Editing Anatomy and Physiology – RN Flashcards (section)

== Renal, Endocrine, and Electrolytes ==

;List five functions of the kidney and the failure state each produces.
:Waste excretion (uremia), fluid and electrolyte regulation (overload and hyperkalemia), acid-base regulation (metabolic acidosis), erythropoietin production (anemia), and vitamin D activation (hypocalcemia with hyperphosphatemia). Renin release adds hypertension.

;Why is creatinine a better marker of kidney function than blood urea nitrogen?
:Creatinine, normally about 0.6 to 1.2 mg/dL, is produced at a steady rate from muscle and is filtered without significant reabsorption. Blood urea nitrogen, normally about 10 to 20 mg/dL, also rises with dehydration, high protein intake, gastrointestinal bleeding, and corticosteroid use, so it is less specific.

;How does insulin affect potassium, and what are the two clinical consequences?
:Insulin drives potassium into cells along with glucose. Clinically, insulin with dextrose is a temporizing treatment for hyperkalemia, and potassium must be monitored and replaced during treatment of diabetic ketoacidosis, where the level can fall sharply once insulin is started.

;Contrast the electrolyte and hemodynamic profiles of Addison disease and Cushing syndrome.
:Addison disease (adrenocortical insufficiency) produces hyponatremia, hyperkalemia, hypoglycemia, hypotension, and hyperpigmentation. Cushing syndrome (cortisol excess) produces hypernatremia, hypokalemia, hyperglycemia, hypertension, immunosuppression, and osteoporosis.

;Distinguish diabetes insipidus from the syndrome of inappropriate antidiuretic hormone.
:Diabetes insipidus is a deficiency of antidiuretic hormone, producing large volumes of dilute urine, hypernatremia, and rising serum osmolality. The syndrome of inappropriate antidiuretic hormone is excess hormone, producing water retention, concentrated urine, dilutional hyponatremia, and neurologic changes.

;Why does a patient develop hypocalcemia after a thyroidectomy?
:The parathyroid glands lie on the posterior thyroid and may be injured or removed. Loss of parathyroid hormone reduces bone resorption, renal calcium reabsorption, and vitamin D activation, so serum calcium falls, producing perioral and digital paresthesias, positive Chvostek and Trousseau signs, tetany, and possible laryngospasm.

;Why do immobilized patients develop hypercalcemia and renal calculi?
:Bone remodeling responds to mechanical stress. Without weight bearing, osteoclastic resorption outpaces osteoblastic formation, releasing calcium into the blood and urine. Urinary stasis in the supine position adds stone risk, which is why mobilization and hydration are therapeutic.

;Which electrolyte disturbances mimic each other by causing increased neuromuscular excitability?
:Hypocalcemia and hypomagnesemia both cause tetany, twitching, positive Chvostek and Trousseau signs, and hyperreflexia. Refractory hypocalcemia often will not correct until magnesium is replaced. Conversely, hypercalcemia and hypermagnesemia both depress excitability, causing lethargy, weakness, and diminished reflexes.