Metabolic Bone Disease Flashcards

1
Q

Bone matrix

A

Made of collagen support surrounded by hydroxyapatite for stregnth

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2
Q

Osteoproroiss
Osteomalacia/rickett’s
Paget’s overview

Formation and resorption

A

Decreased formation, increased resorption…increase due to age/hormonla

Decreased ofrmation, no resorption change…decreased mineralization of collagen matrix

Increased formation but nbigger increased resorption…local overactivation of osteoclasts

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3
Q

Bone strenght is

A

Quantity of bone plus quality of architecture

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4
Q

T score and Z score

A

T score compares to white female

Z score compares to cohort

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5
Q

Osteoporosis pathophys

A

Loss of bone strenght due to altered uqualith and quantity

Loss of collagen support and hydroxyapatite

Imbalance betwen turnover and formation

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6
Q

Osteoporosis types

A

Postmenopausla or primrary - aging/hormonal

Secondary -younger

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7
Q

Notable osteopororiss risk factors

A
Female
Low BW 
Excess alcohol
low Vit D or calcium
Cig
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8
Q

Osteoporosis signs and symptoms

A

Asymptomatic until fragility fracture occurs

Normall thoracic/lumbar spine of hip

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9
Q

Diagnosis of osteoporosis

A

Post menopausal women or men over 50

T score

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10
Q

Osteopenia diagnosis

A

Postmeno women or men over 50

T scroe between -1 and -2.5

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11
Q

Osteomalacia and rickets

A

Impact mineralization of the collagen matrix of bone

Osteomalacia only in adults and involves cortical only
Rickets in children and involves cortical bone, growth plates ,and cartilage

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12
Q

Osteomalacia vs. porosis

A

Malacia - normal matrix with decreased mineralization

Porosis - decreased matrix and mineraliaation

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13
Q

Osteomalacia and ricket presentation

A

Bone and muscle weakness, tenderness, fracture,s wddling

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14
Q

Osteomalacia diagnostic eval

A

DEXA may be normal or show decreased B

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15
Q

Osteomalacia and ricket pathophys

A

Abnormalities in Vit D and calcium

Abnormalitlies in phopshorus

Abnormalities in enzymes needed to mineralize bone (alkaline phosphatase)

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16
Q

Abnormailites in Vit D

A

Vit D deficiency

Inability to produce inactive form - liver dz

Antiepileptics

Inability to convert to active - chronic kidney dz or dependent rickets type 1

17
Q

Osteomalacia and rickets phosphorus abnormalities

A

Decreased dietary
Decreased absorption

Renal phosphate wasting (tubular defect, hypophosphatemia, oncogenic osteomalacia, tenofovir)

18
Q

Familial hypophosphatemia

A

Defect in FGF 23 causing renal phsophate wwasting

Xlinked most common

Hypopohios, slowgrwoth, enthesopathy, dental carries

Tx with calcitrol and phosphorus

19
Q

Osteogenic osteomalacia

A

Tumors that produce FGF23

Low phosphorus and osteomalacia

Remove tumor

20
Q

Hypoposphatasia

A

Decreased alkaline phosphatasia

Pyrophosphate deposits and inhibits mineralization

Enzyme replacemrnt or BMT

21
Q

Paget’s dz pathogenesis

A

Abnormal osteoclasts activity resulting in excessive bone remodeling

Affects speciic areas

Overgrowth in some and under in other

22
Q

Paget’s clinical presentation

A

Arthritis, bleeding, bone pain

Asymptomatic elevation of alkalaine phosphate or incidental rediographic finding**

23
Q

Paget’s most common bones

A

Pelvis, lumbar spine, femur

24
Q

Diagnositc eval of Paget’s

A

Elevation in alkaline phosphatase

X-ray

Bone scan

25
Q

Paget’s dz hallmarks

A

Osteoporosis circumscripta

Blade of grass sign

Cotton wool skull

26
Q

Diagnosis of Paget’s

A

Radiographic evidecne with an elevated alkaline phosphatase

Bone biopsy only need if evidence of osteosarcoma

27
Q

Indication for tx Paget’s

A

Symptomatic OR

asympto with active dz and a lesion

28
Q

Paget’s tx

A

Bisphosphonates - 1st line bc inhibit bone resoprtion by osteoclasts

Calcitrol - 2nd line

Surgery

29
Q

Complications of Paget’s

A

Hyperparathyroidism, osteosarcoma,