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OMS II BECOM Exam 1 > Disorders of MSK I&II - Zaloga > Flashcards

Disorders of MSK I&II - Zaloga Flashcards

1
Q

osteoclasts

A
  • resorb bone causing release of Ca2+
  • remodeling of skeleton
  • macrophages clean up cellular debris
  • has RANK receptor to activate NFkB for survival
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2
Q

osteoblasts

A
  • form new bone
  • activate osteoclasts with RANKL and M-CSF
  • contain LRP5/6 receptor for WNT binding to activate beta-catenin and OPG…inhibited by sclerostin
  • contain RANKL
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3
Q

OPG - osteoprotegrin

A
  • decoy receptor produced by osteoblasts

- binds to RANKL preventing binding to RANK receptor

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4
Q

hereditary bone disorders

A
  1. Achondroplasia
  2. Osteogenesis Imperfecta (Type 1 collagen disease)
  3. osteopetrosis
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5
Q

achondroplasia

A
  • most common dysplasia
  • dwarfism
  • FGFR3 mutation (always active) –> inhibiting endochondral growth –> no ossification in appendicular skeleton
  • short extremities
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6
Q

osteogenesis imperfecta (type 1 collagen disease) aka brittle bone

A
  • most common connective tissue disorder
  • affect type 1 collagen –> brittle bones, fractures
  • blue sclera, hearing loss
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7
Q

osteopetrosis aka marble bone disease

A
  • brittle, fragile bones –> easy fractures
  • mutations of osteoclasts resorption –> reduced resorption –> sclerosis
  • adult is benign and infantile is malignant
  • decreased hematopoiesis –> anemia
  • adult: autosomal dominant –> defect in chloride channel function
  • infant: autosomal recessive: proton pump or chloride channel dysfunction
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8
Q

bone and cartilage acquired disorders

A
  1. osteopenia and osteoporosis
  2. osteomalacia and rickets
  3. Paget disease
  4. osteitis fibrosa cystica
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9
Q

osteoporosis

A
  • severe osteopenia
  • primary, idiopathic, senile - low proliferative osteoblasts (low turnover), postmenopausal - low estrogen, cytokines stimulate osteoclasts with high RANKL and low OPG (high turnover)
  • normal bone content, low quantity, thin trabeculae
  • dexa scan measure density
  • high risk fractures
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10
Q

rickets and osteomalacia

A
  • vit. D deficiency –> under mineralized bone
  • rickets (children) –> interferes with growth plates
  • osteomalacia (adults) –> undermineralized bone
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11
Q

Paget disease aka osteitis deformans

A
  • increase bone, but disordered (risk of fractures)
  • lamellar bone in sclerotic phase
  • high alkaline phosphatase
  • mutations in SQSTM1 gene –> increase NFkB –> increase osteoclast activity

phases:
Osteolytic – osteoclasts resorbing bone

Mixed – osteoblasts enter to repair

Sclerotic – dense, weak bone due to osteoclasts breaking it down

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12
Q

osteitis fibrosa cystica

A
  • loss of bone mass
  • calcified structures replaced with fibrous –> weak bones
  • cyst like brown tumors
  • causes: PTH (increase serum Ca2+ and osteoclasts), renal disease (cannot make vit. D)
  • brown tumor –> decrease in bone density/mass
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13
Q

fracture repair process

A
  • rupture blood vessels –> hematoma fills gap –> fibrin mesh –> influx of inflammatory cells and fibroblasts –> new capillaries
  • 1st week –> hematoma and remodel fractured ends of bone
  • 2nd week –> soft tissue callus to bony callus - stiffness and strength increase with more mineralization
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14
Q

osteonecrosis (avascular necrosis)

A
  • dead bone (necrotic) –> few osteocytes
  • causes: fractures or corticosteroids
  • vascular insufficiency
  • subchondral and medullary infarcts
  • trabeculae collapsed and not repaired
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15
Q

osteomyelitis

A
  • inflammation of bone and marrow, sclerosis
  • usually due to infection
  • dead bone, fibrosis, infiltrate of inflammatory cells
  • pyogenic bacteria and mycobacteria (fungal)
  • mycobacterial –> tuberculous spondylitis (Pott disease)
  • staph 90% cause for pyogenic
  • E. coli, pseudomonas, klebsiella in IV drug and GU tract infections
  • H. influenza in neonates (not vaccinated)
  • sickle cell –> salmonella
  • treatment: antibiotics and drainage
  • acute neutrophils, chronic lymphocytes
  • infection breaks periosteum –> form sinus tract
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16
Q

osteoarthritis aka degenerative joint disease

A
  • degeneration of cartilage, disordered repair
  • previous joint injury and obesity predisposing factors
  • NO FUSION of joints
  • inflammation –> chondrocyte death –> bone eburnation, thickened trabeculae, subchondral sclerosis
  • fracture gaps can form synovial cysts and osteophytes
  • osteophytes in Heberden’s and Bouchard’s nodes**
17
Q

rheumatoid arthritis (RA)

A
  • chronic inflammation, autoimmune
  • attack joints –> synovitis, lose joint space
  • cartilage destruction with ankylosis (FUSION)
  • osteopenia
  • radial deviation of wrist, ulnar deviation of fingers
  • self antigens attacked by antibodies and CD4 T cells
  • cytokines: IFN-gamma (Macs), IL17 (neutrophils), monocytes
  • T cells activate RANKL –> bone resorption w/ osteoclasts
  • anti-CCP (citrullinated peptides) for diagnostic marker - autoantibodies
  • rheumatoid factor –> IgM, IgA binding Fc on IgG activating immune system
  • Pannus destroys cartilage –> fibrous –> bone ankylosis
18
Q

seronegative spondyloarthropies

A
  1. Ankylosing Spondylitis
  2. psoriatic arthritis
  3. reactive arthritis

swelling of fingers/toes, changes in ligament attachments, no rheumatoid factor, HLA-B27, T cell attacks antigen

19
Q

Ankylosing Spondylitis aka rheumatoid spondylitis (Marie-Strumpell)

A
  • destroy articular cartilage
  • bone ankylosis (sacroiliac joints common)
  • 90% HLA-B27 positive
  • low back pain, spinal immobility
20
Q

psoriatic arthritis

A
  • psoriasis, chronic inflammation
  • peripheral and axial joints (ex. hands, feet mainly) - distal joints
  • joint destruction not frequent
  • HLA-B27 and HLA-Cw6 alleles
21
Q

reactive arthritis aka Reiter’s syndrome

A
  • joint pain, swelling due to infection of another part of body
  • triad: urethritis or cervicitis, conjunctivitis, and arthritis
  • GU tract infection (chlamydia)
  • GI tract infection (shigella, salmonella, campylobacter)
  • 80% HLA-B27 positive
22
Q

Gout

A
  • crystals include monosodium urate (needle like)
  • attacks of acute arthritis by crystals in/around joints –> cytokine cascade –> destroy joints
  • hyperuricemia, MSU crystals cause inflammation, cytokines recruit Macs (inflammasome) to recognize crystals and cause inflammation
  • repeated attacks –> tophaceous gout –> pannus destroys cartilage w/ ankylosis
  • cause: hyperuricemia, renal failure, obese, EtOH
  • men more affected
23
Q

Pseudogout aka chondrocalcinosis

A
  • crystals include Ca2+ pyrophosphate dehydrate, CPPD, (rhomboid shape)
  • sexes/races equally affected
  • activation of macrophages inflammasome –> inflammation
  • more mild than gout
24
Q

peripheral nerves neuropathy

A
  • contain axons and myelin sheaths (Schwann cells)
  • damage to proteins that make myelin (MBP, MPZ, PMP22, PRX) or Schwanna cells –> disease and slow nerve conduction
  • pseudotumor if transected ends not close together for repair
25
Q

axon neuropathy

A
  • due to trauma or entrapment (ex. lacerations, fractures)
  • morton neuroma - nerve compression due to painful mass in foot, fibrosis
  • traumatic neuroma - fibrosis around nerve
26
Q

Gullian Barr syndrome

A
  • acute inflammatory demyelinating polyneuropathy
  • T cell immune response –> demyelination by Macs and antibodies attacking nerve fibers
  • ascending paralysis, areflexia, slow conduction velocity
  • begins distally, invades proximally
27
Q

neuromuscular junction

A
  • presynaptic depolarization –> Ca2+ channels release ACh vesicles –> bind to receptors on motor end plate (postsynaptic sarcolemma) –> contraction

Diseases: Myasthenia Gravis, Lambert-Eaton myasthenic syndrome

28
Q

myasthenia gravis (Graves)

A
  • autoantibodies against ACh receptors
  • painless weakness, may affect ventilation
  • associated with thymoma and thymic hyperplasia –> treat with thymectomy in some cases
  • ptosis and diplopia
  • treatment: AChE inhibitors, immunosuppressive to decrease antibodies, thymectomy
29
Q

Lambert-Eaton myasthenic syndrome

A
  • antibodies attack presynaptic Ca2+ channel –> prevent ACh release –> weakness of extremeties
  • repetitive stimulation –> increase muscle response
  • associated with neuroendocrine carcinoma of lungs
30
Q

skeletal muscle atrophy

A
  • normal - one nerve innervates same fiber type
  • denervation when axons are damaged –> myofiber atrophy
  • reinnervation of myofibers –> switch of fiber type and regeneration of fibers –> type grouping
  • degeneration –> release creatine kinase
  • regeneration –> satellite cells fuse with damaged myofibers
  • replaced with fibrosis and fat with chronic disease where regeneration fails
31
Q

inflammatory myopathies

A
  1. polymyositis
  2. dermatomyositis
  3. inclusion body myositis

autoimmune inflammatory disease –> autoantibodies, HLA-DR genotypes

32
Q

Dermatomyositis

A
  • autoimmune –> proximal muscle weakness, skin changes
  • Anti-Mi2 antibodies –> heliotrope rash, Gottron papules
  • Anti-Jo1 antibodies –> interstitial lung disease, mechanic hands, arthritis
  • myalgia, high serum creatine kinase
  • perifascicular atrophy (inflammatory infiltrate of muscle edges) due to CD4 cells –> associated with blood vessel injury
33
Q

Polymyositis

A
  • same as dermatomyositis, but no skin changes
  • muscle weakness and myalgia
  • CD8 T cells infiltrate instead
  • no perifascicular atrophy or vascular injury
34
Q

inherited myopathies

A
  1. congenital: central core disease, NEM, centronuclear, congenital fiber type disproportion –> floppy infant
  2. muscular dystrophies –> progressive muscle damage (ex. Duchenne, Becker)
    - mutated dystrophin –> X linked
    - mutated caveolin and sarcoglycan –> limb-girdle dystrophies
    - genetic testing for dystrophin to confirm
    - + Gower’s sign –> impaired lower extremeties
    - high creatine kinase levels at 1st then drops
    - muscle tissue replaced with collagen and adipose
35
Q

Duchenne muscular dystrophy

A
  • X linked dystrophin mutation –> absent dystrophin
  • faster onset, more severe, most common
  • pseudohypertrophy, wheel chair, respiratory problems, cardiomyopathy
36
Q

Becker muscular dystrophy

A
  • X linked dystrophin mutation –> some dystrophin

- later onset, less severe, slowly progressive, longer lifespan

OMS II BECOM Exam 1 (30 decks)

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