parathyroid disorder/paget dz Flashcards
paget disease
localized disorder of bone remodeling
-begins with excessive bone resorption followed by an increase in bone formation
what is a bone feature of paget disease?
woven bone- structurally disorganizzed mosaic of bone that is weaker, larger, less compact, more vascular and more likely to fracture
what are the clinical features of paget disease?
most are asx;
- bone pain (most common sx)
- secondary osteoarthritis (when it occurs around a joint)
- excessive warmth (due to hypervascularity)
- neurologic complications (compression of neural tz)
what bones are most likely to have paget disease?
single bone but is more frequently multifocal. It has a predilection for the axial skeleton (ie, spine, pelvis, femur, sacrum, and skull, in descending order of frequency), but any bone may be affected.
-After onset, Paget disease does not spread from bone to bone, but it may become progressively worse at preexisting sites.
etiology of paget
widely unknown, maybe genetic/enviormental
- white ppl
- measles, RSV
what are the three phases of Paget dz?
lytic
mixed lytic and blastic
sclerotic
what is the lytic phase of PD?
normal bone is resorbed by abnormal osteoclasts (larger more nuclei)
what is the mixed phase?
rapid increases in bone formation from numerous osteoblasts, but normal looking
BUT new bone is abnormal w/ collagen fibers depositid in a bad fashion, rather than linerally
high degree of bone turnover
what is the sclerotic phase?
woven bone patter- allows bone to be infiltrated by excessive fibrous connective tissue and BV- eventually this burns out (sclerotic) and the condition becomes quiescent
what are some complications if the skull is involved in PD?
Deafness Vertigo Tinnitus Dental malocclusion Basilar invagination Cranial nerve disorders
verterbral involvment of PD?
nerve root compressions or cauda equina syndrome
lab findings in Paget dz?
serum Ca, Phosphorous, and PTH are all normal
*might see hypercalcemia
what are some markers of bone turnover that are usefule to monitor in pt w/ aget dz?
- Bone-specific alkaline phosphatase (marker of bone formation)
- Deoxypyridinoline (marker of bone resorption)
- N -Telopeptide of type I collagen (marker of bone resorption)
- Alpha-alpha type I C-telopeptide fragments
tx of paget dz
tx isn’t curative but control progression
bisphosphonate tx
Ca, vit D , NSAIDs
drug tx of PD
Etidronate
Pamidronate
Alendronate
Tiludronate
Risedronate
Zoledronic acid
Salmon calcitonin
Pamidronate and salmon calcitonin are administered parenterally. (Human calcitonin is no longer available.
what does PTH do?
causes serum Ca to increase by mobilizing osteoclasts, stimulates the kidneys to resorb Ca and increases GI absorption of Ca
what is the main cause of primary hyperparthyroidism?
benign parathyroid gland adenomas
what are other causes of primary HyperPT?
hyperplasia, carcinomas
what is the etiology of hyperPT?
W>M, incidence increases after 50 yo
what is the most common cause of hypercalcemia in hospitalized pts?
malignancy
what other disorders might cause hypercalcemia?
renal failure milk-alkali syndrome multiple myeloma head-neck-lung Ca sarcoidosis TB medications(thiazides, Ca, Vit D, lithium) Hodgkin lymphoma adrenal insufficiency prolonged bed rest hyperthyroidism (secondary hyperPT)
hyperPT and CKD?
secondary hyperPT is caused by hyperphosphatemia that increases ionized Ca levels and decreased renal production of active vit D
sx of hyperPT/
mild-asx
thrist, anorexia, N, V, abdominal pain, constipation, fatigue, anemia, weight loss, PUD, pancreatitis, HTN, depressed tendon reflexes
polydypsia and polyuria caused by hypercalcemia induced nephrogenic DI
“stones bones groans and psychiatric moans”
stones: renal loss of Ca and Phosphate
bones: bone loss from PTH (cortical bone or diffuse bone demineralization=traecular bone increase)
pathologic fractures=cystic bone lesion (jaw)
groans: increased GI absorption and abdominal cramps
moans: irritability, psychosis, depression
