Calcium, Phosphate & Vitamin D in Bone Health Flashcards by Tendai Gwata

Bone Mass

actual amount of osseous tissue in any unit volume of bone.

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Concentration of ionized

calcium in ECF (plasma)

1.2mmol/L

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Calcium in plasma present in

three forms

Combined with plasma proteins-non diffusible
Combined with anionic
substances in plasma – diffusible
but non ionised
Ionised form – diffusible (most
important form)

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Calcium reservoir

About 98 -99% of total body calcium stored in bone
Bones act as the most important reservoir:
✓release calcium when extracellular calcium drops and
✓store excess calcium

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Functions of Calcium

mechanical stability and serves as a reservoir
bone formation and remodeling
important cofactor for several enzymes and signal for signaling pathways
including blood clotting - ensuresthat blood clots normally
✓ muscle contraction; regulates muscle contractions, including heartbeat

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Calcium-Recommended daily allowance

25–30 mmol (1000–1200 mg) for most adults

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Absorption and Excretion of Calcium-Intestinal Absorption

• Vit D dependent

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Absorption and Excretion of Calcium-Bone deposition and

Resorption

Vit D & PTH dependent

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Absorption and Excretion of Calcium-• Excretion in Kidneys

PTH dependent

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Phosphate absorptive efficiency may be enhanced by?

1,25(OH)2D (Vit D)

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Excretion of phosphate is through?

urine – controlled according to plasma

concentration levels which can be overridden by PTH

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Parathyroid Hormone (PTH) - Effects on Calcium and Phosphate Levels

inc . Calcium

involved in Phosphate homeo

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Parathyroid Hormone (PTH) – Effects on Bone

PTH promotes net bone resorption

inc in Calcium

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Parathyroid Hormone (PTH) – Effects on Bone

PTH promotes net bone resorption

inc in Calcium

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Parathyroid Hormone (PTH) - Effects on the Kidneys

Therefore, PTH would facilitate increased
phosphate excretion from the kidneys, thereby
reducing complex formation and facilitating
increase in availability of free ionized calcium.

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PTH increases plasma calcium (Ca++) by:

inc. bone resorption (activates osteoclasts, dec collagen synthesis by osteoblasts).
inc. Ca++ reabsorption in the kidneys
inc. vitamin D synthesis in kidneys,dec. Ca++ absorption in the GIT

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PTH on phosphate levels:

dec plasma levels by inc. bone resorption

dec plasma levels by inc. excretion from kidneys

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vitamin D2

Ergocalciferol

plant origin

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CholecalciferoI

(vitamin D3) of animal origin

precursor for cholecalciferol

synthesis in skin

dehydrocholesterol

Sunlight plays a major role in ?

the conversion of 7-dehydrocholesterol (precursor for cholecalciferol
synthesis in skin) to cholecalciferol

what is 25-hydroxycholecalciferol converted to in the kidney

1,25 – dihydroxycholecalciferol

calcitriol - 1,25-diOH-D3

Actions of -1,25-diOH-D3

-binds to intracellular
receptor proteins
-1,25-diOH-D3
receptor complex
interacts with DNA in the nucleus of
target 
-Can either selectively stimulate gene
expression or repress gene expression
(similar to steroid hormones)

Actions of Vitamin D-On the intestine?

-stimulates intestinal absorption of calcium and phosphate by
increased synthesis of a specific calcium binding protein calbindin
-stimulate an ATP-dependent calcium pump, which
transports calcium into the blood stream

Actions of Vitamin D-On the bone ?

-stimulates the mobilization of calcium and phosphate from the bone by potentiating parathormone

Actions of Vitamin D-On the kidneys

inhibits calcium excretion by stimulating | calcium reabsorption; weak effect

Calcitonin

- Secreted by cells in the thyroid gland - Inhibits osteoclast activity ( decreases bone resorption) - Reduces plasma calcium, opposing the effects of PTH

Vitamin D Deficiency causes :

``` Nutritional deficiency Inadequate skin synthesis Liver disease (reduced 25-hydroxylase activity) Kidney disease (reduced 1-hydroxylase activity) ```

Vitamin D Deficiency clinical correlation :

- Rickets(in children ) - Osteomalacia (adults) - Hypocalcemia, - Hypophosphatemia, - Increased serum alkaline phosphatase (ALP) from bone

Rickets: In children

- Demineralisation of bone – soft pliable bones - Characteristic bow-leg deformity - Overgrowth at costochondral junction – rachitic rosary - Pigeon chest deformity - Frontal bossing

Osteomalacia: In adults

 Weakening of bones – | frequent fractures.

Vitamin D Resistant Rickets

-• Plasma levels of 1,25(OH)2D are elevated. -Caused by mutations in the gene encoding the vitamin D receptor in the intestine - decrease Ca2+ absorption from diet -Treatment: Difficult. Regular, usually nocturnal calcium infusions, which dramatically improve growth but do not restore hair growth.

Hypervitaminosis D

-Vitamin D toxicity - Enhanced calcium absorption and bone resorption results in hypercalcemia, which can lead to deposition of calcium in many organs, particularly the arteries and kidneys (soft tissue calcification).

Hypocalcemia causes

- Low Parathyroid Hormone Levels (Hypoparathyroidism) - High Parathyroid Hormone Levels (Secondary Hyperparathyroidism) - Hungry bone syndrome after parathyroidectomy

Hypocalcemia lab findings

* 25 hydroxyvitamin D levels – low if nutritional deficiency of vitamin D * 1,25 dihydroxyvitamin D levels – low if renal insufficiency * PTH levels – low after parathyroidectomy

Hypocalcemia- clinical features

- hypocalcemic tetany - excitability of periperal nerves - carpopedal spasm ,stridor and convulsions

Treatment of hypocalcemia

Ca supplements and vit D | In emergencies: calcium gluconate IV

Hypercalcemia causes :

-Excessive PTH production • Hypervitaminosis • Excessive 1,25(OH)2D production • Excessive calcium intake

Lab findings of hypercalcemia if its due to hypervitaminosiss D

- increase in calcium ' - increase in phosphate - increase in 1,25 (OH)2 D

Lab findings of hypercalcemia if its due to excessive PTH production

increase in PTH increase in Ca decrease in phosphate

Clinical Manifestations of Hypercalcemia

``` • Non-specific signs and symptoms: – Polyuria & polydipsia – Renal calculi ( colic) – Lethargy, – Anorexia and nausea – Peptic ulceration – Depression – Drowsiness – Impaired cognition ```

Hypophosphatemia Causes:

1) Inadequate intestinal phosphate absorption – vitamin D deficiency, (2) Excessive renal phosphate excretion – PTH excess.

Hypophosphatemia: Symptoms

Nerve, bone, red and white blood cells, membrane, and muscle functional problems Serum levels of phosphate and calcium must be monitored closely (every 6 –12 h) throughout treatment.

Hyperphosphatemia- Causes

-Decreased renal excretion - Impaired kidney function • Hypoparathyroidism • Excessive release of phosphate into the ECF (from the gut, bone or parenteral phosphate therapy)

Hyperphosphatemia-Clinical effects:

-Calcification of soft-tissue, organs (kidney, lungs, heart) • Tetany, • Seizures.

Hyperphosphatemia-Lab finding:

• Fasting serum phosphate concentration >1.8 mmol/L (5.5 mg/dL),