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NMSP Exam 2 > Bones, Joints, Soft Tissues Part 1 > Flashcards

Bones, Joints, Soft Tissues Part 1 Flashcards

1
Q

What is the bone matrix and what is it composed of?

A

Extracellular component of bone

  • Osteoid (organic)
  • Mineral
  • Inorganic (hardness d/t hydroxyapatite, contains majority of calcium and phosphorus in the body)
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2
Q

What is osteoid? What is a major protein in this and what does that do?

A

Type 1 collagen
- Contains the protein osteopontin (osteocalcin) that is produced by osteoblasts; contributes to bone formation, mineralization, calcium homeostatis

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3
Q

What are 2 histologic forms of bone? Where do we see these and what are some characteristics?

A

Woven

  • Fetal development or fracture repair (produced rapidly)
  • Haphazard arrangement of collagen so less structural integrity
  • Abnormal in adults

Lamellar
- Parallel collagen which is stronger but slower to produce

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4
Q

3 types of cells in bone?

What is mechanotransduction and which cell does this?

A

Osteoblasts

  • Blasts build bone
  • Regulate mineralization

Osteocytes

  • Inactive osteoblasts
  • Work through canaliculi
  • Control calcium and phosphate levels
  • Mechanotransduction: Detects mechanical forces & translates them into biological activity

Osteoclasts

  • Multinucleated macrophages that participate in bone resorption
  • Resorption pit: Cell surface integrins attach, secrete metalloproteases, dissolve bone
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5
Q

What is endochondral ossificaiton?

What are radial growth and longitudinal growth?

A

Formation of long bones; cartilage mold is laid down first and then ossified

Radial growth: Osteoblasts deposit cortex beneath periosteum of diaphysis (primary centers of ossificaiton)

Longitudinal growth: New bone is deposited at bottom of growth plates (epiphyses) (secondary centers of ossification)

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6
Q

What is intramembranous ossification?

What is appositional growth?

A

Formation of flat bones; mesenchyme is directly ossified so no cartilage mold
- Appositional growth: Direct deposit of new bone on pre-existing bone

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7
Q

When is peak bone mass achieved?

A

Fourth decade of life; after this resorption > formation and you start losing skeletal mass

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8
Q

What is RANK?

Does this cause breakdown or building of bone?

A

Receptor activator for NF-KB on osteoclast precursors

  • When stimulated by RANKL, activates transcription factor NF-KB which is essential for generation and survival of osteoclasts
  • B/d of bone
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9
Q

What is RANKL?

Does this cause breakdown or building of bone?

A

Expressed on osteoblasts & marrow stromal cells

- B/d of bone

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10
Q

What is OPG?

Does this cause breakdown or building of bone?

A

Osteoprotegerin “decoy” receptor made by osteoblasts

  • Binds to RANKL to prevent its interaction with RANK
  • Builds bone
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11
Q

What are some systemic factors that promote osteoclast differentiation and bone turnover?

A

PTH, IL-1, glucocorticoids

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12
Q

What are some systemic factors that block osteoclast differentiation, promote OPG expression, and favor bone deposition?

A

Bone morphogenic proteins and sex hormones, vitamin D

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13
Q

What role does WNT and beta-catenin play in bone?

What about sclerostin?

A

WNT proteins trigger activation of beta-catenin & production of OPG

Sclerostin inhibits WNT/beta-catenin to suppress bone formation

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14
Q

What role does M-CSF play?

A

Macrophage colony stimulating factor helps generation of osteoclasts

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15
Q

How do osteoclasts and osteoblasts work togeter?

A

Osteoclasts activate a bunch of things in the b/d of the matrix that stimulates osteoblasts

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16
Q

What is dysostosis?

What is Dysplasia?

A

Dysostosis: Localized disruptions of migration & condensation of mesenchyme & differentiation into cartilage anlage
- Often d/t defects in homeobox genes

Dysplasia: Global disorganization of bone &/or cartilage (abn growth, NOT premalignant)
- Mutations in genes controlling entire skeleton

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17
Q

Dysostosis:

What is aplasia?

What are supernumerary digits?

What is syndactyly or craniosynostosis?

A

Aplasia: Absence of entire bone or digit

Supernumerary digits: Extra bones or digits

Syndactyly or craniosynostosis: Abn fusion of bones

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18
Q

What gene mutation is common in brachydactyly types D & E? What do you see in this disorder?

A

HOXD13

Short terminal phalanges of thumb and big toe

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19
Q

What gene mutation is common in cleidocranial dysplasia? What do you see in this disorder?

A

RUNX2

  • Wormian bones (extra cranial bones within cranial sutures)
  • Patent fontanelles
  • Delayed closure of cranial sutures
  • Delayed eruption of secondary teeth
  • Primitive clavicles
  • Short height
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20
Q

What gene mutation is common in achondroplasia? What do you see in this disorder?

A

Major cause of dwarfism; short extremities with normal trunk length, enlarged head
- No change in longevity, intelligence, or reproductive status

FGFR3 gain of fxn mutation

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21
Q

What gene mutation is common in thanatophoric dysplasia? What do you see in this disorder?

A

Most common lethal form of dwarfism; similar to achondroplasia but with small chest cavity (resp insufficiency) and bell-shaped abd leading to death soon after birth

FGFR3 gain of fxn but more sever phenotype than achondroplasia

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22
Q

What causes osteogenesis imperfecta?

What are some common sx?

A

Deficiencies in type 1 collagen synthesis (alpha 1 and 2 chains) leads to no triple helix formation and “brittle bones”

Brittle bones, blue sclera, hearing loss, dental imperfections

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23
Q

What are the different types of osteogenesis imperfecta?

What genes are involved in Types 1 and 2?

A

4 subtypes but mainly:

  • Type 1 has normal life span with childhood fractures that dec in freq following puberty
  • Type 2: Uniformly fatal in utero w intrauterine fractures

Both Types 1 and 2 could have defects in COL1A1, type 2 could have defect in COL1A2

Types 3 and 4 are moderately in between severity of types 1 and 2

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24
Q

What are specific sx of OI Type 1?

A
  • Collagen structure is normal but there is dec amount
  • Most fractures happen before puberty w dec in freq after puberty
  • Loose joints
  • Blue, grey, purple tinted sclera
  • Brittle teeth
  • Hearing loss possible beginning in early 20s or 30s
  • Skeletal fragility
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25
Q

What are specific sx of OI Type 2?

A
  • Most severe form
  • Collagen improperly formed
  • Lethality d/t respiratory problems
  • Numerous fractures and severe bone deformity
  • Small stature w underdeveloped lungs
  • Blue sclera
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26
Q

What is tx for OI?

A
  • Surgical rodding of long bones
  • Exercise, keep healthy weight, good nutrition
  • Don’t smoke, don’t take steroids
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27
Q

What is osteopetrosis?

What is defective in this?

A

Dec bone resorption d/t deficient osteoclast development/fxn leading to diffuse symmetric skeletal sclerosis

Deficiency in carbonic anhydrase 2
- Required by osteoclast & renal tubular cells (renal tubular acidosis) to generate protons from CO2 and water

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28
Q

What is Albers-Schonberg disease? What gene mutation causes this?

A

Mild auto dominant form of osteopetrosis caused by mutation in CLCN7; required for resorption pit acidification

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29
Q

Is osteopetrosis usually auto dominant or recessive? What gene mutation causes this?

A

Usually auto recessive caused by mutation of TCIRG1 which encodes subunit of osteoclast vacuolar hydrogen positive ATPase that is necessary for acidification of resorption pit

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30
Q

What are some sx of osteopetrosis? What are the bones like?

What is the severe infantile form?

A

Bones lack medullary cavity, have bulbous ends, and have small neural foramina that compress nerves; bones tends to be woven vs lamellar

Severe infantile type is autosomal recessive

  • Fractures, anemia & hydrocephaly, repeated (fatal) infections d/t leukopenia
  • Extramedullary hematopoiesis
  • Cranial nerve deficits leading to optic atrophy, deafness, and facial paralysis
31
Q

Tx for osteopetrosis?

A

Hematopoietic stem cell transplant
- Osteoclasts are derived from hematopoietic precursors. Normal osteoclasts produced from donor stem cells reverse many of the skeletal abnormalities

32
Q

What is mucopolysaccaridoses?

What are the clinical sx of this?

A

Lysosomal storage disease

  • Deficiency in enzymes that degrade acid hydrolase enzymes: dermatan sulfate, heparan sulfate, and keratan sulfate
  • Mesenchymal cells, esp chondrocytes, degrade extracellular matrix mucopolysaccharides
  • Mucopolysaccharides accumulate in chondrocytes leading to apoptosis in extracellular space and structural defects in articular cartilage

Leads to short stature, chest wall abnormalities, malformed bones

33
Q

What are the classifications that differentiate osteopenia w osteoporosis?

A

Osteopenia is dec bones mass that is 1-2.5 standard deviations below the mean

Osteoporosis is osteopenia severe enough to inc risk of fracture
- Bone mass that is at least 2.5 standard deviations below peak bones mass in young adults

34
Q

What are some signs of osteoporosis?

What are two common forms?

What can contribute to it?

A

Atraumatic or vertebral compression fractures signify osteoporosis; loss of height d/t lumbar lordosis & kyphoscoliosis

Most common forms are senile & postmenopausal

Physical activity, muscle strength, diet, & hormonal state are important contributions to the development of osteoporosis

35
Q

What is the pathogenesis of osteoporosis?

A

Following peak skeletal mass, small deficits in bone formation happen with every resorption and formation cycle
- Normal age-related bone loss averages at 0.7% per year

36
Q

How do age-related changes and physical activity contribute to osteoporosis?

A

Senile osteoporosis (low turnover variant)

  • Dec in proliferative and biosynthetic potential (dec capacity to make bone)
  • Dec cellular response to growth factors

Dec in physical activity leading to inc rate of bone loss

  • Mechanical forces stimulate inc in normal bone remodeling
  • Bone loss is seen w immobility, paralysis, astronauts in zero gravity
  • Resistance exercises are better than endurance
37
Q

How to genetic factors, calcium, and hormones contribute to osteoporosis?

A

Genetic factors

  • LRP5
  • Polymorphisms in vertian genes
  • RANKL, OPG, RANK, HLA focus, estrogen receptor gene, vitamin D receptor gene

Calcium

  • Adolescent girls w insufficient calcium intake during periods of rapid growth restrict their peak bone mass
  • Ca2+ def, inc in PTH, dec in Vit D all contribute to senile osteoporosis

Hormones

  • Post-menopause accelerates bone loss
  • Estrogen deficiency plays major role; inc resorption more than formation, inc inflammatory cytokines which inc RANKL and dec OPG
38
Q

Important note about breast cancer and osteoporosis?

A

Tx for breast cancer (such as Tamoxifen) inc bone loss and risk for osteoporosis

39
Q

Prevention and tx of osteoporosis?

A

Prevention: Exercise, calcium, vitamin D

  • Eating too much phosphorus in teen years (high amounts in soda, cheese, peanut butter) can dec calcium
  • Smoking is RF

DEXA scan to find osteoporosis

Tx: Bisphosphonates (dec osteoclast activity, induce apoptosis)

40
Q

What are rickets and osteomalacia?

What are the differences?

A

Bone manifestations of Vit D deficiency or abn metabolism

Rickets appears in children and interferes w deposition of bone in growth plate

Osteomalacia appears in adults; bone formed during remodeling is undermineralized which predisposes to fractures

41
Q

Sx of rickets?

A
  • Frontal bossing
  • Squared off head
  • Rachitic rosary
  • Anterior protrusion of chest/pigeon breast deformity
  • Lumbar lordosis
  • Bowed legs
42
Q

What does hyperparathyroidism lead to?

A

PTH is central in calcium homeostasis; inc in PTH leads to inc in serum calcium

  • Osteoclast activation
  • Indirectly mediates effect of osteoblasts by inc RANKL expression
  • Inc resorption of calcium by renal tubules
  • Inc urinary excretion of phosphates
  • Inc synthesis of active Vit D by the kidneys
43
Q

What is primary hyperPTism?

A

Autonomous PT secretion

44
Q

What is secondary hyperPTism and what 3 main things can cause it?

A

Underlying renal disease

  • Chronic renal insufficiency: Dec in Vit D synthesis leading to dec GI calcium absorption
  • Hyperphosphatemia of renal failure also suppresses renal hydroxylase to dec Vit D synthesis
  • Metabolic acidosis & aluminum deposition in bone
45
Q

Important note about hyperPTism control?

A

Bony changes disappear completely

46
Q

What skeletal abnormalities can untx hyperPTism lead to?

A
  • Osteoporosis
  • Brown tumor
  • Von Recklinghausen disease of bone
47
Q

What are some characteristics of osteoporosis in hyperPTism?

A

Inc in osteoclast activity most prominent in cortical bone
- Dissecting osteitis: Osteoclasts tunnel into & dissect centrally along the length of trabeculae, adjacent marrow spaces replaced by fibrovascular tissue; “railroad tracks”

48
Q

What do Brown Tumors in hyperPTism do?

A

Bone loss predisposes to microfractures, secondary hemorrhage, macrophage recruitment, & ingrowth of reparative fibrous tissue leading to mass lesion
- Brown: Vascular, hemorrhage & hemosiderin deposition; can undergo cystic degeneration

49
Q

What is von Recklinghausen disease of bone in hyperPTism?

A

Inc bone cell activity, peritrabecular fibrosis, & cystic brown tumors is hallmark of severe hyperPTism

  • Generalized osteitis
  • Fibrosis cystica
50
Q

What is renal osteodystrophy? What are 4 disorders that we can see this in?

A

Skeletal changes that occur in chronic renal disease, including those w dialysis

  • Osteopenia/osteoporosis
  • Osteomalacia
  • Secondary hyperPTism
  • Growth retardation
51
Q

What are histologic bone changes we could see in renal osteodystrophy?

A
  • High-turnover osteodystrophy: Inc in bone resorption & bone formation
  • Low-turnover osteodystrophy or aplastic disease: Adynamic bone (little osteoclastic & blastic activity) & less commonly osteomalacia
  • Mixed pattern of disease: Areas w high turnover and low turnover
52
Q

Renal osteodystrophy pathogenesis happens through what 3 mechanisms?

A
  • Tubular dysfxn: Renal tubular acidosis; associated systemic acidosis dissolves hydroxyapatite leading to matric demineralization & osteomalacia
  • Secondary hyperPTism: D/t dec in phosphate excretion, chronic hyperphosphatemia, and hypocalcemia
  • Dec biosynthetic fxn: Dec vit D hydroxylation
53
Q

Importance of renal osteodystrophy in kids?

A

More serious in children b/c bones are still growing

  • Slows growth and causes deformities such as legs bending inward or outward (renal rickets)
  • Can lead to short stature

Can be called the “silent crippler” b/c bone changes from renal dystrophy can begin many years before sx appear

54
Q

What is paget disease (aka osteitis deformans)?

What is the pathogenesis and what gene mutation can cause it?

A

Disordered and structurally unsound bone mass

  • Most involve multiple bones (polyostotic)
  • Axial skeleton and femur often involved
  • Avg age of dx is 70yo

Pathogenesis is uncertain but there are both genetic and env contributions

  • 50% of cases are familial
  • 10% of the sporadic cases a/w SQSTM1 gene (inc osteoclast activity)
55
Q

Morphology seen in Pagets?

A

Mosiac pattern of lamellar bone (seen in sclerotic phase)

  • Jigsaw-like appearance w prominent cement lines; haphazardly oriented units of lamellar bone
  • Bone can compress spinal and cranial nerve roots
56
Q

What are the 3 stages of Pagets?

What is a transformation that can happen?

A
  • Initial osteolytic stage: Osteoclasts w 100 nuclei
  • Mixed osteoclastic-blastic stage: Clasts persist but lots of blasts also; at the end of stage primarily blastic
  • Burned-out quiescent osteosclerotic stage: Osteoblast activity predominates

Sarcomatous transformation: Less than 1% will trasform into osteosarcoma or fibrosarcoma in the long bones, pelvis, skull, spine

57
Q

What are some clinical signs of Paget Disease?

A
  • On weight bearing bones, can see bowing of femur and tibia, distortion of femoral head, secondary osteoarthritis
  • Chalk-stick type fractures in long bones of legs
  • Compression fractures of spine leading to spinal cord injuries and kyphosis
  • Hypervascularity of Paget bone will warm overlying skin; inc blood flow acts as arteriovenous shunt leading to high-output heart failure
  • Leontiasis ossea (lion face): Enlargement of craniofacial skeleton making it hard to hold head erect
  • Platybasia: Invagination of skull base d/t weak bone and compression of posterior fossa
58
Q

What are lab values we can see in Paget Disease?

What is tx?

A

Inc serum alkaline phosphate, normal serum calcium and phosphorus

Tx is calcitonin and bisphosphonates

59
Q

Define the follow type of fractures:

  • Simple
  • Compound
  • Comminuted
  • Displaced
  • Stress
  • Greenstick
  • Pathologic
A
  • Simple: Overlying skin intact
  • Compound: Bone communicated w skin surface
  • Comminuted: Bone is fragmented
  • Displaced: Ends of bone at the fracture site are not aligned
  • Stress: Slowly developing fracture that follows a period of inc physical activity in which bone is subjected to repetitive loads
  • Greenstick: Extending only partially through the bone, common in infants when bones are soft
  • Pathologic: Involving bone weakened by underlying disease process such as tumor
60
Q

What is the process of fracture healing? (There’s a lot)

What do you see at the end of the first week?

A
  • Immediately post fracture the rupture of blood vessels results in a hematoma which fills fracture gap and surrounds area of injury
  • Clotted blood will seal site and create framework for inflam cells and new capillaries
  • Degranulated platelets and migratory inflam cells release PDGF, TGF-b, FGF to activate osteoprogenitor and sims osteoclastic and blastic activity

End of first week: Soft tissue callus or procallus

61
Q

What do you see around 2nd and 3rd until end of fracture healing?

When is healing complete?

A
  • Soft tissue callus becomes bony callus
  • Woven bone forms that are oriented perpendicular to cortical axis
  • Bony callus reaches max growth at end of 2nd or 3rd week which helps stabilize fracture site
  • Newly formed cartilage undergoes endochondral ossification

Healing is complete w the restoration of the medullary cavity

62
Q

What is osteonecrosis and what do most cases arise from?

A

Infarction of the bone and marrow

- Most cases from fractures or corticosteroid tx

63
Q

What are the differences in subchondral infarcts and medullary infarcts in osteonecrosis?

A

Subchondral infarcts: Cause pain that is initially only a/w activity, later pain becomes constant
- Often collapse which may lead to severe secondary osteoarthritis

Medullary: Usually small and clinically silent except when they occur in Gaucher disease, dysbarism (“the bends”), and sickle cell anemia

64
Q

Morphology of osteonecrosis in both subchondral and medullary infarcts? What happens to the overlying articular cartilage in each?

What is dead bone?

A

Medullary infarcts involve the tabecular bone and marrow and often do not involve the cortex (d/t its collateral blood flow)
- Articular cartilage remains viable

Subchondral infarcts are often triangular or wedge-shaped w the subchondral bone at its base
- Happen slowly so there is collapse of necrotic bone, fracture, and sloughing off of the articular cartilage

Dead bone: Empty lacunae surrounded by necrotic adipocytes that often rupture
- Trabeculae act as scaffolding of new bone “creeping substitution”

65
Q

What is osteomyelitis?

What most commonly causes it?

A

Inflammation of bone & marrow, usually following infection (can be systemic but more often is a primary solitary focus)
- Can be d/t any kind of inf but most commonly pyogenic bacteria and mycobacteria

66
Q

How do bacteria spread in pyogenic osteomyelitis?

Infants, kids, adults?

A

Infants: Epiphyseal infection can spread to joint leading to septic or suppurative arthritis

Healthy kids: Often hematogenous spread from trivial mucosa injuries or minor skin infections

Adults: Often a complication of open fractures, surgical procedures, and diabetic infections of the feet

67
Q

What are common bacterial pathogens in osteomyelitis and what patient populations do we see this in?

A

S. aureus is most common in all ages

E. coli, pseudomonas, klebsiella: Pts w UTIs or pts w IVDU

H. flu & GBS: Neonates

Salmonella: Sickle cell pts

68
Q

What happens in acute osteomyelitis?

What is sequestrum?

A

Bacteria and neutrophils proliferate

  • Necrosis of bone cells & marrow in 48 hours
  • Kids may have subperiosteal abscess form

Sequestrum is dead bone following subperiosteal abscess
- May crumble and release fragments through the sinus tract

69
Q

What happens in chronic osteomyelitis?

What is an involucrum?

What is a brodie abscess?

What is sclerosing osteomyelitis of Garre?

A

After first week you get chronic inflam cells that release cytokines that stimulate osteoclastic resorption, ingrowth of fibrous tissue, & deposition of reactive bone at the periphery

Involucrum: Newly deposited bone forms a shell of living tissue around the segment of devitalized bone

Brodie abscess: Small interosseous abscess that gets walled off by reactive bone

Sclerosing osteomyelitis of Garre: Affects jaw, a/w extensive new bone formation that obscures much of the underlying osseous structure

70
Q

Acute osteomyelitis:

Clinical signs

Radiograph

Tx

A

Malaise, fever, chills, leukocytosis, throbbing over region, unexplained fever in infants, localized pain in adults

Imaging may show a lytic focus of bone destruction surrounded by zone of sclerosis
- Bx and culture to ID pathogen

Tx with abx and surgical drainage (usually curative)

71
Q

Chronic osteomyelitis:

What causes it?

Clinical course?

Complications?

A

Delay in dx, extensive bone necrosis, inadequate abx or surgical debridement, weakened host defenses

Usually has acute flare-ups that may occur years later

Complications: pathologic fractures, secondary amyloidosis, endocarditis, sepsis, development of squamous cell carcinoma in draining sinus tracts, sarcoma in infected bone

72
Q

Mycobacterial osteomyelitis:

How does it happen?

Clinical course?

Sx?

Histo?

A

Usually blood borne and originating from a focus of active visceral disease

Bone inf may persist for years before detected

Sx: Localized pain, low-grade fevers, chills, weight loss

Histo: Caseous necrosis & granulomas

More resistant & destructive than pyogenic osto

73
Q

What is TB spondylitis (Pott’s disease)?

A

Mycobacterial osteomyelitis involving the spine

- Can causes permanent compression freactures

74
Q

What are two different forms of skeletal syphilis?

A

Congenital syphilis: Bones lesions appear about 5th month gestation & fully developed at birth
- Saber shin: Massive reactive periosteal bone deposition on medial & anterior surfaces of the tibia

Acquired syphilis: Early in tertiary stage, 2-5 years after initial infection
- Saddle nose, palate, skull & extremities (esp long tubular bones like tibia)

NMSP Exam 2 (6 decks)

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