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Year 2 LCRS - Musculoskeletal > Metabolic Bone Disease - Histopathology > Flashcards

Metabolic Bone Disease - Histopathology Flashcards

1
Q

What are the functions of bone?

A

MECHANICAL – support and site for muscle attachment

PROTECTIVE – vital organs and bone marrow (STRONG)

METABOLIC – reserve of calcium (high surface area)

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2
Q

What is the composition of bone?

A

INORGANIC – 65%

  • Calcium hydroxyapatite (10Ca 6PO4OH2)
  • A store house for 99% o f Ca in the body
  • 85% of the phosphorous, 65% Na & Mg

ORGANIC – 35%
- Bone cells and protein matrix (collagen, osteoid

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3
Q

What are the epiphysis, metaphysis and diaphysis?

A

The growth plate (epiphyseal line) fuses in your early 20s. Until then, the bone grows and elongates from the epiphysis (end region of bone)

Below the growth plate, bone is flared slightly – this is the metaphysis

The long, narrow parallel area is the diaphysis

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4
Q

Where does the blood supply to the bone come through?

A

periosteum

  • if periosteal surface is disturbed, the blood supply is cut off and bone becomes necrotic
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5
Q

What are the classifications of bone?

A

anatomical bones:
- flat, long, short/cuboid, irregular, sesamoid

macroscopic structure:
cortical (strong, protective – mechanical): 
- Long bones
- 80% of skeleton
- Appendicular
- 80-90% calcified
- Mainly mechanical and protective

cancellous (trabecular bone – in marrow)

  • Vertebrae & pelvis
  • 20% of skeleton
  • Axial
  • 15-25% calcified
  • Mainly metabolic function
  • Large surface

microscopic structure:

  • woven bone (immature)
  • lamellar bone (mature) - bone is organised into concentric lamellae, which form in response to mechanical forces. They give the bone strength in the cortical bone
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6
Q

What are the functions of different bone cells?

A

Osteoblasts: build bone by laying down osteoid (which is then mineralised)

Osteoclasts: multinucleate cells of macrophage family, resorb or chew bone

Osteocytes: osteoblast like cells, which sit in lacunae in bones – they look inert (imbedded in matrix)

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7
Q

Why would you perform a bone biopsy?

A
  • confirm diagnosis of bone disorder
  • Evaluate bone pain or tenderness
  • Investigate an abnormality seen on x-ray
  • For bone tumour diagnosis (benign vs. malignant)
  • To determine the cause of an unexplained infection
  • To evaluate therapy
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8
Q

What are the different types of bone biopsy?

A

CLOSED – needle – core biopsy (Jamshidi needle)

OPEN – for sclerotic or inaccessible lesions (requires general anaesthetic)

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9
Q

Describe the histology of the femoral head

A

Bone is organised with cartilage on the surface between the two articular surfaces. Trabecular bone is on the inside, with cortical bone on the outside (thick, dense bone)

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10
Q

What are different stains used in histological stains?

A

H&E - looks at morphology of cells

Masson- Goldner Trichrome - labels in different colours mineralsied and non mineralsied bone

Tetracyline/Calcein labelling - bone turnover shown - labels bone as its forming

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11
Q

What is metabolic bone disease?

A

Disordered bone turnover - group of diseases that cause reduced bone mass and reduced bone strength

It occurs due to imbalance of various chemicals in the body (vitamins, hormones, minerals etc.)

causes altered bone cell activity, rate of mienralisation, or changes in bone structure

Patients present with bone pain and difficulty performing normal tasks

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12
Q

What is osteoporosis?

A

defined as bone mineral density T-score of -2.5 or lower (standard deviations different from mean peak bone mass BMD)

aetiology is primarily age related/ due to post menopausal occurrences

secondarily seen with drugs and in systemic disease (long term treatment)

*types of osteoporosis: high turnover and low turnover

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13
Q

What would you see in an osteoporosis bone biopsy?

A

In a bone biopsy, two thirds of the bone is calcified (one third is osteoid)

In osteoporosis, the ratio is the same, but there is less bone present in general (NORMAL, WEAK BONE)

  • IN OSTEOPOROSIS, CALCIUM IS NOT AFFECTED. Calcium is normal. Osteoporosis is the loss of bone mass over time (loss of calcium, phosphate and protein in the same ratios).

** If you don’t use your bones, you will develop osteoporosis earlier.

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14
Q

What is osteomalacia?

A

Defective mineralisatin of normally synthesized bone - bone is bendy and mainly osteoid

Rickets in cildren

two types:

  • deficiency of Vitamin D (leads to hypocalcaemia -> osteomalacia)
  • deficiency of PO4 (usually due to CKD)

*In osteomalacia, only one third is calcified – this is ABNORMAL BONE

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15
Q

What are the sequelae of osteomalacia?

A
  • Bone pain/tenderness
  • Fracture and microfracture
  • Proximal weakness
  • Bone deformity (e.g. tibia bowing in rickets)
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16
Q

What are the sequelae of osteomalacia?

A
  • Bone pain/tenderness
  • Fracture and microfracture
  • Proximal weakness
  • Bone deformity (e.g. tibia bowing in rickets)
  • Vitamin D deficiency is also associated with characteristic horizontal fractures in Looser’s zones
17
Q

What are the features of hyperparathyroidism?

What are primary and secondary causes?

A

EXCESS PTH, causes BONE RESORPTION

  • Increased Ca and PO4 excretion in urine (calcium hydroxyapatite is broken down into its constituents)
  • Hypercalcaemia
  • Hypophosphatemia
  • Skeletal changes of osteitis fibrosa cystica if disease is allowed to progress

4 organs are directly or indirectly affected by PTH and between them control Ca metabolism:

  • Parathyroid glands
  • bones
  • kidneys
  • proximal small intestine

Primarily due to a parathyroid adenoma (85-90%), chief cell hyperplasia

Secondarily due to chronic renal deficiency, vitamin D deficiency

18
Q

What are the symptoms of hyperparathyroidism?

A

mnemonic

  • Stones (Ca oxalate renal stones)
  • Bones (osteitis fibrosa cystica, bone resorption)
  • Abdominal groans Abdominal groans (acute pancreatitis) (acute pancreatitis)
  • Psychic moans (psychosis & depression)
19
Q

Describe the histology of hyperparathyroidism

A

Earliest bone changes : subperiosteal bone erosions in hands -> tunneling erosion in trabecule -> Brown cell tumours

The test for suspected hyperparathyroidism used to be an x-ray of the hand. The hand would show small, brown cell tumours (lytic lesions) usually on the radial side of the digits and thumb.

Brown cell tumour:

  • Composed of osteoclast cells
  • Osteoclasts have become out of control (they are being induced to resorb bone -> form small brown tumours composed of groups of osteoclast cells on a background of fibrous tissue and blood)
20
Q

What is renal osteodystrophy?

A

Bone disease related to CKD

Comprise all the skeletal changes of chronic renal disease:

  1. Increased bone resorption (osteitis fibrosa cystica)
  2. Osteomalacia
  3. Osteosclerosis (osteoblasts aren’t working properly)
  4. Growth retardation
  5. Osteoporosis
21
Q

What is Paget’s disease?

What are some causes?

A

disorder of bone turnover

Paget’s disease of bone is divided into 3 stages:

  1. Osteolytic (osteoclast predominant stage)
  2. Osteolytic-osteosclerotic (osteoblasts will try to build bone)
  3. Quiescent osteosclerotic (there is disorganised, mineralised bone)
  • Onset normally when patients are over the age of 40 (affects 3% of Caucasians > 55 year olds)
  • Slightly more common in men
  • Rare in Asian and African populations
  • Mono-ostotic cases (affects just one bone) only make up 15% (the remainder is polyostotic)

Causes:

  • Aetiology is unknown
  • Familial cases show autosomal pattern of inheritance with incomplete penetrance (mutation in sequestosome 1 gene or RANK)
  • Overuse or previous injury
22
Q

What are clinical symptoms of Paget’s disease?

A

*often asymptomatic and found by chance

Pain
Microfractures
Nerve compression (incl. Spinal N and cord)
Skull changes may put medulla at risk
Deafness – AFFECTS region of temporal bone
Haemodynamic changes (sometimes)
Cardiac failure haemodynamic changes, cardiac failure
Hypercalcaemia
Development of sarcoma in area of involvement, 1% (osteosarcoma)

23
Q

What does Paget’s disease look like histologically?

A

sclerosis of cortises -> thickening
osteolytic regions
osteolytic black spots in cavities

  • in the initial (osteolytic phase), you see the bone being remodelled in a disorganised way
  • We see lots of osteoclast giant cells, and multinucleated osteoclasts
  • Then the osteoblasts fight back and build bone
  • We are left with a paving pattern – there are reversal lines where the bone is being remodelled

Year 2 LCRS - Musculoskeletal (10 decks)

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