Other Bone Problems Flashcards
What is the risk of osteoporosis based on
Peak bone mass
+
Rate of bone loss
What is osteoporosis
Lots of trabecula spongy bone mass – >
form POROUS (porosis..) bone – >
increased risk of fracture
Despite
normal bone mineralisation +
lab values of calcium + phosphate
What age is the peak bone mass occurring
30
What three things determine how high the peak bone mass will be?
Diet
Exercise
Inherited vitamin D receptor
What are the determinants of bone loss rate?
Diet
Exercise
For women – oestrogen:
@menopause – >lose oestrogen – >lose bone mass rapid I.e. increased bone resorbtion
What test is used to check for osteoporosis?
And what is the T score to determine osteoporosis?
Bone mineral density test = DEXA
T score < -2.5
Two types of osteoporosis?
Type 1 = postmenopausal
Type to senile > 70 years
Where do you fractures usually occur in osteoporosis?
Weight-bearing areas:
Vertebrae –> decreased height + kyphosis
Hip - femoral neck
Distal radius - COLLES fracture
In osteoporosis what are the lab works like?
Normal – calcium/phosphate/ALP = HALLMARK
What is the prophylaxis treatment for osteoporosis
Weight-bearing exercise
Decent calcium/vitamin D in adulthood/childhood
Treatments for osteoporosis
Bisphosphonate is:
attach to bone – >osteoclast eat bisphosphonate – > osteoclast apoptosis – > decreased bone resorption
Oestrogen replacement therapy – could cause breast cancer
Denosumsb - monoclonal antibody against RANKL
What drug is contra indicated for osteoporosis
Glucocorticoids
What happens in pagets disease of bone
Osteoclast + osteoblast function in balance
Four stages of pagets disease of bone
1.osteoclastic lytic stage:
Osteoclast goes crazy – resorb bone without permission of osteoblast
- Mixed osteoclast osteoblast stage:
Bone very weak – osteoblast recognises need to lay down bone ASAP to protect - Osteoblastic sclerotic stage:
Osteoclast burns out –> osteoblasts only lays bone in rush -> sclerotic thick bone - Quiescent stage decreased osteoblast osteoclast activity
What age does Padgett’s affect?
Aetiology?
Localisation?
60 years
Unknown – possibly viral – infect osteoblast
Localised = 1+ bones BUT not @ entire skeleton
What do you see on histology for pageants disease of bone
Cement lines @bone = not sealed
-> Thick bone BUT fragile – >
Mosaic pattern of lamellar bone
Clinical features of pagets
Pain ALP⬆️ Grrrrrr lion face Ear - hearing loss Thicken calvarium @school – > ⬆️Hat size
Treatment for Paget bone disease
Calcitonin – inhibit osteoclast
BISPHOSPHONATES
2 complications are Padgett disease of bone
Remodelling of bone – > form arteriovenous shunts
-> hard pushed to aviation – >
high output cardiac failure
Osteoplast produces loads of bone – >
osteoblasts mutate – >osteosarcoma
In Rickets + osteomalacia what is the problem
Defective mineralisation of osteoid due to vitamin D deficiency
What are the risk factors for rickets/osteomalacia
Decreased sun exposure
Shit diet
Malabsorption – vitamin D = fat soluble vitamin
Liver + renal failure – need it to activate vitamin D
How does a child with rickets presents?
Frontal bossing – enlarged forehead = Osteoid deposition
Pigeon breast deformity:
inward bending of ribs +
anterior protrusion of sternum
Rachitic rosary(beads THASBY!!!): Osteoid deposition @costochondral junction
Bowlegged – >1 years start walking
Who get osteomalacia
Vitamin D deficiency in adults
Lab work for osteomalacia/Ricketts
Decreased vitamin D – >decreased serum calcium- >
Increased PTH secretion – >
- decreased phosphate serum
- osteoblast hyperactivity – >increased ALP
What happens in achondroplasia
Disorder of cartilage proliferation @ growth plate
Explain the pathogenesis of achondroplasia
85% – Sporadic mutation
15% – autosomal dominant + full penetrance – lethal
->
Activating mutation @ fibroblast growth factor 3
(FGF – 3) – >
Inhibit chondrocyte proliferation – >impaired cartilage proliferation @growth plate – >
Short extremities only
At embryology what are the two ways to form bone
1.intramembranous:
Connective-tissue matrix –>
form woven bone of skull + chest + flat bones of wrist
- Endochondral bone formation:
Establish cartilage matrix -> cartilage dies -> calcifies + mineralised -> form woven BONE - long
-> lamellar bone
Explain how the chondrocyte make cartilage at the growth plate
Chondrocytes make cartilage – >
growth plate expands – >
Chondrocytes die @ edge of plate – >
dead chondrocytes replaced with bone = longer
In achondroplasia there’s a problem with the chondrocyte proliferation hence why the short extremities
Explain osteogenesis imperfecta
Autosomal dominant defect in collagen type one synthesis – >
Congenital defect in formation – >weak bone
Clinical features of osteogenesis imperfecta
Blue sclera –
thinning of squirrel collagen – >
reveal choroidal veins = blue
Hearing loss – break malleus incus stapes
Multiple fractures because of shit collagen
Explain osteoPETROSIS pathogenesis
Inherited defect of bone result shown due to defective osteoclast – >
thick dense bones prone to fracture
Where is the mutation in osteopetrosis
Carbonic anhydrase 2 mutation –
Need acid environment to resorb bone i.e. remove calcium
What does x-ray reveal osteopetrosis
Bone in bone appearance – can’t see dark space outside of medulla
Explainwhy we get pancytopenia in osteopetrosis
CA deficiency – >bone thickens – >
Fills medullary/marrow space =
MYELOPHTHISIC process – > pancytopenia
Explain why there is vision and hearing loss in osteopetrosis
CA deficiency – >bone thickens – >
compress cranial nerves = vision and hearing decrease
Explain why we get hydrocephalus in osteopetrosis
CA deficiency – >
bone thickens @Foramen Magnum = narrow – >
Hydrocephalus
Explain rather get renal tubular acidosis and osteopetrosis
Decreased CA – >Decreased H+ – >
can’t excrete enough H+ & No net gain of HCO3 ->
Acidotic
Treatment for osteopetrosis and why?
Bone marrow transplant
Haematopoiesis well –>
make normal monocytes – >
make normal macrophages e.g. osteoclasts
Most common reason for dwarfism
Achondroplasia
Explain the relationship between oestrogen and osteoporosis
Oestrogen inhibits apoptosis in osteoblasts
Oestrogen induces apoptosis in osteoclasts
At menopause get XS remodelling cycles and XS bone resorption
