endocrine and metabolic bone disorders Flashcards

1
Q

what bone stores and components of it

A

stores 95% of Ca2+, has osteoids (unmineralised bone made from type 1 collagen) and inorganic mineral component (calcium hydroxyapatite crystals- mostly this)

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

cells of bone

A

osteoblasts (produces osteoid and helps mineralise it) and osteoclasts (releases enzymes to break down/RESORB bone)

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

osteoclast differentiation DIAGRAM

A

RANK receptor of osteoclast precursors bind to RANKL receptor on osteblasts to become activated- thus needs osteoblasts

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

receptors that osteoblasts express

A

those for PTH and calcitriol- hence osteoblasts regulates balance between bone formation and resorption

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

how bone looks like

A

cortical (HARD) bone on outside, with trabecular (spongy) bone inside- they are formed in a LAMELLAR pattern (way collagen laid down to make it strong)

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

effect of vit D deficiency on bone in children and adults

A

not enough mineralisation of bone (osteoids)- can lead to LOOSER ZONES (easily have stress fractures- can’t hold body weight) and WADDLING GAIT (way of walking) rickets- growth plates affected= skeletal abnormalities, pain, growth issues and increased fracture risk osteomalacia- growth plates close so growth not affected, but pain, myopathy and increased fracture risk occurs

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

what is tertiary hyperparathyroidism

A

often occurs in chronic kidney disease- chronic low Ca2+ (as kidney can’t produce calcitriiol), hence gland becomes bigger and bigger, so PTH rises and is AUTONOMOUS, increasing Ca2+

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

renal failure and bone disease DIAGRAM

A

less calcitriol and PO4 excretion, and PO4 binds to calcium, so these 2 things= hypocalcaemia this leads to high PTH= high bone resorption, as well as less bone mineralisation (as not enough calcium), which gobbles up bone and calcifies BLOOD VESSELS; this can lead to brown tumours ie gobbled up bone (osteitis fibrosa cystica)

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

treatment of osteitis fibrosa cystica (hyperparathyroid bone disease)

A

low phosphate diet and phosphate binders to prevent XS phosphate alphacalcidol (active D3) parathyroidectomy for tertiary hyperparathyroidism

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

what is osteoporosis and effect on men/women

A

loss of trabeculae, lower mass of bone and increased RISK OF FRACTURE bone mass goes down for both women and men, but goes down a lot POSTMENOPAUSE

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

define osteoporosis and score threshold

A

bone mineral density ie bone MASS greater than 2.5 SD’S BELOW average value of young healthy adults (T score of -2.5 or lower)

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

how to measure BMD

A

using DEXA scan of lumbar spine and neck- measures mineral content ie bone mass

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

osteoporosis vs osteomalacia

A

although both cause increased fracture risk, malacia is due to vit D deficiency causing less MINERALISATION, whereas osteoporosis is where resorption exceeds formation= less bone MASS also, serum levels normal is osteoporosis, so diagnosis via DEXA scan , but serum levels in malacia bad (low Ca, high PTH), so diagnosis via blood test

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

predisposing conditions for osteoporosis

A

postmenopausal oestrogen deficiency (leads to loss of bone) age related lack of osteoblasts (occurs as u age) hypogonadism (low LH/FSH= low oestrogen) endocrine problems like cushings, hyperthyroidism and primary hyperpara. drugs eg glucocorticoids/heparin

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

consequences of hip fracture

A

20% with the fracture dead within a year, 80% cannot independently do one activity in daily life

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

treatment of osteoporsis

A

oestrogen, bisphosphonates, denosumab, teriparatide

17
Q

oestrogen- what it does, problem

A

treats post menopausal women to prevent bone loss however, its a short term solution- can lead to breast cancer, and must be taken with progestogen to prevent endometrial hyperplasia/cancer

18
Q

bisphosphonates- mechanism

A

binds to hydroxyapatite crystals- osteoclasts ingest this and become paralysed, then death= less gobbling up of bone= less bone turnover

19
Q

uses of bisphosphones

A

FIRST LINE treatment for osteoporosis also for hypercalcaemia of malignancy- reduces bone pain and reduces hypercalcaemia (as osteoclasts die) paget’s disease- reduces pain severe hypercalcaemic emergency (rehydration first)

20
Q

pharmocokinetics of bisphosphonates

A

given as tablet but poorly absorbed- MUST take on empty stomach can paralyse osteoclasts for years

21
Q

side effects of bisphosphonates

A

oesophagitis- can irritate oesophagus when taken orally osteonecrosis of jaw (breaking down)- cancer patients most at risk atypical factures- because bone remodelling has become ADYNAMIC (no longer dynamic as osteoclasts not working), can lead to fractures

22
Q

denosumab DIAGRAM

A

binds to RANKL on ostebblasts, preventing osteoclasts precursor from binding and differentiating 2nd line- taken every 6 months unlike bisphosphonates

23
Q

teriparatide

A

recombinant PTH- increases both formation and resorption/reabsorption, but formation MORE 3rd line treatment as EXPENSIVE

24
Q

what is paget’s disease and how it occurs

A

excessive bone resorption by ABNORMAL osteoclasts- compensate by laying down lots of bone, but in an unorganised way (WOVEN rather than laminar)- thus weaker= hypertrophy and frailty

25
Q

epi of pagets disease- prevalence, who affected

A

prevalence different- more in white countries: disease of elderly in both males and females

26
Q

clinical features of pagets

A

skull, pelvis, spine and leg (tibia/femur) bones most affected- leads to fractures, pain, deformed bone, increased warmth (osteoclasts/blasts active) and deafness (cochlea affected)

27
Q

diagnosis of pagets

A

Ca2+ normal but ALKALINE PHOSPHATASE increased xrays show enlarged deformed bones- radioactivty also shows busy bones

28
Q

treatment of pagets

A

bisphosphonates (switch off osteoclasts) analgesia