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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
Q

What regulates vit D?

A

Kidneys–resorption and excretion

26
Q

Treatments for osteoporosis (5)

A
  • 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
Q

bisphosphonates

  • name
  • function
  • conflicts
A
  • 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
Q

estrogen/estradiol supplement

A
  • induces osteoclast apoptosis

- can lead to increased risk of cancer in women who are post-menopausal

29
Q

teraperatid

A
  • 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
Q

selective estrogen receptor modulate

A
  • induces osteoclast apoptosis

- help with spinal fractures ONLY

31
Q

Hyperparathyroid

  • sxs; labs
  • order?
  • treatment
A
  • recurrent kidney stones, hypercalcemia, bone pain, abdominal pain
  • need imaging
  • only treatment is surgery
32
Q

What can occur with medullary thyroid cancer?

-treatment

A
  • 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
Q

What can occur with chronic kidney disease?

A
  • 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
Q

Pagets disease

  • what is it
  • order?
  • treatment
A
  • increase osteoclast activity and osteoblasts cannot keep up
  • xray will show lytic lesions
  • bisphosphonate to stop osteoclast activity and increase osteoblast activity
35
Q

Woven bone

  • other name
  • collagen organization
  • when is it produced
A
  • primary bone
  • characterized by a haphazard organization of collagen fibers and is mechanically weak.
  • produced when osteoblasts produce osteoid rapidly, which occurs initially in allfetalbones, but is later replaced by more resilient lamellar bone.
36
Q

Lamellar bone

  • other name
  • collagen organization
A
  • (secondary bone)

- has a regular parallel alignment of collagen into sheets (“lamellae”) and is mechanically strong

37
Q

Interstitial growth

A

bone grows longitudinally

38
Q

Appositional growth

A

bone grows in diameter (width)– osteoblasts working on outside, osteoclast working on inside

39
Q

Skeletal envelopes

A
  • periosteal
  • endocortical
  • cancellous
  • intracortical
40
Q

Periosteal

  • parts
  • vascularization?
A

-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
Q

Endocortical

  • surrounds?
  • lined with?
A
  • Surface surrounding marrow cavity
  • Extracellular fluid separates these cells from bone matrix
  • Lined with fenestrated layer (bone lining cells)
42
Q

Cancellous

  • location?
  • nutrients?
A
  • Cells line both surfaces and are exposed to all elements of marrow cavity
  • No vessels
  • Fenestrated layer provide nutrients
43
Q

Intracortical

  • location?
  • vascular?
  • covered with
A
  • Surface of haversian canal
  • Have 1-2 blood vessels in canal
  • Covered by fenestrated layer
44
Q

Runx2 with endochondral ossification

A

-causes proliferation of hypertrophic chondrocytes to dead chondrocytes

45
Q

Runx2 and intramembranous ossification

A

-causes differentiation of mesenchymal cells to osteoblasts

46
Q

Endochondral ossification steps

-and what happens during each step

A
  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
Q

PTHRP

A

released by proliferating cells-limits IHH in pre-hypertrophic cells

48
Q

GH

A

Acts on resting chondroblasts to induce and maintain proliferation through IGF-1

49
Q

IHH

A

released by pre-hypertrophic cells-stimulates proliferation of mesenchymal cells to osteoblasts

50
Q

FGFR3

A

HARD STOP- stop proliferation, only continue hypertrophy–mutation causes achondroplasia

51
Q

Estrogen

A

spike will cause increase in proliferation, and then will work on mesenchymal to stop differentiation and stop chondroblasts form being created

52
Q

Sox 9

A

Expressed by proliferating chondrocytes to differentiate mesenchymal cells to chondroblast

53
Q

NMP13

A

Expressed by hypertrophic cells that die, critical for degradation of transverse septum (removed by osteoclast)

Unit 2: LGS (5 decks)

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