bone path

Question 1

Function of musculoskeletal system

Answer 1

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

Question 2

Describe the normal bone

Answer 2

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

Question 3

What is the function of sodium hydroxyapatite?

Answer 3

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

Question 4

What are the function of bone cells?

Answer 4

Bone forming - osteoblasts and osteocytes

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

Question 5

What is another important function of osteoblasts?

Answer 5

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

Question 6

What are the different tissues of bone?

Answer 6

•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

Question 7

What are the components of long bone

Answer 7

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

Question 8

How does the bone grow and develop?

Answer 8

• Enchondral ossification

* Intramembranous ossification

Question 9

Define endochondral ossification

Answer 9

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

Question 10

Another name for membranous ossification?

Answer 10

periosteum ossification

Question 11

Membranous ossification

Answer 11

•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

Question 12

Where do the fibroblasts come from?

Answer 12

periosteum and differentiate into osteoblasts

Question 13

How do bones grow in membranous ossification vs endochondral ?

Answer 13

Bones in width in Membranous ossification

Bones grow in length in endochondral ossification

Question 14

How do bones form?

Answer 14

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)

Question 15

What are osteoids made up of and what makes it?

Answer 15

Osteoblasts make osteoids

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

Question 16

What is the essential function of VitD?

Answer 16

Increase in serum calcium level

Question 17

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

Answer 17

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

Question 18

What are the functions of parathyroid hormone?

Answer 18

.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

Question 19

Calcitonin function

Answer 19

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

Question 20

List congenital bone disorders

Answer 20

achondroplasia
osteogenesis imperfecta
osteopetrosis

Question 21

Define achondroplasia

Answer 21

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

Question 22

List features of achondroplasia

Answer 22

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

Question 23

Define osteogenesis imperfecta

Answer 23

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

Question 24

Features of osteogenesis imperfecta

Answer 24

–Fractures
–Blue sclera
–Dental abnormalities
–Hearing loss

Question 25

Define osteopetrosis and a/ features | tx?

Answer 25

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

Question 26

List metabolic bone diseases

Answer 26

``` Osteoporosis Osteomalacia Paget’s disease Hyperparathyroidism Renal osteodystrophy ```

Question 27

Compare and contrast pathogenesis of osteoporosis and osteomalacia

Answer 27

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

Question 28

Outline the general procedure to diagnose metabolic bone diseases?

Answer 28

``` Careful history Physical examination Radiographic examination Laboratory tests Bone biopsy may be indicated ```

Question 29

What are the primary and sec causes of osteoporosis?

Answer 29

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

Question 30

Complications of osteoporosis

Answer 30

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

Question 31

Diagnosis of osteoporosis?

Answer 31

Imaging techniques that measures bone density |  X-ray (when 30- 40% of bone mass is lost)

Question 32

Prevention and tx of osteoporosis

Answer 32

``` Exercise Oral calcium and Vitamin D H.R.T Calcitonin Bisphosphonates ```

Question 33

Differentiate rickets and osteomalacia

Answer 33

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

Question 34

Causes of both rickets and osteomalacia

Answer 34

``` 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 ```

Question 35

Clinical features of osteomalacia

Answer 35

Bone pain | Microfractures (Loosers zone)

Question 36

Clinical features of rickets

Answer 36

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

Question 37

Tx for rickets and osteomalacia?

Answer 37

vitamin D

Question 38

Causes of hyperparathyroidism

Answer 38

primary parathyroid adenoma/hyperplasia high calcium secondary prolonged hypocalcaemia low/normal Ca2+

Question 39

Effects of increased PTH on bone

Answer 39

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

Question 40

Define renal osteodystrophy

Answer 40

``` Bone disease secondary to renal failure –Osteitis fibrosa cystica –Osteomalacia –Osteosclerosis –Osteoporosis ```

Question 41

Pathogenesis of renal osteodystrophy

Answer 41

(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)

Question 42

What is another name for Paget's disease?

Answer 42

Osteitis deformans)

Question 43

Paget's disease description

Answer 43

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)

Question 44

Complications of Paget's disease

Answer 44

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

Question 45

Summarise causes of abnormal matrix abnormal mineralization abnormal osteoclasts

Answer 45

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

Question 46

Define avascular necrosis / osteronecrosis

Answer 46

``` 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 ```

Question 47

Types of fractures

Answer 47

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 ```

Question 48

Features of fracture types

Answer 48

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

Question 49

Explain process of bone healing

Answer 49

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

Question 50

Factors that affect healing of bone fractures

Answer 50

``` 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 ```

Question 51

Complications of fracture

Answer 51

``` Delayed union Malunion Fibrous union Non union Aseptic necrosis Osteomyelitis ```

Question 52

Treatment of fracture

Answer 52

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

Question 53

Define osteomyelitis

Answer 53

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

Question 54

Pathogenesis of osteomyelitis

Answer 54

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)

Question 55

Clinical features of osteomyelitis

Answer 55

``` more commonly Children Fever Malaise Bone pain and tenderness Reduced movement of limb ```

Question 56

Dx of osteomyelitis

Answer 56

``` 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’ ```

Question 57

Complications of osteomyelitis

Answer 57

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

Question 58

Tx of osteomyelitis

Answer 58

Antibiotics IV and then PO X weeks | Surgical drainage

Question 59

How do pyogenic organisms spread in osteomyelitis

Answer 59

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

Question 60

What pyogenic organisms are responsible for osteomyelitis

Answer 60

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

Question 61

Describe tuberculous osteomyelitis

Answer 61

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