TEST BANK: ANATOMY &
PHYSIOLOGY: THE UNITY OF FORM
AND FUNCTION
10th Edition | Updated 2026/2027
Authors: Kenneth S. Saladin, Eric Wise, Robin McFarland Resource Type: Comprehensive
Elite Exam Resource Subject: Advanced Human Anatomy and Physiology Assessment Level:
Expert/Clinical Integration
PART ONE: ORGANIZATION OF THE BODY
Question 1: Homeostatic Regulation and Negative Feedback Loops
Topic: Major Themes of Anatomy and Physiology Difficulty: High
Question: A 55-year-old male with a history of untreated Type 1 Diabetes Mellitus presents to
the emergency department in a state of ketoacidosis. His physiological state involves the
catastrophic disruption of standard homeostatic loops. Considering the principles of negative
feedback inhibition described in Saladin’s 10th Edition, which of the following accurately
describes the specific failure of the effector mechanism in this pathology, and how does it
fundamentally differ from a positive feedback loop?
A. The control center (hypothalamus) fails to detect the stimulus (high blood glucose),
preventing the release of insulin, thus acting as an open loop. B. The receptor (pancreatic beta
cells) detects the stimulus, but the effector (skeletal muscle and adipose tissue) fails to receive
the signal due to a lack of insulin secretion, breaking the loop that normally negates the original
stimulus. C. The system has physiologically converted to a positive feedback loop where high
glucose levels trigger glucagon release, further increasing blood glucose in a self-amplifying
cycle similar to the Ferguson reflex in childbirth. D. The effector organs have become
desensitized to the signal (downregulation of tyrosine kinase receptors), despite normal output
from the control center, representing a failure of the receptor level rather than the integration
center. E. The set point for blood glucose has been physiologically reset to a higher level by the
medulla oblongata to accommodate the increased metabolic demand of ketogenesis.
Correct Answer: B
Detailed Rationale: Anatomy and physiology are grounded in the concept of homeostasis, the
body's ability to maintain a dynamic equilibrium despite external fluctuations. In the context of
blood glucose regulation, the system operates via a negative feedback loop. Negative feedback
is the fundamental mechanism that keeps a variable close to its set point; the body senses a
change and activates mechanisms to reverse it.
In a healthy individual, rising blood glucose (the stimulus) is detected by the beta cells of the
pancreas (acting as both sensor and integrator). These cells secrete insulin (the chemical
messenger). Insulin binds to receptors on effectors—primarily skeletal muscle and adipose
tissue—facilitating glucose uptake via GLUT4 transporters. This removal of glucose from the
blood negates the original stimulus, restoring homeostasis.
,In Type 1 Diabetes, the autoimmune destruction of pancreatic beta cells destroys the
sensor/integrator's ability to produce the signal (insulin). Consequently, the effectors never
receive the command to uptake glucose. The negative feedback loop is broken not because the
effectors are resistant (as in Type 2 Diabetes) or because the set point has changed, but
because the transmission of the corrective signal is absent. This results in the persistence of the
stimulus (hyperglycemia) without the "negating" response. The breakdown leads to the
recruitment of alternative metabolic pathways (lipolysis), resulting in ketoacidosis.
Distractor Analysis:
● A is incorrect: The hypothalamus is not the primary control center for acute blood
glucose regulation; the pancreas acts as the sensor and control center for insulin release.
● C is incorrect: While positive feedback loops do exist in the body (e.g., oxytocin in
childbirth or blood clotting), diabetes is not a conversion to a positive feedback loop.
Positive feedback amplifies a change (self-amplifying cycle) to a specific endpoint,
whereas diabetes is a failure of negative feedback.
● D is incorrect: This describes the pathophysiology of Type 2 Diabetes, where the effector
cells become resistant to insulin (receptor downregulation). The question specifies Type
1, which involves a lack of secretion.
● E is incorrect: Set points can change (e.g., fever), but diabetes is defined by the inability
to maintain the set point due to pathology, not a regulated physiological resetting of the
homeostatic range.
Question 2: Membrane Transport and Cystic Fibrosis
Topic: Cellular Form and Function Difficulty: High
Question: Cystic fibrosis (CF) is a genetic disorder resulting from a mutation in the CFTR gene.
This mutation impairs a specific type of membrane transport protein. Based on the fluid mosaic
model and transport kinetics, how does the failure of this specific transporter lead to the
pathognomonic thickened mucus secretions observed in the respiratory and digestive tracts?
A. The failure of primary active transport pumps to move sodium out of the cell leads to
intracellular swelling and lysis of goblet cells, releasing chromatin that thickens the mucus. B.
The inability to actively transport calcium into the sarcoplasmic reticulum prevents ciliary
beating, leading to mucus accumulation and stasis. C. A defect in a chloride channel prevents
chloride efflux; consequently, sodium and water do not follow the osmotic gradient into the
extracellular mucus, resulting in dehydrated, viscous secretions. D. The mutation causes an
overexpression of aquaporins, causing excessive water reabsorption from the mucus back into
the cytoplasm, drying out the airways. E. Facilitated diffusion of glucose is inhibited, starving the
cilia of energy required to clear normal mucus secretions.
Correct Answer: C
Detailed Rationale: The cell membrane regulates the intracellular and extracellular
environments through selective permeability and transport proteins. The Cystic Fibrosis
Transmembrane Conductance Regulator (CFTR) is an ATP-gated chloride channel. Although it
uses ATP, it functions as a gated channel allowing chloride ions to move down their
electrochemical gradient.
Physiologically, the CFTR protein facilitates the transport of chloride ions (Cl^-) out of epithelial
cells into the lumen (e.g., of the airway or pancreatic ducts). The accumulation of negative
charge in the lumen draws sodium ions (Na^+) across the epithelium via paracellular pathways
or other channels to maintain electrical neutrality. The secretion of NaCl into the lumen
increases the osmotic pressure, which draws water out of the cells via osmosis. This hydration
, is critical for maintaining the sol-layer of mucus, keeping it thin and movable by cilia.
In Cystic Fibrosis, the defective CFTR protein fails to transport chloride. Without the chloride
gradient, sodium does not follow, and consequently, water remains within the tissue fluid rather
than hydrating the mucus. This results in dehydrated, sticky, and viscous mucus that clogs
airways and pancreatic ducts, leading to the clinical manifestations of the disease.
Distractor Analysis:
● A is incorrect: This describes the failure of the Na^+/K^+ ATPase, which would affect cell
volume regulation but is not the primary defect in CF. The Na^+/K^+ pump establishes the
gradients used by secondary transport but is not the mutated protein in CF.
● B is incorrect: While calcium is important for ciliary function, CF is specifically a disorder
of chloride transport, not calcium pumps.
● D is incorrect: The pathology is not due to excessive aquaporin activity moving water in,
but rather the failure of salt transport to draw water out.
● E is incorrect: Glucose transport is not the primary deficit in CF; the issue is electrolytic
and osmotic balance in the secretions.
Question 3: Enzymes and Energy of Activation
Topic: The Chemistry of Life Difficulty: Moderate
Question: Metabolic reactions in the human body must occur at 37°C, a temperature generally
too low for rapid spontaneous chemical reactions. How do enzymes, as biological catalysts,
facilitate these reactions without altering the thermodynamic equilibrium?
A. Enzymes increase the kinetic energy of the substrate molecules, effectively raising the local
temperature to physiological levels. B. Enzymes lower the activation energy required for the
reaction by stabilizing the transition state, allowing the reaction to proceed at a faster rate
without being consumed. C. Enzymes alter the free energy change (\Delta G) of the reaction,
making endergonic reactions exergonic. D. Enzymes donate phosphate groups to every
substrate, destabilizing bonds through covalent modification. E. Enzymes decrease the
concentration of products, driving the reaction forward according to Le Chatelier's principle.
Correct Answer: B
Detailed Rationale: Enzymes are protein catalysts that speed up the rate of chemical reactions
in the body. They do not add energy to the reaction or change the net energy difference (\Delta
G) between reactants and products. Instead, they function by lowering the activation
energy—the energy barrier that must be overcome for the reactants to reach the transition state.
By binding to the substrate at the active site (forming an enzyme-substrate complex), the
enzyme induces conformational changes (induced fit) that stress chemical bonds, orient
molecules correctly, or provide a favorable microenvironment. This stabilization of the transition
state reduces the energy required for the reaction to occur, increasing the reaction rate by
millions of times compared to the uncatalyzed rate.
Distractor Analysis:
● A is incorrect: Enzymes do not change temperature; they allow reactions to occur at
body temperature.
● C is incorrect: Catalysts cannot change the \Delta G (thermodynamics); they only
change the kinetics (speed).
● D is incorrect: While some enzymes (kinases) transfer phosphate, this is not the
universal mechanism of catalysis.
● E is incorrect: Enzymes speed up both forward and reverse reactions equally to reach
equilibrium faster; they do not shift equilibrium positions by removing products.
PHYSIOLOGY: THE UNITY OF FORM
AND FUNCTION
10th Edition | Updated 2026/2027
Authors: Kenneth S. Saladin, Eric Wise, Robin McFarland Resource Type: Comprehensive
Elite Exam Resource Subject: Advanced Human Anatomy and Physiology Assessment Level:
Expert/Clinical Integration
PART ONE: ORGANIZATION OF THE BODY
Question 1: Homeostatic Regulation and Negative Feedback Loops
Topic: Major Themes of Anatomy and Physiology Difficulty: High
Question: A 55-year-old male with a history of untreated Type 1 Diabetes Mellitus presents to
the emergency department in a state of ketoacidosis. His physiological state involves the
catastrophic disruption of standard homeostatic loops. Considering the principles of negative
feedback inhibition described in Saladin’s 10th Edition, which of the following accurately
describes the specific failure of the effector mechanism in this pathology, and how does it
fundamentally differ from a positive feedback loop?
A. The control center (hypothalamus) fails to detect the stimulus (high blood glucose),
preventing the release of insulin, thus acting as an open loop. B. The receptor (pancreatic beta
cells) detects the stimulus, but the effector (skeletal muscle and adipose tissue) fails to receive
the signal due to a lack of insulin secretion, breaking the loop that normally negates the original
stimulus. C. The system has physiologically converted to a positive feedback loop where high
glucose levels trigger glucagon release, further increasing blood glucose in a self-amplifying
cycle similar to the Ferguson reflex in childbirth. D. The effector organs have become
desensitized to the signal (downregulation of tyrosine kinase receptors), despite normal output
from the control center, representing a failure of the receptor level rather than the integration
center. E. The set point for blood glucose has been physiologically reset to a higher level by the
medulla oblongata to accommodate the increased metabolic demand of ketogenesis.
Correct Answer: B
Detailed Rationale: Anatomy and physiology are grounded in the concept of homeostasis, the
body's ability to maintain a dynamic equilibrium despite external fluctuations. In the context of
blood glucose regulation, the system operates via a negative feedback loop. Negative feedback
is the fundamental mechanism that keeps a variable close to its set point; the body senses a
change and activates mechanisms to reverse it.
In a healthy individual, rising blood glucose (the stimulus) is detected by the beta cells of the
pancreas (acting as both sensor and integrator). These cells secrete insulin (the chemical
messenger). Insulin binds to receptors on effectors—primarily skeletal muscle and adipose
tissue—facilitating glucose uptake via GLUT4 transporters. This removal of glucose from the
blood negates the original stimulus, restoring homeostasis.
,In Type 1 Diabetes, the autoimmune destruction of pancreatic beta cells destroys the
sensor/integrator's ability to produce the signal (insulin). Consequently, the effectors never
receive the command to uptake glucose. The negative feedback loop is broken not because the
effectors are resistant (as in Type 2 Diabetes) or because the set point has changed, but
because the transmission of the corrective signal is absent. This results in the persistence of the
stimulus (hyperglycemia) without the "negating" response. The breakdown leads to the
recruitment of alternative metabolic pathways (lipolysis), resulting in ketoacidosis.
Distractor Analysis:
● A is incorrect: The hypothalamus is not the primary control center for acute blood
glucose regulation; the pancreas acts as the sensor and control center for insulin release.
● C is incorrect: While positive feedback loops do exist in the body (e.g., oxytocin in
childbirth or blood clotting), diabetes is not a conversion to a positive feedback loop.
Positive feedback amplifies a change (self-amplifying cycle) to a specific endpoint,
whereas diabetes is a failure of negative feedback.
● D is incorrect: This describes the pathophysiology of Type 2 Diabetes, where the effector
cells become resistant to insulin (receptor downregulation). The question specifies Type
1, which involves a lack of secretion.
● E is incorrect: Set points can change (e.g., fever), but diabetes is defined by the inability
to maintain the set point due to pathology, not a regulated physiological resetting of the
homeostatic range.
Question 2: Membrane Transport and Cystic Fibrosis
Topic: Cellular Form and Function Difficulty: High
Question: Cystic fibrosis (CF) is a genetic disorder resulting from a mutation in the CFTR gene.
This mutation impairs a specific type of membrane transport protein. Based on the fluid mosaic
model and transport kinetics, how does the failure of this specific transporter lead to the
pathognomonic thickened mucus secretions observed in the respiratory and digestive tracts?
A. The failure of primary active transport pumps to move sodium out of the cell leads to
intracellular swelling and lysis of goblet cells, releasing chromatin that thickens the mucus. B.
The inability to actively transport calcium into the sarcoplasmic reticulum prevents ciliary
beating, leading to mucus accumulation and stasis. C. A defect in a chloride channel prevents
chloride efflux; consequently, sodium and water do not follow the osmotic gradient into the
extracellular mucus, resulting in dehydrated, viscous secretions. D. The mutation causes an
overexpression of aquaporins, causing excessive water reabsorption from the mucus back into
the cytoplasm, drying out the airways. E. Facilitated diffusion of glucose is inhibited, starving the
cilia of energy required to clear normal mucus secretions.
Correct Answer: C
Detailed Rationale: The cell membrane regulates the intracellular and extracellular
environments through selective permeability and transport proteins. The Cystic Fibrosis
Transmembrane Conductance Regulator (CFTR) is an ATP-gated chloride channel. Although it
uses ATP, it functions as a gated channel allowing chloride ions to move down their
electrochemical gradient.
Physiologically, the CFTR protein facilitates the transport of chloride ions (Cl^-) out of epithelial
cells into the lumen (e.g., of the airway or pancreatic ducts). The accumulation of negative
charge in the lumen draws sodium ions (Na^+) across the epithelium via paracellular pathways
or other channels to maintain electrical neutrality. The secretion of NaCl into the lumen
increases the osmotic pressure, which draws water out of the cells via osmosis. This hydration
, is critical for maintaining the sol-layer of mucus, keeping it thin and movable by cilia.
In Cystic Fibrosis, the defective CFTR protein fails to transport chloride. Without the chloride
gradient, sodium does not follow, and consequently, water remains within the tissue fluid rather
than hydrating the mucus. This results in dehydrated, sticky, and viscous mucus that clogs
airways and pancreatic ducts, leading to the clinical manifestations of the disease.
Distractor Analysis:
● A is incorrect: This describes the failure of the Na^+/K^+ ATPase, which would affect cell
volume regulation but is not the primary defect in CF. The Na^+/K^+ pump establishes the
gradients used by secondary transport but is not the mutated protein in CF.
● B is incorrect: While calcium is important for ciliary function, CF is specifically a disorder
of chloride transport, not calcium pumps.
● D is incorrect: The pathology is not due to excessive aquaporin activity moving water in,
but rather the failure of salt transport to draw water out.
● E is incorrect: Glucose transport is not the primary deficit in CF; the issue is electrolytic
and osmotic balance in the secretions.
Question 3: Enzymes and Energy of Activation
Topic: The Chemistry of Life Difficulty: Moderate
Question: Metabolic reactions in the human body must occur at 37°C, a temperature generally
too low for rapid spontaneous chemical reactions. How do enzymes, as biological catalysts,
facilitate these reactions without altering the thermodynamic equilibrium?
A. Enzymes increase the kinetic energy of the substrate molecules, effectively raising the local
temperature to physiological levels. B. Enzymes lower the activation energy required for the
reaction by stabilizing the transition state, allowing the reaction to proceed at a faster rate
without being consumed. C. Enzymes alter the free energy change (\Delta G) of the reaction,
making endergonic reactions exergonic. D. Enzymes donate phosphate groups to every
substrate, destabilizing bonds through covalent modification. E. Enzymes decrease the
concentration of products, driving the reaction forward according to Le Chatelier's principle.
Correct Answer: B
Detailed Rationale: Enzymes are protein catalysts that speed up the rate of chemical reactions
in the body. They do not add energy to the reaction or change the net energy difference (\Delta
G) between reactants and products. Instead, they function by lowering the activation
energy—the energy barrier that must be overcome for the reactants to reach the transition state.
By binding to the substrate at the active site (forming an enzyme-substrate complex), the
enzyme induces conformational changes (induced fit) that stress chemical bonds, orient
molecules correctly, or provide a favorable microenvironment. This stabilization of the transition
state reduces the energy required for the reaction to occur, increasing the reaction rate by
millions of times compared to the uncatalyzed rate.
Distractor Analysis:
● A is incorrect: Enzymes do not change temperature; they allow reactions to occur at
body temperature.
● C is incorrect: Catalysts cannot change the \Delta G (thermodynamics); they only
change the kinetics (speed).
● D is incorrect: While some enzymes (kinases) transfer phosphate, this is not the
universal mechanism of catalysis.
● E is incorrect: Enzymes speed up both forward and reverse reactions equally to reach
equilibrium faster; they do not shift equilibrium positions by removing products.
