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3 > Calcium metabolism > Flashcards

Calcium metabolism Flashcards

1
Q

Ca distribution in blood

A

45% albumin bound
15% bound to anions - phosphate, citrate
40% free calcium (ionized)

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2
Q

Sources of calcium regulation

A

diet
bone - 99.9% calcium stored
kidney - excretion

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3
Q

Ca hormones

A

PTH - increase Ca
Calcitriol - increase Ca
calcitonin - decrease Ca

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4
Q

Drop in Ca - homeostatic pathway

A

1) sensed by parathyroid glans
2) secrete PTH from parathyroid chief cells
3) in kidney:
- increase calcitriol formation
- decrease Ca excretion
- increase phosphorus excretion
4) PTH effects on bone - increase calcium and phosphorus release
5) calcitriol effects on intestines
- increase Ca and phosphorus absorption

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5
Q

PTH effects - prolonged/sustained

A

bone resorption increased

stimulates osteoblasts to produce RANKL, resulting in increased osteoclast activity

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6
Q

PTH effects - episodic, normal

A

promotes bone growth and mineralization

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7
Q

Calcitonin production

A

parafollictular/C cells of thyroid

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8
Q

Calcitonin action

A

antagonizes PTH

fine control of Ca homeostasis - not essential for maintaining serum Ca

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9
Q

Hypercalcemia causes

A

90%: primary hyperparathyroidism/malignancy
measure iPTH to narrow cause
(high: primary hyperPTism/familial hypercalcemic hypocalciuria
normal/decreased: usually malignancy)

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10
Q

Hyperparathyroidism features

A

Longstanding, asymptomatic hypercalcemia/mild hypercalcemia
Seen in postmenopausal females
normal PE

FHx of hyperPTIism, multiple endocrine dysplasia

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11
Q

DDx of hyperparathyroidism

A

Primary hyperparathyroidism
Hyperparathyroidism related to familial syndromes
familial hypocalciuric hypercalcemia
Secondary and tertiary hyperPTism (CKD leading to metabolic bone disease)

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12
Q

Malignancy (hypercalcemia) features

A

rapid increase in serum Ca
more symptomatic
presents in advanced disease, poorer diagnosis

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13
Q

DDx of hypercalcemia due to malignancy

A

Humoral hypercalcemia of malignancy - 80% (PTH-related peptide, common in squamous cell carcinomas)
Osteolytic bone metastases - 20%
Vitamin D intoxication
Chronic granulomatous disorders - sarcoidosis, TB
Meds

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14
Q

Clinical presentations of hypercalcemia

A

neuropsychiatric: anxiety, depression, cognitive dysfunction
GI: constipation, anorexia, nausea
Renal: polyuria, nephrolithiasis
Muscle weakness, bone pain, osteoporosis

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15
Q

Tx of mild hypercalcemia

A 
<3 mmol/L
avoid aggravating factors - thiazide diuretics, lithium
bed rest
adequate hydration
treat underlying cause
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16
Q

Tx of moderate hypercalcemia

A

3-3.5 mmol/L
depends on symptoms
if acute rise, treat as severe

17
Q

Tx of severe hypercalcemia

A 
>3.5 mmol/L
3-pronged treatment:
IV saline
calcitonin
biphosphonates (zolendronate)
18
Q

Hypocalcemia approach

A

differentiate based on PTH levels

19
Q

Hypocalcemia with low PTH DDx

A

Surgical: thyroidectomy
AI: rare, usually with polygrandular autoimmune syndrome
Congenital: hypoplasia of PT gland (DiGeorge syndrome), mutations
Destruction/infiltration: Wilson’s disease, hemochromatosis, HIV

20
Q

Hypocalcemia with high PTH DDx

A 
Vitamin D deficiency
CKD - usually early
Sepsis/severe illness: pancreatitis
Postsurgical hemorrhage: due to citrate in blood products (chelates calcium)
Osteoblastic metastases
Premature infants
21
Q

Clinical presentations of acute hypocalcemia

A

tetany, seizures
CV dysfunction, prolonged QT interval, ventricular dysrhythmia
Papilledemia - with severe hypocalcemia

22
Q

Clinical presentations of chronic hypocalcemia

A

dental changes
cataracts
extrapyramidal disorders

23
Q

Tx of hypocalcemia

A

treat underlying cause

supplement vit D, magnesium, parathyroidectomy

24
Q

Role of magnesium in hypocalcemia

A

Hypomagnesemia can decrease PTH secretion/cause PTH resistance
Can occur due to malabsorption, diarrhea, alcoholism, malnutrition
Need to check/treat hypomagnesemia

25
Q

Bone resorption time period

A

rapid, ~ 3 weeks

26
Q

Bone formation time period

A

Slow, 3-4 months

mineralization occurs over years

27
Q

Bone resorption mechanism

A

1) Osteocytes signals denuded bone surface with elderly/damaged bone to be removed
2) attracts osteoclasts
3) osteoclasts dissolve material by attaching themselves to bone surface and secreting acid

28
Q

Bone formation mechanism

A

1) signalling through Wnt pathway
- sclerostin: secreted by osteocytes to inhibit Wnt when there is lack of mechanical stress
2) Osteoblasts increase in number, activity and maturity
3) Lay down osteoid, then mineralized

29
Q

Hormones affecting osteoblast

A

Progesterone, PTH, testosterone - increase

GCs - inhibit

30
Q

Local regulators of bone resorption/formation

A

Osteoblasts and osteoblast-derived lining cells (LCs) secrete RANK-ligand osteoprotegrin

  • help stimulate new resorption
  • RANKL interacts with RANK receptor on osteoclast precursors leads to osteoclast maturation

Osteoclasts signalling –> osteoblast maturation mediated through Wnt pathway

31
Q

Systemic regulators of bone resorption/formation

A

PTH, calcitriol, GH, GCs, thyroid hormones, sex hormones

32
Q

estrogen effects on bone density

A

decrease resorption in both genders

33
Q

testosterone effects on bone density

A

decrease resorption

increase formation

34
Q

Cortisol effects on bone density

A

increase resorption at higher than physiological doses (also suppresses estrogen)
decreased formation

35
Q

Resorption markers of bone remodelling

A

C-terminal telopeptide (CTX) - most specific/sensitive
NTX
pyridinoline
Deoxypyridinoline

36
Q

Bone formation markers

A

Alkaline phosphatase - total and bone-specific
Procollagen-1-N peptide - most sensitive and specific
Osteocalcin

37
Q

Vitamin D formation

A

1) cholesterol + acetate –> 7-dehydrocholesterol
2) +UV –> cholecalciferol (D3) (same as ingested form)
3) Liver: converted to 25(OH)D3
4) Kidney: converted to 1,25(OH2)D3 - active form

38
Q

Vitamin D dose in Ca absorption

A

<80 nmol/L, Ca absorption rises with increasing vitamin D

above 80 nmol/L, no effect

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