calcium regulation

Question 1

what substances in the blood can increase serum calcium?

Answer 1

-vitamin D (skin or diet)
-PTH SECRETED by parathyroid gland

Question 2

what subst in blood can decrease serum calcium?

Answer 2

calcitonin, significant effect however its removal (after parathyroid cells removed) doesnt make a difference interestingly

Question 3

what organs are the main regulators of calcium and phospate

Answer 3

gut, kidney, bone

Question 4

(look at ipad) what reactions happen in skin cells in vit d synthetic process?

Answer 4

7- dehydrocholesterol -> pre vitamin D3 -> vitamin D3

Question 5

what is vitamin d3 converted to? where? by what enzyme?

Answer 5

25 (OH) CHOLECALCIFEROL BY 25 HYDROXYLASE IN TH ELIVER

Question 6

what is 25 (OH) cholecalciferol converted to? where? by what enzyme?

Answer 6

1,25 (OH)2 cholecalciferol by 1 alpha hydroxylase in the kidney

Question 7

what is calcitriol?

Answer 7

1,25 (OH)2 cholecalciferol / active vit D

Question 8

what is the measured indicator for vit d?

Answer 8

25-OH cholicalciferol (or 25-OH vit d)

Question 9

how does calcitriol regulate its synthesis?

Answer 9

by decreasing the transcription of 1 alpha hydroxylase

Question 10

what are the effects of lacitriol on calcium and phosphate absorption/ reabsorbtion/ secretion in gut bone and kidn?

Answer 10

kidney and gut both incr serum calcium bc incr reabsorption/ absorption
bone: decreases serum calcium because incr OSTEOBLAST activity

Question 11

what are the direct actions of pth on calcium adn phosphate levels

Answer 11

increases OSTEOCLAST activity in bone so increasing calcium in serum

in kidney:
-incr calcium reabsorption
-incr phosphate EXCRETION

Question 12

what are the indirect effects of pth on calcium and phosphate levels? what substance is involved?

Answer 12

PTH increases 1 a hydroxylase activity :
-> increases 1,25 (OH)2D3 synthesis
-> increases ca and po reabsorption in GUT

(SO OVERALL: PTH: KIDNEY AND BONE: DIRECT, GUT: INDIRECT)

Question 13

what is the effect of hyperparathyroidism on serum phosphate levels? what is the mechanism?

Answer 13

remember: P.T.H: please transporter halt

-phosphate is reabsorbed in the kidney by na/ phosphate co-transporters
-PTH inhibits this transporter
- leads in less phosphate reabsorption so low phosphate in serum and more excreted

Question 14

what is FGF23 derived form? what are its mechanisms for influencing serum phosphate levels?

Answer 14

derived from bone,
1) inhibits same transporters as PTH
2) Inhibits calcitriol ( leads to less phosphate reabsorption form gut) (indirect)

Question 15

signs and sympotms of hypocalcemia

Answer 15

CAT goes numb

convulsions
arrhythmias
tetany

paraesthesia (nmbness in mouth, hands, feet, lips)

Question 16

what is tetany

Answer 16

involuntary contraction of muscles due to LOW calcium levels

Question 17

what are convulsions

Answer 17

rapid uncontrolable muscle movements like spasm

Question 18

what is chvosteks’ sign

Answer 18

a specific facial paresthesia: when you tap check below eye and they close their eye on that side

Question 19

what is trousseaus sign?

Answer 19

a specific type of tetany: carpopedal spasm (basically tetany below wrist/ palm)

Question 20

causes of hypocalcaemia

Answer 20

• Low PTH levels
  -low vitamin D

Question 21

DEFICIENCY in what chemical element/ mineral can cause low pth levels

Answer 21

magnesium

Question 22

causes of low PTH:

Answer 22

SURGery in neck
autoimmune
congenital (agenesis: rare)
MAGNESIUM DEFICIENCY

Question 23

causes of vit d def

Answer 23

poor diet/ malabsorption
low uv exposure
impaired productIon (RENAL FAILURE) !!!

Question 24

what happens to calcium levels in hypoparathyroidism?

Answer 24

decrease (hypocalcaemia)

Question 25

AS a rule of thumb are systems underacting or overacting in hypercalcaemia?

Answer 25

under- so they overeact in hypo

Question 26

what are the specific symptoms in hypercalcaemia?

Answer 26

broken bones, stones, psychic groans and abdominal moans, low muscles tones

Question 27

specific renal effects- what si the medical name of having stones

Answer 27

nephrocalcinosis: kidney stones, renal colic (pain cuased by kidney trying to pass urine when theres kidney stone)

Question 28

specific abdominal symptoms - GI effects

Answer 28

Anorexia (loss of apetite), nausea, dyspepsia, constipation, pancreatitis (mechanism is unclear )

Question 29

Psychic groans - CNS effects specific, in which cases do these usually arise?

Answer 29

Fatigue, depression, impaired concentration, altered mentation, coma (usually >3mmol/L : probably very intense symptoms)

Question 30

causes of hypercalcaemia and most common cause

Answer 30

primary hyperparathyroidism (most common) , malignancy, vit d excess (rare)

Question 31

what happens in primary hyperparathyroidism, what is the cause?

Answer 31

too much pth, usually due to parathyroid gland adenoma (benign tumour) no negative feedback, due to AUTONOMOUS PTH SECRETION from adenoma: (body has enough calcium and pth is still abnormally released: more calcium absorbed)

Question 32

what cancers usually cause hypercalcaemia and how?

Answer 32

bony metastases produce local factors to activate osteoclasts Certain cancers (eg squamous cell carcinomas) secrete PTH-related hormones (like a peptide that acts at PTH receptors

Question 33

HOW TO REMEMBER SPECIFIC LITTLE differences in pth and calcitriol effcets on excretions and absorptions

Answer 33

they both generally increase both calcium and phosphate from everywhere except from: 1) calcitriol: in bone: osteoblasts: steal ca from blood 2) pth: in kidney: increases phosphate EXCRETION - remove from blood

Question 34

effect of primary hyperparathyroidism on phosphate?

Answer 34

low phosphate: increased renal phosphate excretion (inhibition of Na+/PO43- transporter in kidney)

Question 35

what is the treatment of primary hyperparathyroidsim?

Answer 35

Parathyroidectomy is treatment of choice for primary hyperparathyroidism

Question 36

what are the risks of untreated hyperparathyroidism?

Answer 36

Osteoporosis Renal calculi (stones) (Hypercalcemia: bad on bones too much calcium deposition makes them brittle ) Psychological impact of hypercalcaemia – mental function, mood

Question 37

what is secondary hyperparathyroidism? (what pth and ca levels and why)

Answer 37

- clacium low or normal - PTH high as a responce/ secondary to the low calcium

Question 38

difference bwteen prim and secondary hyperparathyroidsim?

Answer 38

both pth high, calcium high in primary, low in secondary (means problem is not in the actual gland-like in primary, its in the calcium level)

Question 39

what is the most common cause of secondary hyperparathyroidism?

Answer 39

vit d deficiency commonly: diet and sunlight less common: renal failure: cant make calcitriol (Active vit d)

Question 39

common type of vit d in food

Answer 39

vit d2- ergocalciferol Ithing of ergo- energy in food)

Question 39

treatment of secondary hyperparathyroidism if renal function normal?

Answer 39

- vit d replacement: Give 25 hydroxy vitamin D: either 1) ergocalciferol: 25 hydroxy vitamin D2 or 2)cholecalciferol: 25 hydroxy vitamin D3

Question 40

treatment of secondary hyperparathyroidism if renal function abnormal?

Answer 40

inadequate 1a hydroxylation, so can’t activate 25 hydroxy vitamin D preparations (no point in giving vit d they cant do anything with it so they need special vit d cant use over counter ) -need alfacalcidol -1a hydroxycholecalciferol

Question 41

what is the difference between secondary and tertiary hyperparathyroidism? describe mechanism of disease in tertiary- treatment?

Answer 41

-the have same biochemistry : high pth low calcium but tertiary is when there is CHRONICALLY low calcium, -so the parathyroids have been overworking for a long time to produce PTH so they start growing (all 4 glands hyperplasia) and releasing "basally" more pth than normal (diseased glands) - this means that in contrast to secondary, parathyroids are damaged and treatment is removal (parathyroidectomy)

Question 42

why does renal failure cause vit d def?

Answer 42

bc a 25 hydrohylase is in kidney and calcitriol produced by it in kidney

Question 43

most common cause of tertiary hyperparathyroidism and on eless common in uk maybe more in developing counr

Answer 43

1) chronic renal failure 2) chronic malnutrition

Question 44

when is there low PTH and hypercalcaemia?

Answer 44

malignancyy (bc parathyroid is doing its job fine, issue is alciujm secretion atopically)

Question 45

Management of hypercalcaemia of malignancy? (bone cancer)

Answer 45

1) hydration 2) if nauseus??: BISPHOSPHONATES – INHIBIT OSTEOCLASTS AND STOP THEM FROM ABSORBING BONE LOWERS CALCIUM, LESS BONY PAIN