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MSK Flashcards

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1
Q

Hyaline cartilage

A
  • Most predominant, primarily made up of type II collagen and proteoglycans with chondrocytes
  • Located at the ends of long bones and nose cartilage
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2
Q
A

Hyaline cartilage

(Homogenous mixture)

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3
Q
A

Elastic cartilage

  • Elastic fibers floating within matrix, helps resist tensile forces
  • Located in ear and epiglottis
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4
Q
A

Fibrocartilage

  • Mostly type I collagen fibers running through matrix, helps resist compressive forces
  • Herringbone pattern (Chevron pattern)
  • Located in intervertebral discs, pubic symphysis, and menisci
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5
Q
A

A - Isogenous Groups

B - Perichondrium

C - Lacunar Space

D - Chondrocyte

E - Territorial Matrix

F - Interterritorial matrix

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6
Q

Molecular components of cartilage matrix

A
  • Type II collagen
  • Proteoglycans and GAGs (like HA) form complexes with negative charges to give matrix its viscosity, strength, and flexibility
  • Water is 60-80% matrix weight (bound to proteoglycans and GAGs)
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7
Q
A
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8
Q

Methods that cartilage develops into bone

Location of Occurence

A
  • Endochondral ossification
    • Mesoderm –> Cartilage –> Bone
    • Long bones, base of skull, short bones in hands/feet
    • Primary and secondary ossification centers
      • Fusion - 12-16(F), 14-18(M)
  • Intramembraneous ossification
    • Mesenchyme –> Bone
    • Flat bones of face, cranial bones, clavicles
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9
Q
A
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10
Q
A

A - Osteocytes (sit in lacunae, connected by canaliculi)

B - Osteoblasts (located on surface of bone)

C - Osteoclasts (multinucleated gianted cells)

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11
Q
A
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12
Q
A

Woven Bone

  • Newly formed (immature) bone without organized lamellae
  • Contains osteoid = gelatinous substance, not yet mineralized
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13
Q
A

Lamellar Bone

  • Mature bone that consists of organized layers of mineralized bone
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14
Q

How is collagen mineralized into bone?

A
  • Collagen is mineralized through exocytosis of small vesicles from the osteoblasts filled with alkaline phosphatase and pyrophatase into newly formed bone (osteoid) to initiate mineralization and bind calcium/phosphate
  • Organic material makes up 30% of bone
    • Other 70% = hydroxyapatite, complex of calcium and phosphate
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15
Q

How do hormones and nutrients play roles in maintenance of bone tissue?

A
  • Low serum Ca sensed by CaSR on parathyroid gland
  • Parathyroid gland releases PTH
  • PTH stimulates bone resorption (and kidney reabsorption) to increase Ca in blood

*Also Vitamin D (abosrbed through skin and intestines) plays a role in regulation of Ca in blood

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16
Q

ESR vs CRP

A

ESR

  • Elevated with age, diabetes, ESRD, pregnancy, obesity, F
  • Lower with CHF, Sickle cell disease

CRP (more sensitive and less variable than ESR)

  • Affected by age and gender
  • Elevated with heart disease, infection, malignancy, obesity, diabetes, and smoking
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17
Q

How do crossbridges (x-bridges) factor into muscle movement?

A
  • Total muscle force is proportional to total number of attached x-bridges
    • Keyword: attached (only those attached can produce force)
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18
Q

Molecule mechanism of muscle movement

A
  • Myosin head attaches to thin filaments (actin monomers + troponin complex)
    • When calcium binds to troponin –> Actin is exposed allowing for myosin head to bind
  • Myosin head contains ATPase which breaks down ATP, using energy for configurational changes
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19
Q

Basic mechanical properites of MSK

A
  • Need sustained APs to cause accumulation of muscle twitches and force outputs
    • There exists a frequency threshold where force output hits a ceiling
  • Operating range of muscles
    • Too far - no crossbridge attachments
    • Too close - all crossbridge attachment sites are filled
  • The faster a muscle shortens, the less the force
  • As sarcomeres stretch out, the elastic properties of muscles kick in
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20
Q

What affects the number of cross bridges (x-bridges)

A
  1. Ca2+ and Neuro system
    • Ca2+ - determines magnitude of muscle movement
    • CNS controls single motor units (100s-1Ks fibers)
  2. Length of the muscle
  3. Velocity (how fast the muscle moves)
  4. X-bridge cycling speed
    • How fast myosin can make attachments and form x-bridges at any given speed
    • Depends on various isozymes of myosin
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21
Q

What are the stubstrates used by muscles for energy and what are their mobilization times + duration

A
  • ATP - Instantaneous, 0-5s
  • CP (Creatinine Phosphate) - <1s mob, 10s
    • CP + ADP –> ATP (via CPK)
  • Glycogen
    • Anaerobic - 5-30s mob, several minutes
    • Aerobic - 30-120s mob, 30m-2hr
  • Anaerobic fat - 20-60m mob, long duration
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22
Q

RA vs OA

A
  • RA - symmetrical inflammatory
    • Middle aged
    • Pain decreases with joint use - MCPs and PIPs
    • Morning stiffness from 30-60min
  • OA - nonsymmetrical bony enlargment at joint
    • Older aged
    • Pain increases with joint use - PIPs and DIPs
    • Morning stiffness <30min
    • Swelling is less pronounced and less persistent
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23
Q

OA Common patterns of joint involvement

A
  • Primary OA
    • Either or in combination of hand, cervical/lumbar spine, feet, knees, and hips
  • Generalized OA
    • Involves hands + at least 1 large joint
      • Multiple finger joints usually involved
  • Secondary OA
    • If OA appears prematurely and/or in joints atypically affected like MCP, wrist, elbow, shoulder, ankle
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24
Q

Herberden’s nodes

A

Bony enlargements in DIP joints, typically seen in OA

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25
Aggregan
Proteoglycan macromolecule linked with HA, consisting of negatively charged GAGs and constrained by type II collagen - _provide tensile strength of cartilage_ With retained water (supports 95% load) --\> compressive stifness
26
OA Pathology
* New bone activity --\> Thickening * Osteophytes, initial increase in chondrocyte number and activity * Cartilage damage/lost * Synovial hyperplasia --\> edematous and inflamed * Capsular thickening --\> edematous --\> fibrosis
27
OA Treatment
* Firstly, simple analgesic like acetaminophen * Anti-inflammatories * Selective COX2is \> NSAIDs (only regarding GI risks) * Others: Intraarticular injections, corticosteroids, HA, Overcounters (glucosamine, chondroiton) * Total joint replacement * Advanced OA * Unclear in mild/moderate OA * No response to conservative therapy * Arthroscopy (maybe) with mechanical symptoms (like locking)
28
Indications for x-ray
* Trauma * Infection (destroyed bone) * Arthritis
29
Indications for CT
* Bone biopsy * Need more fracture details * Ex: Irregularity/depression of articular surface
30
Indications for MRI
* Issues with joints, soft tissue, and cartilage * Ex: Shoulder, rotator cuff injuries
31
Indications for fluoroscopy
* Procedures where real-time dynamic imaging is needed * Ex: Joint injections or biopsies
32
Indications for US
* Involving superficial soft tissue * Ex: Achilles tendon tear * Soft tissue biopsies
33
Indications for nuclear medicine | (DXA, Bone scintigraphy)
* Detection of osteoporosis and fracture risk
34
DXA
Dual x-ray absorptiometry - measure of bone density measured in standard deviations * T score - compared to std yound population * Z score - compared to patients of similar age and gender Scores * \<1 SD = normal * 1-2.4 SD = osteopenia * \>2.5 SD = osteoporosis * Plus at least 1 low trauma fracture = sever osteoporosis
35
Bone scintigraphy
Photon emitting substance (usually technetium) injected via IV * Identifies (via "lighting up") areas of active bone turnover and increased blood flow * Fracture, infection, and blastic metastases
36
Myelography indications
* If MRI is contraindicated * Central canal evaluation \*Contrast injected into central canal (thecal sac) allowing for visibility on _CT and fluoroscopy_
37
Arthrography indication
* More visibility in joints (via contrast injection) during radiography, CT, and fluoroscopy * Cartilage, rotator cuff tendons, instrinc ligaments of wrist, elbow, labrum (shoulder and hip) \*Contraindicated for contrast allergy and MRI contraindication
38
Absolute and relative contraindications of MRI
Relative * Pacemakers, stimulators, metal in the orbit, weight Absolute * Aneursym clips, metal
39
What are the various mechanisms of biologics (BRMs)
1. Cytokine receptor antagonists 2. Monoclonal antibodies 1. Binds both cytokine and cytokine receptor 3. Soluble cytokine receptors
40
Certolizumab
**anti-TNFa** Humanized Fab' fragment
41
Etanercept
**anti-TNFa** Human recombinant receptor/Fc fusion protein
42
TNFa inhibitors
Infliximab - chimeric monoclonal antibody Adalimumab and Golimumab - human recombinant Etanercept - human recombinant receptor/ Fc fusion protein Certolizumab - humanized Fab' fragment
43
Tocilizumab
anti-IL6
44
Abatacept
Binds B7 (CD80/86) preventing co-signaling needed for T cell activation * B7 - CD28
45
Rituximab
Monoclonal antibody that binds CD20 on mature B cells * Induces apoptosis, transiently depleting pre-B and mature B cells * Doesn't affect progenitor and plasma cells \*Rare SFx of progressive multifocal leukoencephalopathy
46
Difference between biologics and small molecules inhibitors
* Biologics * Large protein-based, limited by parenteral administration * Produced in expensive mammalian cell-cultures * Small molecule inhibitors * Can be administered orally * **Target intracellular proteins**
47
Bacterial factors that promote septic arthritis
* Staph auerus - MSCRAMMs (adhesins) permit adherence to cartilage * Endotoxins promote cartilage breakdown
48
Etiology of septic arthritis
* Typically hematogenous * Vascular synovial membrane lacks limiting BM * Direct inoculation * Surgery, trauma, contiguous spread from adjacent infected soft tissue or bone
49
Pathogenesis of septic arthritis
Host inflammatory repsonse * Host-derived extracellular proteins promote bacterial attachment * Protease/cytokines → cartilage + subchondral bone destruction * Joint inflammation → increased intra-articular pressure and reduced capillary blood flow → ischemia and necrosis
50
Pathogenesis of Osteomyelitis
* Bacterial adhesions (like S. aureus MSCRAMMs) promoted adhesion to fibronectin, collagen, and other molecules on cell surfaces * Persistence within osteoblasts (survive and become more antibiotic resistance) - espc S. aureus * Biofilm formation
51
Clinical syndromes of Lyme disease
Early phase * Erythema migrans - expanding annular erythematous * Disseminated - fever and chills, secondary annular skin lesions, meningitis, cranial neuritis, carditis, and migratory arthritis Late phase * Septic arthritis * Chronic encephalopathy
52
Clinical syndromes of parvovirus
AKA 5th disease / erythema infectiosum / slapped cheek virus * Acute, symmetrical polyarthritis of PIP and MCP joints with morning stiffness * W\>M * Self-resolves in 2 weeks (20% women may develop persistent polyarticular arthritis for months)
53
MTX SFx and contraindications
* Transaminitis - elevated of enzymes * Leukopenia, oral ulcers, alopecia, interstitial pneumonia * Contraindicated in pregnant women (or those who want to get pregnant) = teratogenic
54
Prednisone SFx
* HTN * Osteoporosis - vertebral compression fracture via increase in osteoclasts * AVN * GI ulcers * Weight Gain * Lack of Sleep * Contraindicated in children because it can impede/decrease growth
55
What do you check before MTX administration?
* Liver function * Hep C infection
56
Clinical presentation of reactive arthritis (ReA)
* Acute, following GI/GU infection, self-limiting (3-24 weeks) * Chlamydia, shigella, salmonella, yersinia, campylobacter, clostridium * M\>F * Additive, asymmetric mono/oligo-arthritis involving more commonly _large lower extremity joints_ * Dactylitis, enthesitis, sacroiliitis * Extra articular features: scaly plaque-like lesions on hands/feet, mucosal lesions, thicekend/opacified nails, conjunctivits, acute anterior uveitis
57
Clinical presentation of axial spondyloarthritis (AS)
* _Sacroiliitis and inflammatory back pain + stiffness_ * Systemic symptoms: fatigue, impaired sleep * Oligoarthritis, enthesitis, uveitis, IBD, aortitis
58
Clinical presentation of psoriatic arthritis (PsA)
* Cutaneous * Psoriatic plaques, onycholysis, nail bed pitting * Guttate, Pustular, Erythrodermic * Inflammatory polyarthritis (25% of psoriatic patients) * Asymmetric/Symmetric/Axial * Often DIP involvement * Dactylitis, enthesitis, rheumatoid factor negative * M=F * "Pencil in cup" on xray - both destructive+constructive
59
Clinical presentation of IBD SpA
* Associated with diseases like Crohn's * Sacroiliitis + inflammatory back pain/stiffness * Change in bowel habits * Oligoarthritis, enthesitis, dactylitis, systemic symptoms (fatigue, impaired sleep) \*Peripheral arthritis w/ and w/o IBD being active * Arthtiris may be present before bowel disease \*Similar to AS symptoms
60

MSK/DERM (2 decks)

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