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UTA NURS 5315 Advanced Pathophysiology
Questions & Correct Answers with Rationales /
NURS 5315 Endocrine Practice Test with 130
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1. Within a physiologic range, what does an increase in left
ventricular end-diastolic volume (preload) result in?
a. Increase in force of contraction
b. Increase in afterload
c. Decrease in refractory time
d. Decrease in repolarization –
Correct Answer :Increase in force of contraction. This concept is expressed in the Frank-Starling law;
the cardiac muscle, like other muscles, increases its strength of contraction when it is stretched.
1. As stated in the Frank-Starling law, a direct relationship exists between the _____ of the blood in the
heart at the end of diastole and the _____ of contraction during the next systole.
a. Pressure; force
b. Viscosity; force
c. Volume; strength
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d. Viscosity; strength –
Correct Answer :Volume; strength. As stated in the Frank-Starling law, the volume of blood in the heart
at the end of diastole (the length of its muscle fibers) is directly related to the force (strength) of
contraction during the next systole.
1. Pressure in the left ventricle must exceed pressure in which structure before the left ventricle can
eject blood?
a. Superior vena cava
b. Inferior vena cava
c. Aorta
d. Pulmonary veins –
Correct Answer :Aorta. Pressure in the ventricle must exceed aortic pressure before blood can be
pumped out during systole. The aorta is the only structure in which pressure must be less than the
amount of blood in the left ventricle for ejection to occur.
1. When the volume of blood in the ventricle at the end of diastole increases, the force of the
myocardial contraction during the next systole will also increase, which is an example of which law or
theory about the heart?
a. Laplace's law
b. Cross-bridge theory
c. Poiseuille law
d. Frank-Starling law –
Correct Answer :Frank-Starling law. his concept is expressed only in the Frank-Starling law; the cardiac
muscle, like other muscles, increases its strength of contraction when it is stretched.
1. Reflex control of total cardiac output and total peripheral resistance is controlled by what
mechanism?
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a. Parasympathetic stimulation of the heart, arterioles, and veins
b. Sympathetic stimulation of the heart, arterioles, and veins
c. Autonomic control of the heart only
d. Somatic control of the heart, arterioles, and veins –
Correct Answer :Sympathetic stimulation of the heart, arterioles, and veins. Reflex control of total
cardiac output and peripheral resistance includes (1) sympathetic stimulation of the heart, arterioles,
and veins; and (2) parasympathetic stimulation of the heart only. Neither autonomic nor somatic
controls are involved in this process.
1. What is the major effect of a calcium channel blocker such as verapamil on cardiac contractions?
a. Increases the rate of cardiac contractions.
b. Decreases the strength of cardiac contractions.
c. Stabilizes the rhythm of cardiac contractions.
d. Stabilizes the vasodilation during cardiac contractions. –
Correct Answer :Decreases the strength of cardiac contractions. The L-type, or long-lasting, channels
are the predominant type of calcium channels and are the channels blocked by calcium channel-
blocking drugs (verapamil, nifedipine, diltiazem). The major effect of these medications is to decrease
the strength of cardiac contraction. This selection is the only option that accurately identifies the
effect of a calcium channel blocker on the cardiac contractions.
1. What is the initiating event that leads to the development of atherosclerosis?
a. Release of the inflammatory cytokines
b. Macrophages adhere to vessel walls.
c. Injury to the endothelial cells that line the artery walls
d. Release of the platelet-deprived growth factor –
Correct Answer :Injury to the endothelial cells that line the artery walls. Atherosclerosis begins with an
injury to the endothelial cells that line the arterial walls. Possible causes of endothelial injury include
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the common risk factors for atherosclerosis, such as smoking, hypertension, diabetes, increased levels
of low-density lipoprotein (LDL), decreased levels of high-density lipoprotein (HDL), and
autoimmunity.
1. What is the effect of oxidized low-density lipoproteins (LDLs) in atherosclerosis?
a. LDLs cause smooth muscle proliferation.
b. LDLs cause regression of atherosclerotic plaques.
c. LDLs increase levels of inflammatory cytokines.
d. LDLs direct macrophages to the site in the endothelium. –
Correct Answer :LDLs cause smooth muscle proliferation. Oxidized LDLs are toxic to endothelial cells,
cause smooth muscle proliferation, and activate further immune and inflammatory responses.
1. When endothelia cells are injured, what alteration contributes to atherosclerosis?
a. The release of toxic oxygen radicals that oxidize low-density lipoproteins (LDLs).
b. Cells are unable to make the normal amount of vasodilating cytokines.
c. Cells produce an increased amount of antithrombotic cytokines.
d. Cells develop a hypersensitivity to homocysteine and lipids. –
Correct Answer :Cells are unable to make the normal amount of vasodilating cytokines. Injured
endothelial cells become inflamed and cannot make normal amounts of antithrombotic and
vasodilating cytokines.
1. Which factor is responsible for the hypertrophy of the myocardium associated with hypertension?
a. Increased norepinephrine
b. Angiotensin II
c. Adducin
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