MIDTERM EXAM: NUR631 — Advanced Physiology and Pathophysiology | GCU (2026/2027)
MIDTERM EXAM: NUR631 / NUR 631 (LATEST
UPDATE) ADVANCED PHYSIOLOGY AND PATHOPHYSIOLOGY
EXAM | QUESTIONS AND VERIFIED ANSWERS | 100% CORRECT
| GRADE A — GCU
Grand Canyon University — College of Nursing and Health Care Professions
Aligned with NUR 631 Course Syllabus, AACN Essentials of Master's Education, and Advanced Physiology
and Pathophysiology Competencies (2026/2027 Edition)
Total Questions: 120 | Sections: 8 | Cognitive Mix: 20% Recall, 50% Application, 30% Analysis
Section 1: Cellular Physiology & Pathophysiology
Q1: A 58-year-old male with chronic obstructive pulmonary disease exhibits an elevated
hematocrit. Which cellular adaptation best explains the increased red blood cell mass
in response to chronic hypoxemia?
A. Hyperplasia, an increase in the number of cells due to increased hormonal stimulation
B. Hypertrophy, an increase in cell size driven by increased functional demand
[CORRECT]
C. Metaplasia, the reversible replacement of one differentiated cell type by another
D. Dysplasia, disordered cellular growth with atypical morphology suggestive of pre-neoplastic
change
Correct Answer: B
Rationale: Chronic hypoxemia stimulates renal erythropoietin release, which drives erythroid
precursor cells to enlarge and synthesize more hemoglobin—an increase in cell SIZE rather than
number. This is hypertrophy (compensatory). Hyperplasia is ruled out because mature RBCs are
anucleate and cannot divide; metaplasia and dysplasia involve cell-type change and atypical growth,
neither of which occurs in erythroid response to hypoxia.
Q2: A researcher examines a biopsy of bronchial epithelium from a 55-year-old heavy
smoker. Columnar ciliated epithelium has been replaced by stratified squamous
epithelium. Which cellular adaptation is depicted, and what is its primary biological
significance?
A. Hypertrophy; an adaptive response that strengthens tissue contractility
B. Metaplasia; a reversible, protective substitution that is reversible with smoking
cessation but may progress to malignancy [CORRECT]
C. Dysplasia; an irreversible pre-neoplastic transformation that mandates immediate surgical
excision
D. Anaplasia; loss of cell differentiation consistent with frank malignancy
Correct Answer: B
Rationale: Replacement of columnar ciliated epithelium by stratified squamous epithelium in smokers
is classic squamous metaplasia, a reversible adaptive substitution to chronic irritation. It is not yet
malignant (rules out anaplasia), does not increase cell size (rules out hypertrophy), and is not the
disordered atypical proliferation of dysplasia. Continued injury may, however, progress to dysplasia and
squamous cell carcinoma.
Grand Canyon University — College of Nursing and Health Care Professions Page 1
,MIDTERM EXAM: NUR631 — Advanced Physiology and Pathophysiology | GCU (2026/2027)
Q3: A cell is exposed to ischemia. Within minutes, ATP depletion triggers failure of the
Na+/K+-ATPase pump. Which sequence of events best describes the subsequent
pathophysiological cascade leading to irreversible cellular injury?
A. Na+ influx → cellular swelling → K+ efflux → ribosome detachment → reversible injury only
B. Na+ influx → cellular swelling → Ca2+ influx → mitochondrial dysfunction →
activation of phospholipases and proteases → membrane damage → cell death
[CORRECT]
C. K+ influx → cellular dehydration → Cl- efflux → nuclear pyknosis → apoptosis
D. Ca2+ efflux → cytoskeletal stabilization → lysosomal inactivation → necrosis
Correct Answer: B
Rationale: Ischemia depletes ATP, disabling the Na+/K+-ATPase. Sodium enters the cell, water
follows, and the cell swells. Critically, ATP depletion also fails Ca2+ pumps, allowing pathologic calcium
influx into the cytosol and mitochondria. Calcium activates phospholipases (membrane destruction),
proteases (cytoskeleton disruption), and endonucleases (DNA fragmentation), and impairs
mitochondria—collectively producing irreversible injury. K+ efflux and ribosome detachment occur
early but are reversible.
Q4: Which statement most accurately distinguishes apoptosis from necrosis at the
cellular and tissue level?
A. Apoptosis produces a robust inflammatory response due to membrane rupture, whereas
necrosis is inflammation-silent
B. Apoptosis is characterized by cell swelling, membrane rupture, and random DNA digestion,
while necrosis produces cell shrinkage and an inflammatory response
C. Apoptosis is an energy-requiring, programmed process producing cell shrinkage,
nuclear condensation, and apoptotic bodies without significant inflammation;
necrosis is characterized by cell swelling, membrane rupture, and marked
inflammation [CORRECT]
D. Apoptosis can only occur in pathologic states, whereas necrosis is exclusively physiologic
Correct Answer: C
Rationale: Apoptosis is ATP-dependent, programmed cell death involving caspase activation, cell
shrinkage, chromatin condensation (pyknosis), and formation of apoptotic bodies that are phagocytosed
without inflammation. Necrosis is pathologic, characterized by cell swelling (oncosis), membrane
rupture, release of cellular contents, and a vigorous inflammatory response. Options A, B, and D reverse
these features or contain factually incorrect statements.
Q5: A 67-year-old patient receiving doxorubicin chemotherapy develops cardiotoxicity.
The mechanism most directly responsible is:
A. Formation of hydroxyl free radicals via iron-mediated Fenton chemistry, causing
lipid peroxidation of mitochondrial membranes [CORRECT]
B. Inhibition of topoisomerase II exclusively, without oxidative injury
C. Direct competitive inhibition of cardiac beta-1 adrenergic receptors
D. Activation of Bcl-2 with consequent suppression of cardiomyocyte apoptosis
Correct Answer: A
Rationale: Doxorubicin causes dose-dependent cardiotoxicity primarily through iron-catalyzed free
radical generation (Fenton reaction) and lipid peroxidation of mitochondrial membranes, depleting
cardiomyocyte ATP and triggering apoptosis. While doxorubicin also inhibits topoisomerase II in tumor
cells, the cardiotoxic mechanism is predominantly oxidative. The drug does not act on beta-receptors,
Grand Canyon University — College of Nursing and Health Care Professions Page 2
,MIDTERM EXAM: NUR631 — Advanced Physiology and Pathophysiology | GCU (2026/2027)
and it promotes (not suppresses) cardiomyocyte apoptosis via Bcl-2 family modulation.
Q6: Which second messenger system is activated when a ligand binds a
Gq-protein-coupled receptor, and what is the immediate downstream effect?
A. Activation of adenylyl cyclase → increased cAMP → protein kinase A activation
B. Activation of phospholipase C → hydrolysis of PIP2 to IP3 and DAG → Ca2+ release
from ER and protein kinase C activation [CORRECT]
C. Activation of guanylyl cyclase → increased cGMP → protein kinase G activation
D. Direct activation of receptor tyrosine kinase → autophosphorylation → Ras-MAPK cascade
Correct Answer: B
Rationale: Gq-coupled receptors (e.g., alpha-1 adrenergic, muscarinic M1, M3) activate phospholipase
C, which hydrolyzes membrane PIP2 into IP3 (mobilizes intracellular Ca2+ from the ER) and DAG
(activates protein kinase C). Adenylyl cyclase/cAMP is the Gs pathway, guanylyl cyclase/cGMP is
receptor guanylyl cyclase, and receptor tyrosine kinase signaling is independent of G proteins.
Q7: A cell experiences a mutation that disrupts the Rb (retinoblastoma) protein. Which
checkpoint of the cell cycle is most directly affected, and what is the consequence?
A. G2/M checkpoint; cells arrest in G2 and cannot enter mitosis
B. Spindle (M) checkpoint; chromosomal segregation fails
C. G1/S restriction point; cells progress into S phase even without mitogenic signals,
predisposing to uncontrolled proliferation [CORRECT]
D. S-phase checkpoint; DNA replication stalls
Correct Answer: C
Rationale: Rb is the master regulator of the G1/S restriction point. Hypophosphorylated Rb sequesters
E2F transcription factors, preventing S-phase entry. Mitogenic signals activate cyclin D-CDK4/6 and
cyclin E-CDK2, which phosphorylate Rb, releasing E2F and allowing S-phase entry. Mutated or absent
Rb removes this brake, permitting uncontrolled S-phase progression—a hallmark of many cancers.
Q8: A patient with mitochondrial disease demonstrates lactic acidosis with normal
oxygenation. The underlying cellular mechanism is best described as:
A. Impaired glycolysis resulting in pyruvate accumulation and conversion to lactate
B. Defective electron transport chain complexes reducing aerobic ATP production,
forcing anaerobic glycolysis with excessive lactate generation [CORRECT]
C. Excessive gluconeogenesis causing pyruvate overflow into the lactate pool
D. Deficiency of pyruvate carboxylase impairing TCA cycle entry
Correct Answer: B
Rationale: Mitochondrial disease impairs the electron transport chain (ETC), reducing oxidative
phosphorylation. Cells compensate by upregulating anaerobic glycolysis, which generates ATP but
produces pyruvate faster than defective mitochondria can metabolize it via the TCA cycle. Excess
pyruvate is converted to lactate by lactate dehydrogenase, causing lactic acidosis even with normal
tissue oxygenation. Glycolysis itself is not impaired; it is paradoxically increased.
Q9: Which of the following accurately describes the role of the Na+/K+-ATPase pump
in maintaining cellular homeostasis?
A. It moves 2 Na+ out and 3 K+ in, generating a net negative intracellular charge
Grand Canyon University — College of Nursing and Health Care Professions Page 3
, MIDTERM EXAM: NUR631 — Advanced Physiology and Pathophysiology | GCU (2026/2027)
B. It moves 3 Na+ out and 2 K+ in, hydrolyzing one ATP, and contributes to the
resting membrane potential and secondary active transport gradients [CORRECT]
C. It is a passive channel that does not consume ATP
D. It moves Na+ and K+ in a 1:1 ratio with no contribution to membrane potential
Correct Answer: B
Rationale: The Na+/K+-ATPase is an electrogenic primary active transporter that hydrolyzes one ATP
to move 3 Na+ out and 2 K+ in, contributing directly to the negative resting membrane potential (about
-10 mV of the total ~-70 mV) and establishing Na+ and K+ gradients used by secondary active
transporters (e.g., Na+/Ca2+ exchanger, Na+/glucose cotransporter).
Q10: A 72-year-old patient exhibits marked skeletal muscle wasting after prolonged
immobilization following hip surgery. Which cellular process is most directly
responsible?
A. Atrophy due to decreased protein synthesis and increased
ubiquitin-proteasome-mediated protein degradation [CORRECT]
B. Apoptosis of myocytes triggered by tumor necrosis factor-alpha
C. Metaplasia of skeletal muscle to fibrous tissue
D. Necrosis induced by ischemia from disuse
Correct Answer: A
Rationale: Disuse and immobilization produce skeletal muscle atrophy through decreased protein
synthesis and activation of the ubiquitin-proteasome pathway with upregulation of muscle-specific E3
ligases (atrogin-1, MuRF1). This is a reversible decrease in cell size. Apoptosis, metaplasia, and necrosis
are not characteristic of disuse atrophy.
Q11: In cellular signaling, which mechanism describes how a hydrophobic ligand such
as cortisol exerts its effect on target cells?
A. Binds cell-surface G-protein-coupled receptors, activating adenylyl cyclase
B. Diffuses across the plasma membrane and binds intracellular nuclear receptors
that function as ligand-regulated transcription factors [CORRECT]
C. Activates receptor tyrosine kinases at the membrane surface
D. Binds ion-channel linked receptors in the membrane
Correct Answer: B
Rationale: Hydrophobic ligands (steroid hormones, thyroid hormone, vitamin D, retinoic acid) diffuse
across the plasma membrane and bind intracellular receptors in the cytoplasm or nucleus. The
ligand-receptor complex then binds hormone response elements (HREs) on DNA, directly modulating
gene transcription. GPCRs, RTKs, and ion-channel receptors mediate hydrophilic ligand signaling.
Q12: A cell is exposed to ionizing radiation. The predominant mechanism of DNA
damage and subsequent cellular injury is:
A. Direct breakage of phosphodiester bonds exclusively
B. Generation of reactive oxygen species that cause single- and double-strand DNA
breaks, base modifications, and lipid peroxidation [CORRECT]
C. Inhibition of DNA polymerase without strand damage
D. Methylation of CpG islands causing gene silencing
Correct Answer: B
Grand Canyon University — College of Nursing and Health Care Professions Page 4
MIDTERM EXAM: NUR631 / NUR 631 (LATEST
UPDATE) ADVANCED PHYSIOLOGY AND PATHOPHYSIOLOGY
EXAM | QUESTIONS AND VERIFIED ANSWERS | 100% CORRECT
| GRADE A — GCU
Grand Canyon University — College of Nursing and Health Care Professions
Aligned with NUR 631 Course Syllabus, AACN Essentials of Master's Education, and Advanced Physiology
and Pathophysiology Competencies (2026/2027 Edition)
Total Questions: 120 | Sections: 8 | Cognitive Mix: 20% Recall, 50% Application, 30% Analysis
Section 1: Cellular Physiology & Pathophysiology
Q1: A 58-year-old male with chronic obstructive pulmonary disease exhibits an elevated
hematocrit. Which cellular adaptation best explains the increased red blood cell mass
in response to chronic hypoxemia?
A. Hyperplasia, an increase in the number of cells due to increased hormonal stimulation
B. Hypertrophy, an increase in cell size driven by increased functional demand
[CORRECT]
C. Metaplasia, the reversible replacement of one differentiated cell type by another
D. Dysplasia, disordered cellular growth with atypical morphology suggestive of pre-neoplastic
change
Correct Answer: B
Rationale: Chronic hypoxemia stimulates renal erythropoietin release, which drives erythroid
precursor cells to enlarge and synthesize more hemoglobin—an increase in cell SIZE rather than
number. This is hypertrophy (compensatory). Hyperplasia is ruled out because mature RBCs are
anucleate and cannot divide; metaplasia and dysplasia involve cell-type change and atypical growth,
neither of which occurs in erythroid response to hypoxia.
Q2: A researcher examines a biopsy of bronchial epithelium from a 55-year-old heavy
smoker. Columnar ciliated epithelium has been replaced by stratified squamous
epithelium. Which cellular adaptation is depicted, and what is its primary biological
significance?
A. Hypertrophy; an adaptive response that strengthens tissue contractility
B. Metaplasia; a reversible, protective substitution that is reversible with smoking
cessation but may progress to malignancy [CORRECT]
C. Dysplasia; an irreversible pre-neoplastic transformation that mandates immediate surgical
excision
D. Anaplasia; loss of cell differentiation consistent with frank malignancy
Correct Answer: B
Rationale: Replacement of columnar ciliated epithelium by stratified squamous epithelium in smokers
is classic squamous metaplasia, a reversible adaptive substitution to chronic irritation. It is not yet
malignant (rules out anaplasia), does not increase cell size (rules out hypertrophy), and is not the
disordered atypical proliferation of dysplasia. Continued injury may, however, progress to dysplasia and
squamous cell carcinoma.
Grand Canyon University — College of Nursing and Health Care Professions Page 1
,MIDTERM EXAM: NUR631 — Advanced Physiology and Pathophysiology | GCU (2026/2027)
Q3: A cell is exposed to ischemia. Within minutes, ATP depletion triggers failure of the
Na+/K+-ATPase pump. Which sequence of events best describes the subsequent
pathophysiological cascade leading to irreversible cellular injury?
A. Na+ influx → cellular swelling → K+ efflux → ribosome detachment → reversible injury only
B. Na+ influx → cellular swelling → Ca2+ influx → mitochondrial dysfunction →
activation of phospholipases and proteases → membrane damage → cell death
[CORRECT]
C. K+ influx → cellular dehydration → Cl- efflux → nuclear pyknosis → apoptosis
D. Ca2+ efflux → cytoskeletal stabilization → lysosomal inactivation → necrosis
Correct Answer: B
Rationale: Ischemia depletes ATP, disabling the Na+/K+-ATPase. Sodium enters the cell, water
follows, and the cell swells. Critically, ATP depletion also fails Ca2+ pumps, allowing pathologic calcium
influx into the cytosol and mitochondria. Calcium activates phospholipases (membrane destruction),
proteases (cytoskeleton disruption), and endonucleases (DNA fragmentation), and impairs
mitochondria—collectively producing irreversible injury. K+ efflux and ribosome detachment occur
early but are reversible.
Q4: Which statement most accurately distinguishes apoptosis from necrosis at the
cellular and tissue level?
A. Apoptosis produces a robust inflammatory response due to membrane rupture, whereas
necrosis is inflammation-silent
B. Apoptosis is characterized by cell swelling, membrane rupture, and random DNA digestion,
while necrosis produces cell shrinkage and an inflammatory response
C. Apoptosis is an energy-requiring, programmed process producing cell shrinkage,
nuclear condensation, and apoptotic bodies without significant inflammation;
necrosis is characterized by cell swelling, membrane rupture, and marked
inflammation [CORRECT]
D. Apoptosis can only occur in pathologic states, whereas necrosis is exclusively physiologic
Correct Answer: C
Rationale: Apoptosis is ATP-dependent, programmed cell death involving caspase activation, cell
shrinkage, chromatin condensation (pyknosis), and formation of apoptotic bodies that are phagocytosed
without inflammation. Necrosis is pathologic, characterized by cell swelling (oncosis), membrane
rupture, release of cellular contents, and a vigorous inflammatory response. Options A, B, and D reverse
these features or contain factually incorrect statements.
Q5: A 67-year-old patient receiving doxorubicin chemotherapy develops cardiotoxicity.
The mechanism most directly responsible is:
A. Formation of hydroxyl free radicals via iron-mediated Fenton chemistry, causing
lipid peroxidation of mitochondrial membranes [CORRECT]
B. Inhibition of topoisomerase II exclusively, without oxidative injury
C. Direct competitive inhibition of cardiac beta-1 adrenergic receptors
D. Activation of Bcl-2 with consequent suppression of cardiomyocyte apoptosis
Correct Answer: A
Rationale: Doxorubicin causes dose-dependent cardiotoxicity primarily through iron-catalyzed free
radical generation (Fenton reaction) and lipid peroxidation of mitochondrial membranes, depleting
cardiomyocyte ATP and triggering apoptosis. While doxorubicin also inhibits topoisomerase II in tumor
cells, the cardiotoxic mechanism is predominantly oxidative. The drug does not act on beta-receptors,
Grand Canyon University — College of Nursing and Health Care Professions Page 2
,MIDTERM EXAM: NUR631 — Advanced Physiology and Pathophysiology | GCU (2026/2027)
and it promotes (not suppresses) cardiomyocyte apoptosis via Bcl-2 family modulation.
Q6: Which second messenger system is activated when a ligand binds a
Gq-protein-coupled receptor, and what is the immediate downstream effect?
A. Activation of adenylyl cyclase → increased cAMP → protein kinase A activation
B. Activation of phospholipase C → hydrolysis of PIP2 to IP3 and DAG → Ca2+ release
from ER and protein kinase C activation [CORRECT]
C. Activation of guanylyl cyclase → increased cGMP → protein kinase G activation
D. Direct activation of receptor tyrosine kinase → autophosphorylation → Ras-MAPK cascade
Correct Answer: B
Rationale: Gq-coupled receptors (e.g., alpha-1 adrenergic, muscarinic M1, M3) activate phospholipase
C, which hydrolyzes membrane PIP2 into IP3 (mobilizes intracellular Ca2+ from the ER) and DAG
(activates protein kinase C). Adenylyl cyclase/cAMP is the Gs pathway, guanylyl cyclase/cGMP is
receptor guanylyl cyclase, and receptor tyrosine kinase signaling is independent of G proteins.
Q7: A cell experiences a mutation that disrupts the Rb (retinoblastoma) protein. Which
checkpoint of the cell cycle is most directly affected, and what is the consequence?
A. G2/M checkpoint; cells arrest in G2 and cannot enter mitosis
B. Spindle (M) checkpoint; chromosomal segregation fails
C. G1/S restriction point; cells progress into S phase even without mitogenic signals,
predisposing to uncontrolled proliferation [CORRECT]
D. S-phase checkpoint; DNA replication stalls
Correct Answer: C
Rationale: Rb is the master regulator of the G1/S restriction point. Hypophosphorylated Rb sequesters
E2F transcription factors, preventing S-phase entry. Mitogenic signals activate cyclin D-CDK4/6 and
cyclin E-CDK2, which phosphorylate Rb, releasing E2F and allowing S-phase entry. Mutated or absent
Rb removes this brake, permitting uncontrolled S-phase progression—a hallmark of many cancers.
Q8: A patient with mitochondrial disease demonstrates lactic acidosis with normal
oxygenation. The underlying cellular mechanism is best described as:
A. Impaired glycolysis resulting in pyruvate accumulation and conversion to lactate
B. Defective electron transport chain complexes reducing aerobic ATP production,
forcing anaerobic glycolysis with excessive lactate generation [CORRECT]
C. Excessive gluconeogenesis causing pyruvate overflow into the lactate pool
D. Deficiency of pyruvate carboxylase impairing TCA cycle entry
Correct Answer: B
Rationale: Mitochondrial disease impairs the electron transport chain (ETC), reducing oxidative
phosphorylation. Cells compensate by upregulating anaerobic glycolysis, which generates ATP but
produces pyruvate faster than defective mitochondria can metabolize it via the TCA cycle. Excess
pyruvate is converted to lactate by lactate dehydrogenase, causing lactic acidosis even with normal
tissue oxygenation. Glycolysis itself is not impaired; it is paradoxically increased.
Q9: Which of the following accurately describes the role of the Na+/K+-ATPase pump
in maintaining cellular homeostasis?
A. It moves 2 Na+ out and 3 K+ in, generating a net negative intracellular charge
Grand Canyon University — College of Nursing and Health Care Professions Page 3
, MIDTERM EXAM: NUR631 — Advanced Physiology and Pathophysiology | GCU (2026/2027)
B. It moves 3 Na+ out and 2 K+ in, hydrolyzing one ATP, and contributes to the
resting membrane potential and secondary active transport gradients [CORRECT]
C. It is a passive channel that does not consume ATP
D. It moves Na+ and K+ in a 1:1 ratio with no contribution to membrane potential
Correct Answer: B
Rationale: The Na+/K+-ATPase is an electrogenic primary active transporter that hydrolyzes one ATP
to move 3 Na+ out and 2 K+ in, contributing directly to the negative resting membrane potential (about
-10 mV of the total ~-70 mV) and establishing Na+ and K+ gradients used by secondary active
transporters (e.g., Na+/Ca2+ exchanger, Na+/glucose cotransporter).
Q10: A 72-year-old patient exhibits marked skeletal muscle wasting after prolonged
immobilization following hip surgery. Which cellular process is most directly
responsible?
A. Atrophy due to decreased protein synthesis and increased
ubiquitin-proteasome-mediated protein degradation [CORRECT]
B. Apoptosis of myocytes triggered by tumor necrosis factor-alpha
C. Metaplasia of skeletal muscle to fibrous tissue
D. Necrosis induced by ischemia from disuse
Correct Answer: A
Rationale: Disuse and immobilization produce skeletal muscle atrophy through decreased protein
synthesis and activation of the ubiquitin-proteasome pathway with upregulation of muscle-specific E3
ligases (atrogin-1, MuRF1). This is a reversible decrease in cell size. Apoptosis, metaplasia, and necrosis
are not characteristic of disuse atrophy.
Q11: In cellular signaling, which mechanism describes how a hydrophobic ligand such
as cortisol exerts its effect on target cells?
A. Binds cell-surface G-protein-coupled receptors, activating adenylyl cyclase
B. Diffuses across the plasma membrane and binds intracellular nuclear receptors
that function as ligand-regulated transcription factors [CORRECT]
C. Activates receptor tyrosine kinases at the membrane surface
D. Binds ion-channel linked receptors in the membrane
Correct Answer: B
Rationale: Hydrophobic ligands (steroid hormones, thyroid hormone, vitamin D, retinoic acid) diffuse
across the plasma membrane and bind intracellular receptors in the cytoplasm or nucleus. The
ligand-receptor complex then binds hormone response elements (HREs) on DNA, directly modulating
gene transcription. GPCRs, RTKs, and ion-channel receptors mediate hydrophilic ligand signaling.
Q12: A cell is exposed to ionizing radiation. The predominant mechanism of DNA
damage and subsequent cellular injury is:
A. Direct breakage of phosphodiester bonds exclusively
B. Generation of reactive oxygen species that cause single- and double-strand DNA
breaks, base modifications, and lipid peroxidation [CORRECT]
C. Inhibition of DNA polymerase without strand damage
D. Methylation of CpG islands causing gene silencing
Correct Answer: B
Grand Canyon University — College of Nursing and Health Care Professions Page 4
