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Z MCQ Of OrthoBullets > Basic Sciences > Flashcards

Basic Sciences Flashcards

1
Q

What is the difference between Haversian and Volkmann canals?

A

Vascular canals in the bone

  • Haversian canals are oriented along the long axis of the bone
  • Volkmann canals are oriented transversely.
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2
Q

What are the two types of bone (microscopic structural classification)

A
  • Woven bone (not stress oriented)
  • Lamellar bone (stress oriented)
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3
Q

What induces osteoblast differentiation?

A
  • BMP stimulates mesenchymal cells to become osteoprogenitor cells
  • Platelet derived growth factor (PDGF) and Insulin derived growth factor (IDGF) induces osteoblast differentiation
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4
Q

Describe Osteoclast activation

A
  • PTH receptor on osteoblast bind to PTH = Expression of RANKL
  • RANKL binds to RANK receptor on osteoclasts = activates = bone resorption
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5
Q

What binds to the RANKL of osteoblasts and inhibits RANK activation (inhibits osteoclast activity)?

A

Osteoprotegrin (OPG)

  • TRICK: OsteoProtects by binding to RANKL and preventing activation of RANK on osteoclasts.
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6
Q

What are the precursors to osteoclasts?

A

Myeloid hematopeitic cells from monocyte/macrophage lineage cells

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7
Q

Name of site of bone resorption where ruffled borders meet the bone surface

A

Howship’s Lacunae

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8
Q

What is Cathepsin K?

A

Major proteolytic enzyme that digest organic material at the ruffled borders

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9
Q

Mechanism of action of bisphosphonates?

A

Prevents formation of ruffled borders of osteoclasts and prevents production of acid hydrolases

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10
Q

Mutation of Cathepsin K leads to what disease?

A

Pycnodysostosis (increased bone density, short stature, brittle bones)

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11
Q

How do osteocytes communicate with adjacent osteocytes?

A

Gap junctions in canaliculi

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12
Q

Osteoprogenitor cells become different cells under different conditions….in what condition do they become Osteoblast, collagen, fibrous tissue?

A
  • Osteoblast (“the marathon runner”)
    • LOW strain + HIGH oxygen
  • Collagen (“Collagen gets Choked”)
    • INTERMEDIATE strain + LOW oxygen
  • Fibrous tissue
    • HIGH strain
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13
Q

What type of collagen makes up bone?

A

Type 1 (90% of organic material of bone)

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14
Q

What ORGANIC material is responsible for

  • the compressive strength
  • the tensile strength of the bone matrix?
A
  • Collagen = tensile strength
  • Proteoglycans = compressive strength
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15
Q

What is the most abundant non-collagenous protein in bone matrix?

A

Osteocalcin (10-20% of total)

  • Promotes mineralization and bone formation
  • Stimulated by 1,25 dihydroxyvitamin D3
  • Inhibited by PTH
  • MARKER OF BONE TURNOVER (in serum and urine)
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16
Q

What are the inorganic components of bone?

A
  • Calcium Hydroxyapatite (gives compressive strength)
  • Brushite (osteocalcium phosphate)
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17
Q

Blood supply to long bones comes from 3 sources

A
  • Periosteal (low pressure system)
  • Metaphyseal-epiphyseal
  • Nutrient arteries (HIGH pressure system)
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18
Q

Direction of arterial blowflood in bone (mature vs immature)

A
  • Mature = CENTRIFUGAL (inside out)
    • High pressure nutrient arteries inside and low pressure periosteal flow
    • Venous is opposite (centripedal)
  • Immature = Centripedal
    • Low pressure from periosteal blood flow dominates
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19
Q

What % of endosteum is devascularized from reaming during IMN insertion?

A

Reaming nail devascularizes 50-80% of endosteal blood supply

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20
Q

What is the pattern of blood flow in bone after fracture?

A
  • Centripedal (outside in)
    • Nutrient artery blood flow disrupted and periosteal blood floor predominates.
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21
Q

Name factors that stimulate bone resorption

A
  • RANKL
  • PTH
  • IL-1
  • 1,25 - hydroxyvitamin D
  • Prostaglandin E2
  • IL-6 (Myeloma)
  • MIP-1A (Myeloma)
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22
Q

Bone loss per year after 25 yo?

A
  • 0.3-0.5%/ year after skeletal maturity
    • 2-3 % / year for untreated postmenopausal women
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23
Q

IL-1 vs IL-10, which one causes bone resorption which one causes bone formation.

A
  • IL-1 (one finger, fuck you bone)
    • activates osteoclasts and caused bone resorption.
    • PTH stimulate osteoblast to secrete IL-1 and IL-6 activating osteoclasts and increase M-CSF (Macrophage colony-stimulating factor) = more osteoclasts.
  • IL-10 (double high five to bone)
    • Bone formation
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24
Q

What is the affect of PTH on the kidney and intestine?

A
  • Stimulates enzymatic conversion of 25-(OH)-vitamin D3 to 1,25-(OH)2-vitamin D3 (ACTIVE form)
    • Increases absorption of Ca++ in kidney (increase serum Ca++)
    • Increase excretion of Po4- from kidney
    • Increase gut absoprtion of Ca++ (affect of 1,25-(OH) vitamin D3
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25
Q

What are the effects of activated vitamin D (1,25(OH)2 vitamin D3)

A
  • Increase kidney and gut absorption/ resorption of Ca++
  • Promotes the mineralization of osteoid matrix produced by osteoblasts.
  • NOTE: Vitamin D deficiency causes osteomalacia/ Rickets
  • Phenytoin (Dilantin) causes impaired metabolism of vitamin D.
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26
Q

What is the function of Thyroid hormone on bone?

A
  • Regulates skeletal growth at the physis by stimulating:
    • Chondrocyte growth
    • type X collagen synthesis
    • alkaline phosphatase activity
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27
Q

When does the appendicular system form during gestation?

A
  • 4-8 weeks
  • Limb bud development is under the control of fibroblast growth factors (FGF)
  • TRICK: Finger Growth Fast (FGF)
    • Mutation in FGF = Apert syndrome (acrocephalosyndactyly)
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28
Q

What regulates limb bud formation?

A
  • “Shh” (Sonic HedgeHog) is expressed by the notochord and regulates limb bud formation
  • limb bud grows outwards into ectoderm.
    • bud is a combo of the lateral plate mesoderm and somatic mesoderm.
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29
Q

What is the first signaling center to appear (proximodistal) limb patterning? Hint: a defect of ____ will result in proximal limb truncation/ central deficit (ie Cleft hand)

A

AER

TRICK: AEROSMITH—–rock on sign with hand!!

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30
Q

In Anteroposterior (radioulnar - radial = anterior and ulnar = posterior) limb growth, what signaling center appears and determines limb polarity?

A
  • ZPA (Zone of polarizing activity)
  • along posterior (aka ulnar) limb and expresses Shh.
  • ZPA duplication = MIRROR HAND
  • Higher concentration of “Shh” in side of Small finger (ulnar)
  • Lower concentration of “Shh” radially

NOTE:

ULNAR (where Shh supposed to be high)

  • more Shh = more fingers
  • Less Shh = less fingers

RADIAL (where Shh supposed to be low)

more Shh = LOSS OF THUMB

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31
Q

What gene is expressed in dorsal ectoderm and regulates dorsal-ventral growth of limb?

A
  • Wnt genes
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32
Q

The Spinal Column (vertebra) originate from which structures?

A
  • Somites
    • pairs of mesodermal structures that develop cranial to caudal
  • MORE SPECIFICALLY:
    • The sclerotome layer of the somite will become the vertebral bodies and annulus
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33
Q

What does the notochord become?

A
  • Nucleus pulposus and anterior vertebral bodies
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34
Q

What forms the PNS?

What forms the spinal cord?

A
  • Neural crest = PNS
  • Neural tube = spinal cord
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35
Q

What are the 3 ossification centers of the vertebrae?

A
  1. Centrum (anterior body)
  2. Neural Arch (posterior elements, pedicles)
  3. Costal elements (TP or ribs, lateral mass)
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36
Q

What type of collagen is associated with enchondral OSSIFICATION?

A

type X collagen

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37
Q

What is Hueter-Volkmann Law?

A
  • Compression across physis slows longitudinal growth
  • Tension accelerates longitudinal growth
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38
Q

In the hypertrophic zone of physis, what regulates chondrocyte maturation (hypertrophy/calcification)?

A
  • Parathyropid related peptyides
    • Expression regulated by Indian Hedgehog gene
39
Q

Name the zones of the physis and associated diseases

A
40
Q

Name the types of bone formation?

A
  1. Endochondral
    1. (initial production of cartilage gets replaced by bone - secondary # healing, long bone growth, embryonic)
  2. Intramembranous
    1. (direct bone production with mesenchymal diff. into osteoblast, flat bones, primary bone healing, distraction osteogenesis)
  3. Appositional
    1. (width, periosteum)
41
Q

Name a condition with defects in intramembranous ossification?

A
  • Cleidocranial dysplasia
    • Remember that clavicle (considered flat-ish and formed by intramembranous bone formation)
    • Mutation in CBFA1 (aka Runx2) on chromosome 6.
42
Q

What regulates intramembranous bone formation?

A
  • Wnt pathway and Hedgehog signaling
    • beta-catenin = induces cells to form osteoblasts = bone formation
    • Sclerostin = inhibits Wnt Pathway = decrease bone formation

TRICK: Sclerostin Sucks (decrease bone formation)

43
Q

What are the modes of bone healing and there associated strain?

A
  • Primary bone healing = < 2% strain
  • Secondary bone healing = 2-10% strain
44
Q

What are the stages of bone healing?

A
  • Inflammation (aka hematoma formation)
  • Repair
    • Soft Callus
    • Hard Callus
  • Remodelling
45
Q

Type of non-union

A
  • Hypertrophic
    • inadequate stability with adequate blood supply/biology
  • Atrophic
    • Inadequate blood supply/biology and inadequate immobilization
  • Oligotrophic
    • inadequate reduction (wants to heal but too far to go)
46
Q

What is the effect of TGF-B on bony healing?

A
  • Transforming Growth Factor-B
  • Found in # hematoma
  • Stimulates production of Type II collagen and proteoglycans by mesenchymal cells.
  • Induces osteoblasts to synthesize collagen,
47
Q

What are the properties of a bone graft?

A
  • Osteoconductive (scaffold for bone formation)
    • ex: demineralized bone matrices (DBMs)
  • Osteoinductive (factors promoting bone formation)
    • ex: BMP (from the TGF-B superfamily) or DBMs.
  • Osteogenic (actual cells that produce bone)
    • ex: mesenchymal cells, osteoblasts, osteocytes.

NOTE:

  • AUTOGRAFT is GOLD STANDARD (osteoinductive, conductive and genic)
  • Fresh or fresh frozen allograft still have BMP, therefore osteoinductive. vs freeze dried does NOT.

Resorption rate fastest to slowest

calcium sulfate > tricalcium phosphate > hydroxyapatite

48
Q

Explain the antigenicity of allograft

A
  • Class I and II antigen on allograft recognized by host T lymphocytes and elicit immune response.
49
Q

What is the MOA of calcitonin in the treatment of osteoporosis?

A
  • Inhibition of sclerostin formation and inhibition of osteoclast apoptosis. (OITE)
50
Q

Where is PTH secreted?

A
  • Chief cells of parathyroid glands (4)
51
Q

What is the function of PTH?

A
  • response to low serum Ca++
  • Increase bone resorption
    • PTH receptor on osteoblasts which secrete IL-1 to active osteoclasts
  • Increase kidney resorption of calcium (distal convoluted tubule, reminder that most resorption is in proximal c. tubule)
  • Decrease kidney resorption of phosphate
  • Increase activation of 25-OH vitamin D (Calcidiol) to 1,25-dihydroxyvitamin D3 (active, calcitriol) (which in term increases gut/kidney absoprtion of PO4- and Ca++)
52
Q

Describe the sarcomere

  • H band?
  • I band?
  • A band?
  • Z line?
A
  • Actin thin
  • Myosin thick
  • TRICK:
    • A band = A team (both myosin and actin)
      • Only one that stays constant (does NOT shorten with contraction)
    • I band = skinnies (only actin)
    • H band = huge people (myosin only)
    • Z line = site of attachment of actin between side to side sarcomeres
53
Q

How does Botox work?

A
  • Blocks release of Ach (acetylcholine) from end plate (Motor endplate)

as compared to myasthenia gravis which attack receptors and results in shortage of Ach receptors.

54
Q

What are the types of muscle contraction?

A
  • Isometric:
    • constrant length
  • Isokinetic:
    • Constant speed (need cybex machine that keeps speed constant)
  • Plyometric:
    • Rapid lengthening followed by contraction
  • Isotonic:
    • constant tension
    • concentric - shortens during contraction
    • eccentric - lengthens during contraction
55
Q

Force generated by muscle is MOST dependent on_______

A

muscle cross-sectional area

56
Q

What are the components of the stress strain (load-elongation) curve for a ligament/tendon?

A
  • Toe region:
    • tightening of loose fibers to resist stress.
  • Linear region:
    • stiffness = slope (constant)
  • Yield point:
    • Point where elastic (reversible) becomes plastic (irreversible).
57
Q

What is the most predominant proteoglycan in tendon? HINT: it regulates collagen fiber diameter

A

Decorin

TRICK: Decorin regulates Diamter of tenDon

58
Q

Name the 4 transitional tissues that make up tendon’s insertion into bone (firbocartilaginous enthesis)

A
  1. Tendon
  2. Uncalcified fibrocartilage
  3. Calcified firbocartilage
  4. Bone

NOTE:

  • Fibrocartilaginous enthesis (direct attachment) to epiphysis/ apophysis
    • RTC, achilles
  • Fibrous enthesis (indirect attachment)
59
Q

True or false. Tendons are less viscoelastic (less elastin) than ligaments

A

TRUE

60
Q

Name and describe the zones of articular cartilage

A
  • Superficial zone (tangential zone)
    • Collagen oriented PARALLEL to joint (shear stress)
    • High collagen, low proteoglycans
  • Transitional zone (intermediate zone)
    • Random orientation of collagen
    • Round chondrocytes
  • Deep zone (basal layer or radial zone)
    • Collagen oriented perpendicular to joint
    • HIGH proteoglycans (compressive stress)
    • Round chondrocytes in columns
  • TIDEMARK
    • between superfical uncalcified cartilage and deeper calcified cartilage
    • just superficial to subchondral bone
61
Q

What are the changes in articular cartilage seen in OA vs aging?

A
  • OA
    • Increased water content
    • Decreased stiffness
    • Increased chondroitin 4 sulfate: keratan sulfate ratio
  • Aging
    • Decreased water content
    • Increased stiffness
    • Decreased chondroitin 4 sulfate: keratan sulfate ratio

NOTE: Advanced Glycosylation End Products (AGEs) increases with age and their accumulation thought to lead to OA

62
Q

What major transcription factor is involved in differentiation of cells towards the cartilage lineage?

A

SOX-9

63
Q

What are the cell types in synovium and which one produced synovial fluid (hyaluronic acid)?

A
  • Type A cells
    • antigen presenting ability, superficial layer
  • Type B cells
    • PRODUCE SYNOVIAL FLUID
  • Type C cells
    • Unknown function
64
Q

What is the composition of collagen?

A
  • Triple helix of:
    • 2x alpha 1 chains
    • 1x alpha 2 chains

Collagen fiber = multiple collagen fibrils aggregated together.

65
Q

What is an exon (in DNA)?

A
  • an exon is the portion of gene on DNA that codes for mRNA

TRICK:

EXon is EXpressed

66
Q

What is the type of immune response to metallic orthopaedic implants?

A
  • Type IV
    • Delayed-type hypersensitivity reaction
67
Q

What are translocations?

A
  • Translocations allow expression of genes (oncogenes) that are usuallyp NOT active
  • 95% present in sarcomas
68
Q
  • Western blot detects _____
  • Southern blot detects _____
  • Northern blot detects _____
  • SOutwestern blot detects _____
A
  • Western blot detects _____PROTEIN
  • Southern blot detects _____DNA
  • Northern blot detects _____RNA
  • Soutwestern blot detects _____DNA BINDING PROTEIN

Trick:

  • SNoW
  • DRoP
  • Southern = DownNA under
  • Western Ortho = Protein junkies (Joey/Yousif/Sahil)
69
Q

Define toughness of a material and how to calculate it using a stress-strain curve

A
  • Toughness
    • Amount of energy per volume a material can absorb before failure (fracture)
    • AREA UNDER the stress-strain curve
    • J/m3
70
Q

What is hysteresis?

A
  • Energy dissipation
  • characteristic of a viscoelastic material where the loding curve does NOT follow the unloading curve
    • The difference between the curves is the energy that is dissipated.
71
Q

What is Hooke’s law?

A
  • When a material is loaded in the elastic zone:
    • Stress is proportional to the strain
72
Q

Define:

  • Brittle material:
  • Ductile material:
  • Viscoelastic material:
  • Isotropic material:
  • Anisotropic material:
A
  • Brittle material:
    • linear stress strain relationship up until point of failure (elastic only, little to no plastic deformation)
  • Ductile material:
    • large amounts of plastic deformation before failure
  • Viscoelastic material:
    • ​Stress-strain is dependent on duration of applied load and the RATE by which the load is applied (internal friction) - ie ligs and bone
  • Isotropic material:
    • ​same mechanical properties in ALL directions
  • Anisotropic material:
    • ​different mechanical properties DEPENDING on the direction of applied load
73
Q

Which metal is most prone to crevice corrosion (fatigue cracks due to difference in oxygen tension)?

A

Stainless steel

74
Q

How is titanium corrosion resistant?

A
  • Forms a layer of self passivation around it
    • Titanium oxide around it that shields it from outside.
75
Q

Name ways of increasing the stability of an Ex-Fix.

A
  • Contact of ends of #
  • LARGER DIAMETER PINS (most important)
  • Additional pins
  • Decrease bone to rod distance
  • Pins in different planes
  • Incrase size or number of stacking rods
  • Rods in different planes
  • Increased spacing between same sided pins
76
Q

Define antalgic gait

A
  • Gait abnormality secondary to pain resulting in shortened stance phase relative to swing phase.
77
Q

What is the increase in 5 year mortality after a vertebral fragility fracture?

A

15% increase in 5-year mortality

78
Q

What is the FRAX score?

A

WHo fracture risk assessment tool to calculte 10 year risk of hip fracture and osteoporosis-related #

79
Q

Define osteopenia an osteoporosis

A
  • Osteopenia: L2-4 lubar density with T-score -1 to –2.5 –> 1-2.5 SD below peak bone mass of a 25 year old individual
  • Osteoporosis: L2-4 lumbar density with T score < -2.5 –> 2.5 SD below the peak bone mass of a 25 year old individual.
80
Q

What is the classification of osteoporosis?

A
  • Type 1: Post menopausal
  • Type 2: Elderly/ Senile
81
Q

In hypophasphatasia, what are the abnormal labs (serum and urine)?

A
  • Serum
    • decreased serum alkaline phosphatase
  • Urine:
    • presence of “phosphoethanolamine” is diagnostic
82
Q

Describe the types of Rickets and there associated lab values

A
  • X-linked hypophosphatemic rickets (most common, familial)
    • lose phosphate in kidneys (defective resorption)
    • poor mineralization
    • Tx: Calcitriol (1,25 DHvitamin D3))
  • Vitamin D deficient Rickets (Nutritional)
    • Lack of vitamin D (sun/nutrition)
    • Tx: 5000 iu/d Vitamin D
  • Hereditary vitamin D Dependant Rickets
    • Type 1: Can’t make it (can’t make activated vitamin D) - autosomal recessive
    • Type 2: Can’t use it (receptors defective)
  • Hypophasphatasia
    • Can’t make alkaline phosphatase required to make inorganic phosphate require for bone mineralization
83
Q

What is the common mutation in Autosomal Dominant Hypophosphatemic Rickets (ADHR)

A
  • Mutation causing cleavage-resistant FGF23
  • increase in FGF23 = increase renal loss of phosphate
    • This mechanism seen in oncogenic osteomalacia (mutation in phosphatonin gene for FGF23.
  • Much rarer than X-linked dominant Hypophosphatemic Rickets.
84
Q

What is pseudohypoparathyroidism and what condition is associated with it?

A
  • PTH resistance (decrease in target cell response)
  • Type 1a = ALBRIGHT HEREDITARY OSTEODYSTROPHY
    • Short 4th and 5th metacarpals
    • “knuckle, knuckle, dimple, dimple”
85
Q

What are the radiographic findings in scurvy?

A
  • White line of Frankel
    • Sclerotic line at metaphysis
  • Trummerfeld zone
    • Transverse radiolucent band in metaphysis just adjacent to Frankel line
  • Wimberger ring
    • Ring of increased density surrounding epiphysis
  • Pelkin spur and fracture
    • Metaphyseal spurs and #
  • Corner sign of Park
    • metaphysea clefts
  • Decreased trabeculae
    • Ground-glass osteopenia
86
Q

Name bone resorption desorders and their causes

A
  • Osteopetrosis
    • Defective carbonic anhydrase = decrease resorption
  • Pycnodysostosis
    • Defective Cathepsin K = decrease resorption
  • Osteoporosis
    • Decrease estrogen/ postmenopausal
    • Corticosteroids
    • Hyperparathyroidism
    • All increase resorption
  • Familial Expansile Osteolysis (FEO)
    • RANK mutation = increase resorption
  • Hyperostosis
    • “Hyperostosis corticalis deformans juvenilis”
    • Defective/ decrease in osteoprotegerin (mutation) = increase resorption
87
Q

What are makers of bone formation (measured in serum)?

A
  • Osteocalcin (ONLY one that is bone specific)
  • Alkaline Phosphatase
  • C & N propeptides of Type I collagen
88
Q

What type of immune reaction occurs in response to Orthopaedic hardware?

A
  • Type 4 hypersensitivity reaction (excessive cell-mediated immunity, T-lymphocytes, acquired/adaptive)
89
Q

What mutation causes X-linked Hypophosphatemic rickets?

A

Mutation in proteinase PHEX

Trick: peX = X-linked hypophosphatemic rickets

MILLERS

  • PHEX regulates FGF-23, which normally prevents the kidney’s reabsorption of phosphate.
  • The PHEX gene mutation therefore reduces phosphate reabsorption, leading to hypophosphatemia.
90
Q

HLA-B27 is associated with which rheumatologic condictions?

A
  • PAIR
  • Psoriatic arthritis
  • Ank Spond
  • Inflx bowel disease
  • RA

HLA-DR3 = myastenis gravis and SLE

HLA-DR4 = RA

91
Q

What is the Paparika sign?

A
  • Punctate bleeding of bone after debridement of bone (usually in osteomyelitis case or nonunion).
92
Q

What is the Penumbra sign? (Osteomyelitis)

A
  • MR
    • Bright signal in surrounding bone
    • Dark signal in abcess/sclerotic bone
93
Q

Describe the MOA of beta-Lactam abx, aminoglycosides, quinolones.

A
  • beta-Lactam abx (penG, Cephalosporin)
    • Inhibit cross linking of polysaccharides in CELL WALL
  • Aminoglycosides (Gent, Tobramycin)
    • Inhibit protein synthesis (30S ribosomal subunit)
  • Quinolones (cipro, levo, ofloxacin)
    • Inhibits DNA gyrase

Z MCQ Of OrthoBullets (27 decks)

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