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TSM > 1.101 Calcium Homeostasis > Flashcards

1.101 Calcium Homeostasis Flashcards

1
Q

What is 1,25 DHCC?

A

Metabolite of Vitamin D,
Natural form in humans is vitamin D3 - inactive - needs to be turned into 1,25DHCC
Ingested in diet and by UV in skin

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2
Q

What is base the molecule for 1,25 DHCC?

A

Cholesterol - steroid

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3
Q

How is 1,25 DHCC synthesised?

A

1-alpha-hydroxylase - activated by PTH - enzyme used for the synthesis of 1,25 DHCC in kidney

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4
Q

What is the main action of 1,25 DHCC?

A

The main action of 1,25 DHCC is to stimulate absorption of Ca2+ from the intestine
1,25 DHCC induces the production of intracellular calcium binding proteins (CaBP) which sequester Ca2+, thereby buffering the high intracellular Ca2+ concentrations that arise during initial absorption. They allow Ca2+ to be absorbed against a high Ca2+ gradient
Another similarity with steroid hormones with vitamin d - stimulation the transciption of proteins CaBP

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5
Q

What is the mechanism of action of 1,25 DHCC?

A

In the kidney it increases tubular reabsorption of calcium - minor
In bone the primary effect is to promote the actions of the PTH - net effect is resorption of calcium
Net effect - increase calcium plasma concentration

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6
Q

What is the function of calcitonin?

A

Calcitonin acts to decrease plasma Ca2+ levels
While PTH and 1,25 DHCC act to increase plasma Ca2+ only calcitonin causes a decrease in plasma Ca2+
Plays only a minor role in daily Ca2+ balance

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7
Q

Where is calcitonin synthesised?

A

Calcitonin is synthesized and secreted by the parafollicular cells (C cells) of the thyroid gland

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8
Q

What is the main target for calcitonin?

A

• The main target cell for calcitonin is the osteoclast
• Calcitonin acts to inhibit osteoclast motility and cell shape and inactivates them
The major effect of calcitonin administration is a rapid fall in Ca2+ caused by inhibition of bone resorption

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9
Q

What is the action of calcitonin in the kidney?

A

In the kidney calcitonin decreases tubular reabsorption of Ca2+ but this is a weak effect. It has no effect on the intestine

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10
Q

Can chronic excess calcitonin cause hypocalcemia?

A

Chronic excess of calcitonin does not produce hypocalcaemia and removal of parafollicular cells does not cause hypercalcaemia. PTH and 1,25 DHCC regulation dominate

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11
Q

What is osteoporosis?

A

Reduced bone density and mass
Equal loss of mineral and organic matrix
Increase fracture risk

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12
Q

What is the pathogenesis of osteoporosis?

A

Bone resorption exceeds formation
Most frequent in postmenopausal women
natural loss with ageing exacerbated
lack of oestrogen promotes bone resorption (high turnover)
most bone loss in first 10 years after menopause or oophorectomy
Oestrogen stimulates bone formation

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13
Q

What are other risk factors of osteoporosis?

A 
Oestrogen replacement
	anti-resorptive drugs e.g. bisphosphonates, calcitonin, selective oestrogen receptor modulators (SERMs)
Replace sex steroids (androgens in men)
Calcium and vitamin D in diet
Exercise - weight carrying stimulator 
Reduce risk factors
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14
Q

What are osteomalacia and rickets?

A

Inadequate mineralisation of new bone matrix - ratio of mineral to organic matrix is lower than usual
Too much organic phase - lack of strength

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15
Q

What is the pathogenesis of osteomalacia and rickets?

A

Most commonly caused by deficiency in vitamin D activity (hypocalcaemia)
diet, insufficient exposure to sunlight
inability to convert vitamin D to 1,25 DHCC - kidney disease
inability of 1,25 DHCC to act on target tissue e.g. vitamin D-dependent rickets type II

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16
Q

What is vitamin D dependent rickets Type II?

A

Mutation in 1,25DHCC receptor
Impaired intestinal absorption of calcium
Results in osteomalacia despite high levels of 1,25DHCC

17
Q

What are the treatment for osteomalacia and rickets?

A

• Vitamin D analogs (e.g. calcitriol)
• Dietary calcium
Malabsorption if present should be treated - direct vitamin d injection into the blood,

18
Q

What are the symptoms of hypercalcaemia?

A

neuromuscular supression - less permiable to sodium and less firing of action potential - muscle weakness
kidney stones, dehydration, weight loss, nausea, vomiting and fatigue

19
Q

what is the most common cause of hypercalcaemia?

A

Primary hyperparathyroidism (asymptomatic hypercalcaemia)

20
Q

What is primary hyperparathyroidism?

A

• Ca2+ homeostatic loss due to excessive PTH secretion
• Excess PTH secreted from benign parathyroid tumour (adenoma) or hyperplastic parathyroid tissue - a bit larger than they should be
• Hypercalcaemia results from combined effects of PTH-induced bone resorption, intestinal Ca2+ absorption and renal tubular reabsorption
• Pathophysiology related to both PTH excess and concomitant excessive production of 1,25 DHCC
Deposition of Ca2+ in heart, lung, soft tissues

21
Q

What is the treatment of hyperparathyroidism?

A

• Treat with antiresorptive agents e.g. bisphosphonates and salmon calcitonin
• Surgery
• removal of adenoma
• removal of majority of all four glands in hyperplasia
Asymptomatic patients do not require surgery

22
Q

How can malignant disease cause hypercalcaemia?

A

• Most patients with severe hypercalcaemia have cancer
• Malignant cells (metastases) in bone cause destruction of the bone and release Ca2+
• direct tumour invasion
• Local Osteolytic Hypercalcemia (LOH) caused by secretion of osteoclast activating factors
• Metastases not in bone synthesize and secrete parathyroid hormone-related peptide (PTH-rP)
• Structurally similar to PTH, particularly amino terminus
Endogenous levels of PTH are low, in response to hypercalcaemia

23
Q

What are the other causes of hypercalcaemia?

A

• Vitamin D-dependent hypercalcaemia
• overdose on pharmacological preparations
• granulomatous diseases (e.g. TB, leprosy) - over secrete vitamin D
• Hyperthyroidism
• increase bone turnover (osteoclast activity)
• usually asymptomatic
• Acromegaly - over secretion of growth hormone from the pituatary gland
• stimulation of 1a-hydroxylase in kidney by elevated levels of growth hormone - more 1,25 DHCC
• Increase kidney size
• Milk ingestion (Ca2+-containing antacids)
Peptic

24
Q

What is a hypercalcaemic crisis?

A

• The end stage of hypercalcaemia
• may lead to coma and death
• usually associated with malignancy
• Patients usually dehydrated (vomiting)
• rehydrate and use loop diuretic (e.g. furosemide) to promote calciuria
• use anti-resorptive agents e.g. bisphosphonates, calcitonin
Once Ca2+ levels normal, treat underlying disease

25
Q

What is a PTH-deficient hypoparathyroidism (primary hypoparathyroidism)

A

Reduced or absent synthesis of PTH
Often due to inadvertent removal of excessive parathyroid tissue during thyroid or parathyroid surgery
Can occur for no apparent reason (idiopathic)
low PTH levels results in low 1,25 DHCC production in kidney. This leads to decreases in bone resorption, renal Ca2+ reabsorption and GI Ca2+ absorption (low DHCC)

26
Q

What is PTH-ineffective hypoparathyroidism?

A

Synthesis of biologically inactive PTH - something wrong in cleavage process

27
Q

What is PTH-resistant hypoparathyroidism?

A

PTH levels high but symptoms of hypoparathyroidism

Pseudohypoparathyroidism

28
Q

What is Secondary hyperparathyroidism?

A

Malabsorption of vitamin D in GI tract
Or decreased renal production of 1,25 DHCC (kidney disease)
The decrease in plasma Ca2+ stimulates PTH, which returns Ca2+ levels to normal at the expense of significant Ca2+ loss from bone (can accelerate metabolic bone disease)
Hypocalcaemia stimulates PTH

29
Q

What is the treatment of hypoparathyroidism?

A

• Ca2+ and calcitriol (long-term)
• Malabsorption treated with dietary Ca2+ and high doses on vitamin D - higher doses to saturate al the absorptive methods
Injections of vitamin D if malabsorption cannot be ovecome by dietary supplements

30
Q

What can cause hypecalcitoneamia?

A

Tumours of the parafollicular cells
Hereditary
Calcitonin is high, but serum calcium is normal
As is bone architecture

31
Q

What effect does pregnancy have on calcium levels in the body?

A

Increased calcium absorption from the gut
Elevated PTH, calcitonin and 1,25DHCC
During six months prior to birth, calcium accumulates in the foetus
The placenta synthesises 1,25 DHCC, as does foetal kidney and bone - however the foetus requires maternal vitamin D

TSM (67 decks)

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