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Endocrinology > Endocrine Control of Calcium Metabolism (12) > Flashcards

Endocrine Control of Calcium Metabolism (12) Flashcards

1
Q

what form is calcium usually found as in the body

A

calcium salts.

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2
Q

what are the multiple roles of calcium

A

Neuromuscular excitability. Muscle contraction. Strength in bones. Intracellular second messenger. Intracellular co-enzyme.
Hormone/ neurotransmitter stimulus-secretion coupling. Blood coagulation (factor IV)

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3
Q

where is calcium mainly found

A

mainly found in bone (99%, approx. 1kg) as complex hydrated calcium salt (hydroxyapatite crystals).

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4
Q

how is calcium present in the blood

A

as unbound ionised calcium (which is the biologically active component), bound to plasma proteins, or a tiny bit is left as soluble salts. It is present in the blood in dynamic equilibrium

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5
Q

what calcium is bioactive

A

the free unbound Ca2+

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6
Q

what is the total blood [Ca2+]

A

~2.5mM. 1.25mM is unbound, 1.13mM is bound and 0.13mM is a soluble salt

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7
Q

what percentage of calcium is bound, unbound or a soluble salt

A

50% unbound (ionised), 45% bound to plasma proteins and 5% as diffusible salts

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8
Q

how is calcium handled by the body

A

intake via diet (~1000mg/24hr). then absorbed via GI tract into the blood. Some is excreted as faeces (~850mg/24hr). Once in the blood calcium can pass into the kidneys and regulate the content or the blood. A lot of calcium entering into kidney returns into the blood. Some is lost in urine (~150mg/24hr). The hydroxyapatite crystals in the bone can be broken down to increase blood calcium levels. There is invisible loss of calcium via dead cells, hair, nails etc.

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9
Q

what two hormones increase [Ca2+] in the blood

A

parathyroid hormone (PTH) and 1,25 - dihydroxycholecalciferol (calcitriol)

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10
Q

what hormone decreases [Ca2+] in the blood

A

calcitonin

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11
Q

how many parathyroid glands are there

A

four

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12
Q

where is parathyroid hormone PTH released

A

the parathyroid gland

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13
Q

where is calcitonin produced

A

in the parafollicular cells

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14
Q

describe the structure of the parathyroid glands

A

made up of follicles with parafollicular cells

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15
Q

describe the structure of parathyroid hormone / parathormone/ PTH

A

initially synthesised as protein pre-pro-PTH. its 84 aa polypeptide. binds to transmembrane G-protein linked receptors. when it binds to the G-protein linked receptor it leads to activation adenylate cyclase, with phospholipase C acting as a 2nd messenger

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16
Q

what are the actions of PTH on the kidneys

A

Increased Ca2+ reabsorption from tubular fluid in the proximal and distal tubules. Increased PO43- excretion in urine. Stimulates 1a hydroxylase activity which hydroxylases 25 OH Vit D3 to calcitriol (1,25(OH)2D3). The calcitriol then acts on the small intestine

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17
Q

what are the actions of PTH on the small intestine

A

The 1,25 (OH)2D3 acts to increase Ca2+ absorption into the blood and increase absorption of PO43-. these both lead to an influence in the blood calcium conc.

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18
Q

what are the actions of PTH on bones

A

stimulates osteoclasts (breakdown). inhibits osteoblasts (rebuilding). this leads to increased bone reabsorption.

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19
Q

what effect does PTH have on blood

A

PTH causes increased Ca2+ reabsorption and increased PO43- excretion from the kidneys. Increased Ca2+ and PO43- absorption from the small intestine. Increased Ca2+ mobilisation due to increased osteoclast activity. These all lead to increased Ca2+ conc in blood

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20
Q

what is the action of PTH in bone (in detail)

A

PTH leads to inhibition of new bone formation. It binds to PTH receptor on osteoblasts, which stimulates osteoclast activating factors (OAFs e.g RANKL). The OAFS stimulate osteoclasts to increase bone matrix breakdown and release Ca2+ and PO43+ which leads to increased bone reabsorption.

21
Q

why doesn’t PTH have a direct effect on osteoclasts

A

there are no receptors present

22
Q

how is PTH regulated

A

decreased plasma [Ca2+] causes increased PTH production in parathyroid glands. This leads to increased plasma [Ca2+]. The increased Ca2+ has a negative feedback on parathyroid glands.

23
Q

what does increased PTH lead to (with regards to PTH regulaton)

A

synthesis of calcitriol which leads to increased plasma [Ca2+]. Calcitriol also has a -ve feedback effect on the parathyroid glands to reduce PTH production which then reduces [Ca2+]. Catecholamines stimulate the beta receptors on the cells producing PTH so they secrete more PTH.

24
Q

How is calcitriol/ 1,25 (OH)2D3 synthesised

A

its precursor is cholecalciferol (Vitamin D3). Vitamin D3 is a steroid that circulates around the body and is taken up by the liver. enzyme 25-hydroxylase converts it to 25-hydroxy-cholecalciferol which is then stored in the liver. It then circulates from the liver to the kidney. enzyme 1alpha hydroxylase (stimulated by PTH) converts 25-hydroxy-cholecalciferol to calcitriol.

25
Q

what are the two main sources of cholcalciferol/vitamin D3

A

diet and sunlight. UV B works on the skin to convert 7-dehydrocholesterol to cholecalciferol

26
Q

what are the actions of 1,25(OH)2D3 aka calcitriol

A

acts on the small intestine to increase Ca2+ absorption and PO43- absorption. this causes increased osteoblast activity in the bone and therefore increased storage of Ca2+ in bone. In the kidneys it increases Ca2+ and PO43- reabsorption in the proximal tubule

27
Q

How is phosphate reabsorbed

A

there are phosphate ion transporters on the apical membrane. PTH inhibits this transporter so phosphate will not be reabsorbed so it will be excreted in the urine. calcitriol can also block the phosphate transporter through the FGF23 molecule.

28
Q

describe the structure and function of calcitonin

A

Synthesized as pre-procalcitonin. Calcitonin is 32 aa polypeptide. Binds to transmembrane G-protein linked receptor which leads to activation of adenyl cyclase or PLC as second messenger systems

29
Q

how is calcitonin regulated

A

increased plasma [Ca2+] and gastrin stimulates the parafollicular cells of the thyroid to produce calcitonin

30
Q

what is the action of calcitonin

A

in the bone it inhibits osteoclast activity which decreases plasma [Ca2+]. in the kidneys it increases urinary excretion of Ca2+ (Na+, PO43-) which again decreases the plasma conc.

31
Q

what are some endocrine causes of hypocalcaemia

A

hypoparathyroidism (cells respond to PTH) pseudohypoparathyroidism (cells don’t respond to PTH) and vitamin D deficiency

32
Q

what are the two ways hypocalcaemia can be shown

A

trousseau’s sign and chvostek’s sign. These are both forms of tetany, which is where smooth muscle goes into auto-contraction.

33
Q

what are the causes of hypoparathyroidism

A

consequence of thyroid surgery. idiopathic. hypomagnesaemia. suppression by raised plasma [Ca2+]

34
Q

what is Pseudohypoparathyroidism aka allbright hereditary osteodystrophy

A

due to target organ resistance to PTH (multiple underlying causes). believed to be due to defective Gs proteins

35
Q

what are the features Pseudohypoparathyroidism

A

Particular physical appearance (short stature, round face). Low IQ. Subcutaneous calcification and various bone abnormalities (e.g. shortening of metacarpals). Associated endocrine disorders (e.g. hypothyroidism, hypogonadism)

36
Q

what does vitamin D deficiency cause

A

rickets in children. osteomalacia in adults.

37
Q

what is the clinical feature of vitamin D deficiency

A

decreased calcification of bone matrix resulting in softening of bone this leads to bowing of bones in children and fractures in adults

38
Q

describe the differential diagnosis of hypoparathyroidism

A

Decreased Plasma [Ca2+]. Increased Plasma PO43-. Reduced PTH

39
Q

describe the differential diagnosis of pseudohypoparathyroidism

A

Decreased Plasma [Ca2+]. Increased Plasma PO43-. Increased PTH

40
Q

describe the differential diagnosis of vitamin D deficiency

A

Decreased Plasma [Ca2+]. Decreased Plasma PO43-. Increased PTH

41
Q

what are some endocrine causes of hypercalcaemia

A

Primary Hyperparathyroidism. Tertiary Hyperparathyroidism. Vitamin D Toxicosis

42
Q

what is primary hyperparathyroidism

A

a tumour in the parathyroid causes a large increase in PTH secretion. as it is a tumour it is unlikely to be regulated by the normal negative feedback - it will continue to produce large amounts of PTH leading to an increased plasma [Ca2+]

43
Q

what is secondary hyperparathyroidism

A

Some people have low plasma [Ca2+] due to renal failure. renal failure leads to loss of calcium in the urine which will stimulate the parathyroid to release PTH which will do its best to maintain the plasma calcium ion level

44
Q

what is tertiary hyperparathyroidism

A

Initial chronic low plasma calcium ion concentration. The parathyroid gland is being massively stimulated for a long time. The PTH becomes autonomous and it stops responding to the negative feedback
This is similar to primary hyperparathyroidism as it causes an increased plasma calcium ion level

45
Q

what happens when there is parathyroid hormone excess in the kidneys

A

More Ca reabsorption. More PO4 excretion  Polyuria. Renal stones. Nephrocalcinosis. More 1,25 (OH)2 D2 synthesis

46
Q

what happens when there is parathyroid hormone excess in the GI tract

A

gastric acid. duodenal ulcers

47
Q

what happens when there is parathyroid hormone excess in the bone

A

bone lesions. bone rarefraction and fractures

48
Q

what is the clinical feature of primary hyperthyroidism

A

clubbing of the fingers and marked periosteal bone erosion in the terminal phalanges

Endocrinology (12 decks)

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