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Unit 2: LGS > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Osteoblast

  • function
  • derived from
A
  • build bone

- come from mesenchymal cells (lineage with cartilage and muscle cells)

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2
Q

Osteoclast

  • function
  • anatomy
  • lineage
  • signaling molecule
A
  • break down bone (re-absorption)
  • multi-nucleated: fusion of monocytes
  • lineage: Hematopoietic stem cells
  • signaling molecule: RANKL (critical for differentiation of osteoclasts)
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3
Q

RANKL inhibitor

A

-used for cancer

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4
Q

Osteocyte

  • derived from?
  • special feature
  • signaling molecule
A
  • osteoblasts trapped in bone matrix they were creating
  • as bone begins to mineralize the cells will send out dendritic projections to communicate with other osteocytes
  • express RANKL
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5
Q

Bone lining

A
  • quiescent osteoblast
  • after wave of bone formation has occurred they will line bone everywhere
  • activate immediate formation and recruit other cells
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6
Q

Bone perfusion

A
  • arteries that allow for blood to flow through bone

- peripheral arterial disease leads to osteoporosis

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7
Q

Nutrient artery

A

-main entrance of blood in bone

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8
Q

What arteries feed diaphysis?

A
  • ascending and descending medullary artery

- connect to nutrient artery

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9
Q

What other arteries are used to profuse bone?

A
  • periosteal arteries

- epiphyseal arteries

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10
Q

How does vit D effect hypertrophy?

A
  • regulate gene expression
  • work on hypertrophic cells-allowing them to continue to pass into hypertrophy-sets up matrix that will mineralize
  • lack: slows process of mineralization
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11
Q

How does estrogen effect bone growth?

A

-works on proliferating cells; causes increase in proliferation with spike of estrogen and once those cells finish proliferating the growth plate is closed.

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12
Q

Achodroplasia

  • Mutation of?
  • What does it prevent?
  • How often does it occur?
  • Down stream effects
A

-FGFR3
- Prevention of elongation of long bone
-Epidemiology: every one in 30,000–250,000 total
○ Can cause: sleep apnea due to bend of basocranium (endochondral) which causes stenosis of foramen magnum–spinal chord is pinched; Platyspondyly- excessive lordosis of lumbar–treated with laminectomy

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13
Q

Modeling

  • How does it work?
  • What causes change
A

○ Cells work in different areas but at same time; osteoclast in middle, osteoblast on outside
○ Allows for adaptation to increased load or change in shape

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14
Q

Redmodeling

  • How does it work?
  • What causes change?
A

○ Cells work in same area but at different time
○ Allows for replacement of bone; driven by loading because of increase of strain on bone which causes microfractures and dead osteocytes must be removed

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15
Q

Rickets

  • Cause
  • Effect
  • Treatment
A
  • Caused by low vit D and calcium
  • Will cause widend and irregular growth plate
  • Increase calcium and vit D
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16
Q

Intramembranous ossification

  • What is it?
  • What is responsible?
A
  • Mesenchyme to osteoblast
  • Rungsx2 responsible for this type of ossification and mutation in transcription factor of Rungsx2 will cause deficiency in this type of ossification
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17
Q

Endochondral ossifciation

-What is it?

A

-Mesenchyme to chondroblast to osteoblast

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18
Q

Cleidocranial dysplasia

  • Cause
  • Symptoms
A
  • Dysfunction of Rungsx2

- Poor formation/missing clavicle/scapula, anterior fontanelle very large, supernumerary teeth (hyperodontia)

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19
Q

Steps in resorption

A

○ Migration - protosomes
○ Sealing/Ruffle border - Actin ring attaches (creating sealed zone) Ruffle border set up inside sealed zone
○ Acidification- Will demineralize hydroxy epitite,
Enzymatic dissolution - Capescian k- breaks down collagen

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20
Q

Organs involved in bone homeostasis

A
  • Intestines (absorption of Ca)
  • Parathyroid (serum Ca)
  • Thyroid (calcitonin)
  • Kidneys (serum Ca)
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21
Q

3 hormones that control phosphate and calcium in serum?

A
  • PTH
  • Vit D- pre-hormone–vit D leads to calcium absorption in body
  • Fibroblast growth hormone
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22
Q

Secondary hormones that affect Ca and phosphate in serum?

A
  • Calcitonin: neg regulator of bone absorption
  • Insulin
  • Thyroid hormone
  • Sex hormone
23
Q

Why is vit D a pre-hormone

A

-it is activated into active hormone; can make in skin or get from diet

24
Q

Difference detween Vit D3 and D2

A

D3 stays in body longer

25
What regulates vit D?
Kidneys--resorption and excretion
26
Treatments for osteoporosis (5)
- increase cholesterol-- contains vit D - vit D replacement (ergocalciferol) - bisphosphonates: inhibit ruffle border--decrease osteoclast activity - monoclonal antibodies: bind to rank-L; denosumab - teraperatid-PTH analog: increases osteoblasts - estrogen supplement; estradiol/progesterone supplement; selective estrogen receptor modulate
27
bisphosphonates - name - function - conflicts
- end in dodronate; alendronate (oral), ivandronate (IV) - disrupt ruffle border of osteoclasts making them unable to bind and make seal reducing bone resorption - need to be taken for pro-longed period - not well absorbed - GI upset; need to sit up for 30 min - stay in bones for yrs so needs to be stopped after 5 yrs or accumulation will lead to increased fractures
28
estrogen/estradiol supplement
- induces osteoclast apoptosis | - can lead to increased risk of cancer in women who are post-menopausal
29
teraperatid
- PTH analog - increases osteoblastic activity and proliferation - given as shot to stomach; taken once every day - only used for a period of a couple months
30
selective estrogen receptor modulate
- induces osteoclast apoptosis | - help with spinal fractures ONLY
31
Hyperparathyroid - sxs; labs - order? - treatment
- recurrent kidney stones, hypercalcemia, bone pain, abdominal pain - need imaging - only treatment is surgery
32
What can occur with medullary thyroid cancer? | -treatment
- thyroid is removed as well as parathyroid - decrease in PTH--decrease resorption of bone from kidneys---decrease in calcium - increase calcium absorption with vit D or PTH analog
33
What can occur with chronic kidney disease?
- low calcium and vit D due to chronic diuretics - stones produced due to increase in phosphate binding to calcium--even if there is low calcium - treatment: vit D supplement, RANKL inhibitor (don't go through liver or kidneys)
34
Pagets disease - what is it - order? - treatment
- increase osteoclast activity and osteoblasts cannot keep up - xray will show lytic lesions - bisphosphonate to stop osteoclast activity and increase osteoblast activity
35
Woven bone - other name - collagen organization - when is it produced
- primary bone - characterized by a haphazard organization of collagen fibers and is mechanically weak. - produced when osteoblasts produce osteoid rapidly, which occurs initially in all fetal bones, but is later replaced by more resilient lamellar bone.
36
Lamellar bone - other name - collagen organization
- (secondary bone) | - has a regular parallel alignment of collagen into sheets ("lamellae") and is mechanically strong
37
Interstitial growth
bone grows longitudinally
38
Appositional growth
bone grows in diameter (width)-- osteoblasts working on outside, osteoclast working on inside
39
Skeletal envelopes
- periosteal - endocortical - cancellous - intracortical
40
Periosteal - parts - vascularization?
-outer fibrous portion -inner portion with mesenchymal cells § Necessary for growth, development, modeling/remodeling, and fracture repair § Can form into chondrocytes/osteoblasts -Well vascularized, innervated by sympathetic and pain sensitive fibers
41
Endocortical - surrounds? - lined with?
- Surface surrounding marrow cavity - Extracellular fluid separates these cells from bone matrix - Lined with fenestrated layer (bone lining cells)
42
Cancellous - location? - nutrients?
- Cells line both surfaces and are exposed to all elements of marrow cavity - No vessels - Fenestrated layer provide nutrients
43
Intracortical - location? - vascular? - covered with
- Surface of haversian canal - Have 1-2 blood vessels in canal - Covered by fenestrated layer
44
Runx2 with endochondral ossification
-causes proliferation of hypertrophic chondrocytes to dead chondrocytes
45
Runx2 and intramembranous ossification
-causes differentiation of mesenchymal cells to osteoblasts
46
Endochondral ossification steps | -and what happens during each step
1. Resting: mesenchymal cells--differentiate into chondroblasts 2. Proliferative: chondroblasts proliferate 3. Pre-hypertrophic: stage between chondroblast and chondrocyte-continued proliferation but will soon no longer to be able to proliferate 4. Hypertrophic: chondrocytes- no longer proliferating but excreting matrix so that they can die and be calcified 5. Calcification: chondrocyte is dead and begins to be calcified, this is done by osteoclasts coming in to remove transverse septa and osteoblasts coming in to create calcified bone matrix
47
 PTHRP
released by proliferating cells-limits IHH in pre-hypertrophic cells
48
GH
Acts on resting chondroblasts to induce and maintain proliferation through IGF-1
49
IHH
released by pre-hypertrophic cells-stimulates proliferation of mesenchymal cells to osteoblasts
50
FGFR3
HARD STOP- stop proliferation, only continue hypertrophy--mutation causes achondroplasia
51
Estrogen
spike will cause increase in proliferation, and then will work on mesenchymal to stop differentiation and stop chondroblasts form being created
52
Sox 9
Expressed by proliferating chondrocytes to differentiate mesenchymal cells to chondroblast 
53
NMP13
Expressed by hypertrophic cells that die, critical for degradation of transverse septum (removed by osteoclast)

Unit 2: LGS (5 decks)

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