51 Bone diseases + markers Flashcards by user delete

What are the four functions of the bone?

Structural support.
Organ protection.
Blood cell production.
Site of mineral storage.

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What are the two layers of bone?

Characteristics?

Cortical bone: outer, hard.

Trabecular: inner, spongy.

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What does the extracellular matrix of the bone consist of? (4).

Collagen.
Hydroxyapatite.
Calcium.
Phosphate.

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What is osteoid?

Non-mineralised organic matrix consisting of mainly Type 1 collagen.

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What is hydroxyapetite?

Calcium-phosphate-hydroxide salt.

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Differentiate between the function of osteoclasts and osteoblasts:

Osteoblasts: make bone.
Osteoclasts: resorb bone.

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What are osteocytes?

Osteoblasts that are trapped in the bone matrix.

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What do osteoblasts make? (4).

Osteoid.
Hormones (osteocalcin).
Matrix proteins.
Alkaline phosphatase.

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Which enzymes do osteoclasts produce? (2).

TRAP - tartrate resistant acid phosphatase.

Cathepsin K.

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Which hormones regulate osteoclast activity? (3).

PTH.
Calcitonin.
IL-6.

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Which ligands are involved in osteoclast maturation? (2).

RANK ligand.

Osteoprotegrin.

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What are the functions of osteoclasts? (2)

Mechanosensory.

Regulate bone turnover.

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How often is the adult skeleton replaced completely?

10 years.

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Describe the bone cycle: (4)

Resting.
Osteoclast resorption.
Osteoblasts make osteoid.
Mineralisation.

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Describe how bone mass changes with age.

Peaks at 30.

Decreases with age (sudden drop in menopause in women).

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Name the products of active osteoblasts that are measured: (3)

Alkaline phosphatase.
Osteocalcin (OC).
Procollagen type 1 propeptides (P1NP).

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What is produced during bone resorption? (3).

Hydroxyproline.
Pyridinium.
Cross-linked telopeptides of type 1 collagen (NTX, CTX).

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Where is alkaline phosphatase produced?

Bone (50%).

Liver (50%).

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What causes an increase in bone alkaline phosphatase? Generally, then (4).

Increase in bone remodelling.
Growth.
Fractures.
Hyperparathyroidism.
Paget's.

Why is P1NP a good marker of bone production? (2).

Low diurnal and intraindividual variation.

No affected by food intake.

What are the problems with using cross linked collagen molecules as markers?

Diurnal variation.

Not correlated with bone density.

Which marker is used to measure the success and compliance of anti-resorptive therapy?

Cross linked telopeptides of type 1 collagen (CTX, NTX).

Which bone marker is used to monitor compliance with terparatide?

P1NP.

How is bone mass measured and quantified?

DEXA scanning.
T score. Between -1 and -2.5 is osteopenia.
Below -2.5 is osteoporosis.

How is osteoporosis diagnosed?

DEXA scanning. | Bone markers not sensitive enough.

Define osteoporosis:

Decreased bone mass + Deranged micro architecture = Failure of structural integrity.

What is a fragility fracture and where do they normally occur?

Caused by injury insufficient to fracture normal bone. | Spine, neck of femur, wrist.

Which tool is used to assess fracture risk?

FRAX.

What are the risk factors for osteoporosis? (6).

``` Low vitamin D. Early menopause. Steroid use. Alcohol. Smoking. Malabsorption syndromes. ```

What are the antiresorptive treatments for osteoporosis? (6).

``` Bisphosphonates. Denosumab. Raloxifene. Terparataide. Synthetic PTH. Strontium. ```

How do bisphosphonates work?

Mimic pyrophosphate structure. Taken up by osteoclasts. Inhibit their migration and activity, and promoting apoptosis.

What are the drawbacks of bisphosphonate use? (5).

Poor absorption. Difficult to take. Cause GI problems, jaw osteonecrosis and atypical femur fractures.

Which malignancies cause lytic bone mets? (4). | Bone destruction

Brest. Kidney. Lung. Thyroid.

Which malignancies cause sclerotic bone mets? (4). | Bone deposition

Prostate. Lymphoma. Breast. Lung.

Where do bone mets commonly occur? (5).

``` Spine. Pelvis. Femur. Humerus. Skull. ```

How do bone mets present? (5).

``` Pain (worse at night/constant). Fractures. Spinal compression symptoms. Hypercalcaemia symtoms. Anaemia. ```

How does hyperparathyroidism cause hypercalcaemia? (3).

Increases bone breakdown. Increases Ca uptake in intestines. Increase Ca reabsorption by kidneys.

What is tertiary hyperparathyroidism?

After a long time of 2o, thyroid can no longer turn off. Usually due to chronic kidney disease.

What are the causes of primary hyperparathyroidism? (4).

Adenoma (85%). Glandular hyperplasia (6-10%). Parathyroid carcinoma (1-2%). Ectopic adenomas.

What are the symptoms of hypercalcaemia?

Polyuria, mood disturbance, vomiting, anorexia, fatigue and constipation. Progression to cardiac arrhythmia, coma, pancreatitis.

Which genes are associated with glandular hyperplasia of the parathyroid gland?

MEN1. | MEN2.

How does primary hyperparathyroidism present? (4)

Hypercalcaemic symptoms. Renal disease. Bone disease. Proximal muscle wasting.

How do calcimimetics work and what are they used for?

Activate CasR in parathyroid gland, reduce PTH secretion. | Normalise Ca in PHPT unsuitable for surgery.

What are the clinical features of Paget's disease of the bone? (6).

``` High alk phase only. Bone pain and deformity. Fractures. Arthritis. Cranial nerve defects. Osteosarcoma risk. ```

What is osteomalacia?

Lack of mineralisation of bone du to deficiency in Vitamin D, Ca or phosphate.

How does osteomalacia present in children vs adults?

Children: widened epiphyses and poor growth. Adults: widened osteoid seams and low mineralisation.

What bone marker changes are seen in osteomalacia? (2) | If 2o? (2)

High alk phos. Low vit D. If 2o HPT low Ca + high PTH.