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Basic Science > Miller's Review Basic Science > Flashcards

Miller's Review Basic Science Flashcards

Ortho basic science

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1
Q

Linear force types

A

Normal = perpendicular to surface, tangential = parallel to surface, compressive = shrinks object, tensile = elongates object

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2
Q

Rotational force types

A

Moment = rotational effect of force, Torque = moment perpendicular to long axis causing rotation, Bending moment = force parallel to long axis, mass moment of intertia = resistance to rotation

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3
Q

Stress =

A

Force that causes a shape to change, it is a property of the object. Stress = Force/Area.

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4
Q

Srain =

A

Deformation of an object due to stress. Strain = change in length/length. It has no unit measurement.

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5
Q

Hooke’s law

A

Stress is directly proportional to the strain up to the yield point, where permanent deformation occurs.

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6
Q

Elastic zone

A

When stress is removed, the object goes back to its same original shape and form.

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7
Q

Young’s modulus of elasticity

A

Defines a materials specific stiffness. Measured by the slope of the stress/strain line. Materials with a steeper slope are more stiff and can withstand more force before permanent deformation.

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8
Q

Plastic deformation

A

Material does not return to original shape and size once stress is removed because molecular bonds have been broken.

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9
Q

Ultimate strength

A

Maximize stress material can tolerate before breaking…but it isn’t the breaking point. It has to go through necking (material cross sectional area reduces, overall stress reduces, but increases focally at the fracture point)

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10
Q

Breaking point

A

Point where material actually fails

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11
Q

Fatigue

A

Repetitive loading cycles cause material to fail below the ultimate strength

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12
Q

Stiffness vs strength

A

Stiffness = resistance to change in shape, depends on elastic deformation (slope)

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13
Q

Hardness vs ductility

A

Hardness = resistance to localized surface plastic deformation (scratches and dents)

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14
Q

Toughness =

A

The whole area under the stress/strain curve. Ability of a material to absorb energy

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15
Q

Which is stiffest? Which is strongest? Which is toughest? Which is most ductile? Which is most brittle?

A

Stiffest = A. Strongest = A. Toughest = B. Ductile = C. Brittle = A.

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16
Q

Creep

A

Constant stress on a material over prolonged period of time causes the strain to slowly increase, the material plasticly deforms and can fail well below its ultimate tensile srength.

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17
Q

Stress relaxation

A

Constant strain on a material (keeping it the same length) over time, decreases stress levels, puts the material in equilibrium and prevents creep

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18
Q

How do material properties change when the load is applied quickly?

A

When stress is applied over a short period of time, materials are stiffer, stronger and tougher

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19
Q

What is hysteresis?

A

Ability of viscoelastic material to dissipate energy between loading and unloading cycles. This happens in the vertebral disc and meniscus. Note there is no change in the curve in a purely elastic material.

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20
Q

What is an isotropic material

A

Materials that behave the same regardless of the direction the force is applied (golf ball, woven bone)

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21
Q

What is an anisotropic material

A

Materials that behave different depending on the direction they are loaded (cortical bone, cartilage)

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22
Q

Microstructure of metal alloys

A

Metal ions in a crystalline lattice structure, solid-solution strengthening, impurity ions distort the lattice and increase resistance to movement of lattice defects

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23
Q

What determines the hardness of a metal alloy?

A

Grain size, smaller grain = harder material

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24
Q

Components of stainless steel

A

316L = iron, chromium, nickel (16%), molybdenum (3%) and carbon (L)

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25
Q

Components of titanium

A

Titanium, aluminum (6%) and vanadium (4%)

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26
Q

Components of cobalt-chrome

A

Cobalt, chrome, molybdenum, nickel, carbon, tungsten

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27
Q

Top 3 metallergies

A

Nickel > Cobalt > Chromium

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28
Q

In what order are metal materials least to most adherent to bacteria

A

Least = Tantalum, pure titanium, stainless steel, Titanium alloy = most adherent

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29
Q

Galvanic corrosion

A

Combining dissimilar metals like stainless steel with CoCr

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30
Q

Fretting corrosion

A

Micromotion during loading of an implant that is not loose. Ex at the head-neck junction of a hip replacement.

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31
Q

Passivation

A

Coating stainlees steel with chromium oxide creates barrier that prevents rust

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32
Q

What is a ceramic and how are its properties different from metal.

A

Metals covalently bound to non-metals (inert = alumina and zirconia, bioactive = beta-tricalcium phosphate and HA). It is brittle and stiff. It is sensitive to notches and cracks. It is insoluble and wettable (hydrophilic, achieves fluid film lubrication and low wear rate).

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33
Q

Why is zirconia preferred over alumina?

A

Lower hardness and it can’t be used on both sides of THA; however, it has superior wear rates when used on polyethylene.

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34
Q

What determines mechanical properties of a polymer?

A

Long and linear chains are stronger. Cross-linking these chains make the material stiffer, harder and stronger.

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35
Q

UHMWPE processing

A

Gamma irradiation to cross link chains (not in O2 to limit free radicals) -> anneal to just below melting point to decrease free radicals but not disrupt crystalline struction

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36
Q

UHMWPE minimal thickness

A

6mm or greater

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37
Q

How does cement work?

A

It is a space filler, like a grout. Strongest in compression.

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38
Q

Why don’t you want a 4mm cement mantle?

A

Heat generated can cause tissue necrosis

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39
Q

How does vacuum mixing help cement biomechanically?

A

Reduces porosity and increases strength

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40
Q

Suture anchor material to avoid

A

Dextro (D) lactide monomer associated with rapid degradation and potential for inflammation

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41
Q

How are biodegradable polymers metabolized?

A

Polymer chain breaks down, inflammatory process begins, PMNs and macrophages eat up monomers and implant becomes amorphous, lactic acid enters Krebs cycle and you breath it out as CO2 or eliminate it as water.

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42
Q

How to biocomposite anchors induce ingrowth?

A

They are biodegradable polymers with ceramic that releases a base that buffers acidic monomer (lactic acid)

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43
Q

Property that provides compressive strength to bone

A

Hydroxyapatite reinforced collaged fibers

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44
Q

Bones are weakest when loads are applied in ____?

A

Shear

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45
Q

Toe region

A

Region of stress/strain curve with nonlinear behavior due to crimped elastin fibers that straighten out as stress is applied

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46
Q

What determines the stiffness of a screw?

A

Core diameter

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47
Q

What determines the pullout strength of a screw

A

The outer diameter

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48
Q

Stiffness of a plate is proportional to the ____ power

A

3rd . More screws and shorter working length also increase stiffness

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49
Q

Stiffness of a nail is proportional the ___ power

A

4th

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50
Q

What increases the stiffness of your ex-fix the most?

A

1) Reduce the fracture 2) Larger pins 3) Pin spread 4) More pins 5) Rods closer to bone 6) Add more rods

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51
Q

Plane of freedom in intercarpal and intertarsal joints

A

Translation

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52
Q

Joint reaction force

A

Force within a joint responds to the forces acting on the joint

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53
Q

What is the difference between rolling and sliding?

A

Rolling maintains an instant center of rotation. In sliding, there is no instand center of rotation.

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54
Q

What is the difference between friction and lubrication?

A

Friction = resistance between two objects as they slide over one another. Lubrication is decreased resistance between the surfaces.

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55
Q

How is articular cartilage lubricated?

A

Elastohydrodynamic lubrication

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56
Q

Coefficient of friction in native joints vs arthroplasty?

A

Native = 0.002, arthroplasty = 0.1

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57
Q

How can you decrease joint reaction forces around the hip?

A

Increase offset (A) or decrease moment arm (B). A cane in the contralateral hand decreases joint reaction forces by 60%

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58
Q

Screw-home mechanism

A

Tibia externally rotates on femur going into extension

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59
Q

Which meniscus has the most excursion?

A

Lateral (1.1cm) > medial (0.5cm)

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60
Q

How do the transverse tarsal joints lock during toe off?

A

The TN and CC joint are no longer parallel, which makes them rigid

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61
Q

What is the primary structure that transmits loads from the hindfoot to the forefoot?

A

Plantar aponeurosis

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62
Q

What is the instant center of rotation of the ankle?

A

Talus

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63
Q

Biomechanical property that allows spine deformity over time

A

Creep

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64
Q

Biomechanical property that allows intervertebral disc energy absorption

A

Hysteresis

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65
Q

Part of the intervertebral disc that provides tensile strength? Compressive strength?

A

Tensile = annulus fibrosus. Compressive = nucleus pulposus.

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66
Q

Ratio of glenohumeral motion to scapulothoracic motion when moving the shoulder?

A

2:1 glenohumeral to scapulothoracic

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67
Q

Center of rotation of elbow

A

Center of trochlea

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68
Q

Secondary restraint to valgus stress in the elbow

A

Radial head. Primary is anterior bundle of MCL in 30-60 degrees elbow flexion. Posterior bundle of MCL in max elbow flexion.

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69
Q

Center of rotation of the wrist

A

Capitate

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70
Q

Primary wrist stabilizer after PRC

A

RSC ligament

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71
Q

Why is woven bone so weak?

A

It is oriented randomly, isotropic and pathologic, seen in infection, malignancy and stress reaction.

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72
Q

Why is lamellar bone stronger?

A

Organized in layers and stress oriented (Wolff’s law). Includes cortical and cancellous bone.

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73
Q

How do strain and O2 levels determine mesenchymal stem cell differentiation?

A

High strain -> fibroblast. Medium strain/low O2 = chondroblast. Low strain/high O2 = osteoblast.

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74
Q

Signaling pathway that promotes osteoblast development.

A

Osteoprogenitor cells release Wnt -> Wnt binds to active osteoblasts -> osteoblasts make and stabilize B-catenin -> production of RUNX2 increases -> RUNX2 increases Osx production -> Osx triggers terminal differentiation into osteocytes

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75
Q

Factors that promote chondrocyte development vs osteoblast development?

A

Sox-9 = chondrocytes. RUNX2/Osx/B-catenin = osteoblasts

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76
Q

Factor that triggers adipocyte development?

A

PPARy

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77
Q

How do osteoblasts make bone?

A

Pulsed PTH triggers type I collagen, alk phos and RANK-L production by the osteoblast.

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78
Q

Mediator for cell signaling from PTH receptor on osteoblasts?

A

Adenylyl cyclase

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79
Q

Two bone forming receptors on osteoblasts?

A

Intermittent PTH builds bone and Vitamin D.

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80
Q

Osteocyte negative feedback on osteoblast via ___?

A

Osteocytes secrete sclerostin via gap junctions in the bone canaliculi that antagonizes the Wnt pathway. PTH increases sclerostin release, calcitonin decreases sclerostin release.

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81
Q

Osteoclast cell lineage

A

Hematopoietic stem cell -> myeloid progenitor -> pre-osteocyte -> fuses with macrophage and becomes multi-nuclear osteoclast

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82
Q

How do osteoclasts resorb bone?

A

Binds to bone and seals ruflled border via integrin aVB3 and vibronectin (Arg-Gly-Asp RGD sequence). After sealed, tartrate resistance acid phosphatase (TRAP) is released, carbonic anhydrase lowers the pH and increases solubility of HA crystals. Organic material is removed by proteolytic enzyme cathepsin K at the ruffled border.

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83
Q

Disease with defective carbonic anhydrase

A

Osteopetrosis

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84
Q

Disease with defective cathepsin K

A

Pyknodysostosis

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85
Q

Factors that activate and inactivate osteoclasts?

A

Activate = RANKL. Inactivate = OPG, calcitonin.

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86
Q

Positive and negative feedback in osteoblast signalling?

A

B-catenin increases production of RUNX2 and OPG -> bone formation. PTH increases production of RANK-L -> bone resorption.

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87
Q

How do tumors cause bone resorption?

A

They stimulate osteoblasts to produce more RANK-L that activates osteoclasts and resorbs bone.

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88
Q

What provides compressive strength to bone? What provides tensile strength to bone?

A

Compressive = HA & proteoglycans. Tensile = type I collagen.

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89
Q

Most abundant noncollagenous matrix protein made by osteoblasts?

A

Osteocalcin, high in Paget’s and hyperparathyroidism

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90
Q

How does enchondral bone formation occur?

A

Chondrocytes in the proliferative zone express CBFA1 and RUNX2, chondrocytes become hypoertrophic. The ossification front approaches the physis and is composed of osteoclasts and osteoprogenitor cells. The osteoclasts destroy the hypertrophic chondrocytes and the surrounding cartilage matrix calcifies. The OPGs generate osteoblasts that lay down bone. The remaining chondrocytes grow away from the ossification front and the bone lengthens.

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91
Q

What is Indian hedgehog? What stimulates vascular invasion in the physis?

A

Protein secreted by chondrocytes in the proliferative zone that increases production of PTHrP -> PTHrP stimulates reserve zone chondrocytes to proliferate and inhibits proliferative zone chondrocytes from hypertrophy.

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92
Q

What cells secrete calcitonin?

A

Parafollicular (Clear cells) in the thyroid gland

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93
Q

Chondroprotective signalling pathways

A

PTH, PTHrP and Ihh

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94
Q

Reserve zone associated diseases

A

Diastrophic dwarfism (defective type II collagen synthesis), pseudoachondroplasia (defective processing and transport of proteoglycans), Kneist syndrome (defective proteoglycan processing)

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95
Q

Proliferative zone associated diseases

A

Gigantism (increased cell proliferation from hGh), achondroplasia (deficient cell proliferation), hypochondroplasia (less severe deficiency in cell proliferation), malnutrition, XRT, injury and excess glucocorticoids (decreased cell proiferation and matrix synthesis)

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96
Q

Hypertrophic pre-calcification zone diseases

A

Mucopolysaccharidosis (Morquio, Hurler = defcient lysosomal storage)

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97
Q

Zone of provisional calcification diseases

A

Rickets, osteomalacia (insufficient Ca for matrix calcification), Salter-Harris I fractures, little league shoulder

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98
Q

Primary spongiosum diseases

A

Metaphyseal chondrodysplasia (Jansen and Schmid), osteomyelitis

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99
Q

Secondary spongiosum diseases

A

Osteopetrosis, osteogensis imperfecta, scurvy, metaphyseal dysplasia (Pyle disease)

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100
Q

Where does appositional bone growth occur?

A

Groove of Ranvier, wedge shaped zone of chondral cells at the periphery

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101
Q

Dense fibrous tissue providing support to the physis

A

Perichondral fibrous ring of La Croix, also provides blood supply to the physis

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102
Q

Strain rate that determines primary vs secondary bone healing

A

<2% = primary. 2-10% = secondary

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103
Q

Phases of secondary bone healing

A

1) Inflammatory = osteoblasts and fibroblasts proliferate via BMP signalling, granulation tissue forms around fracture ends, this tolerates greatest strain before failure

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104
Q

How do u/s and electrical bone stimulators work?

A

U/s = increases callus via nano motion. Electrical bone stimulator = increases osteoblast activity by reducing O2 concentration and increasing pH

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105
Q

Fastest resorbing synthetic bone graft

A

Ca-sulfate

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106
Q

Synthetic bone graft with highest compressive strength

A

Ca-PO4

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107
Q

Ca daily requirements

A

1500mg/day

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108
Q

Peak bone mass age

A

3rd decade

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109
Q

Lab test for Vitamin D

A

25-Vit D

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110
Q

Vitamin D effect on gut

A

Increases Ca and PO4 absorption

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111
Q

Etiology of renal osteodystrophy

A

Impaired kidneys retain PO4 which decreases 1,25-Vit D production and bones demineralize.

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112
Q

Cause of vitamin D deficient rickets

A

Inadequate vitamin D = low calcium = elevated PTH/low PO4. Osteoclasts activate, Alk Phos increases and you see physeal cupping.

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113
Q

Cause of familial hypophosphatemic rickets.

A

X-linked PHEX gene mutation -> unable to resorb phosphate. Will have NORMAL CALCIUM

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114
Q

Cause of Type I hereditary Vitamin D dependent rickets

A

AR defect in 25-OH Vitamin D 1a-hydroxylase that normally activates 25-Vit D. Mutation on Chr 12q14. Labs show elevated 25-OH Vit D, low 1-25-OH Vit D.

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115
Q

Cause of type II hereditary vitamin D dependent rickets

A

Defect in intracellular receptor for 1,25-OH Vit D3

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116
Q

Medications that limit bone healing

A

NSAIDs, prednisone, PPIs, antiepileptics, SSRIs and heparin

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117
Q

Risk factors for osteoporosis

A

White, female, sedentary, low BMI, tobacco use, EtOH, phenytoin, history of breastfeeding, FHx of osteoporosis, premature menopause and clonazepam (increases Sclerostin)

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118
Q

Type I vs type II osteoporosis

A

Type I = post menopausal. Type II = senile age > 70

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119
Q

Strongest predictor of fragility fracture?

A

2 vertebral compression fractures. 1 VCF increases risk of hip fracture by 5x.

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120
Q

Osteoporosis histology

A

Decreased osteon size and enlarged marrow space

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121
Q

FRAX calculator use

A

If 10-year risk of hip fracture is >3% or major osteoporosis -related fracture >20%, you have osteoporosis.

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122
Q

Indications for medical therapy in osteoporosis in post-menopausal women and men > 50

A

Any hip or vertebral fracture

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123
Q

Types of bisphosphonates

A

Nitrogen containing – 1000x more potent, block farnesyl pyrophosphate synthase -> loss of GTPase formation in osteoclast ruffled border -> cell apoptosis

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124
Q

Atypical femur fractures usually occur how many years after treatment start?

A

4 years

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125
Q

How do teriparatide and estrogen work on bone?

A

Teriparatide induces osteoblast formation and new bone formation. Estrogen directly blocks osteoclast activity.

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126
Q

Contraindications to teriparatide use?

A

Paget’s disease and prior bone mets (risk of secondary osteosarcoma)

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127
Q

What is denosumab?

A

IgG2 antibody to RANK-L

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128
Q

What is romosozumab?

A

Sclerostin antibody to treat osteoporosis

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129
Q

Functional unit of muscle

A

Sarcomere. Thick filament = myosin, thin filmament = actin, A band = myosin, I band = actin. Allows fibers to slide past each other

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130
Q

Sliding filament theory

A

Ach released from presynaptic vesicles -> sarcolemma depolarizes and Ca is released from the sarcoplasmic reticulum -> Ca binds to troponin -> tropomysin moves to expose myosin binding sites on actin -> myosin crossbridges bind to actin and produce a power stroke -> ATP breaks actin-myosin link in preparation for next cycle

131
Q

Isotonic

A

Constant muscle tension, length changes. Divides into eccentric anc concentric contraction.

132
Q

Isometric

A

Constant length, tension changes

133
Q

Isokinetic

A

Velocity changes, tension changes

134
Q

Metabolism in 1st 10 seconds, first 4 mintues and 4+ minutes

A

0-10s = ATP and creatine phophate, 1-4 minutes = glycogen and lactic acid via glycolysis. 4+ minutes = glycogen and fatty acids

135
Q

Cells responsible for muscle tear repair

A

Satellite cells

136
Q

Types of nerve fibers

A

A = Fast, heavy myelin, touch. B = Medium, intermediate myelination, autonomic fibers. C = slow, unmyelinated, pain.

137
Q

1st sensation to return after nerve injury

A

Sympathetic activity, then pain, then temperature, then touch, then proprioception, then motor

138
Q

Level of nerve that needs to be intact for full recovery

A

Endoneurium

139
Q

Proteoglycans in tendons

A

Decorin (most prominent, cross links fibrils, regulates tendon diameter and transfers load) and bglycan, rest is type I collagen (95%)

140
Q

Fibers responsible for pain in tendonitis

A

Free nerve endings at the bone-tendon interface

141
Q

Collagen type seen first in tendon healing

A

Type III in the proliferation phase

142
Q

When is tendon healing the weakest

A

7 days

143
Q

Difference between tendon and ligament

A

Less type I collagen in ligament, more proteoglycans and water in ligaments, uniform vascularity in a ligament

144
Q

Histologically, where do ligament injuries occur?

A

Between the unmineralize and mineralized fibrocartilage layers

145
Q

Types of ligament insertion into bone

A

Indirect = superficial fibers into periosteum and deep fibers into bone, seen more at midsubstance. Direct, both superficial and deep fibers go into bone.

146
Q

What structure in the knee is anisotropic

A

Cartilage, mechanical properties vary depending on the direction it is loaded

147
Q

Top 3 components that make up articular cartilage

A

74% water, 15% collagen, 10% proteoglycan. Dry weight is 60% collagen and 30% proteoglycan.

148
Q

What is the structure of collagen made up of

A

Chains of hydrox-proline and hydroxy-lysine. The OH group is added via vitamin C. 3 alpha procollagen chains wind together in a triple helix. Half life ~20 years. Provides tenside strength and stiffness.

149
Q

Where do you find type X collagen

A

Near calcified cartilage (landmark, hypertophic zone and fracture callus)

150
Q

Type II genetic collagen disorder

A

Achondrogenesis (lethal at birth). Pondyloepiphyseal dysplasia congenita (short trunk and limbs, normal hands/feet, normal mentation), precocioius arthritis (12qw13.11=q13.2, OA before age 40, otherwise normal)

151
Q

Proteoglycans that make up healthy cartilage

A

95% chondroitin SO4, keratin and hyaluronic acid

152
Q

What is aggrecan

A

Long chain of negatively charge chondroitin, keratin and hyaluronic acid that is negatively charged.

153
Q

How does the negative change of aggrecan affect cartilage properties?

A

The negative charges repel each other, attract negative cations and water

154
Q

Disease when sulfate transporter does not work in cartilage?

A

Diastrophic dysplasia DTDST = dwarfism, hitchhikers thumb, cauliflower ears, clubfoot, scoliosis and DDH.

155
Q

Transcription factor that leads to chondrocyte differentiation

A

SOX9

156
Q

How do cartilage cells sense mechanical changes

A

Primary cilia

157
Q

What is the metabolic pathway used by chondrocytes

A

Anaerobic metabolism

158
Q

How does the metabolic activity of chondrocytes differ in the superficial and deep layer?

A

Deep = more active, makes mor proteoglycan. Superficial makes more collagen

159
Q

Where in the chondrocyte is type II collagen made?

A

Synthesized in the cell, assembled outside the cell

160
Q

How does cartilage matrix change with weight bearing

A

Weight bearing = H2O moves out, lubricates the joint. Non-weight bearing = H2O moves in, feeds cartilage

161
Q

MRI sequences that can show cartilage

A

DGEMRIC, sodium and T1rho

162
Q

Layers of cartilage

A

Superficial layer (horizontal/tangential orientation of collagen, highest collagen %, containes lubricin, highest water %, least proteoglycan synthesis)

163
Q

Types of cells in synovial membrane

A

No epithelial cells or basement membrane. Type A cells (macrophage, removes debris from the joint), type B cells (fibroblast, make synovial fluid, hyaluronic acid, lubricin, RANK-L, connects to injured cartilage)

164
Q

Main molecule responsible for synovial viscosity

A

Hyaluronic acid = nonsulfate mucopolysaccharide D-glucuronic acide N-acetyl-D-glucosamine

165
Q

Synovial fluid lubricants

A

Lubricin = boundary lubricant. Hyaluronic acid = fluid-film lubrication

166
Q

How does OA cartilage different from normal aging cartilage

A

OA has increases proteoglycans and increased water that decreases its modulus of elasticity. Aging has increased AGEs and decorin, decreased H2O that increases its modulus of elasicity.

167
Q

How does OA activate the innate immune system?

A

Extracellular matrix debris (DAMPS) activate TLRs 2 and 4. This increases IL-1 levels, activates MMPs and ADAMTS proteolytic enzymes

168
Q

Cytokine that triggers liver to release ESR and CRP

A

IL-6

169
Q

TNFa blockers

A

Etanercept (receptor fusion protein), infliximab (chimeric IgG ab) and adalimumab (monocolonal ab)

170
Q

IL-1 inhibitor

A

Anakinra (IL-1 receptor antagonist)

171
Q

IL-6 inhibitor

A

Tocilizumab (humanized anti IL-6 ab)

172
Q

B cell C20 antibody

A

Rituximab

173
Q

Macrophage’s role in osteolysis

A

Eats poly/metal/ceramin -> releases cytokins (RANK-L, stimulates osteoblasts to release RANK-L)

174
Q

Patient presents with this x-ray and minimal pain. What is your diagnosis?

A

Tabetic arthropathy from syphilis infection 20-30 years prior, this is a type of neuropathic arthropathy

175
Q

Most common cause of upper extremity neuropathic joint

A

Syrinx, think spine MRI if neuropathic upper extremity joint to look for syrinx

176
Q

Diagnosis?

A

Ochronosis. Autosomal recessive defect of homogentistic acid oxidase -> alkaptonuria

177
Q

Hemochromatosis triad

A

Cirrhosis, DM and skin pigmentation. 50-80% get arthritis secondary to CPPD crystals and hemosiderein deposition in synovium and cartilage

178
Q

Causes of CPPD

A

Hyperparathyroidism, hemochromatosis, hypothyroidism and hypomagnesemia

179
Q

Crystals in CPPD vs gout

A

CPPD = box shaped blue cars, positively birefringent. Gout = needle shaped, yellow, negatively birefringent

180
Q

Differntiating caldium hydroxyapatite shoulder arthropathy from neuropathic arthropathy in the shoulder?

A

Neuropathic arthropathy is painless, Ca-HA arthropathy is very painful

181
Q

What causes tumoral calcinosis?

A

Elevated serum PO4 from chronic renal failure or genetic mutation (decreased FGF-23 activity)

182
Q

Chikungunya presentation

A

Fever, maculopapular rash, myalgias and arthraglias acutely. Longer term may mimic seronegative RA and develop Raynaud phenomena.

183
Q

Synovial biopsy findings in chikunguya

A

Macrophages with CHICV RNA and NK cells

184
Q

What do NK cells do

A

Cytotoxic lymphocyte that identifies cells without an HLA MHC I identifyer. It is activated by interferon and macrophages and releases perforin which pokes holes in its target.

185
Q

HLA-B27 disorders

A

AS, reactive arthritis, IBD, psoriatic arthritis and JRA

186
Q

HLA in SLE

A

HLA DR3

187
Q

HLA in RA

A

HLA DR4

188
Q

Symptoms in RA

A

Morning stiffness >60 min, symmetric joint involvement

189
Q

Pathophysiology of RA

A

Antigen triggers cell damage -> cell protein modified (citrullinated) -> dendritic cell presents to B cells -> B lymphocytes make auto-antibodies (RF, CCP) -> CD4 T lymphocytes infiltrate joints and release cytokines -> inflammatory synovial proliferation (pannus, CD4 T-lymphoctye, macrophages and fibroblasts) and destruction

190
Q

Most sensitive lab for RA

A

Anti-CCP

191
Q

What is an epitope?

A

Smallest part of an antigen that an antibody can recognize

192
Q

Two types of antibodies

A

Opsonizing (coat antigen for macrophage target), neutralizing (activate cytotoxic lymphocyts and complement system)

193
Q

What type of antibody is RF

A

IgM -> IgG

194
Q

What type of allergy is latex?

A

IgE, type I hypersensitivity

195
Q

What type of allergies are HIT and acute hemolytic transfusion reaction

A

Type II, IgM or IgG antibodies against PF4 and non-self RBCs, respectively.

196
Q

Antibody testing in SLE

A

+ANA for screening (sensitive) -> +Anti-ds DNA and anti-Sm antibodies to confirm (specific)

197
Q

What type of hypersensitivity is SLE?

A

Type III, Ag-Ab immune complex deposition

198
Q

ANA in RA?

A

Most are ANA negative

199
Q

Drug induced Lupus antibody test?

A

Anti-histone

200
Q

Lymphocytes involved in Sjogren’s

A

CD4 T-lymphocytes target salivary and lacrimal glands. B plasma cells make IgA antibodies to SS-A(ro) and SS-B(la) ribonucleoproteins

201
Q

Lympocytes involved in scleroderma

A

CD4 T-lymphocytes activate fibroblasts which increase type I collagen production leading to microvascular injury

202
Q

Antibody testing for scleroderma

A

Anti-centromere if localized (CREST) and anti-DNA topoisomerase I (diffuse)

203
Q

Antibody testing of mixed connective tissue disease

A

Anti-U1snRNP

204
Q

Types of T-lymphocytes

A

Killer (CD8, cytotoxic, activated by antigen presenting cells, duplicate and attack with toxins and enzyme to destroy cell membrane). Helper (CD4, activat Killer cells, macrophages and direct B cell antibody production). Regulatory (suppress immune system).

205
Q

Lymphocyte depleted in HIV

A

CD4+ T-cell

206
Q

Lymphocyte involved in ALVAL

A

Killer T-cells

207
Q

What type of hypersensitivity is ALVAL?

A

Type IV, delayed type

208
Q

Most common initial symptom in ankylosing spondylitis

A

Sacroilitis

209
Q

Most common physical exam finding in patients with psoriatic arthritis

A

Skin lesions and nail lesions (present in 90%)

210
Q

Baterial causes of reactive arthritis

A

Intracellular bacteria: Chlamydia, Shigella, Yersinia, Salmonella

211
Q

Cytokine implicated in septic joints

A

IL-1 triggers proteolytic enzymes

212
Q

Most common location of osteomyelitis in adults

A

Vertebra and ribs

213
Q

Infectious differential for chondroblastoma in kids

A

PEASAO: Pediatric epiphysial apophyseal subacute osteomyelitis. Typically Kingella if <5 and S. aureus if >5

214
Q

Pathology differences in chronic vs acute osteomyelitis

A

There will be PMNs infiltrating trabecular bone. In acute osteomyelitis, there will be osteocytes within the trabeculae still alive. In chronic osteo, there will be no osteocytes because the bone is dead.

215
Q

Newborn osteomyelitis bugs

A

GBS, S. aureus and enteric gram negative rods. Empiric tx = nafcillin + gent or nafcillin + 3rd gen cephalosporin

216
Q

1 cause of osteo-articular infection in kids <5 if diagnosed by PCR?

A

B-hemolytic gram negative coccobacillus, K. kingae

217
Q

Antibiotic for K. kingella

A

PCN

218
Q

Most common osteomyelitis in sickle cell

A

S. aureus, sickle cell is also associated with salmonella (gram negative motile rod)

219
Q

Sickle cell increased risk for infection by encapsulated bacteria because?

A

Auto-spelenctomy from thrombi

220
Q

Prophylactic abx for foot puncture wound through shoe?

A

3rd gen cephalosporin or cipro, give tetanus. Higher risk of pseudomonas infection (gram negative rod)

221
Q

Gram negative intracellular bacteria seen in patients with late stage HIV and associated lesions

A

B. henselae, seen in 90% of HIV patients who own a cat. Skin lesion is bacillary angiomatosis (below) and painful long bone lytic lesions.

222
Q

Stains for B. henselae

A

Warthin-Starry-stain (silver), IFA igG PCR

223
Q

Most common location for extra-pulmonary Tb?

A

Spine (50%)

224
Q

Fungal infections seen in PNW? SW? Midwest? SE?

A

PNW = cryptococcus, SW = coccidiomycosis, Midwest = histoplasmosis, SE = blastomycosis

225
Q

Cause of erysipelas

A

Group A beta hemolytic strep pyogenes infects superficial layers of dermis and turns it bright red

226
Q

Most common bug involved in cellulitis

A

Group A strep

227
Q

Most common bug involved in NSTI

A

Gram + group A strep (exotoxin), polymicrobial in immunocompromised

228
Q

NSTI bug in salt water lacerations

A

Gram negative vibrio vulnificus

229
Q

NSTI bug in fresh water lacerations

A

Gram negative aeromonas hydrophilia

230
Q

Late physical exam findings in NSTI

A

Numb and non-blancheable skin

231
Q

Early physical exam findings in NSTI

A

Blisters, bullae, violet skin

232
Q

Bug involved in gas gangrene

A

Gram + rod C. perfringens, seen in contaminated wounds, has potent alpha and theta toxins that breaks down cell membrane.

233
Q

Treatment of gas gangrene

A

Urgent open debridement (obligate anaerobe, can’t survive in presence of O2), hyperbaric O2 is actually effective for this

234
Q

PCN mechanism of action

A

Inhibits peptidoglycan cell wall synthesis in gram positive bacteria by binding and blocking transpeptidase

235
Q

Beta lactamase

A

B-lactamase breaks PCN’s B-lactam ring and are resistant to PCN, this is why 80% of S. aureus are PCN resistant

236
Q

MecA gene

A

Provides methicillin resistance to S. aureus via coding for a different transpeptidase that doesn’t bind to PCNs or cephalosporins

237
Q

Difference between hospital acquired and community acquired MRSA

A

Hospital acquired has larger cassette mecA gene that allows for greater abx resistance. Community acquired may be more susceptible to abx; however, it has the PVL cytotoxin that causes boils and hemorrhage PNA.

238
Q

Gene that increases bacterial adherence to titanium

A

Fnb

239
Q

Protein A mechanism of action in infection

A

Inactivates IgG

240
Q

Gram positive drum stick shaped rod and its exotoxin

A

C. tetani, tetanospasmin blocks inhibitory nerves and results in spasm/lock jaw

241
Q

Treatment of tetanus

A

Immunize every 5-10 years. If unsure of vaccination in contaminated wound, give Tdap vaccine and tetanus Ig

242
Q

Most common rabies bite in US

A

Bats

243
Q

Atypical mycobacteria that grows at colder temperatures from fresh or salt water

A

Mycobacterium marinum. Causes noncaseating granulomas (fish tank granulomas)

244
Q

Gram negative motile curved rod found in shellfish in warm brackish water

A

Vibrio, can cause NSTI

245
Q

Fish handler’s disease

A

Erysipelothrix rhusiopathiae, common in pigs, self limited gram + bacilli that causes pain, itching and ring-shaped hand lesions with purple border

246
Q

CREST syndrome

A

Anti-centromere antibodies cause calcinosis, Raynaud’s, esophageal dysmotility, sclerodactyly and telangiectasias

247
Q

Mechanism of action of fluoroquinolones

A

Act on DNA topoisomerase

248
Q

Mechanism of action of refampin

A

Binds bacteria RNA polymerase, inhibiting bacterial mRNA synthesis from DNA.

249
Q

Does an exon or intron code for proteins?

A

Exon, intron does not, they are regulatory proteins or junk DNA that get snipped out by snRNPs

250
Q

Antibodies agains snRNPs?

A

Anti-Sm (lupus) and Anti-U(1)RNP (mixed connective tissue disease)

251
Q

Diffences between human ribosome and bacterial ribosome

A

Human = 80S ribosome with 60S and 40S subunits. Bacterial = 70S ribosome with 50S and 30S subunits

252
Q

Antibiotics that act on bacteria 50S subunit

A

Clindamycin, macrolides and linezolid (also 23s RNA)

253
Q

Antibiotics that act on bacterial 30S subunit

A

Aminoglycosides and tetracycline

254
Q

What part of the bacteria does PCR amplify to identify bacteria?

A

The 16S ribosomal RNA gene

255
Q

Condition with bilateral scapular winging and progressive facial nerve paralysis? Mutation? Treatment?

A

DUX4 junk DNA is usually hypermethylated and silent, when undermethylated it causes progressive facial and shoulder weakness in fascioscapulohumeral muscular dystrophy. Treatment is scapulothoracic fusion.

256
Q

Neurofibromin gene activator or suppressor?

A

Suppressor, inhibits Ras protein. In NF1 the mutation turns it off and allows uncontrolled growth of neurofibromas.

257
Q

McCune-Albright gene activator or suppressor?

A

Activator, GNAS mutation upregulates cAMP and cell activity -> fibrous dysplasia, precocious puberty and café au lait spots

258
Q

Most common inheritance pattern in structural protein mutations like achondroplasia, pseudoachondroplasia, MED, SED, Kneist, Stickler, Schmid, OI, Ehler’s Danlos, Marfan’s and Jansens?

A

AD

259
Q

Most common inheritance pattern in enzyme mutations like diastrophic dysplasia, Hurler’s, Sanfilippo, Morquio, Gaucher’s, osteopetrosis and homocystinuria?

A

AR – Except for Hunter’s disease (iduronate sulfatase is XLR)

260
Q

X-linked recessive disorders

A

Hunter’s (iduronate sulfatase), SED tarda (TRAPPC2), Hemophilia A (factor VIII) and B (factor IX), Duchenne and Becker muscular dystrophy (Xp21 dystrophin)

261
Q

X-linked dominant disorder

A

Hypophosphatemic rickets (vitamin D resistant rickets, most common cause of rickets in US). Mutation is PHEX that no longer suppresses FGF23. FGF23 increases renal PO4 wasting

262
Q

Treatment for XLD hypophosphatemic rickets

A

PO4, calcitriol supplement and burosumab (anti-FGF23 monoclonal ab)

263
Q

Carter effect example

A

Sex-dependent polygenic inheritance, females need more gene expression to have clubfoot than males, so female have lower rates of clubfoot and higher rate of transmission to offspring

264
Q

Genetic basis of laxity in Down Syndrome patients

A

COL 6 overexpression (lives on Chr 21)

265
Q

Genetic cause of Prader-Willi syndrome

A

Paternal genes from Chr15(q11-13) are deletes and materal genes activated (imprinting)

266
Q

Embryonic layer that gives risk to the musculoskeletal system

A

Mesoderm

267
Q

BMPs are apart of what superfamily of transcription factors?

A

TGF-beta

268
Q

Marker of osteoblastic differentiation and new bone formation

A

Alkaline phosphatase

269
Q

Genetic disease with high levels of alk phos

A

Paget’s and rickets

270
Q

Genetic disease with low levels of alk phos

A

Phosphatasia. Genetic mutation of TNSALP makes alk phos non-functional. Pyrophyosphate levels rise and bone formation is inhibited, patients develop osteomalacia and rickets (only rickets with low alk phos)

271
Q

Genetic defect in stone man syndrome

A

Fibrodysplasia ossificans progressive is from an AD gain of function mutation in the BMP receptor ACVR1, it is always on and BMP4 is overexpressed, causing excess bone formation secondary to injury.

272
Q

Stone man syndrome treatment

A

Don’t resect because it stimulates more bone formation

273
Q

Disease associated with monophalangeal hallux valgus?

A

Fibrodysplasia ossificans progressively.

274
Q

Signaling molecules involved in limb formation

A

FGF (distal to proximal growth), Hedgehog (ulnar vs radial), Wnt (dorsal vs ventral then bone homeostasis)

275
Q

FGF effect on limb buds

A

Expressed at apical ectodermal ridge and increases the length of the limb bud

276
Q

Hypochondroplasia mutation

A

FGFR3, milder form of achondroplasia

277
Q

Thanatophoric dysplasia mutation

A

FGFR3, fatal, no proliferative zone in physis

278
Q

Tumoral-induced osteomalacia mutation

A

Increased expression of ectopic FGF23 -> creation of phosphaturic tumors

279
Q

Normal function of FGF23

A

Decreases renal reabsorption of phosphate and decreases serum phosphate levels and increases urin PO4

280
Q

Hyperphosphatemia genetic mutation

A

Deactivating mutation in FGF23 -> increased PO4 resorption in kidneys and tumoral calcinosis, commonly seen in renal failure

281
Q

Hedgehog signaling pathways

A

Sonic hedgehog: expressed at ZPA and determines radial-ulnar development. Indian hedgehog promotes osteoblast differentiation via Wnt/B catenin pathway.

282
Q

Limb deformities that occur secondary to over-expression of sonic hedgehog protein

A

Post-axial polydactyly and ulnar dimelia (2 pinkies, 2 ulnas)

283
Q

Limb deformities that occur secondary to under-expression of sonic hedgehog protein

A

Fibular hemimelia results with postaxial hypoplasia

284
Q

Anterolateral, anteromedial and posteromedial tibial bowing

A

AL= NF, AM= Fibular hemimelia, PM= physiologic

285
Q

Indian hedgehog pathway

A

Induces early bone transcription factors RUNX2 and osterix, also matures cartilage in endochondral ossification by inducing type X collagen, MMP13 and PTHrP in perichondrium, pathologic pathway in osteophyte formation, triggers Wnt/B catenin pathway

286
Q

Limb deformities that result from disruption of the Wnt pathway

A

Wnt is responsible for dorsal/ventral limb development. Nail-patella synrome (LMX1B in Wnt pathway)

287
Q

What is your diagnosis?

A

Nail patella syndrome = iliac horns, absent patella nd hypoplastic nails

288
Q

Wnt/B catenin signaling pathway

A

Wnt binds Fizzleds and LRP5/6, prevents B-catenin breakdown so it can travel to the nucleus and induce transcription factors RUNX2, Osx and osteocalcin to promote ossification.

289
Q

Type of bone healing seen in distraction osteogenesis

A

Intramembranous, no cartilage model, high expression of Wnt increases RUNX2, inhibits SOX9 and bone is formed directly from osteoblasts

290
Q

Wnt signaling in endochondral ossification

A

Wnt is low initially, favoring SOX9 and chondrocyte development, Wnt increases later to calcify the soft callus

291
Q

Strain seen in endochondral ossification

A

2-10%

292
Q

Osteocyte function when bone is loaded vs. not loaded.

A

Loaded = sclerostin decreased. Unloaded = increased. Sclerostin blocks the LRP/Fz receptor in the Wnt/B-catenin pathway and reduces bone formation and stimulates osteoblast apoptosis.

293
Q

Antibody to sclerostin

A

Romosozumab

294
Q

Diseases with genetic defects in the SOST gene

A

Results in non-functiong Sclerostin and overproduction of bone with low risk of fractures in sclerosteosis and Van Buchem disease

295
Q

Dickkopf-related protein (DKK1) function

A

Blocks LRP 5/6 in Wnt-B catenin pathway and decreases bone mass… increased expression seen in multiple myeloma cells

296
Q

Genetic defect in juvenile Paget’s disease?

A

Osteoprotegrin

297
Q

Receptors found on osteoclasts

A

C-sf1 (binds M-CSF), RANK (binds RANK-L), calcitonin and aVB integrin (binds vitronectin on bone)

298
Q

Nitrogen containing bisphosphonate mechanism

A

Blocks farnesyl phyrophosphate synthase in the mevalonate pathway (Risedronate, Alendronate, Zolendronate, Pamidronate).

299
Q

Non-nitrogen containing bisphosphonates mechanism of action

A

Competes with osteoclast ATP and induces apoptosis (Tiludronate, Clodronate, Etidronate)

300
Q

How do osteoclasts resorb bone?

A

CO2 + H2O made into H2CO3 by carbonic anhydrase, then HCl- is released into Howship’s lacunae to acidfy the environment to pH of 4.5 and dissolve HA crystals. Cathespin K dissolves the collagen matrix. TRAP levels increase and can be measured in serum

301
Q

Genetic diseases of non-functioning osteoclasts

A

Osteopetrosis (most common Cl channelopathy or CA II deficiency = no ruffled border) and pyknodysostosis (cathepsin K deficiency). These have increased risk of fractures as opposed to sclerosteosis and Van Buchem’s that have rare fractures.

302
Q

Virchow’s triad

A

Hypercoaguability, stasis and endothelial damage

303
Q

Most common inherited clotting disorder

A

Facotor V Leiden

304
Q

TXA mechanism of action

A

Lysine analog that binds plasminogen and prevents fibrinolysis

305
Q

Drug that inhibits prostaglandin E2 via IL-1B

A

Acetaminophen

306
Q

Drug that irreversibly binds COX in platelets

A

ASA

307
Q

Drug that preferentially inhibits COX-2

A

Celicoxib

308
Q

Drug that inhibits Vitamin K gamm carboxylation? Reversal?

A

Coumadin, reverse with Vit K or FFP

309
Q

Drug that reversibly inhibits Xa, ATIII, factors II, IX, XI and XII? Reversal?

A

Heparin, reverse with protamine sulfate. Acts by increasing ATIII activity.

310
Q

Drug that reversibly inhibits Xa, ATIII and factor II?

A

LMWH. Acts by increasing ATIII activity.

311
Q

Drug that irreversibly inhibits factor X and ATIII? Reversal?

A

Fondaparinux. Reverse with Andexanet.

312
Q

Drug that inhibits thrombin IIa only?

A

Hirudin/dabagatran. Reverse with Idracizumab.

313
Q

Effort thrombosis etiology? Treatment?

A

Upper extremity DVT from strenuous exercise. Axillary subclavian vein thrombosis. Treat with thrombolysis and/or 1st rib resection.

314
Q

Do you need to anticoagulated patients who had DVT after knee arthroscopy or casting?

A

No based on the NEJM RCT in 2017

315
Q

Fat Embolism Syndrom

A

Petechial rash, neurologic symptoms and pulmonary collapse (ARDS)

316
Q

Best prophylaxis in prevention of fat emboli syndrome

A

Fix within 24 hours, higher risk if fixed after 48 hours

317
Q

CO and PVR in hypovolemic shock

A

CO decreased, PVR increased

318
Q

Stages of hypovolemic blood loss

A

I) 0-15%, normal vitals 2) 15-30%, tachycardia, increased DBP 3) 30-40%, decreased SBP, oliguria, MS changes 4) >40%, narrowed pulse pressure, life threatening, no UOP

319
Q

Best clinical and lab indicators for adequate perfusion

A

UOP >30cc/hr and lactate >2.5

320
Q

PVR in septic shock

A

Decreased due to systemic vasodilation

321
Q

Etiology of neurogenic shock

A

High cord injury -> loss of sympathetic tone and peripheral blood pooling -> hypotension and bradycardia

322
Q

Earliest sign of malignant hyperthermia

A

Unexplained rise in EtCO2

323
Q

Mutations associated with malignant hyperthermia?

A

Familial = RYR1 gene mutation. DMD muscular dystrophy as well.

Basic Science (1 decks)

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