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.
,Question 4: Protein Synthesis and Translation
Topic: Genes and Cellular Function Difficulty: Moderate
Question: Ricin is a potent toxin that irreversibly inactivates the ribosomes of eukaryotic cells. If
a cell is exposed to ricin, which specific cellular process is immediately halted, and what is the
downstream consequence for cell survival?
A. Transcription of DNA into mRNA stops, preventing the creation of new genetic templates. B.
DNA replication is blocked, preventing the cell from entering the S-phase of the cell cycle. C.
Translation is inhibited because the ribosome can no longer catalyze peptide bond formation
between amino acids, leading to a cessation of protein production. D. Post-translational
modification in the Golgi apparatus ceases, leading to misfolded proteins. E. The
sodium-potassium pump is blocked, leading to immediate depolarization and lysis.
Correct Answer: C
Detailed Rationale: The ribosome is the cellular machinery responsible for translation—the
process of decoding mRNA to synthesize a polypeptide chain. Ricin specifically inactivates the
60S subunit of the eukaryotic ribosome by depurating a specific adenine residue in the 28S
rRNA.
Without functional ribosomes, the cell cannot form peptide bonds between amino acids.
Consequently, protein synthesis halts completely. Since proteins are required for essentially all
cellular functions (enzymes, structural components, signaling molecules), the inability to replace
degrading proteins leads to rapid cell death. This targets the central dogma of biology at the
translation step.
Distractor Analysis:
● A is incorrect: Transcription occurs in the nucleus via RNA polymerase; ribosomes are
located in the cytoplasm/RER.
● B is incorrect: DNA replication involves DNA polymerase, not ribosomes.
● D is incorrect: The Golgi modifies proteins after they are synthesized; if synthesis stops,
the Golgi has nothing to modify, but it is not the primary target.
● E is incorrect: While pumps are proteins, the toxin stops their synthesis, not their
immediate function (though they will eventually degrade).
Question 5: Epithelial Tissue Characteristics
Topic: The Human Tissues Difficulty: Moderate
Question: A defining characteristic of epithelial tissue is its polarity. Consider the simple
columnar epithelium lining the small intestine. How does the structural difference between the
apical and basal surfaces functionally support the tissue's role in absorption?
A. The apical surface contains desmosomes to anchor the cell to the basement membrane,
while the basal surface contains microvilli for absorption. B. The apical surface features
microvilli that increase surface area for nutrient interaction, while the basal surface contains
hemidesmosomes and integrins for attachment to the underlying connective tissue. C. The
apical surface is lined with cilia to move mucus, while the basal surface facilitates gap junction
communication with smooth muscle. D. The epithelium is non-polar, with uniform distribution of
transport proteins on all sides to maximize passive diffusion. E. The apical surface secretes
collagen to form the basement membrane, while the basal surface absorbs nutrients from the
blood.
Correct Answer: B
, Detailed Rationale: Epithelial polarity refers to the unequal distribution of organelles and
membrane proteins between the exposed (apical) surface and the attached (basal) surface. In
the small intestine, the primary function is absorption.
● Apical Surface: Faces the lumen. It is covered in microvilli (forming the brush border),
which vastly increase the surface area available for transporter proteins to absorb
glucose, amino acids, and lipids.
● Basal Surface: Faces the basement membrane. It contains anchorage proteins like
integrins and hemidesmosomes to secure the epithelium to the underlying connective
tissue (lamina propria) and transport proteins to move absorbed nutrients into the
interstitial fluid/blood.
Distractor Analysis:
● A is incorrect: It reverses the locations. Microvilli are apical; anchors are basal.
● C is incorrect: Cilia are found in the respiratory tract (for motility), not the small intestine
(which needs surface area for absorption).
● D is incorrect: Polarity is a fundamental definition of epithelia; non-polar cells would lose
directional transport capability.
● E is incorrect: The basement membrane is secreted basally, and nutrients are absorbed
apically from the lumen, not the blood.
PART TWO: SUPPORT AND MOVEMENT
Question 6: Burn Pathophysiology and Fluid Shifts
Topic: The Integumentary System Difficulty: High
Question: A 30-year-old patient is admitted with partial and full-thickness burns covering 40%
of their Total Body Surface Area (TBSA). In the first 24 hours, the patient is at high risk for
hypovolemic shock. According to the pathophysiology of severe burns described in Saladin,
what is the primary cellular and histological mechanism driving the massive fluid shift from the
intravascular to the interstitial compartment (fluid sequestration)?
A. Heat-induced denaturation of albumin increases blood colloid osmotic pressure, pulling fluid
into the capillaries, which then rupture. B. The release of inflammatory mediators like histamine
and vasoactive kinins causes a systemic increase in capillary permeability, allowing plasma
proteins to leak into the interstitial space, reversing the oncotic gradient. C. Destruction of the
epidermis eliminates the waterproof keratin barrier, leading to immediate evaporation of 5 liters
of blood volume directly into the atmosphere. D. Systemic vasoconstriction caused by the
sympathetic nervous system forces plasma out of the high-pressure arterioles into the tissue
spaces. E. The hypermetabolic state consumes intracellular water for hydrolysis, depleting the
intravascular volume to support catabolism.
Correct Answer: B
Detailed Rationale: A major burn injury (>30% TBSA) triggers a systemic inflammatory
response syndrome (SIRS). The direct thermal injury and the subsequent release of
inflammatory cytokines (e.g., histamine, bradykinin, prostaglandins) cause a catastrophic failure
of the capillary endothelial barrier. Normally, the endothelial lining prevents large plasma
proteins (like albumin) from escaping the bloodstream. This protein retention maintains the
blood colloid osmotic pressure (BCOP), which holds water in the vessels.
In severe burns, the capillaries become leaky (increased permeability). Plasma proteins escape
into the interstitial space (the "third space"). As proteins move out, they carry the oncotic pulling
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.
,Question 4: Protein Synthesis and Translation
Topic: Genes and Cellular Function Difficulty: Moderate
Question: Ricin is a potent toxin that irreversibly inactivates the ribosomes of eukaryotic cells. If
a cell is exposed to ricin, which specific cellular process is immediately halted, and what is the
downstream consequence for cell survival?
A. Transcription of DNA into mRNA stops, preventing the creation of new genetic templates. B.
DNA replication is blocked, preventing the cell from entering the S-phase of the cell cycle. C.
Translation is inhibited because the ribosome can no longer catalyze peptide bond formation
between amino acids, leading to a cessation of protein production. D. Post-translational
modification in the Golgi apparatus ceases, leading to misfolded proteins. E. The
sodium-potassium pump is blocked, leading to immediate depolarization and lysis.
Correct Answer: C
Detailed Rationale: The ribosome is the cellular machinery responsible for translation—the
process of decoding mRNA to synthesize a polypeptide chain. Ricin specifically inactivates the
60S subunit of the eukaryotic ribosome by depurating a specific adenine residue in the 28S
rRNA.
Without functional ribosomes, the cell cannot form peptide bonds between amino acids.
Consequently, protein synthesis halts completely. Since proteins are required for essentially all
cellular functions (enzymes, structural components, signaling molecules), the inability to replace
degrading proteins leads to rapid cell death. This targets the central dogma of biology at the
translation step.
Distractor Analysis:
● A is incorrect: Transcription occurs in the nucleus via RNA polymerase; ribosomes are
located in the cytoplasm/RER.
● B is incorrect: DNA replication involves DNA polymerase, not ribosomes.
● D is incorrect: The Golgi modifies proteins after they are synthesized; if synthesis stops,
the Golgi has nothing to modify, but it is not the primary target.
● E is incorrect: While pumps are proteins, the toxin stops their synthesis, not their
immediate function (though they will eventually degrade).
Question 5: Epithelial Tissue Characteristics
Topic: The Human Tissues Difficulty: Moderate
Question: A defining characteristic of epithelial tissue is its polarity. Consider the simple
columnar epithelium lining the small intestine. How does the structural difference between the
apical and basal surfaces functionally support the tissue's role in absorption?
A. The apical surface contains desmosomes to anchor the cell to the basement membrane,
while the basal surface contains microvilli for absorption. B. The apical surface features
microvilli that increase surface area for nutrient interaction, while the basal surface contains
hemidesmosomes and integrins for attachment to the underlying connective tissue. C. The
apical surface is lined with cilia to move mucus, while the basal surface facilitates gap junction
communication with smooth muscle. D. The epithelium is non-polar, with uniform distribution of
transport proteins on all sides to maximize passive diffusion. E. The apical surface secretes
collagen to form the basement membrane, while the basal surface absorbs nutrients from the
blood.
Correct Answer: B
, Detailed Rationale: Epithelial polarity refers to the unequal distribution of organelles and
membrane proteins between the exposed (apical) surface and the attached (basal) surface. In
the small intestine, the primary function is absorption.
● Apical Surface: Faces the lumen. It is covered in microvilli (forming the brush border),
which vastly increase the surface area available for transporter proteins to absorb
glucose, amino acids, and lipids.
● Basal Surface: Faces the basement membrane. It contains anchorage proteins like
integrins and hemidesmosomes to secure the epithelium to the underlying connective
tissue (lamina propria) and transport proteins to move absorbed nutrients into the
interstitial fluid/blood.
Distractor Analysis:
● A is incorrect: It reverses the locations. Microvilli are apical; anchors are basal.
● C is incorrect: Cilia are found in the respiratory tract (for motility), not the small intestine
(which needs surface area for absorption).
● D is incorrect: Polarity is a fundamental definition of epithelia; non-polar cells would lose
directional transport capability.
● E is incorrect: The basement membrane is secreted basally, and nutrients are absorbed
apically from the lumen, not the blood.
PART TWO: SUPPORT AND MOVEMENT
Question 6: Burn Pathophysiology and Fluid Shifts
Topic: The Integumentary System Difficulty: High
Question: A 30-year-old patient is admitted with partial and full-thickness burns covering 40%
of their Total Body Surface Area (TBSA). In the first 24 hours, the patient is at high risk for
hypovolemic shock. According to the pathophysiology of severe burns described in Saladin,
what is the primary cellular and histological mechanism driving the massive fluid shift from the
intravascular to the interstitial compartment (fluid sequestration)?
A. Heat-induced denaturation of albumin increases blood colloid osmotic pressure, pulling fluid
into the capillaries, which then rupture. B. The release of inflammatory mediators like histamine
and vasoactive kinins causes a systemic increase in capillary permeability, allowing plasma
proteins to leak into the interstitial space, reversing the oncotic gradient. C. Destruction of the
epidermis eliminates the waterproof keratin barrier, leading to immediate evaporation of 5 liters
of blood volume directly into the atmosphere. D. Systemic vasoconstriction caused by the
sympathetic nervous system forces plasma out of the high-pressure arterioles into the tissue
spaces. E. The hypermetabolic state consumes intracellular water for hydrolysis, depleting the
intravascular volume to support catabolism.
Correct Answer: B
Detailed Rationale: A major burn injury (>30% TBSA) triggers a systemic inflammatory
response syndrome (SIRS). The direct thermal injury and the subsequent release of
inflammatory cytokines (e.g., histamine, bradykinin, prostaglandins) cause a catastrophic failure
of the capillary endothelial barrier. Normally, the endothelial lining prevents large plasma
proteins (like albumin) from escaping the bloodstream. This protein retention maintains the
blood colloid osmotic pressure (BCOP), which holds water in the vessels.
In severe burns, the capillaries become leaky (increased permeability). Plasma proteins escape
into the interstitial space (the "third space"). As proteins move out, they carry the oncotic pulling
