Renal--Ca++, Mg++, And P

Front 1

Which type of calcium is active--plasma protein bound, complexed to anions, or ionized?

Back 1

IONIZED(48%)
Measuring this tells if you have true hypocalcemia or not

Front 2

True/False: Lower serum albumin will give a lower ionized Ca++.

Back 2

FALSE--it will only give a lower total Ca++

Front 3

Where does Ca++ reabsorption happen?

Back 3

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

Front 4

A decrease in plasma calcium triggers what in the body?

Back 4

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

Front 5

What are the signs of hypercalcemia?

Back 5

Stones, bones, moans, abdominal groans, and psychiatric overtones

Front 6

How do you evaluate hyperCa++?

Back 6

Normal/elevated = PTH mediated hyperCa++
Low = non-PTH mediated

Front 7

What are the THREE types of PTH mediated hyperCa++?

Back 7

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

Front 8

What are the three non-PTH mediated hyperCa++ causes?

Back 8

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

Front 9

What is the proper treatment for hyperCa++?

Back 9

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)

Front 10

What do bisphosphonates do?

Back 10

1st line therapy for hypercalcemia--they reduce the activity of osteoclasts

Front 11

True/False: Hypocalcemia must involve a decrease in ionized calcium.

Back 11

FALSE--it can be a decrease in total calcium with or without a low level of ionized calcium

Front 12

What are the symptoms of hypocalcemia?

Back 12

Spasm/seizures, Chvostek sign, Trousseau's sign, ECG changes, hypotension

Front 13

How do you evaluate hypocalcemia?

Back 13

check PTH levels

Front 14

What are the three causes of hypoCa++?

Back 14

Parathyroidectomy(often from hyperCa++) causing hungry bone syndrome
Hypoparathyroidism
Hypomagnesemia--prevents PTH secretion and action

Front 15

What are the five non-PTH causes of hypoCa++?

Back 15

VitD deficiency
GI malabsorption
HyperPhosphatemia--chronic kidney disease
Rhabdomyolysis
Pseudohypoparathyroidism--genetic decrease in cell response to PTH

Front 16

What are the treatments for hypoCa++?

Back 16

IV Calcium replacement, hemodialysis, and if it is chronic then a high Ca++ diet, vit. D, and correct low Mg++ levels

Front 17

True/False: most phosphorus is protein bound

Back 17

FALSE--most is complexed in the tissues

Front 18

What hormonal changes occur when phosphate levels rise?

Back 18

PTH secretion increases and FGF23 increases--both stimulate phosphate excretion by decreased NaPi levels in the PT(primarily FGF23)

Front 19

The symptoms of hyperphosphatemia stem from what?

Back 19

HypoCa++

Front 20

What causes hyperphosphatemia?

Back 20

Kidney disease, excess ingestion or enemas, tumor lysis syndrome, rhabdomyolysis, and hemolytic anemia(RBC's contain phosphate)

Front 21

What is the treatment for HyperPhosphatemia?

Back 21

Acute = oral phosphate binders in the gut or hemodialysis in the case of tumor lysis syndrome
Chronic = low phosphate diet or phosphate binders

Front 22

What are the symptoms of hypoPhosphatemia?

Back 22

Muscle problems, bone pain, rhabdomyolysis, heart failure

Front 23

What are the causes of hypophosphatemia?

Back 23

Hyperparathyroidism, malnutrition, DM ketoacidosis, refeeding syndrome, and Fanconi syndrome(PT dysfunction with glucosuira, bicarbonaturia, and uricosuria)

Front 24

What are the treatments for hyperphosphatemia?

Back 24

Acute = IV phosphate replacement therapy
Chronic = phosphate supplements OR parathyroidectomy

Front 25

True/False: Most magnesium is freely ionized in the plasma

Back 25

False--only 1% is found in the ECF

Front 26

Where is magnesium reabsorbed?

Back 26

20% in the PT
70% in the TAL
10% in the DCT

Front 27

What can lead to hypermagnesemia?

Back 27

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

Front 28

What is the most common cause of hypomagnesemia?

Back 28

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)

Front 29

What are the symptoms of hypomagnesemia?

Back 29

NM--hyperreflexia, carpopedal spasm, tetany, seizures, chvostek, and trousseau's
ECG widening of the QRS, QT prolongation, T wave peaking, Vtach, and Torsade

Front 30

What is the treatment for hypomagnesemia?

Back 30

Oral MgCl in 3-4 divided doses
Severe = IV MgSO4