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bone path Flashcards

1
Q

Function of musculoskeletal system

A 
•Provides mechanical support
•Protects organs
•Allows for efficient movement
•Stores salts and other materials needed for
metabolism
•Produces haematopoietic elements
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2
Q

Describe the normal bone

A 
Composed of organic matrix (Type 1 collagen and proteoglycans aka osteoids )35% and inorganic elements (calcium hydroxyapatite)65% 
Also contains cells in organic matrix - 
osteoprogenitor cells
osteoblasts
osteoclasts
osteocytes
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3
Q

What is the function of sodium hydroxyapatite?

A

Provides hardness and strength to bone
Stores salts - 99% calcium , 85% phosphorus
65% sodium and magnesium

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4
Q

What are the function of bone cells?

A

Bone forming - osteoblasts and osteocytes

Bone clearing/digesting- osteoclasts (both mature and precursor)

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5
Q

What is another important function of osteoblasts?

A 
To produce two types of osteoids ( unmineralized organic bone) 
- woven bone
feotal skeleton
a/w pathology in adults  
-lamellar bone 
compact/cortical 
cancellous/trabecular
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6
Q

What are the different tissues of bone?

A

•Periosteum:- Fibrous tissue that forms the outermost
covering of bone
•Compact (cortical) bone:- Hard and dense bone that forms
the outer layer of the bones
•Spongy (cancellous) bone:- Lighter bone, commonly found
in ends and inner portions of long bones
•Medullary Cavity: Located in the shaft of a long bone and is
surrounded by compact bone
•Cartilage:- Connective tissue that provides a smooth
articulation surface for other bones

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7
Q

What are the components of long bone

A

Epiphysis - End of bone
Metaphysis - Middle of epiphysis and diaphysis // growth plate
Diaphysis- shaft
Medullary canal - contain bone marrow

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8
Q

How does the bone grow and develop?

A
  • Enchondral ossification

* Intramembranous ossification

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9
Q

Define endochondral ossification

A

bone formed from cartilage •Foetal development: bones are composed of
cartilage
–flexible and less dense due to lack of calcium salts
•As
development continues: ossification occurs
–Gradual replacement of cartilage and deposition of calcium
•Occurs in the epiphysis of long bones, facial bones
and vertebrae

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10
Q

Another name for membranous ossification?

A

periosteum ossification

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11
Q

Membranous ossification

A

•Bone is formed from connective tissue
•Fibroblasts from the periosteum differentiate to
osteoblasts
•Occurs in the cranial bones and beneath the
periosteum throughout postnatal growth

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12
Q

Where do the fibroblasts come from?

A

periosteum and differentiate into osteoblasts

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13
Q

How do bones grow in membranous ossification vs endochondral ?

A

Bones in width in Membranous ossification

Bones grow in length in endochondral ossification

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14
Q

How do bones form?

A

Production of osteoid
Mineralization of osteoid
Remodelling via resorption and reformation
Several factors involved in bone formation and destruction (exercise, hormones,vitamins, growth factors and cytokines)

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15
Q

What are osteoids made up of and what makes it?

A

Osteoblasts make osteoids

Osteoids are made up of type 1 collagen and other proteins/proteoglycans

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16
Q

What is the essential function of VitD?

A

Increase in serum calcium level

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17
Q

What are the strategies that Vit D uses to achieve the essential function?

A

Increases intestinal reabsorption of CA2+ and phosphate
Increases Ca2+ reabsorption in in distal tubules of kidney
Increases resorption of
Stimulates osteoclastic bone resorption(very high VIT d) ;; required for normal mineralization of bone

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18
Q

What are the functions of parathyroid hormone?

A

.Secreted by parathyroid in response to a fall in
serum calcium
.Stimulates osteoclastic bone resorption Ca
.Increases renal tubular reabsorption of Ca

.Increases synthesis of 1,25(OH)D

Increases urinary
PO4
excretion

.Increases GI calcium absorption

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19
Q

Calcitonin function

A

opposite of PTH
produced by follicular cells and is in response to high plasma calcium
-reduces bone resorption by suppressing osteoclastic activity

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20
Q

List congenital bone disorders

A

achondroplasia
osteogenesis imperfecta
osteopetrosis

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21
Q

Define achondroplasia

A

a.w dwarfism
reduction in chondrocyte(cells which secrete cartilage matrix and become embedded in it) proliferation in the growth plate and cause premature ossification(i.e bone remodelling–laying down of bone)

can be hereditary AD/ spontaneous
heterozygotes- normal longevity (normal mental and sexual development)
homozygotes die shortly after

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22
Q

List features of achondroplasia

A

Shortening of long bones
Normal skull
Severe spinal canal stenosis with severe pain

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23
Q

Define osteogenesis imperfecta

A 
Disorder of collagen type 1
Hereditary (most are autosomal dominant) or spontaneous mutations
Several forms (I-IV)
Some lethal in utero
Others normal lifespan
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24
Q

Features of osteogenesis imperfecta

A

–Fractures
–Blue sclera
–Dental abnormalities
–Hearing loss

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25
Q

Define osteopetrosis and a/ features

tx?

A

aka marble bones

Osteoclast dysfunction-> failure of bone resorption-> increase in bone mass (“marble bones”)
–Sclerosis and bone fractures
–Hydrocephalus and cranial nerve palsies

Bone fills the medullary cavity
–Anaemia and neutropenia (infections)
–Hepatosplenomegaly due to extramedullary haematopoiesis

tx bone marrow transplant

26
Q

List metabolic bone diseases

A 
Osteoporosis
Osteomalacia
Paget’s disease
Hyperparathyroidism
Renal osteodystrophy
27
Q

Compare and contrast pathogenesis of osteoporosis and osteomalacia

A

Osteoporosis - reduction in bone mass;; mineralization is normal
Increase in resorption of bone by osteoclasts (which is normally inhibited by calcitonin) and a decrease in new bone formation by osteoblasts

Osteomalacia- inadequate mineralization of bone, normal osteoid formation - disease of adults. osteoclasts are rare as unmineralized osteoid does not stimulate an osteoclastic reaction. Wide osteoid seams with prominent osteoblasts seen

28
Q

Outline the general procedure to diagnose metabolic bone diseases?

A 
Careful history
Physical examination
Radiographic examination
Laboratory tests
Bone biopsy may be indicated
29
Q

What are the primary and sec causes of osteoporosis?

A 
Primary
–Senile
–Post menopausal (oestrogen deficiency)
–Genetic factors (Vit D receptors polymorphism)
–Idiopathic
Secondary
–Immobility
–Insufficient Ca intake
–Hormones
–Drugs (steroid)
–Neoplasia
30
Q

Complications of osteoporosis

A

Bone Pain
Bone fracture
Loss of height (compression #) esp elderly
Deformity

31
Q

Diagnosis of osteoporosis?

A

Imaging techniques that measures bone density

 X-ray (when 30- 40% of bone mass is lost)

32
Q

Prevention and tx of osteoporosis

A 
Exercise
Oral calcium and Vitamin D
H.R.T
Calcitonin
Bisphosphonates
33
Q

Differentiate rickets and osteomalacia

A

Rickets occurs in children
inadequate mineralization of epiphyseal cartilage - lack of osteoid mineralization
Osteomalacia occurs in adults

34
Q

Causes of both rickets and osteomalacia

A 
Due to deficiency of Vitamin D and the exacerbating effects of a compensatory increase in PTH
–Dietary lack
–Malabsorption
–Chronic renal failure
–Liver disease
–Inadequate exposure to sunlight
–End organ resistance to vitamin D
–Drugs
35
Q

Clinical features of osteomalacia

A

Bone pain

Microfractures (Loosers zone)

36
Q

Clinical features of rickets

A

deformities a/w rickets

Deformity of the skull (craniotabes), frontal bossing and a squared appearance of the head
Thickening of the knees, wrists
Enlargement of costochondral junctions of the ribs (ricketic rosary)
Protrusion of the sternum- pigeon-breast
Retraction of softened rib- Harrison’s grove
Lumbar lordosis
Bowing of the long bones of the legs

37
Q

Tx for rickets and osteomalacia?

A

vitamin D

38
Q

Causes of hyperparathyroidism

A

primary
parathyroid adenoma/hyperplasia
high calcium

secondary
prolonged hypocalcaemia
low/normal Ca2+

39
Q

Effects of increased PTH on bone

A

PTH induces osteoclast activity
–Bone resorption
Cavities in the trabeculae of cancellous bone
Fibrosis
Microfractures and hemorrhage
–= osteitis fibrosa cystica = brown “tumours” = von Reckilnghausen disease of bone

changes regress after control of hyperPT

40
Q

Define renal osteodystrophy

A 
Bone disease secondary to renal failure
–Osteitis fibrosa cystica
–Osteomalacia
–Osteosclerosis
–Osteoporosis
41
Q

Pathogenesis of renal osteodystrophy

A

(kidneys- site to make vit D , low Vit D, low Ca)

Chronic renal disease
–Hypocalcaemia
–Retention of phosphate
Compensatory increase in PTH->osteitis fibrosa cystica
Loss of renal mass-> ↓ conversion of 25-hydroxyvitamin D to 1,25-hydroxyvitamin D-> osteomalacia
Aluminum present in dialysis solutions can bind to osteoid and inhibit mineralisation of the osteoid->osteomalacia
Metabolic acidosis-> bone resorption and release of calcium hydroxyapatite from the matrix->osteomalacia
Steroid therapy-> osteoporosis
Deposition of amyloid in bone (β2-microglobulin)

42
Q

What is another name for Paget’s disease?

A

Osteitis deformans)

43
Q

Paget’s disease description

A

multiple bone involvement 85%, affecting 5% of elderly
commonly affects whites
unknown cause , possibly slow virus like paramyxovirus- cytoplasm and nuclei of osteoclasts of affected pts contain viral particles
hereditary - mut in chr 18q

The hallmark is the “mosaic pattern”
Initial phase- osteoclastic activity->bone resorption
Mixed phase- osteoclasts persist + osteoblasts-> haphazard bone production (collagen matrix madness)
Fibrosis of bone marrow spaces
Late stage- coarse thickened trabeculae (osteosclerotic phase aka gain in bone mass)

44
Q

Complications of Paget’s disease

A 
Bone pain
Fractures
Deformity
Nerve or cord compression
Deafness
Osteoarthritis
Heart failure
Malignant transformation (osteosarcoma)
45
Q

Summarise causes of abnormal matrix
abnormal mineralization
abnormal osteoclasts

A 
Abnormal Matrix
–Collagen disorders (osteogenesis imperfecta)
–Osteoporosis
Abnormal mineralisation
–Ricketts (Vit D deficiency)
–Hyperparathyroidism
–Renal osteodystrophy
Abnormal osteoclasts
–Paget’s disease
–Osteopetrosis
46
Q

Define avascular necrosis / osteronecrosis

A 
Infarction of bone and marrow
Due to ischaemia
–Vascular injury (trauma)
–Thrombosis/embolism
–Steroid therapy
–Radiation
–Alcoholism
–Idiopathic
Major sites
–Head of femur
–Scaphoid
May be asymptomatic or associated with pain
If untreated may predispose to severe arthritis
47
Q

Types of fractures

A

Complete vs. greenstick

  • Greenstick (incomplete:- the bone is cracked but not broken into two pieces)
  • A split in a young, immature bone (common in children).

Simple vs. compound

  • Simple (closed:- the overlying skin is unbroken)
  • Compound (open:- the skin is broken and the bone may protrude through)
Comminuted
-The bone is splintered- multiple bone fragments
Displaced
-The ends of the bone are not aligned
Spiral
-Twisting injury
Complicated
–Injury to adjacent tissues (blood vessels and nerves)
Depressed
–Fracture of the skull with risk of damaging the brain
Stress fracture
–Bone fracture after repetitive stress
–Tibia, fibula and metatarsals (athletes, dancers, army recruits)
Pathologic fractures
–Fracture of a diseased bone
–Osteoporosis
–Osteomalacia
–Paget’s Disease
–Tumours
Primary
Secondary
–Congenital bone disorders
48
Q

Features of fracture types

A

Incomplete simple fractures heal most rapidly
Comminuted fractures are characterised by shattered bone fragments at the site of fracture (which must be resorbed and thus delay healing)
Compound fractures communicate with the overlying skin and are more likely to become infected

49
Q

Explain process of bone healing

A

Haematoma formation
Organisation of haematoma (inflammatory infiltrate and granulation tissue formation)-> procallus formation (soft tissue callus)
Osteoprogenitor cells-> osteoblasts which migrate into the granulation tissue, proliferate and produce osteoid
External callus bridges the fracture site outside the bone
Internal callus bridges the fracture in the medullary cavity
Ossification
Replacement of woven bone by lamellar bone
Remodelling

50
Q

Factors that affect healing of bone fractures

A 
Type (simple heals more quickly than comminuted and compound)
Alignment
Degree of immobilization
Interposition of soft tissue
Blood supply
Steroids
DM
Nutrition (Vit C, D)
Infection
Age
Malignant tumor
51
Q

Complications of fracture

A 
Delayed union
Malunion
Fibrous union
Non union
Aseptic necrosis
Osteomyelitis
52
Q

Treatment of fracture

A

Immobilisation
–Internal fixation (plates, screws)
–External (POP)

53
Q

Define osteomyelitis

A 
Inflammation of bone and marrow due to infection
Pathogenic microorganisms
–Pyogenic bacteria (most common)
–Mycobacteria
–Fungi
–Viruses
–Parasites
54
Q

Pathogenesis of osteomyelitis

A

The initial focus of inflammation is in the metaphysis (best vascularized part of bone in children) or vertebrae in adults
Necrosis of bone (sequestrum)
Reactive new bone formation (involucrum)

55
Q

Clinical features of osteomyelitis

A 
more commonly Children
Fever
Malaise
Bone pain and tenderness
Reduced movement of limb
56
Q

Dx of osteomyelitis

A 
Blood culture
Blood tests (↑ WCC, ↑ESR, C-reactive protein)
Radiography
–Lytic lesions surrounded by zone of sclerosis
–Bone changes are late
US
MRI
Bone scan ‘hot spot’
57
Q

Complications of osteomyelitis

A

Abscess formation (Brodie’s)
Continuous bone formation ( Garré sclerosing osteomyelitis)
Drainage of pus and necrotic debris (sinus formation)
Chronic osteomyelitis
Fractures
Amyloidosis
Bacteraemia

58
Q

Tx of osteomyelitis

A

Antibiotics IV and then PO X weeks

Surgical drainage

59
Q

How do pyogenic organisms spread in osteomyelitis

A

Organisms gain access to the bone via
–Bloodstream from an extra-osseous site
–Direct extension from a contiguous site
–Direct inoculation (traumatic or surgical) of the bone

60
Q

What pyogenic organisms are responsible for osteomyelitis

A

Most cases of haematogenous osteomyelitis are caused by Staphylococcus aureus
E-coli, Pseudomonas and Klebsiella in patients with genitourinary tract infection and drug abusers
Patients with sickle cell disease are prone to osteomyelitis and it is commonly due to Salmonella
Group B streptococci are the most common organisms in the neonates
Many of the non haematogenous cases are caused by mixed flora and/or anaerobes

61
Q

Describe tuberculous osteomyelitis

A

Occurs by haematogenous seeding from these extra-osseous sites
rare in developed countries

Tuberculous infection of the spine (Pott’s disease) can cause compression fractures and spinal deformities
Granulomatous inflammation of the affected bone
Can be very difficult to treat

bone pathology (4 decks)

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