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CBE > Week 8 Calcium > Flashcards

Week 8 Calcium Flashcards

1
Q

Intracellular Ca2+ concentration and function

A

very low concentration (1microM)
reversible increase of Ca2+ can bind proteins -> cell processes

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2
Q

Extracellular Ca2+ concentration and function

A

High concentration (1mM)
1. bone mineralisation
2. maintain activity of excitable tissue

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3
Q

2 main types of Calcium in plasma

A
  1. ionised Ca2+ (free)
  2. albumin-bound Ca2+ (inactive)
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4
Q

which type of calcium is actively regulated

A

ionised calcium:
Its concentration is constant

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5
Q

which organs contribute to calcium balance

A

GI, Kidney, Bone

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6
Q

negative calcium balance leads to….

A

decrease in bone density

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7
Q

osteocytes

A

mechanosensor cells for bones
stimulates bone growth
may become osteoblasts

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8
Q

osteoclasts

A

bone resorption

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9
Q

osteoblasts

A

make bone

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10
Q

osteoblast - bone formation process - osteoid (bone matrix)

A
  1. osteoblast precursor
  2. osteoblast
  3. osteoid
  4. calcified osteoid
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11
Q

how long does it take for osteoid to mineralise

A

several days

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12
Q

how long for full mineralisation

A

several months

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13
Q

mineralisation main component

A

hydroxyapatite(calcium phosphate)

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14
Q

what is hydroxyapatite

A

calcium phosphate (& OH)
tiny crystals around collagen fibres, provides rigidity

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15
Q

what does mineralisation depend on?

A

calcitriol (active form of Vitamin D)

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16
Q

calcitriol deficiency leads to??

A

osteomalacia
rickets (kids)

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17
Q

alkaline phosphate (ALP) and mineralisation

A

An enzyme expressed by osteoblasts:
1. hydrolysis and releases inorganic phosphate ions
2. hydrolyses pyrophosphate (2 phosphate - inhibitor of mineralisation

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18
Q

osteoclast and bone resorption

A

multinucleate:
border adjacent to bone releases H+ and enzymes
enzyme:
carbonic anhydrase II, H+ generation.

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19
Q

which cells have RANK ligand

A

bone marrow stromal cells

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20
Q

which cells have RANK (receptor)

A

precursor osteoclasts

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21
Q

Characteristics of osteopetrosis

A

Increased bone density/mass
Increased fragility due to brittle structure.

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22
Q

cause of osteopetrosis

A

failure of matrix degradation by osteoclasts.

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23
Q

most common cause of osteoporosis

A

oestrogen drop after menopause

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24
Q

main cause of osteoporosis

A

increased bone resorption

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25
Q

what is Paget’s disease

A

overactive osteoclasts

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26
Q

calcitriol comes from?

A

steroid hormone -> from vitamin D

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27
Q

what does PTH regulate/how fast

A

-regulate ionised calcium levels
-minute-by-minute
increased in response to falling Ca2+

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28
Q

what controls PTH secretion

A

calcium receptors on cell -> senses calcium concentration

29
Q

what receptor is the calcium receptor

A

G protein coupled receptors

30
Q

PTH biochemical effects and what organs:

A
  1. calcium efflux from bone
  2. Ca2+ reabsorption (distal)
  3. bicarbonate and phosphate loss (proximal)
  4. Ca2+ absorption (intestinal)
31
Q

what stimulates/suppresses PTH system

A

(urinary calcium loss, decreased bone resorption, decreased calcitriol) will stimulate PTH release -> to reverse this action.

32
Q

principal function of calcitonin

A

to reduce osteoclast activity, treat high serum calcium.

33
Q

calcitonin as a biomarker(where is it secreted)

A

Secreted from thyroid gland:
1. medullary cancer of the thyroid
2. will increase when serum Ca2+ increases

34
Q

cholecalciferol (Vitamin D) to calcitriol production pathway

A
  1. Has a precursor on skin, converted through sunlight UV
  2. cholecalciferol is converted to calcitriol in the liver and kidney
35
Q

calcitriol synthesis pathway

A
  1. 25 hydroxylase adds OH to cholecalciferol (Liver)
  2. 25-OH vitamin D functions constitutively
  3. 1alpha-hydroxylse adds another OH to 25-OH vit D. (Kidney)
  4. 1,25 (OH)2 vitamin D is stimulated by PTH, calcium can affect its activity.
36
Q

calcitriol effect, and affect what organs

A

Maintain calcium and phosphate levels:
By itself:
- increase Ca2+ and PO4- absorption (GI)

with PTH:
- Increases bone resorption and stimulate osteoclast (RANKL).
- Increases renal Ca2+ reabsorption.

37
Q

difference between calcitriol (VitD) and PTH

A

PTH leads to phosphate loss (renal - proximal tubule)
Calcitriol leads to phosphate increase (GI absorption)

PTH is short term, calcitriol is long term Ca2+ regulation.

38
Q

how does PTH affect calcitriol

A

PTH stimulates 1alpha hydroxylase

39
Q

how does calcitriol affect PTH

A

calcitriol deficiency -> impaired PTH signalling
calcitriol can switch off PTH gene transcription via vitamin D receptor.

40
Q

how does calcitriol promote its own inactivation

A

activates 24 hydroxylase

41
Q

hypercalcaemia clinical manifestations

A

stones: renal stones
bones
muscle weakness: competition with inward Na+ flux.
abdominal moans: pain
psychic groans: depression…

42
Q

non-pathological hypercalcaemia

A

Due to high plasma albumin -> raised calcium:
1. dehydration
2. intravenous injection albumin
3. venous stasis

43
Q

Primary hyperparathyroidism causes

A

(90%) solitary adenoma
hyperplasia
(rare) carcinoma

44
Q

Secondary hyperparathyroidism cause

A

PTH increase due to low calcium. (appropriate)

45
Q

Tertiary hyperparathyroidism causes

A

Results from chronic secondary hyperparathyroidism:
secondary gland becomes overactive

46
Q

1y hyperparathyroidism biochemistry

A

Increased calcium, Increased PTH
Low bicarbonate and phosphate
normal ALP
moderately elevated ALP when severe

47
Q

treatment of 1y hyperparathyroidism

A

Immediate - treat high calcium:
1. rehydration
2. drugs
Definitive:
Remove of adenoma

48
Q

imaging of hypercalcaemia

A

renal stones

49
Q

treatment of hypercalcaemia

A
  1. calcitonin - reduce osteoclast activity
  2. bisphosphonates - inhibits bone resorption and osteoclast activity.
  3. furosemide - diuretic, inhibit Ca2+ reabsorption
  4. glucocorticoid: prolong calcitonin effect
50
Q

why are hypercalcaemias common in malignancies

A
  1. Metastasis deposit on bone and directly activate osteoclasts
  2. release endocrine factors that act on bone
51
Q

what disease affects calcitriol levels

A

Hodgkin’s lymphoma and Sarcoidosis
Has 1 hydroxylase activity, so it will contribute to calcitriol synthesis.

52
Q

solid tumours and endocrine factors

A

some solid tumours secrete PTH-related peptide
but PTHrP is difference from PTH, PTH level is also suppressed.

53
Q

name when PTHrP is the cause of hypercalcaemia

A

humoral hypercalcaemia of malignancy

54
Q

metastatic breast tumour and hypercalcaemia

A

locally produce PTHrP

55
Q

multiple myeloma and hypercalcaemia

A

activate osteoclasts through cytokines like RANKL

56
Q

Malignancy biochemistry diagnosis - hypercalcaemia

A

Raised calcium & ALP
High phosphate
Low PTH

57
Q

Hypercalcaemia - malignancy vs adenoma - biochemistry

A

Adenoma will have high PTH, low phosphate
Malignancy will have low PTH, high phosphate.

Adenomas rarely have elevated ALP due to a modest bone turnover.
Whereas malignancy may have very high ALP due to a much less controlled bone turnover.

58
Q

sarcoidosis and hypercalcaemia

A

has 1hydroxylase activity, synthesise calcitriol, high calcium, normal PTH.

59
Q

familial hypocalciuric hypercalcaemia (FHH)

A

Ca2+ sensing receptors are less sensitive.
PTH and Ca2+ have a higher set point now.
elevated PTH and Ca2+ in blood.
Low urine calcium (excretion) is due to PTH elevation.

60
Q

factitious hypocalcaemia

A

low albumin, less calcium:
1. nephrotic syndrome
2. liver disease, less protein synthesis
3. malnutrition

61
Q

causes of low 1,25 vitamin D

A
  1. malabsorption
  2. inadequate sunlight
  3. diet factors
  4. chronic renal disease

rarely enzyme issues

62
Q

what does calcitriol deficiency lead to (steps)

A
  1. low calcium
  2. high PTH (2ndary hyperp)
  3. low phosphate
  4. high bone resorption
  5. high ALP
63
Q

osteomalacia and calcitriol

A

low calcitriol meaning that osteoid cannot be calcified properly

64
Q

inherited causes of osteomalacia

A
  1. deficient 1 hydroxylase (low calcitriol)
  2. low ALP
  3. low phosphate
  4. defective calcitriol receptor
65
Q

causes of hypoparathyroidism

A
  1. surgical damage or removal of parathyroid.
  2. suppressed secretion (maternal hypercalcaemia)
66
Q

hypocalcaemia biochemical effects

A

low Ca2+ and low PTH. Phosphate may be elevated

67
Q

treatment of hypocalcaemia

A

doses of calcium and vitamin D or calcitriol

68
Q

(aging) osteoporosis vs osteomalacia

A

osteoporosis has a normal histology (less bone density) and relatively normal biochemistry.
osteomalacia has an abnormal histology and biochemistry

69
Q
A

CBE (16 decks)

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