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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
How can hypocalcmia be treated?
**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
**T/F:** in assessing for hypercalcemia, must correct lab value for albumin?
**True**! Total Ca is protein bound, so must correct abnormal value for albumin
27
What can cause hypercalcemia?
_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
What is the clinical presentation of hypercalcemia?
**"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
How can hypercalcemia affect the kidney?
**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
How to treat hypercalcemia?
_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 l**oop diuretics** _Inhibit bone resorption_ - Calcitonin - Bisphosphonates (e.g. pamidronate)
31
What are the most common causes of hypercalcemia?
- Primary hyperparathyroidism - Malignancy
32
What is the most important initial treatment for hypercalcemia?
Aggressive volume replacement
33
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
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
What is the body's response to hypocalcemia?
Decreased plasma Ca -\> **in**activation of Ca-sensing receptor - Decreased fractional renal Ca excretion - Increased PTH release - Increased renal 25,hydroxy Vitamin D enzyme
35
What is the body's response to hypercalcemia?
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
Excretion of Ca (stool vs. urine)? P?
**Ca** - Stool: 2/3 - Urine: 1/3 **P** - Stool: 1/3 - Urine: 2/3
37
Describe P absorption in GIT? - Absorption affected by what - By region - What happens to complexed P?
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
Describe kidney handling of P? - How much filtered? - What affects reabsorption?
- 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
What can cause hypophosphatemia?
**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
How is hypophosphatemia defined?
\< 3.5 mg/dL - Critical hypophosphatemia when \< 1 mg/dL
41
What are the clinical symptoms of hypophosphatemia?
_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
Treatment for hypophosphatemia?
_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
What can cause hyperphosphatemia?
**Cell shifts** - Tumor lysis - Rhabdomyolysis **Renal** - Kidney disease
44
How can hyperphosphatemia be measured/evaluated? What are consequences of hyperphosphatemia?
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
What can cause secondary hyperparathyroidism?
- Hypocalcemia secondary to Ca x Phos binding -\> release of PTH - Osteitis Fibrosa Cystica and metastatic calcifications
46
Treatment for hyperphosphatemia?
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
What affects Mg movement (cell efflux/influx)?
Cell efflux of Mg: **beta stimulation** Cell influx of Mg: - **Insulin** - **Calcitriol** - **Vitamin B6**
48
What is the role of Mg in the body?
**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
What are dietary sources of Mg?
Plants (central metal iron in chlorophyll)
50
Describe renal handling of Mg in the kidney?
tAL: paracellular movement (like Ca)
51
What can cause hypomagnesemia?
- Malnutrition - Alcoholism - GI malabsorpotion - Renal wasting after nephrotoxic drugs: cisplatin, Amphotericin B, cyclosporin
52
How can hypogmagnesemia present?
- Muscle weakness, tremors, fasciculations, arrhythmias - Neuropsychiatric changes - Hypocalcemia, hypokalemia
53
Treatment for hypomagnesemia?
- IV or IM supplements - Oral Mg (side effect is diarrhea, which can -\> GI Mg loss!)
54
What can cause hypermagnesemia?
- Iatrogenic (given to prevent contractions in pregnancy) - Mg containing antacids in pts with CKD or AKI
55
Manifestations of hypermagnesemia?
_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
What is the treatment for hypermagnesemia?
- Initial treatment: **IV Ca** (stabilize cardiac membrane) - Loop diuretics - Hemodialysis
57
Putting it all together: CKD
58
Treatment options in CKD?
**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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