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endocrinology > endocrine control of calcium metabolism > Flashcards

endocrine control of calcium metabolism Flashcards

1
Q

describe Ca

A

most abundant metal in human body
5th most abundant element
essential
diet should meet all the requirements - people eat more than they need, as long as no GI or kidney problems

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2
Q

role of Ca

A

neuromuscular excitability - signal in neurons to
muscle contraction, reduce excitability so muscles not hyperactive
strength in bones - made of Ca salts
intracellular secondary messenger - something change Ca signalling, keep low so can be increased with secondary messenger
intracellular co-enzyme
hormone/NT stimulus-secretion coupling - release of hormones reflux Ca to edge, Ca at bouton of neuron, couple vesicle to membrane eg B cell releasing insulin
blood coagulation (factor IV) - vital for binding to phospholipids

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3
Q

how is Ca in the body

A

most as Ca salts
99% in bone as hydrated Ca salt - hydroxyapatite crystals, salt of calcium and phosphorus, their metabolism is closely linked
some ionised as Ca2+
some bound to protein
tiny bit - soluble and unsoluble eg citrate and lactate salt
only unbound Ca2+ is active - the rest is sequestered away

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4
Q

proportions of different stores of Ca

A

50% ionised - 1.25mM - biologically active component
45% - bound to plasma proteins -1.13mM
5% - diffusible salts -0.13mM

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5
Q

total Ca vol

A

2.5mM

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6
Q

describe Ca handling by the body

A

intake 1000mg/24hr into GI tract
850mg/24hr lost faeces
rest go to the blood
balance between bone and blood - as long as rate of growth and destruction of blood is the same
some secretions from blood back to GI
minute amounts - invisible loss - in dead cells, hair nails
most regulation of Ca through kidney, as long as no major differences in bone turnover - excretion 150mg/reabsorption
only when homeostasis of Ca changes that you need to stop some being secreted or absorb/ingest more

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7
Q

what increases Ca conc

A 
parathyroid hormone (PTH)/parathormone 
1,25 (OH)2 Vitamin D3 - active form is dihydroxycholecalciferol or Calcitriol
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8
Q

what decreases Ca conc

A

calcitonin - regulation of this is less pronounced

biological effect less significant

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9
Q

what releases PTH

A

parathyroid glands

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10
Q

how many parathyroid glands are there

A

4

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11
Q

what produces calcitonin

A

parafollicular cells, part of thyroid gland - surround follicles and release calcitonin when Ca is too high

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12
Q

describe the Ca sensing receptor

A

system for detecting Ca conc - cell surface receptor
G coupled protein receptor, transmembrane region
ligand (Ca) bind to external binding site
cause conformational change in receptor - change how associates and activates G protein and how they go and act as cell signalling by activating cAMP
if high levels of Ca - inhibit PTH
if low Ca/antagonist for receptor is used - g protein change - PTH

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13
Q

what is parathyroid hormone

A

initially synthesised as pre-proPTH
cleaved in an intracellular process
PTH polypeptide = 84AA
binds to transmembrane G protein linked receptors
activation of adenyl cyclase and PLC as a second messenger
the G protein receptor depends on the type of tissue

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14
Q

PTH action on kidney

A

increases Ca reabsorption
increase phosphorus secretion
this homeostasis is co-regulated
stimulates 1alpha hydroxylase activity - increases 1,25 (OH)2 Vitamin D3 synthesis - acts on small intestine - increase Ca absorption, increase phosphorus absorption

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15
Q

PTH action in bone

A

osteoclast stimulated
osteoblast inhibited
increase bone resorption - free Ca trapped in bone is released
3Ca + 2PO4 – Ca3(po4)2 equilibrium

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16
Q

PTH effect on blood

A

preserves circulating Ca conc for muscle and neurone effect
sacrifice bone
in break down of bone phosphorus is released and not needed so it is got rid of

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17
Q

explain the mechanism of PTH action in bone

A

PTH bind to PTH receptor on osteoblast
releases osteoclast activating factors eg RANKL - regulate osteoclast
OAF bind to receptor on osteoclast - activate it - cause bone resorption

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18
Q

what does RANKL stand for

A

receptor activator of nuclear factor kappa-B ligand

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19
Q

describe PTH regulation

A

catecholamines (via B receptors) decrease Ca stimulate PTH - increases plasma Ca conc and causes synthesis of 1,25 (OH)2D3, which also increases plasma Ca conc
1,25(OH)2D3 -ve feedback on parathyroid gland - reduce PTH production

20
Q

describe the synthesis of 1,25(OH)2D3

A

from diet and 7-dehydrocholesterol in skin (with UV light) – cholecalciferol (vit D3)
25 hydroxy- cholecalciferol 25 (OH) vitD3, this is synthesised in the liver and stored in this form
enzyme 1 alpha hydroxylase - (stimulated by PTH) catalyse production of
1,25(OH)2 D3 - synthesised in kidneys and is the main active form
[need kidney and liver functioning normally to get the active form]

21
Q

what else does calcium receptor detect

A

kidney - ca excretion
GI - bind to AA
other cells - nutritional purposes

22
Q

vitamin D3 deficiency

A

because of where people come from and dress code
don’t know what normal range is and if it is different in different ethnicities
no signs of nationwide problems but a lot of ‘deficiency’

23
Q

action of 1,25(OH)2 D3

A

in kidney increase Ca and phosphorus reabsorption
Ca that is reabsorbed goes into bone
increases osteoblast activity of the bone ]in mall intestine increase Ca and phosphorus absorption
phosphorus reabsorbed from kidney inhibit absorption from SI
attempts to restore bone but has a longer, chronic effect - lays down salt
if you treat people just with this it isn’t necessarily good for the bone

24
Q

describe phosphate levels

A

pretty static

excreted in kidney

25
Q

what is fibroblast growth factor 23

A

regulates phosphate metabolism

high vit D stimulate FGF-23 production from osteocytes - stops phosphorus level in the blood getting to high

26
Q

describe phosphate reabsorption

A

Na/phosphorus cotransporter move both inside kidney
PTH and FGF-23 inhibit this
FGF-23 inhibit calcitriol
calcitriol stimulate FGF23

27
Q

what is calcitonin

A

synthesised as pre-procalcitonin - cleaved
calcitonin is 32aa polypeptide
bind to transmembrane G protein linked receptor
activation of adenyl cyclase/PLC as secondary messenger (depends on cell type)

28
Q

calcitonin regulation

A

increased plasma Ca and gastrin stimulate parafollicular cells - calcitonin
gastrin: from stomach - stimulates stomach acid release - sign of high Ca

29
Q

calcitonin actions

A

inactivation of osteoclast activity and increase urinary excretion of ca na and phosphorus
decrease plasma Ca - more difficult to knock it down than bring it up
human calcitonin has little effect

30
Q

endocrine causes of hypoglycaemia

A

hypoparathyroidism - too little PTH
pseudohypoparathyroidism
vit D deficiency

31
Q

signs of hypocalcaemia

A

tetany - trousseau’s sign - neuromuscular spasem@: easier for Na to enter when low Ca - neuron depolarises more - more AP and contraction
Chvostek’s sign - twitch in nose and lips when flick behind the ear

32
Q

causes of hypoparathyroidism

A

idiopathic - low circulating levels of PTH
hypomagnesaemia - low mg - GI, kidney and diet problem, chronic alcohol. Low mg - low ca - need mg for parathyroid function and downstream affect of PTH
suppression by raised plasma Ca levels

33
Q

what is pseudohypoparathyroidism known as

A

allbright hereditary osteodystrophy

34
Q

what happens in pseudohypothyroidism

A

target organ resistance to PTH

defective G protein

35
Q

features of pseudohypoparathyroidism

A

short stature, round face
low IQ - developmental and learning difficulties
subcutaneous calcification and various bone abnormalities - shortening of metacarpals
associated endocrine disorders - hypothyroidism, hypogonadism

36
Q

how can you diagnose pseudohypoparathyroidism

A

cells don’t respond to PTH when added artificially (they would in hypoparathyroidism)

37
Q

describe vitamin D deficiency

A

rickets in children - bow leg bone
osteomalacia - adults
clinical feature - decreased calcification of bone matrix resulting in softening of bone - fractures in adults

38
Q

ca, phosphorous and PTH levels in hypocalcaemia

A

hypopara - low Ca, high phos, low PTH
pseudo - low Ca, high phos, high PTH
vit D - low Ca, low phos, high PTH (low ca -ve feedback stim PTH)

39
Q

endocrine causes of hypercalcaemia

A

primary hyperparathyroidism
tertiary hyperparathyroidism
vit D toxicosis - have to take in a lot, eg if you take supplements

40
Q

primary hyperparathyroidism

A

adenoma

parathyroid - increase PTH - increase Ca - parathyroids not regulated by feedback mechanism

41
Q

secondary hyperparathyroidism

A

renal failure - parathyroids hyperplastic - produce a lot of PTH and cure renel failure
parathyroids - high PTH - low Ca - kidney disease stop kidney resporption - continue to produce PTH

42
Q

tertiary hyperparathyroidism

A

initial chronic low plasma ca

autonomous parathyroids - increase OTH - increase Ca - parathyroids grown so don’t respond to -ve feedback

43
Q

what happens in parathormone excess

A

kidney - high Ca, high phos excretion, polyurea, renel stones, nephrocalcinosis, high vit d3 synthesis
in GI - gastric acid can’t be neutralised - duodenal ulcers - high Ca stimulate the secretion of gastric acid - Ach and gastrin amplified by Ca - release more acid
bone - bone lesion, bone rarefraction, fractures

44
Q

effect of primary parathyroidism

A

clubbed fingers

marked periosteal bone erosion in terminal phalanges

45
Q

what is the endosteum

A

layer of connective tissue that line the bone marrow cavities

46
Q

what is renal calculi

A

stones in kidneys from crystallisation of minerals that normally dissolve

47
Q

where is calcitonin produced

A

the parafollicular cells

endocrinology (12 decks)

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