Basic Science Flashcards

0
Q

Fibular hemimelia?

A

Not an isolated entity. Can be associated w femur shortening

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1
Q

Where is the primary ossification centre?

A

Linea aspera of femur @ 1 year, but it’s present in all long bones

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2
Q

Syndactyly?

A

Failure of differentiation

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3
Q

Growth plate zones?

A

Resting, proliferative, hypertrophic, primary spongiosa, secondary spongiosa

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4
Q

Distal femur and proximal tibia growth cm per year?

A

0.9cm femur, 0.6cm tibia

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5
Q

What hormone regulates the process of growth plate closure?

A

Estrogen

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6
Q

Growth hormone - insulin growth factor

A

Most important for linear bone growth

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7
Q

Effects of juvenile hypothyroidism?

A

Delayed ossification, short stature, scfe

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8
Q

Vitamin d indirect and direct?

A

Indirect - absorption of calcium in intestine

Direct - on growth plate chondrocytes

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9
Q

Rickets is caused by?

A

Lack of calcium, vitamin d and phosphate

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10
Q

Heuter volkmann law?

A

Increased pressure on a physis stimulates growth

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11
Q

Skeletal dysplasia - 4 d’s

A

Dwarfism, dysmorphic features, deformities, disproportionate features

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12
Q

What zone of growth plate does achondroplasia affect?

A

Proliferative

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13
Q

Marfan’s syndrome?

A

A type of skeletal dysplasia, rule out cardiac and ocular complications, cartilage disorder characterised by hyper laxity

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14
Q

Diastrophic dysplasia? What thumb deformity?

A

Hitchhikers thumb. Different then the large space between 2nd and 3rd fingers you see in achondroplasia

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15
Q

Most common cause of teratologic DDH?

A

Arthrogryposis

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16
Q

How does varus/values deformity progress in children?

A

Genu varum until 1.5 then neutral. Progress to maximum valgus by age 3-4 then reach adult valgus at age 7.

If not either skeletal dysplasia or bone metabolic disease

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17
Q

Why is 8yo a critical age in ddh?

A

There is no capacity for hip to remodel beyond this age, so not the right answer to simply reduce a dislocated hip

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18
Q

Pathoanatomy in ddh - 6 things?

A

Inverted limbus, ligamentum teres, Iliopsoas, pulvinar, transverse acetabular ligament,

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19
Q

What “packaging problems” are associated w ddh?

A

Torticollis, metatarsus adductus

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20
Q

Three causes of ddh?

A
  1. Ligamentous laxity - females - Estrogen
  2. Mechanical causes - first born, oligohydramnious, cultural etc.
  3. Primary acetabular dysplasia
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21
Q

Why do we take a Pavlik harness off if it’s not working?

A
AVN 
Risk factors include
No ossific nucleus
High dislocation
Extreme abduction in cast
Acetabular inlet constriction
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22
Q

How do bisphosphonates work? Which type are more effective?

A

Inhibit osteoclast resorption of bone. Nitrogen containing 1000x

23
Q

How do nitrogen containing bisphosphonates work?

A

Inhibit protein prenylation - block farnesyl pyrophosphate synthase leading to decrease GTPase

24
Q

Osteoconductive matrix?

A

Scaffold or framework for bone growth

25
Q

Osteoinductive factors?

A

Growth factors such as bmp that stimulate bone formation

26
Q

Osteogenic cells?

A

Primitive mesenchymal cells, osteoblasts, osteoclasts

27
Q

Hyperaemia in inflammatory arthritis activates?

A

Osteoclasts, periarticular osteopenia.

the inflammatory cells are called pannus

28
Q

Gouty arthropathy? Fluid stains?

A

Needle like crystals, brightly birefringent

29
Q

Pseudogout?

A

Episodic inflammation of joints. CPPD deposits. Positively birefringement

30
Q

Uniform joint space narrowing is predictive of what type of arthritis?

A

Inflammatory arthritis

31
Q

Erosion and joint space narrowing?

A

Spondyloarthropathy

32
Q

If you have a sausage digit? What type of arthritis?

A

Spondyloarthropathy - reactive vs psoriatic

Cause is flexor tenosynovitis and entheslopathy

33
Q

If a patient has polymyositis what do you need to rule out?

A

Malignancy

34
Q

Osteoarthritis what type of joint space narrowing?

A

Asymmetrical jsn. (inflammatory is symmetrical)

35
Q

Whats the difference between oncogene and tumour suppressor gene?

A

Both lead to cancer - oncogene cell function turned on. Tsg gene function turned off

36
Q

Name 5 causes of an Erlenmeyer flask deformity as seen on xray.

A

Mnemonic CHONG
C- Craniometaphyseal Dysplasia (Pyle Disease)
H- Hemoglobinopathies (Thalassemia/Sickle Cell)
O- Osteopetrosis
N- Niemann Pick Disease
G- Gaucher’s Disease

37
Q

Which disease is characterized by a hereditary deficiency of glucocerebrosidase?

A

Gaucher’s disease. Lysosomal storage disorder resulting in fatty deposits in many organs, especially bone marrow.

38
Q

Name 7 molecules that stimulate bone resorption

A
RANKL
PTH (activates adenylyl cyclase)
IL-1
1-25 Dihydroxyvitamin D3
Prostaglandin E2
IL-6 (myeloma)
MIP-1A (myeloma)
39
Q

Name 5 molecules that inhibit bone resorption

A
Osteoprotegrin (binds RANKL)
Calcitonin (direct binding of receptor on osteoclast)
Estrogen
TGF beta
IL-10
40
Q

PTH increases serum calcium and decreases serum phosphate. List three effects of PTH on the osteoblast. What does PTH do in the kidney? Where is PTH made?

A

Effects of PTH on Osteoblast:

  1. Increases synthesis of IL-1 and IL-6
  2. Increases synthesis of RANKL
  3. Increases M-CSF (macrophage colony stimulating factor; this promotes more osteoclasts)

PTH effect on kidney:
Causes 25-hydroxyvitamin D3 to be activated to 1,25dihydroxyvitamin D3 (this in turn increases absorption of calcium and excretion of phosphate)

PTH is made in the chief cells of the parathyroid gland.

41
Q

Calcitonin: Where is it made? How does it influence bone resorption?

A

Made in C-cells of the thyroid gland.

It directly binds receptors on the osteoclast and decreases bone resorption by decreasing the number of osteoclasts and decreasing osteoclast activity.

42
Q

List RFs for osteoporosis (10)

A
older age
female gender
early menopause
fam hx of hip fracture
low body weight
smoking/etoh
fair skinned
low protein intake
use of anticonvulsants/antidepressants
use of glucocorticoids
43
Q

Indirect ligament insertion (ie. MCL) occurs via Sharpey’s fibers. Describe zones of direct ligament insertion.
Bonus: give an example of a tendon which inserts via direct insertion.

A

Zone 1. Ligament.
Zone 2. Fibrocartilage
Zone 3. Mineralized fibrocartilage
Zone 4. Bone

Bonus: Supraspinatus

44
Q

Effect of age on hyaline cartilage

A
Larger cells
Fewer cells
Less water
Higher ratio of keratin sulfate to chondroitin sulfate
Higher protein content
Smaller proteoglycan size
Stiffer (increased modulus of elasticity)
Less elasticity
45
Q

Effect of osteoarthritis on hyaline cartilage

A
Increased water
Increased chondroitin sulfate
Decreased PG content
Decreased keratin sulfate
Decreased collagen content
Less stiff (Decreased modulus of elasticity)
46
Q

Function of Type A and Type B synovial cells

A

A: phagocytosis
B: produce synovial fluid

47
Q

List factors contributing to stability of an Ex Fix construct.

A
Bone ends in contact
Larger pins (rigidity proportional to radius to 4th power)
More pins
Pins spaced further
Bicortical pins
Pins in different planes
Rods closer to bone
Thicker rods
Multiple rods (ie. stacked rods)
Rods in different planes
48
Q

List 4 indications for use of a locked plate

A

Osteoporotic bone
Bridging comminuted fracture
Short articular segment with comminuted metaphysis
When anatomic constraints do not permit plating tension side.

49
Q

List layers of physis

A
Reserve
Proliferative
Maturation (hypertrophic zone)
Degeneration (hypertrophic zone)
Provisional Calcification (hypertrophic zone)
Spongiosa
50
Q

List 9 indications and 2 contratindications for bisphosphonate use

A
Osteogenesis Imperfecta
Polyostotic fibrous dysplasia
Paget's disease
Early AVN
Osteoporosis
Metastatic disease
Multiple myeloma
Malignant hypercalcemia
CRPS

**DON’T use if severe renal disease or postop lumbar fusion

51
Q

Outline the Lankford and Evans stages of CRPS

Differentiate between type I and II CRPS

A
Stage 1 (0-3mos from onset)
Red, swollen, warm, sweaty, painful. Decreased ROM. Xray often normal.
Stage 2 (3-12 mos)
Worse pain. Dry skin, maybe cyanosis. Stiffness. Osteopenia on xray.
Stage 3 (>12 mos)
Pain diminished. Contractures and shiny skin. Extreme osteopenia on xray.

Type I: “RSD” no demonstrable nerve lesion
Type 2: “causalgia” has involved nerve dysfunction

52
Q

Outline pharmacologic mgmt of CRPS

A

NSAIDS and alpha blockers.
Bisphosphonates
Antidepressants/Anticonvulsants

53
Q

Outline non pharmacologic, non surgical mgmt of CRPS (3)

A

Gentle physiotherapy
Tactile discrimination training
Graded motor imagery

54
Q

Outline surgical mgmt of CRPS

A

Sympathectomy

55
Q

Which experiences more tourniquet damage - directly compressed tissue or distal ischemic tissue?

A

Both directly compressed muscle/nerve is more damaged than the distal ischemic tissue.

56
Q

EMG changes with tourniquet use? How long?

A

Yes - in 62% of postop ortho patients.

Lasted 51 days