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Clinical Biochemistry: Introduction to Clinical Biochemistry > Parathyroid, Vitamin D and Bone > Flashcards

Parathyroid, Vitamin D and Bone Flashcards

1
Q

What is Bone Growth and Turnover influenced?

A
  • Calcium, phosphate, and magnesium metabolism
  • PTH
  • Vitamin D
  • Other hormones and factors such as thyroid hormones, oestrogens, androgens, cortisol, insulin, GH, IGFs, TGFb, FGF, PDGF
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2
Q

Which hormones regulate calcium?

A
  • PTH
  • 1,25(OH)2D (calcitriol)
  • Calcitonin (minor role in Ca homeostasis)

Calcium in the ECF is tightly controlled. Also used to regulate phosphate concentration.

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3
Q

Which cells are used to secrete Parathyroid Hormones?

A

Secreted by parathyroid glands

  • Chief and Oxyphil cells.
  • PTH synthesised, stored and secreted by chief cells.
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4
Q

Which organs does PTH acts upon?

A
  • PTH acts directly Bone and Kidney
  • Indirectly on intestine to regulate [Ca] and [PO4]

Metabolism and clearance determined by liver and kidneys

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5
Q

What is the effect of PTH acting on the receptors in cells?

A

PTH exerts its influence by interacting with PTH/PTHrPreceptors on plasma membrane of target cells. This initiates a cascade of intracellular events

  • Generation of cAMP
  • Activation of kinasesl
  • Phosphorylation of proteins
  • Increased entry of calcium and intracellular calcium
  • Stimulated phospholipase C activity. Generation of DAG and PI activate enzyme transport systems
  • Secretion of lysosomal enzymes
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6
Q

What are the forms of Vitamin D?

A
  • Several forms of Vitamin D occur (vitamers): Vitamin D1 – D5
  • Two major forms parent molecules, known collectively as Calciferol: Vitamin D2 (Ergocalciferol) and Vitamin D3 (Cholecalciferol)
  • 25(OH) Vitamin D: Calcidiol, Calcifediol, 25-hydroxycholecalciferol, 25-hydroxyvitamin D
  • Calcitriol (1,25(OH)2D): 1,25-dihydroxycholecalciferol, 1,25-dihydroxyvitamin D
  • Alphacalcidol: 1-hydroxycholecalciferol which is Vitamin D analogue with less of an effect on calcium than calcitriol
  • Calcichew D3 Forte: Vitamin D3 with calcium
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7
Q

What is 25(OH) Vitamin D, D2 and D3?

A
  • Effectively a pre-cursor of active form of Vitamin D
  • t1/2= 3 weeks
  • Direct indicator of available Vitamin D
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8
Q

What is 1,25(OH) Vitamin D?

A
  • Active form, very short t1/2= 4hrs
  • Limited clinical utility
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9
Q

What is the action of PTH in the kidneys?

A
  • Induces 25-OH Vit D-1a-hydroxylase which increases production 1,25(OH)2D which stimulates intestinal absorption of calcium and phosphate
  • Increases calcium reabsorption in the DCT
  • Decreases reabsorption of phosphate in PT
  • Inhibits Na+-H+ antiporter activity which favours a mild hyperchloremic metabolic acidosis in hyperparathyroid states
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10
Q

What are the effects of PTH to the bone?

A

Chronic exposure to high [PTH] leads to increased bone resorption

  • Osteolysis
  • Differentiation of osteoclasts
  • PTH acts directly by altering the activity or number of osteoblasts and indirectly on osteoclasts. This leads to bone remodelling
  • Bone resorption, a quick response is important for maintenance of calcium homeostasis
  • Delayed effects are important for extreme systemic needs and skeletal homeostasis
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11
Q

What are the signs of Renal Failure in relation to the Calcium system?

A
  • Fall in calcium. Lesss conversion of 25(OH)D to 1,25(OH)D
  • Increase in phosphate. Kidneys not excreting excess
  • Increase in PTH. Stimulated by low Ca and continual stimulation of parathyroid glands leads to 2° hyperparathyroidism
  • Patients with end stage renal failure become hypercalcaemiac. Probably due to development of autonomous PTH secretion from prolonged hypocalcaemic stimulus
  • Such hypercalcaemia may manifest for the first time in a renal transplant patient who becomes able to metabolise vitamin D normally. Results in 3° hyperparathyroidism
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12
Q

How can PTH mobilisation be described?

A

PTH mobilisation of calcium is biphasic

  • A rapid phase involving existing cells
  • Long term response dependent on proliferation of osteoclasts
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13
Q

How does PTH affect the Urine and the Serum?

A

Serum

  • In serum total and free calcium are increased, phosphate decreased

Urine

  • In urine, inorganic phosphate and cAMP are increased
  • Calcium is usually increased. Larger filtered load of calcium from bone resorption and intestinal reabsorption overrides increased tubular reabsorption of calcium
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14
Q

Which molecules aside from Calcium affect PTH release?

A
  • Mild hypomagnasaemia stimulates PTH secretion
  • More severe hypomagnasaemia reduces PTH secretion as it is a Mg dependent process
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15
Q

What are some functions of the bone?

A
  • Support: Framework of body supporting softer connective tissues and muscles
  • Protection: Mechanical protection for internal organs
  • Assisting in movement: Muscles attached to bones so when they contract bones will move
  • Mineral storage: Calcium and phosphate reservoirs
  • Production of blood cells: Bone marrow inside some long bones
  • Storage of energy: With age, bone marrow changes from ‘red’ to ‘yellow’ and is predominantly adipose cells providing a chemical energy reserve
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16
Q

What are the types of Bone?

A

Long bones

  • Greater length than width, shaft (diaphysis) with variable number of endings, curved for strength
  • Predominantly compact bone with lesser amounts of marrow and spongy bone e.g. femur, tibia, ulna and radius

Short bones

  • Roughly cube shaped with approximately equal length and width
  • Thin layer of compact bone surrounding spongy interior e.g. ankle and wrist bones

Flat bones

  • Thin structure providing mechanical protection and extensive surface area for muscle attachment
  • Two parallel layers of compact bone surrounding spongy interior e.g. cranial bones, sternum, shoulder blades

Irregular bones

  • Complicated shapes due to function they fulfil within body
  • Thin layers of compact bone surrounding spongy interior e.g. vertebrae and some facial bones

Sesamoid bones

  • Develop in some tendons where there is considerable friction, tension and physical stresses; quantity varies considerably person to person e.g. common to all are patellae (kneecaps)
17
Q

What are the types of bone tissue?

A

Compact Bone Tissue

  • Forms outer shell of bones consisting of very hard bones arranged in concentric layers (Haversian systems)
  • Accounts for 80% of total bone mass of adult

Cancellous (trabecular, spongy bone) Tissue

  • Located beneath the compact bone
  • Consists of a meshwork of bony trabeculae with many interconnecting spaces containing bone marrow
  • Accounts for remaining 20% of total bone mass but nearly 10x surface area of compact bone
18
Q

What are the Types of Bone Cells?

A

Osteoblasts

  • Produce matrix which mineralises to form ‘osteoid’
  • Become quiescent and flatten to become lining cells
  • Respond to hormonal control to activate osteoclasts

Osteocyctes

  • Cells inside the bone which sense mechanical stress to initiate remodelling
  • Transports mineral into and out of bone

Osteoclasts

  • Dissolve bone by solubilising mineral - resorption
  • Effects change in bone structure
19
Q

What is the purpose of Bone Remodelling?

A

It is a lifelong process. In the 1st of year of life, 100% of bone is replaced and in adults 10% per year. Its purpose is to:

  • Regulates calcium homeostasis
  • Repairs micro-damaged bones (everyday stress)
  • Shapes and sculptures skeleton during growth

Imbalance leads to metabolic bone disorders

20
Q

What is the molecular structure of the bone?

A

Matrix - 40% organic

  • Type 1 collagen (tensile strength)
  • Proteoglycans (compressive strength)
  • Osteocalcin / osteonectin
  • Growth factors / cytokines

Inorganic

  • 60% inorganic - hydroxyapatite

Organic

  • Osteoblasts / osteocytes / osteoclasts
21
Q

What is the cycle of Bone Remodelling?

A
  • Osteoclast Resorption
  • Osteoblast activity matrix formation (osteoid)
  • Mineralization
  • Resting Phase
22
Q

What are the two process that occur in ossification of Bone?

A

Begins 3rd month foetal life and completed late adolescence

Intramembranous ossification

  • Occurs during flat bone formation
  • Formed from mineralisation of connective tissue rather than cartilage

Endochondral ossification

  • Occurs in long bones
  • Involves initial hyaline cartilage model which continues to grow (growth plate) and mineralise at the metaphysis
  • Once skeletal maturity is reached, bones stop growing in length and the plate is replaced with an epiphyseal line
  • Defects in the continued division of these plates can lead to growth disorders e.g. achondroplasia where there is a defect in cartilage formation leading to dwarfism
23
Q

What are some disorders of Bone?

A
  • Osteomalacia – inadequate mineralisation of bone
  • Osteoporosis – Reduced bone mineral density
  • Pagets disease – excessive resorption and formation leading to weak and misshapen bones
  • Renal osteodystrophy – kidneys fail to maintain Ca and PO4
  • Rheumatoid osteoarthritis – systemic inflammatory disease
  • Malignancy
24
Q

What causes Osteomalacia?

A
  • Insufficient Ca absorption due to lack Ca or Vit D def
  • Phosphate deficiency caused by increased renal loss
25
Q

What is Osteomalacia in Children?

A

Rickets

Clinical Biochemistry: Introduction to Clinical Biochemistry (11 decks)

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