Msk: Metabolic Bone Disease

Front 1

T or F: Intrinsic bone diseases present w/ serum Calcium abnormalities

Back 1

FALSE

Front 2

name 4 intrinsic bone diseases

Back 2

osteoporosis
osteogenesis imperfecta
osteopetrosis
Paget disease

Front 3

T or F: Extrinsic bone diseases often present w/ serum Ca2+ abnormalities

Back 3

TRUE

Front 4

name 4 extrinsic bone diseases

Back 4

primary hyperparathyroidism
secondary hyperparathyroidism
osteomalacia/rickets
renal osteodystrophy

Front 5

what is the primary purpose of PTH?

Back 5

increase serum Ca++

Front 6

what is the action of PTH on bone?

Back 6

increases Ca++ release
increases PO4--- release

Front 7

what is the action of PTH in the kidney?

Back 7

increases Ca++ resorption (in the distal tubule)
decreases PO4 resorption
This is how you get a net increase in serum Ca++

Front 8

what is the action of PTH in the gut?

Back 8

indirectly increases Ca++ absorption
Note: No direct effects

Front 9

where are the PTH receptors in the bone?

Back 9

on the osteoblasts

Front 10

how does PTH lead to the stimulation of osteoclasts?

Back 10

osteoblasts secrete osteoclast activating factors (OAFs) when PTH is bound

Front 11

In normal Ca++ homeostasis, what compensates for small fluctuations in serum Ca?

Back 11

Lining Cell-Osteocyte Complex (LCOC)

Front 12

what happens if the threshold of the LCOC is surpassed?

Back 12

the Bone Multicellular Unit (BMU) is recruited to raise serum Ca++ often at the expense of the structural integrity of the bone

Front 13

define osteopenia

Back 13

a general term used to refer to states of low absolute amounts of bone mineral (this includes osteoporosis and osteomalacia)

Front 14

define osteoporosis

Back 14

there is normal mineralization in a decreased amount of total bone

Front 15

define osteomalacia

Back 15

decreased mineralization of a normal amount of total bone

Front 16

a state of high absolute amounts of bone mineral -->

Back 16

osteosclerosis

Front 17

a disease state characterized by an increase in the number of BMUs is __ and is seen in __ and __

Back 17

high turnover osteoporosis seen in hyperPTH and postmenopausal bone loss

Front 18

__ is characterized by a normal number of BMUs but impaired recruitment of osteoblasts.

Back 18

low turnover osteoporosis

Front 19

__ occurs in normal aging and accounts for the bone losses seen in men and women as they get older

Back 19

low turnover osteoporosis

Front 20

at physiologic or slightly elevated levels of PTH __ responds by increasing the efflux of Ca++ from bone

Back 20

LCOC

Front 21

subperiosteal bone resporption and large cystic lesions referred to as Brown tumors -->

Back 21

high turnover osteoporosis

Front 22

stones, bones, groans, psych overtones -->

Back 22

hyperparathyroidism

Front 23

what is the most common cause of hypoPTH?

Back 23

damage or removal of the PTH glands during surgery

Front 24

decreased serum Ca++, increased serum PO4, decreased urinary PO4 excretion -->

Back 24

hypoPTH

Front 25

what is pseudohypoparathyroidism?

Back 25

then the kidneys and bone can't respond to PTH --> hypoCa++ and hyperPO4 occur despite elevated PTH

Front 26

What are some features of Albright hereditary osteodystrophy?

Back 26

pseudohypoPTH, short stature, round facies, shortened 4th fingers

Front 27

ergocalciferol -->

Back 27

D2

Front 28

cholecalciferol -->

Back 28

D3

Front 29

in what range are serum levels of Ca++ in pts w/ Vit D deficiency?

Back 29

low-normal

Front 30

for normal hydroxyapatite formation, the product of the serum __ and __ must exceed __

Back 30

Ca++ * PO4 > 30

Front 31

when Ca * PO4 < 30 what occurs?

Back 31

osteomalacia (decreased mineralization in a normal amount of bone)

Front 32

what are the histological hallmarks of osteomalacia?

Back 32

widened osteoid seams in regions of bone remodeling

Front 33

in skeletally immature pts, osteomalacia is referred to as __

Back 33

rickets

Front 34

in early stage renal failure, what happens to serum PO4 levels?

Back 34

they increase

Front 35

how does renal disease lead to secondary hyperparaPTH (osteomalacia)?

Back 35

high serum PO4 directly stimulates release of PTH, inhibits hydroxylation of VitD and directly lower serum Ca++ levels

Front 36

what is renal osteodystrophy?

Back 36

the combination of secondary hyperPTH, osteomalacia, and osteosclerosis

Front 37

mineralization of previously osteomalatic bone leads to __

Back 37

osteosclerosis

Front 38

what is the most common metabolic bone disease?

Back 38

involutional osteoporosis

Front 39

T or F: postmenopausal osteoporosis is characterized by greater loss of cortical bone over trabecular

Back 39

FALSE

Front 40

post menopausal osteoporosis: high or low turnover state?

Back 40

high

Front 41

vertebral and Colles fractures -->

Back 41

postmenopausal osteoporosis

Front 42

vertebral and proximal femur fractures -->

Back 42

age-related osteoporosis

Front 43

T or F: hyperthyroidism can cause secondary osteoporosis

Back 43

TRUE

Front 44

what would serum Ca++ in thyrotoxicosis?

Back 44

elevated!!!

Front 45

osteogenesis imperfecta results from the inability to form __

Back 45

Type 1 collagen

Front 46

the __ result from a primary defect in osteoblastic function in which the cells form abnormal extracellular glycoproteins

Back 46

mucopolysaccharidoses

Front 47

what is the inheritance of the most common OI?

Back 47

AD

Front 48

what is the primary defect in osteopetrosis?

Back 48

lack of osteoclastic bone resorption

Front 49

why are pts w/ osteopetrosis prone to infection?

Back 49

b/c they lose marrow space

Front 50

high alk phos w/ normal Ca++ and PO4 with rapid remodelling -->

Back 50

Paget's Disease of Bone

Front 51

primary or secondary hyperPTH: hypophosphatemia

Back 51

Primary

Front 52

hyperCa++ and hypoPO4 -->

Back 52

primary hyperPTH

Front 53

what is an example of an osteoclast activating factor you should know for a test?

Back 53

Rank ligand

Front 54

what is the main mechanism of steroid-induced osteoporosis?

Back 54

osteoblast precursor inhibition