39: Ca/Phosphate Homeostasis Flashcards

1
Q

Distribution of Ca in ECF, ICF, and bones/teeth

A

ECF: 0.1%
ICF: 1%
Bones and teeth: 99%

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2
Q

Total Ca that is protein bound vs ultrafilterable

A

Protein bound: 40%

Ultrafilterable: 60%

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3
Q

Normal range for Ca and Pi in the blood

A

Ca: 10mg/dL
Pi: 2.5-4.5 mg/dL

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4
Q

Two things that occur with Ca as we age

A
  1. Decrease amount we absorb from dietary intake

2. Existing bones reabsorb faster than new bone is made -> osteopenia or osteoporosis

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5
Q

S/S hypocalcemia

A

Hyperreflexia, spontaneous twitching, muscle cramps, tingling and numbness

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6
Q

Two signs that are indicators of hypocalcemia (explain them)

A
  1. Chvostek sign: twitch in facial muscle elicited by tapping facial nerve
  2. Trousseau sign: carpopedal spasm upon inflation of BP cuff
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7
Q

How does hypocalcemia cause tetany?

A

Reduces activation threshold for Na channels -> increased membrane excitability

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8
Q

S/S hypercalcemia

A

Decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyperreflexia, lethargy, coma

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9
Q

Concentration of Pi vs Ca in ECF

A

Are inversely related

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10
Q

Distribution of Pi in bone, ICF, and plasma

A

Bone: 85%
ICF: 15%
Plasma: <1%

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11
Q

Plasma Pi: % ionized, bound to protein, and complexed

A

84% ionized
10% bound to protein
6% complexed to cations

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12
Q

What happens to PTH with chronic hypercalcemia?

A

Decreased synthesis and storage of PTH + breakdown of stored PTH

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13
Q

What happens to PTH/parathyroids during chronic hypocalcemia

A

Increased synthesis and storage of PTH + hyperplasia of parathyroid glands

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14
Q

What binds vitamin D in plasma?

A

Vitamin D binding protein

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15
Q

Where are vitamin D receptors

A

In nucleus

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16
Q

What does vitamin D do once it meets its receptor in order to be effective?

A

Receptor + vitamin D dimerize with another set -> become hydroxylated -> modulate gene transcription

17
Q

What happens with calcitonin with thyroidectomy and thyroid tumors

A

Thyroidectomy: decreased calcitonin, but no effect on Ca metabolism
Thyroid tumors: increased calcitonin, but no effect on Ca metabolism

18
Q

One of the most potent regulators of osteoblasts and osteoclast function

A

Estradiol-17B

19
Q

What can happen to pts treated with high levels of glucocorticoids?

A

Glucocorticoid induced osteoporosis

20
Q

How does PTH cause bone resoprtion in the long term?

A

Sustained levels shift balance to a relative increase in osteoclasts

21
Q

PTH role in SI

A

No direct action, works indirectly via vitamin D

22
Q

TRPV6 channel

A

Channel for Ca entry into intestinal ep from lumen

23
Q

Calbindin

A

Binds Ca to maintain Ca reservoir + shuttles it into blood

24
Q

The saying for primary hyperparathyroidism symptoms

A

Stones, bones and groans

25
Q

Treatment for primary hyperparathyroidism

A

Usually requires parathyroidectomy

26
Q

Treatment for hypoparathyroidism

A

Oral Ca supplement + active form of vitamin D

27
Q

Other name for Albright Hereditary Osteodystrophy

A

Pseudohypoparathyroidism Type 1A

28
Q

Type I and II of pseudovitamin D deficient rickets

A

Type I: decreased 1a-hydroxylase

Type II: decreased vitamin D receptor

29
Q

Nutritional osteomalacia

A

From GI disorder or suboptimal nutrition and inadequate sunlight, can also be caused by gastric bypass