, adrenal, pituitary disorders - feedback loops
Musculoskeletal, GI & Exam 1 High-Yield
• Stress response: Selye GAS, HPA axis
• Pain: nociceptive vs neuropathic, gate control
• GI: liver failure, portal HTN, pancreatitis basics
• 2026/2027 Wilkes Exam 1 high-yield: cellular adaptation, inheritance patterns
NSG 530 Exam 1 Wilkes Advanced Pathophysiology 2026/2027 | Comprehensive Study Quiz Page 2
, QUESTION 1: NSG 530: What is difference between apoptosis and necrosis?
A) Apoptosis programmed cell death, neat, no inflammation; Necrosis uncontrolled cell death from
injury, inflammation present
B) Same thing
C) Apoptosis always pathological
D) Necrosis always programmed
CORRECT ANSWER: A) Apoptosis programmed cell death, neat, no inflammation;
Necrosis uncontrolled cell death from injury, inflammation present
RATIONALE: Apoptosis: programmed, physiologic or pathologic, cell shrinkage, chromatin condensation,
apoptotic bodies, no inflammation, caspases. Necrosis: pathologic from injury hypoxia toxins, cell swelling,
membrane rupture, inflammation, types coagulative, liquefactive, caseous, fat, fibrinoid.
QUESTION 2: ABG: pH 7.30, PaCO2 50, HCO3 24 - interpretation?
A) Respiratory acidosis - pH low, PaCO2 high, HCO3 normal acute
B) Metabolic acidosis
C) Respiratory alkalosis
D) Normal ABG
CORRECT ANSWER: A) Respiratory acidosis - pH low, PaCO2 high, HCO3 normal acute
RATIONALE: ABG interpretation: pH 7.35-7.45 normal, pH <7.35 acidosis, >7.45 alkalosis. Respiratory
opposite pH and PaCO2. Metabolic same direction pH and HCO3. This pH 7.30 low, PaCO2 50 high
(normal 35-45) respiratory acidosis - hypoventilation, COPD, respiratory depression.
QUESTION 3: Type II hypersensitivity example?
A) Hemolytic transfusion reaction, Goodpasture syndrome - IgG/IgM against cell surface antigens
B) Anaphylaxis
C) Serum sickness
D) Contact dermatitis
CORRECT ANSWER: A) Hemolytic transfusion reaction, Goodpasture syndrome -
IgG/IgM against cell surface antigens
RATIONALE: Hypersensitivity: Type I IgE mediated anaphylaxis, allergic rhinitis. Type II cytotoxic IgG/IgM
against cell surface hemolytic transfusion, Goodpasture, myasthenia gravis. Type III immune complex
serum sickness, SLE. Type IV delayed T cell contact dermatitis, TB test.
QUESTION 4: Left heart failure vs right heart failure pathophysiology?
A) Left HF: pulmonary congestion dyspnea crackles, decreased CO; Right HF: systemic congestion
JVD edema hepatomegaly due to backup
B) Same symptoms
C) Only right causes pulmonary edema
D) Only left causes peripheral edema
CORRECT ANSWER: A) Left HF: pulmonary congestion dyspnea crackles, decreased
CO; Right HF: systemic congestion JVD edema hepatomegaly due to backup
RATIONALE: Left HF: impaired LV pumping causes pulmonary congestion - dyspnea orthopnea PND
crackles. Right HF: impaired RV causes systemic congestion JVD peripheral edema hepatomegaly ascites.
Often left leads to right. Systolic HF reduced EF <40% impaired contractility; diastolic HF preserved EF
NSG 530 Exam 1 Wilkes Advanced Pathophysiology 2026/2027 | Comprehensive Study Quiz Page 3
, impaired relaxation.
QUESTION 5: DKA vs HHS pathophysiology differentiation?
A) DKA: Type 1 absolute insulin deficiency, hyperglycemia >250, ketosis, acidosis pH <7.3,
Kussmaul; HHS Type 2 relative deficiency, glucose >600, no ketosis, more dehydration, osm >320
B) Same condition
C) DKA only Type 2
D) HHS always has ketosis
CORRECT ANSWER: A) DKA: Type 1 absolute insulin deficiency, hyperglycemia >250,
ketosis, acidosis pH <7.3, Kussmaul; HHS Type 2 relative deficiency, glucose >600, no
ketosis, more dehydration, osm >320
RATIONALE: DKA: Type 1 absolute insulin lack, hyperglycemia >250, ketosis from lipolysis, metabolic
acidosis pH <7.3 HCO3 <15, Kussmaul respirations. HHS Type 2 relative deficiency, glucose >600,
no/minimal ketosis, severe dehydration hyperosmolarity >320, altered mental status. Both triggered by
infection, noncompliance.
QUESTION 6: What causes increased intracranial pressure ICP?
A) Hematoma, edema, hydrocephalus, tumor increase volume in rigid skull - Monroe-Kellie doctrine
B) Only low BP
C) Only anemia
D) No cause
CORRECT ANSWER: A) Hematoma, edema, hydrocephalus, tumor increase volume in
rigid skull - Monroe-Kellie doctrine
RATIONALE: ICP normal 5-15 mmHg. Monroe-Kellie: skull rigid, increase in one component blood, brain,
CSF must decrease in another or ICP rises. Causes hematoma, edema, hydrocephalus, tumor. Cushing
triad late sign increased ICP: bradycardia, hypertension widened pulse pressure, irregular respirations.
QUESTION 7: NSG 530: What is difference between apoptosis and necrosis?
A) Apoptosis programmed cell death, neat, no inflammation; Necrosis uncontrolled cell death from
injury, inflammation present
B) Same thing
C) Apoptosis always pathological
D) Necrosis always programmed
CORRECT ANSWER: A) Apoptosis programmed cell death, neat, no inflammation;
Necrosis uncontrolled cell death from injury, inflammation present
RATIONALE: Apoptosis: programmed, physiologic or pathologic, cell shrinkage, chromatin condensation,
apoptotic bodies, no inflammation, caspases. Necrosis: pathologic from injury hypoxia toxins, cell swelling,
membrane rupture, inflammation, types coagulative, liquefactive, caseous, fat, fibrinoid.
QUESTION 8: ABG: pH 7.30, PaCO2 50, HCO3 24 - interpretation?
A) Respiratory acidosis - pH low, PaCO2 high, HCO3 normal acute
B) Metabolic acidosis
C) Respiratory alkalosis
D) Normal ABG
NSG 530 Exam 1 Wilkes Advanced Pathophysiology 2026/2027 | Comprehensive Study Quiz Page 4
NSG 530 EXAM 1
ADVANCED PATHOPHYSIOLOGY
WILKES 2026/2027
Comprehensive Study Quiz 2026/2027 UPDATE | Wilkes University
EXAM 1 ADV PATHO WILKES 2026/2027 UPDATE
, EXAM COVERAGE AREAS
Advanced Pathophysiology - Exam 1 Domains | NSG 530 Wilkes | 2026/2027 Update
Cellular Biology, Genetics & Fluid Electrolytes
• Cellular injury: hypoxia, free radicals, apoptosis vs necrosis
• Genetics: Mendelian, autosomal dominant/recessive, X-linked, epigenetics
• Fluid & electrolytes: Na, K, Ca, Mg, Phos - regulation & imbalances
• Acid-base: metabolic acidosis/alkalosis, respiratory, ABG interpretation
Inflammation, Immunity & Infection
• Acute vs chronic inflammation: mediators, cardinal signs, healing
• Innate vs adaptive immunity: B cells, T cells, antibodies, complement
• Hypersensitivity: Type I-IV, autoimmunity, immunodeficiency
• Infection: bacterial, viral mechanisms, sepsis pathophysiology
Cardiovascular & Hematologic Pathophysiology
• HTN, atherosclerosis, CAD, MI: plaque rupture, ischemia-reperfusion
• Heart failure: systolic vs diastolic, left vs right, compensation
• Shock: cardiogenic, hypovolemic, distributive, obstructive - stages
• Anemia, coagulation disorders, leukemia basics
Pulmonary & Renal Pathophysiology
• Ventilation/perfusion mismatch, hypoxemia mechanisms
• Obstructive vs restrictive lung diseases: asthma, COPD, pulmonary edema
• AKI vs CKD: prerenal, intrinsic, postrenal, GFR, azotemia
• Glomerular disorders, nephrotic vs nephritic
Neurologic & Endocrine Pathophysiology
• Intracranial pressure, cerebral edema, herniation
• Stroke: ischemic vs hemorrhagic, seizure pathophysiology
• Diabetes: Type 1 vs Type 2, DKA vs HHS, metabolic syndrome
• Thyroid, adrenal, pituitary disorders - feedback loops
Musculoskeletal, GI & Exam 1 High-Yield
• Stress response: Selye GAS, HPA axis
• Pain: nociceptive vs neuropathic, gate control
• GI: liver failure, portal HTN, pancreatitis basics
• 2026/2027 Wilkes Exam 1 high-yield: cellular adaptation, inheritance patterns
NSG 530 Exam 1 Wilkes Advanced Pathophysiology 2026/2027 | Comprehensive Study Quiz Page 2
, QUESTION 1: NSG 530: What is difference between apoptosis and necrosis?
A) Apoptosis programmed cell death, neat, no inflammation; Necrosis uncontrolled cell death from
injury, inflammation present
B) Same thing
C) Apoptosis always pathological
D) Necrosis always programmed
CORRECT ANSWER: A) Apoptosis programmed cell death, neat, no inflammation;
Necrosis uncontrolled cell death from injury, inflammation present
RATIONALE: Apoptosis: programmed, physiologic or pathologic, cell shrinkage, chromatin condensation,
apoptotic bodies, no inflammation, caspases. Necrosis: pathologic from injury hypoxia toxins, cell swelling,
membrane rupture, inflammation, types coagulative, liquefactive, caseous, fat, fibrinoid.
QUESTION 2: ABG: pH 7.30, PaCO2 50, HCO3 24 - interpretation?
A) Respiratory acidosis - pH low, PaCO2 high, HCO3 normal acute
B) Metabolic acidosis
C) Respiratory alkalosis
D) Normal ABG
CORRECT ANSWER: A) Respiratory acidosis - pH low, PaCO2 high, HCO3 normal acute
RATIONALE: ABG interpretation: pH 7.35-7.45 normal, pH <7.35 acidosis, >7.45 alkalosis. Respiratory
opposite pH and PaCO2. Metabolic same direction pH and HCO3. This pH 7.30 low, PaCO2 50 high
(normal 35-45) respiratory acidosis - hypoventilation, COPD, respiratory depression.
QUESTION 3: Type II hypersensitivity example?
A) Hemolytic transfusion reaction, Goodpasture syndrome - IgG/IgM against cell surface antigens
B) Anaphylaxis
C) Serum sickness
D) Contact dermatitis
CORRECT ANSWER: A) Hemolytic transfusion reaction, Goodpasture syndrome -
IgG/IgM against cell surface antigens
RATIONALE: Hypersensitivity: Type I IgE mediated anaphylaxis, allergic rhinitis. Type II cytotoxic IgG/IgM
against cell surface hemolytic transfusion, Goodpasture, myasthenia gravis. Type III immune complex
serum sickness, SLE. Type IV delayed T cell contact dermatitis, TB test.
QUESTION 4: Left heart failure vs right heart failure pathophysiology?
A) Left HF: pulmonary congestion dyspnea crackles, decreased CO; Right HF: systemic congestion
JVD edema hepatomegaly due to backup
B) Same symptoms
C) Only right causes pulmonary edema
D) Only left causes peripheral edema
CORRECT ANSWER: A) Left HF: pulmonary congestion dyspnea crackles, decreased
CO; Right HF: systemic congestion JVD edema hepatomegaly due to backup
RATIONALE: Left HF: impaired LV pumping causes pulmonary congestion - dyspnea orthopnea PND
crackles. Right HF: impaired RV causes systemic congestion JVD peripheral edema hepatomegaly ascites.
Often left leads to right. Systolic HF reduced EF <40% impaired contractility; diastolic HF preserved EF
NSG 530 Exam 1 Wilkes Advanced Pathophysiology 2026/2027 | Comprehensive Study Quiz Page 3
, impaired relaxation.
QUESTION 5: DKA vs HHS pathophysiology differentiation?
A) DKA: Type 1 absolute insulin deficiency, hyperglycemia >250, ketosis, acidosis pH <7.3,
Kussmaul; HHS Type 2 relative deficiency, glucose >600, no ketosis, more dehydration, osm >320
B) Same condition
C) DKA only Type 2
D) HHS always has ketosis
CORRECT ANSWER: A) DKA: Type 1 absolute insulin deficiency, hyperglycemia >250,
ketosis, acidosis pH <7.3, Kussmaul; HHS Type 2 relative deficiency, glucose >600, no
ketosis, more dehydration, osm >320
RATIONALE: DKA: Type 1 absolute insulin lack, hyperglycemia >250, ketosis from lipolysis, metabolic
acidosis pH <7.3 HCO3 <15, Kussmaul respirations. HHS Type 2 relative deficiency, glucose >600,
no/minimal ketosis, severe dehydration hyperosmolarity >320, altered mental status. Both triggered by
infection, noncompliance.
QUESTION 6: What causes increased intracranial pressure ICP?
A) Hematoma, edema, hydrocephalus, tumor increase volume in rigid skull - Monroe-Kellie doctrine
B) Only low BP
C) Only anemia
D) No cause
CORRECT ANSWER: A) Hematoma, edema, hydrocephalus, tumor increase volume in
rigid skull - Monroe-Kellie doctrine
RATIONALE: ICP normal 5-15 mmHg. Monroe-Kellie: skull rigid, increase in one component blood, brain,
CSF must decrease in another or ICP rises. Causes hematoma, edema, hydrocephalus, tumor. Cushing
triad late sign increased ICP: bradycardia, hypertension widened pulse pressure, irregular respirations.
QUESTION 7: NSG 530: What is difference between apoptosis and necrosis?
A) Apoptosis programmed cell death, neat, no inflammation; Necrosis uncontrolled cell death from
injury, inflammation present
B) Same thing
C) Apoptosis always pathological
D) Necrosis always programmed
CORRECT ANSWER: A) Apoptosis programmed cell death, neat, no inflammation;
Necrosis uncontrolled cell death from injury, inflammation present
RATIONALE: Apoptosis: programmed, physiologic or pathologic, cell shrinkage, chromatin condensation,
apoptotic bodies, no inflammation, caspases. Necrosis: pathologic from injury hypoxia toxins, cell swelling,
membrane rupture, inflammation, types coagulative, liquefactive, caseous, fat, fibrinoid.
QUESTION 8: ABG: pH 7.30, PaCO2 50, HCO3 24 - interpretation?
A) Respiratory acidosis - pH low, PaCO2 high, HCO3 normal acute
B) Metabolic acidosis
C) Respiratory alkalosis
D) Normal ABG
NSG 530 Exam 1 Wilkes Advanced Pathophysiology 2026/2027 | Comprehensive Study Quiz Page 4
