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Clinical Pathology > Bone and new markers > Flashcards

Bone and new markers Flashcards

1
Q

What part of the bone is corticoid bone?

A

Hard, out layer

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2
Q

What part of the bone is the trabecular bone?

A

Spongy, inner layer

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3
Q

What do osteoblasts do?

A

Secrete bone

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4
Q

What do osteoclasts do?

A

absorb bone

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5
Q

What is the function of the trabecular bone?

A

Bone marrow -

-Haemopoesis

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6
Q

What is the extracellular part of bone composed of?

A

Inorganic matrix - hydroxyapatite, minerals e.g. calcium, phosphate

Organic matrix - collagen

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7
Q

What is bone before it is mineralised?

A

Osteoid

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8
Q

What mineralises bone?

A

Hydroxyapatite

calcium-phosphate, hydroxide salt

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9
Q

Why is bone considered a dynamic tissue?

A

Constantly being remodelling

High vascular

Metabolically active

Osteoblasts produce and secrete metric and help with mineralisation

Osteoclasts reabsorb (both clasts/blast actions = linked)

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10
Q

What do osteoblasts do?

A

Make osteoid (non-mineralised organic matrix - mainly collagen)

Make hormones (osteocalcin), matrix proteins and alkaline phosphatase

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11
Q

What are osteoblasts called when buried underneath/trapped within matrix?

A

Osteocytes

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12
Q

What enzymes do osteocytes produce?

A

Tartrate resistant acid phosphatase (TRAP)

Cathespin K

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13
Q

What main hormone is osteoclasts regulated by?

A

PTH

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14
Q

What ligands/proteins helps with osteoclast maturation and activity

A

RANK (produced by osteoblasts)

Osteoprotegrin

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15
Q

What are the function of osteocytes?

A

Maintain bone matrix turnover

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16
Q

What is the bone remodelling process?

A

Osteocyte -> reabsorption pit -> osteoblast -> produce osteoids -> mineralisation (hydroxyapatite) -> osteocyte

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17
Q

Why is reduced bone mass related to menopause?

A

Loss of oestrogen

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18
Q

What also happens as you get older (i.e. osteoclastic - osteoblastic activity)

A

Osteoclastic activity increases - balance tipped to bone reabsorption

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19
Q

What diagnostic test is used to investigate bone gross structure?

A

X-rays

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20
Q

What investigative technique is used to assess bone mass? (I.e. calcium levels)

A

DEXA scan

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21
Q

What biomarkers indicate bone formation (i.e. pro-osteoblastic activity)

A

Osteocalcin

Pro collagen type I phosphatase (P1NP)

Alkaline phosphatase

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22
Q

What markers could be used for bone reabsorption

A

Cross linked telopeptides of type 1 collagen (CTX/NTX)

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23
Q

What markers could be used for osteoclastic activity? (i.e. enzymes)

A

TARP (tartrate acted resistant phosphatase)

Cathespin K

24
Q

What produces alkaline phosphatase?

A

Osteoblasts - indicator of bone remodelling

25
Q

When is high levels of all pos observed?

A
  • Fractures
  • Hyperthyroidism
  • Pagets disease of bone
26
Q

What is pro collagen type I phosphatase an indicator of? what is it a particularly good marker?

A

Indicates osteoblastic activity

Good because it is a very stable marker - no diurnal variation/no affected by food intake

27
Q

What does cross linked telopeptides of Type I collagen indicate? What can their use be problematic?

A

Indicates bone reabsorption e.g. adolescence, menopause, hyperthyroidism

However diurnal variation/affected by food intake

28
Q

What are the problems with using bone markers?

A

Not disease specific

Not specific - type I collagen which is widely distributed in body

Intra-individual variability

29
Q

What is a DEXA scan used to determine? What do the T scores indicate

A

Bone mass/density

T score - number of SD’s away

normal = -1+
Osteopenia = -1 - -2.5
Osteoporosis =

30
Q

What are the risk factors for osteoporosis?

A 
Age
Early menopause 
Malnutrition
Alcohol/smoking
Steroids
31
Q

What is osteoporosis? What is it marketed by?

A

Generalised loss of bone

Reduced bone mass + deranged bone architecture = failure of structural integrity (propensity to fracture)

Lighter X-ray, DEXA scan (

32
Q

What is a fragility fracture?

A

Fracture of bone by force that would usually be insufficient to fracture a normal bone (minimal trauma)

33
Q

What anti-reabsorptive drug is used to treat osteoporosis? what cell does it act on?

A

Bisphosponates

Anti-resorptive - osteoclasts

34
Q

What anabolic drug is used to treat osteoporosis? What cell does it act on?

A

Terparatide

Anabolic - synthetic PTN

35
Q

Where are the common places for bone metastasis occur?

A 
Femur
spine
pelvis
skull
Humerus
36
Q

What are the two types of bone metastasis? Where do they originate from usually?

A

Lytic - osteoclastic breakdown - lung/breat

Sclerotic - osteoblastic - deposition of new bone =- prostate, lymphoma, breast/lung

37
Q

What are the symptoms of bone metastasis?

A
  • Pain
  • Fractures
  • Paralysis, numbness, trouble urinating - spinal cord compression
  • Hypercalcaemia - thirsty, loss of appetite, confusion, fatigue
  • anaemia - disrupted bone marrow function
38
Q

What are the symptoms of hypercalcaemia?

A 
Polyuria/polydipsa
Dehydration
Fatigue
Confusion
Mood disturbance
Nausea
Abdo pain
Vomiting 
Coma
Dehydration
Cardiac arrthymias
39
Q

What are the main causes of hypercalcaemia?

A
  • Malignancy

- Hyperparathyroidism

40
Q

What regulates blood calcium? What is produced and by what cells?

A

Parathyroid gland

Produces PTH by chief cells

41
Q

What does PTH do?

A

increases Ca in blood by increasing decomposition of bone, and increasing absorption from intestines and kidney

42
Q

What other factors act on the parathyroid gland?

A 
Vit D (low increase PTH)
Magnesium
43
Q

What is secondary hyperparathyroidism usually caused by?

A

Vit D deficiency (marked by normal calcium levels but too high PTH)

44
Q

What is tertiary hyperparathyroidism usually caused by?

A

When secondary hyperparathyroidism has gone on for too long

45
Q

What is primary hyperparathyroidism usually caused by?

A

Calcium and PTH inappropriately high

Disease of

46
Q

What are the main causes of primary parathyroidism

A

Adenoma - chief cells producing too much PTH

Also parathyroid carcinoma - malignant - aggressive but rare

Hyperplasia of glands - sporadic or genetic (MEN1, MEN2a, familial hyperparathyroidism)

Ectopic adenomas

47
Q

What are the clinical manifestations of primary hyper parathyroidism?

A
  • Renal failure
  • Hypercalcaemia
  • Bone disease
  • proximal muscle wasting
48
Q

What is the treatment for PHPT?

A

Surgery

Cinacalcet - activates the CaSR receptor - results in reduced PTH secretion

49
Q

What is Pagets disease? What is it marked by?

A

Excessive bone turnover and formation resulting in abnormal remodelling

  • Marked by elevated Alkaline phosphatase
50
Q

What are the clinical features of Paget’s disease?

A
  • Bone pain
  • Bone deformity
  • Fractures
  • Arthritis
  • Risk of osteosarcoma
  • Pelvis, femur, lumber vert
51
Q

Whats the best treatment for pages disease?

A

Bisphosphonates - slow down osteoclasts

52
Q

What is the osteomalacia commonly referred to as?

A

Rickets

53
Q

What is osteomalacia usually caused by?

A

Lack of mineralisation of osteoid

Insufficient calcium absorption from intestine e.g. lack of dietary calcium or vit D deficiency

Excessive renal excretion of phosphate

54
Q

What are the presentations of osteomalacia?

A
  • Symmetrical bone pain
  • Muscle weakness
  • Bone weakness
  • Low Ca, low bit D
  • Secondary hyperparathyroidism
55
Q

What is the biochemistry (increase/decreased Alk pos, Ca, phosphate, PTH) for the following conditions…

a) HyperPTH
b) osteomalacia
c) osteoporosis
d) Pagets
e) Bone mets

A

a) High alk phos, high calcium, low phosphate, high PTH
b) High alk phos, low calcium, low phosphate, high PTH
c) no change
d) high alk phos,
e) high alk phos, high calcium, low PTH

Clinical Pathology (50 decks)

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