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Blwyddyn 1; Tymor 3 > 137; Calcium Homeostasis > Flashcards

137; Calcium Homeostasis Flashcards

1
Q

Why is VitD considered a hormone?

A

It is produced intrinsically and acts as different sites within the body

(Other vitamins acquired through diet)

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2
Q

What VitD derived from?

A

7-dehydrocholesterol

(A sterol)

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3
Q

What is the first step in VitD activation? Where does this occur?

A

7-dehydrocholesterol

–>

*UVlight @ skin*

–>

VitaminD3

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4
Q

What is the next step in VitD activation following formation of VitD3?

Where does this occur?

A

VitD3

–>

*25-hydroxylase, liver*

–>

25(OH)VitD3

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5
Q

What regulates the activity of 25-hydroxylase?

A

Nothing, it is active regardless of PTH/Ca levels

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6
Q

What is the next step in VitD activation following formation of 25(OH)VitD3?

Where does this occur?

A

25(OH)VitD3

–>

*renal 1-a-hydroxylase, kidneys*

–>

1,25(OH)VitD3

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7
Q

What regulates the activity of renal 1-a-hydroxylase?

A

PTH is stimulatory

Ca stimulates to a lesser extent

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8
Q

What is the best screening test for VitD adequacy?

A

25(OH)VitD3 blood test

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9
Q

Diagram fo VitD synthesis

A
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10
Q

Rocaltrol, Calcijex, Decostriol, Biowoz, Vectical… are market names for what?

A

VitaminD

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11
Q

On what type of receptor does VitD act?

A

Transmembrane GPCR

They exist internally and on cell surfaces (evolutionary similarities with steroid receptors)

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12
Q

What is the role of VitD in the gut?

A

Small intestine- stimulates trans-epithelial movement of Ca and PO4

This increases serum Ca levels

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13
Q

What is the role of VitD in bones?

A

Stimulate terminal differentiation of OsteoClasts (directly, and via OsteoBlasts), which resorb bone

…Increases serum Ca

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14
Q

What is the role of VitD on the Parathyroid glands?

A

Decreases transcription of the PTH gene;

PTH increases VitD production through its stimulatory action on renal 1-a-hydroxylase

Negative feedback

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15
Q

Where is PTH produced?

A

Parathyroid glands

It is an 84aa peptide hormone

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16
Q

On what organs within the body does VitD act?

A

GIT

Bones

Parathyroids

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17
Q

List 5 majorfunctions of PTH

A
  1. Maintain normal Ca and PO4 levels
  2. Activates VitD (VitD -ve feedback on PTH)
  3. Stimulates bone resorption
  4. Stimulates renal tubular reabsorption of Ca
  5. Stimulates activity of renal 1-a-hydroxylase (indirectly causing Ca absorption in gut)
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18
Q

What stimulates PTH secretion?

A

Falling Ca levels

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19
Q

What supresses PTH secretion?

A

VitD

Rising Ca levels

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20
Q

On what type of receptor does PTH act?

A

GPCR

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21
Q

The PTH receptor binds to PTH with the same affinity as which other protein?

A

PTHrP

ParaThyroid Hormone related Protein

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22
Q

What effect does PTH have on tubular reabsorption of minerals?

A

PTH promotes Ca reabsorption

PTH internalises and degrades Phosphate receptors leading to reduced reabsorption

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23
Q

How are Ca levels detected in various organs?

A

Via Ca-sensing receptors

…on the kidneys and parathyroids

24
Q

Where is Calcitonin produced and secreted?

A

Parafollicular cells of the thyroid glands

(C-cells)

25
Q

How is Calcitonin regulated?

A

Directly by Calcium

S T I M U L A T O R Y

26
Q

What is the role of Calcitonin?

A

Inhibits OsteoClast function; thus reducing resorption

At high Ca levels, calcitonin decreases bone resorption It has no role in daily maintenance of Ca homeostasis

27
Q

What is Hypercalcaemia?

A

Blood Ca level above 2.1 - 2.5 mmol/l

28
Q

What are the signs and symptoms of Hypercalcaemia?

A

Stones; renal- diuresis, dehydration and kidney (&biliary) stones

Bones; bone resorption, bone pain, inc. fractures

Groans; nausea, vomiting, anorexia, abdominal pain

Thrones; constipation, polyuria

Phsychiatric Overtones; depression, anxiety, decreased alertness, coma, confusion

CV risks; cause/exacerbate hypertension, shorten QT interval

29
Q

What are the hormonal causes for Hypercalcaemia?

A
  1. Primary hyperParathyroidism (eg Parathyroid tumour)
  2. Hypervitaminosis D
  3. Praneoplastic; PTHrP, cytokines…
30
Q

What are the non-hormonal causes of Hypercalcaemia?

A
  1. Milk-alkali syndrome
  2. Renal failure
  3. Medications; Thiazide diuretics, Lithium
31
Q

What is Hypocalcaemia?

How is it measured?

A

Blood Ca level below 2.1mmol/l

Measured through ionised Ca;

cannot be accurately measured without knowing serum albumin levels

32
Q

What are the signs and symptoms of Hypocalcaemia?

A

Lowers depolarisation threshold; associated with increased activity

  1. Perioral tingling and parasthesia
  2. Tetany
  3. Facial spasms
  4. Hyper-reflexia
  5. Laryngospasm
  6. Cardiac arrhythmias
33
Q

What are the hormonal causes of Hypocalcaemia?

A

Hypoparathyroidism ee. Surgical removal

Autoimmune

Pseudo hypoparathyroidism (PTH receptor dysfunction)

Idiopathic

34
Q

What are the non-hormonal causes of Hypocalcaemia?

A

HypovitaminosisD; diet, rickets, osteomalacia

Organ dysfunction; GI mamabsorption, renal loss

Genetic; Ca-sensing receptor dysfunction

Or an endocrine response to a non-hypoparathyroid hypocalcaemia, causing secondary hyperparathyroidism?

35
Q

What is Rickets?

A

VitD deficiency in children

36
Q

What are the signs and symptoms of rickets?

A

Bowed legs

Abnormal amounts of unmineralised osteoid

Soft bones; easily fractured, loss of rigidity

37
Q

What is Osteomalacia?

A

VitD deficiency in adults

38
Q

What are the signs and symptoms of Osteomalacia?

A

Increased amounts of unmineralised osteoid

Reduced bone strength, easily fractured

Adults with VitD deficiency do not have bowed legs because epiphyses are fused, bone growth complete

39
Q

What does Ca-sensing receptor dysfunction cause?

A

Hypocalcuric-Hypercalcaemia (familial)

An inactivating mutation desensitises the receptor for Ca; higher Ca levels required to supress PTH

Mild in Hetero-, lethal in Homo- children due to extreme Hypercalcaemia

Also causes reduced Ca loss from urine

40
Q

What does PTH receptor dysfunction cause?

A

Pseudo-Hypoparathyroidism Hypocalcaemia

PTH levels are high but receptors are resistant. Caused by mutation i one of G subunits

41
Q

What 2 major factors are required for Ca absorption?

A

VitD

Sunlight

42
Q

Give examples of GI dysfunctions that reduce Ca absorption

A

Short bowel

Malabsorptive disorders

IBS

43
Q

Why might a high phosphate diet compromise Ca absorption?

A

Phosphate binds with high affinity for Ca;

With high PO4 less Ca is available for absorption

44
Q

Give examples of Renal dysfunctions that cause Hypocalcaemia

A

Abnormal response to PTH;

  • 1-a-hydroxyl activation
  • Ca reabsorption in tubules

Insufficiency of 1,25(OH)D3

Genetic tubular Ca leak;

  • hypercalciuria
  • secondary hyperparathyroidism
45
Q

What is the main cause of Hypercalcaemia?

A

Primary hyperparathyroidism;

Adenoma or hyperplasia of parathyroids

46
Q

What are the clinical features of primary hyperparathyroidism?

A

Hypercalcaemia

High PTH

Hypercalciuria

Increased fractures

Increased risk of kidney stones

47
Q

Renal failure-associated hypercalcaemia…

A

Renal failure can cause hyper- and hypo- calcaemia.

Hypercalcaemia due to;

Reduced tubular Ca clearance

Increased resorption from bones (high PTH)

Renal failure causes:

PTH elevation

Low endogenous 1,25(OH)D3

Abolished Ca and PO4 clearance (dialysis filters these poorly also)

48
Q

What are the causes of hypervitaminosis D?

A

Excess dietary intake; through supplements

Excess intrinsic production; Extra-renal 1-a-hydroxylase activity

Granulomas (MO) or lymphomas

1-a-OH not regulated by PTH or Ca

49
Q

What are the clinical features of Hypervitaminosis D?

A

HypoPTH

Hypercalcaemia

50
Q

Study this diagram of Ca homeostasis

A
51
Q

Study this diagram of VitD synthesis

A
52
Q

Name a population at risk of VitD deficiency

A

Finnish

Anyone with lack of sunlight

53
Q

What are the problems with using VitD and PTH as medications?

A

They are peptides; Will be digested if taken orally

54
Q

Ca, PTH & VitD feedback loops:

A
55
Q

Detailed Ca homeostasis diagram

A

Blwyddyn 1; Tymor 3 (13 decks)

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