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Semester 3 - urinary > 7. Regulation of calcium and phosphate > Flashcards

7. Regulation of calcium and phosphate Flashcards

1
Q

How much Ca is there in the whole body?

A

2.1-2.6mmol/L

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2
Q

How much ionised Ca2+ is there?

A

1.1-1.4mmol/L

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3
Q

What proportions of Ca in the body are found where?

A

90% in the bones

  1. 99% extracellular
  2. 01% intracellular (toxic to cells)
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4
Q

What are the 2 types of extracellular Ca?

A

Diffusible

Non-diffusible

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5
Q

What is diffusible Ca?

A

• Free ionized Ca2+ (cellular processes e.g. neuronal action potentials, contraction muscles, hormone
secretion, blood coagulation)
• Complexed calcium – bound to negatively charged molecules like oxalate. Not involved in cellular
processes

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6
Q

What is non-diffusible Ca?

A

Ca2+ bound to negatively charged proteins e.g. albumin

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7
Q

Where is most of the Ca reabsorbed?

A

PCT

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8
Q

How is Ca absorbed in the PCT?

A

80% by solvent drag/paracellularly with water
20% transcellularly - Actively pumping out Calcium at basolateral membrane into blood, maintaining conc gradient for diffusion from lumen into blood

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9
Q

What is solvent drag?

A

As a solvent crosses a semipermeable membrane, it drags larger solutes along with it

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10
Q

Where is 25% of the Ca reabsorbed?

A

Thick ascending limb

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11
Q

How is Ca absorbed in the TAL?

A

Half/half:
• Paracellularly - Na+K+2Cl cotransporter on apical membrane brings in the ions from lumen into tubular cell. Na+ moved out of cell at basolateral membrane into blood by Na+K+ATPase maintaining Na+ gradient. K+ moved out into lumen of tubule by K+Cl- channel. K+ also moved out into lumen via ROMK-many positive ions are pumped into lumen which repels Ca2+/Mg2+ and causes it to move paracellularly to blood.
• Transcellularly - Actively pumping out Calcium at basolateral membrane into blood, maintaining conc gradient for diffusion

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12
Q

What stimulates the reabsorption of Ca in the TAL by the transcellular route?

A

PTH

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13
Q

Where is 8% of the Ca reabsorbed? How?

A

DCT

Transcellularly

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14
Q

Where is 1.5% of the Ca reabsorbed?

A

Collecting duct

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15
Q

How much calcium is excreted in urine?

A

~0.5%

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16
Q

Where is PO4^3- found in the body?

A

80% in bone

20% in interstitial fluid

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17
Q

How is phosphate reabsorbed?

A

Reabsorbed with 2 Na+ ions at the apical membrane in the PCT

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18
Q

What increases the excretion of PO4^3-?

A

Anything that causes an increase in its plasma conc e.g. PTH, acidosis, glucocorticoids, reduced GFR (CKD)

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19
Q

What decreases the excretion of PO4^3-?

A

Vitamin D

20
Q

What will a fall in FR cause in relation to phosphate?

A

• A fall in GFR will result in increased plasma PO4

3- concentration and is a common cause of itching in CKD.

21
Q

What is the relationship between the concentrations of calcium and phosphate? Why?

A

Inversely proportional
Because their concentrations in the blood are close to saturation point, meaning that adding more of one of the ions results in formation of CaPO4, thus removing some of the other ion

22
Q

What happens when decreased calcium conc is detected by PT gland?

A

increased PTH secretion

23
Q

What two structure are affected by PTH?

A

kidney and bone

24
Q

How does PTH affect bone?

A

increased bone resorption –> increased calcium released into plasma

25
Q

How does PTH affect kidney?

A
  • increased calcium reabsorption in distal tubules so plasma calcium conc increases and decreased urinary excretion of calcium
  • decreased phosphate reabsorption in proximal tubule so plasma phosphate conc decreases and increased excretion
  • increased active vitamin d formation –> increased calcium absorption in intestines –> increased plasma calcium conc
26
Q

Causes of hypocalcaemia

A 
CKD
Hypoparathyroidism
Rickets & osteomalacia
Tissue injury
Alkalosis
27
Q

Why can CKD cause hypocalcaemia?

A

Causes hyperphosphatemia, thus Ca levels fall

Also low levels of activated vitamin D, so less Ca absorpted in the gut

28
Q

Why can tissue injury cause hypocalcaemia?

A

Release of intracellular phosphate, causing Ca levels to fall

29
Q

Why can alkalosis lead to hypocalcaemia?

A

Reduced H+ available to bind to protein, so more Ca2+ binds

Even though the total Ca remains same, there is decreased Ca2+ so there is less for cellular processes

30
Q

Treatment of hypocalcaemia

A

Oral/IV Ca

Alfacalcidol - vitamin D analogue

31
Q

Signs/symptoms of hypocalcaemia

A

Decreased Ca2+ results in neuromuscular excitability leading to tetany with convulsions, hand and feet muscle cramps and cardiac arrythmias

32
Q

Signs/symptoms of hypercalcaemia

A 
• Hypercalcemia makes cells less excitable resulting in slow reflexes, muscle weakness and constipation
• Symptoms and signs of hypercalcemia
are:
• Polyuria
• Polydipsia
• ‘Bones’ (bone pain and fractures
• ‘Stones’ (renal calculi)
• ‘Groans’ (abdominal pain, vomiting and constipation)
• ‘Moans’ (depression or confusion)
33
Q

Causes of hypercalcaemia

A

• Primary hyperparathyroidism
• Sudden acidosis, resulting in the release of bound calcium, which becomes ionized Ca2+
• Increased intestinal absorption due to excess vitamin D or ingestion of calcium
• Bone destruction resulting in increased Ca2+
release from bone – usually caused by secondary deposits from malignancy or myeloma
• Granulomatous disease
• Drugs e.g. thiazides
• Tertiary hyperparathyroidism in CKD
• Hypermagnesem

34
Q

Treatment of hypercalcaemia

A

Treatment is of the underlying cause, with fluids for rehydration and bisphosphonates

35
Q

Causes of hypophosphatemia

A

• Hypophosphatemia is caused by an excessive loss of PO4 3-
• Causes include:
• Hyperparathyroidism
• Reduced absorption from GI (alcohol and medications such as antacids)
• Significantly reduced intake
- Malnourished
- Anorexia nervosa
• Refeeding syndrome - shift of phosphate from blood to cells when start to eat
• Diabetic ketoacidosis – insulin given
• Respiratory alkalosis

36
Q

Why can respiratory alkalosis lead to hypophosphataemia?

A

Decreased CO2
Intracellular CO2 diffuses out
pH in the cell increases, which stimulates glycolysis
Glycolysis uses up phosphate

37
Q

signs of hypophosphatemia

A
  • ‘Stones’ – kidney and gallbladder
  • ‘Thrones’ - polyuria
  • ‘Bones’ – pain
  • ‘Groans’ – constipation and muscle weakness
  • ‘Psychiatric overtones’ – depressed mood and confusion
38
Q

Treatment of hypophosphataemia

A

involves oral or intravenous phosphate and close
monitoring of blood levels
• In severe malnutrition it is important to increase caloric intake gradually to avoid refeeding syndrome

39
Q

Causes of hyperphosphataemia

A
  • Chronic kidney disease (↓GFR)
  • Secondary hyperparathyroidism (kidneys unable to reabsorb Ca2+)
  • Pseudohypoparathyroidism
  • Hypoparathyroidism
  • Excessive intake (diet or phosphate based laxities)
  • Cell death (crush syndrome, tumor lysis, rhabdomyolysis)
  • Respiratory acidosis
  • Diabetic ketoacidosis
40
Q

Why can respiratory acidosis lead to hyperphosphataemia?

A

[CO2] very high, so it diffuses into cells
Reacts with water to become carbonic acid
Carbonic acid breaks down into H+ and HCO3-
This lowers the pH inside the cell, which inhibits glycolysis
Hence, less P used up

41
Q

What is Crush syndrome?

A

Crushing injury to skeletal muscle which leads to major shock and kidney failure
AKA traumatic Rhabdomyolysis

42
Q

Signs/symptoms of hyperphosphataemia

A
  • No symptoms with mild hyperphosphatemia
  • Signs and symptoms of severe hyperphosphatemia include:
  • Spontaneous firing of neurons
  • Tetany
  • Involuntary contraction of muscles
  • Calcium phosphate crystal formation – kidney stones
43
Q

Treatment of hyperphosphataemia

A

Reduced dietary intake
Phosphate binders
Forced diuresis using loop diuretics to reduce reabsorption in the PCT

44
Q

What is pseudohypoparathyroidism?

A

Genetic defect where the kidney is unresponsive to PTH

45
Q

Why can diabetic ketoacidosis lead to hyperphosphataemia?

A

Low insulin

So P not removed from the blood

Semester 3 - urinary (33 decks)

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