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18 Musculoskeletal System > 1.1 Skeletal System > Flashcards

1.1 Skeletal System Flashcards

1
Q

Achondroplasia

  • clinical findings
  • etiology
A

-dwarfism

  • poor endochondral bone (long bones) formation
  • intramembranous (head, chest) not affected
  • mutation of FGFR3
  • fibroblast growth factor receptor 3
  • auto dominant
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2
Q

osteogenesis imperfecta

  • what is it
  • clinical findings (3 big ones)
A
  • congenital defect in Type I collagen synthesis, weak bone
  • auto dom.
  1. multiple fractures–mimic child abuse
  2. blue sclera–loss of type I collagen reveals underlying blue choroidal veins
  3. hearing loss–middle ear bones fracture
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3
Q

Osteopetrosis

  • what is it, etiology
  • Tx
A

“rock like”

  • inherited defect of bone resorption
  • results in thick bone that is paradoxically weak.

-Carbonic Anhydrase II mutation–normally required in osteoclasts to excrete H+, providing acidic environment for bone resporption.

  • Bone marrow transplant
  • osteoclasts come from monocytes
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4
Q

Osteopetrosis

-clinical findings (5 big ones)

A
  1. bone fractures
  2. bone impinges into bone marrow–anemia, thrombocytopenia, leukopenia
  3. bone impinges on cranial nerves–vision/hearing loss
  4. bone narrows foramen magnum–hydrocephalus
  5. Renal tubular acidosis–lack of carbonic anhydrase II leads to metabolic acidosis. (CAII required to excrete H+ and reabsorb HCO3-)
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5
Q

Why is bone marrow transplant the Tx for osteopetrosis?

A

Osteopetrosis is genetic loss of CAII inside osteoclasts, which come from monocytes.
-bone marrow will replace faulty monocytes, which develop into osteoclasts

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6
Q

Osteomalacia (Ricketts)

  • etiology
  • clinical findings
A

-low Vit D, leads to low Ca2+ and phosphate, which leads to defective mineralization osteoid

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7
Q

osteoid

A
  • what osteoblasts produce.

- osteoid is then mineralized with calcium and phosphate to become bone.

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8
Q

Vit D:

  • how is it acquired and activated?
  • what does is act on?
A

-diet and UV light

  • must be activated:
    1. first in liver (to 25-OH-D)
    2. then in kidney (to 1,25-OH-D) active form
  • increases Ca and phosphate reabsorption from:
    1. GI
    2. Bone
    3. Kidney
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9
Q

Osteomalacia (Ricketts)

-clinical findings, child vs adult

A

-adult: weak bone

  • child:
    1. pigeon-breast deformity
    2. frontal bossing (enlarged forehead)
    3. Rachitic rosary (“beads”) in costochondral junction
    4. bowing of legs
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10
Q

osteomalacia (Ricketts)

  • lab findings:
  • calcium
  • phosphate
  • PTH
  • alkaline phosphatase
A
  • calcium: low
  • phosphate: low
  • PTH: high
  • alkaline phosphatase: high because basic environment necessary for osteoid mineralization by osteoclast (secreted by osteoclast)
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11
Q

Osteomalacia (Ricketts)

-causes (5)

A
  1. Diet
  2. Malabsorption
  3. Low sun exposure
  4. Liver disease
  5. Kidney disease
    - both liver and kidney required to activate Vit D.
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12
Q

Osteoporosis

-what test used to measure

A

-DEXA scan to measure bone density

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13
Q

Osteoporosis

  • lab values:
  • calcium
  • phosphate
  • PTH
  • alkaline phosphatase
A

all normal

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14
Q

Osteoporosis:

  • tx
  • contraindications
A
  1. Vit D, Calcium, exercise
  2. bisphosphonates–induce apoptosis of osteoclasts that eat them
  3. estrogen replacement–not recommended
  4. glucocorticoids–contraindicated
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15
Q

Paget Disease of Bone

  • etiology, mech
  • stages
A

‘paget’s puzzle pieces’

  • imbalance btwn osteoclast and osteoblast function
  • 3 stages:
    1. osteoclast overactive
    2. osteoblast tries to lay down bone in a rush
    3. osteoclasts burn out, osteblasts still lay down bone
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16
Q

bisphosphonates

A
  • induce apoptosis in osteoclasts when they eat them. reduce bone resorption
  • tx in:
  • Paget’s disease of bone
  • Osteoporosis
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17
Q

Osteomyelitis

  • etiology
  • clinical findings
  • difference child vs adult
A
  • infection of bone and marrow
  • inside bone–abscess (sequestrum) surrounded by sclerosis of bone (involucrum)
  • child: metaphysis seeded
  • adult: epiphysis seeded
18
Q

involucrum

A

-sclerotic bone tissue that surrounds abscess in osteomyelitis

19
Q

sequestrum

A

-abscess in bone from osteomyelitis

20
Q

what can gas emboli do to bone?

A

cause ischemia, leading to avascular necrosis

21
Q

osteomyelitis:

categories

A
  1. hematogenous
  2. direct implantation (penetrating injury)
  3. contiguous (direct infection from wound/ulcer)
  4. prosthetic infection
22
Q

direct implantation osteomyelitis

-what pathogens?

A
  • pseudomonas

- enjoys living in damp foot under socks and shoes

23
Q

contiguous osteomyelitis

  • common cause?
  • what pathogens?
A
  • diabetic foot ulcer
  • think bugs that live in pressure ulcers:
  • S aureus, G-‘s, strep, anaerobes, candida
24
Q

hematogenous osteomyelitis

-what pathogens?

A

-S aureus, strep, G-, TB, salmonella

25
Q

prosthetic osteomyelitis

-what is main pathogen?

A
  • coagulase negative S Aureus.

- likes to adhere to foreign surfaces.

26
Q

what antibiotic is useful in tx of biofilm organisms?

A

Rifampin.

-think rifampin for prosthetic infections

27
Q

osteomyelitis

-describe tx

A
  • difficult tx
    1. 6 weeks of Abx (not useful in exposed bone)
    2. surgery to remove sequestra or prostheses (if Abx fail)
    3. Rifampin for biofilm organisms
28
Q

cell origin of:

  • osteoblasts
  • osteocytes
  • osteoclasts
A
  1. mesenchymal stem cells
  2. osteoblasts
  3. monocytes
29
Q

What is master regulator of bone formation?

A

RUNX2

aka CBFA-1

30
Q

what do osteocytes secrete to resorb bone?

2 things

A
  1. H+

2. cathepsin K

31
Q

sclerostin

A
  • secreted by osteocytes to reduce anabolic function of osteoblasts.
  • mech related to sensation of bone loading
  • problem can cause sclerosteosis
32
Q

sclerosteosis

  • mech
  • clinical findings (2)
A
  • osteocytes have mutation in sclerostin
  • bone think it’s being loaded when not–so overgrown bone!
  • nerve entrapment (facial palsy)
  • syndactyly
33
Q

what is more active:

trabecular or cortical remodeling?

A
  • trabecular (cancellous)
  • 80% of turnover
  • high surface-volume ratio
34
Q
  • what imaging test can be done to measure bone mineralization rate? and how does it work?
  • what disease can you dx from abnormal result?
A

Double tetracycline labeling.

  • label with tetracycline 2x in 2 different times. measure distance btwn lines.
  • if lines are not well-defined, you have osteomalacia
35
Q

list:

  • osteoblast/cyte diseases
  • osteocyte diseases
A
  • osteogenesis imperfecta
  • osteomalacia
  • sclerosteosis
  • osteopetrosis
  • paget’s disease
36
Q

BMP

A

bone morphogenic proteins

  • induce patterns of bone/cartilage formation
  • take effect after ‘switch’ of RUNX2
37
Q

fracture repair:

-steps (4)

A
  1. macrophages remove debris
  2. chrondroblasts secrete hyaline cartilage callus
  3. osteoblasts replace cartilage with bone
  4. primary bone is replaced by lamellar secondary bone.
38
Q

PTH induces secretion of what 3 things to activate osteoclasts?

A
  1. M-CSF (macrophage colony stimulating factor)
    - induce macrophage proliferation
  2. RANK-L
    - induce differentation into osteoclasts
  3. OPG–osteoprotegerin
    - blocks RANK-L, regulation.
39
Q

integrin alpha-5-beta-3

A
  • allows osteoclasts to attach to bone

- new clinical target to block osteoclast activity

40
Q

What is PTH paradox?

A
  1. spurts of PTH: induce osteoblasts

2. constant PTH: induce osteoclasts

18 Musculoskeletal System (11 decks)

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