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Basic Science 1 Flashcards

1
Q

Toughness

A

Amt energy absorbed before failure
= area under stress/strain curve

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2
Q

Fatigue strength

A

Breaking after many load cycles

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3
Q

Osteopoikilosis
- What is it
- Inheritence

A

Bone islands, benign, often around joints
AD
No treatment needed

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4
Q

What is fretting corrosion

A

Micro motion at metal/metal interface
Think modular implants (aka not loose)

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5
Q

What is crevice corrosion

A

Pitting leading to ion release

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6
Q

What is glavanic corrosion

A

2 dissimilar metals in contact -> electrochem rxn -> ion release

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7
Q

What is adhesive wear

A

2 surface rub together and remove material from the less wear resistant surface

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8
Q

Mutation Marfans

A

Fibrillin 1 mutation - AD
Elevated TGF-beta

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9
Q

What do the following tests measure
- Northern blot
- Southern blot
- PCR

A

North: RNA
South: DNA
PCR: amplifies DNA fragments

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10
Q

What is the difference between the organization of woven vs lamellar bone?

A

Woven (frx callus, pathologic states)
- Randomly organized
- High cellularity

Lamellar (cortical, cancellous)
- Layers oriented by stress (Wolff’s law)
- Less cellular

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11
Q

What is the strain environment for each of the following osteoprogenitor cells?
- Fibroblast
- Chondroblast
- Osteoblast/cyte

A

Strain = change length/length

Fibroblast - high strain
(Why high strain fractures ie bridging a simple pattern results in a fibrous union)
Chondroblast - med strain, low O2
Osteoblast/cyte - low strain, high O2
(Why want low strain and good blood flow for frx healing)

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12
Q

What are 3 TF critical for osteoblast development?

A

Wnt signaling pathway
1. In response to mechanical stress, progenitor cells release Wnt proteins that cause production of B-Catenin
2. B-catenin -> Runx2 -> Osx

Runx2
B-catenin
Osx

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13
Q

What cells do the following TFs control?
1. Sox9
2. PPARgamma

A

Sox9 - chondrocytes
(Sox sux for making bone)
PPARgamma - adipoctyes

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14
Q

What 3 substances do osteoblasts produce? What 2 receptors on osteoblasts control this?

A
  1. PTH - via adenylyl cyclase, if pulsed anabolic effect on bone
  2. Vit
    - Bind to:
    BLASTS
    - Make:
  3. Type 1 collagen
  4. Alk phos
  5. RANK-L
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15
Q

How do osteocytes inhibit osteoblasts?

A

Sclerostin - inhibits bone formation via Xs osteoblasts
Want LOW levels if supplementing a patient with Vitamin D

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16
Q

What molecules increase vs decrease sclerostin?

A

PTH increases sclerostin = less bone
- PTH reduces bone if chronically high (vs pulsed is anabolic)
- High serum Ca, low PO4
Calcitonin deceases sclerostin = more bone

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17
Q

Where do osteoclasts come from?
How/where does resorption occur?

A

Hematopoietic cells aka macrophage lineage
- Don’t worry about TFs

Resorption:
- At ruffled border (capthesin K = enzyme here)
- Forms Howships lacunae
- TRAP (tartrate resistant acid phosphate) lowers pH w/ carbonic anhydrase to dissolve hydroxyapatite crystals

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18
Q

How do osteoclasts bind to bone?

A

Binds via integrins -> vibronectin
- Vibronectin: Arg - Gly - Asp (RGD) sequence

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19
Q

Carbonic anhydrase mutation disease
- Mechanism of disease
- Inheritance
- Clinical presentation
- XRs
- Trt

A

CA: osteopetrosis
- Osteoclasts can’t acidify Howship lacuna = high bone density
- Don’t see a ruffled border on the histo

AR form of the disease (vs AR proton pump dysfxn that is fatal)

Progressive blind/deaf, anemia as bone marrow gets squashed (bleeding)

XRs: rugger jersey spine (aka v dense bone), erlenmeyer flask prox hum/dist fem, coxa vara

Trt:
- Definitive: bone marrow transplant
- Plate frx (avoid IM fixation) - surg fixation has high union rates

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20
Q

What 2 molecules made by osteoblasts regulate osteoclasts?

A

OPG - inactivates RANK to inactivate clasts
- B-catenin is TF that stimulates blasts to release OPG to shut down clasts
- OPG = decoy receptor for RANK

RANKL - activates clasts
- PTH stimulates blasts to release RANK to stimulate clasts

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21
Q

How does calcitonin regulate bone?

A

From parafollicular cells thyroid
Binds to clasts to shut down

Decreases serum Ca bc keeping it in bone

Calcitonin is the opposite of PTH
- PTH increases Ca, decrease PO4

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22
Q

How does cancer cause lytic lesions in bone?

A

IL 1 and PTHrP stimulates RANK

RANK resorbs!

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23
Q

What 2 molecules suppress osteoblasts?

24
Q

How does cortical vs cancellous bone remodel?

A

Cortical: cutting cones in osteons
Cancellous: on bone surface via blast/clast cycle

25
What are the 3 types of bone formation?
Intramemb - no cartilage model, flat bones - Haversian remodeling - Primary bone healing Enchondral - calcified cartilage (bone replaces cartilage), long bones / callus / physis Appositional - on top of old bone, periosteal bone enlargement by width
26
What collagen do chondrocytes secrete in the hypertrophic zone of the growth plate?
Type X col VEGF also here to induce vascular invasion
27
What part of the growth plate do salter harris fractures occur through
Zone of provisional Ca WITHIN the hypertrophic zone
28
What are the 3 stages of 2ary bone healing?
Inflam - Osteo/fibroblasts - In theory, COX2 inhibition represses runx2/osterix here, changes the differentiation pathway for blasts Repair - If stable environment (low strain) - get blasts - If unstable environment (higher strain) - get chondrocytes (medium) or fibroblasts (high) - MMPs degrade the ECM - Enchondral oss changes soft -> hard callus : T 2/9/10 col -> T1 col Remodel according to Wolffs law
29
What is the theory behind electrical bone stimulators
Increase blasts - Decrease O2 - Increase pH
30
Define the following + give examples 1. Osteoconductive 2. Osteoinductive 3. Osteogenic
1. Conductive = scaffold - Cancellous allo 2. Inductive = GFs to stim bone - DBM, BMP 3. Geneic = cellular elements to make new bone - AUTOGRAFT
31
How do cancellous graft incorporate?
Creeping substitution
32
Vitamin D - What is the active form - How does it work
1,25 Vit D = active 25 vit D = lab study to det vit D def Resorbs Ca in kidneys
33
What is the structure of T1 col
Triple helix 2 alpha1 chains 1 alpha 2 chain
34
What are the labs for renal osteodystrophy
Kidneys are impaired - Can't excrete PO2 -> high PO4 (uremia) - Can't make 1,25 vit D -> low Ca Changes PTH Sx are of low Ca: stones, groans, psychiatric overtones
35
What are the 2 forms of renal osteodystrophy?
1. High PTH - low Ca = 2ary hyper PT - Brown tumors -> pathologic frx Labs: low Ca, high PO4 / alk phos / PTH 2. Normal PTH - No hyperPT
36
What is Rickets? 4 major causes/types?
Can't mineralize bone @ ZPA (in hypertrophic zone) In kids = Rickets = problem at cartilage matrix In adults = osteomalacia = problem at bone matrix 1. Nutritional (vit D def) 2. Hereditary vit D dep 3. Familial hypophos rickets 4. Hypophosphatasia
37
Mutation + labs familial hypophos rickets
X-dom PHEX gene Can't absorb PO4 **Normal serum Ca
38
What are the levels of T score for osteopenia vs osteoporosis?
DEXA tells you your T score > 1 = normal -1 to -2.5 = penia < -2.5 = porosis
39
Who do you treat for osteoporosis?
T score < -2.5 If post meno women or men >50yo have: - Hip or vertebral fracture - Penia w/ hx frx, FRAX score for hip frx risk >3% and other osteoporotic frx risk >20%
40
What are the Ca and vit D doses when treating osteoporosis? What is the goal serum vit D?
Ca: 1200-1500 mg/d Vit D: 800-1000 IU/d Want serum 25 vit D to be 41-250 ng/mL Think 1000/1000/50-250
41
What hormones are bone metabolic vs anabolic?
Metabolic: estrogen - Raloxifene - reduces osteoclast activity Anabolic: PTH - Teriparatide (CI Pagets for 2ary osteosarcoma)
42
Bisphos 1. General mechanism 2. Nitrogen mechanism 3. Non-nitrogen mechanism
Mechanism: taken up by clasts -> clast apoptosis Nitrogen: 1000x more potent - Xs farnesyl pyrophosphate synthase - Lose GTPase formation at ruffled border Non-nitrogen - Breakdown into a non-useable form of ATP -> apoptosis
43
What is denosumab (Prolia)
IgG vs RANKL No RANK = no clasts
44
What is the structure of a sarcomere?
Individual muscle unit Thick filament = myosin (A band) Thin filament = actin (I band)
45
Define the following Isotonic Isometric Isokinetic
Isotonic = length changes, tension constant Isometric = length constant, tension changes Isokinetic = VELOCITY constant, tension changes
46
How does muscle change with strength conditioning
Increase fiber size If increase fiber size -> increase cross sectional area = proportional to force
47
What is the order of energy substrate used in muscle
1. <10s = ATP + creatine phosphate (no O2 use so no lactate) 2. 1-4 min = glycogen + lactic acid 3. >4min = glycogen + fatty acid (O2 system)
48
What cells repair muscle injury
Satellite cells Heal w/ dense fibrosis via TGF beta Tears at MT jxn > mid substance
49
Order of nerve structure (small to large)
Axon Myelin sheath - made by Schwann cells CNS, glial cells PNS Endoneurium Fascicles Perineurium Epineurium - cushions against external pressure
50
Name the nerve cell type for the following sensations: 1. Touch 2. Autonomic NS 3. Pain
1. Type A - heavy myelin, fast conduction speed - TOUCH 2. Type B - intermediate myelin, medium speed - ANS 3. Type C - no myelin, slow conduction - pain
51
Order the following in the way in which they RECOVER after nerve injury (aka first to come back -> last) Loss of function would be opposite order
Recover first: sympathetic Pain Temp Touch Proprioception Recover last: motor - endoneurium must be intact for full recovery
52
Define the following Neurapraxia Axonotmesis Neurotmesis
Neurapraxia - reversible nerve injury Axonotmesis - disrupt the axon and myelin sheath but the epineurium is intact (aka very outside) Neurotmesis - complete nerve division, worst prognosis
53
What is the role of decorin and aggregan in tendon?
Decorin = regulates diameter - Transfers loads as cross links between fibers Aggregan @ points of tendon compression
54
What are Sharpey's fibers?
Mineralized fibrocartilage that binds tendon to bone Tendon -> fibrocart -> mineralized fibrocart (Sharpey) -> bone
55
Timeframe for tendon repair strength
7-10d weakest 21d original strength 6mo max strength = 2/3 original strength

Millers (29 decks)

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