Bone Disorders (osteoporosis, etc) Flashcards
osteoporosis is due to loss of what kind of bone
loss of trabecular (spongy) bone and inteconnections
MC type of fracture in osteoporosis
vertebral crush fractures–> acute back pain, loss of height, kyphosis (forward bending of the spine)
Type II osteoporosis
senile osteoporosis–> seen in men and women over 70 years old
causes of type II osteoporosis (2)
- progressive decline in osteoblast function and increased osteoclast function (more resorption than formation
- decreased activity
what causes type I, or postmenopausal osteoporosis (mechanism)
- ↓ estrogen leads to increased IL-1, IL-6 and TNF by monocytes and cells in marrow
- these enhance expression of RANKL (on osteoblasts) and RANK (on osteoclast precursor) ⇒ increased production of osteoclasts
*also ↓ expression of OPG, which is a soluble receptor that binds RANK-L and prevents stimulation of osteoblast precursor
what are two other fracture other than vertebral that osteoporosis characterisically causes
- femoral neck fx
- Colles’ fx–> fx of distal radius
*these occur after falls from normal height, not harsh trauma
Serum Ca, Phos, Alk phos, and PTH in osteoporosis
all normal
treatment of osteoporosis
- Stop smoking, drinkin, using corticosteroids
- weight-bearing exercise
- Vitamin D and Ca supplements
- Bisphosphonates
- PTH tx (anabolic agent on bone)
drug that is an analogue of PTH
teriperatide–> cant use for more than 3 years
how do bisphosphonates work
pyrophosphate analogues–> bind hydroxyapetite in bone, inhibiting osteoclast resorption of bone
denosunab MOA (used for extreme osteoporosis)
RANK-L inhibitor (like OPG), inhibits osteoclast activity
which SERM can be used in osteoporosis to reduce risk of vertebral fracture
raloxifene–> only helpful for vertebral fx, also reduces risk of Breast CA
2 AEs of bisphosphonate use
- erosive esophagitis (wash down with lots of water)
2. osteonecrosis of the jaw
disease with thickened, dense bones that are prone to fx
osteopetrosis (marble bone disease)
what is the defect in osteopetrosis and what cells does it affect
defective carbonic anhdrase II–> failure of normal bone resorption due to impaired osteoclast function (need it to generate acidic environment for bone resorption)
what x-ray finding is seen in osteopetrosis
“bone in bone” appearance–> bones will flare at the end
- erlenmeyer flask deformity–> distal metaphysis of radius and ulna are flared
what two complications can be seen with osteopetrosis
- pancytopenia/ extramedullary hematopoiesis (due to bone marrow being replaced by more bone)
- cranial nerve impingement/ palsy–> compression by increased bone (vision or hearing loss!!)
serum Ca, Phos, Alk phos, and PTH in osteopetrosis?
usually normal; possible mild increases in Ca, Alk phos, or PTH, but serum Ca is usually NORMAL
bone pain, enlargement of bone, headaches, hearing loss
Paget’s disease of bone (osteitis deformans)
what kind of pt would be most likely to present with Paget’s
man over 50 with pain and poorly fitting hats, maybe trouble hearing; esp white dudes
what three bones affected in Paget’s
pelvis, skull, femur
characteristic bone pattern in Paget;s
mosaic “woven” bone–>
what goes wrong in Paget’s
LOCALIZED disorder of bone remodeling caused by increase in both osteoblast and osteoclast activity
serum Ca, Phos, Alk phos, PTH in Pagets
↑ Alk phos only–> highly characterisitic!!
3 complications of Paget’s
- pathologic fractures
- risk of osteogenic sarcoma
- risk of high-output heart failure (due to arteriovascular connections in bone)
osteomalacia/ rickets causes
Vitamin D deficiency
what does vitamin D deficiency do to cause trouble
leads to impaired minerlaization/ calcification of osteoid–> soft bones
What are serum Ca, Phos, Alk phos and PTH in vitamin D deficiency
- ↓ serum Ca (leads to–>)
- ↑ serum PTH (leads to–>)
- ↓ serum Phos
- ↑ Alk phos (due to increased osteoblast activity)
disease caused by hyperparathyroidism
Osteitis fibrosa cystica (von Recklinghausen disease of bone)
how does increased PTH lead to trouble in bone
increased PTH–> increased osteoclast activity (have PTH receptors), particulary when PTH levels are very high
characteristic lesions in osteitis fibrosa cystica
“Brown tumors”–> are cystic spaces in bone that are lined by osteoclasts filled with fibrous stroma and blood
*remember cysts= lined by epithelial tissue
labs in osteitis fibrosa cystica
- ↑ serum Ca
- ↓ serum PTH
- ↑ Alk phos (indicates bone turnover)
- ↑↑ PTH
Type 1 psuedohypoparathyroidism__. other name
Albright hereditary osteodystrophy
what is the issue in Apbright heridiatry osteodystrophy
PTH resisitance at the renal tubules–> dump calcium and keep phosphate (since cant respond to PTH) = get low serum calcium, high phosphate, but with a high PTH level
*can look a lot like osteitis fibrosa cystica; labs are the same
Serum Ca, Phos, Alk phos, and PTH in renal insufficiency
- ↓ Ca
- ↑ Serum Phos
- normal or increased Alk phos
- ↑ PTH
- decreased calcium because no vitamin D is being made in the kidney, also cant excrete phosp, due to poor renal function
serum Ca, Phosp, Alk phos, and PTH in vitamin D toxicity
- ↑ Ca
- ↑ Phos
- normal Alk phos
- ↓ PTH
*Vit D causes lots of calcium, since it causes Ca to be resorbed in kidney and intestines and also causes release from bone (resorption). High Ca causes PTH to decrease, which causes phos to be high (PTH is phos dumping hormone)
