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MSK Flashcards

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Dermatology Board Prep flashcards
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
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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
Q

Aggregan

A

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
Q

OA Pathology

A
  • 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
Q

OA Treatment

A
  • 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
Q

Indications for x-ray

A
  • Trauma
  • Infection (destroyed bone)
  • Arthritis
29
Q

Indications for CT

A
  • Bone biopsy
  • Need more fracture details
    • Ex: Irregularity/depression of articular surface
30
Q

Indications for MRI

A
  • Issues with joints, soft tissue, and cartilage
    • Ex: Shoulder, rotator cuff injuries
31
Q

Indications for fluoroscopy

A
  • Procedures where real-time dynamic imaging is needed
    • Ex: Joint injections or biopsies
32
Q

Indications for US

A
  • Involving superficial soft tissue
    • Ex: Achilles tendon tear
  • Soft tissue biopsies
33
Q

Indications for nuclear medicine

(DXA, Bone scintigraphy)

A
  • Detection of osteoporosis and fracture risk
34
Q

DXA

A

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
Q

Bone scintigraphy

A

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
Q

Myelography indications

A
  • If MRI is contraindicated
  • Central canal evaluation

*Contrast injected into central canal (thecal sac) allowing for visibility on CT and fluoroscopy

37
Q

Arthrography indication

A
  • 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
Q

Absolute and relative contraindications of MRI

A

Relative

  • Pacemakers, stimulators, metal in the orbit, weight

Absolute

  • Aneursym clips, metal
39
Q

What are the various mechanisms of biologics (BRMs)

A
  1. Cytokine receptor antagonists
  2. Monoclonal antibodies
    1. Binds both cytokine and cytokine receptor
  3. Soluble cytokine receptors
40
Q

Certolizumab

A

anti-TNFa Humanized Fab’ fragment

41
Q

Etanercept

A

anti-TNFa Human recombinant receptor/Fc fusion protein

42
Q

TNFa inhibitors

A

Infliximab - chimeric monoclonal antibody

Adalimumab and Golimumab - human recombinant

Etanercept - human recombinant receptor/ Fc fusion protein

Certolizumab - humanized Fab’ fragment

43
Q

Tocilizumab

A

anti-IL6

44
Q

Abatacept

A

Binds B7 (CD80/86) preventing co-signaling needed for T cell activation

  • B7 - CD28
45
Q

Rituximab

A

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
Q

Difference between biologics and small molecules inhibitors

A
  • 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
Q

Bacterial factors that promote septic arthritis

A
  • Staph auerus - MSCRAMMs (adhesins) permit adherence to cartilage
  • Endotoxins promote cartilage breakdown
48
Q

Etiology of septic arthritis

A
  • Typically hematogenous
    • Vascular synovial membrane lacks limiting BM
  • Direct inoculation
    • Surgery, trauma, contiguous spread from adjacent infected soft tissue or bone
49
Q

Pathogenesis of septic arthritis

A

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
Q

Pathogenesis of Osteomyelitis

A
  • 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
Q

Clinical syndromes of Lyme disease

A

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
Q

Clinical syndromes of parvovirus

A

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
Q

MTX SFx and contraindications

A
  • Transaminitis - elevated of enzymes
  • Leukopenia, oral ulcers, alopecia, interstitial pneumonia
  • Contraindicated in pregnant women (or those who want to get pregnant) = teratogenic
54
Q

Prednisone SFx

A
  • 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
Q

What do you check before MTX administration?

A
  • Liver function
    • Hep C infection
56
Q

Clinical presentation of reactive arthritis (ReA)

A
  • 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
Q

Clinical presentation of axial spondyloarthritis (AS)

A
  • Sacroiliitis and inflammatory back pain + stiffness
  • Systemic symptoms: fatigue, impaired sleep
  • Oligoarthritis, enthesitis, uveitis, IBD, aortitis
58
Q

Clinical presentation of psoriatic arthritis (PsA)

A
  • 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
Q

Clinical presentation of IBD SpA

A
  • 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
Q
A

MSK/DERM (2 decks)

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