NUR 521 Exam 2 Blueprint and Study Guide with Accurate Solutions-
University of Alabama
Module Q Topic
s
Module 4: 15 • Hemodynamics
Cardio o Review the circulatory system and cardiac output regulation.
vascular I • Diuretics
o Review the PPT slide that shows where each class of diuretics work in the kidney.
Sites of Diuretic action
• PCT: The PCT has a high resorptive capacity. A large fraction (about 65%) of filtered sodium and
chloride is reabsorbed at the PCT. In addition, essentially all of the bicarbonate and potassium in
the filtrate is reabsorbed here. Solutes and water are reabsorbed at equal rations, so this urine
remains isotonic.
• Loop of Henle: The descending limb of the loop of Henle is freely permeable to water. Hence, as
tubular urine moves down the loop and passes through the hypertonic environment of the renal
medulla, water is drawn from the loop into the interstitial space. This process decreases the volume of
the tubular urine and causes the urine to become concentrated (tonicity increases to about 1200
mOsm/L).
• Early segment of distal convoluted tubule: About 10% of filtered sodium and chloride is reabsorbed
in the early segment of the distal convoluted tubule. Water follows passively.
• Distal Nephron: The distal nephron is the site of two important processes. The first involves
exchange of sodium for potassium and is under the influence of aldosterone. The second determines
the final concentration of the urine and is regulated by antidiuretic hormone (ADH).
• Sodium-Potassium Exchange: Aldosterone, the principal mineralocorticoid of the adrenal cortex,
stimulates reabsorption of sodium from the distal nephron. At the same time aldosterone causes
potassium to be secreted. Although not directly coupled, these two processes—sodium retention
and potassium excretion—can be viewed as an exchange mechanism. Aldosterone promotes
sodium–potassium exchange by stimulating cells of the distal nephron to synthesize more of the
pumps responsible for sodium and potassium transport
Compare and contrast the diuretics presented in the module.
• How do they work?
o Furosemide (LOOP diuretic) MOA: acts in the thick segment of the ascending limb of the loop
of Henle, blocks reabsorption of Na and Cl, preventing reabsorption of water which = profound
diuresis even when renal blood flow and GFR are low. If tx is insufficient with just Lasix, it can
, be combined with a thiazide diuretic (no use in combining with any other loop diuretic).
o Hydrochlorothiazide/Microzide (Thiazide diuretic) MOA: steroid derivative, promotes
urine production by blocking reabsorption of Na and Cl in the early segment of the distal
convoluted tubule water retention in nephron and increased flow of urine
o Spironolactone/ Aldactone (Aldosterone Antagonist, potassium-sparring diuretic): blocks the
action of aldosterone in the distal nephron retention of K and excretion of Na. Diuresis is scanty
because most Na has already been reabsorbed before reaching the distal tubule.
o Triamterene/ Dyrenium (non-aldosterone antagonist, potassium-sparring diuretic): disrupts
Na-K exchange in the distal nephron by direct inhibition decreased Na reabsorption and reduced
K secretion Na excretion is increased K is conserved. Minimal diuresis.
• What is the indication of use?
o Furosemide USE: when rapid or massive mobilization of fluid is required such as pulmonary
edema associated with CHF, edema from heart, liver, or kidney that haven’t responded to
other drugs, and/or HTN
o Thiazide USE: HTN, edema in CHF, hepatic, or renal disease
o Spironolactone USE: HTN, edema, CHF (blocking aldosterone creates protective
effects), counteracts K-wasting diuretics, off-label: acne, hair loss, hirsutism, hormone
therapy for transgender females.
o Triamterene USE: HTN, edema, combo drug can augment Lasix and counteract K
wasting effects
• What factors should be considered when choosing which diuretic to prescribe a patient? Produce
some example scenarios of when you would prescribe one versus the other. How does renal function
come into play?
o Furosemide: more loss of fluid and electrolytes than any other diuretic, K wasting, do not give
if K is low, beer criteria use in caution in pts over 65 who are at higher risk for hyponatremia
o Thiazide: MUST have an adequate kidney function to work (minimum 20-30mL/min), CI
with digoxin, lithium, and other HTN meds.
• BBW?
o ALL diuretics can cause profound diuresis with fluid and electrolyte depletion
o Loop & thiazide AE: hyponatremia, hypochloremia, dehydration, hypotension,
hypokalemia, ototoxicity (loop), hyperglycemia, hyperuricemia, reduced HDL, increased
LDL
o Spironolactone BBW: shown to cause tumors in rats, avoid unnecessary use.
, o Spironolactone AE: hyperkalemia (dysrhythmias), deep voice, impotence,
menstrual irregularities, hirsutism
o Triamterene BBW: hyperkalemia
• How would you know if your patient was experiencing AE like ototoxicity, dehydration, hypo
or hyperkalemia, and hypotension. What would be subjective and objective findings?
• What important information would you teach your patient about each of these
drugs? HTN
• What is included in the workup for HTN?
o EKG
o Urinalysis
o H&H
o BMP: Electrolytes, Kidney function, and Glucose
o Uric acid
o Triglycerides and cholesterol
• What lifestyle modifications should you discuss with your patient?
o Sodium restricted diet
o Restrict alcohol consumption
o Aerobic exercise, Healthy body weight
o Smoking cessation
Know about the RAAS and how this affects fluid and blood pressure changes in the body.
• RAAS: Decreased perfusion pressure in the afferent arteriole stimulates secretion of renin by
juxtaglomerular cells renin reacts with Angiotensin in liver to make Angiotensin I Angiotensin I
converts to Angiotensin II in the lungs Angiotensin II causes vasoconstriction in the blood vessels
Angiotensin II becomes III in the adrenal cortex stimulating aldosterone release Aldosterone increases
Na and water reabsorption by kidney tubules which = increased blood volume & increased BP (slide
35)
•
Review HTN guidelines presented in PPT and module.
• Drug of choice for pregnant women with mild pre-eclampsia: labetalol and methyldopa, MgSO4
used for seizures
• In older adults, avoid central acting alpha agonists and peripheral alpha 1 antagonists, start low
doses, risk of orthostatic hypotension is high
University of Alabama
Module Q Topic
s
Module 4: 15 • Hemodynamics
Cardio o Review the circulatory system and cardiac output regulation.
vascular I • Diuretics
o Review the PPT slide that shows where each class of diuretics work in the kidney.
Sites of Diuretic action
• PCT: The PCT has a high resorptive capacity. A large fraction (about 65%) of filtered sodium and
chloride is reabsorbed at the PCT. In addition, essentially all of the bicarbonate and potassium in
the filtrate is reabsorbed here. Solutes and water are reabsorbed at equal rations, so this urine
remains isotonic.
• Loop of Henle: The descending limb of the loop of Henle is freely permeable to water. Hence, as
tubular urine moves down the loop and passes through the hypertonic environment of the renal
medulla, water is drawn from the loop into the interstitial space. This process decreases the volume of
the tubular urine and causes the urine to become concentrated (tonicity increases to about 1200
mOsm/L).
• Early segment of distal convoluted tubule: About 10% of filtered sodium and chloride is reabsorbed
in the early segment of the distal convoluted tubule. Water follows passively.
• Distal Nephron: The distal nephron is the site of two important processes. The first involves
exchange of sodium for potassium and is under the influence of aldosterone. The second determines
the final concentration of the urine and is regulated by antidiuretic hormone (ADH).
• Sodium-Potassium Exchange: Aldosterone, the principal mineralocorticoid of the adrenal cortex,
stimulates reabsorption of sodium from the distal nephron. At the same time aldosterone causes
potassium to be secreted. Although not directly coupled, these two processes—sodium retention
and potassium excretion—can be viewed as an exchange mechanism. Aldosterone promotes
sodium–potassium exchange by stimulating cells of the distal nephron to synthesize more of the
pumps responsible for sodium and potassium transport
Compare and contrast the diuretics presented in the module.
• How do they work?
o Furosemide (LOOP diuretic) MOA: acts in the thick segment of the ascending limb of the loop
of Henle, blocks reabsorption of Na and Cl, preventing reabsorption of water which = profound
diuresis even when renal blood flow and GFR are low. If tx is insufficient with just Lasix, it can
, be combined with a thiazide diuretic (no use in combining with any other loop diuretic).
o Hydrochlorothiazide/Microzide (Thiazide diuretic) MOA: steroid derivative, promotes
urine production by blocking reabsorption of Na and Cl in the early segment of the distal
convoluted tubule water retention in nephron and increased flow of urine
o Spironolactone/ Aldactone (Aldosterone Antagonist, potassium-sparring diuretic): blocks the
action of aldosterone in the distal nephron retention of K and excretion of Na. Diuresis is scanty
because most Na has already been reabsorbed before reaching the distal tubule.
o Triamterene/ Dyrenium (non-aldosterone antagonist, potassium-sparring diuretic): disrupts
Na-K exchange in the distal nephron by direct inhibition decreased Na reabsorption and reduced
K secretion Na excretion is increased K is conserved. Minimal diuresis.
• What is the indication of use?
o Furosemide USE: when rapid or massive mobilization of fluid is required such as pulmonary
edema associated with CHF, edema from heart, liver, or kidney that haven’t responded to
other drugs, and/or HTN
o Thiazide USE: HTN, edema in CHF, hepatic, or renal disease
o Spironolactone USE: HTN, edema, CHF (blocking aldosterone creates protective
effects), counteracts K-wasting diuretics, off-label: acne, hair loss, hirsutism, hormone
therapy for transgender females.
o Triamterene USE: HTN, edema, combo drug can augment Lasix and counteract K
wasting effects
• What factors should be considered when choosing which diuretic to prescribe a patient? Produce
some example scenarios of when you would prescribe one versus the other. How does renal function
come into play?
o Furosemide: more loss of fluid and electrolytes than any other diuretic, K wasting, do not give
if K is low, beer criteria use in caution in pts over 65 who are at higher risk for hyponatremia
o Thiazide: MUST have an adequate kidney function to work (minimum 20-30mL/min), CI
with digoxin, lithium, and other HTN meds.
• BBW?
o ALL diuretics can cause profound diuresis with fluid and electrolyte depletion
o Loop & thiazide AE: hyponatremia, hypochloremia, dehydration, hypotension,
hypokalemia, ototoxicity (loop), hyperglycemia, hyperuricemia, reduced HDL, increased
LDL
o Spironolactone BBW: shown to cause tumors in rats, avoid unnecessary use.
, o Spironolactone AE: hyperkalemia (dysrhythmias), deep voice, impotence,
menstrual irregularities, hirsutism
o Triamterene BBW: hyperkalemia
• How would you know if your patient was experiencing AE like ototoxicity, dehydration, hypo
or hyperkalemia, and hypotension. What would be subjective and objective findings?
• What important information would you teach your patient about each of these
drugs? HTN
• What is included in the workup for HTN?
o EKG
o Urinalysis
o H&H
o BMP: Electrolytes, Kidney function, and Glucose
o Uric acid
o Triglycerides and cholesterol
• What lifestyle modifications should you discuss with your patient?
o Sodium restricted diet
o Restrict alcohol consumption
o Aerobic exercise, Healthy body weight
o Smoking cessation
Know about the RAAS and how this affects fluid and blood pressure changes in the body.
• RAAS: Decreased perfusion pressure in the afferent arteriole stimulates secretion of renin by
juxtaglomerular cells renin reacts with Angiotensin in liver to make Angiotensin I Angiotensin I
converts to Angiotensin II in the lungs Angiotensin II causes vasoconstriction in the blood vessels
Angiotensin II becomes III in the adrenal cortex stimulating aldosterone release Aldosterone increases
Na and water reabsorption by kidney tubules which = increased blood volume & increased BP (slide
35)
•
Review HTN guidelines presented in PPT and module.
• Drug of choice for pregnant women with mild pre-eclampsia: labetalol and methyldopa, MgSO4
used for seizures
• In older adults, avoid central acting alpha agonists and peripheral alpha 1 antagonists, start low
doses, risk of orthostatic hypotension is high
