ADVANCED PATHOPHYSIOLOGY | EXAM 2 | 2026/2027 LATEST UPDATE
NSG 530 EXAM 2
ADVANCED PATHOPHYSIOLOGY
QUIZ 2026/2027
Comprehensive Study Quiz 2026/2027 LATEST UPDATE | Wilkes University
EXAM 2 ADV PATHO WILKES 2026/2027 LATEST
, EXAM COVERAGE AREAS
Advanced Pathophysiology - Exam 2 Domains | NSG 530 | 2026/2027 LATEST
Cardiovascular II - Advanced Cardiac Pathophysiology
• Coronary artery disease: stable angina vs unstable vs MI - plaque progression
• Valvular disorders: stenosis vs regurgitation pathophysiology
• Cardiomyopathy: dilated, hypertrophic, restrictive
• Pericardial disease, infective endocarditis pathophysiology
Pulmonary II - Advanced Pulmonary Pathophysiology
• Pulmonary hypertension: WHO groups, pathophysiology
• ARDS: Berlin criteria, diffuse alveolar damage
• Pulmonary embolism: Virchow triad, hemodynamic consequences
• Lung cancer & pleural effusion pathophysiology
Renal & Urologic Pathophysiology Advanced
• Glomerulonephritis vs nephrotic syndrome: proteinuria, hematuria
• Tubular disorders: ATN, interstitial nephritis
• Urolithiasis, UTI, BPH pathophysiology
• Electrolyte disorders advanced: hyper/hyponatremia, hyper/hypokalemia mechanisms
Gastrointestinal & Hepatobiliary Advanced
• GERD, peptic ulcer, IBD Crohn vs ulcerative colitis
• Liver: hepatitis, cirrhosis, portal hypertension, hepatic failure
• Pancreatitis: acute vs chronic, gallstones pathophysiology
• Intestinal obstruction, ischemia, malabsorption
Endocrine & Reproductive Advanced
• Pituitary: acromegaly, DI vs SIADH - water balance
• Adrenal: Cushing vs Addison, pheochromocytoma
• Reproductive: PCOS, infertility, menopause pathophysiology
• Metabolic bone disease: osteoporosis pathophysiology
Neurologic, Musculoskeletal & Integration
• Neurodegenerative: Alzheimer, Parkinson, MS, ALS pathophysiology
• Musculoskeletal: RA vs OA, gout, osteoporosis
• Hematologic: clotting disorders DIC, thrombocytopenia
• Integration: multisystem failure, stress, compensatory mechanisms - Exam 2 high-yield
NSG 530 Exam 2 Advanced Pathophysiology Quiz 2026/2027 LATEST UPDATE Page 2
, QUESTION 1: NSG 530 Exam 2: Difference between stable angina and unstable
angina/MI pathophysiology?
A) Stable: fixed plaque, exertional, reversible ischemia. Unstable/MI: plaque rupture, thrombosis,
unstable, may cause infarction
B) Same pathophysiology
C) Stable is plaque rupture
D) Unstable is only exertional
CORRECT ANSWER: A) Stable: fixed plaque, exertional, reversible ischemia.
Unstable/MI: plaque rupture, thrombosis, unstable, may cause infarction
RATIONALE: Stable angina: fixed atherosclerotic plaque >70% stenosis, demand ischemia exertional,
reversible. Unstable angina/NSTEMI/STEMI: plaque rupture, platelet aggregation, thrombosis, partial or
complete occlusion - unstable, may cause necrosis. Troponin elevated in MI.
QUESTION 2: ARDS Berlin criteria pathophysiology?
A) Acute onset within 1 week, bilateral opacities not fully explained by effusion, PaO2/FiO2 <300 with
PEEP, diffuse alveolar damage increased permeability pulmonary edema
B) Only cardiac edema
C) Only unilateral
D) No criteria
CORRECT ANSWER: A) Acute onset within 1 week, bilateral opacities not fully
explained by effusion, PaO2/FiO2 <300 with PEEP, diffuse alveolar damage increased
permeability pulmonary edema
RATIONALE: ARDS: Berlin 2012 acute within 1 week known insult, bilateral opacities, PaO2/FiO2 <300
mmHg with PEEP >=5, not cardiac failure. Patho diffuse alveolar damage, increased alveolar-capillary
permeability, non-cardiogenic pulmonary edema, hyaline membranes, V/Q mismatch.
QUESTION 3: Nephrotic vs nephritic syndrome differentiation?
A) Nephrotic: heavy proteinuria >3.5g/day, hypoalbuminemia, edema, hyperlipidemia, minimal
hematuria. Nephritic: hematuria, HTN, oliguria, mild proteinuria, RBC casts
B) Same syndrome
C) Nephrotic has hematuria always
D) Nephritic has heavy proteinuria >3.5g
CORRECT ANSWER: A) Nephrotic: heavy proteinuria >3.5g/day, hypoalbuminemia,
edema, hyperlipidemia, minimal hematuria. Nephritic: hematuria, HTN, oliguria, mild
proteinuria, RBC casts
RATIONALE: Nephrotic: podocyte injury heavy proteinuria >3.5g/day, hypoalbuminemia, edema,
hyperlipidemia, lipiduria. Causes minimal change, FSGS, membranous. Nephritic: glomerular inflammation
hematuria, HTN, oliguria, azotemia, RBC casts. Causes post-strep GN, IgA nephropathy, lupus nephritis.
QUESTION 4: DI vs SIADH pathophysiology - water balance?
A) DI: ADH deficiency or resistance - polyuria, hypernatremia, dilute urine. SIADH: excess ADH -
water retention, hyponatremia, concentrated urine
B) Same disorder
C) DI causes hyponatremia
NSG 530 Exam 2 Advanced Pathophysiology Quiz 2026/2027 LATEST UPDATE Page 3
, D) SIADH causes hypernatremia
CORRECT ANSWER: A) DI: ADH deficiency or resistance - polyuria, hypernatremia,
dilute urine. SIADH: excess ADH - water retention, hyponatremia, concentrated urine
RATIONALE: DI: ADH deficiency (central) or resistance (nephrogenic) - polyuria 3-20 L/day, polydipsia,
hypernatremia, low urine osmolality, high serum osmolality. SIADH: excess ADH secretion - water retention,
hyponatremia, hypo-osmolality serum, high urine osmolality, euvolemic. Causes: CNS disorders, drugs,
tumors.
QUESTION 5: RA vs OA pathophysiology differentiation?
A) RA: autoimmune synovitis, pannus, symmetric small joints, systemic, inflammatory. OA:
degenerative cartilage wear, asymmetric weight-bearing joints, non-inflammatory
B) Same disease
C) RA is degenerative
D) OA is autoimmune
CORRECT ANSWER: A) RA: autoimmune synovitis, pannus, symmetric small joints,
systemic, inflammatory. OA: degenerative cartilage wear, asymmetric weight-bearing
joints, non-inflammatory
RATIONALE: RA: autoimmune systemic, synovial inflammation pannus formation, symmetric small joints
MCP PIP, morning stiffness >1 hr, RF anti-CCP, systemic features. OA: degenerative cartilage loss, bone
spurs, asymmetric weight-bearing hips knees, Heberden Bouchard nodes, morning stiffness <30 min,
non-inflammatory.
QUESTION 6: Virchow triad for PE/DVT?
A) Stasis, endothelial injury, hypercoagulability - all increase clot risk
B) Only stasis
C) Only injury
D) Only hypercoagulability
CORRECT ANSWER: A) Stasis, endothelial injury, hypercoagulability - all increase clot
risk
RATIONALE: Virchow triad: venous stasis (immobility, HF), endothelial injury (trauma, surgery, central line),
hypercoagulability (factor V Leiden, OCP, cancer, pregnancy). PE pathophysiology clot lodges pulmonary
artery increases dead space, V/Q mismatch, increased pulmonary vascular resistance, RV strain.
QUESTION 7: NSG 530 Exam 2: Difference between stable angina and unstable
angina/MI pathophysiology?
A) Stable: fixed plaque, exertional, reversible ischemia. Unstable/MI: plaque rupture, thrombosis,
unstable, may cause infarction
B) Same pathophysiology
C) Stable is plaque rupture
D) Unstable is only exertional
CORRECT ANSWER: A) Stable: fixed plaque, exertional, reversible ischemia.
Unstable/MI: plaque rupture, thrombosis, unstable, may cause infarction
RATIONALE: Stable angina: fixed atherosclerotic plaque >70% stenosis, demand ischemia exertional,
reversible. Unstable angina/NSTEMI/STEMI: plaque rupture, platelet aggregation, thrombosis, partial or
NSG 530 Exam 2 Advanced Pathophysiology Quiz 2026/2027 LATEST UPDATE Page 4
NSG 530 EXAM 2
ADVANCED PATHOPHYSIOLOGY
QUIZ 2026/2027
Comprehensive Study Quiz 2026/2027 LATEST UPDATE | Wilkes University
EXAM 2 ADV PATHO WILKES 2026/2027 LATEST
, EXAM COVERAGE AREAS
Advanced Pathophysiology - Exam 2 Domains | NSG 530 | 2026/2027 LATEST
Cardiovascular II - Advanced Cardiac Pathophysiology
• Coronary artery disease: stable angina vs unstable vs MI - plaque progression
• Valvular disorders: stenosis vs regurgitation pathophysiology
• Cardiomyopathy: dilated, hypertrophic, restrictive
• Pericardial disease, infective endocarditis pathophysiology
Pulmonary II - Advanced Pulmonary Pathophysiology
• Pulmonary hypertension: WHO groups, pathophysiology
• ARDS: Berlin criteria, diffuse alveolar damage
• Pulmonary embolism: Virchow triad, hemodynamic consequences
• Lung cancer & pleural effusion pathophysiology
Renal & Urologic Pathophysiology Advanced
• Glomerulonephritis vs nephrotic syndrome: proteinuria, hematuria
• Tubular disorders: ATN, interstitial nephritis
• Urolithiasis, UTI, BPH pathophysiology
• Electrolyte disorders advanced: hyper/hyponatremia, hyper/hypokalemia mechanisms
Gastrointestinal & Hepatobiliary Advanced
• GERD, peptic ulcer, IBD Crohn vs ulcerative colitis
• Liver: hepatitis, cirrhosis, portal hypertension, hepatic failure
• Pancreatitis: acute vs chronic, gallstones pathophysiology
• Intestinal obstruction, ischemia, malabsorption
Endocrine & Reproductive Advanced
• Pituitary: acromegaly, DI vs SIADH - water balance
• Adrenal: Cushing vs Addison, pheochromocytoma
• Reproductive: PCOS, infertility, menopause pathophysiology
• Metabolic bone disease: osteoporosis pathophysiology
Neurologic, Musculoskeletal & Integration
• Neurodegenerative: Alzheimer, Parkinson, MS, ALS pathophysiology
• Musculoskeletal: RA vs OA, gout, osteoporosis
• Hematologic: clotting disorders DIC, thrombocytopenia
• Integration: multisystem failure, stress, compensatory mechanisms - Exam 2 high-yield
NSG 530 Exam 2 Advanced Pathophysiology Quiz 2026/2027 LATEST UPDATE Page 2
, QUESTION 1: NSG 530 Exam 2: Difference between stable angina and unstable
angina/MI pathophysiology?
A) Stable: fixed plaque, exertional, reversible ischemia. Unstable/MI: plaque rupture, thrombosis,
unstable, may cause infarction
B) Same pathophysiology
C) Stable is plaque rupture
D) Unstable is only exertional
CORRECT ANSWER: A) Stable: fixed plaque, exertional, reversible ischemia.
Unstable/MI: plaque rupture, thrombosis, unstable, may cause infarction
RATIONALE: Stable angina: fixed atherosclerotic plaque >70% stenosis, demand ischemia exertional,
reversible. Unstable angina/NSTEMI/STEMI: plaque rupture, platelet aggregation, thrombosis, partial or
complete occlusion - unstable, may cause necrosis. Troponin elevated in MI.
QUESTION 2: ARDS Berlin criteria pathophysiology?
A) Acute onset within 1 week, bilateral opacities not fully explained by effusion, PaO2/FiO2 <300 with
PEEP, diffuse alveolar damage increased permeability pulmonary edema
B) Only cardiac edema
C) Only unilateral
D) No criteria
CORRECT ANSWER: A) Acute onset within 1 week, bilateral opacities not fully
explained by effusion, PaO2/FiO2 <300 with PEEP, diffuse alveolar damage increased
permeability pulmonary edema
RATIONALE: ARDS: Berlin 2012 acute within 1 week known insult, bilateral opacities, PaO2/FiO2 <300
mmHg with PEEP >=5, not cardiac failure. Patho diffuse alveolar damage, increased alveolar-capillary
permeability, non-cardiogenic pulmonary edema, hyaline membranes, V/Q mismatch.
QUESTION 3: Nephrotic vs nephritic syndrome differentiation?
A) Nephrotic: heavy proteinuria >3.5g/day, hypoalbuminemia, edema, hyperlipidemia, minimal
hematuria. Nephritic: hematuria, HTN, oliguria, mild proteinuria, RBC casts
B) Same syndrome
C) Nephrotic has hematuria always
D) Nephritic has heavy proteinuria >3.5g
CORRECT ANSWER: A) Nephrotic: heavy proteinuria >3.5g/day, hypoalbuminemia,
edema, hyperlipidemia, minimal hematuria. Nephritic: hematuria, HTN, oliguria, mild
proteinuria, RBC casts
RATIONALE: Nephrotic: podocyte injury heavy proteinuria >3.5g/day, hypoalbuminemia, edema,
hyperlipidemia, lipiduria. Causes minimal change, FSGS, membranous. Nephritic: glomerular inflammation
hematuria, HTN, oliguria, azotemia, RBC casts. Causes post-strep GN, IgA nephropathy, lupus nephritis.
QUESTION 4: DI vs SIADH pathophysiology - water balance?
A) DI: ADH deficiency or resistance - polyuria, hypernatremia, dilute urine. SIADH: excess ADH -
water retention, hyponatremia, concentrated urine
B) Same disorder
C) DI causes hyponatremia
NSG 530 Exam 2 Advanced Pathophysiology Quiz 2026/2027 LATEST UPDATE Page 3
, D) SIADH causes hypernatremia
CORRECT ANSWER: A) DI: ADH deficiency or resistance - polyuria, hypernatremia,
dilute urine. SIADH: excess ADH - water retention, hyponatremia, concentrated urine
RATIONALE: DI: ADH deficiency (central) or resistance (nephrogenic) - polyuria 3-20 L/day, polydipsia,
hypernatremia, low urine osmolality, high serum osmolality. SIADH: excess ADH secretion - water retention,
hyponatremia, hypo-osmolality serum, high urine osmolality, euvolemic. Causes: CNS disorders, drugs,
tumors.
QUESTION 5: RA vs OA pathophysiology differentiation?
A) RA: autoimmune synovitis, pannus, symmetric small joints, systemic, inflammatory. OA:
degenerative cartilage wear, asymmetric weight-bearing joints, non-inflammatory
B) Same disease
C) RA is degenerative
D) OA is autoimmune
CORRECT ANSWER: A) RA: autoimmune synovitis, pannus, symmetric small joints,
systemic, inflammatory. OA: degenerative cartilage wear, asymmetric weight-bearing
joints, non-inflammatory
RATIONALE: RA: autoimmune systemic, synovial inflammation pannus formation, symmetric small joints
MCP PIP, morning stiffness >1 hr, RF anti-CCP, systemic features. OA: degenerative cartilage loss, bone
spurs, asymmetric weight-bearing hips knees, Heberden Bouchard nodes, morning stiffness <30 min,
non-inflammatory.
QUESTION 6: Virchow triad for PE/DVT?
A) Stasis, endothelial injury, hypercoagulability - all increase clot risk
B) Only stasis
C) Only injury
D) Only hypercoagulability
CORRECT ANSWER: A) Stasis, endothelial injury, hypercoagulability - all increase clot
risk
RATIONALE: Virchow triad: venous stasis (immobility, HF), endothelial injury (trauma, surgery, central line),
hypercoagulability (factor V Leiden, OCP, cancer, pregnancy). PE pathophysiology clot lodges pulmonary
artery increases dead space, V/Q mismatch, increased pulmonary vascular resistance, RV strain.
QUESTION 7: NSG 530 Exam 2: Difference between stable angina and unstable
angina/MI pathophysiology?
A) Stable: fixed plaque, exertional, reversible ischemia. Unstable/MI: plaque rupture, thrombosis,
unstable, may cause infarction
B) Same pathophysiology
C) Stable is plaque rupture
D) Unstable is only exertional
CORRECT ANSWER: A) Stable: fixed plaque, exertional, reversible ischemia.
Unstable/MI: plaque rupture, thrombosis, unstable, may cause infarction
RATIONALE: Stable angina: fixed atherosclerotic plaque >70% stenosis, demand ischemia exertional,
reversible. Unstable angina/NSTEMI/STEMI: plaque rupture, platelet aggregation, thrombosis, partial or
NSG 530 Exam 2 Advanced Pathophysiology Quiz 2026/2027 LATEST UPDATE Page 4
