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Pathology > Lecture 2: Bone And Ligament > Flashcards

Lecture 2: Bone And Ligament Flashcards

1
Q

3 basic functions of bone

A
  • mechanical
  • metabolic
  • blood production
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2
Q

Mechanical functions of bone

A
  • protect body’s vital organs (trunk, pelvis, head)
  • muscle ligament, organ attachment
  • means of movement with muscle contractions
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3
Q

Metabolic bone functions

A

-maintains precise ca2+ and phosphorus levels (mineral homeostasis)

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4
Q

Blood production bone function

A
  • RBC for oxygen delivery
  • WBC for infection control
  • platelets (megakaryocytes for blood clotting)

*this mostly occurs in the long bones, not much from flat bones

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5
Q

What type of tissue is bone

A

Highly specialized connective tissue

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6
Q

Basic elements of bone

A
  • osteopenia cells: osteoblasts, osteoclasts, osteocytes
  • collagen fibers
  • ground substance: HA, glycoprotein, calcium phosphate
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7
Q

Two basic types of bones

A

Long bones and flat bones (some are irregular)

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8
Q

The engineering properties of bone

A

Strength/Stiffness
-Pound for pound, a tube is the best design for optimizing strength, resilience, and weight
-resists bending as well as steel (has some give but wont break)
Flexibility: prevents fracture with most stress
Fatigue resistant: average hip joint will sustain 1.8mil cyclical loads per year

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9
Q

Compact bone

A

Cortical bone, arranged in concentric ovals (lamellae)

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10
Q

Periosteum

A

the sheath outside your bones that supplies them with blood, nerves and the cells that help them grow and heal

  • outer fibrous layer
  • inner layer: osteogenic cells
  • highly vascular
  • highly innervated (free nerve endings= pain transmission)
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11
Q

Spongy bone

A

Cancellous bone, trabecular bone, thin intersecting plates, spicules of bone

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12
Q

Osteocytes

A

Living element of bone tissue, derived from osteoblasts

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13
Q

Osteoblasts

A

New bone formation within cellular matrix

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14
Q

Osteoclasts

A

Cells designed to resorb old bone, or damaged bone

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15
Q

Endosteum

A

The lining membrane of spongy bone. Mainly osteogenic cells

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16
Q

Bone formation via osteoblasts (two steps)

A
  1. Ossification
    - formation of osteoid (pre bone)
    - osteoblasts synthesize collagen and other proteins to make osteoid tissue
  2. Calcification
    - deposition of calcium salts in the osteoid tissue
    - osteoblasts secrete the enzyme alkaline phosphates, especially following fracture
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17
Q

Haversian canal

A

The network of tubes in the bone that house nerves, arteries, veins, and lymphatic vessels

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18
Q

What factors impact bone remodeling

A
  • Mechanical stress
  • Level of calcium and phosphate
  • hormone levels: parathyroid, calcitonin, vitamin D, cortisol, growth hormones, thyroid hormone, sex hormones
  • primary cell type: osteoclasts
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19
Q

How does Growth during development work

A

It is thought that osteoblast activity is actually controls osteoclast activity and the balance is tipped toward bone formation

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20
Q

parathyroid hormones role in bone formation

A
  • maintains serum levels of ionized ca2+
  • increases release of ca2+ and Ph from bone
  • conservation of ca2+ and elimination of ph by kidney
  • intestinal reabsorption of ca2+ through vitamin D
  • increases number and amplification of osteoclasts, breaks down bone, increases plasma calcium
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21
Q

Calcitonin role in regulation of bone formation

A
  • inhibits release of ca2+ from bone
  • increases renal elimination of ca2+ and ph which lowers serum ca2+ levels
  • reduces osteoclasts activity
  • inhibits calcium released from the bone and tells osteoclasts to quiet down, builds bone, decreases plasma calcium
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22
Q

Vitamin Ds role in regulation of bone formation

A
  • functions as a hormone in regulating calcium
  • it increases absorption of ca2+ from intestine and promotes the actions of PTH on bone
  • regulates calcium; increases calcium absorption from the gut; increases PTH activity
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23
Q

Wolff’s law

A

Bone remodels in response to the mechanical stresses it experiences
-to produce an anatomical structure best able to resist the applied stress

  • increase demands= hypertorphy (tuberosity, osteophytes (bone spurs)
  • decrease demand=atrophy (disuse osteoporosis)
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24
Q

Bone stress on the proximal femur (wards triangle)

A
  • an area of bone that breaks frequently

- it is near the femoral neck

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25
Q

How are bones able to support high stress

A
  • muscles allow us to absorb more stress
  • when we are tired/muscles fatigued, you are more likely to get a stress reaction or a break in the bone (there is loss of energy and an altered gait pattern)
  • when muscles are weak this leads to an abnormally high bone load and then breakage
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26
Q

Abnormal conditions of the bone

A
  • local death: necrosis due to fracture or disease
  • increased deposition
  • decreased deposition
  • increased resorption
  • decreased resorption
  • common: increased deposition and decreased resorption
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27
Q

Reasons for increased deposition in bone

A
  • work hypertrophy- Wolff’s law (increase stress leads to increase in bone deposition)
  • degenerative joint disease- subchondral bone takes increase pressure and reacts by increasing bone deposition
  • healing fracture: callus formation
  • infections
  • some bone tumors
28
Q

Reasons for decreased bone deposition

A
  • rickets (children) and osteomalacia (adults) = vitamin D deficiency
  • disuse osteoporosis- Wolff’s law (immobilization post fracture, paraplegia, quadriplegia, weightlessness (astronauts))
29
Q

Abnormal conditions that increase resorption (increase osteoclasts activity)

A
  • infection within bone

- most bone tumors

30
Q

Abnormal conditions that decrease resorption (decrease osteoclasts activity)

A

-osteopetrosis (marble bones): inherited bone disorder, decrease resorption therefore increase bone density which makes bones brittle and fracture more readily

31
Q

Conditions causing an increase in deposition or an increase/decrease resorption (combo)

A
  • systemic osteoporosis: rehab with low impact weight bearing in invoke wolfs law (happens often to neck of femur, vertebral bodies, and wrist), post menopausal women who have a decrease in estrogen and therefore a decrease in absorption of ca2+ through the gut
  • rheumatoid arthritis: periarticular inflammation to which bone reacts by decreasing deposition and increasing resorption (rehab implication: do not stimulate further inflammation)
32
Q

Osteopenia

A
  • Loss in bone mineral density that is 1-2.5 standard deviations from the mean of the norm of the peak BMD of the reference young adult
  • at the spine and hips, a 1 st dev decrease in bone mass is associated with 2x increase fracture risk
33
Q

Osteoporosis general definition and definition of type 1 and 2

A

-when osteopenia reaches 2.5 SD from reference, then it is classified as osteoporosis

Type 1: post menopausal/decreased estrogen, increased osteoclastogenesis. Biggest impact is on trabecular bone

Type 2: senile- in both men and women equally. Decreased osteoblasts activity, decrease calcium absorption

34
Q

Osteogenesis imperfecta

A

Brittle bones (very fragile), Humpty Dumpty

35
Q

Paget’s disease

A
  • long bone bending and flat bone thickening

- too much bone resorption and reformation

36
Q

Fracture definition

A
  • structural break in bone
  • always associated with some degree of soft tissue injury (muscle, connective tissue, brain/spinal cord, vascular, lymphatic, nerve tissue)
37
Q

The job of PTs when it comes to fractures

A

Minimize deterrents to healing (can’t actually speed up healing)

38
Q

Fracture sites

A
  • proximal, middle, distal third
  • diaphyseal, metaphyseal, epiphyseal (only in kids)
  • Intra articular
  • fracture-dislocation
39
Q

Types of incomplete fractures

A

Greenstick, buckle, torus, non displaced (impacted)

40
Q

Types of complete fractures

A

Transverse, oblique, spiral, segmental, displaced, comminuted

41
Q

Classification of fractures by severity: uncomplicated

A

No other serious injury or serious reaction associated with the fracture

42
Q

Classification of fractures by severity: complicated

A

Other significant injury or serious reaction to the fracture

Ex. Pneumothorax, kidney puncture, spleen injury

43
Q

Slater Harris fracture prognosis based on type

A
  • Type I: excellent, provided blood flow in intact (separation of entire epiphysis)
  • type II: Excellent, provided blood flow is intact
  • Type III: ORIF usually necessary, prognosis good, so long as blood flow not disrupted
  • type IV: bad, unless perfect reduction is both obtained and maintained
  • type V- decidedly poor because premature cessation of bone growth almost inevitable
44
Q

Clinical presentations of fractures

A
  • bone pain
  • loss of motion
  • unable to bear weight (lower extremity)
  • obvious deformity
  • amount of discoloration
  • amount of discoloration
  • amount of swelling
45
Q

Normal bone healing stages

A
  • hematoma formation
  • fibrocartilaginous callus formation (soft callus)
  • bony callus formation (hard callus, can see on x ray)
  • remodeling
46
Q

Hematoma stage of bone healing (inflammation)

A
  • hematoma facilitates formation of fibrin mesh work
  • this serves as the framework for inflammatory cells, fibroblasts, and capillary buds
  • time frame: begins during first 1-2 days (can be within hours)
  • periosteum is key!
47
Q

Fibrocartilaginous callus formation stage of bone healing (proliferation stage)

A

-hematoma -> granulation tissue (pro callus)
- fibroblasts proliferate and invade the pro- callus
-peaks at 2-3 weeks
-not strong enough for weight bearing
(Piezo electric effect)

48
Q

Bony callus formation stage of bone healing

A
  • consolidation of fraction fragments
  • conversion of the fibrocartilaginous cartilage to bony callus
  • osteoblasts are key
  • begins 3-4 weeks after injury and continues for months
  • weight bearing, resistance tolerated
  • visible on x-ray
49
Q

Remodeling stage of bone healing

A
  • complete consolidation of fracture fragments
  • osteoclasts are key
  • compact bone replaces spongy bone
  • thickened bone often remains in perpetuity
  • may continue for years (often kids bones go back to looking normal quickly)
50
Q

Two main pathways for bone healing

A

Intramembranous and endochondral ossification

51
Q

Types of fracture imaging

A

Standard x rays, CT scan, MRI, bone scan

52
Q

Treatments for fractures

A

Fracture reduction, immobilization, casting, ORIF, external fixation, bone stimulator, bone graft

53
Q

General casting principle

A

One joint above and one joint below the break

54
Q

Complications of fractures

A
  • death from diffuse fat embolism
  • avascular necrosis
  • fracture blisters
  • compartment syndrome (can lose a limb)
  • nerve injury, neurogenic inflammation
  • permanent bony deformation
  • Complex regional pain syndrome (CRPS)
  • DJD, stiff joint
55
Q

Volkmann’s ischemic contracture

A

Etiology: upper extremity- supracondylar fracture, lower extremity: femur fracture

Signs/symptoms: exquisite pain with passive flex ion and extension of fingers, loss of color, parenthesis, pulslessness, paralysis, muscle necrosis/nerve injury

56
Q

Myositis ossificans

A

Etiology: supracondylar numeral fractures (brachial is muscle), posterior elbow dislocations, trauma leads to excessive osteoblast activity

57
Q

Complications following a fracture

A
  • delayed union
  • mail union (not angled right)
  • non union (can lead to pseudo arthrosis, creation of joint)

Treatment: patience, bone stimulator, bone graft

58
Q

Contributors to abnormal healing

A
  • Severe damage to periostea sleeve
  • loss of blood flow to fracture fragments
  • too much shear during healing
  • not enough time for mobilization
  • too much traction during reduction
  • infection in soft tissue
  • infection in bone
  • bone disease
  • massive soft tissue damage in area
59
Q

PT treatment while bone is healing

A
  • muscle co contraction (pumping action) to avoid edema accumulation
  • pendulum exercises for upper extremity
  • if ORIF, ROM, gait training
  • work on areas not injured to prepare for things like crutch walking (think ahead)
60
Q

PT treatment once bone has reached clinical union

A
  • PROM, AAROM, AROM
  • gentle joint mobilization
  • modality use: high amplitude E stim, ultrasound, TENS
  • Strength development
  • endurance work
  • coordination, proprioception work
61
Q

Bone forming tumors

A
  • woven bone formed by neoplasticism cells
  • in general, 1degree bone tumors are rare
  • osteoid osteopathic and osteoblastoma: most common benign bone tumors
  • osteosarcoma: most common malignant tumor of bone
62
Q

Osteosarcoma

A
  • a malignant mesenchymal tumor, most commonly is intramedullary in the long bones
  • most occur in adolescence, most occur around the knee
  • increased risk in older adults
  • spread through medullary canal
  • painful and results in necrotic bone
63
Q

Osteoid osteosarcoma/ osteoblastoma

A

-Benign bone tumors
-similar histologically but vary in size, location, and clarity of margins
-can become malignant if given enough stimulation
-

64
Q

Ligament sprain grades

A
  • Grade 1: no loss of ligamentous integrity
  • Grade 2: many fibers torn, significant c/o pain, clinical evidence of instability
  • Grade 3: complete disruption, instability
  • Grade 4: same as grade 3 but with a upsilon of bone
65
Q

Treatment of ligament injuries

A
  • ligaments embedded in capsule: heal well
  • 1st and second degree: RICE, ROM exercise, PREs, protection from instability

-3rd and 4th degree: prolonged immobilization of surgical correction

66
Q

Effects of immobilization on ligament

A
  • decreases numbers and organizations of collagen fibers
  • decreases water content of ground substance
  • weakening of bone and ligament at insertion site

Pathology (4 decks)

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