NURS 6501 Advanced Pathophysiology Exam
3 QUESTIONS AND VERIFIED ANSWERS
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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
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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?
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
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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 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
d. Insulin resistance - Correct Answer :Angiotensin II. Of the available options, only angiotensin II is responsible
for the hypertrophy of the myocardium and much of the renal damage associated with hypertension.
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1. What pathologic change occurs to the kidney's glomeruli as a result of hypertension?
a. Compression of the renal tubules
b. Ischemia of the tubule
c. Increased pressure from within the tubule
d. Obstruction of the renal tubule –
Correct Answer :Ischemia of the tubule. n the kidney, vasoconstriction and resultant decreased renal perfusion
cause tubular ischemia and pre-glomerular arteriopathy. This selection is the only option that accurately
identifies the pathologic change to the kidney that occurs as a result of hypertension.
1. What effect does atherosclerosis have on the development of an aneurysm?
a. Atherosclerosis causes ischemia of the intima.
b. It increases nitric oxide.
c. Atherosclerosis erodes the vessel wall.
d. It obstructs the vessel. –
Correct Answer :Atherosclerosis erodes the vessel wall. Atherosclerosis is a common cause of aneurysms
because plaque formation erodes the vessel wall.
1. What change in a vein supports the development of varicose veins?
a. Increase in osmotic pressure
b. Damage to the venous endothelium
c. Damage to the valves in veins
d. Increase in hydrostatic pressure - Correct Answer :Damage to the valves in veins. If a valve is damaged,
permitting backflow, then a section of the vein is subjected to the pressure exerted by a larger volume of blood
under the influence of gravity. The vein swells as it becomes engorged, and the surrounding tissue becomes
edematous because increased hydrostatic pressure pushes plasma through the stretched vessel wall.
1. Which description is consistent with chronic lymphocytic leukemia (CLL)?
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