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#1 ( 12411 )
CORRECT: E
The cutaneous senses for which separate receptors exist are touch, warmth, cold, pain, and
possibly itching. Combination of these sensations plus, in some cases, cortical components
are synthesized into the sensations of vibratory sensation, two-point discrimination, and
stereognosis (= identification of objects by the sense of touch).

#2 ( 13019 )
CORRECT: E
Sinus arrhythmia is seen in healthy young individuals breathing at normal rate, especially if the
depth of breathing is increased.

#3 ( 13030 )
CORRECT: E
Hypoxic hypoxia is the most common form of hypoxia seen clinically. The diseases that cause
it can be roughly divided into those in which the gas exchange apparatus fails, those such as
congenital heart disease in which large amounts of blood are shunted from venous to the
arterial side of the circulation, and those in which the respiratory pump fails.

#4 ( 13032 )
CORRECT: E
Clearance of inulin = Concentration in urine (Uin) x urine flow (V)
(Cin) arterial plasma level of inulin (Pin)

#5 ( 13035 )
CORRECT: E
Angiotensin II, vasopressin, norepinephrine, platelet-activating factor, platelet-derived growth
factor, thromboxane A2, PGF2, leukotrienes C and D, and histamine cause contraction of
glomerular mesangial cells. Insulin-like growth factor 1 (somatomedin C) causes the growth,
but not contraction or relaxation. ANP, dopamine, PGE2, cyclic AMP cause relaxation of
glomerular mesangial cells.

#6 ( 13070 )
CORRECT: E
Glycine, γ-aminobutyric (GABA), glutamate and aspartate are amino acids involved in neurons
mediation (retina, cerebellum, cerebral cortex, brain stem, spinal cord).

#7 ( 13073 )
CORRECT: E
The causes of orthostatic (postural) hypotension are multiple. It’s common after surgical
sympathectomy and in patients receiving sympatholytic drugs. It also occurs in diabetes and
syphilis, in which there is damage to sympathetic nervous system. Another cause of orthostatic
hypotension is autonomic insufficiency. In other cases, the defect is peripheral, and resting
norepinephrine values are low with little or no response to baroreceptor stimulation.
Baroreceptor reflexes are also abnormal in patients with primary hyperaldosteronism.

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#8 ( 13081 )
CORRECT: B
Toxins from bacteria such as endotoxin act on monocytes, and Kupffer cells to produce
interleukin 1 (IL-1), a polypeptide also known as EP. IL-1 has widespread effects in the human
body. It enters the brain, and produces fever by a direct action on the preoptic area of the
hypothalamus. It also acts on lymphocytes to activate immune system, stimulates release of
neutrophils, and causes proteolysis in muscle. The fever produced by IL-1 may be due to local
release of prostaglandins. Injection of prostaglandins into the hypothalamus produces fever.

#9 ( 13723 )
CORRECT: A
The chylomicrons are cleared from the circulation by the action of lipoprotein lipase, which is
located on the surface of the endothelium of capillaries. This enzyme catalyzes the breakdown
of the triglyceride in the chylomicrons to FFA and glycerol, which then enter adipose cells and
are re-esterified.

#10 ( 13724 )
CORRECT: B
The intracellular hormone-sensitive lipase of adipose tissue catalyzes the breakdown of stored
triglycerides into glycerol and FFA, with the latter entering the circulation.

#11 ( 13727 )
CORRECT: D
The plasma cholesterol level is decreased by thyroid hormones, which increase LDL receptors,
and by estrogens, which lower LDL and increase HDL. If bile acid reabsorption in the intestine
is decreased by resins, more cholesterol is diverted to bile acid formation. Big doses of niacin
also decrease LDL and increase HDL.

#12 ( 13732 )
CORRECT: H
Arachidonic acid is also converted to lipoxins A and B. Lipoxin A dilates the microvasculature.
Lipoxin A and lipoxin B both inhibit the cytotoxic effects of natural killer cells.

#13 ( 13743 )
CORRECT: E
Water and ethanol inhibit vasopressin secretion. Furosemide inhibits Na+-K+-2Cl- reabsorption
in the medullary thick ascending limb of the loop of Henle. Thiazides inhibit Na+-K+-2Cl-
cotransport in the early portion of the distal tubule. Diamox as a carbonic anhydrase inhibitor,
decreases H+ secretion, with resultant increase in Na+ and K+ secretion. Spironolactone and
triamterene are K+-retaining natriuretics. They inhibit Na+-K+ exchange in the distal portion of
the diatal tubule and the collecting duct by inhibiting the action of aldosterone (spironolactone)
or by inhibiting Na+ reabsorption (triamterene). Antagonists of V2 vasopressin receptors inhibit
action of vasopressin on collecting duct.

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#14 ( 13747 )
CORRECT: E
The mechanism responsible for obliteration of ductus arteriosus is incompletely understood.
There is evidence that a rise in arterial PO2 and asphyxia are both capable of making the
ductus arteriosus constrict. Bradykinin has been shown to constrict ductus while dilating the
pulmonary vesicular bed. Prostacyclin appears to have a role in maintaining the patency of
ductus arteriosus before birth, and administration of indomethacin, a drug that inhibits
prostacyclin synthesis, closes the ductus in many infants.

#15 ( 13748 )
CORRECT: E
Fatty acids and amino acids in the duodenum release CCK, which causes gallbladder
contraction. Acid and Ca2+ also stimulate the secretion of CCK. Substances that cause
contraction of gallbladder are called cholagogues.

#16 ( 13750 )
CORRECT: D
Calcium acts directly on the parathyroid glands in a feedback fashion to regulate the secretion
of parathyroid hormone. When it is low, secretion is increased, and Ca2+ is mobilized from the
bones.

An increase in the extracellular phosphate level produces a proportional decrease in

calcium concentration, because the product of the calcium and phosphate levels is a constant.

Magnesium also appears to have a direct effect, with an acute decrease in plasma Mg2+
concentration stimulating parathyroid secretion.

Secretion of PTH is also increased by β-adrenergic discharge and cyclic AMP.

#17 ( 14430 )
CORRECT: E
The lymphatic system consists of a widely distributed network of permeable, close-ended
vessels that run in parallel with tissue capillary networks. Lymphatic capillaries function in the
retrieval of fluid, proteins and cells that have escaped across the vascular bed. Fluid removal
by lymphatics is stimulated by increases in tissue hydrostatic pressure (increased fluid
volume). Fluids collected by the lymphatic capillaries eventually drain back into the circulation
through the right and left subclavian veins.

The lymphatic system transports a volume of fluid about equal to the entire plasma volume
and about 25-50% of the plasma protein every 24 hours. Inadequate lymphatic function
results in the loss of plasma volume and the accumulation of fluid and protein in the tissues.
Alone, fluid accumulation would be self-limiting since increased interstitial pressure acts to
decrease the hydrostatic pressure gradient across the capillary wall. However the continued
accumulation of proteins in the interstitium acts as an osmotic force thereby enhancing tissue
fluid accumulation (edema).

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#18 ( 15011 )
CORRECT: E
The dorsal respiratory group (DRG) of neurons in the medulla repetitively discharges to
stimulate the muscles of inspiration. The basic cause of the rhythmic bursts of action
potentials is not understood, but it is known that the nature of the discharge is a ramp signal,
rather than an instantaneous burst of activity. If the DRG exhibited an instantaneous burst of
action potentials of equal magnitude, rapid filling of the lungs would occur, producing an abrupt
inspiratory gasp. Instead, the inspiratory signal from the DRG begins weakly and then steadily
increases to full intensity over a period of around two seconds. This progressive discharge
results in a steady increase in lung volume during the inspiration phase. At the end of the
inspiratory ramp signal, the action potentials abruptly cease, and the DRG remains inactive for
approximately three seconds before beginning another cycle. (Inspiratory activity probably
oscillates between sets of neurons in the DRG, but such neural nets have not been
demonstrated in humans.)

The inspiratory ramp signal is controlled by the rate of increase of the signal and the limiting
point at which the ramp ceases. If the ramp is shortened, as occurs with the Hering-Breuer
inflation reflex or pneumotaxic center activity, the duration of inspiration is shortened. Through
an unknown mechanism, the duration of expiration is also shortened by this inspiratory activity,
thus reducing the overall period of respiration and increasing the respiratory rate to
accommodate active respiration.

#19 ( 15012 )
CORRECT: A
The ventral respiratory group (VRG) of medullary neurons remains inactive during normal quiet
breathing and is not involved in the basic rhythmic pattern that controls breathing. When
respiratory drive rises above normal, however, respiratory signals from the oscillation
mechanism of the dorsal respiratory group (DRG) of medullary neurons begin to affect the
motor neurons of the VRG. The VRG nerve cells respond by sending powerful motor impulses
to the abdominal group of muscles to increase expiration and pulmonary ventilation.

#20 ( 15016 )
CORRECT: B
The work of breathing (WOB) is due to several factors. Energy must be expended in order to
overcome:
• airway resistance within the conducting passages of the respiratory system;
• elasticity of the thoracic cage and lungs (elastic work); and
• inertia of inelastic tissues (viscous resistance).

By contrast, maintenance of airway patency does not contribute to the WOB. Airway patency
in larger passages is mainly a function of cartilaginous elements in the airway wall; the integrity
of smaller noncartilaginous passages is maintained primarily by the radial traction of
peribronchial collagen fibers within the surrounding parenchymal tissue. The work of breathing
increases dramatically with pulmonary diseases such as asthma, emphysema, and heart
failure with severe dyspnea. These conditions require extra muscular effort to overcome the
reduced compliance and increased resistance of an impaired respiratory system.

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#21 ( 15017 )
CORRECT: A
Gaseous exchange in the respiratory system occurs only in the respiratory zone, that is, within
the alveoli that make up the acini, or primary lobules of the lung (this tissue is also known as
the lung parenchyma). The alveoli serve as the sites of external respiration and are found in
various structural configurations, including several branches, or generations, of respiratory
bronchioles, alveolar ducts, and alveolar sacs. Such respiratory units represent a continuation
of the terminal bronchioles of the tracheobronchial tree of conducting passages. The terminal
bronchioles are very small-diameter branches of the bronchioles and mark the end of the
conducting zone of the respiratory system.

The volume of gas contained in the various classes of the conducting airway is not available
for exchange with pulmonary capillary blood. The gas contained in this anatomic dead space
volume, therefore, is nonfunctional. As a general rule, the anatomic dead space volume, in
milliliters, is approximately equal to the body weight, in pounds, of a man. Thus, in a 150-
pound subject with a tidal volume of 500 mL, the anatomic dead space volume will be
approximately 150mL. Consequently, only the first 350mL of inspired air reaches the alveoli
for gaseous exchange; during expiration, the first 150mL of gas expired occupied the
conducting zone, whereas only the last 350mL of gas exhaled was in contact with the alveoli.
For these reasons, alveolar ventilation (or the alveolar minute volume), is always less than the
respiratory minute volume; e.g. 150-lb male, rapid shallow breathing pattern:

Respiratory rate: 30 breaths / min.

Tidal volume: 200mL.
Respiratory minute volume = 200 mL × 30 / min = 6000 mL / min.
Alveolar minute volume = (200 mL - 150 mL) × 30 / min = 1500 mL / min.

Since anatomic dead space volume (e.g. 150 mL) is fixed for an individual of a particular size,
alveolar ventilation is dramatically affected by the depth of ventilation. Therefore, for a given
respiratory minute volume, slow deep respirations produce greater alveolar ventilation than
rapid shallow breathing; e.g. 150-lb male, slow deep breathing pattern:

Respiratory rate: 10 breaths / min.

Tidal volume: 500mL.
Respiratory minute volume = 500 mL × 10 / min = 5000 mL / min.
Alveolar minute volume = (500 mL - 150 mL) × 10 / min = 3500 mL / min.

The physiologic dead space volume is the volume of gas in the respiratory system that does
not equilibrate with blood. In pulmonary pathophysiologic states, this non equilibrating gas
volume includes the volume of gas in nonperfused alveoli, as well as, any volume of gas in the
alveoli that is in excess of that needed to properly exchange with the blood in pulmonary
capillaries. Such ventilation-perfusion inequalities in the lung may lead to hypoxemia. In
healthy lungs, however, ventilation-perfusion matching is optimal, and the physiologic dead
space volume equals the anatomic dead space volume. In other words, virtually all of the gas
that reaches the alveoli is available for equilibration with blood in the pulmonary capillaries.
Only that volume of gas in the conducting passages, the anatomic dead space, is non-

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equilibrating and nonfunctional. Such a volume, in a healthy individual, is identical to the

physiologic dead space.

#22 ( 15020 )
CORRECT: D
Gaseous exchange in the respiratory system occurs only in the respiratory zone, that is, within
the alveoli that make up the acini, or primary lobules of the lung (this tissue is also known as
the lung parenchyma). The alveoli serve as the sites of external respiration and are found in
various structural configurations, including several branches, or generations, of respiratory
bronchioles, alveolar ducts, and alveolar sacs. Such respiratory units represent a continuation
of the terminal bronchioles of the tracheobronchial tree of conducting passages. The terminal
bronchioles are very small-diameter branches of the bronchioles and mark the end of the
conducting zone of the respiratory system.

The volume of gas contained in the various classes of the conducting airway is not available
for exchange with pulmonary capillary blood. The gas contained in this anatomic dead space
volume, therefore, is nonfunctional. As a general rule, the anatomic dead space volume, in
milliliters, is approximately equal to the body weight, in pounds, of a man. Thus, in a 150-
pound subject with a tidal volume of 500 mL, the anatomic dead space volume will be
approximately 150mL. Consequently, only the first 350mL of inspired air reaches the alveoli
for gaseous exchange; during expiration, the first 150mL of gas expired occupied the
conducting zone, whereas only the last 350mL of gas exhaled was in contact with the alveoli.
For these reasons, alveolar ventilation (or the alveolar minute volume), is always less than the
respiratory minute volume; e.g. 150-lb male, rapid shallow breathing pattern:

Respiratory rate: 30 breaths / min.

Tidal volume: 200mL.
Respiratory minute volume = 200 mL × 30 / min = 6000 mL / min.
Alveolar minute volume = (200 mL - 150 mL) × 30 / min = 1500 mL / min.

Since anatomic dead space volume (e.g. 150 mL) is fixed for an individual of a particular size,
alveolar ventilation is dramatically affected by the depth of ventilation. Therefore, for a given
respiratory minute volume, slow deep respirations produce greater alveolar ventilation than
rapid shallow breathing; e.g. 150-lb male, slow deep breathing pattern:

Respiratory rate: 10 breaths / min.

Tidal volume: 500mL.
Respiratory minute volume = 500 mL × 10 / min = 5000 mL / min.
Alveolar minute volume = (500 mL - 150 mL) × 10 / min = 3500 mL / min.

The physiologic dead space volume is the volume of gas in the respiratory system that does
not equilibrate with blood. In pulmonary pathophysiologic states, this non-equilibrating gas
volume includes the volume of gas in nonperfused alveoli, as well as, any volume of gas in the
alveoli that is in excess of that needed to properly exchange with the blood in pulmonary
capillaries. Such ventilation-perfusion inequalities in the lung may lead to hypoxemia. In

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healthy lungs, however, ventilation-perfusion matching is optimal, and the physiologic dead
space volume equals the anatomic dead space volume. In other words, virtually all of the gas
that reaches the alveoli is available for equilibration with blood in the pulmonary capillaries.
Only that volume of gas in the conducting passages, the anatomic dead space is non-
equilibrating and nonfunctional. Such a volume, in a healthy individual, is identical to the
physiologic dead space.

#23 ( 15021 )
CORRECT: E
Gaseous exchange in the respiratory system occurs only in the respiratory zone, that is, within
the alveoli that make up the acini, or primary lobules of the lung (this tissue is also known as
the lung parenchyma). The alveoli serve as the sites of external respiration and are found in
various structural configurations, including several branches, or generations, of respiratory
bronchioles, alveolar ducts, and alveolar sacs. Such respiratory units represent a continuation
of the terminal bronchioles of the tracheobronchial tree of conducting passages. The terminal
bronchioles are very small-diameter branches of the bronchioles and mark the end of the
conducting zone of the respiratory system.

The volume of gas contained in the various classes of the conducting airway is not available
for exchange with pulmonary capillary blood. The gas contained in this anatomic dead space
volume, therefore, is nonfunctional. As a general rule, the anatomic dead space volume, in
milliliters, is approximately equal to the body weight, in pounds, of a man. Thus, in a 150-
pound subject with a tidal volume of 500 mL, the anatomic dead space volume will be
approximately 150mL. Consequently, only the first 350mL of inspired air reaches the alveoli
for gaseous exchange; during expiration, the first 150mL of gas expired occupied the
conducting zone, whereas only the last 350mL of gas exhaled was in contact with the alveoli.
For these reasons, alveolar ventilation (or the alveolar minute volume), is always less than the
respiratory minute volume; e.g. 150-lb male, rapid shallow breathing pattern:

Respiratory rate: 30 breaths / min.

Tidal volume: 200mL.
Respiratory minute volume = 200 mL × 30 / min = 6000 mL / min.
Alveolar minute volume = (200 mL - 150 mL) × 30 / min = 1500 mL / min.

Since anatomic dead space volume (e.g. 150 mL) is fixed for an individual of a particular size,
alveolar ventilation is dramatically affected by the depth of ventilation. Therefore, for a given
respiratory minute volume, slow deep respirations produce greater alveolar ventilation than
rapid shallow breathing; e.g. 150-lb male, slow deep breathing pattern:

Respiratory rate: 10 breaths / min.

Tidal volume: 500mL.
Respiratory minute volume = 500 mL × 10 / min = 5000 mL / min.
Alveolar minute volume = (500 mL - 150 mL) × 10 / min = 3500 mL / min.

The physiologic dead space volume is the volume of gas in the respiratory system that does
not equilibrate with blood. In pulmonary pathophysiologic states, this non-equilibrating gas

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volume includes the volume of gas in nonperfused alveoli, as well as, any volume of gas in the
alveoli that is in excess of that needed to properly exchange with the blood in pulmonary
capillaries. Such ventilation-perfusion inequalities in the lung may lead to hypoxemia. In
healthy lungs, however, ventilation-perfusion matching is optimal, and the physiologic dead
space volume equals the anatomic dead space volume. In other words, virtually all of the gas
that reaches the alveoli is available for equilibration with blood in the pulmonary capillaries.
Only that volume of gas in the conducting passages, the anatomic dead space is non-
equilibrating and nonfunctional. Such a volume, in a healthy individual, is identical to the
physiologic dead space.

#24 ( 15023 )
CORRECT: D
Carbon dioxide has no ability to “displace” either carbon monoxide or nitrous oxide from the
alveoli or from the bloodstream. In fact, carbon monoxide has a pronounced affinity for oxygen
binding sites on hemoglobin molecules and is, therefore, particularly difficult to “displace” by
any means. Carbon monoxide and nitrous oxide do not combine chemically; therefore, they
exert independent partial pressures both in alveoli and in arterial blood. Diffusion of gas
across the alveolar-capillary membrane from the alveolus to the pulmonary capillary must
occur within the relatively short transit time (approximately 0.75 sec) that an erythrocyte has as
it passes through a capillary adjacent to an alveolus.

The ability of a gas in an alveolus to reach partial pressure equilibrium with capillary blood is
dependent on factors, such as the ease with which the gas reacts with components in the
blood. For example, the incomplete anesthetic gas, nitrous oxide (N2O), quickly diffuses out of
the alveolus but does not combine with hemoglobin. As a result, it reaches equilibrium in
arterial blood very rapidly (0.1 sec). Therefore, the “limiting factor” that determines how much
nitrous oxide can enter the bloodstream is not the diffusion of the gas, but the rate of blood
flowing through the pulmonary capillaries. In order for the diffusion of such a high-solubility
gas to continue, more blood must enter the alveolar-capillary system. Cardiac output,
therefore, limits the diffusion of a gas such as nitrous oxide; its uptake is said to be perfusion-
limited. By contrast, the coupling of carbon monoxide (CO) to hemoglobin in red blood cells
occurs with such avidity, that the partial pressure of CO (in the plasma) remains very low. As a
result, equilibrium of carbon monoxide with arterial blood is not reached in the 0.75 second
transit time of blood through the alveolar-capillary system. The uptake of carbon monoxide
into arterial blood is described as being diffusion-limited. Such a mechanism is not affected
by the perfusion of pulmonary capillaries.

The uptake of oxygen by pulmonary capillaries is both perfusion-limited and diffusion-limited.

Therefore, the transfer of such a gas can be affected by ventilation-perfusion mismatches in
the lung. Under normal resting conditions, the transfer of oxygen is perfusion-limited. Partial
pressure equilibrium with alveolar gas normally occurs in the first one-third of the transit time of
arterial blood through the alveolar-capillary system (approximately 0.3 sec). Therefore, once
hemoglobin molecules are saturated, oxygen molecules subsequently entering the plasma
quickly elevate the partial pressure of oxygen (Pao2) to the same value as alveolar partial
pressure (PAo2). Clearly, increased transfer of oxygen to red blood cells to form
oxyhemoglobin can only occur if pulmonary perfusion is increased. Individuals with decreased

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cardiac output (e.g. heart failure), decreased pulmonary blood flow, or decreased hemoglobin
levels (e.g. various anemias) exhibit the perfusion-limited aspect of oxygen uptake. In
addition, oxygen has a marked affinity for hemoglobin (although only a fraction of that of
carbon monoxide for hemoglobin), and can be affected by the integrity of the alveolar-capillary
membrane and alterations in the rate of diffusion of the gas through the membrane. When the
alveolar-capillary membrane is impaired, as in pulmonary fibrosis or pulmonary edema, the
diffusion of gas is reduced and the Pao2 will be less than the PAo2, given the normal transit
time of 0.75 second. In this instance, oxygen uptake is said to be diffusion-limited.

#25 ( 15024 )
CORRECT: D
Carbon dioxide has no ability to “displace” either carbon monoxide or nitrous oxide from the
alveoli or from the bloodstream. In fact, carbon monoxide has a pronounced affinity for oxygen
binding sites on hemoglobin molecules and is, therefore, particularly difficult to “displace” by
any means. Carbon monoxide and nitrous oxide do not combine chemically; therefore, they
exert independent partial pressures both in alveoli and in arterial blood. Diffusion of gas
across the alveolar-capillary membrane from the alveolus to the pulmonary capillary must
occur within the relatively short transit time (approximately 0.75 sec) that an erythrocyte has as
it passes through a capillary adjacent to an alveolus.

The ability of a gas in an alveolus to reach partial pressure equilibrium with capillary blood is
dependent on factors, such as the ease with which the gas reacts with components in the
blood. For example, the incomplete anesthetic gas, nitrous oxide (N2O), quickly diffuses out of
the alveolus but does not combine with hemoglobin. As a result, it reaches equilibrium in
arterial blood very rapidly (0.1 sec). Therefore, the “limiting factor” that determines how much
nitrous oxide can enter the bloodstream is not the diffusion of the gas, but the rate of blood
flowing through the pulmonary capillaries. In order for the diffusion of such a high-solubility
gas to continue, more blood must enter the alveolar-capillary system. Cardiac output,
therefore, limits the diffusion of a gas such as nitrous oxide; its uptake is said to be perfusion-
limited. By contrast, the coupling of carbon monoxide (CO) to hemoglobin in red blood cells
occurs with such avidity, that the partial pressure of CO (in the plasma) remains very low. As a
result, equilibrium of carbon monoxide with arterial blood is not reached in the 0.75 second
transit time of blood through the alveolar-capillary system. The uptake of carbon monoxide
into arterial blood is described as being diffusion-limited. Such a mechanism is not affected
by the perfusion of pulmonary capillaries.

The uptake of oxygen by pulmonary capillaries is both perfusion-limited and diffusion-limited.

Therefore, the transfer of such a gas can be affected by ventilation-perfusion mismatches in
the lung. Under normal resting conditions, the transfer of oxygen is perfusion-limited. Partial
pressure equilibrium with alveolar gas normally occurs in the first one-third of the transit time of
arterial blood through the alveolar-capillary system (approximately 0.3 sec). Therefore, once
hemoglobin molecules are saturated, oxygen molecules subsequently entering the plasma
quickly elevate the partial pressure of oxygen (Pao2) to the same value as alveolar partial
pressure (PAo2). Clearly, increased transfer of oxygen to red blood cells to form
oxyhemoglobin can only occur if pulmonary perfusion is increased. Individuals with decreased
cardiac output (e.g. heart failure), decreased pulmonary blood flow, or decreased hemoglobin

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levels (e.g. various anemias) exhibit the perfusion-limited aspect of oxygen uptake. In
addition, oxygen has a marked affinity for hemoglobin (although only a fraction of that of
carbon monoxide for hemoglobin), and can be affected by the integrity of the alveolar-capillary
membrane and alterations in the rate of diffusion of the gas through the membrane. When the
alveolar-capillary membrane is impaired, as in pulmonary fibrosis or pulmonary edema, the
diffusion of gas is reduced and the Pao2 will be less than the PAo2, given the normal transit
time of 0.75 second. In this instance, oxygen uptake is said to be diffusion-limited.

#26 ( 15025 )
CORRECT: C
Carbon dioxide has no ability to “displace” either carbon monoxide or nitrous oxide from the
alveoli or from the bloodstream. In fact, carbon monoxide has a pronounced affinity for oxygen
binding sites on hemoglobin molecules and is, therefore, particularly difficult to “displace” by
any means. Carbon monoxide and nitrous oxide do not combine chemically; therefore, they
exert independent partial pressures both in alveoli and in arterial blood. Diffusion of gas
across the alveolar-capillary membrane from the alveolus to the pulmonary capillary must
occur within the relatively short transit time (approximately 0.75 sec) that an erythrocyte has as
it passes through a capillary adjacent to an alveolus.

The ability of a gas in an alveolus to reach partial pressure equilibrium with capillary blood is
dependent on factors, such as the ease with which the gas reacts with components in the
blood. For example, the incomplete anesthetic gas, nitrous oxide (N2O), quickly diffuses out of
the alveolus but does not combine with hemoglobin. As a result, it reaches equilibrium in
arterial blood very rapidly (0.1 sec). Therefore, the “limiting factor” that determines how much
nitrous oxide can enter the bloodstream is not the diffusion of the gas, but the rate of blood
flowing through the pulmonary capillaries. In order for the diffusion of such a high-solubility
gas to continue, more blood must enter the alveolar-capillary system. Cardiac output,
therefore, limits the diffusion of a gas such as nitrous oxide; its uptake is said to be perfusion-
limited. By contrast, the coupling of carbon monoxide (CO) to hemoglobin in red blood cells
occurs with such avidity, that the partial pressure of CO (in the plasma) remains very low. As a
result, equilibrium of carbon monoxide with arterial blood is not reached in the 0.75 second
transit time of blood through the alveolar-capillary system. The uptake of carbon monoxide
into arterial blood is described as being diffusion-limited. Such a mechanism is not affected
by the perfusion of pulmonary capillaries.

The uptake of oxygen by pulmonary capillaries is both perfusion-limited and diffusion-limited.

Therefore, the transfer of such a gas can be affected by ventilation-perfusion mismatches in
the lung. Under normal resting conditions, the transfer of oxygen is perfusion-limited. Partial
pressure equilibrium with alveolar gas normally occurs in the first one-third of the transit time of
arterial blood through the alveolar-capillary system (approximately 0.3 sec). Therefore, once
hemoglobin molecules are saturated, oxygen molecules subsequently entering the plasma
quickly elevate the partial pressure of oxygen (Pao2) to the same value as alveolar partial
pressure (PAo2). Clearly, increased transfer of oxygen to red blood cells to form
oxyhemoglobin can only occur if pulmonary perfusion is increased. Individuals with decreased
cardiac output (e.g. heart failure), decreased pulmonary blood flow, or decreased hemoglobin
levels (e.g. various anemias) exhibit the perfusion-limited aspect of oxygen uptake. In

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addition, oxygen has a marked affinity for hemoglobin (although only a fraction of that of
carbon monoxide for hemoglobin), and can be affected by the integrity of the alveolar-capillary
membrane and alterations in the rate of diffusion of the gas through the membrane. When the
alveolar-capillary membrane is impaired, as in pulmonary fibrosis or pulmonary edema, the
diffusion of gas is reduced and the Pao2 will be less than the PAo2, given the normal transit
time of 0.75 second. In this instance, oxygen uptake is said to be diffusion-limited.

#27 ( 15178 )
CORRECT: C
Drug potency refers to the ability of a drug to produce a specified effect at a given dose. If
Drug A produces this specified response at a lower dose than Drug B, then Drug A is
considered more potent than Drug B.

Drug efficacy refers to the intrinsic ability of a drug to produce a response relative to the
number of drug-receptor complexes formed. (At the 50% response level, efficacy is usually
expressed as ED50, or median effective dose, the dose that produces a specified intensity of
effect in 50% of individuals.) Some drugs are not as effective, or efficacious, as others, even
at higher doses. If a drug produces a desired therapeutic effect by forming relatively few drug-
receptor complexes, the drug is said to have high efficacy. However, if a drug simply exhibits
high potency, this is no guarantee that the drug will be efficacious.

High potency allows a drug to be administered at a lower dose, but this feature is only valuable
and significant if the drug also exhibits efficacy. A drug must be capable of forming a sufficient
number of drug-receptor complexes in order to be therapeutically useful. Potency alone is not
enough.

#28 ( 15179 )
CORRECT: B

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The hydrogen ion concentration of a fluid dramatically affects the amount of dissociation of a
substance placed into that fluid. The degree of dissociation of the substance, in turn,
influences the rate of transfer of the substance through cell membranes. For example, an
orally administered drug that is a weak acid tends to remain nonionized, or undissociated, in
an acidic fluid such as gastric juice (pH = 1.6-2.4). This occurs because the large numbers of
H+ in the acidic environment readily combine with any anions being generated by the limited
dissociation of the weak acid. This combining tendency drives the reaction “to the left”, i.e.,
back towards the formation of nonionized reactant, thus opposing further ionization of the drug.

Alkaline solutions contain relatively few H+, therefore, a weak acid drug or drug metabolite
readily ionizes when placed into an alkaline fluid such as intestinal juice (pH = 7.6-8.2), thus
generating hydrogen ions and anions. The hydrogen ions rapidly bind with the hydroxide ions
(OH-) of the alkaline fluid to form water and drive the reaction “to the right”, i.e., towards the
formation of more product.

The pH factors described above also influence the ionization kinetics and absorption of an
alkaline drug or drug metabolite. For example, a drug that is a weak base tends to ionize and
form water when placed in an acidic environment such as gastric juice, thus driving the
reaction “to the right”; a drug that is a weak base placed in an alkaline medium tends to remain
in the undissociated state, thus driving the reaction “to the left”.

The degree of dissociation of a drug or drug metabolite affects the movement of the drug or
metabolite through cell membranes. Cell membranes are more permeable to nonionized
drugs, therefore, transfer of such drugs through cell membranes, as occurs in absorption,
takes place more readily. In summary, acidic drugs placed in an acidic fluid remain
nonionized, whereas alkaline drugs in an alkaline environment remain nonionized. In either
case, more rapid transfer of drug through cell membranes occurs.

In order to reduce the rate of absorption through cell membranes, drugs or drug metabolites
need to be maintained in an ionized state. Maintaining a drug in such an ionized state is useful
in the kidney in order to slow tubular reabsorption and keep the drug in the glomerular filtrate,
thus promoting its removal in the urine in some cases of drug overdose. See the attached
image.

#29 ( 15180 )
CORRECT: C

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The hydrogen ion concentration of a fluid dramatically affects the amount of dissociation of a
substance placed into that fluid. The degree of dissociation of the substance, in turn,
influences the rate of transfer of the substance through cell membranes. For example, an
orally administered drug that is a weak acid tends to remain nonionized, or undissociated, in
an acidic fluid such as gastric juice (pH = 1.6-2.4). This occurs because the large numbers of
H+ in the acidic environment readily combine with any anions being generated by the limited
dissociation of the weak acid. This combining tendency drives the reaction “to the left”, i.e.,
back towards the formation of nonionized reactant, thus opposing further ionization of the drug.

Alkaline solutions contain relatively few H+, therefore, a weak acid drug or drug metabolite
readily ionizes when placed into an alkaline fluid such as intestinal juice (pH = 7.6-8.2), thus
generating hydrogen ions and anions. The hydrogen ions rapidly bind with the hydroxide ions
(OH-) of the alkaline fluid to form water and drive the reaction “to the right”, i.e., towards the
formation of more product.

The pH factors described above also influence the ionization kinetics and absorption of an
alkaline drug or drug metabolite. For example, a drug that is a weak base tends to ionize and
form water when placed in an acidic environment such as gastric juice, thus driving the
reaction “to the right”; a drug that is a weak base placed in an alkaline medium tends to remain
in the undissociated state, thus driving the reaction “to the left”.

The degree of dissociation of a drug or drug metabolite affects the movement of the drug or
metabolite through cell membranes. Cell membranes are more permeable to nonionized
drugs, therefore, transfer of such drugs through cell membranes, as occurs in absorption,
takes place more readily. In summary, acidic drugs placed in an acidic fluid remain
nonionized, whereas alkaline drugs in an alkaline environment remain nonionized. In either
case, more rapid transfer of drug through cell membranes occurs.

In order to reduce the rate of absorption through cell membranes, drugs or drug metabolites
need to be maintained in an ionized state. Maintaining a drug in such an ionized state is useful
in the kidney in order to slow tubular reabsorption and keep the drug in the glomerular filtrate,
thus promoting its removal in the urine in some cases of drug overdose. See the attached
image.

#30 ( 15350 )
CORRECT: A
Creatine is synthesized in the liver from methionine, glycine, and arginine. In skeletal muscle,
it is phosphorylated to form phosphorylcreatine, which is an important energy store for ATP
synthesis.

The creatinine in the urine is formed from phosphorylcreatine. Creatine is not converted
directly to creatinine. The rate of creatinine excretion is relatively constant from day to day.

There is very little creatine in the urine of normal men, but appreciable quantities are excreted
in any condition associated with extensive muscle breakdown. Thus, creatinuria occurs in
starvation, thyrotoxicosis, poorly controlled diabetes mellitus, and the various primary and

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secondary diseases of muscle (myopathies).

#31 ( 15351 )
CORRECT: A
Creatine is synthesized in the liver from methionine, glycine, and arginine. In skeletal muscle,
it is phosphorylated to form phosphorylcreatine, which is an important energy store for ATP
synthesis.

The creatinine in the urine is formed from phosphorylcreatine. Creatine is not converted
directly to creatinine. The rate of creatinine excretion is relatively constant from day to day.

There is very little creatine in the urine of normal men, but appreciable quantities are excreted
in any condition associated with extensive muscle breakdown. Thus, creatinuria occurs in
starvation, thyrotoxicosis, poorly controlled diabetes mellitus, and the various primary and
secondary diseases of muscle (myopathies).

#32 ( 15352 )
CORRECT: B
Creatine is synthesized in the liver from methionine, glycine, and arginine. In skeletal muscle,
it is phosphorylated to form phosphorylcreatine, which is an important energy store for ATP
synthesis.

The creatinine in the urine is formed from phosphorylcreatine. Creatine is not converted
directly to creatinine. The rate of creatinine excretion is relatively constant from day to day.

There is very little creatine in the urine of normal men, but appreciable quantities are excreted
in any condition associated with extensive muscle breakdown. Thus, creatinuria occurs in
starvation, thyrotoxicosis, poorly controlled diabetes mellitus, and the various primary and
secondary diseases of muscle (myopathies).

#33 ( 15353 )
CORRECT: C
Creatine is synthesized in the liver from methionine, glycine, and arginine. In skeletal muscle,
it is phosphorylated to form phosphorylcreatine, which is an important energy store for ATP
synthesis.

The creatinine in the urine is formed from phosphorylcreatine. Creatine is not converted
directly to creatinine. The rate of creatinine excretion is relatively constant from day to day.

There is very little creatine in the urine of normal men, but appreciable quantities are excreted
in any condition associated with extensive muscle breakdown. Thus, creatinuria occurs in
starvation, thyrotoxicosis, poorly controlled diabetes mellitus, and the various primary and
secondary diseases of muscle (myopathies).

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#34 ( 15354 )
CORRECT: E
Much more RT3 and much less T3 are formed during fetal life, and the ratio shifts to that of
adults about 6 weeks after birth. Various drugs inhibit the 5'-deiodinase that converts T4 to T3
and RT3 to 3,3'-diiodothyronine, producing a fall in plasma T3 and a rise in plasma RT3. A wide
variety of nonthyroidal illnesses also depress 5'-deiodinase. These include burns, trauma,
advanced cancer, cirrhosis, renal failure, myocardial infarction, and febrile states.

#35 ( 15355 )
CORRECT: E
Much more RT3 and much less T3 are formed during fetal life, and the ratio shifts to that of
adults about 6 weeks after birth. Various drugs inhibit the 5'-deiodinase that converts T4 to T3
and RT3 to 3,3'-diiodothyronine, producing a fall in plasma T3 and a rise in plasma RT3. A wide
variety of nonthyroidal illnesses also depress 5'-deiodinase. These include burns, trauma,
advanced cancer, cirrhosis, renal failure, myocardial infarction, and febrile states.

#36 ( 15356 )
CORRECT: A
Each muscle spindle consists of 2-10 muscle fibers enclosed in a connective tissue capsule.
These fibers are more embryonal in character and have less distinct striations than the rest of
the fibers in the muscle. They are called intrafusal fibers to distinguish them from the
extrafusal fibers, the regular contractile units of the muscle. The intrafusal fibers are in parallel
with the rest of the muscle fibers because the ends of the capsule of the spindle are attached
to the tendons at either end of the muscle or to the sides of the extrafusal fibers.

#37 ( 15357 )
CORRECT: A
Each muscle spindle consists of 2-10 muscle fibers enclosed in a connective tissue capsule.
These fibers are more embryonal in character and have less distinct striations than the rest of
the fibers in the muscle. They are called intrafusal fibers to distinguish them from the
extrafusal fibers, the regular contractile units of the muscle. The intrafusal fibers are in parallel
with the rest of the muscle fibers because the ends of the capsule of the spindle are attached
to the tendons at either end of the muscle or to the sides of the extrafusal fibers.

#38 ( 15358 )
CORRECT: B
Each muscle spindle consists of 2-10 muscle fibers enclosed in a connective tissue capsule.
These fibers are more embryonal in character and have less distinct striations than the rest of
the fibers in the muscle. They are called intrafusal fibers to distinguish them from the
extrafusal fibers, the regular contractile units of the muscle. The intrafusal fibers are in parallel
with the rest of the muscle fibers because the ends of the capsule of the spindle are attached
to the tendons at either end of the muscle or to the sides of the extrafusal fibers.

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#39 ( 15359 )
CORRECT: A
There are two types of intrafusal fibers in mammalian muscle spindles. The first type contains
many nuclei in a dilated central area and is therefore called a nuclear bag fiber. The second
type, the nuclear chain fiber, is thinner and shorter and lacks a definite bag. The ends of the
nuclear chain fibers connect to the sides of the nuclear bag fibers. The ends of the intrafusal
fibers are contractile, whereas the central portions probably are not.

#40 ( 15360 )
CORRECT: A
There are two types of intrafusal fibers in mammalian muscle spindles. The first type contains
many nuclei in a dilated central area and is therefore called a nuclear bag fiber. The second
type, the nuclear chain fiber, is thinner and shorter and lacks a definite bag. The ends of the
nuclear chain fibers connect to the sides of the nuclear bag fibers. The ends of the intrafusal
fibers are contractile, whereas the central portions probably are not.
__________________________________________________________________________
NOTE:
F a c t o r s a f f e c tin g th e s e c r e t io n o f h u m a n Questions 41 through 49 refer to
h o rm o the table on the left.
FACTO PRO LAC GROW
R T IN HT O
HR M O
NE I - moderate increase
S le e I+ I+ I+ - marked increase
N u r s in I+ N I++ - very marked increase
B re a s t I N N - no change
n o n la c t a t in g
D - moderate decrease
S tr e s I+ I+ D+ - marked decrease
H y p o g ly c e I I+
S tr e n u o u s I I
S exual I N
w om e
P re g n a n I+ N
E s tro g e I I
H y p o t h y r o id I N
TR I+ N
P h e n o th ia z i I+ N
b u tyro p h e n o
O p ia t I I
G lu c o N D
S o m a to s t N D+
L- D+ I+
DOPA
A p o m o rp h D+ I+
B r o m o c r ip tin e D+ I
r e la t e d e r g o t

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#41 ( 15370 )
CORRECT: C

#42 ( 15371 )
CORRECT: B

#43 ( 15372 )
CORRECT: A

#44 ( 15373 )
CORRECT: B

#45 ( 15374 )
CORRECT: C

#46 ( 15375 )
CORRECT: A

#47 ( 15376 )
CORRECT: A

#48 ( 15377 )
CORRECT: B

#49 ( 15378 )
CORRECT: C

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