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Millers > Basic Science 1 > Flashcards

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?

A

TNF
DKK1

24
Q

How does cortical vs cancellous bone remodel?

A

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

25
Q

What are the 3 types of bone formation?

A

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
Q

What collagen do chondrocytes secrete in the hypertrophic zone of the growth plate?

A

Type X col

VEGF also here to induce vascular invasion

27
Q

What part of the growth plate do salter harris fractures occur through

A

Zone of provisional Ca WITHIN the hypertrophic zone

28
Q

What are the 3 stages of 2ary bone healing?

A

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
Q

What is the theory behind electrical bone stimulators

A

Increase blasts
- Decrease O2
- Increase pH

30
Q

Define the following + give examples
1. Osteoconductive
2. Osteoinductive
3. Osteogenic

A
  1. Conductive = scaffold
    - Cancellous allo
  2. Inductive = GFs to stim bone
    - DBM, BMP
  3. Geneic = cellular elements to make new bone
    - AUTOGRAFT
31
Q

How do cancellous graft incorporate?

A

Creeping substitution

32
Q

Vitamin D
- What is the active form
- How does it work

A

1,25 Vit D = active
25 vit D = lab study to det vit D def

Resorbs Ca in kidneys

33
Q

What is the structure of T1 col

A

Triple helix
2 alpha1 chains
1 alpha 2 chain

34
Q

What are the labs for renal osteodystrophy

A

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
Q

What are the 2 forms of renal osteodystrophy?

A
  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
Q

What is Rickets? 4 major causes/types?

A

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
Q

Mutation + labs familial hypophos rickets

A

X-dom
PHEX gene
Can’t absorb PO4
**Normal serum Ca

38
Q

What are the levels of T score for osteopenia vs osteoporosis?

A

DEXA tells you your T score
> 1 = normal
-1 to -2.5 = penia
< -2.5 = porosis

39
Q

Who do you treat for osteoporosis?

A

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
Q

What are the Ca and vit D doses when treating osteoporosis?
What is the goal serum vit D?

A

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
Q

What hormones are bone metabolic vs anabolic?

A

Metabolic: estrogen
- Raloxifene - reduces osteoclast activity
Anabolic: PTH
- Teriparatide (CI Pagets for 2ary osteosarcoma)

42
Q

Bisphos
1. General mechanism
2. Nitrogen mechanism
3. Non-nitrogen mechanism

A

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
Q

What is denosumab (Prolia)

A

IgG vs RANKL
No RANK = no clasts

44
Q

What is the structure of a sarcomere?

A

Individual muscle unit
Thick filament = myosin (A band)
Thin filament = actin (I band)

45
Q

Define the following
Isotonic
Isometric
Isokinetic

A

Isotonic = length changes, tension constant
Isometric = length constant, tension changes
Isokinetic = VELOCITY constant, tension changes

46
Q

How does muscle change with strength conditioning

A

Increase fiber size
If increase fiber size -> increase cross sectional area = proportional to force

47
Q

What is the order of energy substrate used in muscle

A
  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
Q

What cells repair muscle injury

A

Satellite cells
Heal w/ dense fibrosis via TGF beta

Tears at MT jxn > mid substance

49
Q

Order of nerve structure (small to large)

A

Axon
Myelin sheath - made by Schwann cells CNS, glial cells PNS
Endoneurium
Fascicles
Perineurium
Epineurium - cushions against external pressure

50
Q

Name the nerve cell type for the following sensations:
1. Touch
2. Autonomic NS
3. Pain

A
  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
Q

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

A

Recover first: sympathetic
Pain
Temp
Touch
Proprioception
Recover last: motor - endoneurium must be intact for full recovery

52
Q

Define the following
Neurapraxia
Axonotmesis
Neurotmesis

A

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
Q

What is the role of decorin and aggregan in tendon?

A

Decorin = regulates diameter
- Transfers loads as cross links between fibers

Aggregan @ points of tendon compression

54
Q

What are Sharpey’s fibers?

A

Mineralized fibrocartilage that binds tendon to bone

Tendon -> fibrocart -> mineralized fibrocart (Sharpey) -> bone

55
Q

Timeframe for tendon repair strength

A

7-10d weakest
21d original strength
6mo max strength = 2/3 original strength

Millers (29 decks)

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