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Y2 LCRS 2 - NMH, Psych, Anatomy of Limbs, Head, Neck & Spine, Musculoskeletal > MSK; Lecture 1, 2 and 3 - Intro and biochemistry, Histopathology and Radiology > Flashcards

MSK; Lecture 1, 2 and 3 - Intro and biochemistry, Histopathology and Radiology Flashcards

1
Q

What is metabolic bone disease?

A

Group of diseases that cause change in bone density and strength -> by increasing bone resorption, decreasing bone formation and altering bone structure (ass.. w/disturbances in mineral met)

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2
Q

What are the 5 common metabolic bone disorders?

A

1ry hyperPTHism, Rickets/osteomalacia, osteoporosis, Paget’s disease, renal osteodystrophy

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3
Q

What are the symptoms of the common metabolic bone disorders?

A

Met: hypo/hypercalcaemia, hyper/hypophosphataemia. Bone specific: deformity, fractures causing bone pain

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4
Q

What Ca is present in bone?

A

Hydroxyapatite; cancellous bone is met active

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5
Q

Which processes occur in the bone?

A

Remodelling -> 5% anytime with the total skeleton over 7y; continuous exchange of ECF with bone fluid reserve

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6
Q

What makes bone strong?

A

Mass, Material properties (matrix and mineral), Microarchitecture, Macroarchitecture

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7
Q

How can bone structure and function be assessed?

A

Bone histology, biochemical tests, BMD, radiology

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8
Q

How does bone mass change with age?

A

Peak in 20s with men and women decreasing after their 40s, women much faster in early menopause

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9
Q

What is the 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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10
Q

What is bone composed of?

A

Inorganic (65%) - Ca hydroxyapatite, storehouse for 99% of Ca in body, 85% of PO4 and 65% in Na/Mg; organic 35% (bone cells and protein matrix)

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11
Q

What are cortical bones?

A

Skull and long bones, 80% of skeleton, appendicular, 80-90% calcified and mainly mechanical/protective

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12
Q

What are cancellous bones?

A

Vertebrae and pelvis; 20% of skeleton, axial, 15-25% calcified; mainly metabolic with large SA to allow for easy release of Ca

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13
Q

Why would you take a bone biopsy?

A

Indications -> evaluate bone pain/tenderness, investigate an abnormality seen on xray; for bone tumour diagnosis (benign/malignant); determine cause of unexplained infection; evaluate therapy

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14
Q

What types of bone biopsy available?

A

Usually in anterior superior iliac crest for marrow; closed: needle core biopsy; open: for sclerotic/inaccessible lesions

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15
Q

What are osteoblasts?

A

Build bone by laying down osteoid

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16
Q

What are osteoclasts?

A

Multinucleate cells of macrophage family; resorb/chew bone

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17
Q

What are osteocytes?

A

Osteoblast like cells which sit in lacunae in bone

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18
Q

How do you form an osteoblast?

A

RANK and RANKL

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19
Q

What is RANK?

A

Receptor activator for nuclear factor kB

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20
Q

What is osteoprotegerin?

A

Inhibits RANK/L binding and therefore inhibits osteoclastogenesis

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21
Q

What are the types of bone?

A

Anatomically flat/long/cuboid bones (intramembranous ossification (flat) and endochondral ossification (long)); trabecular (cancellous); compact bone (cortical); woven bone (immature), lamellar bone (mature)

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22
Q

What are reversal lines?

A

You can see where there has been resorption and building up of bone - like a fossil

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23
Q

What is metabolic bone disease?

A

Disordered bone turnover due to imbalance of various chemicals in the body (vit, hormones, minerals); overall effect is reduced bone mass (osteopoenia) often resulting in fractures with little/no trauma

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24
Q

What are the 3 main categories of metabolic bone disease?

A

Related to endocrine abnormality (vit D, PTH); non-endocrine (Age related osteoporosis); disuse osteopoenia (in bed for a long time/space)

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25
Q

What can cause osteoporosis?

A

1ry: age, post menopause; 2ry: drugs, systemic disease

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26
Q

What features do patients present with?

A

Bone pain, pathological fracture; weakness in bone

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27
Q

What is the pathological bone in osteoporsis?

A

Less dense bone

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28
Q

What happens to mineralisation of bone in osteoporosis?

A

Mineralisation is the same

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29
Q

What is osteomalacia?

A

Defective bone mineralisation -> 1ry from deficiency of vit D; 2ry from deficiency of PO4

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30
Q

What are the functions of Vit D?

A

Bone metabolism, intestinal/renal Ca absorption, cell proliferation, cell differentation, immune regulation

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31
Q

What are the symptoms of osteomalacia?

A

Sequelae; bone pain/tenderness, fracture, proximal weakness, bone deformity

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32
Q

What occurs in rickets?

A

The growth plates expand but aren’t strong enough to support soft tissue weight, so bow to the side.

Cupping of metaphyses and fraying/splying of the bones occurs.

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33
Q

What are Looser’s zone?

A

Horizontal fractures in osteomalacia

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34
Q

What is hyperPTHism?

A
  • Excess PTH;
  • increased Ca/PO4 excretion in urine hyperCa,
  • hypoPO4;
  • skeletal changes of osteitis fibrosa cystica (pain as bone is broken down too quickly, and holes are forming in the bone)
  • 1ry due to pit adenoma -> BONE RESORPTION
  • 2ry due to other systemic background -> BONE RESORPTION AND BONE MINERALISATION (higher PO4 in 2ry)
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35
Q

What is osteitis fibrosa cystica?

A

Pain as bone is broken down too quickly, and holes are forming in the bone - cysts seen in xray and fibrous tissue in bone where it is breaking

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36
Q

What are the organs affected by hyperPTHism?

A

PTH glands, bones, kidneys, proximal small intestine

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37
Q

What are the causes of Hyperpthism?

A

1ry: PTH adenoma; chief cell hyperplasia; 2ry chronic renal deficiency/ vit D deficiency

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38
Q

What is a simple diagnosis method of HyperPTHism?

A

X-ray of hand; causes small lesion in bones of hand -> brown cell tumours (bone broken down and replaced by fibrous tissue)

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39
Q

What is renal osteodystrophy?

A

Comprises all skeletal changes of chronic renal disease,->

  • increased bone resorption (OFC);
  • osteomalacia;
  • osteosclerosis;
  • growth retardation;
  • osteoporosis
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40
Q

What are the features of renal osteodystrophy?

A
  • PO4 retention – hyperphosphataemia
  • Hypocalcaemia as a result of ↓vit D
  • 2ry hyperparathyroidism
  • Metabolic acidosis
  • Aluminium deposition
  • subperiosteal erosions,
  • brown tumours,
  • sclerosis
  • soft tissue calcification (vesels, cartilage)
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41
Q

What is Paget’s disease?

A

Disorder of bone turnove -> 3 stages:

  • osteolytic;
  • osteolytic-osteosclerotic;
  • Quiescent osteosclerotic
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42
Q

What is the pathogenesis of Paget’s?

A

Onset: >40y mainly in caucasians; M=F; rare in asians and africans; mono-ostotic (15%) and rest polyostotic; Familial cases show autosomal patter of inheritance with incomplete penetrance; parvomyxovirus type particles found

43
Q

What is the site predilection in Paget’s disease?

A

x

44
Q

What are the symptoms of paget’s?

A

Pain; microfractures; nerve compression (incl. Spinal N and cord); Skull changes may put medulla at risk; deafness; +/-haemodynamic changes, cardiac failure haemodynamic changes, cardiac failure • hypercalcaemia • Development of sarcoma in area of involvement 1%

45
Q

How does each substance in biochem investigations change in each of the 5 main metabolic diseases of bone?

A
46
Q

What is normal Ca homeostasis?

A
47
Q

How is Ca distributed in the body and how is it corrected?

A
48
Q

How does PTH regulate sCa levels?

A

Has predominant role in minute regulation -> highest regulation from kidneys

49
Q

What is relevant about PTH?

A

84a.a. peptide but N1-34 active; Mg dependent (low in alcoholics); T1/2: 8min; PTH receptor activated by PTHrP

50
Q

Slide 23

A

x

51
Q

What is the function of PTH in the kidney?

A
52
Q

What is the function of PTH in the bone?

A

Bone resorption through RANK system

53
Q

What are the causes of 1ry HyperPTHism?

A

50s; 3F:1M; Parathyroid adenoma 80%; Parathyroid hyperplasia = 20%; Parathyroid CA = <1%. Familial Syndromes: MEN 1 = 2%; MEN 2A = rare; HPT-JT = rare

54
Q

How do you diagnose hyperPTHism?

A

An elevated total/ionised calcium with PTH levels frankly elevated or in the upper half of the normal range’; (ie. Corrected Calcium > 2.60 mmol/l with PTH > 3.9 pmol/l (nr 1.0 - 6.8)). Subjects with hypercalcaemia and a PTH in the upper half of the normal range are physiologically not normal. It is important to note that such ‘non-suppressed’ concentrations are entirely compatible with the diagnosis of Primary HPT

55
Q

What is the clinical features of 1ry HyperPTHism due to high Ca?

A

Thirst, polyuria, Tiredness, fatigue, muscle weakness, Renal colic, nephrocalcinosis, CRF, Dyspepsia, pancreatitis, Constipation, nausea, anorexia, Depression, impaired concentration, Drowsy, coma. Patients may also suffer fractures secondary to bone resorption

56
Q

How does high sCa cause diuresis?

A

Ca >3 is medical emergency as they become acutely dehydrated

57
Q

What does chronically elevated PTH increase the risk of?

A

Renal stones; cortical bone resorption (Increased bone turnover; Acute/ pulsed PTH; anabolic; Chronic: catabolic (Cortical > cancellous)

58
Q

What are the biochemical findings in 1ry hyperPTHism?

A
  1. Increased serum calcium - by absorption from bone/gut 2. Decreased serum phosphate - renal excretion in proximal tubule 3. PTH in the upper half of the normal range or elevated 4. Increased urine calcium excretion 5. Cr may be elevated NB: FHH needs to be ruled out before
59
Q

How is Vit D metabolised?

A

Metabolised by liver and kidney -> vit D binding protein: t1/2 = 3d, filtered by kidney but reabsorbed by PCT (activates it too); if you have too much then it is converted into 24,25 D and this is inactive;

60
Q

Where is Ca absorbed?

A

Activated Vit D increases gut Ca absorption; 20-60% load DDM/JJM and colon; passive in paracellular space (linear with diet); active (up to 40% saturable DDM)

61
Q

What are the actions of Vit D?

A

x

62
Q

What is the definition of Vit D deficiency?

A

At a nadir 25 OH D = 30 ng/ml (75nmol/l) PTH levels start to rise. Muscle function optimal >70nmol/l. Gut Ca absorption increases up to 80 nmol/l

63
Q

What is rickets?

A

Inadequate Vitamin D activity leads to defective mineralisation of the cartilagenous growth plate (before a low calcium)

64
Q

What are the S+S of rickets?

A

Symptoms: Bone pain and tenderness (axial); Muscle weakness (proximal); Lack of play Signs:Age dependent deformity; Myopathy; Hypotonia; Short stature; Tenderness on percussion

65
Q

What are the causes of rickets/osteomalacia?

A

Lack of sunlight

66
Q

What is the biochem of rickets/osteomalacia?

A

x

67
Q

What is FGF-23 and where is PTH reabsorbed?

A

FGF-23; 32KD protein Produced by osteoblast, lineage cells, long bones. LIKE PTH causes P loss UNLIKE PTH inhibits activation of Vit D by 1 α OH ase; PO4 fully filtered and reabsorbed ony in PCT

68
Q

*Describe this picture and explain why 2 systems are needed for PO4

A
  • PTH activates vit D in kidney and causing increase absorption of Ca and PO4;
  • which then causes PTH to shut down
  • which causes increased Ca and PO4 in blood
  • which would lead to crystals forming (not good) so bones detect this and FGF-23 is produced to release it
69
Q

How is osteomalacia and phosphate linked and what are the causes?

A

Can also get with renal phosphate loss, when calcium and Vitamin D levels are usually normal

70
Q

How can FGF-23 excess cause rickets/osteomalacia?

A
71
Q

What happens if the PCT is damaged?

A

Causes phosphaturia and stops 1α hydroxylation of Vit D. Fanconi syndrome: multiple myeloma, heavy metal poisoning: lead, mercury; drugs: tenofovir, gentamycin; congenital disease: Wilsons, glycogen storage diseases

72
Q

What is osteoporosis and the causes?

A

Low bone density

73
Q

How does oestrogen deficiency cause menopausal bone loss?

A
74
Q

How does cancellous bone loss differ in men vs women?

A

Disproportionate loss of cancellous bone in women

75
Q

What does osteoporosis do to fracture rates?

A

Increased -> hip fracture has a mortality rate of 3months in elderly

76
Q

How do you exclude other causes using biochem in osteoporosis?

A
77
Q

How do you asses osteoporosis?

A

Bone density - single best predictor of fracture risk; BMD represents 70% of total risk

78
Q

What is DEXA?

A

Uses t-score = BMD - young adult mean BMD/ young adult s.d. -> how many SD off the average for 25yo -> -2.5 = osteoporosis; -1 to -2.5 osteopaenia; >-1 normal; 1SD is a 2.5 increase risk of fracture

79
Q

Why would you use central measurements to measure osteoporosis?

A

Risk over 20% - leads to treatment recommendations

80
Q

What are bone markers?

A

Give insight into activity (resoption and formation); dynamic (unlike BMD); divided into markers of formation and resorption

81
Q

How is collagen synthesised?

A

x

82
Q

What bone resorption markers are used in monitoring osteoporosis treatment?

A

Monitoring of response to treatment with anti- resorptive drugs (BMD change 18mnths); bone resorption markers fall in 4-6 weeks; expect a 50% drop of urine NTx by 3 months

83
Q

What are the problems with cross-links in osteoporosis?

A
84
Q

What are the clinical use of bone formation markers?

A
85
Q

What is BSAP?

A
86
Q

What happens to alkaline phosphatase with age?

A
87
Q

What is CKD-MBD?

A
  • Skeletal remodeling disorders caused by CKD contribute directly to to heterotopic calcification, especially vascular.
  • The disorders in mineral metabolism that accompany CKD are key factors in the excess mortality caused by CKD.
  • CKD impairs skeletal anabolism, decreasing osteoblast function and bone formation rates .
88
Q

What is the biochemistry of renal osteodystrophy?

A
89
Q

How does secondary hyperparathyroidism progress?

A
90
Q

What is the difference between osteopenia, osteoporosis and osteomalacia?

A

Osteopenia is poverty of the bone -> seen in both osteoporosis and osteomalacia. Porosis is decreased bone mass; malacia decreased mineralisation

91
Q

What are the radiological signs of osteomalacia (and rickets)?

A

Vit D deficiency -> vit D and Ca are decreased, PTH is increased -> Radiology = age/growth plate closure -> codfish vertebra (biconcave, loss of height, osteopenic and pencilled-in margin)

92
Q

How can you describe osteomalacia?

A

Too little mineral = osteopenic. too much osteiod = Looser’s zones

93
Q

What are Looser’s zones and where are they found?

A

Narrow lucency, perpendicular to bone cortex -> pubic rami, proximal femur, scapula, lower ribs

94
Q

What is the difference between osteomalacia and osteoporosis?

A

Malacia: less mineral, osteopenia, bend and bow before breaking, codfish vertebra with uniform spine deformity. Porosis: less bone, osteopenia, break and anterior wedging

95
Q

What is the difference between osteomalacia and rickets?

A

Malacia: changes in mature bone, osteopenia, Looser’s zones, codfish vertebrae and bending vertebrae. Rickets: Before growth plate closure, changes related to growth plates (MAINLY), changes of osteomalacia co-exist

96
Q

Where are the most obvious changes seen in rickets?

A

Metaphysis is where the most rapid growth occurs, so where the most obvious changes will be -> indistinct frayed metaphyseal margin, with widened growth plate (no calcification) -> cupping/splaying of metaphyses due to weight bearing

97
Q

What are the radiological findings in rickets?

A

Indistinct frayed metaphyseal margin, with widened growth plate (no calcification) -> cupping/splaying of metaphyses due to weight bearing. Rickety rosary (splayed and cupped ends of ribs), bowing of weight bearing bones

98
Q

What is the radiological finding of primary hyperparathyroidism?

A

Bone resorption

99
Q

Where are the main sites of bone resorption in hyperPTHism?

A

Subperiosteal (radial aspect middle and ring finger phalanges), subchondral (distal clavicle and pubis), intracortical (pepper-pot skull), brown tumours (bigger, shows increased osteoclastic activity)

100
Q

What are the 2 types of bone loss and which disease have each type?

A

SLOW: involutional osteoporosis, bone has time to remodel/bone loss occurs according to mechanical needs. FAST: HyperPTHism/Disuse osteoporosis, bone loss is too rapid, so loss doesn’t cater to mechanical needs

101
Q

What are the radiological findings in renal osteodystrophy?

A

Osteomalacia, Osteoporosis, 2ry HPTH -> sub-periosteal erosions, brown tumours, sclerosis, axial skeleton/vertebral end plates, rugger jersey spine, and soft tissue calcification (arteries and cartilage)

102
Q

What are the mediators of bone metabolism?

A

Ca/P/Vit D/ PTH/calcitonin; other hormones: T4, GH, glucocorticoids, oestrogens, androgens, insulin; other factors: vit c and other nutrients, cytokines, prostaglandin, several GF

103
Q

What are codfish vertebrae?

A

Biconcave deformity of vertbrae seen in osteoporosis and osteomalacia

Y2 LCRS 2 - NMH, Psych, Anatomy of Limbs, Head, Neck & Spine, Musculoskeletal (17 decks)

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