Non-neoplastic Bone Flashcards
What is the main function of osteoblasts?
Bulit + lay down of Bone
Osteo B lasts B uilt bone
What is the main function of osteoclasts?
Resorb bone
Multinucleate cells of macrophage family
In What categories can metabolic bone disease be classified (different aetiologies) ?
- non-endocrine (e..g age-related osteoporosis)
- Related to endocrine abnormality
- Disuse osteopenia
What is the usual aetiology of osteoporosis?
Age related (post-menopausal/ age)
or secondary to systemc diseases/ drugs (steroids!)
What is the pathophysgioloy of osteoporosis?
What test would you do and what do you expect?
Different processes leading to
↓bone mass
DEXA scan: T score > 2.5 SD below normal (1-2.5 = osteopaenia)
What are the typical clinicla features of osteoporosis?
Low impact fractures (#)
(hip - NOF, vertebrae; wrists - Colles’)
Pain (back) (vertebra # +/- nerve pain)
What are the expected x-ray changes in a patient with osteoporosis?
None
What does histology of osteoporosis show?
Loss of calcellous bone
What is osteomalacia/ rickets? (pathophysiology)
Overall calcium deficiency leading to
Reduced bone mineralisation
What are characteristic features of osteopenia on X-ray?
Looser’s zones
(pseudo-fractures)
Splaying of metaphysis
What are histological features of osteomalcia and rickets?
Excess of unmineralized bone (osteoids)
What are the biochemical findings of Osteomalacia/ Rickets?
Normal/ Low calcium
Low Po4
High ALP
Explanation:
Overall calcium is low –> activation of osteoclasts and increased bone resobtion to even out low calcium (can be corrected to normal biochemical levels and explains the high ALP due to high bone turnover)
Phosphate is low due to incereased renal excretion of phosphate due to higher PTH levels
What are the causes of primary hyperparathyroidism?
Parathyroid adenoma
Parathyroid hyperplasia
carcinoma
MEN
What are the symptoms of primary hyperparathyroidism?
Symptoms of Hypercalcaemia
Moans (abdominal pain), constipation
Stones: renal stones
Bone pains + fractures
Groans: psychological changes (depression, confusion)
What are common x-ray changes of Primary hyperparathyroidism?
Brown’s tumours
(collection of multinucleate giant cells)
Salt and pepper skull
Subperiosteal bone resorption in phalanges
Brow’s tumour
What is osteitis fibrosa cystica?
A rare skeletal disorder seen in advanced hyperparathyroidism characterized by replacement of calcified bone with fibrous tissue
(Most often seen in primary Hyperparathyroidism)
What are the biochemical findings in primary hyperparathyroidism?
High calcium
Low/Normal P04
High/normal ALP
High/ normal PTH (inappripriartely normal)
What are the disease features of Paget’s disease of the bone?
Idiopathig high bone turnover
Seeing initally increased lysis (lytic lesions), then mixed (lytic + sclerotic) and sclerosis (sclorotic lesions)
What are the symptoms of Paget’s disease?
Bone pain
Microfractures
Nerve compression (due to expansion of bone: sensorineural hearing loss, sciatica)
infreased head size
high output cardiac failure
Whatare histological findings of Paget’s disease of the bone?
Huge osteoclasts
w > 100 nuclei Mosaic pattern of lamellar bone (like jigsaw puzzle)
What are the biochemical findings of Paget’s disease of the bone?
Normal Calcium, Normal phosphate
High ALP
What are the 4 stages of bone repair (after #)?
- Organisation of haematoma (pro-callus)
- Formation of fibrocartilaginous callous
- Mineralisation of fibrocartilaginous callous
- remodeling of bone among weight bearing lines
What are the most common site of infection for osteomyelitis?
Vertebrae
Jaw (dental abscess)
toe (diabetic ulcers)
Long bones
Whatare the expected X-ray changes in osteomyelitis?
Early: sub-periostel new bone formaion
Later (10 days) lytic destruction of bone
What is the most common organism causing Osteomyelitis in adults?
S.aureus
What is the most common organism causing osteomyelitis in children?
What bone are more commonly involved?
Haemophilus influenza
Group B strep
often affecting long bones
Which orgnaisms cause osteomyelsitis in the following patient populations
1. SIckle cell patients
2. Immunocompromised
3. Congenital osteomyelitis
- Sickle cell - Salmonella
- Immunocompromised -TB
- Congenital - Syphilis
What are the expected X-ray changes of Osteoarthritis?
LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
What chagnes of the Hands can be seen in a patient with Osteoarthrits?
Hberden’s nodes (DIPJ)
Bouchard’s nodes (PIPJ)
What are common x-ray changes see in Rheumatoid arthritis?
Early: juxta-articular osteopenia
Later: joint space narrowing, marginal erosions of cartilage and bone, osteopenia (generalized), subchondral cysts
What would a hand-exmaination of a patient with RA show?
Overall DIPJ sparing
Radial deviation of wrist and ulnar deviation of fingers
- “swan neck” and “Boutonniere” deformity of fingers
- Swan neck = hyperextension of PIPJ & flexion of DIPJ
- Boutonniere = flexion of PIPJ & hyperextension of DIPJ
● “Z” shaped thumb
● Synovial swelling
What are histophatologicla findings of Rheumatoid Arthritis?
thickening of synovial membran
hyperplasia of surface synoviocytes
intense inflammatory cell infiltrate & fibrin deposition & necrosis
What is the epidemiology in Gout compared to pseudo-gout?
Gout: middle aged-obese men
Pseudo-grout: Women >50
What joints are most commonly affected in a patient with gout?
Acute monoarthritis
- Classically 1st MTP (big toe)
- Precipitated by
trauma/infection
Although there is a chronic form that is polyarticular: Chronic tophaceous gout
What are classical features of Chronic tophaceous gout?
- Polyarticular arthritis
- Tophi deposits in ear lobes, fingers and elbows
- Urate kidney stones
What joints are commonly affected in pseudo-gout?
Acute monoarthritis
- Knee and shoulder
- Precipitated by
trauma/infection
Chronic
- Polyarticular arthritis
How would gout and pseudo-gout differentiated on an x-ray?
In gout: rat-bite erosions
Pseudogrout: Chondrocalcinosis on X-ray
What would the crystals look in gout and pseudo-gout?
Gout: Urate crystals, needle shaped - negatively bierefringent
Pseudo-gout: Calcium pyrophosphate crystals,
rhomboid shaped - positively bierefringent
How is an acute attack of gout managed?
Colchicine (+NSAIDs)
(Rest + ice affected joint)
binds and stabilizes tubulin subunits → inhibits microtubule polymerization → inhibits phagocytosis of urate crystals, neutrophil activation, migration, and degranulation
How is gout chronically managed?
What is the MOA?
Allopurinol
Inhibition of xanthine oxidase → hypoxanthine and xanthine are not degraded into uric acid
Conservative: ↓ETOH and purine intake e.g. sardines, liver
How is pseudo-gout managed?
NSAIDs or intra-articular steroids
What is the aetiology of pseudo-gout?
The primary (idiopathic) form is most common, risk Factor: age
Secondary forms
- joint trauma/ damage, e.g. surgery, JIA, OA
- Metabolic: Hyperparathyroidism, haemochromasism others
- Familial chondrocalcinosis
What are different aetiologies of pseudo-gout?
- increased production: tumour lysis syndrome, inherited metabolic abnormalities
- Increasd intake: high dietary, alcohol intake
- Decreased excretion: diuretics
