Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 Endocrinology > Endocrine and metabolic bone disorders > Flashcards

Endocrine and metabolic bone disorders Flashcards

1
Q

What components make up bone?

A

Organic components - osteoid - unmineralised bone mainly type 1 collagen fibres
Inorganic mineral components - calcium hydroxyapatite crystals filling the spaces between collagen fibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the cells that break down bone and how do they do that?

A

Osteoclasts - release lysosomal enzymes which break down bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the cells that build up bone and how do they do that?

A

Osteoblasts - synthesise osteoid and participate in mineralisation/calcification of osteoid (bone formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are osteoclasts made from? How are they activated?

A

They originate as osteoblasts and when RANKL (ligand) binds to RANKR (receptor) it forms an osteoclast precursor. Then differentiation and fusion forms an activated osteoclast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What hormones do osteoblasts express receptors for? What do they do?

A

PTH and calcitrol

- regulate balance between bone formation and resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the different types of bone found in the bone?

A

Cortical - hard bone

Trabecular - spongey bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What kind of pattern is bone formed in healthy bone? Why is it formed this way?

A

Lamellar pattern - collagen fibrils laid down in alternating orientations making it mechanically strong

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is woven bone?

A

Disorganised collagen fibrils which are weaker than the lamellar pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does vitamin D deficiency lead to? - what are the effects on the bone

A

Inadequate mineralisation of newly formed bone matrix - osteoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does rickets affect? What does it lead to?

A

Affects cartilage of epiphysial growth plates and bone. Leads to skeletal abnormalities and pain, growth retardation and increased fracture risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does osteomalacia affect? What does it lead to?

A

It happens after epiphyseal closure as adults aren’t growing anymore, it affects the bone and leads to skeletal pain, increased fracture risk and proximal myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the effects of vitamin D deficiency on the bone?

A

Can cause stress fractures on parts of bone that hold up a lot of weight eg femur - PAINFUL
Waddling gait - typical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the causes of hyperparathyroidism

A

primary - adenoma
secondary - vit d deficiency
tertiary - chronic low plasma ca2+ eg renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can an adenoma cause primary hyperparathyroidism?

A

Parathyroids release PTH which increases Ca2+. Gland makes too much PTH with an adenoma - autonomous secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does PTH increase Ca2+ reabsorption

A

increases reabsorption of Ca2+ from bone, kidney and 1alphahydroxylases inactive vit D making active vitamin D aka calcitriol so increases Ca2+ from the gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does secondary hyperparathyroidism happen due to vit D deficiency

A

Vit D is needed to reabsorb calcium from the gut. Lack of vit D = calcium falls = more PTH made to increase Ca2+ = doesnt work but PTH up!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does tertiary hyperparathyroidism happen

A

Chronic kidney disease = kidneys important for activation of vitamin D by 1alphahydroxylase so no calcitriol so patient very vit D deficient so eventually because PTH made so often, the parathyroid glands become completely autonomous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the effects of lack of phosphate excretion

A

Phosphate rises, binds to calcium which decreases serum Ca2+ . 1. can’t mineralise bone. 2. PTH up leading to boen resorption leading to cysts. 3. phosphate causes vascular calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Osteitis fibrosa cystica (hyperparathyroid bone disease)

A

XS osteoclastic bone resorption secondary to high PTH

‘Brown tumours’ = radiolucent bone lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are treatments for Osteitis fibrosa cystica?

A

Hyperphosphataemia - low phosphate diet, and phosphate binders to reduce GI phosphate absorption
Alphacalcidol – ie calcitriol analogues
Parathyroidectomy in 3o hyperparathyroidism
Indicated for hypercalcaemia &/or hyperparathyroid bone disease

21
Q

What is osteoporosis

A

Loss of bony trabeculae, reduced bone mass, weaker bone so predisposed to fracture after minimal trauma

22
Q

What is the bone mineral density of someone with osteoporosis?

A

Bone mineral density > 2.5 standard deviations below the average value for young healthy adults (usually referred to as a T-score of -2.5 or lower)

23
Q

What can bone mineral density (BMD) be used to predict

A

Future fracture risk

24
Q

What does a DEXA scan do?

A

Measure BMD - dual energy xray absorptiometry of the femoral neck and lumbar spine. It measures the calcium content of the bone and the more calcium, the greater the bone density

25
Q

What is a similarity between osteomalacia and osteoporosis?

A

Both predispose to fracture

26
Q

What is the difference between osteoporosis and osteomalacia?

A

Osteomalacia is due to vit D deficiency and there is an abnormal serum biochemistry but osteoporosis has an increased bone reabsorption, normal serum biochemistry and diagnosis is via DEXA scan

27
Q

How is post menopausal oestrogen deficiency a predisposing conditions for osteoporosis

A

Post menopausal oestrogen deficiency as oestrogen deficiency leads to a loss of bone matrix leading to subsequent increased risk of fracture

28
Q

What are pre disposing conditions for osteoporosis

A

Postmenopausal oestrogen deficiency
Age-related deficiency in bone homeostasis (men and women) eg osteoblast senescence
Hypogonadism in young women and in men
Endocrine conditions: Cushing’s syndrome, Hyperthyroidism, Primary hyperparathyroidism
Iatrogenic: Prolonged use of glucocorticoids, Heparin

29
Q

What are treatment options for osteoporosis

A
  • Oestrogen/Selective Oestrogen Receptor -
  • Modulators
  • Bisphosphonates
  • Denosumab
  • Teriparatide
30
Q

When is oestrogen given as treatment for osteoporosis?

A

Treatment of post menopausal women with pharmacological doses of oestrogen due to it’s anti-resorptive effects on the skeleton and preventing bone loss. Women with intact uterus need additional progestogen to prevent endometrial hyperplasia/cancer

31
Q

Why is oestrogen HRT useage limited as a treatment for osteoporosis

A

Increased risk of breast cancer and venous thromboembolism

32
Q

How do bisphosphonates work as oestoporosis treatment?

A

Bind avidly to hydroxyapatite and ingested by osteoclasts – impair ability of osteoclasts to reabsorb bone.
Decrease osteoclast progenitor development and recruitment
Promote osteoclast apoptosis (programmed cell death)
Net result = reduced bone turnover.

33
Q

When are bisphosphonates used as treatment?

A
  • Osteoporosis – first line treatment
  • Malignancy: Associated hypercalcaemia, Reduce bone pain from metastases
  • Paget’s disease – reduce bony pain
  • Severe hypercalcaemic emergency – i.v. initially (+++ re-hydration first)
34
Q

When should patients take bisphosphonates?

A

Orally active but poorly absorbed; take on an empty stomach (food, especially milk, reduces drug absorption generally)

35
Q

Where do bisphosphonates accumulate? Why is this a problem if given to younger patients?

A

Accumulates at site of bone mineralisation and remains part of bone until it is resorbed - months, years. A worry if will lead to long term effects on younger patients on their bones due to accumulation

36
Q

What are unwanted effects of bisphosphonates

A

Oesophagitis (may need to switch from oral to iv)
Osteonecrosis of the jaw
Atypical fractures

37
Q

What patients have the biggest risk of osteonecrosis of the jaw due to bisphosphonate treatment

A

greatest risk in cancer patients receiving iv bisphosphonates

38
Q

What can atypical fractures reflect in bisphosphonate treatment?

A

may reflect over-suppression of bone remodelling in prolonged bisphosphonate use

39
Q

How does denosumab work as an osteoporosis treatment?

A

Human monoclonal antibody
Binds RANKL, inhibiting osteoclast formation and activity
Hence inhibits osteoclast-mediated bone resorption

40
Q

How is denosumab administered to treat osteoporosis?

A

s.c injection 6/12ly

41
Q

How does teriparatide work as a treatment for osteoporosis?

A

Recombinant PTH fragment - amino-terminal 34 amino acids of native PTH
Increases bone formation and bone resorption, but formation outweighs resorption

42
Q

How is teriparatide administered to treat osteoporosis? Why isn’t it often used?

A

Daily s.c injection but is expensive!

43
Q

What is paget’s disease?

A

Accelerated, localised but disorganised bone remodelling due to excessive bone resorption (osteoclastic overactivity) followed by a compensatory increase in bone formation (osteoblasts) making WOVEN bone which is mechanically weaker so causes bone fragility and hypertrophy and deformity

44
Q

Where is Paget’s disease most prevalent?

A

Highest in UK, N America, Australia and NZ
Lowest in Asian and Scandinavia
Men and women affected equally
Disease usually not apparent under age 50y

45
Q

What is Paget’s disease characterised by

A

Abnormal large osteoclasts that are excessive in number

46
Q

What are clinical features of Paget’s disease of bone?

A 
Skull, thoracolumbar spine, pelvis, femur and tibia most commonly affected
Arthritis
Fracture
Pain
Bone deformity
Increased vascularity  (warmth over affected bone) 
Deafness – cochlear involvement
Radiculopathy – due to nerve compression
47
Q

How is Paget’s disease of bone diagnosed?

A

Plasma [Ca2+] normal
Plasma [alkaline phosphatase] usually increased
Plain x rays =
Lytic lesions (early), thickened, enlarged, deformed bones (later)
Radionuclide bone scan demonstrates extent of skeletal involvement

48
Q

What are treatment options for Paget’s disease?

A

Bisphosphonates – very helpful for reducing bony pain and disease activity
Simple analgesia

Year 2 Endocrinology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions