NSG 3850 Pathophysiology II Exam 3 2026 | Questions
with Answers & Detailed Explanations | Renal, GI,
Endocrine & Neurologic Disorders | Latest Version
Description
Complete NSG 3850 Pathophysiology II Exam 3 2026 preparation guide containing 150 multiple-
choice practice questions with verified answers and detailed explanations in italic.
This comprehensive study resource covers all essential topics from the NSG 3850 Exam 3 :
✅ Renal Pathophysiology – Glomerular Disorders – Acute glomerulonephritis (post-strep, cola-colored
urine, hematuria, hypertension, edema), nephrotic syndrome (massive proteinuria >3.5g/day,
hypoalbuminemia, hyperlipidemia, edema, thromboembolism risk), Goodpasture syndrome, IgA
nephropathy (Berger disease), Alport syndrome, rapidly progressive glomerulonephritis (crescents)
✅ Renal Pathophysiology – Tubular & Infectious Disorders – Acute pyelonephritis (fever, chills, flank
pain, CVA tenderness, E. coli), chronic pyelonephritis (scarring, atrophy), polycystic kidney disease
(ADPKD, liver cysts, cerebral aneurysms), nephrolithiasis (calcium oxalate stones, dehydration), acute
kidney injury (oliguric phase, hyperkalemia), chronic kidney disease (anemia due to decreased EPO, renal
osteodystrophy from hyperphosphatemia, ESRD with 75% nephron loss)
✅ Gastrointestinal Pathophysiology – Peptic ulcer disease (duodenal: pain 2-3h after meals relieved by
eating; gastric: pain 1h after meals worsened by eating, H. pylori), GERD (LES incompetence, Barrett's
esophagus), Crohn's disease (transmural inflammation, skip lesions, fistulas), ulcerative colitis (continuous
colonic inflammation, toxic megacolon), cirrhosis (portal hypertension, esophageal varices, hepatic
encephalopathy from ammonia accumulation), acute pancreatitis (epigastric pain radiating to back,
gallstones), celiac disease (villous atrophy, gluten avoidance, steatorrhea), dumping syndrome (rapid
gastric emptying), diverticulitis (LLQ pain, perforation risk)
✅ Endocrine Disorders – Type 1 diabetes (autoimmune beta-cell destruction, DKA, hypoglycemia), Type
2 diabetes (insulin resistance, metformin contraindicated if eGFR<30), Cushing's syndrome (central
obesity, moon facies, buffalo hump, purple striae, hypertension), Cushing's disease (pituitary adenoma,
elevated ACTH), Addison's disease (hyperpigmentation, hypotension, hyponatremia, hyperkalemia),
adrenal crisis (IV hydrocortisone, IVF, dextrose), diabetes insipidus (polyuria, polydipsia, hypernatremia),
SIADH (oliguria, hyponatremia), thyroid storm (hyperthermia, tachycardia, agitation), myxedema coma
(hypothermia, bradycardia, lethargy), hyperaldosteronism (hypertension, hypokalemia),
, hyperparathyroidism (hypercalcemia, kidney stones), hypoparathyroidism (hypocalcemia, tetany, Chvostek
sign)
✅ Fluid & Electrolyte Physiology – Intracellular (K+, Mg2+, phosphates), extracellular (vascular &
interstitial spaces), transcellular fluid, oncotic pressure (albumin), hydrostatic pressure, osmotic diuresis,
metabolic acidosis (low pH, low HCO3), metabolic alkalosis (high pH, high HCO3), respiratory acidosis (low
pH, high PaCO2), respiratory alkalosis (high pH, low PaCO2), mixed acid-base imbalances, ABG
interpretation
✅ Neurologic Disorders – Increased intracranial pressure (head elevation 30°, Cushing's triad:
hypertension/bradycardia/irregular respirations, unequal pupils), status epilepticus (IV benzodiazepines),
phenytoin (gingival hyperplasia), Parkinson's disease (substantia nigra degeneration, dopamine deficiency),
Alzheimer's disease (amyloid plaques, neurofibrillary tangles), multiple sclerosis (CNS demyelination,
relapsing-remitting), ALS (progressive muscle weakness without sensory loss), Guillain-Barré (ascending
paralysis), myasthenia gravis (weakness improves with rest), stroke (ischemic vs hemorrhagic, tPA window
3 hours), GCS scoring, bacterial meningitis (fever, headache, nuchal rigidity, S. pneumoniae)
📚 Section 1: Renal Pathophysiology – Glomerular Disorders (Questions 1–35)
1. A patient presents with hypertension, edema, hematuria, and cola-colored urine
following a recent streptococcal throat infection. Which condition is most likely?
A) Acute pyelonephritis
B) Acute glomerulonephritis
C) Nephrotic syndrome
D) Polycystic kidney disease
Answer: B
Explanation: Acute glomerulonephritis often follows a streptococcal infection by 1-3 weeks.
Antigen-antibody complexes deposit in glomeruli, causing inflammation, hematuria,
, proteinuria, hypertension, and fluid retention. The cola-colored urine results from RBCs in
the urine .
2. Which finding is characteristic of nephrotic syndrome?
A) Hematuria and red blood cell casts
B) Hypertension and azotemia
C) Massive proteinuria (>3.5 g/day) and hypoalbuminemia
D) White blood cell casts and fever
Answer: C
Explanation: Nephrotic syndrome results from increased glomerular permeability to proteins.
Key features include massive proteinuria, hypoalbuminemia, generalized edema,
hyperlipidemia, and lipiduria. Hematuria and hypertension are more characteristic of
nephritic syndrome [citation:10,14].
3. A patient with nephrotic syndrome is at increased risk for which complication?
A) Hypokalemia
B) Hyperkalemia
C) Thromboembolism
D) Hypocalcemia
Answer: C
Explanation: Loss of anticoagulant proteins (protein C, protein S, antithrombin III) in the
, urine, along with increased hepatic synthesis of procoagulant factors, creates a
hypercoagulable state. Renal vein thrombosis is a particular risk in nephrotic syndrome .
4. Which statement accurately distinguishes acute glomerulonephritis from nephrotic
syndrome?
A) Glomerulonephritis typically presents with nephrotic-range proteinuria
B) Nephrotic syndrome typically presents with hypertension and hematuria
C) Glomerulonephritis involves inflammation; nephrotic syndrome involves increased
permeability
D) Nephrotic syndrome is caused by streptococcal infection
Answer: C
Explanation: The key distinction is pathophysiology: glomerulonephritis is primarily
inflammatory (causing hematuria, RBC casts, hypertension), while nephrotic syndrome
results from podocyte injury causing massive protein loss .
5. In nephrotic syndrome, the generalized edema is caused by:
A) Excessive renal retention of potassium ions
B) Loss of plasma albumin through the glomerulus, reducing capillary oncotic pressure
C) Increased systemic hydrostatic pressure
D) Lymphatic obstruction
with Answers & Detailed Explanations | Renal, GI,
Endocrine & Neurologic Disorders | Latest Version
Description
Complete NSG 3850 Pathophysiology II Exam 3 2026 preparation guide containing 150 multiple-
choice practice questions with verified answers and detailed explanations in italic.
This comprehensive study resource covers all essential topics from the NSG 3850 Exam 3 :
✅ Renal Pathophysiology – Glomerular Disorders – Acute glomerulonephritis (post-strep, cola-colored
urine, hematuria, hypertension, edema), nephrotic syndrome (massive proteinuria >3.5g/day,
hypoalbuminemia, hyperlipidemia, edema, thromboembolism risk), Goodpasture syndrome, IgA
nephropathy (Berger disease), Alport syndrome, rapidly progressive glomerulonephritis (crescents)
✅ Renal Pathophysiology – Tubular & Infectious Disorders – Acute pyelonephritis (fever, chills, flank
pain, CVA tenderness, E. coli), chronic pyelonephritis (scarring, atrophy), polycystic kidney disease
(ADPKD, liver cysts, cerebral aneurysms), nephrolithiasis (calcium oxalate stones, dehydration), acute
kidney injury (oliguric phase, hyperkalemia), chronic kidney disease (anemia due to decreased EPO, renal
osteodystrophy from hyperphosphatemia, ESRD with 75% nephron loss)
✅ Gastrointestinal Pathophysiology – Peptic ulcer disease (duodenal: pain 2-3h after meals relieved by
eating; gastric: pain 1h after meals worsened by eating, H. pylori), GERD (LES incompetence, Barrett's
esophagus), Crohn's disease (transmural inflammation, skip lesions, fistulas), ulcerative colitis (continuous
colonic inflammation, toxic megacolon), cirrhosis (portal hypertension, esophageal varices, hepatic
encephalopathy from ammonia accumulation), acute pancreatitis (epigastric pain radiating to back,
gallstones), celiac disease (villous atrophy, gluten avoidance, steatorrhea), dumping syndrome (rapid
gastric emptying), diverticulitis (LLQ pain, perforation risk)
✅ Endocrine Disorders – Type 1 diabetes (autoimmune beta-cell destruction, DKA, hypoglycemia), Type
2 diabetes (insulin resistance, metformin contraindicated if eGFR<30), Cushing's syndrome (central
obesity, moon facies, buffalo hump, purple striae, hypertension), Cushing's disease (pituitary adenoma,
elevated ACTH), Addison's disease (hyperpigmentation, hypotension, hyponatremia, hyperkalemia),
adrenal crisis (IV hydrocortisone, IVF, dextrose), diabetes insipidus (polyuria, polydipsia, hypernatremia),
SIADH (oliguria, hyponatremia), thyroid storm (hyperthermia, tachycardia, agitation), myxedema coma
(hypothermia, bradycardia, lethargy), hyperaldosteronism (hypertension, hypokalemia),
, hyperparathyroidism (hypercalcemia, kidney stones), hypoparathyroidism (hypocalcemia, tetany, Chvostek
sign)
✅ Fluid & Electrolyte Physiology – Intracellular (K+, Mg2+, phosphates), extracellular (vascular &
interstitial spaces), transcellular fluid, oncotic pressure (albumin), hydrostatic pressure, osmotic diuresis,
metabolic acidosis (low pH, low HCO3), metabolic alkalosis (high pH, high HCO3), respiratory acidosis (low
pH, high PaCO2), respiratory alkalosis (high pH, low PaCO2), mixed acid-base imbalances, ABG
interpretation
✅ Neurologic Disorders – Increased intracranial pressure (head elevation 30°, Cushing's triad:
hypertension/bradycardia/irregular respirations, unequal pupils), status epilepticus (IV benzodiazepines),
phenytoin (gingival hyperplasia), Parkinson's disease (substantia nigra degeneration, dopamine deficiency),
Alzheimer's disease (amyloid plaques, neurofibrillary tangles), multiple sclerosis (CNS demyelination,
relapsing-remitting), ALS (progressive muscle weakness without sensory loss), Guillain-Barré (ascending
paralysis), myasthenia gravis (weakness improves with rest), stroke (ischemic vs hemorrhagic, tPA window
3 hours), GCS scoring, bacterial meningitis (fever, headache, nuchal rigidity, S. pneumoniae)
📚 Section 1: Renal Pathophysiology – Glomerular Disorders (Questions 1–35)
1. A patient presents with hypertension, edema, hematuria, and cola-colored urine
following a recent streptococcal throat infection. Which condition is most likely?
A) Acute pyelonephritis
B) Acute glomerulonephritis
C) Nephrotic syndrome
D) Polycystic kidney disease
Answer: B
Explanation: Acute glomerulonephritis often follows a streptococcal infection by 1-3 weeks.
Antigen-antibody complexes deposit in glomeruli, causing inflammation, hematuria,
, proteinuria, hypertension, and fluid retention. The cola-colored urine results from RBCs in
the urine .
2. Which finding is characteristic of nephrotic syndrome?
A) Hematuria and red blood cell casts
B) Hypertension and azotemia
C) Massive proteinuria (>3.5 g/day) and hypoalbuminemia
D) White blood cell casts and fever
Answer: C
Explanation: Nephrotic syndrome results from increased glomerular permeability to proteins.
Key features include massive proteinuria, hypoalbuminemia, generalized edema,
hyperlipidemia, and lipiduria. Hematuria and hypertension are more characteristic of
nephritic syndrome [citation:10,14].
3. A patient with nephrotic syndrome is at increased risk for which complication?
A) Hypokalemia
B) Hyperkalemia
C) Thromboembolism
D) Hypocalcemia
Answer: C
Explanation: Loss of anticoagulant proteins (protein C, protein S, antithrombin III) in the
, urine, along with increased hepatic synthesis of procoagulant factors, creates a
hypercoagulable state. Renal vein thrombosis is a particular risk in nephrotic syndrome .
4. Which statement accurately distinguishes acute glomerulonephritis from nephrotic
syndrome?
A) Glomerulonephritis typically presents with nephrotic-range proteinuria
B) Nephrotic syndrome typically presents with hypertension and hematuria
C) Glomerulonephritis involves inflammation; nephrotic syndrome involves increased
permeability
D) Nephrotic syndrome is caused by streptococcal infection
Answer: C
Explanation: The key distinction is pathophysiology: glomerulonephritis is primarily
inflammatory (causing hematuria, RBC casts, hypertension), while nephrotic syndrome
results from podocyte injury causing massive protein loss .
5. In nephrotic syndrome, the generalized edema is caused by:
A) Excessive renal retention of potassium ions
B) Loss of plasma albumin through the glomerulus, reducing capillary oncotic pressure
C) Increased systemic hydrostatic pressure
D) Lymphatic obstruction
