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Metabolic Bone Disease Flashcards

1
Q

How is Paget’s disease diagnosed?

A

On X-ray - shows enlargement of bone and patchy cortical thickening and deformity.

  • Affinity for the axial skeleton and skull.
  • Sabre tibia
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2
Q

What is Vitamin D dependant Rickets?

A

A syndrome caused by a deficiency in 1-alpha hydroxylase.

  • Type 1: 1-alpha hydroxylase defiency which means body can’t convert inactive VitD into the active form in the kidney.
  • Type 2: Inactive vitamin D receptor.
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3
Q

What is the primary cause of Osteomalacia?

A

Vitamin D deficiency

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4
Q

Excess of what causes hypophosphatemic rickets?

A

FGF23 which inhibits 1-alpha hydroxylase and promotes phosphate excretion.

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5
Q

Treatment for Pagets?

A

Biphosphontes which bind to the surface of bone and slow down resorption by osteoclasts.

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6
Q

RANK L

A

RANK L activates RANK receptor stimulating osteoclast genesis and resorption.

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7
Q

Sclerostin is secreted by what?

A

Osteocytes causing bone resorption.

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8
Q

How does Paget’s disease clinically present?

A

Asymptomatic in 70% Bone pain and deformity Fractures Osteosarcoma Suspect if there is a sudden onset or worsening of one pain.

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9
Q

Reverse RANK RANK L signalling

A

RANK binds to RANKL receptor on osteoblasts stimulating osteoblast genesis and production of osteoid.

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10
Q

Paget’s disease

A

Increased bone turnover associated with increased osteoblast and osteoclast activity resulting in poor quality woven bone. Leads to enlargement, deformity and weakness.

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11
Q

Trendenlenberg’s gait indicates a problem with which nerve?

A

Superior gluteal nerve

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12
Q

What are the steps of bone remodelling?

A
  1. Quiscence
  2. Resorption by osteoclasts
  3. Reversal - osteoblasts lay osteoid (unmineralised bone).
  4. Osteoblasts become trapped in ECM and differentiate into osteocytes.
  5. Osteoid is mineralised by Ca2+ and PO34- to form hydroxyappetite crystals.
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13
Q

What is the difference between osteomalacia and rickets?

A

Ricket’s occurs in children during bone growth, osteomalacia occurs after fusion of the epiphyses.

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14
Q

What are the clinical features of osteoporosis?

A

Height loss, thoracic kyphosis, lumbar lordosis, protuberant abdomen, decreased lung capacity, oesophageal reflux, weight loss.

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15
Q

How is blood chemistry altered in Paget’s?

A

Elevated ALP alkaline phosphatase.

Ca2+ and PO34- normal.

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16
Q

In type 1 VitD dependant rickets 25(OH)D is high and 1,25(OH)2 is low.

-Treatment?

A

Treatment is to give the active form of vitamin D.

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17
Q

What can cause excess FGF23 to be produced?

A

Tumours can produce excess FGF23 production causing hypophosphatemic rickets and osteomalacia.

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18
Q

How do you diagnose osteoporosis?

A

DXA scans - diagnosis made on bone mineral density.

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19
Q

How does oestrogen affect bone health?

A
  1. Promotes osteoblastogenesis
  2. Pro-anabolic effect on bone formation
  3. Inhibits sclerostin promoting bone formation
  4. Inhibits osteclastogenesis
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20
Q

Causes of Rickets and Osteomalacia:

A

Vit D deficiency

Renal osteodystrophy - failure to produce calcitriol.

Drug induced - Anti-convulsants may induce liver enzymes leading to breakdown of 25-VitD.

Inherited VitD resistance.

Liver disease - 25 Vit D production affected e.g in Cirrhosis.

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21
Q

What is the treatment for osteoporosis?

A

Anti-resorptives, denosumab, Anti RANK L, Romosozumab, anti-sclerostin.

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22
Q

How long does bone remodelling take?

A

3-6 months

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23
Q

Hypophosphatemic rickets

A

Characterised by excessive renal phosphate losses which results in low serum phosphate which is to low for bone mineralisation.

  • diagnosed in children.
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24
Q

Actions of Vit D

A
  1. Inc Ca2+ intestinal absorption
  2. Decrease Ca2+ kidney excretion
  3. Inc bone resorption to increase serum Ca2+
25
Q

What are the signs and symptoms of Rickets?

A

Growth retardation, hypotonia, and apathy in children.

Once walking knock-kneed, bow-legged and deformities of the epiphyseal metaphyseal junction are present e.g the rachitic rosary.

Features of low Ca2+ are mild.

Children with Ricket’s are ill.

26
Q

OPG (Osteoprotegerin)

A

OPG inhibits RANK L preventing activation of RANK so you get no osteoclast genesis.

27
Q

RANK

A

RANK is a receptor expressed on osteoclast precursors.

28
Q

Osteomalacia

A

Softening of bone due to defective mineralisation of newly formed bone in the mature skeleton.

29
Q

Synthesis of vitamin D

A
  1. UVB light in skin
  2. Liver
  3. Kidney converts to dihydroxy 1-25 the active form.
30
Q

What are common fragility fractures of osteoporosis?

A

Wrist , kohlers fracture. vertebral fractures, neck of femur.

31
Q

What are high osteocalcin levels a sign of?

A

Osteocalcin levels are increased in metabolic bone diseases with increased bone or osteoid formation including osteoporosis, osteomalacia, rickets, hyperparathyroidism, renal osteodystrophy, thyrotoxicosis, and in individuals with fractures, acromegaly and bone metastasis.

32
Q

Lack of sclerostin leads to what?

A

Conditions characterised by high bone mass.

33
Q

What drugs can be linked to bone loss?

A

Corticosteroids, aromatase inhibitors, glitazones.

34
Q

PTH function

A

Increases serum Ca2+ through resorption of bone and promotes phosphate excretion.

35
Q

Rickets

A

Bone disease associated with decreased serum calcium/phosphate leading to widening and delay of mineralisation of growth plates in bones.

  • affects children as it affects growth plates.
36
Q

What is osteoporosis?

A

A disease characterised by low bone mass and detereoration of bone tissue. Leads to inc bone fragility and inc fracture risk.

37
Q

What are the normal calcium and ionised calcium ranges in the blood?

A
  1. 2-2.6mmol for total calcium.
  2. 1-1.3mmol for ionised calcium.
38
Q

What are the clinical features of hypercalcemia?

A

• Lethargy and general aches • Polyuria, polydipsia • Anorexia, nausea, vomiting • Dehydration • Constipation • Psychosis • Bradycardia and heart block • Kidney failure

‘Stones, bones, abdominal moans and psychic groans’

39
Q

What are the investigations of hypercalcemia?

40
Q

Primary hyperparathyroidism:

41
Q

What are the PTH independant causes of hypercalcemia?

A

Humoral hypercalcaemia of malignancy (HHM) - Due to production of PTH-related protein (PTHrP), which promotes osteoclastic bone resorption.

Hypercalcaemia associated with local osteolysis.

1,25(OH)2D secreting lymphomas.

42
Q

What is the only immunoglobulin can cross the placenta?

43
Q

What are the symptoms of hypocalcemia?

A

Symptoms due to neuromuscular excitability:

  • paraesthesia
  • carpopedal spasm / cramps
  • laryngospasm (stridor)
  • bronchospasm (wheeze)
  • seizures
44
Q

Chvostek’s sign

A
  • Tap over the area of facial nerve
  • Observe twitching of facial muscles
45
Q

Trousseau’s sign

A
  1. Inflate blood pressure cuff 10 mm Hg above systolic blood pressure .
  2. Leave cuff inflated for 3 mins.
  3. Aim to induce local hypoxia.
  4. Observe flexion at wrist – occurs slowly.
  5. Present in 94% hypocalcaemic cases
46
Q

Investigation of Hypocalcemia:

47
Q

Hypocalcemia due to sepsis:

A

Hypocalcaemia affects 20% of patients with sepsis.

48
Q

A deficiency in what other ion can cause hypocalcemia?

A

Mg2+ hypomagnesia <0.5mmol

49
Q

How does hypomagnesaemia cause hypocalcemia?

A
  1. Impaired PTH secretion.
  2. End organ resistance to PTH.
50
Q

Causes of hypomagnesaemia:

A
  1. Decreased consumption - Malnutrition and alcohol.
  2. Intestinal losses - Short bowel syndrome, diarrhoea.
  3. Renal losses - diuretics and alcohol.
51
Q

What causes autoimmune hypoparathyroidism?

A

Polyglandular autoimmune syndrome type 1

52
Q

Causes of hypoparathyroidism:

A
  1. Parathyroid destruction.
  2. Autoimmune - Polyglandular autoimmune syndrome type 1.
  3. Parathyroid agenesis - DiGeorge syndrome.
  4. Reduced parathyroid function - Hypomagnesaemia.
53
Q

What are the symptoms of DiGeorge syndrome?

  • CATCH22
A
  1. HypoCalcemia
  2. Abnormalities of the face
  3. Thymus hypoplasia
  4. Cleft palate
  5. Hypoparathyroidism thus hypocalcemia
  6. 22 - location of deletion.
54
Q

Causes of vitamin D deficiency:

55
Q

Management of hypocalcemia:

56
Q

What are the major causes of hypercalcemia?

A

Major causes of hypercalcaemia: primary hyperparathyroidism and malignancy.

57
Q

What are the major causes of hypocalcaemia?

A

Major causes of hypocalcaemia: sepsis, hypomagnesaemia, hypoparathyroidism and vitamin D deficiency.

58
Q

Management of hypercalcaemia:

MSK 2 (20 decks)

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