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MS2 Renal > 9/15- Ca, Phosphorus, Mg > Flashcards

9/15- Ca, Phosphorus, Mg Flashcards

1
Q

What is the “Rule of 3s”?

A

For the 3 electrolytes: Ca, P, Mg

Controlled by 3 hormones

  • Parathyroid hormone (PTH)
  • Vitamin D
  • Phosphatonins (FGF23)

(- Calcitonin)

Affect 3 target organs

  • Bone
  • Intestine
  • Kidney
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2
Q

How does Parathryoid hormone function?

What stimulates it? Inhibits it?

A

Stimulated by low Ca; functions to increase Ca!

Stimulated by:

  • Low ionized Ca (INactivates Ca sensing receptor, CaSR)
  • Increased serum P and low serum Mg

Inhibited by:

  • Increase in ionized Ca levels
  • Calcitriol (1,25(OH)2D)
  • Hypomagnesia is associated with hypocalcemia
  • Hypomagnesemia -> increased IC Ca levels, thus inhibiting PTH secretion
  • Skeletal PTH receptors are also less sensitive in hypomagnesia
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3
Q

Describe synthesis of PTH?

A
  • Pre-pro PTH -> pro-PTH -> intact PTH (iPTH)
  • Catabolized to N-terminal (active) and C-terminal fragments
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4
Q

How does PTH increase serum Ca (broadly: direct and indirect)

A
  • Direct action on bone
  • Indirect action on kidney
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5
Q

How does PTH affect bone?

A

Increases resorption (mobilization of Ca from bone); direct

  • Ca and P released
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6
Q

How does PTH affect kidney?

A

Indirect

Proximal tubule: inhibits posphate reabsorption and stimulation of renal 25(OH)D-1-hydroxylase

  • Less phosphate to bind Ca -> more free Ca
  • 1,25OH vitamin D reabsorbs Ca from GIT

Distal tubule: increases reabsorption of Ca

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7
Q

Describe the Ca Sensing Receptors (CaSR)

  • Location
  • Describe pathway (kidney specifics)
A

Location:

  • Kidney
  • Parathyroid gland (less PTH produced)
  • Intestine

Kidney: thick ascending loop

  • Hypercalcemia activates CaSR
  • Inhibition of apical K channel
  • Ca absorption stops
  • End result = mechanism analogous to furosemide or Bartter’s and -> calciuresis (high urine Ca)

Any transporter blocked -> Ca loss

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8
Q

How is hyperparathyroidism treated?

A

Cinacalcet (Sensipar)- binds to the CaSR

  • Tricks the receptor into thinking that Ca level is higher than it really is

Other treatments:

  • Calcitriol (1,25 Vitamin D) – feedback inhibition
  • Surgical parathyroidectomy
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9
Q

Flowchart of Vitamin D production

A
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10
Q

What stimulates 1,25OH2 Vitamin D (Calcitriol)? Inhibits?

A

Stimulated by (1αHydroxylase stimulation):

  • PTH (FEEDBACK)
  • Low phosphorus / low calcium
  • Estrogen, Prolactin, Calcitonin, Growth Hormone

Inhibited by: Calcitriol (1,25-OH2 Vitamin D) (FEEDBACK)

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11
Q

What does Calcitriol do? (1,25OH2 Vitamin D)

A
  • Increases Ca, Mg and Phos reabsorption in the GIT
  • Inhibit PTH secretion of parathyroid
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12
Q

What are phosphotonins?

  • Secreted by what cells
  • High levels when?
A

Fibroblast GF 23 (FGF-23)

  • Tells the kidney to dump phosphorus
  • Secreted by the bone cells
  • Levels are high in CKD due to phosphorus retention
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13
Q

Role of calcitonin?

A

Calcitonin “tones down” calcium

  • Net effect = lowering serum Ca levels
  • Opposite effect on serum Ca as PTH
  • Inhibits osteoclast-mediated bone resorption
  • Increases renal excretion of Ca
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14
Q

When in calcitonin indicated?

A

- Hypercalcemia

- Osteoporosis

(Salmon is more potent!)

Not used because:

  • High cost
  • Inconvenience (nasal, parenteral)
  • Resistance development (tachyphylaxis)
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15
Q

Major Ca stores are where?

A

Bone (99%)

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16
Q

How is Ca found in extracelllar fluid

A
  • Bound to protein (mostly albumin), 45%
  • Complexed (bound to anions such as citrate, phosphate, sulfate), 10%
  • Free (ionized), 45%
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17
Q

Acidosis -> ____ (increase/decrease) in ionized Ca

A

Acidosis -> increase in ionized Ca

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18
Q

Alkalosis -> ____ (increase/decrease) in ionized Ca

A

Alkalosis -> decrease in ionized Ca

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19
Q

How does the nephron handle Ca (renal Ca transport)?

A

- PCT: reabsorption coupled to Na, convection flow

- DCT: VitD and PTH increase reabsorption (only segment that is hormone dependent)

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20
Q

How does a low sodium diet help with kidney stones?

A

Kidney trying to maximally reabsorb Na in the proximal tubule and Ca follows (less Ca -> less risk of kidney stones)

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21
Q

How do thiazide diuretics affect Ca levels?

A
  • Thiazide diuretics block apical Na-Cl exchanger
  • Cell wants to increase IC Na concentration, so basolateral Na/Ca exchanger kicks up
  • Allows Ca to travel over apical membrane through ECaC channels
  • Less Ca in lumen/excreted (?)
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22
Q

Lab values for Ca assume what? How can this be corrected?

A

Values assume normal serum protein

  • Must correct for albumin
  • Corrected Ca = Ca + (4 - alb) x 0.8
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23
Q

What can cause hypocalcemia?

A

Absence of PTH gland or function

  • Hypoparathyroid
  • Hypomagnesemia

Ineffective PTH

  • Vit D deficiency
  • Intestinal malabsorption of Ca
  • Hypogmagnasemia

PTH overwhelmed

  • Hyperphosphatemia (e.g. tumor lysis and rhabdomyolysis)
  • Ca and P complexing
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24
Q

What is the clinical presentation of hypocalcemia?

A

Neuromuscular:

  • Tetany
  • Trousseau’s and Chvostek’s signs
  • Seizures
  • Neuropsychiatric changes

Cardiovascular

  • Prolonged QT inteval
  • Arrhythmias
  • Hypotension
  • Heart failure

Ectodermal

  • Coarse scaly skin
  • Cataracts
25
Q

How can hypocalcmia be treated?

A

Correct underlying disease process

Treat with Ca

- IV Ca: CaCl2 of Ca gluconate

- Oral Ca: complexed either to carbonate, citrate, or acetate

- Vitamin D: Calcitriol (active) or Calcifediol (inactive)

26
Q

T/F: in assessing for hypercalcemia, must correct lab value for albumin?

A

True!

Total Ca is protein bound, so must correct abnormal value for albumin

27
Q

What can cause hypercalcemia?

A

Bone:

  • Hyperparathyroidism
  • Acidemia and Ca release
  • Immobilization GIT
  • Vitamin D and Ca reabsorption
  • Milk: alkali (Ca ingestion)

Kidney

  • Thiazide diuretics
  • Familial hypercalcemia

Other:

  • Granulomatous production of 1,25 OH
28
Q

What is the clinical presentation of hypercalcemia?

A

“Bones, stones, groans, abdominal moans”

Cardiovascular

  • Vasoconstriction
  • HTN
  • short QT interval

GI

  • Ulcers
  • Constipation
  • Pancreatitis

Neuropsychiatric

  • Lethargy
  • Obtundation
  • Psychosis
  • Muscle weakness

Extraskeletal calcifications:

  • Dermal
  • Ocular
  • Vascular (+/- infarction)
  • Visceral organs
29
Q

How can hypercalcemia affect the kidney?

A

Acute kidney injury

  • Vasoconstriction and decreased renal plasma flow and GFR

Nephrogenic Diabetes Insipidus

  • Blocks ADH actions at CD and -> inability to concentrate urine Nephrolithiasis Nephrocalcinosis
30
Q

How to treat hypercalcemia?

A

Optimize renal excretion of Ca

  • Avoid Ca resabsorption at PCT: correct volume depletion by giving salt/saline (remember Na and Ca absorbed together)
  • Promote Ca loss at TAL via loop diuretics

Inhibit bone resorption

  • Calcitonin
  • Bisphosphonates (e.g. pamidronate)
31
Q

What are the most common causes of hypercalcemia?

A
  • Primary hyperparathyroidism
  • Malignancy
32
Q

What is the most important initial treatment for hypercalcemia?

A

Aggressive volume replacement

33
Q

Case)

  • 65 yo man presents with altered mental status
  • Serum Ca 10 mg/dL and serum albumin is 1.2 mg/dL
  • He appears volume depleted and gives a 10 day Hx of polyuria

What is his corrected Ca?

What should be done first?

A. IV fluids (normal saline- salt)

B. Furosemide

C. 1,25 OH Vitamin D

D. Hydrochlorothiazide

What is the most likely diagnosis?

A. Multiple myeloma (bone malignancy)

B. Kidney failure

C. Migraines

D. Sarcoidosis

A

Corrected Ca = 0.8 x (4 - albumin) + current Ca

= 12.2 mg/dL This is hypercalcemia

What should be done first?

A. IV fluids (normal saline- salt)

B. Furosemide

C. 1,25 OH Vitamin D

D. Hydrochlorothiazide

What is the most likely diagnosis?

A. Multiple myeloma (bone malignancy)

B. Kidney failure

C. Migraines

D. Sarcoidosis

34
Q

What is the body’s response to hypocalcemia?

A

Decreased plasma Ca -> inactivation of Ca-sensing receptor

  • Decreased fractional renal Ca excretion
  • Increased PTH release
  • Increased renal 25,hydroxy Vitamin D enzyme
35
Q

What is the body’s response to hypercalcemia?

A

Increased plasma Ca -> activation of Ca-sensing receptor

  • Increased fractional renal Ca excretion
  • Decreased PTH and increased calcitonin release
  • Decreased renal 25,hydroxy Vitamin D enzyme
36
Q

Excretion of Ca (stool vs. urine)? P?

A

Ca

  • Stool: 2/3
  • Urine: 1/3

P

  • Stool: 1/3
  • Urine: 2/3
37
Q

Describe P absorption in GIT?

  • Absorption affected by what
  • By region
  • What happens to complexed P?
A

Absorption enhanced by calcitriol

- Duodenum: P absorption coupled to Na

- Jejunum/Ileum: P absorption is passive

Complexed phosphorus (e.g. Ca-P, Mg-P) is not absorbed and is lost in stool

38
Q

Describe kidney handling of P?

  • How much filtered?
  • What affects reabsorption?
A
  • Not protein bound, so > 50% enters filtrate
  • 55-75% of filtered P is reabsorbed in the proximal tubule
  • P reabsorption is inhibited by PTH and FGF-23 via reducing NPT2A (transporter expression)
39
Q

What can cause hypophosphatemia?

A

Cell shift:

  • Severe alcoholism
  • Glucose infusion after starvation

Renal loss

  • Elevated PTH
  • Fanconi’s syndrome (proximal tubular cell defect)

Malabsorption

  • Phosphorus binding antacids

Vitamin D

  • Deficiency and decreased GI absorption
  • Certain tumors and neoplastic syndrome
40
Q

How is hypophosphatemia defined?

A

< 3.5 mg/dL

  • Critical hypophosphatemia when < 1 mg/dL
41
Q

What are the clinical symptoms of hypophosphatemia?

A

Acute: inadequate ATP production

  • Skeletal muscle weakness and necrosis
  • Cardiac failure, neurological dysfunction
  • Hemolysis, tissue hypoxia
  • Impaired platelet and macrophage function

Chronic:

  • Increased bone resorption and hypercalcemia
  • Bone demineralization and pain
42
Q

Treatment for hypophosphatemia?

A

Oral:

  • Milk, cheese, eggs
  • Na and K phosphate supplements

IV

  • Use in emergencies or critical hypophosphatemia (recall: under 1 mg/dL)
  • Can cause severe and symptomatic hypocalcemia (complexes with Ca)
43
Q

What can cause hyperphosphatemia?

A

Cell shifts

  • Tumor lysis
  • Rhabdomyolysis

Renal

  • Kidney disease
44
Q

How can hyperphosphatemia be measured/evaluated? What are consequences of hyperphosphatemia?

A

Calcium phosphorus product: Ca x Phos

  • Normal = 30
  • Pts with kidney disease = 60-70

Result:

  • Ca-Phos deposition in vessels, tissues, visceral organs
  • “Calciphylaxis”– VERY high mortality
45
Q

What can cause secondary hyperparathyroidism?

A
  • Hypocalcemia secondary to Ca x Phos binding -> release of PTH
  • Osteitis Fibrosa Cystica and metastatic calcifications
46
Q

Treatment for hyperphosphatemia?

A

Correct underlying disease process!

The 3 Ds:

  • Diet: Avoid high phos foods
  • Dietary Binders: Oral phosphate binding agents (take with meals to bind the P in food)
  • Magnesium, aluminum (not for long term use), calcium, and non-calcium based binders
  • Dialysis (extra-corporeal removal)
47
Q

What affects Mg movement (cell efflux/influx)?

A

Cell efflux of Mg: beta stimulation

Cell influx of Mg:

  • Insulin
  • Calcitriol
  • Vitamin B6
48
Q

What is the role of Mg in the body?

A

DNA and protein synthesis

Neurologic:

  • Neuronal activity
  • Cardiac excitability
  • Neuromuscular transmission
  • Vasomotor tone and BP

Necessary cofactor for transport systems that affect potassium and calcium levels

  • Leaky ROMK channel: low intracellular Mg levels keeps it open
  • PTH needs Mg to facilitate calcium release from bone
49
Q

What are dietary sources of Mg?

A

Plants (central metal iron in chlorophyll)

50
Q

Describe renal handling of Mg in the kidney?

A

tAL: paracellular movement (like Ca)

51
Q

What can cause hypomagnesemia?

A
  • Malnutrition
  • Alcoholism
  • GI malabsorpotion
  • Renal wasting after nephrotoxic drugs: cisplatin, Amphotericin B, cyclosporin
52
Q

How can hypogmagnesemia present?

A
  • Muscle weakness, tremors, fasciculations, arrhythmias
  • Neuropsychiatric changes
  • Hypocalcemia, hypokalemia
53
Q

Treatment for hypomagnesemia?

A
  • IV or IM supplements
  • Oral Mg (side effect is diarrhea, which can -> GI Mg loss!)
54
Q

What can cause hypermagnesemia?

A
  • Iatrogenic (given to prevent contractions in pregnancy)
  • Mg containing antacids in pts with CKD or AKI
55
Q

Manifestations of hypermagnesemia?

A

3-5 mg/dL

  • Thirst, nausea, vomiting

5-7 mg/dL

  • Drowsiness, hypotension, depressed DTR

> 12 mg/dL

  • Coma, respiratory paralysis, hypotension, cardiac arrest
56
Q

What is the treatment for hypermagnesemia?

A
  • Initial treatment: IV Ca (stabilize cardiac membrane)
  • Loop diuretics
  • Hemodialysis
57
Q

Putting it all together: CKD

A
58
Q

Treatment options in CKD?

A

Remove phosphorus

  • Dietary phosphate reduction
  • Dietary binders (bind P and remove via GIT)
  • Dialysis (extra-corporeal removal)

Reduce PTH levels

  • Cinacalcet
  • 1,25 Vitamin D (Calcitriol)

25-Vitamin D supplementation

MS2 Renal (25 decks)

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