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Electrolytes, Acid/base disturbances, endocrinology > Disorders of Calciume and phosphorus and Mg > Flashcards

Disorders of Calciume and phosphorus and Mg Flashcards

1
Q

what are the mechanisms for calcium and phosphorus maintained by?

A

Vit D, the small intestine, renal tubles, PTH, and bone

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2
Q

what cells secrete PTH in the PT?

A

Chief Cells

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3
Q

what does PTH do to the bone?

A

stimulates osteoclasts and osteoblasts (bone resorbed and Ca released into blood stream)

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4
Q

renal actions of PTH?

A

increases reabsorption of Ca

  • passively in the proximal tubule
  • actively transported in cortical TAL of LOH and DCT

2) Inhibits reabsorption of phosphate: Occurs in the proximal tubule
3) Synthesis of calcitriol: Stimulates synthesis of 1-alpha hydroxylase to convert calcidiol to calcitriol

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5
Q

Intestinal Actions of PTH?

A

ntestinal Actions

Increases the intestinal absorption of calcium by calcitriol
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6
Q

what does increased levls of PTH cause?

A

increased serum calcium and decreased Ph

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7
Q

what does decreased levels of PTH cause?

A

decreased serum Ca and increased Ph

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8
Q

what are he most common causes of disorders of Ca and phosphorus?

A

parathyroid disorders, renal failure, malignancy

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9
Q

what is one of the most common disorders of calcium and phosphorus in hospitalized pts w/ malignancies?

A

hypercalcemia

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10
Q

what tpes of maligancies might pts get hypercalcemia w/

A

lung cancer, SCC of head, neck, and esophagus, femal genital tract carcinoma, multiple myeloma, lymphoma, renal cell carcinoam

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11
Q

what are some other causes of hyperca

A

vit D intoxication
hyperparathyroidims
sarcoidosis

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12
Q

CF of hyperca

A

anorexia, N, constipation, polyuria, polydipsia, dehydration, change in levelof consciousness

-volume depletion: orthostatic hypotension, tachycardia

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13
Q

what dx studies need to be done in a hyper cc workup

A

corrected calcium (albumin)

  • CXR: pulmonary mass
  • UA for hematuria (early sign of RCC)
  • ESR: monoclonal gammopathy
  • vita D
  • 24 hours urine collection
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14
Q

what does an elevated urine clacium suggest?

A

malignant neoplastic or paraneoplastic process or hyperparathyroidims

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15
Q

what does an decreased uring Ca suggest?

A

primary hyperparathyroidms

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16
Q

tx of hyperCa

A

isotonic saline for volume repletion,

  • loop diuretics if pt is hypervolemic after volume repletion
  • bisphosphonates in severy hyperca
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17
Q

what is the more common disorder? hyper Ca or hypoCa?

A

hypoCa!

critically ill ps

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18
Q

what does hypoCa commonly result from

A

CKD or hypoparathyroidism

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19
Q

what can sever hyopcalcemia cause?

A

compmelete cardiovascular collaps

20
Q

what are clinical features of hypocalemia?

A

dry skin, brittle nails, pruritis, muscle cramping, SOB, numbness and tinglin in the extremeites

21
Q

what are some sever cardiovasuble manifestation of hypoca

A

syncope and angina

22
Q

what are some dlinical signs of hypocalcemia?

A

psroiasis, dry skin, perioral numbness,

-wheezing, bradycardia, crackles, 3rd heart sound

23
Q

what are classic neurologic findings in hyopca?

A

trousseau sign, chvostek sign (facial nerve),

irritabilyt, confusion, dementaion, sz

24
Q

what dx studies need to be done?

A

Ca < 8.5

ionized Ca, Mg, Ph albumine, LFts,

BUN and creatinine

25
Q

tx of hypocalemia

A

tx any emergent CV states

-severe hypoca; I V calcium gluconate or Ca Cl

26
Q

hyperphosatemia is most common secondary to what disorder?

A

CKD or excessiv euse of phosphate-containing laxitives or enemas

27
Q

what is hypophosphatemia secondary to?

A

deminished supply or absorption, increased urinary loss,

-vit D deviciency,
-respiratory alkalosis
burns
-hyperparathyroidism

28
Q

how is hypoPh classifed?

A

based on serum level

  • moderate: 1-2.5 and is usually ax
  • severe: 1 or less
29
Q

what can severe hypoPh lead to?

A

rhabdomyolysis, paresthesia, encephalopathy

30
Q

tx of hyperphopahtemia

A

if secondary to CKD- dietary phophorous restriction and oral phosphate binders
-calcium carb tablest

31
Q

hypomagensemia

A

denfined as plasma Mg levels of les than 1.8 mEq/L

*plasma levels do not reflect total storage

32
Q

when does hypoMg usually prsent?

A

when totat body stors are severly depleted- results from diminished intake and imparied absorbtion

33
Q

what are some common causes of hypoMg?

A

chronic alcoholism, chronic D, hypopartathyroidism, hyperaldosteronis, diuretic therapy, osmotic diureses, and nutritional deficiencies

34
Q

what OTC drug can cause hypomg?

A

PPI (greater than 5 yrs)

35
Q

what are clinical features of hypomag?

A

lethargy, anorexia, N, V, wkns, tetany, seizure

36
Q

what lab test should be checked along side HyopMg?

A

K, Ca, urine calcium

hypoaK, hyopCa, and hypocalciuria sheen w.hypoMg

37
Q

what might an EKG show with hypoMg?

A

polonged PR and QT intervals, or widening of the QRS

38
Q

how do you tx hypomg?

A

oral mg oxide

in severe- Mg sulfate solution via IV, can used IM

39
Q

hyper mg?

A

> 2.2

Mg stored in bones and muscles

40
Q

CFof hypermg

A

sx are rare- except in pts w/ CKD who are given Mg containing products such as laxatives or antacids

41
Q

what conditions can iatrogenically induce hypermg?

A

eclampsia or preterm labor

42
Q

what are sgns and symptoms of hyperMg?

A

impaired neruomuscular transmission

  • reduced deep tendon reflexes
  • muscle weaknessm hypotenson
  • respiratory depression- cardiac arrest
  • N,V, flusing
43
Q

what may been seen on an EKG w/ hypermg?

A

widened QRs, prolonged PR, prolonged QT

44
Q

lab studies of hypermg?

A

bleeding and clotting times are incraeased

45
Q

tx of hypermg?

A

calcium gluconate IV
=saline diuresis and IV furosemide
-dialysis

Electrolytes, Acid/base disturbances, endocrinology (7 decks)

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