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MET2 > Calcium > Flashcards

Calcium Flashcards

1
Q

Explain what happens to serum Ca2+ levels during acidosis and alkalosis [2]

A

Acidosis: causes Ca2+ to increase

Alkolosis: causes Ca2+ to decrease

Ca2+ and H+ bind to same place on albumin: acidosis the H= competes with Ca2+ and causes more ionised Ca2+ in the blood

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2
Q

What is the difference in extracellular and intracellular Ca2+ levels? [1]

What does low Ca2+ mean with regards to membrane excitatbility? [1]

A

What is the difference in extracellular and intracellular Ca2+ levels? [1]
Ca2+ greater extracellularly [1]
(Intracellular calcium: 99% is in complexes within the mitochondrial compartment)

What does low Ca2+ mean with regards to membrane excitatbility? [1]
Low Ca -> high membrane excitability.

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3
Q

Explain which is worse out of hyper or hypocalcemia

A

Very low Ca2+ is more dangerous immediately:

As serum calcium falls, there is less blockage of Na+ channels by Ca2+ in cardiac cells causing cardiac AP
Fall in Ca2+ makes AP easier to fire / lowers threshold which causes: arrhythmias and tetany

= SUDDEN CARDIAC DEATH

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4
Q

Explain the importance of Ca2+ in cardiac AP [1]

How does low

A

Calcium is involved in maintaining the plateau phase:
- Na in
- Ca out.

Extracellular Ca2+: blocks the voltage gated Na channels in the cardiac cell membrane.

Low Ca2+ levels: less blockade of VGNaCs = tachyarrhythmias

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5
Q

Parathyroid hormone (PTH) is secreted from which hormone? [1]

Effect of PTH secretion? [3]

A

PTH from parathyroid

PTH causes: overall increase in Ca2+ serum levels by:

  • Increased renal Ca2+ reabsorption.
  • Increased bone Ca2+ release.
  • Increased gut absorption via release of vitamin D (1,25vitD).
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6
Q

What inhibits the release of PTH? [1]

A

Ca2+ levels being too high (-ve feedback)

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7
Q

What are the two cells of the parathyroid and what are their functions? [2]

A

Parathyroid gland:
- Chief cell: produces PTH
- Oxyphil cells: unknown

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8
Q

What is the precursor to PTH ? [2]

A

Prepro PTH –> ProPTH –> PTH

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9
Q

What type of molecule is Ca2+ sensing receptor in parathyroid gland?

Enzyme linked
Tyrosine Kinase
GPCR
Nucleus binding

A

What type of molecule is Ca2+ sensing receptor in parathyroid gland?

Enzyme linked
Tyrosine Kinase
GPCR
Nucleus binding

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10
Q

What is the effect of Ca2+ binding to Ca2+ sensing receptor on parathyroid? [3]

A

Ca2+ binds to Ca2+ sensing receptor on parathyroid. Causes:
* Reduces PTH secretion
* Increases breakdown of stored PTH in vesicles
* Suppresses transcription of PTH gene.

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11
Q

What is the activated form of vitamin D? [1]

A

1α,25-dihydroxyvitamin D

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12
Q

Name 3 determinants of PTH secretion and how the effect PTH [6]

A

1,25-dihydroxycholecalciferol: aka Calcitriol Suppresses PTH secretion (which lowers Ca2+ levels)

Phosphate: stimulates PTH gene transcription

Cincalcet: activaates CaSR: reduces Ca2+

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13
Q

What effect does the inactivaton of CaSR have? [1]

What effect does the overactivation of CaSR have? [1]

A

What effect does the inactivaton of CaSR on parathyroid gland have? [1]
Hypercalcemia: no -ve feedback

What effect does the overactivation of CaSR on parathyroid gland have? [1]
Hypocalcaemia: too much -ve feedback

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14
Q

Why does PTH cause an increase in phosphate excretion?

A

Bone is broken down to release Ca2+, but also P is released

Therefore the kidney needs to excrete P to compensate

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15
Q

Effect of PTH on

a) Kidney [2]
b) Bone [2]
c) Intestine [2]

A

Effect of PTH on

a) Kidney: decreases Ca2+ excretion AND increases P excretion (one is broken down to release Ca2+, but also P is released. Therefore the kidney needs to excrete P to compensate)
b) Bone: Increases Ca2+ and phosphate reabsorbtion
c) Intestine: Increases Ca2+ and phosphate

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16
Q

Which areas of nephron cause reabsorbtion of Ca2+ dependently / independently of PTH? [3]

A

PCT: independent
LoH: independent
DCT: PTH dependent

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17
Q

Explain how Ca2+ is reabsorbed at PCT [2]

A

At PCT:
- independent of PTH
- Driven by NaKCl2 channel causing a voltage gradient paracellularly which Ca2+ flows (coupled with Na+ reabsorbtion)

18
Q

Explain how Ca2+ is reabsorbed at LoH [2]

A

Driven by voltage gradient: Para/transcellular
Coupled with Na+ reabsorbtion: NKCC2 channel

19
Q

Why do thiazide diuretics raise serum calcium?

A

Increase Ca2+ reabsorbtion into the blood / raises Ca2+ serum levels:

  • Blocks Na/Cl symporter on luminal side
  • This drops the Na conc. In tubular cell
  • This creates Na diffusion gradient
  • Na diffusion increases from capillary into tubular
    cell - across Na/Ca exchanger -> takes Na into cell and transports Ca2+ into blood. -> increase in blood Ca levels.
20
Q

inhibition of Na/Cl symporter: causes what to serum Ca2+ levels? [1]

A

Increases serum Ca2+ levels

21
Q

Effect of PTH on:

  • NaPi transporters (and therefore P reabsorbtion)? [1]
  • Vit. D activation? [1]
  • PCT GNG? [1]
  • Na/H20/HCO3- reabsorbtion? [1]
A
  • Down-regulation of NaPi transporters: Reduced phosphate reabsorption
  • Vitamin D Activation Stimulation of 25(OH) D3 –> 1,25(OH)2 D3 (inactivates 1,25-dihydroxyvitamin D)
  • Proximal tubule gluconeogenesis
  • Inhibits sodium/water/bicarbonate reabsorption via effects on Na/H exchanger and Na/K ATPase
22
Q

What effect does PTH have on bone tissue? [2]

A

COME BACK

23
Q

What effect does PTH have on bone tissue? [2]

A

COME BACK

24
Q

Where do you find vit. D receptors? [2]

Role of vit D? [2]

A

Receptors: nucleus and cytoplams
Role: Upregulates Ca2+ transporters

25
Q

Effect of PTH on bone remodelling xx

A
26
Q

The conversion of vit. D to WHAT is regulated? [1]

The conversion of vit. D to WHAT is unregulated? [1]

What are the enzymes used for each? [2]

A

Conversion of vit D to 25(OH)D in the liver is an unregulated process, under the action of p450 enzymes. The half life of 25(OH)D is 2-3 weeks.

The conversion of vit D to 1,25(OH)D is highly regulated, via 1αhydroxylase

27
Q

How does negative feedback of activation of vitamin D receptor work?

A

In most cells there is a negative feedback inhibition: activation of the VDR inhibits the action of 1α hydroxylase (which converts vit D to active form), therefore reducing the amount of activated vitamin D able to bind to the VDR.

28
Q

Why would chronic infection (e.g from sarcoidosis / TB granuloma) cause hypercalcemia?

A
  • Macrophages produce vitamin D
  • Release of vitamin D is converted to 1 25 dihydroxyvitamin dby 1α hydroxylase
  • Causes increase in serum calcium
29
Q

The major role of calcitriol is [2]?

A

The major role of calcitriol is in increasing gut calcium and phosphate absorption.

30
Q

other vit d effects

A
31
Q

What does the hormone FGF23 do? [1]
Which cells are they secreted from? [1]
What does FGF23 do to 1-a-hydroxylase? [1]

A

What does the hormone FGF23 do? [1]
Reduces serum P levels USED FOR WHEN GET P EXCRETED FROM FROM BONE BUT NEED TO EXCRETE VIA RENAL SYSTEM

Which cells are they secreted from? [1]
Secreted by osteocytes

What does FGF23 do to 1-a-hydroxylase? [1]
**reduces 1-a-hydroxylase: less activated vit. D **

32
Q

FYI

A

Activating mutation in FGF23 - Autosomal dominant hypophosphataemic rickets
Tumour induced osteomalacia - paraneoplastic FGF23
Familial tumoral calcinosis - low levels FGF23

33
Q

Explain 3 classes of symptoms seen in hypercalcemia

A

Hypercalcemia
Symptoms

Neuropsychiatric disorders: due to reduced membrane excitibility causing reduced nerve transmisison in the brain

GI abnormalities:
* Constipation / pancreatitis: reduced membrane excitibility causes less muscle contraction

Renal dysfunction:
* Nephrogenic Diabetes Insipidus: Ca2+ binds to CaSR in nephrone, which down regulates NaKCL2 symporter
Renal stones & Renal failure due to XS Ca2+ in urine

34
Q

What is primary cause of hypercalcemia? [1]

A

Malignancy in parathyroid gland is main cause, usually from bone metastasis

35
Q

How do you treat hypercalcemia?

A

Expand plasma volume - reduce voltage gradient in tubular cells -> less Ca ++ reabsorbed
Reduce Ca release from bone
Treat underlying cause

36
Q

What are primary, secondary and tertiary causes of hyperparathyroidism?

A

Primary: Parathyroid adenoma/carcinoma/hyperplasia

Secondary: Physiological compensation for hypocalcemia or Vitamin D deficiency. Can create tertiary

Tertiary: Autonomous PTH production following chronic secondary.

37
Q

What is the effect of primary hyperparathyroidism? [1] and why? [2]

A

hypercalcaemia + excess PTH -> osteoporosis.

38
Q

How can you ID if have primary Hyperparathyroidism? [4]

A

Neck USS
MIBI scan
CT scan
Parathyroid Venous Sampling

39
Q

How do you treat hypoparathyroidism acutely and chronically? [2]

A

Acutely: give Ca2+
Chronically: Give activated vit D: increased gut absorb

40
Q

How would hypoT present? [4]

A

Neuromuscular Excitability:
Cardiac tachyarrhythmia
Tetany
Seizures
Psychiatric manifestations

41
Q

What would be overall causes of Hypocalcemia? [3]

A

PTH problems
Vit D problems (e.g. nutritional deficiency)
Compartment shifts

42
Q

kidney, [] converts 25-hydroxyvitamin-D into 1,25-dihydroxyvitamin-D

A

kidney, 1-α-hydroxylase converts 25-hydroxyvitamin-D into 1,25-dihydroxyvitamin-D

MET2 (52 decks)

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