MARYVILLE NURS 611 FINAL PAPER 2025/2026 QUESTIONS
WITH SOLUTIONS GRADED A+
✔✔How does the Renin-Angiotensin-Aldosterone System (RAAS) function? - ✔✔When
renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor -
prorenin, already present in the blood into renin and secrete it directly into the
circulation. Plasma renin then carries out the conversion of angiotensinogen, released
by the liver, to angiotensin I.
[2] Angiotensin I is subsequently converted to angiotensin II by the angiotensin-
converting enzyme (ACE) found in the lungs. Angiotensin II is a potent vasoconstrictive
peptide that causes blood vessels to narrow, resulting in increased blood pressure.
[3] Angiotensin II also stimulates the secretion of the hormone aldosterone from the
adrenal cortex. Aldosterone causes the renal tubules to increase the reabsorption of
sodium and water into the blood, while at the same time causing the excretion of
potassium (to maintain electrolyte balance). This increases the volume of extracellular
fluid in the body, which also increases blood pressure.
✔✔Increased plasma osmolality - ✔✔Secretion of antidiuretic hormone (ADH) and the
perception of thirst are stimulated by __________
✔✔Normal Na+ levels - ✔✔135-145 meq/L
✔✔Clinical manifestations of severe hypernatremia - ✔✔confusion, convulsions,
cerebral hemorrhage, and coma
✔✔Causes of hyponatremia - ✔✔Diuretics, vomiting, diarrhea, kidney failure, liver
failure, to much of hypotonic IV solutions
✔✔Clinical manifestations of hyponatremia - ✔✔headaches, lethargy, confusion, coma.
✔✔What electrolyte is the major determinant of the resting membrane potential
necessary for transmission of nerve impulses? - ✔✔K+
✔✔Causes of hyperkalemia - ✔✔Renal failure, Addison's disease, massive trauma,
insulin deficiency, use of potassium salt substitutes, or metabolic acidosis
✔✔Addison's disease - ✔✔Adrenal glands produce too little cortisol and often
insufficient levels of aldosterone
✔✔Clinical manifestations of hyperkalemia - ✔✔increased cell excitability, ECG
changes with tall-peaked T waves., acidosis
, ✔✔What happens in acidosis? - ✔✔H+ ions shift into the cells in exchange for ICF
potassium
✔✔What is a treatment of hyperkalemia - ✔✔Insulin
✔✔How does Insulin treat hyperkalemia? - ✔✔Insulin transports K+ from the blood to
the cell along with glucose. Insulin contributes to the regulation of plasma potassium
levels by stimulating the Na+, K+, -ATPase pump, thereby promoting the movement of
potassium into liver and muscle cells simultaneously with glucose transport after eating.
The intracellular movement of K+ prevents an acute hyperkalemia related to food intake
✔✔Causes of hypokalemia - ✔✔Hyperaldosteronism, hypernatremia, and fluid volume
excess
✔✔Manifestations of Hypokalemia - ✔✔ECG: flattened T-wave, AV block, Bradycardia,
paralytic ileus
✔✔Hypocalcemia causes - ✔✔Inadequate intestinal absorption, massive blood
administration, decreases in PTH and vit D levels; nutritional deficiencies-malnutrition;
alkalosis, elevated calcitonin level; pancreatitis; hypoalbuminemia
✔✔Hypocalcemia manifestations - ✔✔Increased neuromuscular excitability; tingling,
muscle spasms (particularly in hands, feet, and facial muscles), intestinal cramping,
hyperactive bowel sounds; osteoporosis and fractures; severe cases show convulsions
and tetany; prolonged QT interval cardiac arrest
✔✔Hypercalcemia causes - ✔✔Hyperparathyroidism; bone metastases with calcium
resorption from breast, prostate, renal, and cervical cancer; sarcoidosis; excess vit D;
many tumors that produce PTH; calcium-containing antacids
✔✔Hypercalcemia manifestations - ✔✔Many nonspecific; fatigue, weakness, lethargy,
anorexia, nausea, constipation; impaired renal function, kidney stones dysrhythmias,
bradycardia, cardiac arrest; bone pain, osteoporosis, fractures
✔✔Hypophosphatemia causes - ✔✔Intestinal malabsorption related to vitamin D
deficiency, use of magnesium- and aluminum- containing antacids, long-term alcohol
abuse, and malabsorption syndromes; respiratory alkalosis; increased renal excretion of
phosphate associated with hyperparathyroidism.
✔✔Hypophosphatemia manifestations - ✔✔Conditions related to reduced capacity for
oxygen transport by red blood cells and disturbed energy metabolism; leukocyte and
platelet dysfunction; deranges nerve and muscle function; in severe cases, irritability,
confusion, numbness, coma, convulsions; possibly respiratory failure (because of
muscle weakness), cardiomyopathies, bone resorption ( leading to rickets or
osteomalacia)
WITH SOLUTIONS GRADED A+
✔✔How does the Renin-Angiotensin-Aldosterone System (RAAS) function? - ✔✔When
renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor -
prorenin, already present in the blood into renin and secrete it directly into the
circulation. Plasma renin then carries out the conversion of angiotensinogen, released
by the liver, to angiotensin I.
[2] Angiotensin I is subsequently converted to angiotensin II by the angiotensin-
converting enzyme (ACE) found in the lungs. Angiotensin II is a potent vasoconstrictive
peptide that causes blood vessels to narrow, resulting in increased blood pressure.
[3] Angiotensin II also stimulates the secretion of the hormone aldosterone from the
adrenal cortex. Aldosterone causes the renal tubules to increase the reabsorption of
sodium and water into the blood, while at the same time causing the excretion of
potassium (to maintain electrolyte balance). This increases the volume of extracellular
fluid in the body, which also increases blood pressure.
✔✔Increased plasma osmolality - ✔✔Secretion of antidiuretic hormone (ADH) and the
perception of thirst are stimulated by __________
✔✔Normal Na+ levels - ✔✔135-145 meq/L
✔✔Clinical manifestations of severe hypernatremia - ✔✔confusion, convulsions,
cerebral hemorrhage, and coma
✔✔Causes of hyponatremia - ✔✔Diuretics, vomiting, diarrhea, kidney failure, liver
failure, to much of hypotonic IV solutions
✔✔Clinical manifestations of hyponatremia - ✔✔headaches, lethargy, confusion, coma.
✔✔What electrolyte is the major determinant of the resting membrane potential
necessary for transmission of nerve impulses? - ✔✔K+
✔✔Causes of hyperkalemia - ✔✔Renal failure, Addison's disease, massive trauma,
insulin deficiency, use of potassium salt substitutes, or metabolic acidosis
✔✔Addison's disease - ✔✔Adrenal glands produce too little cortisol and often
insufficient levels of aldosterone
✔✔Clinical manifestations of hyperkalemia - ✔✔increased cell excitability, ECG
changes with tall-peaked T waves., acidosis
, ✔✔What happens in acidosis? - ✔✔H+ ions shift into the cells in exchange for ICF
potassium
✔✔What is a treatment of hyperkalemia - ✔✔Insulin
✔✔How does Insulin treat hyperkalemia? - ✔✔Insulin transports K+ from the blood to
the cell along with glucose. Insulin contributes to the regulation of plasma potassium
levels by stimulating the Na+, K+, -ATPase pump, thereby promoting the movement of
potassium into liver and muscle cells simultaneously with glucose transport after eating.
The intracellular movement of K+ prevents an acute hyperkalemia related to food intake
✔✔Causes of hypokalemia - ✔✔Hyperaldosteronism, hypernatremia, and fluid volume
excess
✔✔Manifestations of Hypokalemia - ✔✔ECG: flattened T-wave, AV block, Bradycardia,
paralytic ileus
✔✔Hypocalcemia causes - ✔✔Inadequate intestinal absorption, massive blood
administration, decreases in PTH and vit D levels; nutritional deficiencies-malnutrition;
alkalosis, elevated calcitonin level; pancreatitis; hypoalbuminemia
✔✔Hypocalcemia manifestations - ✔✔Increased neuromuscular excitability; tingling,
muscle spasms (particularly in hands, feet, and facial muscles), intestinal cramping,
hyperactive bowel sounds; osteoporosis and fractures; severe cases show convulsions
and tetany; prolonged QT interval cardiac arrest
✔✔Hypercalcemia causes - ✔✔Hyperparathyroidism; bone metastases with calcium
resorption from breast, prostate, renal, and cervical cancer; sarcoidosis; excess vit D;
many tumors that produce PTH; calcium-containing antacids
✔✔Hypercalcemia manifestations - ✔✔Many nonspecific; fatigue, weakness, lethargy,
anorexia, nausea, constipation; impaired renal function, kidney stones dysrhythmias,
bradycardia, cardiac arrest; bone pain, osteoporosis, fractures
✔✔Hypophosphatemia causes - ✔✔Intestinal malabsorption related to vitamin D
deficiency, use of magnesium- and aluminum- containing antacids, long-term alcohol
abuse, and malabsorption syndromes; respiratory alkalosis; increased renal excretion of
phosphate associated with hyperparathyroidism.
✔✔Hypophosphatemia manifestations - ✔✔Conditions related to reduced capacity for
oxygen transport by red blood cells and disturbed energy metabolism; leukocyte and
platelet dysfunction; deranges nerve and muscle function; in severe cases, irritability,
confusion, numbness, coma, convulsions; possibly respiratory failure (because of
muscle weakness), cardiomyopathies, bone resorption ( leading to rickets or
osteomalacia)
