Metabolic bone disease flashcards

Question 1

Osteoporosis pathogenesis

Answer 1

rate of bone reabsorption > bone formation

Question 2

Bone remodelling unit

Answer 2

BRU Osteoblasts, osteoclasts

Question 3

At what age does complete bone replacement cease to occur?

Answer 3

Unit 35-40 years old

Question 4

How much bone is lost every reabsorption cycle?

Answer 4

Loss of bone mass is incremental with every reabsorption cycle (0.7%/year)

Question 5

Classification of osteoporosis

Answer 5

Localised: following limb disuse Systemic

Question 6

Primary systemic osteoporosis

Answer 6

Post-menopausal (type I), age related (type II - both sexes)

Question 7

Secondary systemic osteoporosis

Answer 7

Endocrinopathies Neoplasias Nutritional Drugs Miscellaneous

Question 8

Pathogenesis of primary osteoporosis

Answer 8

Question 9

Contributing factors to primary osteoporosis

Answer 9

Genetic factors Nutritional status (calcium, vitamin D, high quality protein) Physical activity Environment

Question 10

Osseous morphology post menopausal

Answer 10

Increased osteoclast activity Thinning out of trabeculae Loss of inter-connections

Question 11

Osseous morphology of age related osteoporosis

Answer 11

Subperiosteal and endosteal resorption Thinning out of compact bone and trabeculae

Question 12

Diagnosis of osteoporosis

Answer 12

Bone mineral density testing (i) Dual-emission X-ray absorptiometry (DEXA) (ii) Quantitative computered tomography (QCT) Biopsy: not used for routine diagnosis

Question 13

Bone mineral dentidy T-score criteria for osteopenia and osteoporosis

Answer 13

Normal = >-1.0 Low bone mass (osteopenia) = between -1.0 and -2.5 Osteoporosis = <-2.5 and frigility A Z score is needed to avoid overestimation of bone mineral deficits.

Question 14

Osteomalacia

Answer 14

Inadequate mineralisation of skeletal matrix. Outcome is defective osseous structure. In children there is also defective mineralisation of the cartilaginous matrix of the growth plate, and it is known as rickets.

Question 15

Types of osteomalacia (according to causes)

Answer 15

Vitamin D-related Malabsorption syndromes Renal diseases Drug induced Others (poisons, tumours).

Question 16

Pathogenesis of osteomalacia

Answer 16

(1) Deficiency of vitamin D causes hypocalcaemia
(2) Parathyroid hormone (PTH) secretion is activated, renal alpha1-hydroxylase is activated, Ca2+ is mobilised from bone, renal excretion of Ca2+ is decreased, HPO34 renal excretion increases.
(3) Serum levels of Ca2+ are restored nearly to normal.
(4) Hypophosphatemia persists with impairment of osseous mineralisation.

Question 17

Paget’s disease of bone.

Answer 17

Osteitis deformans Bone resorption, intense bone formation, skeletal deformity. Uncommon before 40y. Male<female></female>

Question 18

Developmental stages of Paget’s disease

Answer 18

1. Osteoclastic activity 2. Osteoclastic x osteoblastic proliferation 3. Osteosclerotic phase

Question 19

Pathogenesis of Paget’s disease

Answer 19

Obscure cause (environmental? Genetic?) Increased osteoclast recruitment

Question 20

Pathology of Paget’s disease

Answer 20

In Paget’s disease large, abnormal, multinucleated osteoclasts cause excessive bone erosion with destruction of trabeculae and cortical bone. Each wave of bone destruction is followed by a vigorous but uncoordinated osteoblastic response, producing new osteoid to fill the defects left by the osteoclasts. The result is greatly disordered bone architecture.

There are three pathological phases: (1) Lytic phase (2) Mixed phase (3) Sclerotic phase

Question 21

Lytic phase of Paget’s

Answer 21

Large osteoclasts with many nuclei (up to 100) Woven aspect with resorption pits

Question 22

Mixed phase of Paget’s

Answer 22

Presence of osteoclasts Prominent osteoblasts Marrow replaced by LCT Osteoprogenitor cells Richness in blood vessels Woven and lamellar pattern

Question 23

Sclerotic phase of Paget’s

Answer 23

Reduction in fibro-vascular pattern Normal marrow Coarse trabeculae (thick) Cortical fragility

Question 24

Diagnosis of Paget’s disease

Answer 24

(1) X-ray: thick, coarse cortex and cancellous bone; wedge-shaped lytic edge (2) Serum alkaline phosphatase (ALP): is elevated >5x upper limit than normal (ULN) in association with osteoblastic activity. (3) Hydroxyproline: increased urinary excretion (4) Osteocalcin: serum elevation when osteoblastic activity is increased.

Question 25

What may neoplastic formations follow?

Answer 25

(1) Osteosarcoma (most common) (2) Giant cell tumour (3) Giant cell tumour reparative granuloma (4) Malignant fibrous histiosarcoma (5) Chondrosarcoma