Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Basic Science > Basics of BScience > Flashcards

Basics of BScience Flashcards

1
Q

5 things osteoblasts make

A 
Col 1 (collagen)
Osteocalcin
Osteonectin
Alk phos - basic environment to build bone
RANK L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some TFs that push mes stem cells to become osteoblasts

A 
CBFA / RUNX
WNT / B catenin
IHH / IGF 2
LRP 5/6 / Osterix
BMP / SMAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What cells do mes stem cells becomes in 1. high strain 2. med strain 3. low strain environments

A
  1. High strain -> fibroblast
  2. Med strain + low O2 + SOX 9 -> chondroblasts
  3. Low strain + high O2 (think absolute stability + good BF) -> osteoblast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 2 receptors on osteoblasts

A

PTH-R: binds PTH and PTHrP (tumors)

1,25 vit D - R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 3 main products of osteoclasts?

A

MMP
Cathepsin K
TRAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do osteoclasts bind to bone?

A

alpha V beta 3 on blasts bind Vitronectin on bone

RGD sequence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do osteoblasts make to DOWNREG osteoclasts?

A

OPG = decoy for RANK L receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What inflammatory markers activate osteoclasts?

A 
IL 1
IL 6
TNF alpha
PG E2
Vit D and PTH via blasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What 5 factors inhibit osteoclasts?

A 
Calcitonin 
TGF beta (opposite of activating alpha)
IL 10
OPG xs RANK L from blasts
Estrogen " "
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What molecule do osteocytes make -> what does this do?

A

Sclerostin (SOST gene)
via DKK 1 pathway
Xs WNT / B catenin TF - fewer mes stem cells become osteoblasts = decreased bone mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name 2 diseases that have sclerostin deficiency

A
  1. Sclerosteosis
  2. Van Buchem disease
    Sclerostin def
    More WNT/B cat -> more blasts = increased bone mass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is cleidocranial dysplasia?

A

AD
Mutated CBFA / RUNX TF - less mes stem cell to osteoblasts
Problem with intramem oss
Missing clavicles (hyper mobile shoulders) + teeth
STRANGER THINGS
Op: inter-troch osteotomy for coxa vara (neck shaft angle <100 deg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is intra-membranous ossification?

A

Bone healing w/o cartilage model

Mes stem cells -> osteoblasts -> organic matrix deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the pathophys and presentation of osteopetrosis

A

CLAST malfunction - can’t acidify Howship lacuna (broken carbonic anhydrase) - can’t resorb bone
Very dense bone but fragile w/o medullary canal
- Frx
- Skull - CN palsy
- Decreased vascularity = higher risk osteomyelitis
- Coxa vara
XR: bone-in-bone w/o med canal, erlenmeyer flask prox hum/distal femur, rugger jersey spine
Trt varies by inheritance pattern
- AD = Albers Schonger ds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do tumors cause osteolysis? What do labs show? Trt?

A 
Make 
1. RANK-L -> direct activate clasts
2. PTHrP -> blasts activate clasts
Net: hyperCa of malig
Trt: bisphos
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Labs for Pagets

A

High urine N & C telopeptides
High ALP
NORMAL Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathophys Pagets

A 
"Focally increased remodeling of bone"
More clast activity 
Spontaneous >> AD
3 phases that may co-exist:
1. Lytic 
2. Mixed
3. Sclerotic - blast predom
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Presentation Pagets

A 
Often asx
Bone pain
Fractures 
Intense pain + swelling - worry about Paget sarcoma
Cardiac - high output cardiac failure 
XR: bone bowing, cotton wool skull
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Comp Pagets

A 
2ary sarcoma (osteosarc)
VERY poor prognosis - chemo, wide res
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Trt Pagets

A

Bisphos - ONLY if sx
2nd line - calcitonin
CI = teriparatide (recombinant PTH), increases risk 2ary sarcoma
Bone bowing refractory to bracing - osteotomy and plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the most common comp of TKA vs THA in Paget’s patients?

A

TKA: Malalignment
THA: Hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the pathophys and presentation of osteopetrosis

A

CLAST malfunction - can’t acidify Howship lacuna (broken carbonic anhydrase) - can’t resorb bone
Very dense bone but fragile w/o medullary canal
- Frx
- Skull - CN palsy
- Decreased vascularity = higher risk osteomyelitis
- Coxa vara
XR: bone-in-bone w/o med canal, erlenmeyer flask prox hum/distal femur, rugger jersey spine
Trt varies by inheritance pattern
- AD = Albers Schonger ds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do tumors cause osteolysis? What do labs show? Trt?

A 
Make 
1. RANK-L -> direct activate clasts
2. PTHrP -> blasts activate clasts
Net: hyperCa of malig
Trt: bisphos
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Labs for Pagets

A

High urine N & C telopeptides
High ALP
NORMAL Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pathophys Pagets

A 
"Focally increased remodeling of bone"
More clast activity 
Spontaneous >> AD
3 phases that may co-exist:
1. Lytic 
2. Mixed
3. Sclerotic - blast predom
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What cell do chondrocytes come from? What 2 molecules do chondrocytes make?

A

From chondroblasts
Collagen + PG = cartilage
Collagen = tensile strength, increases via cross linking
PG = hydrophilic, keratin + chondrotin sulfate bound to a protein core on a HA backbone, compressive strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Is collagen make intra or extra cellular

A

Make intra cell

Assembled extra-cell - makes sense BIG molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Trt Pagets

A

Bisphos - ONLY if sx
2nd line - calcitonin
CI = teriparatide (recombinant PTH), increases risk 2ary sarcoma
Bone bowing refractory to bracing - osteotomy and plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the most common comp of TKA vs THA in Paget’s patients?

A

TKA: Malalignment
THA: Hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 2 types of bisphos?

A

N containing - X clast GTPase

Non-N: toxic ATP analog -> clast apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Mechanism of denosumab

A

mAB OPG analog

Xs RANK L - can’t bind receptor on clasts - less clast activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What disease would result from loss of OPG?

A

OPG blocks RANK L from binding and activating clasts
No OPG = more clasts
OSTEOPOROSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are 3 cartilage promoting growth factors (mnemonic TIP)

A

TGF beta
IGF 1
PDGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What cell do chondrocytes come from? What 2 molecules do chondrocytes make?

A

From chondroblasts
Make
collagen + PG = cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Is collagen make intra or extra cellular

A

Make intra cell

Assembled extra-cell - makes sense BIG molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Type 1 collagen makes up what + disease

A

BONES, lig, tendon

Osteogenesis imperfecta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Type 2 collagen makes up what + disease

A

Articular cartilage, nucleus pulposus

SED congenita

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Type 3 collagen makes up what + disease

A

Tendon + lig initial healing

Dupuytrens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Type 5 collagen makes up what + disease

A

Stabilizes col 1

Ehlers Danlos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Type 9 collagen makes up what + disease

A

Stabilizes col 2

Multiple epiphyseal dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Type 10 collagen makes up what + disease

A

Initial fracture healing

Schmid chondrodysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Type 11 collagen makes up what + disease

A

Collagen glue

Stickler syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are 2 key molecules in synovial fluid?

A

Lubricin

HA - shock absorbers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Describe type 1 vs 2 muscle fibers

A

T1: slow, oxidative = slow twitch = aerobic, endurance
Smaller, less force, slower but fatigue resistant
RECRUITED FIRST
T2 = fast twitch = anaerobic (ATP-CP), speed
2a: fast ox-glyc
2b: fast glycolytic
More forceful muscle contraction, more fatigue-able

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe collagen changes (up or down) w/ OA:

  1. H2O
  2. PG
  3. Collagen quantity
  4. Collagen cross linking
  5. Elastic modulus
A

OA: “wet + soft”
1. More water
2-5. Less PG, collagen amt and cross linking, elastic modulus

46
Q

Describe collagen changes w/ aging:

  1. H2O
  2. PG
  3. Collagen quantity
  4. Collagen cross linking
  5. Elastic modulus
A

Aging: “dry + stiff”

  1. Less water
  2. Less PG
  3. No change in coll quantity***
  4. More coll cross linking (stiffer) => 5. Higher modulus
47
Q

What chemokines are pro-OA?

A

IL 1/6 & TNF alpha [pro-clast]
Turn on
1. Collagenase/MMPs - decrease collagen
2. Stromelysin - degrade PG

48
Q

What are the tissues/molecules in ligaments?

A

Col 1 (70%) - col 3 for early healing
PG
H2O
Elastin

49
Q

How do ligaments heal - what changes to the fibers?

A

Increase # fibers

But lower x linking, diameter, and mass

50
Q

What are the 3 types of collagen in tendons?

A

Col 1 (95%) > col 3 > col 5

51
Q

When in the healing phase are tendons the weakest?

A

Inflam phase: days 7-10

52
Q

What type of collagen increases in early OA

53
Q

What are the 2 molecules in a sarcomere?

A

Thick = myosin

Thin - actin

54
Q

What do satellite cells do in muscle?

A

Repair muscle w/ fibrosis - reduces strength

55
Q

Mechanism of lidocaine

A

x Na+ channels - can’t initiate nerve AP via Na/K channels

56
Q

Mechanism of botox

A

Xs ACh release from nerve endings -> can’t bind to muscle on post-synapse

57
Q

What is the Ab in myasthenia gravis?

A

Ab vs ACh-R

58
Q

What type of exercise is best for building muscle?

A

Eccentric (lengthening) + isokinetic (constant speed)

59
Q

What type of collagen increases in early OA

60
Q

What are the 5 regions of the growth plate

A 
Reserve zone
Proliferative zone
3 parts hypertrophic zone:
1. Zone of maturation
2. Zone of degeneration
3. Zone of provisional calcification
61
Q

What happens in the reserve zone? Diseases? (PKGD)

A 
Matrix production
PKGD (packaged)
P = pseudoachondroplasia (COMP gene)
K= Kniest syndrome (col defect)
G = Gaucher (beta glucocerebrosidase)
D = diastrophic dysplasia (AS, sulfate transport gene)
62
Q

What happens in the proliferative zone? Diseases? (MEGA)

A 
Cellular division
See columnar organization
MEGA:
ME = MHE (AD, EXT gene)
G = gigantism
A = achondroplasia (AD, FGFR3 mutation)
63
Q

How does 2ary bone healing occur? What type of collagen is involved?

A 
Enchondral ossification 
Blasts lay cartilage frame 
Remodeled through Howship lacunae 
2-10% strain -> callus 
Type X = early frx healing
64
Q

What is the mechanism that lead poisoning affects bones?

A

Lead xs PTHrP
PTHrP stops physeal maturation @ hypertrophic zone
x PTHrP -> physis matures -> decreased peak bone mineral density

65
Q

What is the difference between 1ary and 2ary spongiosa of the metaphysis?

A 
1ary = WOVEN bone 
2ary = LAMELLAR bone
66
Q

What does AER pattern

A

Prox-distal
Apex = most proximal aspect
Go distal down the ridge

67
Q

What does ZPA pattern

A

Radial-ulnar

Radial and ulnar are polar opposites

68
Q

What does WNT pattern

A

Dorsal-ventral

WANT front and back!

69
Q

How does 1ary bone healing occur?

A

Intra-mem oss
Cutting cone/Haversian remodeling
1ary bone healing = NO strain = absolute stability (compression plating)
No callus

70
Q

How does 2ary bone healing occur? What type of collagen is involved?

A 
Enchondral ossification 
Blasts lay cartilage frame 
Remodeled through Howship lacunae 
2-10% strain -> callus 
Type X = early frx healing
71
Q

Mechanism that PTH works

A

LESS PO4 resorption @kidney
Increase 1,25 vit D prod at kidney
Increase blast -> blast activation -> increase Ca + PO4 in blood
Increase Ca from kidney and gut, PO4 gut resorption

72
Q

Name the disease: high Ca, PTH, alk phos / low PO4

A

Hyper PTH
binds blasts -> high alk phos makes sense
Sx: stones, groans, mona, psychiatric overtones

73
Q

What bone changes do you see with hyper PTH

A

Brown tumors = focal demineralization

74
Q

Name the disease: low Ca and PTH, high PO4

75
Q

Name the disease: low Ca and PO4, high PTH and alk phos

A

Nutritional rickets = vit D def

PTH high b/c trying to compensate -> binds blasts -> high alk phos

76
Q

Which zone of the growth plate does rickets affect

A

ZPC/hypertrophic

77
Q

Name the disease: normal Ca and PTH, high alk phos, low PTH

A 
X linked hypo PO4 rickets
XL dom
PHEX gene
Can't resorb PO4 @ kidney
Wide prox tibial physis -> bowing
Trt: PO4 &amp;&amp;&amp;&amp; vit D
78
Q

Name the disease: low Ca / high PO4, PTH, alk phos

A

Renal osteodystrophy
Kidney retaining PO4
Can’t make vit D
High PTH to compensate -> high alk phos

79
Q

What leg deformity is seen with renaL osteodystrophy

A

Genu vaLgum

80
Q

What T score is osteoporosis vs osteopenia

A

< -2.5 = porosis

-1 - -2.5 = penia

81
Q

What is the highest risk factor for osteoporosis fracture

A

Prior fragility frx

Vert > hip > wrist

82
Q

What is osteomalacia? Labs?

A

Decreased mineralization -> bone QUALITY problem

Low vit D

83
Q

What bone supplements should you give pts over >50yo

A

Ca 1K - 1500 mg/d
Vit D 1K IU/d
Reduces frx risk

84
Q

Which disease as MARGINAL syndesmophytes

85
Q

Which disease has non-marginal flowing wax syndesmophytes

86
Q

What C spine condition should you check for w/ DISH

A

Hyper-ext inj w/o frx - CENTRAL CORD sx

87
Q

What is creep

A

Constant load get increased deformation/displacement over time
Ex: plastic

88
Q

What is anisotropy

A

Material properties change w/ direct of load applied on bone

89
Q

3 antibiotics that target transcription

A

Rifampin - DNA dep RNA pol
Quinolones - DNA gyrase
Metronidazole - DNA

90
Q

Define material toughness

A

Amt energy a material can absorb before failure

91
Q

Equation for bending rigidity of a solid cylinder (ex fix)

92
Q

Mechanism of rivaroxaban and apixaban

A

Xa inhibitors (-xaban)

93
Q

HST 4

A

T cells

Ex: METAL ALLERGY

94
Q

Mechanism of daigatran

A

2a inhibition

95
Q

What vit K def clotting factors does Lorelai miss

A

2, 7, 9, 10, C &S

96
Q

HST rxn 1

A

IgE -> mast cell

Allergies (Asthma)

97
Q

HST rxn 2

A

IgG - Complement mediated

auto Abs

98
Q

What is a disease that changes lubricin in synovial fluid

A 
CACP
Camptodactyly - fixed flexion of fingers
Arthropathy 
Coxa vara - waddle gait  
Pericarditis - cardiac rub
99
Q

HST 4

A

T cells

Ex: METAL ALLERGY

100
Q

What part of the nerve recovers first after injury

A

Sympathetic

101
Q

What is the main difference between freeze dried and frozen allogran

A

Freeze dried less torsional and bending strength
Longer shelf life
- Similar compressive + tensile strength
- None are osteoconductive aka don’t have viable cells (vs osteoinductive)

102
Q

What does each of these structures do:

  1. Golgi organs
  2. Ruffini endings
  3. Pacini corpuscles
  4. Free nerve endings
A
  1. Proprioception
  2. Deep pressure
  3. Rapid vibration
  4. Nociception, often at bone-tendon junction
103
Q

How do psych meds affect bones

A

Early osteoporosis
Phenytoin/others - change vit D metab
Clonazepam - increase sclerostin -> decrease blasts

104
Q

What is a disease that changes lubricin in synovial fluid

A 
CACP
Camptodactyly - fixed flexion of fingers
Arthropathy 
Coxa vara - waddle gait  
Pericarditis - cardiac rub
105
Q

What is the fxn of aggrecan in articular cartilage

A

Aggrecan attracts water
“Exerts swelling pressure against the restraint of collagen”
Provides cartilage the capability to dispense contact forces evenly to underlying bone

106
Q

What is the role of decorin in articular cartilage

A

Controls collagen fibril size

107
Q

What is the main difference between freeze dried and frozen allogran

A

Freeze dried less torsional and bending strength

  • Similar compressive + tensile strength
  • None are osteoconductive aka don’t have viable cells (vs osteoinductive)
108
Q

What does each of these structures do:

  1. Golgi organs
  2. Ruffini endings
  3. Pacini corpuscles
  4. Free nerve endings
A
  1. Proprioception
  2. Deep pressure
  3. Rapid vibration
  4. Nociception, often at bone-tendon junction
109
Q

What nuclear TF is important for tendon and ligament formation

110
Q

What biomaterial has the highest rate of bacterial adherence

A

Titanium alloy > stainless steel > pure titanium

Basic Science (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions