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30 Cards in this Set

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Which type of calcium is active--plasma protein bound, complexed to anions, or ionized?
IONIZED(48%)
Measuring this tells if you have true hypocalcemia or not
True/False: Lower serum albumin will give a lower ionized Ca++.
FALSE--it will only give a lower total Ca++
Where does Ca++ reabsorption happen?
80% in PT
Some in tAL
TAL--Triple transporter and ROMK set up +15 Vte and drive paracell
DISTAL NEPHRON--active reab stimulated by Vit. D and PTH
A decrease in plasma calcium triggers what in the body?
Increase in PTH from parathyroid--this triggers increased Ca++ reab in the DCT, increased Vit D conversion to active form so it can work in the gut, and increased bone BREAKdown and release of Ca++ to plasma
What are the signs of hypercalcemia?
Stones, bones, moans, abdominal groans, and psychiatric overtones
How do you evaluate hyperCa++?
Normal/elevated = PTH mediated hyperCa++
Low = non-PTH mediated
What are the THREE types of PTH mediated hyperCa++?
Primary hyperparathyroidism--usually a para-adenoma causing glands to lose sensitivity to Ca++ and oversecrete PTH
Medication induced = LITHIUM
Familial hyperCa++ = high serum Ca++ with a low urine output NOT FINISHED
What are the three non-PTH mediated hyperCa++ causes?
Malignancy--mets cause bone breakdown that releases Ca++ to the system OR they release PTHrP which has the same effects as PTH
Medicine induced--vit. D overdose, thiazide therapy, or milk-alkali syndrome
Immobilization
Granulomatous disease/Sarcoid--ectopic production of 1,25 (OH)2D
What is the proper treatment for hyperCa++?
Treat if symptomatic or if there is end organ failure
Acute: increase urinary Ca++ excretion with IV NS and a loop diuretic(Ca++ wasting), give bisphosphonates(first line to decrease osteoclast activity) or calcitonin or glucocorticoids, or give hemodialysis
Chronic Therapy: Decreased Ca++ intakeand adjust drugs(thiazides)
What do bisphosphonates do?
1st line therapy for hypercalcemia--they reduce the activity of osteoclasts
True/False: Hypocalcemia must involve a decrease in ionized calcium.
FALSE--it can be a decrease in total calcium with or without a low level of ionized calcium
What are the symptoms of hypocalcemia?
Spasm/seizures, Chvostek sign, Trousseau's sign, ECG changes, hypotension
How do you evaluate hypocalcemia?
check PTH levels
What are the three causes of hypoCa++?
Parathyroidectomy(often from hyperCa++) causing hungry bone syndrome
Hypoparathyroidism
Hypomagnesemia--prevents PTH secretion and action
What are the five non-PTH causes of hypoCa++?
VitD deficiency
GI malabsorption
HyperPhosphatemia--chronic kidney disease
Rhabdomyolysis
Pseudohypoparathyroidism--genetic decrease in cell response to PTH
What are the treatments for hypoCa++?
IV Calcium replacement, hemodialysis, and if it is chronic then a high Ca++ diet, vit. D, and correct low Mg++ levels
True/False: most phosphorus is protein bound
FALSE--most is complexed in the tissues
What hormonal changes occur when phosphate levels rise?
PTH secretion increases and FGF23 increases--both stimulate phosphate excretion by decreased NaPi levels in the PT(primarily FGF23)
The symptoms of hyperphosphatemia stem from what?
HypoCa++
What causes hyperphosphatemia?
Kidney disease, excess ingestion or enemas, tumor lysis syndrome, rhabdomyolysis, and hemolytic anemia(RBC's contain phosphate)
What is the treatment for HyperPhosphatemia?
Acute = oral phosphate binders in the gut or hemodialysis in the case of tumor lysis syndrome
Chronic = low phosphate diet or phosphate binders
What are the symptoms of hypoPhosphatemia?
Muscle problems, bone pain, rhabdomyolysis, heart failure
What are the causes of hypophosphatemia?
Hyperparathyroidism, malnutrition, DM ketoacidosis, refeeding syndrome, and Fanconi syndrome(PT dysfunction with glucosuira, bicarbonaturia, and uricosuria)
What are the treatments for hyperphosphatemia?
Acute = IV phosphate replacement therapy
Chronic = phosphate supplements OR parathyroidectomy
True/False: Most magnesium is freely ionized in the plasma
False--only 1% is found in the ECF
Where is magnesium reabsorbed?
20% in the PT
70% in the TAL
10% in the DCT
What can lead to hypermagnesemia?
GFR lower than 30 and a large Mg++ load
Preeclampsia treatment, TPN, oral laxatives, oral antacids, Mg++ enemas, epsom salts, renal failure, or chronic disease
What is the most common cause of hypomagnesemia?
Magnesium wasting due to diuretic use(will also have hypokalemia and hypocalcemia)
ALSO
malnutrition
genetics--Gitelman's(thiazide disease) and Bartter's(loop diuretic disease)
What are the symptoms of hypomagnesemia?
NM--hyperreflexia, carpopedal spasm, tetany, seizures, chvostek, and trousseau's
ECG widening of the QRS, QT prolongation, T wave peaking, Vtach, and Torsade
What is the treatment for hypomagnesemia?
Oral MgCl in 3-4 divided doses
Severe = IV MgSO4