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ABOS > Basic Science HY > Flashcards

Basic Science HY Flashcards

1
Q

Bone

Growth Plate: What is the major source of nutrition to the growth plate?
After fracture, what is the blood flow immediate, hours to days?
IMN effect on blood flow?
What are the 3 sources of blood supply to bone?
Which way is arterial flow?

A

Blood supply to the growth plate is supplied both via the perichondrial artery, which is the main source of nutrients, and the epiphyseal artery, which supplies the proliferative zone of the growth plate

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2
Q

Bone

compressive strength from?
tensile strenth from?

A
  • Compressive strength from proteoglycans & calcium hydroxyapatite (Ca10(PO4)6(OH)2)
  • tensile strength from type I collagen
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3
Q

Bone metabolism: Calcium and Phosphate

% stored in bone, dietary intake?

A

Calcium: 99% in bone, hydroxyapatite, absorption in GI, resorption in Kidneys, Bone. Intake= adults 750 mg/day for adults; postmenopausal/fractures = 1500 mg/day for adults

Phosphate: 86% in bone, majority is hydroxyapatite, dietary intake= 1000-1500 mg/day

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4
Q

Bone Metabolism: PTH

increases/decrease?
synthesized in?
effect on bone?
in kidney?

A
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5
Q

Bone Metabolism: calcitonin

synthesized in?
action on bone?
recombinant calcitonin used for?

A

parafollicles of the thyroid gland (C cells);

inhibits osteoclastic bone resorption by decreasing number and activity of osteoclasts,

Inc. serum Ca > secretion of calcitonin > inhibition of osteoclasts > dec. Ca (transiently).

Recombinant calcitonin used to treat Paget disease, osteoporosis, and hypercalcemia in malignancy.

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6
Q

VitD

active form?
effect on bone?
lab test?
goal of treatment?

A
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7
Q

Estrogen in bone metabolism

what is the effect on bone?
benefits and risks of therapeutic estrogen?
lab findings in therapeutic estrogen?

A

prevents bone loss by decreasing the frequency of bone resorption and remodeling.

Therapeutic estrogen: decreases bone loss if started w/in 5-10 years of menopause, gains in bone mass limited to 2-4% annually in first 2 years of treatment

Risks: increased heart disease, breast cancer, decreased hip fx, endometrial fx.

Lab findings: decrease in urinary pridoline, serum alkaline phosphatase.

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8
Q

Bone metabolism: thyroid hormone

effect on bone?

A
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9
Q

Bone metabolism: GH

how does it regulate growth in bone?
In Gigantism, what effect does increased GH have on bone?

A
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10
Q

Steroids on bone:

increase bone loss by?

A
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11
Q

how does Teriparatide work?

A

intermittent Teriparatide, a PTH analog, is an anabolic anti-osteoporosis drug. Intermittent PTH has anabolic actions

bisphosphonates, estrogen, estrogen receptor modulators, denosumab, and calcitonin, all of which downregulate osteoclastic activity and are antiresorptive

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12
Q

limb development

Limb development Limb buds are first seen at ? weeks of gestation

Sonic hedge-hog (SHH) gene regulates ?

Zone of polarizing activity (ZPA): controls ?

Apical ectodermal ridge (AER): controls ?

Wnt controls ?

A

Limb development Limb buds are first seen at 8 weeks of gestation

Sonic hedge-hog (SHH) gene regulates limb bud formation / development

Zone of polarizing activity (ZPA): controls AP axis (radioulnar axis, or thumb to small finger; great toe to small toe)

Apical ectodermal ridge (AER): controls longitudinal limb growth

Wnt controls dorsoventral axis

Limb buds develop at 4 weeks and are first able to be visualized by transvaginal ultrasound at 8 weeks. During embryologic development, the limb bud has several defined regions. Two important regions are the apical ectodermal ridge (AER) and the zone of polarizing activity (ZPA). The AER controls longitudinal growth. Abnormal developement or loss of the AER will lead to a truncated limb (exact deformity depends on when in development the AER was affected). The ZPA acts via the sonic hedgehog (SHH) pathway to control anterior-posterior and radio-ulnar growth.

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13
Q
A
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14
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A
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15
Q

Decreased sun exposure leads to decreased bone health via?

A

Ultraviolet light from the sun is needed for skin cells to transform 7-dehydrocholesterol into cholecalciferol (vitamin D3). Once in the cholecalciferol form, it will then go to the liver and get hydroxylated into 25-hydroxyvitamin D and then to the kidneys to become 1,25-dihydroxyvitamin D. Lack of sunlight does not influence the ability of the liver or kidneys to perform hydroxylation, but it does affect the ability of the skin to create cholecalciferol, which in turn means no 1,25-vitamin D. Lack of 1,25 vitamin D has a direct impact on the GI tract’s ability to absorb calcium because the GI tract is an end organ affected by active vitamin D. The absence of 1,25 vitamin D would lead to increased levels of PTH, not decreased production of PTH.

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16
Q

What is the mechanism of action of calcitonin?

A

Interferes with osteoclast maturation
* reduces serum calcium concentration by directly interfering with osteoclast maturation via receptors

By attenuating cartilage breakdown and stimulating cartilage formation via inhibitory pathways of matrix metalloproteinases, calcitonin also has a chondro-protective effect on articular cartilage. Calcitonin has no major effects on intestinal absorption of calcium, but may aid in small-bowel secretion of sodium, potassium, chloride, and water. Calcitonin also has no receptor effect on osteoblasts.

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17
Q

Phosphate

administration decreases urinary calcium excretion through which of the following actions?

A

Phosphate reduces urine calcium excretion through several extrarenal mechanisms

  • it creates a complex with calcium in the intestine to decrease available calcium for absorption.
  • An increase in phosphate will directly stimulate PTH secretion and can reduce ionized calcium, also enhancing PTH secretion. The increased PTH will enhance calcium resorption. Phosphate will complex with calcium in the intestine, decreasing the amount of calcium for absorption. It can also complex with calcium in the bone and soft tissues, decreasing the filtered load of calcium. Decreased phosphate will result in hypercalcuria. There appears to be a direct effect of phosphate to decreased calcium reabsorption in the distal nephron.
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18
Q

excessive cortisol effect on

calcium?

A

Excessive cortisol
decreases intestinal calcium absorption
increases calcium loss from the kidney,
inhibits bone matrix formation
causes secondary hyperparathyroidism

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19
Q

TNF alpha effect on bone

inhibits and enhances?

A

TNF-alpha inhibits osteoblastic activity and enhances osteoclastic bone resorption

20
Q

what are the 3 laws of bone remodeling?

A
21
Q

Bone remodeling mechanism

cortical bone
cancellous bone
how does sclerostin affect bone formation

A
22
Q

Bone morphenetic protein (BMP)

what receptor and path way?
effect on fx healing?
which one is approved and what for?
properties?
effect on embrology/development?

A
  • promotes deferentiation of mesechymal cells into chondrocytes and osteoblasts
  • inflammatory phase of healing BMPs target undifferentiated mesenchymal stem cells through extracellular serine-threonine receptors.

  • has been found to increase chondrogenic phenotype and matrix synthesis in intervertebral discs
  • uses: single-­level ALIF from L2 to ­S1 levels in degenerative disc disease together with the lumbar tapered fusion device (LT Cage; Medtronic)
    open tibial shaft fractures stabilized with an IM nail and treated within 14 days of the initial injury
  • Mutations in BMP-4 are associated with Fibrodysplasia ossificans progressiva
23
Q

TGF beta function on bone remodeling

A

*function stimulates undifferentiated mesenchymal cell proliferation. stimulates production of Type II collagen and proteoglycans by mesenchymal cells
* souce: platelets, bone ECM, cartilage matrix
* seronine theonince sulfate
* TGF-B is used to coat porous coated implants to promote bone ingrowth

24
Q

IGF 1 effects on bone

A

Increased amounts of the active steroid hormone metabolite promote proliferation and maturation of the growth plate. active metabolite that enters target cells and signals a nuclear receptor to stimulate both proliferation and maturation of the growth plate.

signal mechanism involves tyrosine kinase receptors

25
Q

thiazolidinediones effect on bone

A

Thiazolidinediones (TZDs) are agonists of peroxisome proliferator-activated receptor-γ (PPAR-γ) which has been reported to lead to an increase in bone marrow adiposity and a decrease in osteoblastogenesis, leading to an overall decrease in BMD

TZDs have been demonstrated to improve insulin sensitivity and currently represent a widely prescribed elective treatment for type 2 diabetes. They increase insulin sensitivity by their binding to the nuclear receptor and transcription factor, PPAR-γ. Activation of PPAR-γ by TZDs causes an increase in bone marrow adiposity and a decrease in osteoblastogenesis, resulting in reduced bone formation. Recent clinical data have found that intake of thiazolidinediones by older patients with type 2 diabetes correlates with both the decrease of bone mineral density in the femoral neck and hip and a higher risk for fractures.

26
Q

PPAR-y

A

PPAR-gamma is a regulator of mesenchymal progenitor cell that induces adipocyte formation

27
Q

BMP induces ? differentiation
RUNX2 induces ? differentiation
SOX9 induces ? differentiation
Wnt-beta-catenin induces ? differentiation

A

BMP induces OSTEOGENIC differentiation
RUNX2 induces OSTEOGENIC differentiation
SOX9 induces CHONDROGENIC differentiation
Wnt-beta-catenin induces OSTEOGENIC differentiation

28
Q

resorption rates of bone graft substitutes

fastest to slowest ?

A

calcium sulfate > tricalcium phosphate > hydroxyapatite

29
Q

allograft articular cartilage 5 years after implantation will show?

A

5 years after implantation, allograft articular cartilage is completely acellular - no donor or recipient chondrocytes will be present

30
Q

Bone graft properties

osteoconductive
osteoinductive
osteogenic

A

Osteoconductive: structure frame work, DBM

Osteoinduction: growth factors that stimulare growth and induction of stem cells down bone forming lineage. BMP

Osteogenic: cells that will produce bone including mesenchymal stem cells, osteoblast, chondrocytes (mesenchymal stem cells can potentially differentiate down any cell line
osteoprogenitor cells differentiate to osteoblasts and then osteocytes). cancellous bone has a greater ability than cortical bone to form new bone due to its larger surface area. autologous bone graft (fresh autograft and bone marrow aspirate) is the only bone graft material that contains live mensenchymal precursor cells

31
Q

Antigenecity to graft

class of antigens?
what cells elicit the greatest response?
what does not elicit a response?

A

Class I and Class II antigens on graft are recognized by host T lymphocytes and elicit an immune response

immunogenic cells are marrow-based, endothelium, and retinacular-activating cells

bone marrow cells elicit the greatest immune response

extracellular matrix also acts as an antigen:
— type I collagen stimulates both humoral and cell-mediated responses
— noncollagenous matrix (proteoglycans, osteocalcin)

hydroxyapatite has not been shown to elicit an immune response
primary rejection is cell-mediated related to the major histocompatibility complex (MHC) incompatibility

32
Q

types of autograft

cancellous
cortical
vasc bone graft

A
33
Q

allograft

Fresh
Fresh Froxen
Freeze dried

What has the highest/lowest risk of disease transmision? what kind of properties does each have?

A

Fresh allograft: rarely used do to disease transmission

**frozen or freeze-dried **
* reduces immunogenicity while maintaining osteoconductive properties
* reduces osteoinductive capabilities

shelf life
two years for fresh frozen stored at -20 degrees C
five years for fresh frozen stored at -70 degrees C
indefinite for freeze-dried

34
Q

Demineralized Bone Matrix

DBM

A

Acidic extraction of bone matrix from allograft
removes the minerals and leaves the collagenous and noncollagenous structure and proteins. Acid extraction, removes calcium and phosphate but leaves the extracellular matrix.

Properties
osteoconductive without structural support
osteoinductive despite loss of some osteoinductive molecules

35
Q

Level I evidence of calcium phosphate

A

Level I evidence shows that calcium-phosphate bone substitutes allow for bone defect filling, early rehabilitation, and prevention of articular subsidence in distal radius and tibial plateau fractures

36
Q

Reamer aspirate Irrigator

union rates vs ICA?
benefits compared to ICA?
possible complications?

A
  • Union rates comparable to iliac crest autologous bone grafting
  • benefits: Shorter operative time
    Fewer immediate postoperative complications
    Higher volume of graft harvested
  • higher volume blood loss and transfusion rate compared to iliac crest autologous bone grafting,
    femoral shaft fracture due to eccentric reaming,
    insertion site pain (hip abductors)
37
Q

risks and complications with bone grafting

Hep B
Hep C
HIV
allografts are all tested for?
Serous wound drainage?

A

Hep B 1:63k
Hep C 1:100k
HIV 1:1-1.6 million
Serous wound drainage: calcium sulfate bone graft

38
Q

Cytokines that have been identified as factors that promote osteolysis in response to inflammation include

A

IL-6, IL-1, TNF-alpha, RANK

39
Q

Phases of Bone healing

inflammatory phase:
early callous:
mature callous:
remodeling:

A
  • hematoma formation with inflammatory cell invasion into the fracture site describes the immediate inflammatory stage of bone healing
  • early callous: beginning of chondrogenesis at the fracture site with the formation of a zone of provisional preliminary calcification is consistent with the early callus phase of bone healing in which the initial bone callus is a non-ossified cartilaginous matrix that becomes ossified in the mature callus phase of bone healing.
  • mature callous: apoptosois of cartilage cells with mineralization and ossification of the cartilaginous matrix
  • remodeling: mature callus is then remodeled and reorganized into mature lamellar bone in the remodeling phase of bone healing
40
Q

class II medical device
de novo pathway
humanitarian device exception

A

class II medical device regulated through the 510(k) pathway should demonstrate substantial equivalence to a legally marketed predicate device.

Establishing that the probable benefits outweigh the probable risks is part of the regulatory framework for the De Novo pathway

limitation to a patient population of 8000 individuals per year is part of the regulatory framework for the Humanitarian Device Exemption pathway.

(i.e., a predicate device)

41
Q

In designing a study it is important for the results to be applicable across a large patient population:
external validity means,

A

outcomes of the study can be expected to apply to a large population.

Having strict inclusion criteria may improve the internal validity of a study, that is showing a true cause and effect relation, but at the cost of generalizability.

42
Q

alpha vs beta error

A

Alpha error refers to accepting a hypothesis as true when in reality it is false. The P value is set at 5% as a matter of convention, which means 5% of the time when statistical significance is achieved this will be actually false. Beta error is the opposite. The hypothesis is rejected when it is in reality true. This is seen in underpowered studies that lack the numbers and effect sizes in treatment groups demonstrate statistical significance.

43
Q

What connective tissue portion of a peripheral nerve must be intact for the full recovery of a damaged peripheral nerve?

A

Axonotmesis, or second-degree injury, is a nerve injury resulting in damage to the axon, leading to Wallerian degeneration distally and regeneration with axonal sprouting at the proximal nerve stump. The supporting endoneurium and perineurium remain intact and are available to direct the mechanisms of regeneration along the proper path. Concomitantly, a Tinel sign is apparent at the level of injury and advances distally as the nerve regenerates. The classic rate of nerve recovery is 1 inch per month or 1.5 mm per day. Most importantly, the Schwann cell basement membrane is not damaged; therefore, full recovery of motor and sensory function to preinjury levels may occur. Diagnosis of this extent of nerve injury is made only after recovery occurs.

Sunderland’s third-degree nerve injury differs from a second-degree injury (axonotmesis) in that it includes endoneurial damage and subsequent scarring. Regeneration will be incomplete, because fibrotic scar tissue becomes a barrier that prevents the nerve fibers from reaching their end organs or receptors.

44
Q

ossification of the carpus

A

capitate: 1 to 3 months
hamate: 2 to 4 months
triquetrum: 2 to 3 years, lunate: 2 to 4 years
scaphoid: 4 to 6 years,
trapezium: 4 to 6 years, trapezoid: 4 to 6 years
pisiform: 8 to 12 years.

45
Q

energy substrates for skeletal muscle at 10s, 1-4 minutes, longer than 4 minutes

A

In strictly anaerobic activities lasting less than 10 seconds, skeletal muscles use ATP and creatine phosphate

During activities that are aerobic and anaerobic (typically lasting 1 to 4 minutes), skeletal muscle uses glycogen and lactic acid as a substrate.

longer than 4 minutes, glycogen and fatty acids are the preferred substrate.

46
Q
A

ABOS (16 decks)

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