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Clinical Pathology > bone > Flashcards

bone Flashcards

1
Q

What is bone composed of? Describe each layer

A
  • Cortical bone (hard, outer layer)
  • Trabecular bone (spongy, inner layer)
  • Cells (bone forming/resorbing cells)
  • Extracellular (organic matrix- collagen, inorganic compounds)
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2
Q

Describe osteoblasts

A
  • Terminally differentiated
  • Products of mesenchymal stem cells
  • Make osteoid, hormones, matrix proteins, alkaline phosphotase
  • Prerequisite for mineralisation
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3
Q

Describe osteoclasts

A
  • Large
  • Multi nucleated
  • Ruffled resorption border
  • Break down bone
  • Found in bone pits (resorption bays)
  • Produce enzymes- tartrate resistant acid phosphatase & cathepsin K= breakdown ECM
  • Help enhance blood Ca levels
  • Regulated by hormones (PTH, Calcitonin, IL-6)
  • Help with osteoclastic maturation & activity
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4
Q

Describe osteocytes

A
  • Star shaped
  • Trapped/buried osteoblasts
  • Communicate via cytoplasmic extensions
  • Mechanosensory
  • Involved in regulating bone matrix turnover
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5
Q

How is normal bone formed?

A
  • Resorption by osteoclasts

- Formation by osteoblasts

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6
Q

What are the stages in bone formation?

A
  • Resting
  • Resorption
  • Osteoid formation
  • Mineralisation
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7
Q

Give some examples of biochemical markers of bone turnover

A
  • Formation: Alkaline phosphatase, procollagen type 1 propeptides
  • Resorption: Crosslinked telopeptides of type 1 collagen
  • Osteoclast enzymes: tartrate resistant acid phosphatase, cathepsin K
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8
Q

What is bone alkaline phosphatase?

A
  • Released by osteoblasts
  • Involved in mineralisation
  • Release stimulated by increased bone remodelling
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9
Q

Describe P1NP

A
  • Synthesised by osteoblasts
  • Precursor molecule of type 1 collagen
  • Increases with increased osteoblast activity
  • Decreased by reduced osteoblast activity
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10
Q

Why are bone markers used?

A
  • Evaluation of bone turnover & bone loss
  • Evaluation of treatment effect
  • Compliance with mediation
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11
Q

How is bone mass investigated?

A

DEXA

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12
Q

What are T scores and what do certain values mean?

A
  • Bone density
  • -1+ normal bone density
  • -2.5- -1 osteopenia
  • -4- -2.5 osteoporosis
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13
Q

Name some bone disorders

A
  • Metastic disease
  • Paget’s disease
  • Osteoporosis
  • Osteomalacia/rickets
  • Hyperparathyroidism
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14
Q

Describe osteoporosis

A
  • Dec bone mass & deranged bone micro architecture= failure of structural integrity
  • Loss of bone
  • Propensity to fractures- spine & hip
  • Diagnosis by DEXA/Xray
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15
Q

What are common sites of fragility fractures?

A
  • Spine
  • Neck of femur
  • Wrist
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16
Q

What are secondary causes of osteoporosis?

A
  • Endocrine: Early menopause, diabetes, Cushings,
  • GI: Coeliac, IBD, chronic liver disease
  • Haematological: myeloma, haemoglobinopathies
  • Respiratory: COPD, CF
  • Drugs: steroids, heparin, anti-convulsants, ciclosporin
  • Rheumatological: RA
  • Metabolic: homocysturia
17
Q

What investigations can be carried out for secondary causes of osteoporosis?

A
  • Ca & bone profile
  • TFTs
  • FBC (U&Es- estimated GFR)
  • Vit D
  • PTH
  • Coeliac screen
  • Plasma viscosity
18
Q

What are the types of treatments for osteoporosis?

A
  • Anabolic

- Antiresorptives: bisphosphonates

19
Q

What is the mechanism of action for bisphosphonates?

A
  • Mimic pyrophosphate structure
  • Taken up by skeleton
  • Concentrated in newly mineralising bone under osteoclasts
  • Local release during bone resorption
  • Modulate signalling from osteoblasts to osteoclasts
  • Ingested by osteoclasts
  • Inhibit osteoclast formation, migration, activity, promote apoptosis
20
Q

What are problems with using bisphosphonates?

A
  • Poor absorption
  • Cause oesophageal/ upper GI problems
  • Flu-like side effects
  • Osteonecrosis of jaw
  • Atypical femur fractures
21
Q

What types of bone metastases are there?

A
  • Lytic: breast, lung, destruction of normal bone (osteoclasts)
  • Sclerotic/osteoblastic: deposition of new bone, prostate, lymphoma
22
Q

What is the clinical presentation of bone metastasis?

A
  • Pain: worse at night, better with movement, constant
  • Broken bones: femur, humerus, vertebral, pathological
  • Numbness/paralysis/trouble urinating: spinal cord compression
  • Loss of appetite/nausea/thirst/fatigue/confusion: symptoms of hypercalcaemia
  • Anaemia: disruption of bone marrow
23
Q

What are the symptom of hypercalcaemia?

A
  • Severe: abdo pain, vomiting, coma, pancreatitis, dehydration, arrhythmias
  • Mild: nausea, fatigue, constipation, anorexia, mood changes, polyuria/dipsia
24
Q

Which cells secrete PTH?

A

Chief cells of parathyroid gland

25
Q

What are the roles of PTH?

A
  • Inc decomposition of bone releasing Ca
  • Inc absorption of Ca from food by intestines
  • Inc reabsorption of Ca from urine by kidneys
  • All lead to inc levels of blood Ca
26
Q

What are the causes and signs of primary hyperparathyroidism?

A
  • Sporadic or familial
  • Ca high
  • PTH high
  • Low phosphate
  • High alkaline phosphatase
  • Adenomas: encapsulated & consist of chief cells
  • Parathyroid carcinoma: aggressive, severe hypercalcaemia
  • Glandular hyperplasia: all 4 glands enlarged, sporadic or genetic MEN1, MEN2A
  • Ectopic adenomas: in mediastinum/thymus gland, migrate during embryogenesis
27
Q

What are the causes and signs of secondary hyperparathyroidism?

A
  • CKD, vit D deficiency
  • Normal/low Ca
  • PTH high
  • High phosphate if due to kidney problems
28
Q

What are the causes and signs of tertiary hyperparathyroidism?

A
  • prolonged secondary hyperparathyroidism, CKD
  • High Ca
  • High PTH
  • High or low phosphate
29
Q

What are the classical symptoms of primary hyperparathyroidism?

A
  • Hypercalcaemic symptoms
  • Renal disease/ CKD/ nephrolithiasis
  • Bone disease/ osteoporosis/osteitis/fibrosa cystica
  • Proximal muscle wasting
30
Q

What are Calcimimetics used for and how do they work?

A
  • Normalise Ca in sympotmatic patients/not fit for surgery

- Activates CaSR in PT gland leading to reduced PTH secretion

31
Q

Describe Paget’s disease of the bone

A
  • Rapid bone turnover & formation
  • Abnormal bone remodelling
  • 50+
  • Polyostotic or monostotic
  • Elevated alkaline phosphatase reflecting inc bone turnover
32
Q

What are clinical features of Page’s disease?

A
  • Bone pain
  • Bone deformity
  • Fractures
  • Arthritis
  • Cranial nerve defects if skull affected (hearing/vision loss)
  • Risk of osteosarcoma
33
Q

Which bones are most commonly affected by Paget’s disease?

A
  • Pelvis
  • Femur
  • Lower lumbar vertebrae
34
Q

What is osteomalacia?

A
  • Lack of mineralisation of bone due to it D deficiency/lack of Ca/phosphate
  • Widened osteoid seams
  • Childhood rickets: widened epiphyses & poor skeletal growth
35
Q

What are the main causes of osteomalacia?

A
  • Insufficient Ca absorption from intestines (diet or resistance)
  • Excessive renal phosphate excretion (genetic)
36
Q

What are clinical features of osteomalacia?

A
  • Muscle & bone weakness
  • Diffuse bone pains (symmetrical)
  • High alkaline phosphatase & PTH
  • Low vit D & Ca
  • Secondary hyperparathyroidism

Clinical Pathology (56 decks)

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