bone

Question 1

effect of corticosteroids on bone

Answer 1

direct

• reduction of osteoblast activity + lifespan
• suppression of replication of osteoblast precursors
• reduction in calcium absorption

indirect
- inhibition of gonadal + adrenal steroid production

Question 2

which type of collagen is affected in osteogenesis imperfecta?

Answer 2

type 1

genetic mutation that affect maturation + organisation of type 1 collagen

Question 3

osteogenesis imperfecta

Answer 3

brittle bones brone to fractures - due to mutations affecting matuaration + organisation of type 1 collagen

8 types depending on mutation - vary in severity, mild may present in adult
most autosomal dominant

Question 4

osteogenesis imperfecta presentation

Answer 4

recurrent + inappropriate fractures
blue/grey sclera (whites of eyes)

dental problems
deafness
short stature
triangle face
hypermobility
bone deformities - bowed legs, scoliosis

Question 5

diagnosis of osteogenesis imperfecta

Answer 5

clinical
genetic testing can be done but not routine

xrays for fractures

Question 6

management of osteogenesis imperfecta

Answer 6

no cure - fix + prevent further fractures

bisphosphonates - increase bone density
vit D supplementation

MDT - physio, occ, paeds, social workers

Question 7

which bones are most affected in paget’s disease?

Answer 7

axial skeleton

pelxis
lumbar spine
skull
long bones

may be single site (monostotic) or multiple (polyostotic)

Question 8

Paget’s disease

Answer 8

disorder of excessive bone turnover - overactivity of osteoblasts + osteoclats

uncoordinated, leads to patchy areas of sclerosis + lysis

increased risk of pathological fractures

Question 9

Paget’s presentation

Answer 9

older patients
bone pain
bone deformity + fractures

hearing loss - bones of ear affected

Question 10

Paget’s appearance on x-ray

Answer 10

bone enlargement + deformity - patchy
osteoporosis crcumscripta = well defined osteolytic lesions that appear less dense

cotton wool appearance of skull - patchy sclerosis + lysis
V-shaped defects in long bones

Question 11

biochemistry in paget’s

Answer 11

raised alkaline phophatase - other LFTs normal

normal calcium
normal phosphate

Question 12

Pagets investigations

Answer 12

X-ray - patchy, less dense bones

biochemistry - raised alkaline phosphatase

Question 13

management of Paget’s

Answer 13

bisphosphonates

NSAIDs for pain
calcium + vit D - esp when on bisphosphonates

Question 14

Paget’s complications

Answer 14

osteogenic sarcoma (osteosarcoma)

spinal stenosis + spinal cord compression

Question 15

osteogenic sarcoma (osteosarcoma)

Answer 15

key complication of Paget’s

poor prognosis
increased focal pain, bone swelling, pathological fractures

Question 16

what type of receptor is the calcium sensing receptor in the parathyroids?

Answer 16

G-protein couple receptor

plays an essential role in regulation of extracellular calcium homeostasis

Question 17

osteoclasts

Answer 17

multinucleated cells responsible for bone resorption

derived from haematopoietic progenitors

Question 18

osteoblasts

Answer 18

mononuclear cells derived from mesenchymal cells in the bone marrow stroma

–> responsible for bone formation

Question 19

osteocytes

Answer 19

primary cell of mature bone + most common bone cell type

derived from osteoblasts
thought to sense mechanical strain on skeleton

Question 20

common osteoporotic fracture sites

Answer 20

neck of femur
vetebral body
distal radius
humeral neck

Question 21

osteoporosis investigations

Answer 21

DEXA scan

normal serum calcium + phosphate

Question 22

indications for DEXA scan

Answer 22

> 50 yrs
< 50yrs with risk factors

FRAX / Qfracture >10%risk of fracture over 10yrs

Question 23

osteoporosis treatment

Answer 23

lifestyle - diet, sun exposure

calcium + vit D supplements

Question 24

what type of cells produce parathyroid hormone?

Answer 24

chief cells

produces parathyroid hormone in response to hypocalcaemia

Question 25

how does parathyroid act to raise blood calcium?

Answer 25

increases osteoclast activity (reabsorbing calcium from bones0 increasing calcium absorption from the gut increasing calcium absorption from kidneys increasing vit D activity (increases calcium absorption from intestine)

Question 26

symptoms of hyperparathyroidism

Answer 26

(hypercalcaemia) renal stones painful bones abdominal groans - constipation, N+V psychiatric moans - fatigue, depression, psychosis

Question 27

primary hyperparathyroidism

Answer 27

uncontrolled parathyroid hormone produced directly by tumour of the parathyroid glands - leads to hypercalcaemia treatment = surgically removing tumour

Question 28

secondary hyperparathyroidism

Answer 28

where insufficient vit D or chronic renal failure leafs to low absorption of calcium from intestines, kidneys and bones --> causes hypOcalcaemia treatment = correcting vit D deficiency / renal transplant

Question 29

tertiary hyperparathyroidism

Answer 29

when secondary continues for a long period of time causing hyperplasia of the glands --> causes hypercalcaemia treatment = surgically removing part of parathyroid tissue to return parathyroid hormone to appropriate level