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Block 5 - Pulm and Skeletal > Skeletal Path > Flashcards

Skeletal Path Flashcards

0
Q

What does bone consist of?

A

Cells

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

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1
Q

What are the two different kinds of bone?

A 
Trabecular = spongy 
Compact = cortical - has concentric haversian patterns, predominates near the periosteum
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2
Q

What are osteoblasts?

A

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

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3
Q

What are osteocytes?

A

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

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4
Q

What are osteoclasts?

A

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

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5
Q

What is the difference between woven bone and lamellar bone?

A

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

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6
Q

What is the first step in the remodeling process?

A

Activation

Signals from osteocyte responding to physical stress in skeleton = mechanotransduction

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7
Q

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

A

2-3 weeks for osteoclasts to remove one unit

3 months for osteoblasts to replace one unit

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8
Q

How does bone modeling contrast to bone remodeling?

A

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

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9
Q

How does RANK signaling in bone remodeling happen?

A

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

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10
Q

What can increase expression of RANKL on osteoblasts?

A

PTH, vitamin D3, or prostaglandins

Would result in increased osteoclasts and increased resorption of bone

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11
Q

What besides osteoblasts produces RANKL?

A

Activated T cells

Involved with bone loss around joint affected with RA

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12
Q

What is osteoprotegerin?

A

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

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13
Q

How do osteoclasts activate osteoblasts?

A

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

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14
Q

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

A

Local hemorrhage

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

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15
Q

What is the first phase of bone repair?

A

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

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16
Q

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

A

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

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17
Q

What is the second phase of bone repair?

A

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

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18
Q

What is the last phase of bone fracture repair?

A

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

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19
Q

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

A 
Infection
Instability at fracture site
Poor bone quality 
Remnants of necrotic bone
Poor nutrition
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20
Q

What are the two ways to get osteomyelitis?

A

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

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21
Q

How does age of patient affect the pattern of osteomyelitis?

A

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

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22
Q

What are clinical manifestations of osteomyelitis?

A

Fever and pain at site of infection

Overlying soft tissue is swollen and erythematous

23
Q

What is present on radiographs in osteomyelitis?

A

Early stages unremarkable - bone not resorbed yet

After a week or so - upregulation of RANKL and down regulation of OPG produce radiolucent lesion

24
Q

What is sequestrum and involucrum?

A

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
Q

What is granulomatous osteomyelitis?

A

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
Q

How does Potts disease present?

A 
Pain
Low grade fever
Chills
Weight loss 
Possible scoliosis or kyphosis from vertebral fractures compressing spinal nerves
27
Q

What is osteopetrosis?

A

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
Q

What are effects of osteopetrosis?

A

Thickening of bones can compress cranial nerves

Hematopoiesis moves to spleen and liver - hepatosplenomegaly

29
Q

What goes wrong in osteopetrosis?

A

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

30
Q

What is osteogenesis imperfecta?

A

Synthesis of type I collagen is defective - defects in alpha 1 and 2 chains
Large spectrum of phenotypes from lethal to mild

31
Q

What are clinical features of osteogenesis imperfecta?

A

Osteopenia
Brittle bone - fracture common and heal slowly
Thin blue sclera, small misshapen teeth, of hearing deficits

32
Q

What is osteomalacia?

A

Softening of bone caused by defective mineralization
Bones weak and prone to fracture from weight bearing
Widened seams line trabeculae

33
Q

What is osteomalacia in children?

A

Rickets
Soft bones as well as overgrowth of growth plates since mineralization of cartilage doesn’t occur - line rib cage = rachitic rosary

34
Q

What causes osteomalacia and rickets?

A

Commonly secondary to vitamin d deficiency

Partly affected by lack of PTH activity

35
Q

When does the growing skeleton reach a peak bone mass?

A

By the third decade
Higher in men than women
Higher in blacks than whites

36
Q

What is type I osteoporosis?

A

Postmenopausal
Increased osteoclast activity - Associated with abrupt loss of estrogen that increases lifespan and reduces lifespan of osteoblasts
Trabecular bone lost more quickly - fractures of vertebra and proximal femur predominate

37
Q

How does estrogen normally keep osteoclasts in check?

A

By up regulating Fas ligand, activating apoptosis program in osteoclasts
By decreasing sensitivity of mature osteoclasts to RANKL

38
Q

What is an additional effect of estrogen deficiency in post menopausal osteoporosis?

A

Increased production of inflammatory cytokines such as IL-7 and TNF - decreases activity of osteoblasts and has antiapoptotic effects in osteoclasts

39
Q

What is type II osteoporosis?

A

Senile - Begins around 30 in men and women
Decreased osteoblasts activity
Slower bone loss than in type I

40
Q

What is secondary osteoporosis?

A

Cushing and prolonged use of exogenous steroids accelerate bone loss - compromise osteoblasts function and decrease calcium absorption from gut –> stimulates release of PTH that activates osteoclasts
Immobilization of limb
Periarticular osteoporosis with RA

41
Q

What is Paget disease of bone?

A

Basic MCU uncoupled - regions of bone where osteoclasts predominate and others where osteoblasts predominate
Classic histologic mosaic pattern

42
Q

What happens in Paget disease of bone?

A

Begins with furious osteoclastic activity producing lytic lesion
Followed by profound osteoblasts activity
In time lesions become quiescent and leave sclerotic deformed bones that are structurally abnormal and weak

43
Q

How does Paget disease of bone present?

A

Begins in mid adulthood and increases with age
Usually asymptomatic
Pain from microfractures most common sign
Weight bearing can cause degenerative secondary joint problems in the hips
Overgrowth of vertebra can compress spinal nerves

44
Q

What are important facts to remember about degenerative joint disease/osteoarthritis?

A

It is asymmetrical
Stereotypically affects a few joints severely
Produces decreased mobility in fingers, spine, and affected joints
Ankylosis typically does not occur

45
Q

How does degenerative joint disease present?

A

First appears in DIP joint of index finger
Spreads gradually to other digits
DIP joints distorted by osteophytes called heberden nodules
Knees, hips, and vertebra involved as disease progresses
No fever or malaise, no prominent inflammation

46
Q

What is the leading cause of bilateral degenerative joint disease of the knees?

A

Obesity

47
Q

What does destruction of articular cartilage in degenerative joint disease result from?

A

Uncontrolled loss of extra cellular cartilaginous matrix
Loss of aggrecan thought to be primary event
ADAMTS 1, 4, 5 capable of degrading aggrecan

48
Q

What are the two main constituents of extra cellular cartilaginous matrix?

A

Type II collagen - tensile strength
Aggrecan - highly hydrated and resists compression
Constantly remodeled like bone

49
Q

What happens in degenerative joint disease once the cartilage starts to break down?

A

Chondrocytes die and articular surface becomes shaggy = fibrillation
Underlying bone becomes sclerotic
Cracks can form and synovial fluid goes through to form subchondral cysts
Eventual all cartilage goes away and bone on bone creates eburnated bone

50
Q

What is important to remember about RA?

A

Dramatically inflammatory
Symmetrical
Affects small joints
Ankylosis occurs

51
Q

How does RA present?

A

Fever and malaise
Symptoms range from sore stiff joints to chest pain or SOB from inflammation of heart and lungs
Begins in 3rd or 4th decade of life
Starts in PIP joints

52
Q

What are rheumatoid nodules?

A

In about 1/4 of patients
Under skin or in lung or heart
Central zone of fibrinoid necrosis surrounded by epithelioid macrophages, lymphocytes, plasma cells

53
Q

What is the pathophysiology of RA?

A

Intimal lining of synovium is hyperplastic and synovium is infiltrated with lymphocytes including cd4 T cells, B cells, macrophages, and plasma cells
Macrophages produce inflammatory cytokines
Synoviocytes produce proteases, prostaglandins, and cytokines that perpetuate inflammation

54
Q

Why do synoviocytes do in RA?

A

Invade joint space forming a sheet or pannus that covers articular cartilage and isolates it from metabolites in synovial fluid

55
Q

What happens to bone and cartilage in RA?

A

Release of IL-1 and TNFalpha from reactive synovium encourages breakdown of cartilage matrix
RANKL from activated lymphocytes stimulates osteoclasts

Block 5 - Pulm and Skeletal (19 decks)

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