,CHAPTER LIST Chapter 26: Acid–Base Disorders
Chapter 27: Physiology of Blood and
Chapter 1: Basic Principles of Physiology
Hemostasis
Chapter 2: Basic Principles of Pharmacology
Chapter 28: Blood Products and Blood
Chapter 3: Neurophysiology Components
Chapter 4: Inhaled Anesthetics Chapter 29: Procoagulants
Chapter 5: Intravenous Sedatives and Chapter 30: Anticoagulants
Hypnotics
Chapter 31: Physiology and Management of
Chapter 6: Pain Physiology Massive Transfusion
Chapter 7: Opioid Agonists and Antagonists Chapter 32: Gastrointestinal Physiology
Chapter 8: Centrally Acting Nonopioid Chapter 33: Metabolism
Analgesics
Chapter 34: Antiemetics
Chapter 9: Peripherally Acting Analgesics
Chapter 35: Antacids and Gastrointestinal
Chapter 10: Local Anesthetics Motility Drugs
Chapter 11: Neuromuscular Physiology Chapter 36: Nutrition
Chapter 12: Neuromuscular-Blocking Drugs Chapter 37: Normal Endocrine Function
and Reversal Agents
Chapter 38: Drugs that Alter Glucose
Chapter 13: Neurologically Active Drugs Regulation
Chapter 14: Circulatory Physiology Chapter 39: Drugs for the Treatment of
Hypothyroidism and Hyperthyroidism
Chapter 15: Cardiac Physiology
Chapter 40: Other Endocrine Drugs
Chapter 16: Renal Physiology
Chapter 41: Antimicrobials, Antiseptics,
Chapter 17: Intravenous Fluids and
Disinfectants, and Management of
Electrolytes
Perioperative Infection
Chapter 18: Sympathomimetic Drugs
Chapter 42: Chemotherapeutic Drugs
Chapter 19: Sympatholytics
Chapter 43: Psychopharmacologic Drugs
Chapter 20: Vasodilators
Chapter 44: Physiology of the Newborn
Chapter 21: Antiarrhythmic Drugs
Chapter 45: Maternal and Fetal Physiology
Chapter 22: Diuretics and Pharmacology
Chapter 23: Lipid-Lowering Drugs Chapter 46: Physiology and Pharmacology of
the Elderly
Chapter 24: Gas Exchange
Chapter 47: Physiology and Pharmacology of
Chapter 25: Respiratory Pharmacology
Resuscitation
,CHAPTER 1 — TEST BANK (20 MCQs)
Basic Principles of Physiology
1.
During induction of anesthesia, rapid IV bolus of propofol causes a transient decrease in systemic
vascular resistance. Which cellular mechanism MOST directly explains this effect?
A. Inhibition of L-type calcium channels in vascular smooth muscle
B. Activation of voltage-gated sodium channels
C. Increased intracellular IP3 and calcium release
D. Enhanced myosin–actin crossbridge formation
Answer: A
Rationale: Propofol decreases SVR largely by inhibiting L-type calcium channels in vascular smooth
muscle, reducing intracellular calcium and causing vasodilation.
Key words: propofol vasodilation, L-type Ca²⁺ channel, SVR drop
2.
The resting membrane potential of most excitable cells is closest to the equilibrium potential of which
ion?
A. Sodium
B. Potassium
C. Calcium
D. Chloride
Answer: B
Rationale: Resting membrane potential is largely determined by potassium permeability via leak
channels; thus it approximates EK (−90 mV).
Key words: resting membrane potential, potassium equilibrium potential, leak channels
3.
During hypothermia, the anesthetist notes reduced MAC and slowed drug redistribution. Which
physiologic principle MOST contributes to this?
A. Increased membrane fluidity
,B. Decreased enzymatic metabolism and diffusion kinetics
C. Increased cardiac output
D. Enhanced neuronal firing
Answer: B
Rationale: Hypothermia reduces metabolic enzyme activity and slows molecular diffusion, decreasing
clearance and redistribution of anesthetic agents.
Key words: hypothermia, MAC reduction, slowed redistribution, enzyme activity
4.
Which component of the cell membrane MOST determines selective permeability during anesthesia-
induced ion channel modulation?
A. Cholesterol
B. Integral membrane proteins
C. Phospholipid hydrophilic heads
D. Peripheral proteins
Answer: B
Rationale: Integral membrane proteins—especially ion channels—govern selective permeability and
are major anesthetic drug targets.
Key words: ion channels, selective permeability, anesthetic targets
5.
An increase in extracellular potassium from 3.5 to 6.0 mEq/L does which of the following to neuronal
resting potential?
A. Hyperpolarizes the membrane
B. Makes the membrane more negative
C. Has no effect on resting membrane potential
D. Depolarizes the membrane
Answer: D
Rationale: Higher extracellular K⁺ decreases the gradient for K⁺ efflux, making the resting membrane
potential less negative (depolarized).
Key words: hyperkalemia, depolarization, resting potential shift
6.
,Which physiological process MOST limits the accumulation of inhalational anesthetics in highly
perfused tissues after prolonged exposure?
A. Zero-order elimination
B. Fick’s law of diffusion
C. Declining tissue–blood partial pressure gradients
D. Increased MAC with time
Answer: C
Rationale: As tissues equilibrate with arterial blood, the gradient driving further anesthetic uptake
decreases, limiting continued accumulation.
Key words: tissue perfusion, partial pressure gradient, inhaled anesthetics
7.
A patient becomes acidotic during surgery. Which change in cellular physiology is expected?
A. Increased efficacy of sodium-potassium ATPase
B. Decreased excitability due to altered ion channel gating
C. Increased chloride influx producing depolarization
D. Enhanced calcium channel opening
Answer: B
Rationale: Acidosis decreases neuronal excitability by altering gating of voltage-gated ion channels,
especially sodium channels.
Key words: acidosis, neuronal excitability, Na⁺ channel gating
8.
Homeostatic maintenance of blood pressure following induction is primarily mediated by which
mechanism?
A. Positive feedback through vasodilation
B. Negative feedback via baroreceptor reflex
C. Feed-forward stimulation of myocardial oxygen demand
D. Autoregulation of cerebral blood flow only
Answer: B
Rationale: The baroreceptor reflex uses negative feedback to maintain blood pressure via
sympathetic and parasympathetic modulation.
Key words: baroreceptor reflex, negative feedback, BP homeostasis
, 9.
During sepsis, increased capillary permeability leads to third-spacing. What cellular structure is MOST
disrupted?
A. Tight junctions
B. Desmosomes
C. Gap junctions
D. Hemidesmosomes
Answer: A
Rationale: Inflammatory mediators disrupt tight junctions in endothelial cells, increasing permeability
and promoting fluid extravasation.
Key words: tight junctions, endothelial permeability, sepsis
10.
An anesthetist administers a drug that increases intracellular cAMP in cardiac myocytes. Which effect
is expected?
A. Reduced calcium influx
B. Increased contractility
C. Prolonged action potential plateau
D. Decreased heart rate
Answer: B
Rationale: cAMP activates protein kinase A, which increases calcium channel opening and boosts
contractility.
Key words: cAMP, PKA, contractility increase
11.
Which best explains the rapid onset of effect for intravenous anesthetics compared with oral agents?
A. Avoidance of hepatic metabolism during distribution
B. Higher lipid solubility only
C. Direct entry into systemic circulation with 100% bioavailability
D. Increased renal clearance
Answer: C
Rationale: IV administration bypasses absorption barriers and first-pass metabolism, giving
immediate systemic bioavailability.
Key words: IV bioavailability, first-pass effect, onset
Chapter 27: Physiology of Blood and
Chapter 1: Basic Principles of Physiology
Hemostasis
Chapter 2: Basic Principles of Pharmacology
Chapter 28: Blood Products and Blood
Chapter 3: Neurophysiology Components
Chapter 4: Inhaled Anesthetics Chapter 29: Procoagulants
Chapter 5: Intravenous Sedatives and Chapter 30: Anticoagulants
Hypnotics
Chapter 31: Physiology and Management of
Chapter 6: Pain Physiology Massive Transfusion
Chapter 7: Opioid Agonists and Antagonists Chapter 32: Gastrointestinal Physiology
Chapter 8: Centrally Acting Nonopioid Chapter 33: Metabolism
Analgesics
Chapter 34: Antiemetics
Chapter 9: Peripherally Acting Analgesics
Chapter 35: Antacids and Gastrointestinal
Chapter 10: Local Anesthetics Motility Drugs
Chapter 11: Neuromuscular Physiology Chapter 36: Nutrition
Chapter 12: Neuromuscular-Blocking Drugs Chapter 37: Normal Endocrine Function
and Reversal Agents
Chapter 38: Drugs that Alter Glucose
Chapter 13: Neurologically Active Drugs Regulation
Chapter 14: Circulatory Physiology Chapter 39: Drugs for the Treatment of
Hypothyroidism and Hyperthyroidism
Chapter 15: Cardiac Physiology
Chapter 40: Other Endocrine Drugs
Chapter 16: Renal Physiology
Chapter 41: Antimicrobials, Antiseptics,
Chapter 17: Intravenous Fluids and
Disinfectants, and Management of
Electrolytes
Perioperative Infection
Chapter 18: Sympathomimetic Drugs
Chapter 42: Chemotherapeutic Drugs
Chapter 19: Sympatholytics
Chapter 43: Psychopharmacologic Drugs
Chapter 20: Vasodilators
Chapter 44: Physiology of the Newborn
Chapter 21: Antiarrhythmic Drugs
Chapter 45: Maternal and Fetal Physiology
Chapter 22: Diuretics and Pharmacology
Chapter 23: Lipid-Lowering Drugs Chapter 46: Physiology and Pharmacology of
the Elderly
Chapter 24: Gas Exchange
Chapter 47: Physiology and Pharmacology of
Chapter 25: Respiratory Pharmacology
Resuscitation
,CHAPTER 1 — TEST BANK (20 MCQs)
Basic Principles of Physiology
1.
During induction of anesthesia, rapid IV bolus of propofol causes a transient decrease in systemic
vascular resistance. Which cellular mechanism MOST directly explains this effect?
A. Inhibition of L-type calcium channels in vascular smooth muscle
B. Activation of voltage-gated sodium channels
C. Increased intracellular IP3 and calcium release
D. Enhanced myosin–actin crossbridge formation
Answer: A
Rationale: Propofol decreases SVR largely by inhibiting L-type calcium channels in vascular smooth
muscle, reducing intracellular calcium and causing vasodilation.
Key words: propofol vasodilation, L-type Ca²⁺ channel, SVR drop
2.
The resting membrane potential of most excitable cells is closest to the equilibrium potential of which
ion?
A. Sodium
B. Potassium
C. Calcium
D. Chloride
Answer: B
Rationale: Resting membrane potential is largely determined by potassium permeability via leak
channels; thus it approximates EK (−90 mV).
Key words: resting membrane potential, potassium equilibrium potential, leak channels
3.
During hypothermia, the anesthetist notes reduced MAC and slowed drug redistribution. Which
physiologic principle MOST contributes to this?
A. Increased membrane fluidity
,B. Decreased enzymatic metabolism and diffusion kinetics
C. Increased cardiac output
D. Enhanced neuronal firing
Answer: B
Rationale: Hypothermia reduces metabolic enzyme activity and slows molecular diffusion, decreasing
clearance and redistribution of anesthetic agents.
Key words: hypothermia, MAC reduction, slowed redistribution, enzyme activity
4.
Which component of the cell membrane MOST determines selective permeability during anesthesia-
induced ion channel modulation?
A. Cholesterol
B. Integral membrane proteins
C. Phospholipid hydrophilic heads
D. Peripheral proteins
Answer: B
Rationale: Integral membrane proteins—especially ion channels—govern selective permeability and
are major anesthetic drug targets.
Key words: ion channels, selective permeability, anesthetic targets
5.
An increase in extracellular potassium from 3.5 to 6.0 mEq/L does which of the following to neuronal
resting potential?
A. Hyperpolarizes the membrane
B. Makes the membrane more negative
C. Has no effect on resting membrane potential
D. Depolarizes the membrane
Answer: D
Rationale: Higher extracellular K⁺ decreases the gradient for K⁺ efflux, making the resting membrane
potential less negative (depolarized).
Key words: hyperkalemia, depolarization, resting potential shift
6.
,Which physiological process MOST limits the accumulation of inhalational anesthetics in highly
perfused tissues after prolonged exposure?
A. Zero-order elimination
B. Fick’s law of diffusion
C. Declining tissue–blood partial pressure gradients
D. Increased MAC with time
Answer: C
Rationale: As tissues equilibrate with arterial blood, the gradient driving further anesthetic uptake
decreases, limiting continued accumulation.
Key words: tissue perfusion, partial pressure gradient, inhaled anesthetics
7.
A patient becomes acidotic during surgery. Which change in cellular physiology is expected?
A. Increased efficacy of sodium-potassium ATPase
B. Decreased excitability due to altered ion channel gating
C. Increased chloride influx producing depolarization
D. Enhanced calcium channel opening
Answer: B
Rationale: Acidosis decreases neuronal excitability by altering gating of voltage-gated ion channels,
especially sodium channels.
Key words: acidosis, neuronal excitability, Na⁺ channel gating
8.
Homeostatic maintenance of blood pressure following induction is primarily mediated by which
mechanism?
A. Positive feedback through vasodilation
B. Negative feedback via baroreceptor reflex
C. Feed-forward stimulation of myocardial oxygen demand
D. Autoregulation of cerebral blood flow only
Answer: B
Rationale: The baroreceptor reflex uses negative feedback to maintain blood pressure via
sympathetic and parasympathetic modulation.
Key words: baroreceptor reflex, negative feedback, BP homeostasis
, 9.
During sepsis, increased capillary permeability leads to third-spacing. What cellular structure is MOST
disrupted?
A. Tight junctions
B. Desmosomes
C. Gap junctions
D. Hemidesmosomes
Answer: A
Rationale: Inflammatory mediators disrupt tight junctions in endothelial cells, increasing permeability
and promoting fluid extravasation.
Key words: tight junctions, endothelial permeability, sepsis
10.
An anesthetist administers a drug that increases intracellular cAMP in cardiac myocytes. Which effect
is expected?
A. Reduced calcium influx
B. Increased contractility
C. Prolonged action potential plateau
D. Decreased heart rate
Answer: B
Rationale: cAMP activates protein kinase A, which increases calcium channel opening and boosts
contractility.
Key words: cAMP, PKA, contractility increase
11.
Which best explains the rapid onset of effect for intravenous anesthetics compared with oral agents?
A. Avoidance of hepatic metabolism during distribution
B. Higher lipid solubility only
C. Direct entry into systemic circulation with 100% bioavailability
D. Increased renal clearance
Answer: C
Rationale: IV administration bypasses absorption barriers and first-pass metabolism, giving
immediate systemic bioavailability.
Key words: IV bioavailability, first-pass effect, onset
