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Kat's Pathology > Metabolic Bone Disease > Flashcards

Metabolic Bone Disease Flashcards

1
Q

Non-neoplastic bone pathology

A

Congenital/Acquired: trauma, infection, degeneration, inflammation, metabolic

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2
Q

Neoplastic bone pathology

A

Benign/malignant tumours

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3
Q

Function of bone

A

Mechanical - support and site for muscle attachment
Protective - vital organs and bone marrow
Metabolic - reserve of calcium

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4
Q

Composition of bone

A

Inorganic - 65% (calcium hydroxyapetite, is storehouse for 99% of calcium in the body, 85% of the phosphorus, 65% of the sodium and magnesium)

Organic - 35% (bone cells and protein matrix)

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5
Q

Bone structure medial to lateral

A

Medulla
Cortex
Periosteum

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6
Q

Bone structure proximal to distal (e.g. arm)

A

Diaphysis
Metaphysis
Epiphysis (epiphyseal line, subchondral bone)
Articular cartilage

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7
Q

Small synovial joints

A

Facet joints of fovea

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8
Q

What percentage of mineralisation does bone need to have for it to be visible on X-ray

A

50%

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9
Q

Types of bone

A

Cortical

Cancellous

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10
Q

Features of cortical bones

A 
Long bones 
80% of skeleton 
Appendicular 
80-90% calcified 
mainly mechanical and protective 
Less metabolically active
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11
Q

Features of cancellous bone

A 
Vertebra and pelvis 
20% of skeleton 
Axial skeleton 
15-25% calcified 
Mainly metabolic 
Large surface area
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12
Q

Structure of cortical bone

A

Trabecular lamellae
Interstitial lamella
Concentric lamellae
Circumferential lamellae

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13
Q

Bone cells

A

Osteoblasts
Osteoclasts
Osteocytes

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14
Q

Features of osteoblasts

A

Build bone by laying down osteoid

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15
Q

Feature of osteoclasts

A

Multinucleate cells of macrophage family

Resorb or chew bone

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16
Q

Features of osteocytes

A

Osteoblast like cells which sit in the lacunae in bone

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17
Q

Stain used to view osteocytes and canaliculae

A

Silver stain

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18
Q

What promotes osteoblast activity

A

Osteoclast activity released matrix bound growth factors in bone, which allows osteoprogenitor cells to differentiate into osteoblasts.

NB: mechanical factors, hormones and cytokines activate surface osteoblasts which promote activity of osteoclasts

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19
Q

Activation of osteoclasts

A

RANK is expressed on the surface of osteoclast lineage cells.
RANKL is expressed on multipotential stem cells (MSCs) of osteoblast lineage and on T- and B- lymphocytes.
When RANKL binds to RANK this causes the osteoclast precursor cell to differentiate and thus increase bone resorbtion.

OPG competes with RANK for RANKL. OPG is also expressed by MSCs and osteoblast cells.

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20
Q

How are bony metastases formed

A

Oncogene products produced by tumour cells metastasising to bone influence the bone cells to resorb bone and promote local growth of the tumour. This is mediated by the RANK /OPG signalling pathway.
I.e. when tumour growth is promoted, the bone is destroyed.

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21
Q

What can tumours do to bone

A

Induce bone resorption

Induce bone formation

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22
Q

What cancer causes more bone growth than destruction

A

Metastatic prostate carcinoma

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23
Q

Types of bone

A

Woven/lanellar
Anatomically - flat bones/long bones (intramembranous and endochondrial ossification)
Trabecular (cancellous)/compact (cortical)

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24
Q

Features of lamellar bone

A

Cortical and cancellous bone are lamellar and this is particularly evident when viewed under polarised light
Collagen fibres are arranged in alternating orientations allowing for the highest density of collagen per unit of tissue

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25
Q

Features of woven bone

A

In woven bone the lamellar are absent. Collagen fibres are laid down in a disorganized fashion: such as states of high bone turnover(Pagets disease of bone, certain stages of flouride treatment, tumours) not so tightly packed, random bundles

26
Q

Metabolic bone disease

A

Disordered bone turnover due to imbalance of various chemicals in the body (vitamins, hormones, minerals etc)
Overall effect is reduced bone mass (osteopaenia) often resulting in fractures with little or no trauma

27
Q

Categories of bone disease

A

Non-endocrine (e.g. age related osteoporosis)
Related to endocrine abnormality (vitamin D, parathyroid hormone)
Disuse osteopaenia

28
Q

Diagnosis of metabolic bone disease

A

Histology requires bone biopsy from iliac crest,

processed undecalcified for histomorphometry.

29
Q

Studies performed on bone biopsy to diagnose metabolic bone disease

A

Static parameters: cortical thickness and porosity, trabecular bone volume, thickness, number and separation of trabeculae
Bone mineralisation studied using osteoid parameters
Histodynamic parameters obtained from fluorescent tetracycline labelling

30
Q

Aetiology of osteoporosis

A

Primary - age, post-menopausal
Secondary - drugs, systemic disease

90% of cases are due to insufficiency calcium intake and post-menopausal oestrogen deficiency

31
Q

Pathogenesis of osteoporosis

A

Low initial bone mass or accelarated bone loss can reduce bone mass below the fracture threshold

32
Q

Turnover classification of osteoporosis

A

High turnover results from increased bone resorption

Low turnover results from reduced bone formation

33
Q

Influencing factors in osteoporosis

A

Nutrition & social practices (etoh, smoking, malabsorption, vit C&D deficiency)

Endocrine abnormalities (menopause, hyperthyroidism, hyperparathyroidism, cushings, DM)

Immobilisation

Iatrogenic (corticosteroids, long-term heparin or phenytoin therapy, castration, XS thyroid therapy)

34
Q

Risk factors for osteoporosis

A 
Advanced age 
Female 
Smoking 
Alcohol 
Early menopause 
Long-term immobility 
Low BMI
Poor diet (low vitamin D, low calcium)
Malabsorption 
Thyroid disease 
Low testosterone 
Chronic renal disease 
Steroids
35
Q

Osteoporosis in UK figures

A

1/3 women, 1/12 men >50

50% of fracture patients cannot live independently post fracture, 20% die

36
Q

Osteoporosis presentation

A

Patients commonly present with back pain and #

wrist (Colles’), hip (NOF and intertrochanteric) & pelvis may be the first sign of disease

> 60% vertebral # are asymptomatic

Compression # usually in T11-L2 distribution

37
Q

Investigations in osteoporosis

A

Lab investigations: serum calcium, phosphorus and alkaline phosphate (usually all normal)

Imaging

Bone density:
T score between -1 and -2.5 = osteopaenia
T score >-2.5 = osteporosis

38
Q

DEXA scores for osteopaenia and osteoporosis

A

T score between -1 and -2.5 = osteopaenia

T score >-2.5 = osteporosis

39
Q

What is required for proper evaluation of osteoporosis/metabolic bone disease

A

Quantitative analysis. Parameters measured are percentage of bone tissue as opposed to marrow and the percentage of bone tissue actively laying down bone or resorbing bone compared with inactive surfaces.

40
Q

Organs involved in Hypo/Hyper-PTH

A

Parathyroid glands
Bones
Kidneys
Proximal small intestine

41
Q

Low vitamin D effect on PTH

A

Vit D deficiency from whatever cause results in increased parathyroid hormone (PTH) release and subsequent increased bone resorption.

42
Q

Most common cause of hypocalcaemia

A

Low vitamin D

43
Q

Hypocalcaemia clinical manifestation

A

Muscle twitching
Spasms
Tingling
Numbness

44
Q

Osteomalacia

A

Defective bone mineralisation

45
Q

Causes of osteomalacia

A

Deficiency of vitamin D

Deficiency of phosphate

46
Q

Sequelae in osteomalacia

A

Bone pain/tenderness
Fracture
Proximal weakness
Bone deformity

47
Q

Osteomalacia in children

A

Rickets - bowing of the legs and widening of the ephiphysis

48
Q

What condition are looser’s zones seen in

A

Ostemalacia

49
Q

Biochem of hyperparathyroidism

A

Excess PTH
Increased calcium and phosphate excretion in the urine
Hypercalcaemia
Hypophosphataemia
Skeletal changes of osteitis firbosa cystica

50
Q

Causes of hyperparathyroidism

A

Primary: parathyroid adenoma (85-90%), chief cell hyperplasia
Secondary: chronic renal deficiency, vitamin D deficiency, malabsorption

51
Q

Symptoms of hyperparathyroidism

A

Manifestation of hypercalcaemia

STONES (calcium oxalate renal stones)
BONES (osteitis fibrosa cystica, bone resporption)
Abdominal GROANS (pain, acute pancreatitis)
Psychic MOANS (psychosis and depression)

52
Q

Bone lesion in hyperparathyroidism

A

Brown cell tumour

53
Q

Renal osteodystrophy

A

Comprises all the skeletal changes of chronic renal disease:

Increased bone resportion (osteitis fibrosa cystica) 
Ostemalacia 
Osteosclerosis 
Growth retardation 
Osteoporosis
54
Q

Biochem of renal osteodystrophy

A 
Phosphate retention - hyperphosphataemia
Hypocalcaemia as a result of decreased vitamin D 
Secondary hyperparathyroidism 
Metabolic acidosis 
Aluminium deposition
55
Q

Stages of Paget’s disease

A

Osteolytic
Ostelytic-osteosclerotic
Quiescent osteosclerotic

56
Q

Paget’s disease

A

Disorder of bone turnover

57
Q

Who is affected by Paget’s disease

A 
Onset >40 years 
M=F
Rare in Asians and Africans 
Mono-ostotic 15%
Remainder polyostotic
58
Q

Aetiology of Paget’s disease

A

Aetiology is unknown
Familial cases show autosomal pattern of inheritance with incomplete penetrance (mutation 5q35-qter - sequestosome 1 gene)
Parvomyxovirus type particles have been seen on EM in Pagetic bone

59
Q

Sites affected in Paget’s disease

A 
Skull 
Spine 
Pelvis 
Humerus 
Femur 
Tibia
60
Q

Clinical presentation of Paget’s disease

A

Pain
Microfractures
Ner compression (including spinal nerves and cord)
Skull changes may put medulla at risk
+/- haemodynamic changes, cardiac failure
Development of sarcoma in area of involvement in 1%

61
Q

Indications for bone biopsy

A

Suspected osteomalacia
Diagnostic classification of renal osteodystrophy
Osteopaenia in young patients <50y
Osteopaenia associated with abnormal Ca metabolism
Classification of hereditary childhood bone disease

Evaluation of treatment (osteomalacia, hypophosphatasia)

Kat's Pathology (105 decks)

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