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Ca/K regulation Flashcards

1
Q

What is the largest reservoir for calcium in the body?

A

bone

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2
Q

Which fraction of calcium in the body is most tightly regulated?

A

ionized calcium

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3
Q

Where and how is dietary calcium absorbed in the GI tract?

A

duodenum and jejunum, active/passive and dependent on gastric acid secretion

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4
Q

What effect does vitamin D have on phosphorus absorption? Calcium?

A

it increases it’s absorption

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5
Q

Where and how does most calcium reabsorption occur in the kidneys?

A

proximal convoluted tubule, passive

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6
Q

Where does active calcium transport occur in the kidney?

A

TAL and DCT

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7
Q

What ion(s) is calcium transport dependent on in the TAL and DCT?

A

magnesium and sodium

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8
Q

What effect does PTH have on calcium reabsorption in the kidney? Vit D?

A

both increase renal reabsorption

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9
Q

What effect does CaSR have on serum calcium?

A

it binds excess serum Ca

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10
Q

What effect does CaSR binding serum calcium have on GI and renal absorption, specifically? PTH?

A

Reduces GI absorption and renal reabsorption.

Decreases PTH production

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11
Q

What effect does PTH have on the bone during hypocalcemia?

A

it increases bone resorption to raise serum Ca levels

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12
Q

During hypercalcemia, what does PTH do to bones?

A

decreases bone resorption

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13
Q

What is the largest body reservoir for phosphorus?

A

bone!

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14
Q

With low dietary intake of phosphorus, what happens to intestinal absorption?

A

efficiency increases to 80 or 90%

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15
Q

What part of the GI system is responsible for phosphorus resorption?

A

jejunum

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16
Q

What channel is responsible for phosphorus transport in the GI tract? is it active or passive?

A

NaPi2b - sodium dependent

active

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17
Q

What effect does Vit D have on GI absorption of phosphorus?

A

increases it

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18
Q

Where does the majority of phosphorus reabsorption happen in the kidney?

A

proximal convoluted tubule

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19
Q

What channels are responsible for active phosphorus reabsorption in the kidney?

A

NaPi2a and c

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20
Q

What effect does PTH and FGF23 have on renal reabsorption of phosphorus?

A

decreases it

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21
Q

How does FGF23 reduce serum phosphorus levels?

A

decreasing renal reabsorption

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22
Q

What is the first step in determining the cause of hypercalcemia?

A

Measuring PTH

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23
Q

If PTH is high in hypercalcemia, what is the next step?

A

measure urine Ca/Cr ratio

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24
Q

if both PTH and urine Ca/Cr are high in hypercalcemia, what is the diagnosis?

A

primary hyperparathyroidism

25
If PTH is high and urine ca/cr is low in hyper calcemia, what is the diagnosis? what is the next step?
possibly FHH - confirm with genetic CaSR testing and family history
26
if PTH is high and urine Ca/Cr are low, but the history is not consistent with a CaSR mutation, what is the diagnosis for hypercalcemia?
primary hyperparathyroidism
27
If PTH is low in hypercalcemia, what is the next step in diagnosis?
measuring PTHrP and Vit D levels
28
in the setting of hypercalcemia, what diagnosis would a low PTH and high PTHrP signify?
possible malignancy
29
in the setting of hypercalcemia, what diagnosis would a low PTH and elevated 1, 25(OH)D suggest? (3)
lymphoma sarcoid granulomatous disorders
30
in the setting of hypercalcemia, what diagnosis would a low PTH and elevated 25(OH)D suggest?
excessive vitamin D intake
31
in the setting of hypercalcemia, what diagnosis would a low PTH and normal PTHrP/Vit D levels indicate?
myeloma Vit A issues thyrotropin
32
What 2 causes can hypocalcemia be divided into?
high and low PTH
33
In addition to issues of PTH, what are some causes of hypocalcemia?
loop diuretics and hypomagnesemia
34
What is the first step in assessing hyperphosphatemia?
looking at kidney function
35
if a patient has hyperphosphatemia and normal kidney function, what possible DDX's are we looking at?
true hyperphosphatemia or spurious hyperphosphatemia (ie paraproteinemia)
36
if a patient has hyperphosphatemia and reduced kidney function, what possible DDX's are we looking at?
Excess intake or cellular breakdown
37
What two channels are responsible for calcium movement into the capillary in the GI?
Na/Ca exchanger or Ca ATPase
38
What effect does decreased albumin have on ionized calcium fraction?
no effect - it only decreases total body and bound calcium
39
What effect does alkalemia have on calcium fractions?
no change in total body calcium, but ionized calcium will decrease and protien bound will increase
40
In the DCT, what is different about the role and location of CaSR?
it is on the apical side, where it is preventing high lumenal calcium to prevent kidney stones. It does this by increase phosphorus uptake and thus, ca uptake
41
What is the catchy phrase for hypercalcemia clinical presentation?
painful bones renal stones abdominal groans psychic moans
42
if PTH is low but a patient is hypercalcemic, what does that imply about calcium handling?
it's a physiologic response to high calcium in the body - something else is the problem
43
What is the most common cause of low PTH hypocalcemia?
post surgical thyroidectomy
44
what are neurological signs of hypocalcemia?
twitching, positive carpopedal spasm test, seizures
45
what are cardiac consequences of hypocalcemia?
long QT and arrhythmias
46
What happens to coagulability in a hypocalcemic state?
hypercoagulable
47
what are symptoms of hyperphosphatemia?
all the hypocalcemia sx + itching and metastatic calcifications
48
In CKD, what are relative levels of phosphorus, PTH, FGF23 and calcium?
phosphorus is high pTH is high FGF23 is high Calcium is low
49
Define refeeding syndrome in the context of hypophosphatemia
increases in metabolism following a calorie starved period will use up all the phosphorus in the body, such as in starvation, alcoholism, or anorexia
50
What are neuro symptoms of hypophosphatemia?
lethargy and seizures
51
what are cardiac symptoms of hypophosphatemia?
low blood pressure and arrhythmias
52
what are hematologic and ortho symptoms of hypophosphatemia?
hemolysis and bone fractures
53
What factors affect GI absorption of calcium?
Gastric acid enhances absorption, biliary and pancreatic insufficiency decrease absorption due to calcium binding to unabsorbed fat, Vitamin D enhances absorption, serum hypercalcemia decreases absorption by binding with Calcium sensing receptor on the basolateral membrane of the intestinal cells which in turn inhibits the effect of Vitamin D
54
45 year old female presents with abdominal and flank pain, polyuria, muscle aches and fatigue. Further evaluation demonstrates serum Ca = 15 and serum Creatinine = 2.5. Patient states that she takes a diuretic for hypertension but doesn’t recall the names. What class of diuretics could cause hypercalcemia. Explain the mechanism.
Thiazide diuretics can lead to hypercalcemia by increasing calcium reabsorption at the distal tubule. By lowering the sodium concentration in the tubule epithelial cells, thiazides indirectly increase the activity of the basolateral Na+/Ca2+ antiporter to maintain intracellular Na+ level, facilitating Ca2+ to leave the epithelial cells into the renal interstitium. Thus, intracellular Ca2+ concentration is decreased, which allows more Ca2+ from the lumen of the tubules to enter epithelial cells via apical Ca2+-selective channels (TRPV5). In other words, less Ca2+ in the cell increases the driving force for reabsorption from the lumen. Thiazides are also thought to increase the reabsorption of Ca2+ by a mechanism involving the reabsorption of sodium and calcium in the proximal tubule in response to sodium depletion. Some of this response is due to augmentation of the action of parathyroid hormone.
55
45 year old female presents with abdominal and flank pain, polyuria, muscle aches and fatigue. Further evaluation demonstrates serum Ca = 15 and serum Creatinine = 2.5. Patient states that she takes a diuretic for hypertension but doesn’t recall the names. What would be the next test that you perform in your diagnostic algorithm
PTH level
56
45 year old female presents with abdominal and flank pain, polyuria, muscle aches and fatigue. Further evaluation demonstrates serum Ca = 15 and serum Creatinine = 2.5. Patient states that she takes a diuretic for hypertension but doesn’t recall the names. If this patient is diagnosed with primary hyperparathyroidism, how would you expect the serum levels of calcium, phosphorus and 1,25 OH Vitamin D to be affected.
In primary hyperparathyroidism, the elevated PTH leads to hypercalcemia (due to enhanced renal reabsorption of calcium and increased bone turnover of calcium). With regards to phosphorus, there is decreased renal reabsoprtion of phosphorus due to PTH effect on NaPi channels, leading to hypophosphatemia. The effect on Vitamin D can vary – PTH enhances the activation of vitamin D in the kidney. However, many studies have shown that primary hyperparathyroidism is often associated with Vitamin D deficiency.
57
How would you expect renal handling of calcium and phosphorus to change in hypoparathyroidism (decreased PTH)
Deficiency of PTH will lead to decreased renal reabsorption of calcium leading to hypocalcemia. There is also a decreased activation of Vitamin D in the kidney, further decreasing renal reabsorption of calcium. There is a lesser impact on renal reabsorption of phosphorus, which is increased, potentially leading to hyperphosphatemia. However, at that point FGF23 acts to reverse this effect, decreasing renal phosphorus reabsorption and bringing serum phosphorus back to near normal.
58
A 50 year old male with Chronic kidney disease stage 5 (estimated GFR = 9), DM type 2 and hypertension presents for routine follow up with his nephrologist. Labs reveal a markedly elevated serum phosphorus. All of the following interventions would help treat his hyperphosphatemia EXCEPT: a. Low phosphorus diet b. Low sodium diet c. Vitamin D supplementation
vitamin D supplementation

Renal (28 decks)

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