,CONTENT
Chapter 1 Medical Physiology: An Overview
Chapter 2 Cell Signaling, Membrane Transport, and Membrane Potential
Chapter 3 Action Potential, Synaptic Transmission, and Nerve Function
Chapter 4 Sensory Physiology
Chapter 5 Motor System
Chapter 6 Autonomic Nervous System
Chapter 7 Integrative Functions of the Central Nervous System
Chapter 8 Skeletal and Smooth Muscle
Chapter 9 Blood Composition and Function
Chapter 10 Immunology, Organ Interaction, and Homeostasis
Chapter 11 Overview of the Cardiovascular System and Hemodynamics
Chapter 12 Electrical Activity of the Heart
Chapter 13 Cardiac Muscle Mechanics and the Cardiac Pump
Chapter 14 The Systemic Circulation
Chapter 15 Microcirculation and Lymphatic System
Chapter 16 Special Circulations
Chapter 17 Control Mechanisms in Cardiovascular Function
Chapter 18 Ventilation and the Mechanics of Breathing
Chapter 19 Gas Transfer and Transport
Chapter 20 Pulmonary Circulation and Ventilation/Perfusion
Chapter 21 Control of Ventilation
Chapter 22 Kidney Function
Chapter 23 Regulation of Fluid and Electrolyte Balance
Chapter 24 Acid–Base Homeostasis
Chapter 25 Gastrointestinal System Functions
Chapter 26 Liver Functions and Immune Surveillance
Chapter 27 Motility and Gastrointestinal Regulation
Chapter 28 Regulation of Body Temperature
Chapter 29 Exercise Physiology
Chapter 30 Endocrine Control Mechanisms
Chapter 31 Hypothalamus and the Pituitary Gland
Chapter 32 Thyroid Gland
Chapter 33 Adrenal Gland
Chapter 34 Endocrine Pancreas
Chapter 35 Endocrine Regulation of Calcium, Phosphate, and Bone Homeostasis
Chapter 36 Male Reproductive System
Chapter 37 Female Reproductive System
Chapter 38 Fertilization, Pregnancy, and Fetal Development
,Chapter 1 — Medical Physiology: An Overview
Each question aligns with the chapter 1. Four options (A–D). Correct answer shown exactly as
Answer: X. After each question: Deep rationale for the correct choice and Key words.
1. A 55-year-old patient has chronic exogenous glucocorticoid therapy and develops adrenal
atrophy. Which physiological principle best explains why the adrenal cortex atrophied?
A. Positive feedback on the hypothalamic–pituitary–adrenal (HPA) axis
B. Feedforward activation of ACTH secretion
C. Loss of negative feedback on the hypothalamus and pituitary
D. Suppression of endogenous ACTH via negative feedback by administered
glucocorticoid
Answer: D
Rationale: Exogenous glucocorticoids raise circulating cortisol-equivalents, which are sensed by
the hypothalamus and pituitary. That causes decreased CRH and ACTH secretion (classic
negative feedback), reducing trophic stimulation of the adrenal cortex → disuse atrophy. This
demonstrates homeostatic endocrine feedback and how pharmacologic replacement can suppress
endogenous hormone axes. Choice C is the opposite (loss of negative feedback would increase
ACTH), A and B are incorrect mechanisms.
Keywords: negative feedback, HPA axis, ACTH suppression, adrenal atrophy, exogenous
steroids.
2. Which statement best distinguishes homeostasis from allostasis in clinical physiology?
A. Homeostasis emphasizes active anticipatory change; allostasis emphasizes fixed set
points.
B. Homeostasis maintains constant internal variables; allostasis emphasizes adaptive
change of set points under stress.
C. Homeostasis applies only to endocrine systems; allostasis applies only to neural
systems.
D. Homeostasis and allostasis are synonymous and interchangeable.
Answer: B
Rationale: Homeostasis traditionally describes maintenance of internal variables near set points
via feedback (e.g., blood pH). Allostasis emphasizes adaptive changes in set points and
activation of multiple systems to meet anticipated demands (e.g., stress response shifting
,cardiovascular parameters). Clinically, chronic allostatic load (persistent adaptation) can cause
disease. A is reversed, C is false, D is wrong.
Keywords: homeostasis, allostasis, set point, allostatic load, adaptation.
3. A patient with hemorrhage has an immediate tachycardia and peripheral vasoconstriction.
Which control mechanism primarily mediates this response within seconds?
A. Renin–angiotensin–aldosterone system (RAAS) increase
B. Baroreceptor reflex via autonomic nervous system
C. Increased aldosterone release from adrenal cortex
D. Renal sodium retention increasing blood volume
Answer: B
Rationale: The baroreceptor (aortic/carotid) reflex produces rapid (seconds) changes in
sympathetic/parasympathetic outflow to increase HR and vasoconstriction when arterial pressure
falls. RAAS and aldosterone act over minutes–hours. Renal sodium retention is a longer
compensation. This highlights time-scale distinctions in homeostatic responses.
Keywords: baroreceptor reflex, autonomic, hemorrhage, rapid compensation, time scales.
4. Which example best illustrates feedforward control rather than feedback control?
A. Increased breathing rate in response to hypercapnia.
B. Pancreatic insulin release triggered by anticipatory autonomic signals at smelling food.
C. Aldosterone secretion in response to low sodium concentration.
D. Sweating when core temperature rises above set point.
Answer: B
Rationale: Feedforward control anticipates a change and adjusts before the regulated variable
deviates (cephalic phase insulin release when smelling/seeing food). A and C are classic
feedback responses to change in chemical variables; D is a feedback response to increased
temperature. Feedforward reduces overshoot and improves efficiency of regulation.
Keywords: feedforward, cephalic insulin release, anticipatory control, homeostasis.
5. A clinician wants to interpret an arterial blood gas (ABG). Which pair of organ systems
primarily provides acute vs chronic compensation for primary respiratory acidosis?
A. Lungs (acute) — Kidneys (chronic)
B. Kidneys (acute) — Lungs (chronic)
, C. Heart (acute) — Liver (chronic)
D. Adrenal glands (acute) — Bone (chronic)
Answer: A
Rationale: Respiratory acidosis (increased PaCO₂) is caused by hypoventilation. The lungs
cannot compensate for their own failure; acute buffering occurs via intracellular and extracellular
buffers, and the kidneys provide slower (hours–days) compensation by increasing H⁺ excretion
and HCO₃⁻ reabsorption. Thus lungs are the primary problem and kidneys are the chronic
compensator. B reverses timing; C and D are irrelevant.
Keywords: respiratory acidosis, acute vs chronic compensation, renal compensation, ABG
interpretation.
6. Which clinical scenario best demonstrates physiological redundancy that preserves
function after partial organ loss?
A. Single-kidney donors maintaining near-normal GFR through hyperfiltration of
remaining nephrons.
B. Sudden myocardial infarction producing immediate total loss of left ventricular output.
C. Complete transection of a spinal cord causing loss of autonomic reflexes below the
lesion.
D. Acute hepatic necrosis leading to immediate loss of all metabolic functions.
Answer: A
Rationale: Redundancy and reserve mean remaining functional units can compensate—after
nephrectomy, remaining nephrons hyperfilter and increase single-nephron GFR to maintain
overall renal function. MI and hepatic necrosis produce catastrophic loss without redundancy
sufficient to maintain function; spinal transection removes integrated pathways.
Keywords: redundancy, reserve, hyperfiltration, nephron adaptation, organ compensation.
7. Which statement about set points and hysteresis is most accurate in physiology?
A. Set points are immutable; hysteresis has no role in biological systems.
B. Biological set points can shift (hysteresis) so response thresholds differ depending on
prior state.
C. Hysteresis refers to instantaneous feedback without time dependence.
D. Hysteresis is only relevant in mechanical systems and not in physiology.
Answer: B
,Rationale: Set points can change according to prior exposures (e.g., fever resets hypothalamic
thermostat—different thresholds during rising vs falling temperature). Hysteresis describes path-
dependent behavior where the system's response depends on its history, important in
endocrinology and thermoregulation. A, C, D are incorrect.
Keywords: set point, hysteresis, fever, path dependency, thermoregulation.
8. A trial drug blocks peripheral vasodilation to histamine but leaves hypothalamic
temperature sensing intact. After endotoxin exposure, which pattern would you expect?
A. Normal fever development because hypothalamic set point rises.
B. No fever because peripheral vasodilation is essential to generating fever.
C. Exaggerated fever because vasodilation typically cools the body.
D. Hypothermia because drug blocks central sensing.
Answer: C
Rationale: Fever results from hypothalamic set-point increase (pyrogens) and peripheral
mechanisms (vasoconstriction shunting to conserve heat; later vasodilation allows heat loss). If
drug blocks vasodilation, the normal heat-loss phase is blunted—so once set point rises, the body
conserves heat and may show exaggerated hyperthermia because one route of heat dissipation is
impaired. A ignores peripheral effect; B is false; D is wrong.
Keywords: fever, hypothalamic set point, peripheral vasodilation, thermoregulation, heat
dissipation.
9. Which best describes why understanding integrated physiology improves diagnostic
specificity compared with isolated lab abnormalities?
A. Integrated physiology is less predictive but easier to memorize.
B. Integration allows causal linking of multi-system findings (e.g., hyperkalemia +
hypotension + metabolic acidosis → acute adrenal insufficiency).
C. Lab tests are always sufficient for diagnosis without physiological context.
D. Physiology and lab values are unrelated; only imaging is definitive.
Answer: B
Rationale: Integrated physiology connects multiple abnormal findings into coherent syndromes,
improving diagnostic accuracy—e.g., primary adrenal insufficiency causes hyperkalemia,
hyponatremia, hypotension, metabolic acidosis due to mineralocorticoid loss. Understanding
causality across systems avoids misattribution to isolated lab errors. A, C, D are false.
Keywords: integration, diagnostic specificity, multi-system approach, adrenal insufficiency,
pattern recognition.
, 10. A patient with chronic heart failure has increased sympathetic tone chronically. Which
statement best explains why this is initially compensatory but ultimately maladaptive?
A. Sympathetic activation decreases preload and always improves cardiac output long
term.
B. Chronic sympathetic drive increases afterload, myocardial oxygen demand, and
promotes remodeling that worsens pump function.
C. Chronic sympathetic tone directly increases kidney function and permanently corrects
fluid balance.
D. Sympathetic activation has no effect on cardiac remodeling.
Answer: B
Rationale: Acute sympathetic activation increases HR and contractility, maintaining perfusion.
Chronically, elevated catecholamines increase afterload, myocardial oxygen consumption, and
trigger pathologic remodeling (hypertrophy, fibrosis), worsening heart failure. This demonstrates
the difference between short-term homeostatic compensation and long-term maladaptation. A
and C are incorrect; D is false.
Keywords: sympathetic activation, compensation vs maladaptation, heart failure, remodeling.
11. In the context of integrated homeostasis, which pair of hormones are most directly
antagonistic in acute regulation of plasma glucose?
A. Insulin (β-cells) and thyroid hormone (thyroxine)
B. Insulin (β-cells) and glucagon (α-cells)
C. Growth hormone and aldosterone
D. Cortisol and parathyroid hormone
Answer: B
Rationale: Insulin lowers plasma glucose by promoting uptake and glycogen synthesis;
glucagon raises plasma glucose via glycogenolysis and gluconeogenesis. They form a classic
antagonistic endocrine pair for acute glucose homeostasis. The other pairs are not primary direct
antagonists of glucose in acute regulation.
Keywords: insulin, glucagon, glucose homeostasis, antagonistic hormones.
12. Which description of feedforward and feedback is most useful for designing a drug that
minimizes overshoot?
A. A drug that increases feedback gain always eliminates overshoot.
B. Incorporating feedforward control (anticipatory dosing relative to predicted
Chapter 1 Medical Physiology: An Overview
Chapter 2 Cell Signaling, Membrane Transport, and Membrane Potential
Chapter 3 Action Potential, Synaptic Transmission, and Nerve Function
Chapter 4 Sensory Physiology
Chapter 5 Motor System
Chapter 6 Autonomic Nervous System
Chapter 7 Integrative Functions of the Central Nervous System
Chapter 8 Skeletal and Smooth Muscle
Chapter 9 Blood Composition and Function
Chapter 10 Immunology, Organ Interaction, and Homeostasis
Chapter 11 Overview of the Cardiovascular System and Hemodynamics
Chapter 12 Electrical Activity of the Heart
Chapter 13 Cardiac Muscle Mechanics and the Cardiac Pump
Chapter 14 The Systemic Circulation
Chapter 15 Microcirculation and Lymphatic System
Chapter 16 Special Circulations
Chapter 17 Control Mechanisms in Cardiovascular Function
Chapter 18 Ventilation and the Mechanics of Breathing
Chapter 19 Gas Transfer and Transport
Chapter 20 Pulmonary Circulation and Ventilation/Perfusion
Chapter 21 Control of Ventilation
Chapter 22 Kidney Function
Chapter 23 Regulation of Fluid and Electrolyte Balance
Chapter 24 Acid–Base Homeostasis
Chapter 25 Gastrointestinal System Functions
Chapter 26 Liver Functions and Immune Surveillance
Chapter 27 Motility and Gastrointestinal Regulation
Chapter 28 Regulation of Body Temperature
Chapter 29 Exercise Physiology
Chapter 30 Endocrine Control Mechanisms
Chapter 31 Hypothalamus and the Pituitary Gland
Chapter 32 Thyroid Gland
Chapter 33 Adrenal Gland
Chapter 34 Endocrine Pancreas
Chapter 35 Endocrine Regulation of Calcium, Phosphate, and Bone Homeostasis
Chapter 36 Male Reproductive System
Chapter 37 Female Reproductive System
Chapter 38 Fertilization, Pregnancy, and Fetal Development
,Chapter 1 — Medical Physiology: An Overview
Each question aligns with the chapter 1. Four options (A–D). Correct answer shown exactly as
Answer: X. After each question: Deep rationale for the correct choice and Key words.
1. A 55-year-old patient has chronic exogenous glucocorticoid therapy and develops adrenal
atrophy. Which physiological principle best explains why the adrenal cortex atrophied?
A. Positive feedback on the hypothalamic–pituitary–adrenal (HPA) axis
B. Feedforward activation of ACTH secretion
C. Loss of negative feedback on the hypothalamus and pituitary
D. Suppression of endogenous ACTH via negative feedback by administered
glucocorticoid
Answer: D
Rationale: Exogenous glucocorticoids raise circulating cortisol-equivalents, which are sensed by
the hypothalamus and pituitary. That causes decreased CRH and ACTH secretion (classic
negative feedback), reducing trophic stimulation of the adrenal cortex → disuse atrophy. This
demonstrates homeostatic endocrine feedback and how pharmacologic replacement can suppress
endogenous hormone axes. Choice C is the opposite (loss of negative feedback would increase
ACTH), A and B are incorrect mechanisms.
Keywords: negative feedback, HPA axis, ACTH suppression, adrenal atrophy, exogenous
steroids.
2. Which statement best distinguishes homeostasis from allostasis in clinical physiology?
A. Homeostasis emphasizes active anticipatory change; allostasis emphasizes fixed set
points.
B. Homeostasis maintains constant internal variables; allostasis emphasizes adaptive
change of set points under stress.
C. Homeostasis applies only to endocrine systems; allostasis applies only to neural
systems.
D. Homeostasis and allostasis are synonymous and interchangeable.
Answer: B
Rationale: Homeostasis traditionally describes maintenance of internal variables near set points
via feedback (e.g., blood pH). Allostasis emphasizes adaptive changes in set points and
activation of multiple systems to meet anticipated demands (e.g., stress response shifting
,cardiovascular parameters). Clinically, chronic allostatic load (persistent adaptation) can cause
disease. A is reversed, C is false, D is wrong.
Keywords: homeostasis, allostasis, set point, allostatic load, adaptation.
3. A patient with hemorrhage has an immediate tachycardia and peripheral vasoconstriction.
Which control mechanism primarily mediates this response within seconds?
A. Renin–angiotensin–aldosterone system (RAAS) increase
B. Baroreceptor reflex via autonomic nervous system
C. Increased aldosterone release from adrenal cortex
D. Renal sodium retention increasing blood volume
Answer: B
Rationale: The baroreceptor (aortic/carotid) reflex produces rapid (seconds) changes in
sympathetic/parasympathetic outflow to increase HR and vasoconstriction when arterial pressure
falls. RAAS and aldosterone act over minutes–hours. Renal sodium retention is a longer
compensation. This highlights time-scale distinctions in homeostatic responses.
Keywords: baroreceptor reflex, autonomic, hemorrhage, rapid compensation, time scales.
4. Which example best illustrates feedforward control rather than feedback control?
A. Increased breathing rate in response to hypercapnia.
B. Pancreatic insulin release triggered by anticipatory autonomic signals at smelling food.
C. Aldosterone secretion in response to low sodium concentration.
D. Sweating when core temperature rises above set point.
Answer: B
Rationale: Feedforward control anticipates a change and adjusts before the regulated variable
deviates (cephalic phase insulin release when smelling/seeing food). A and C are classic
feedback responses to change in chemical variables; D is a feedback response to increased
temperature. Feedforward reduces overshoot and improves efficiency of regulation.
Keywords: feedforward, cephalic insulin release, anticipatory control, homeostasis.
5. A clinician wants to interpret an arterial blood gas (ABG). Which pair of organ systems
primarily provides acute vs chronic compensation for primary respiratory acidosis?
A. Lungs (acute) — Kidneys (chronic)
B. Kidneys (acute) — Lungs (chronic)
, C. Heart (acute) — Liver (chronic)
D. Adrenal glands (acute) — Bone (chronic)
Answer: A
Rationale: Respiratory acidosis (increased PaCO₂) is caused by hypoventilation. The lungs
cannot compensate for their own failure; acute buffering occurs via intracellular and extracellular
buffers, and the kidneys provide slower (hours–days) compensation by increasing H⁺ excretion
and HCO₃⁻ reabsorption. Thus lungs are the primary problem and kidneys are the chronic
compensator. B reverses timing; C and D are irrelevant.
Keywords: respiratory acidosis, acute vs chronic compensation, renal compensation, ABG
interpretation.
6. Which clinical scenario best demonstrates physiological redundancy that preserves
function after partial organ loss?
A. Single-kidney donors maintaining near-normal GFR through hyperfiltration of
remaining nephrons.
B. Sudden myocardial infarction producing immediate total loss of left ventricular output.
C. Complete transection of a spinal cord causing loss of autonomic reflexes below the
lesion.
D. Acute hepatic necrosis leading to immediate loss of all metabolic functions.
Answer: A
Rationale: Redundancy and reserve mean remaining functional units can compensate—after
nephrectomy, remaining nephrons hyperfilter and increase single-nephron GFR to maintain
overall renal function. MI and hepatic necrosis produce catastrophic loss without redundancy
sufficient to maintain function; spinal transection removes integrated pathways.
Keywords: redundancy, reserve, hyperfiltration, nephron adaptation, organ compensation.
7. Which statement about set points and hysteresis is most accurate in physiology?
A. Set points are immutable; hysteresis has no role in biological systems.
B. Biological set points can shift (hysteresis) so response thresholds differ depending on
prior state.
C. Hysteresis refers to instantaneous feedback without time dependence.
D. Hysteresis is only relevant in mechanical systems and not in physiology.
Answer: B
,Rationale: Set points can change according to prior exposures (e.g., fever resets hypothalamic
thermostat—different thresholds during rising vs falling temperature). Hysteresis describes path-
dependent behavior where the system's response depends on its history, important in
endocrinology and thermoregulation. A, C, D are incorrect.
Keywords: set point, hysteresis, fever, path dependency, thermoregulation.
8. A trial drug blocks peripheral vasodilation to histamine but leaves hypothalamic
temperature sensing intact. After endotoxin exposure, which pattern would you expect?
A. Normal fever development because hypothalamic set point rises.
B. No fever because peripheral vasodilation is essential to generating fever.
C. Exaggerated fever because vasodilation typically cools the body.
D. Hypothermia because drug blocks central sensing.
Answer: C
Rationale: Fever results from hypothalamic set-point increase (pyrogens) and peripheral
mechanisms (vasoconstriction shunting to conserve heat; later vasodilation allows heat loss). If
drug blocks vasodilation, the normal heat-loss phase is blunted—so once set point rises, the body
conserves heat and may show exaggerated hyperthermia because one route of heat dissipation is
impaired. A ignores peripheral effect; B is false; D is wrong.
Keywords: fever, hypothalamic set point, peripheral vasodilation, thermoregulation, heat
dissipation.
9. Which best describes why understanding integrated physiology improves diagnostic
specificity compared with isolated lab abnormalities?
A. Integrated physiology is less predictive but easier to memorize.
B. Integration allows causal linking of multi-system findings (e.g., hyperkalemia +
hypotension + metabolic acidosis → acute adrenal insufficiency).
C. Lab tests are always sufficient for diagnosis without physiological context.
D. Physiology and lab values are unrelated; only imaging is definitive.
Answer: B
Rationale: Integrated physiology connects multiple abnormal findings into coherent syndromes,
improving diagnostic accuracy—e.g., primary adrenal insufficiency causes hyperkalemia,
hyponatremia, hypotension, metabolic acidosis due to mineralocorticoid loss. Understanding
causality across systems avoids misattribution to isolated lab errors. A, C, D are false.
Keywords: integration, diagnostic specificity, multi-system approach, adrenal insufficiency,
pattern recognition.
, 10. A patient with chronic heart failure has increased sympathetic tone chronically. Which
statement best explains why this is initially compensatory but ultimately maladaptive?
A. Sympathetic activation decreases preload and always improves cardiac output long
term.
B. Chronic sympathetic drive increases afterload, myocardial oxygen demand, and
promotes remodeling that worsens pump function.
C. Chronic sympathetic tone directly increases kidney function and permanently corrects
fluid balance.
D. Sympathetic activation has no effect on cardiac remodeling.
Answer: B
Rationale: Acute sympathetic activation increases HR and contractility, maintaining perfusion.
Chronically, elevated catecholamines increase afterload, myocardial oxygen consumption, and
trigger pathologic remodeling (hypertrophy, fibrosis), worsening heart failure. This demonstrates
the difference between short-term homeostatic compensation and long-term maladaptation. A
and C are incorrect; D is false.
Keywords: sympathetic activation, compensation vs maladaptation, heart failure, remodeling.
11. In the context of integrated homeostasis, which pair of hormones are most directly
antagonistic in acute regulation of plasma glucose?
A. Insulin (β-cells) and thyroid hormone (thyroxine)
B. Insulin (β-cells) and glucagon (α-cells)
C. Growth hormone and aldosterone
D. Cortisol and parathyroid hormone
Answer: B
Rationale: Insulin lowers plasma glucose by promoting uptake and glycogen synthesis;
glucagon raises plasma glucose via glycogenolysis and gluconeogenesis. They form a classic
antagonistic endocrine pair for acute glucose homeostasis. The other pairs are not primary direct
antagonists of glucose in acute regulation.
Keywords: insulin, glucagon, glucose homeostasis, antagonistic hormones.
12. Which description of feedforward and feedback is most useful for designing a drug that
minimizes overshoot?
A. A drug that increases feedback gain always eliminates overshoot.
B. Incorporating feedforward control (anticipatory dosing relative to predicted
