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Endocrinology > Disorders of calcium regulation > Flashcards

Disorders of calcium regulation Flashcards

1
Q

What 3 things does the body use to regulate it’s calcium levels and how do they affect calcium levels?

A
  1. Parathyroid hormone = increases calcium
  2. Vitamin D = increases calcium
  3. Calcitonin = decreases calcium
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2
Q

What is a normal calcium range?

A

8.5 - 10mg/dL

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3
Q

How is parathyroid hormone release controlled?

A
  1. Changes in calcium levels are detected by calcium-sensing surface receptors on parathyroid cells
  2. Calcium sensing receptor is connected to an enzyme on the intracellular surface (phospholipase C)
  3. When extracellular levels are high or normal = calcium binds to the receptor and activates phospholipase C
  4. Phospholipase C splits PIP2 into DAG and IP3
  5. IP3 diffuses through the cytoplasm to get to the ER and binds to inositol triphosphate receptor on lignad-gated Ca channel
  6. This opens the calcium channel and stored calcium is released into the cytoplasm (increasing intracellular Ca)
  7. High intracellular ca stops secretory granules holding PTH from binding to chief cells’ membrane and stops them from releasing PTH outside the cell = less calcium released
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4
Q

What happens in the parathyroid gland when there is low blood calcium levels?

A
  1. Less extracellular calcium binds to receptor
  2. Less calcium remains in ER
  3. Secretory granules containing PTH bind to the cell membrane
  4. PTH is released and calcium levels rise
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5
Q

What 3 places in the body does PTH work on?

A

Bone
Kidney
Gut

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6
Q

What is the effect of PTH on bone? Why does this happen?

A

Increases bone remodelling

How?

  • PTH binds to receptors on osteoblasts and they release cytokines (RANKL & M-CSF)
  • These cytokines make macrophage precursors fuse together to form a single osteoclast (breaks bone)
  • As bones are broken down, calcium and phosphate are released and increased in the blood (as phosphate and calcium are minerals which make bone)
  • In the blood, phosphate will bind to calcium (complex calcium which can’t be used for cellular processes)
  • To stop this from happening, PTH also binds to receptors on the tubular cells of kidneys’ proximal convoluted tubules…
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7
Q

What is the effect of PTH in the kidneys? Why does this happen?

A

Increases calcium reabsorption, decreases phosphate reabsorption

How?

  • PTH binds to receptors on the tubular cells of the kidneys’ proximal convoluted tubules
  • This stops sodium and phosphate co-transporters on apical surface of tubular cells from resorbing phosphate from the urine
  • This increases phosphate being lost in urine (phosphaturia)
  • Caldidiol also travels to the tubular cells where enzyme 1-alpha-hydroxylase (also activated by PTH) converts it into calcitriol (active vitamin D)
  • PTH also binds to principle cells in distal convoluted tubules
  • This makes tubular cells make for sodium and calcium channels which become embedded on the surface and resorb more calcium from the urine
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8
Q

What is the effect of PTH in the gut, and how does it happen?

A

Converts Vitamin D and increases calcium absorption in the gut

How?

  • PTH helps convert D3 into active vitamin D3
  • Cholecalciferol is synthesised by keratinocytes in the skin when exposed to sunlight (also comes from food)
  • Cholecalciferol travels to the liver where it is converted into calcidiol
  • Calcidiol travels to the proximal tubular cells of the kidney where it is converted into calcitriol (active vitamin D) using enzyme 1-alpha-hydroxlyase
  • Active vitamin D then goes to the GI tract where it enters enterocytes in the small intestine and increases activity of the calcium channels on the cell membrane allowing it to absorb more calcium from food
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9
Q

What do we mean by appropriate and inappropriate PTH response?

A

Appropriate = changes in PTH are to maintain calcium balance

Inappropriate = changes in PTH are causing the calcium imbalance

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10
Q

Causes of hypoparathyroidism?

A
  1. Parathyroid gland removal during thyroid or parathyroid surgery (most common cause)
  2. Autoimmune polyendocrine syndrome type 1 (destruction of parathyroid gland)
  3. Di George syndrome (causes a variety of disorders as well as non-functioning parathyroid glands)
  4. Autosomal-dominant hypoparathyroidism (mutation in parathyroid calcium sensing receptor)
  5. Pseudohypoparathyroidism (PTH resistance in bones and kidneys due to defective PTH receptor)
  6. Magnesium deficiency (need magnesium to get PTH out of the cell)
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11
Q

What are the signs & symptoms of low PTH?

A

Hypocalcaemia and hyperphosphataemia

  • Trousseau’s sign (BP cuff inflated occluding brachial artery and putting pressure on nerve causes flexion of wrist and. metacarpophalangeal joint)
  • Chvostek’s sign (twitching of the facial muscles in response to tapping over the facial nerve)
  • Paraesthesia
  • Changes in cardiac output
  • Calcification in places like basal ganglia (Fahr’s syndrome)
  • Calcification of eye lens
  • Seizures and cardiac arrhythmias if severe hypocalcaemia
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12
Q

What is the treatment for hypoparathyroidism?

short and long term

A

Calcium and vitamin D supplements to bring calcium levels back to normal

Long term = recombinant human parathyroid hormone

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13
Q

What is primary hyperparathyroidism & what would the lab findings be?

A

The parathyroid gland as it is making PTH independent of calcium levels

  • Hypercalcaemia
  • Hypophosphataemia (as PTH stimulates osteoclasts to break bone and kidneys to retain calcium and get rid of phosphate)
  • High PTH levels
  • High Alkaline Phosphatase (increased bone resorption)
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14
Q

What are the causes of primary hyperparathyroidism?

A
  1. Single parathyroid adenoma (most common)

2. Hyperplasia of parathyroid cells (rare)

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15
Q

Symptoms of hyperparathyroidism?

A

‘Stones, groans, thrones, bones, psychiatric overtones’

  • Stones = gall stones (dehydration)
  • Groans = constipation and muscle weakness (decreased muscle contractions)
  • Thrones = polyuria (impaired sodium and water reabsorption)
  • Bones = bone pain from chronic demineralisation to release calcium (osteoporosis)
  • Psychiatric overtones = depressed mood and confusion
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16
Q

What is secondary hyperparathyroidism? What would the lab findings be?

A

Normal parathyroid gland but makes excess PTH due to hypocalcaemia from another cause

  • Hypocalcaemia
  • Hyperphosphataemia
  • Low vitamin D
  • High PTH
  • High ALP
17
Q

Causes of secondary hyperparathyroidism?

A

Kidney problems = most common cause where the kidneys aren’t filtering the phosphate properly into urine or making enough calcitriol

  • hyperphosphataemia which reduces the amount of free calcium in blood
  • lack of calcitriol = less calcium absorbed by the intestine

2nd cause is chronic lack of calcitriol due to poor intake of vit D or lack of sunlight

18
Q

What is tertiary hyperparathyroidism and what lab findings would you expect to find?

A

Those who have secondary hyperparathyroidism develop primary hyperparathyroidim
- parathyroid begins making PTH independent of calcium levels (hypercalcaemia)

Lab findings:

  • very high PTH
  • Hypercalcaemia
  • level of phosphate can vary (pt with CKD phosphate will be high, in those will good kidneys, phosphate will be low)
19
Q

Lab findings to diagnose primary, secondary and tertiary hyperparathyroidism?

A

Primary hyperparathyroidism = hypercalcaemia and hypophosphataemia

Secondary = hypocalcaemia, hyperphosphataemia and low vitamin D

Tertiary = hypercalcaemia - but it’s distinguished from primary hyperthyroidism if the person has, or used to have CKD and phosphate levels will depend on whether the person has had a kidney transplant.

20
Q

Treatment for primary, secondary and tertiary hyperparathyroidism?

A

Primary & tertiary =

  • Removal of abnormal parathyroid gland
  • Calcimimetics

Secondary =

  • normally treated by managing hyperphosphataemia with phosphate binders and increasing vit D with supplements
  • sometimes surgery
21
Q

How can ‘true’ calcium levels be altered depending on blood pH?

A

Total calcium can vary depending on bloods pH and protein levels

  • albumin has acidic amino acids which have COO- and COOH carboxyl groups which change depending on the pH of the blood
  • When there is high pH (alkalosis), there are few protons so they will be in the COO- form
  • COO- makes albumin negatively charged and since calcium is positively charged, they will bind
  • This means the level of calcium is the same but there is more bound calcium and less free ionised calcium (which is used for cellular processes)
22
Q

How does albumin affect calcium levels?

A

As most calcium is bound to albumin, Increased or decreased albumin will affect calcium levels

  • hypoalbuminaemia would lead to loss of bound calcium but free ionised calcium might remain the same due to hormonal regulation (pseudohypocalcaemia)
23
Q

Causes of true hypocalcaemia?

A
  1. Too much calcium entering blood = most common
  2. Too much calcium leaving the blood

Too much calcium entering:

  • can be due to hypoparathyroidism (surgical removal, autoimmune destruciton, congenital problems, magnesium deficiency)
  • can be due to low levels or lower activity of PTH
  • can be due to low vit D

Too much calcium leaving blood:

  • Too much ionised calcium secreted in kidney failure
  • Tissue injury (burns) where large number of cells die and release intracellular phosphate into blood - phosphate binds to calcium making it insoluble and decreasing total available in blood
  • Acute pancreatitis - free fatty acids bind to ionised calcium which are insoluble and precipitates
  • Too many blood transfusions - additives with EDTA and citrate can chelate or bind to calcium forming complex calcium (which is inactive)
24
Q

Signs and symptoms of hypocalcaemia?

A

Lower calcium means resting state of voltage gated sodium channels is less stable and more likely to open and depolarise (more excitable cells)

  • paraesthesia
  • Chvostek’s sign
  • Trousseaeu’s sign
  • muscle spasms (hands, feet, larynx, premature labour)
  • abdominal pain
  • perioral tingling
  • seizures (extreme cases)
  • basal ganglia calcification
  • cataracts
  • ECG may show prolonged QT, prolonged ST and arrhythmias (AF)
25
Q

Treatment of hypocalcaemia?

A

Normalise calcium levels using calcium gluconate and if appropriate, vitamin D supplementation

26
Q

Symptoms of hypercalcaemia?

A
  • Can be asymptomatic
  • Constipation
  • Nausea
  • Muscle weakness
  • Renal symptoms (polyuria, followed by thirst)
  • High risk of developing kidney stones so might have pain
  • Neurological symptoms = depression and anxiety
27
Q

Most common causes of hypercalcaemia? (2)

How do you differentiate between them?

A

90% of hypercalcaemia will be due to

  1. Malignancy (bone mets, myeloma, lymphoma) - PTH will be LOW
  2. Primary hyperparathyroidism - PTH will be HIGH, phosphate LOW.
28
Q

What does a DEXA scan measure & what scores do you get?

A

Type of X-ray that measures bone mineral density and bone loss.
T score is obtained from the scan

T score between -1 and +1 = normal bone density
T score between -1 and -2.5 = osteopenia
T score <2.5 = osteoporosis

29
Q

What condition would these lab results indicate?

  • Low PTH
  • Low Calcium
  • High Phosphate
A

Hypoparathyroidism

30
Q

What condition would these lab results indicate?

  • High PTH
  • High Calcium
  • Low Phosphate
A

Primary hyperparathyroidism

31
Q

What condition would these lab results indicate?

  • High PTH
  • Low Calcium
  • Low phosphate
A

Secondary hyperparathyroidism due to vitamin D deficiency

Endocrinology (16 decks)

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