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GERR > Lecture 25: Calcium Metabolism > Flashcards

Lecture 25: Calcium Metabolism Flashcards

1
Q

how is calcium homeostasis maintained

A

tightly regulated ion transport by GIT, bone and kidneys

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2
Q

what % of total plasma Ca2+ is free

A

50%

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3
Q

which form of Calcium is metabolically active and has biological effects

A

ionised (free) calcium

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4
Q

list the molecules that calcium binds to in the plasma

A
  • anions
  • albumin
  • globulin
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5
Q

what are the 2 variables that affect the proportion of calcium that is free or bound

A
  • albumin conc.

- blood pH

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6
Q

how does pH affect the proportion of free or bound plasma Ca2+

A
  • H+ ions also bind to albumin
  • H+ can displace Ca2+
  • iCa2+ ^
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7
Q

name the 3 hormones that act to regulate Ca2+ homeostasis

A
  • parathyroid hormone (parathormone)
  • activated Vit D
  • calcitonin
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8
Q

what are the 2 other names for activated Vit D

A
  • -> 1,25-dihydroxycholecalciferol

- -> calcitriol

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9
Q

what stimulates release of parathyroid hormone

A
  • low Ca2+
  • ^ phosphate
  • low Mg2+
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10
Q

name the cells on parathyroid glands that detect low calcium levels

A

chief cells

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11
Q

describe the action of parathyroid hormone in Ca2+ homeostasis

A

main role is to ^ Ca2+ levels in the blood

Bone

  • short term: rapid exchange from bone pool to ECF
  • long term: resorption by osteoclasts

Kidney

  • reabsorption of Ca2+
  • excretion of phosphate (reciprocal relationship)
  • formation of 1,25-dihydroxycholecalciferol

Intestine
- Ca2+ reabsorption

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12
Q

name regulators for active Vit D

A
  • PTH

- low phosphate

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13
Q

what type of hormone is Vit D

A

steroid hormone –> derived from cholesterol

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14
Q

name the main enzyme involved in Vit D activation in the kidneys

A

1 a-hydroxylase

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15
Q

describe the action of activated Vit D in Ca2+ homeostasis

A

Intestine

  • ^ Ca2+ absorption
  • ^ Ca2+ transport prots –> calbindin-D prots

Kidneys
- facilitates Ca2+ absorption

Bone
- ^ calcification and mineralisation

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16
Q

what mediates Vit D action

A
  • receptors
  • Vit D is a steroid hormone w/ genomic effects
  • binds to receptor on nucleus
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17
Q

describe the difference between rickets and osteomalacia

A

rickets = Vit D deficiency in child

osteomalacia = Vit D deficiency in adult

18
Q

list some causes of rickets and osteomalacia

A
  • lack of dietary Vit D and/or sunlight
  • malabsorption of fats
  • failure to form calcitriol –> chronic renal failure
  • mutation in 1 a-hydroxylase
  • mutations in VDR
19
Q

what are the 4 fat soluble vitamins

A

A,D,E,K

20
Q

outline a basic difference between osteoporosis and osteomalacia

A

osteoporosis = normal bone just not enough

osteomalacia = abnormal soft bone which hasn’t been mineralised

21
Q

what people are at risk of Vit D deficiency

A
  • elderly people
  • house-bound people
  • those who cover up a lot in the sun
  • those who where sunscreen all year
  • those with dark skin
22
Q

why are people with dark skin at risk of Vit D deficiency

A
  • they require more sun exposure to make as much Vit D

- sunlight needs to penetrate through layer of melanin to layer that manufactures Vit D

23
Q

where is calcitonin produced

A

in thyroid gland by C cells

24
Q

name a regulator of calcitonin secretion

A

^ Ca2+

25
Q

describe the action of calcitonin

A

Bone
- inhibits resorption

Kidneys
- ^ Ca2+ excretion

26
Q

list some other hormones that influence bone (inc. or dec. bone growth)

A

increase

  • androgens
  • growth hormone and IGF
  • thyroid hormone
  • prolactin

decrease

  • glucocorticoids
  • inflammatory cytokines
27
Q

what is a major pathogenic factor that causes faster bone loss in women over men

A

oestrogen deficiency

28
Q

what is normal calcium levels

A

2.35-2.55 mmol/L

29
Q

what is abnormal calcium levels

A

> 3.5 mmol/L –> hypercalcaemia

<1.9 mmol/L –> hypocalcaemia

30
Q

what is hypocalcaemia

A

dec. serum Ca2+

31
Q

give some causes of hypocalcaemia

A
  • hypoparathyroidism
  • pseudohypoparathyroidism
  • Vit D deficiency
32
Q

what are some clinical signs of hypocalcaemia

A
  • neuromuscular excitability followed by tetany
  • Chvostek’s sign
  • Trousseau’s sign
33
Q

explain how hypocalcaemia can result in tetany

A
  • normally Ca2+ block Na+ from entering cells
  • when Ca2+ low it’s easier for Na+ to enter cells
  • cells depolarise easier
  • tetany
34
Q

explain how hypocalcaemia can result in tetany

A
  • normally Ca2+ block Na+ from entering cells
  • when Ca2+ low it’s easier for Na+ to enter cells
  • cells depolarise easier
  • reduced AP threshold
  • tetany
35
Q

what is Chvostek’s sign

A

tapping on face anterior to ear and below zygomatic bone causes ipsilateral facial twitching

36
Q

what is Trousseau’s sign

A

inflation of BP cuff above SBP for several mins causes muscle contraction incl. flexion of wrist and MCP joints, hyperextension of fingers, and flexion of thumb on palm

37
Q

what is hyperparathyroidism

A

^ PTH

38
Q

what causes primary, secondary and tertiary hyperparathyroidism

A

1st = problem in gland itself e.g. PTH secreting adenoma

2nd = (stimulus is low Ca2+) problem in kidney/ kidney failure

3rd = chronic secondary hyperparathyroidism –> PT glands become autonomous and keep secreting PTH

39
Q

give some clinical signs of hypercalcaemia

A
  • bone pain
  • kidney stones
  • GI disruption e.g. abdominal pain, constipation
  • CNS disturbance e.g. muscle weakness, lethargy
40
Q

what would be seen on an ECG trace for hypo/hypercalcaemia

A

hypo = long QT interval

hyper = short QT interval

GERR (46 decks)

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