Wilkes University
O H TAP · 3 3 5 G S N
W
Passan School of Nursing
EST. 1933
UNITY AMIDST DIVERSITY
NSG 533 Exam 1 — Pathophysiology Foundations
C E L L I N J U RY, F LU I D & E L E CT R O LYT E S , AC I D - B A S E , R E N A L PAT H O P H YS I O LO G Y
INSTITUTION Wilkes University COURSE CODE NSG 533
PROGRAM Advanced Pathophysiology — EXAM Exam 1 — Comprehensive
Graduate Nursing Pathophysiology
EXAM TITLE NSG 533 Exam 1 — TOTAL QUESTIONS 100 Questions
Pathophysiology Foundations
COURSE TITLE Advanced Pathophysiology FORMAT Multiple Choice — Select the
Single Best Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question.
▸ Pathophysiology foundations, cell injury, necrosis, apoptosis, fluid/electrolyte balance, acid-base
disorders, and renal pathophysiology are all testable content.
▸ Correct answers and detailed pathophysiological rationales appear below each question.
▸ All content reflects NSG 533 Advanced Pathophysiology course objectives.
, SECTION I — PATHOPHYSIOLOGY: CELLULAR
Questions 1 – 100
FOUNDATIONS THROUGH RENAL DISEASE
1. The five essential components of pathophysiology are:
A. Diagnosis, treatment, prognosis, prevention, and rehabilitation
B. Etiology, epidemiology, pathogenesis, clinical manifestations, and outcomes
C. History, physical examination, laboratory tests, imaging, and consultation
D. Genetics, environment, lifestyle, nutrition, and immunity
CORRECT ANSWER B — Etiology, epidemiology, pathogenesis, clinical manifestations, and
outcomes
RATIONALE The five core components provide the framework for understanding any disease:
Etiology (cause — idiopathic/cryptogenic if unknown, iatrogenic if from medical
intervention), Epidemiology (incidence = new cases; prevalence = all cases),
Pathogenesis (mechanism of disease development), Clinical manifestations (signs
and symptoms), and Outcomes (results including recovery, chronicity, or death).
The NSG 533 emphasizes applying this framework to every disease studied.
,2. What are the four common mechanisms of cell injury and death?
A. Infection, inflammation, immune response, and neoplasm
B. ATP depletion, oxygen and oxygen-derived free radicals, intracellular calcium and loss of
calcium state, and defects in membrane permeability
C. Apoptosis, necrosis, autophagy, and senescence
D. Hypoxia, ischemia, infarction, and reperfusion
CORRECT ANSWER B — ATP depletion, free radicals, calcium dysregulation, and membrane
defects
RATIONALE The four fundamental mechanisms are: (1) ATP depletion (most common
stressor) — impairs Na⁺/K⁺-ATPase pump → cellular swelling, increased glycolysis
→ glycogen depletion, lactate accumulation, decreased pH; (2) Free radicals —
unstable compounds with unpaired electrons that damage membrane
phospholipids; (3) Intracellular calcium dysregulation — loss of calcium
homeostasis damages mitochondria and activates destructive enzymes; (4)
Membrane permeability defects — compromise cellular integrity. ATP is produced
via anaerobic glycolysis (2 ATP) and aerobic oxidative phosphorylation (36 ATP).
3. How many ATP does glycolysis yield?
A. 36 ATP
B. 2 ATP — glycolysis is the anaerobic phase of ATP production
C. 4 ATP
D. 0 ATP
CORRECT ANSWER B — 2 ATP; oxidative phosphorylation yields 36 ATP
RATIONALE Glycolysis (anaerobic) yields only 2 ATP per glucose. Oxidative phosphorylation
(aerobic) yields 36 ATP. When ATP depletion occurs, cells shift toward increased
anaerobic glycolysis — glycogen is depleted, lactate increases, intracellular pH
decreases, causing nuclear changes: pyknosis (clumping), karyorrhexis
(fragmentation), and karyolysis (dissolution).
, 4. Define apoptosis and list the three mechanisms.
A. Uncontrolled cell death with inflammation — necrosis, autophagy, and lysis
B. Programmed cell death not associated with inflammation — mitochondrial pathway,
death receptor pathway, and apoptosis-inducing factor (AIF)
C. Cell swelling and rupture — osmotic, chemical, and mechanical
D. Cell adaptation to stress — atrophy, hypertrophy, and hyperplasia
CORRECT ANSWER B — Programmed cell death without inflammation; three pathways:
mitochondrial, death receptor, AIF
RATIONALE Apoptosis is orderly, non-inflammatory cell death. Three mechanisms: (1)
Mitochondrial (intrinsic) — Bax blocks Bcl-2, releasing cytochrome c → Apaf-1 →
apoptosomes → caspase 9 → caspase cascade → phagocytosis; (2) Death
receptor (extrinsic) — FAS/TNF activated by ligands → caspase 8 → caspase
cascade; (3) AIF — released from mitochondria, migrates to nucleus, binds DNA,
triggers cell death. HPV and EBV can evade apoptosis.
5. What is the function of aldosterone?
A. Promote renal excretion of sodium and retention of potassium
B. Retain sodium and promote renal excretion of potassium — secreted from the adrenal
cortex in response to angiotensin II
C. Increase urine output and decrease blood pressure
D. Stimulate red blood cell production
CORRECT ANSWER B — Retain sodium, excrete potassium — secreted from adrenal cortex
RATIONALE Aldosterone (mineralocorticoid from adrenal cortex) is secreted in response to
angiotensin II. Primary functions: retain sodium (and water follows) and excrete
potassium. The RAAS cascade: low BP/perfusion/Na → renin from JG cells →
angiotensin I → ACE → angiotensin II → vasoconstriction + aldosterone + ADH.
The three sodium-regulating systems: RAAS (increase BP), Natriuretic Peptide
System (decrease BP), ADH System (water conservation).
O H TAP · 3 3 5 G S N
W
Passan School of Nursing
EST. 1933
UNITY AMIDST DIVERSITY
NSG 533 Exam 1 — Pathophysiology Foundations
C E L L I N J U RY, F LU I D & E L E CT R O LYT E S , AC I D - B A S E , R E N A L PAT H O P H YS I O LO G Y
INSTITUTION Wilkes University COURSE CODE NSG 533
PROGRAM Advanced Pathophysiology — EXAM Exam 1 — Comprehensive
Graduate Nursing Pathophysiology
EXAM TITLE NSG 533 Exam 1 — TOTAL QUESTIONS 100 Questions
Pathophysiology Foundations
COURSE TITLE Advanced Pathophysiology FORMAT Multiple Choice — Select the
Single Best Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question.
▸ Pathophysiology foundations, cell injury, necrosis, apoptosis, fluid/electrolyte balance, acid-base
disorders, and renal pathophysiology are all testable content.
▸ Correct answers and detailed pathophysiological rationales appear below each question.
▸ All content reflects NSG 533 Advanced Pathophysiology course objectives.
, SECTION I — PATHOPHYSIOLOGY: CELLULAR
Questions 1 – 100
FOUNDATIONS THROUGH RENAL DISEASE
1. The five essential components of pathophysiology are:
A. Diagnosis, treatment, prognosis, prevention, and rehabilitation
B. Etiology, epidemiology, pathogenesis, clinical manifestations, and outcomes
C. History, physical examination, laboratory tests, imaging, and consultation
D. Genetics, environment, lifestyle, nutrition, and immunity
CORRECT ANSWER B — Etiology, epidemiology, pathogenesis, clinical manifestations, and
outcomes
RATIONALE The five core components provide the framework for understanding any disease:
Etiology (cause — idiopathic/cryptogenic if unknown, iatrogenic if from medical
intervention), Epidemiology (incidence = new cases; prevalence = all cases),
Pathogenesis (mechanism of disease development), Clinical manifestations (signs
and symptoms), and Outcomes (results including recovery, chronicity, or death).
The NSG 533 emphasizes applying this framework to every disease studied.
,2. What are the four common mechanisms of cell injury and death?
A. Infection, inflammation, immune response, and neoplasm
B. ATP depletion, oxygen and oxygen-derived free radicals, intracellular calcium and loss of
calcium state, and defects in membrane permeability
C. Apoptosis, necrosis, autophagy, and senescence
D. Hypoxia, ischemia, infarction, and reperfusion
CORRECT ANSWER B — ATP depletion, free radicals, calcium dysregulation, and membrane
defects
RATIONALE The four fundamental mechanisms are: (1) ATP depletion (most common
stressor) — impairs Na⁺/K⁺-ATPase pump → cellular swelling, increased glycolysis
→ glycogen depletion, lactate accumulation, decreased pH; (2) Free radicals —
unstable compounds with unpaired electrons that damage membrane
phospholipids; (3) Intracellular calcium dysregulation — loss of calcium
homeostasis damages mitochondria and activates destructive enzymes; (4)
Membrane permeability defects — compromise cellular integrity. ATP is produced
via anaerobic glycolysis (2 ATP) and aerobic oxidative phosphorylation (36 ATP).
3. How many ATP does glycolysis yield?
A. 36 ATP
B. 2 ATP — glycolysis is the anaerobic phase of ATP production
C. 4 ATP
D. 0 ATP
CORRECT ANSWER B — 2 ATP; oxidative phosphorylation yields 36 ATP
RATIONALE Glycolysis (anaerobic) yields only 2 ATP per glucose. Oxidative phosphorylation
(aerobic) yields 36 ATP. When ATP depletion occurs, cells shift toward increased
anaerobic glycolysis — glycogen is depleted, lactate increases, intracellular pH
decreases, causing nuclear changes: pyknosis (clumping), karyorrhexis
(fragmentation), and karyolysis (dissolution).
, 4. Define apoptosis and list the three mechanisms.
A. Uncontrolled cell death with inflammation — necrosis, autophagy, and lysis
B. Programmed cell death not associated with inflammation — mitochondrial pathway,
death receptor pathway, and apoptosis-inducing factor (AIF)
C. Cell swelling and rupture — osmotic, chemical, and mechanical
D. Cell adaptation to stress — atrophy, hypertrophy, and hyperplasia
CORRECT ANSWER B — Programmed cell death without inflammation; three pathways:
mitochondrial, death receptor, AIF
RATIONALE Apoptosis is orderly, non-inflammatory cell death. Three mechanisms: (1)
Mitochondrial (intrinsic) — Bax blocks Bcl-2, releasing cytochrome c → Apaf-1 →
apoptosomes → caspase 9 → caspase cascade → phagocytosis; (2) Death
receptor (extrinsic) — FAS/TNF activated by ligands → caspase 8 → caspase
cascade; (3) AIF — released from mitochondria, migrates to nucleus, binds DNA,
triggers cell death. HPV and EBV can evade apoptosis.
5. What is the function of aldosterone?
A. Promote renal excretion of sodium and retention of potassium
B. Retain sodium and promote renal excretion of potassium — secreted from the adrenal
cortex in response to angiotensin II
C. Increase urine output and decrease blood pressure
D. Stimulate red blood cell production
CORRECT ANSWER B — Retain sodium, excrete potassium — secreted from adrenal cortex
RATIONALE Aldosterone (mineralocorticoid from adrenal cortex) is secreted in response to
angiotensin II. Primary functions: retain sodium (and water follows) and excrete
potassium. The RAAS cascade: low BP/perfusion/Na → renin from JG cells →
angiotensin I → ACE → angiotensin II → vasoconstriction + aldosterone + ADH.
The three sodium-regulating systems: RAAS (increase BP), Natriuretic Peptide
System (decrease BP), ADH System (water conservation).
