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Block 5 - Pulm and Skeletal > Skeletal Path > Flashcards

Flashcards in Skeletal Path Deck (56)
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0

What are the two different kinds of bone?

Trabecular = spongy
Compact = cortical - has concentric haversian patterns, predominates near the periosteum

1

What does bone consist of?

Cells
Matrix - type 1 collagen, non collagenous proteins, hydroxyapatite (calcium and phosphorous)

2

What are osteoblasts?

Synthesize type I collagen and non collagenous proteins of matrix called osteoid until it is mineralized
Osteoid seam eventually mineralized by deposition of hydroxyapatite
Create local alkaline environment favorable for mineral deposition
Receptors for PTH, estrogen and vitamin d

3

What are osteocytes?

Pseudopodia communicate with each other and osteoblasts to control calcium and phosphorous homeostasis
Sensitive to mechanical forces and microfractures and send signals to osteoblasts to initiate remodeling or repair

4

What are osteoclasts?

Differentiate in response to M-CSF, RANKL, interleukin 1, and TNF
Dissolve mineral in matrix by acidifying extra cellular space
Excavations are called Howship's lacunae

5

What is the difference between woven bone and lamellar bone?

Lamellar - collagen fibers parallel and small uniform osteocytes throughout
Woven - formed quickly in response to injury, osteocytes more numerous and variable in size, collagen fibers not as arranged - low tensile strength, replaced by lamellar bone in time
Woven is abnormal in adult skeleton except a tendon insertions

6

What is the first step in the remodeling process?

Activation
Signals from osteocyte responding to physical stress in skeleton = mechanotransduction

7

How long does removing a unit of bone and replacing it take in middle age trabecular bone?

2-3 weeks for osteoclasts to remove one unit
3 months for osteoblasts to replace one unit

8

How does bone modeling contrast to bone remodeling?

Predominantly in developing and growing skeleton
As bone grows metaphysis must narrow to width of diaphysis - osteoblasts and osteoclasts key but not coupled as in remodeling

9

How does RANK signaling in bone remodeling happen?

RANKL on surface of osteoblasts - binds to RANK on osteoclast precursors to make them differentiate and mature

10

What can increase expression of RANKL on osteoblasts?

PTH, vitamin D3, or prostaglandins
Would result in increased osteoclasts and increased resorption of bone

11

What besides osteoblasts produces RANKL?

Activated T cells
Involved with bone loss around joint affected with RA

12

What is osteoprotegerin?

Decoy receptor for RANKL produced by osteoblasts and other cells - blocks interaction of RANK with RANKL
Competes with RANK and ratio regulates osteoclasts

13

How do osteoclasts activate osteoblasts?

Release anabolic cytokines like ILGF-1 and TGFbeta from digested bone matrix

14

What is one of the first things that happens after a bone fracture and why?

Local hemorrhage
Complete fracture disturbs periosteal, medullary and cortical vessels traversing haversian system

15

What is the first phase of bone repair?

Inflammatory
Produced when hematoma from hemorrhage is source of kinins, prostaglandins, and inflammatory mediators such as FGF, PDGF, and TGFbeta

16

What happens towards the end of the inflammatory phase of bone repair?

After one week influx of angioblasts and fibroblasts produce procallus - soft and does not stabilize fracture

17

What is the second phase of bone repair?

Reparative phase
Blood clot is organized
Over several weeks osteoclasts remove necrotic bone at ischemic ends of fracture as chondroblasts and osteoblasts from progenitor cells in periosteum and medullary cavity produce cartilage (outside) and woven bone (inside) to form hard callus

18

What is the last phase of bone fracture repair?

Remodeling phase
Cartilage and woven bone replaced by lamellar bone
Lasts from months to years

19

What are the common causes of delayed healing of bone fractures?

Infection
Instability at fracture site
Poor bone quality
Remnants of necrotic bone
Poor nutrition

20

What are the two ways to get osteomyelitis?

Organisms delivered hematogenously (s aureus most common)
Infection directly from overlying ulcers, periodontal disease, or protrusion of fractures bone through skin (polymicrobial)

21

How does age of patient affect the pattern of osteomyelitis?

In hematogenous, depends on vascular pattern at physis
Neonate - metaphyseal vessels penetrate physis and extend into epiphysis so bacteria can lodge on either side
Actively growing - vessels don't penetrate growth plate - osteomyelitis develops in metaphysis
Adult skeleton - vessels communicate with epiphysis again

22

What are clinical manifestations of osteomyelitis?

Fever and pain at site of infection
Overlying soft tissue is swollen and erythematous

23

What is present on radiographs in osteomyelitis?

Early stages unremarkable - bone not resorbed yet
After a week or so - upregulation of RANKL and down regulation of OPG produce radiolucent lesion

24

What is sequestrum and involucrum?

S - fragments of necrotic bone left over in osteomyelitis that need to be removed
I - sleeve of new bone made by periosteal osteoblasts around dead infected bone once exudate penetrates cortex and elevates periosteum

25

What is granulomatous osteomyelitis?

Occurs in small percentage of tb
Most commonly thoracic and lumbar vertebrae - affected collapse and inf spreads into adjacent bones and soft tissue
More destructive than pyogenic osteomyelitis

26

How does Potts disease present?

Pain
Low grade fever
Chills
Weight loss
Possible scoliosis or kyphosis from vertebral fractures compressing spinal nerves

27

What is osteopetrosis?

Group of genetic diseases with decreased osteoclast function
Sclerosis or hardening of skeleton
Bones dense but abnormally brittle and fractures common
Can be cured by hematopoietic stem cell transplantation

28

What are effects of osteopetrosis?

Thickening of bones can compress cranial nerves
Hematopoiesis moves to spleen and liver - hepatosplenomegaly

29

What goes wrong in osteopetrosis?

Loss of carbonic anhydrase II prevents osteoclasts from acidifying extra cellular environment