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Test Bank for Pathophysiology 6th Edition by Banasik Complete Questions and Answers Study Guide for Nursing and Allied Health Students Preparing for Disease Processes Clinical Concepts Patient Assessment Medical Conditions and Healthcare Examinations

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This Test Bank for Pathophysiology 6th Edition by Banasik is a comprehensive study resource designed to support nursing and allied health students studying disease processes, altered physiology, clinical manifestations, and the relationship between normal and abnormal body function. It provides practice material that can help learners reinforce important pathophysiology concepts, strengthen clinical reasoning, review disease mechanisms, and prepare for course examinations. Students can use the resource to study how diseases and disorders affect different body systems while connecting physiological changes with signs, symptoms, assessment findings, and potential complications. It can be used alongside the textbook, lectures, classroom notes, assignments, and instructor-provided learning materials as a supplementary study aid. The material supports independent revision, structured study sessions, practice-question review, and examination preparation. It is particularly useful for nursing students and healthcare learners preparing for pathophysiology courses and assessments that require an understanding of cellular processes, systemic disorders, disease mechanisms, and the clinical consequences of altered body function.

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Pathophysiology 6th Edition Banasik Tes Bank Y1 1 Y1 1 Y1 1 Y1 1 JY1 1




Chapter 26: Renal Function
Y11 Y11 Y11




Banasik:Pathophysiology,6thEdition
1
Y 1
Y 1
Y




MULTIPLE CHOICE Y11




1. The primary selectivity barrier for glomerular filtration is the
Y11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




a. glomerular basement membrane. JY11 JY1 1




b. endothelial tight junctions. JY1 1 JY1 1




c. epithelial fenestra. JY11




d. mesangial cells. JY11




ANS: J Y 1 1 A
The basement membrane is an important selectivity barrier of the glomerulus, preventing plas
JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1




ma proteins, RBCs, WBCs, and platelets from passing through the glomerulus.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




Endothelial tight junctions, epithelial fenestra, and mesangial cells are not the primary selectivi JY11 JY11 JY11 JY11 JY11 JY1 1 JY11 JY11 JY11 JY11 JY11 JY1 1




ty barriers for glomerular filtration.
JY1 1 JY1 1 JY1 1 JY1 1




2. The glucose transporter in the proximal tubule
JY11 JY11 JY1 1 JY1 1 JY1 1 JY1 1




a. has no transport maximum. JY1 1 JY1 1 JY1 1




b. does not depend on sodium reabsorption. JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




c. is ATP-dependent. JY1 1




d. may be saturated at high filtered glucose loads. JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY1 1 JY1 1




ANS: J Y 1 1 D
The glucose transporter in the proximal tubule may be saturated at high filtered glucose loads;
JY11 JY11 JY1 1 JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




glycosuria then results. A transport maximum does exist beyond which glycosuria occurs. A so JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY1 1




dium-dependentproteinc oN- tU raR poIrN
nsS teG sB
r iTne.
edCeO
d.MThe transporter is not ATP-dependent. JY1 JY1 JY1 1 JY1 JY1 1 JY11 JY11 JY11




3. The primary function of the vasa recta is to
JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY1 1




a. secrete renin. JY1 1




b. reabsorb NaCl. JY1 1




c. reabsorb interstitial fluid. JY1 1 JY1 1




d. secrete urea. JY1 1




ANS: J Y 1 1 C
The vasa recta are capillaries that surround the loops of Henle and collecting ducts and absorb intersti
JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY11 JY1 1 JY1 1 JY1 1 JY11 JY11 JY1 1




tial fluid. The vasa recta do not secrete rennin or urea, nor do they reabsorb NaCl.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




4. Approximately two thirds of the water and electrolytes filtered by the kidney are reabsorbed by JY11 JY11 JY1 1 JY11 JY11 JY1 1 JY11 JY11 JY1 1 JY11 JY11 JY11 JY11 JY1 1




JY1 1 the
a. loop of Henle. JY1 1 JY1 1




b. collecting tubule. JY1 1




c. distal tubule. JY1 1




d. proximal tubule. JY1 1




ANS: J Y 1 1 D
Approximately two thirds of the water and electrolytes filtered by the kidney are reabsorbed by JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1




the proximal tubule. Two thirds of the water and electrolytes filtered by the kidney are not reabso
1 JY11 JY1 1 JY11 JY11 JY11 JY11 JY1 1 JY11 JY11 JY11 JY1 1 JY11 JY11 JY11 JY11 JY1 1




rbed by the loop of Henle, collecting tubule, or distal tubule.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




NURSINGTB.COM

, Pathophysiology 6th Edition Banasik Tes Bank Y1 1 Y1 1 Y1 1 Y1 1 JY1 1




5. Which finding on urinalysis should prompt further evaluation? JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY11




a. pH 4.5 JY1 1




b. Red blood cells 2 per high-power field JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY1 1




c. Specific gravity of 1.015 JY11 JY1 1 JY1 1




d. White blood cells 20 per high-power field JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY1 1




ANS: J Y 1 1 D
This many WBCs in the urine indicate urinary tract infection; 5 or more is not expected. 4.5 is a n
JY1 1 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY11 JY11 JY11 JY1 1 JY11




ormal pH. Fewer than 5 RBCs is insignificant. 1.015 is a normal specific gravity.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY11 JY1 1 JY1 1




6. Renin is released from JY11 JY11 JY11




a. the posterior pituitary gland. JY1 1 JY11 JY1 1




b. the liver. JY1 1




c. juxtaglomerular cells. JY11




d. macula densa cells. JY11 JY1 1




ANS: J Y 1 1 C
Renin is released from the juxtaglomerular cells. Renin is not released from the posterior pituit
JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY1 1




ary gland, liver, or macula densa cells.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




7. It is true that glucose reabsorption in the tubules
JY1 1 JY1 1 JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




a. occurs passively. JY1 1




b. occurs in the proximal convoluted tubule. JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




c. is unlimited. JY1 1




d. simply does not occur. JY1 1 JY1 1 JY1 1




ANS: J Y 1 1 B
Glucose reabsorption occursNi n t hRe pI
SNT G Bis.required.
ro xi m a l c o nCv o lMu t e d tubule. Glucose reabsorption is notpassi
ve; a sodium-dependent proteinUco-transporter O
JY1 1 JY 1 1 JY1 JY 1 1 JY 1 1 JY 1 1 JY 1 1 JY1 1 JY 1 1 JY 1 1 JY1




JY1 1 JY11 Glucose reabsorption in the JY1 1 JY1 1
1
Y 1
Y 1
Y


JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




tubules is limited by the number of co- JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




transporters; a threshold exists beyond which glycosuria will result. Glucose reabsorption occur JY1 1 JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY11 JY11 JY11 JY11 JY11




s in the proximal convoluted tubule with the assistance of a sodium-dependent protein co-
JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY1 1




transporter.

8. Serious renal impairment generally does not occur until JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




of the total nephrons have been d
JY11 JY11 JY11 JY11 JY11 JY1 1




amaged.
a. 20%
b. 40%
c. 60%
d. 80%
ANS: J Y 1 1 D
Serious renal impairment generally does not occur until 75% to 90% of the total nephrons have
JY11 JY11 JY1 1 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY1 1 JY1 1 JY




been damaged. The other answer options are incorrect.
11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




9. An important sign of glomerular basement membrane dysfunction is
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




a. proteinuria.
b. hematuria.
c. glycosuria.
d. urinary casts. JY1 1




ANS: J Y 1 1 A




NURSINGTB.COM

, Pathophysiology 6th Edition Banasik Tes Bank Y1 1 Y1 1 Y1 1 Y1 1 JY1 1




Proteinuria is an important sign of basement membrane dysfunction. Hematuria can be found in gJY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY1 1 JY1 1




lomerular disorders but it is not specific to this; it can be caused by many disorders.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




Glycosuria is found primarily in diabetes mellitus. Urinary casts do not necessarily mean base
JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1




ment membrane dysfunction.
JY1 1 JY1 1




10. The main driving force for glomerular filtration is
JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY11 JY1 1




a. oncotic pressure in the Bowman’s capsule. JY11 JY1 1 JY11 JY1 1 JY1 1




b. hydrostatic pressure in glomerular capillaries. JY1 1 JY1 1 JY11 JY11




c. permeability of the glomerular membrane. JY1 1 JY1 1 JY11 JY1 1




d. solute content of the blood in the glomerular capillaries. JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




ANS: J Y 1 1 B
Hydrostatic pressure within the glomerular capillaries is the main driving force for filtration. A s JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY11 JY11 JY1 1 JY1 1




ignificant drop in blood pressure such as in shock severely reduces glomerular filtration. Onco
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




tic pressure in the Bowman’s capsule, permeability of the glomerular membrane, and solute c
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




ontent of the blood in the glomerular capillaries are not the main driving forces for filtration.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




11. Factors that increase the glomerular filtration rate include
JY1 1 JY11 JY11 JY1 1 JY1 1 JY11 JY1 1




a. fluid volume excess. JY1 1 JY1 1




b. increased hydrostatic pressure in the Bowman’s capsule. JY1 1 JY1 1 JY11 JY1 1 JY1 1 JY1 1




c. high oncotic pressure in glomerular capillary blood. JY1 1 JY1 1 JY11 JY1 1 JY1 1 JY1 1




d. obstruction in the renal tubules. JY1 1 JY11 JY1 1 JY1 1




ANS: J Y 1 1 A
Fluid volume excess increases blood volume which increases glomerular filtration. Increased hydrost
JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1




atic pressure in the Bowman’s capsule, high oncotic pressure in the glomerular
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




capillary, and obstruction ofN naR
r eU tuI
lS buNleGs T
opBp.
osCeO
fiM
ltration. JY11 JY1 1 JY1 1 JY1 JY1




12. The underlying mechanism which directly results in glycosuria is
JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




a. filtration of glucose from the glomerulus. JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




b. exceeding the threshold for glucose reabsorption. JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




c. secretion of glucose into the distal tubule. JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




d. the mechanism is unknown. JY11 JY1 1 JY1 1




ANS: J Y 1 1 B
Glucose is normally freely filtered but then reabsorbed from the tubules into the peritubular cap
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 J Y1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




illaries. If the threshold for reabsorption is exceeded as in uncontrolled diabetes mellitus, glyco
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




suria results. Glucose is freely filtered from the glomerulus; this is not the direct cause of glycosur
JY11 JY1 1 JY11 JY11 JY11 JY1 1 JY1 1 JY11 JY11 JY1 1 JY11 JY11 JY11 JY11 JY11 JY1 1




ia. Glucose is not secreted into the distal tubule. The underlying mechanism that directly results
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY




in glycosuria is exceeding the threshold for glucose reabsorption.
11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




13. Excess potassium is excreted from the body by the renal system primarily via
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY1 1




a. glomerular filtration based on blood level of potassium. JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




b. reabsorption based on blood level of potassium. JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




c. secretion based on aldosterone level. JY1 1 JY1 1 JY1 1 JY1 1




d. an unknown mechanism. JY1 1 JY1 1




ANS: J Y 1 1 C




NURSINGTB.COM

, Pathophysiology 6th Edition Banasik Tes Bank Y1 1 Y1 1 Y1 1 Y1 1 JY1 1




Potassium is secreted from the distal tubule and collecting ducts into the tubule lumen under th JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




e influence of aldosterone. Excess potassium is not excreted from the body by the renal system
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY11




via glomerular filtration or the renal system based on the blood level of potassium, nor is it excret
JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY1 1 JY11 JY11 JY1 1 JY1 1 JY1 1




ed from the body by the renal system based on the aldosterone level.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




14. The glomerular filtration rate is most accurately reflected in the
JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY11




a. blood urea nitrogen level. JY1 1 JY11 JY1 1




b. urinary output. JY1 1




c. serum osmolality. JY1 1




d. serum creatinine level. JY1 1 JY11




ANS: J Y 1 1 D
Serum creatinine is a fairly reliable indicator of glomerular filtration as it is stable. The blood ure
JY11 JY11 JY11 JY11 JY11 JY1 1 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1




a nitrogen level, urinary output, and serum osmolality are affected by factors that make them le
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




ss reliable as indicators of glomerular filtration.
JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




15. Serum creatinine may be increased by JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




a. carbohydrate intake. JY11




b. fat intake. JY1 1




c. muscle breakdown. JY1 1




d. fluid intake. JY1 1




ANS: J Y 1 1 C
Creatinine is an end product of muscle metabolism; muscle breakdown will increase the seru JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




m creatinine level. Serum creatinine is not affected by carbohydrate, fat, or fluid intake. Fluid v
JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY1 1




olume deficit can increase the serum creatinine if it leads to acute renal failure.
JY1 1 JY1 1 JY1 1 JY1 1 J Y1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




NURSINGTB.COM
MULTIPLE RESPONSE JY11




1. Hormones that increase sodium reabsorption from the tubular fluid include (Select all that a JY11 JY11 JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY11 JY1 1 JY11 JY11 J Y11 JY 11




pply.)
a. aldosterone.
b. atrial natriuretic peptide. JY11 JY11




c. antidiuretic hormone. JY11




d. urodilatin.
e. angiotensin II. JY11




ANS: J Y 1 1 A, E JY1 1




Aldosterone and angiotensin II result in sodium reabsorption. Atrial natriuretic peptide and urodilatin JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY11 JY1 1 JY11 JY1 1 J




decrease sodium reabsorption. Antidiuretic hormone does not affect sodium reabsorption.
Y1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1




2. The blood urea nitrogen (BUN) level is affected by (Select all that apply.)
JY11 JY1 1 JY11 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 JY1 1 J Y11 J Y1 1




a. protein intake. JY1 1




b. fat intake. JY1 1




c. fluid intake. JY1 1




d. catabolism.
e. renal function. JY11




ANS: J Y 1 1 A, C, D, E JY11 JY11 JY1 1





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