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MSK πŸ’ͺ🏾 > Calcium, Phosphate & Vitamin D in Bone Health > Flashcards

Calcium, Phosphate & Vitamin D in Bone Health Flashcards

1
Q

Bone Mass

A

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

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2
Q

Concentration of ionized

calcium in ECF (plasma)

A

1.2mmol/L

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3
Q

Calcium in plasma present in

three forms

A 
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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4
Q

Calcium reservoir

A

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

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5
Q

Functions of Calcium

A

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
βœ“ muscle contraction; regulates muscle contractions, including heartbeat

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6
Q

Calcium-Recommended daily allowance

A

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

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7
Q

Absorption and Excretion of Calcium-Intestinal Absorption

A

β€’ Vit D dependent

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8
Q

Absorption and Excretion of Calcium-Bone deposition and

Resorption

A

Vit D & PTH dependent

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9
Q

Absorption and Excretion of Calcium-β€’ Excretion in Kidneys

A

PTH dependent

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10
Q

Phosphate absorptive efficiency may be enhanced by?

A

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

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11
Q

Excretion of phosphate is through?

A

urine – controlled according to plasma

concentration levels which can be overridden by PTH

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12
Q

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

A

inc . Calcium

involved in Phosphate homeo

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13
Q

Parathyroid Hormone (PTH) – Effects on Bone

A

PTH promotes net bone resorption

inc in Calcium

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13
Q

Parathyroid Hormone (PTH) – Effects on Bone

A

PTH promotes net bone resorption

inc in Calcium

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14
Q

Parathyroid Hormone (PTH) - Effects on the Kidneys

A

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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15
Q

PTH increases plasma calcium (Ca++) by:

A

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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16
Q

PTH on phosphate levels:

A

dec plasma levels by inc. bone resorption

dec plasma levels by inc. excretion from kidneys

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17
Q

vitamin D2

A

Ergocalciferol

plant origin

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18
Q

CholecalciferoI

A

(vitamin D3) of animal origin

19
Q

precursor for cholecalciferol

synthesis in skin

A

7-

dehydrocholesterol

20
Q

Sunlight plays a major role in ?

A

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

21
Q

what is 25-hydroxycholecalciferol converted to in the kidney

A

1,25 – dihydroxycholecalciferol

calcitriol - 1,25-diOH-D3

22
Q

Actions of -1,25-diOH-D3

A 
-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)
23
Q

Actions of Vitamin D-On the intestine?

A

-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

24
Q

Actions of Vitamin D-On the bone ?

A

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

25
Q

Actions of Vitamin D-On the kidneys

A

inhibits calcium excretion by stimulating

calcium reabsorption; weak effect

26
Q

Calcitonin

A
  • Secreted by cells in the thyroid gland
  • Inhibits osteoclast activity ( decreases bone resorption)
  • Reduces plasma calcium, opposing the effects of PTH
27
Q

Vitamin D Deficiency causes :

A 
Nutritional deficiency
Inadequate skin synthesis
Liver disease (reduced 25-hydroxylase activity)
Kidney disease (reduced 1-hydroxylase activity)
28
Q

Vitamin D Deficiency clinical correlation :

A
  • Rickets(in children )
  • Osteomalacia (adults)
  • Hypocalcemia,
  • Hypophosphatemia,
  • Increased serum alkaline phosphatase (ALP) from bone
29
Q

Rickets: In children

A
  • Demineralisation of bone – soft pliable bones
  • Characteristic bow-leg deformity
  • Overgrowth at costochondral junction – rachitic rosary
  • Pigeon chest deformity
  • Frontal bossing
30
Q

Osteomalacia: In adults

A

ο‚— Weakening of bones –

frequent fractures.

31
Q

Vitamin D Resistant Rickets

A

-β€’ 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.

32
Q

Hypervitaminosis D

A

-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).

33
Q

Hypocalcemia causes

A
  • Low Parathyroid Hormone Levels (Hypoparathyroidism)
  • High Parathyroid Hormone Levels (Secondary Hyperparathyroidism)
  • Hungry bone syndrome after parathyroidectomy
34
Q

Hypocalcemia lab findings

A
  • 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
35
Q

Hypocalcemia- clinical features

A
  • hypocalcemic tetany
  • excitability of periperal nerves
  • carpopedal spasm ,stridor and convulsions
36
Q

Treatment of hypocalcemia

A

Ca supplements and vit D

In emergencies: calcium gluconate IV

37
Q

Hypercalcemia causes :

A

-Excessive PTH production
β€’ Hypervitaminosis
β€’ Excessive 1,25(OH)2D production
β€’ Excessive calcium intake

38
Q

Lab findings of hypercalcemia if its due to hypervitaminosiss D

A
  • increase in calcium β€˜
  • increase in phosphate
  • increase in 1,25 (OH)2 D
39
Q

Lab findings of hypercalcemia if its due to excessive PTH production

A

increase in PTH
increase in Ca
decrease in phosphate

40
Q

Clinical Manifestations of Hypercalcemia

A 
β€’ Non-specific signs and symptoms:
– Polyuria & polydipsia
– Renal calculi ( colic)
– Lethargy,
– Anorexia and nausea
– Peptic ulceration
– Depression
– Drowsiness
– Impaired cognition
41
Q

Hypophosphatemia Causes:

A

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

42
Q

Hypophosphatemia: Symptoms

A

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.

43
Q

Hyperphosphatemia- Causes

A

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

44
Q

Hyperphosphatemia-Clinical effects:

A

-Calcification of soft-tissue, organs (kidney, lungs, heart)
β€’ Tetany,
β€’ Seizures.

45
Q

Hyperphosphatemia-Lab finding:

A

β€’ Fasting serum phosphate concentration >1.8 mmol/L (5.5 mg/dL),

MSK πŸ’ͺ🏾 (36 decks)

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