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Metabolism, Endocrinology, Haematology > Endocrinology Session 4 > Flashcards

Endocrinology Session 4 Flashcards

1
Q

What cellular processes is calcium involved in?

A
  • Hormone secretion
  • Muscle contraction
  • Nerve conduction
  • Exocytosis
  • Intracellular second messenger
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2
Q

How is the calcium sequestrated in bone?

A

Hydroxyapatite crystals (within collagen fibres)

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3
Q

What is the function of phosphate?

A
  • Cellular energy metabolism (ATP)

- Levels fluctuate

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4
Q

How are calcium and phosphate regulated?

A
  • Parathyroid hormone
  • 1,25-dihydroxyvitamin D / calcitriol
  • Calcitonin (less)
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5
Q

What is the function of the skeleton?

A
  • Providing structural support
  • Major reserve of calcium
  • Buffering serum levels
  • Releasing calcium phosphate into interstitium
  • Taking up calcium phosphate
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6
Q

What do the 3 hormones ac on?

A

Bone, kidneys, GI tract

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7
Q

How much calcium does the adult human have?*

A

1000g

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8
Q

What are the main dietary sources of calcium?

A

Dairy

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9
Q

What is protein bound calcium used for?

A
  • Not easily moved across cell membranes
  • Not biologically active
  • Serves as a reserve
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10
Q

How much calcium is reabsorbed in the kidneys?

A

About 98%

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11
Q

What three physiochemical forms of calcium in plasma?

A

1) Free ionised species (45%)
2) Bound to anionic sites on serum proteins (albumins) 45%
3) Complexed with low-molecular weight organic ions (10%)

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12
Q

What is the total concentration of all three forms of calcium in plasma?

A

2.2-2.7 mmol/L

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13
Q

Which plasma calcium is measured and which one is physiologically active?

A
  • Free ionised is physiologically active

- Total calcium is commonly measured and then levels are corrected

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14
Q

What is hypocalcaemia and what does it result in?

A

Low calcium concentration

  • Hyperexcitability of the nervous system (+ NMJ)
  • Paraesthesia
  • Tetany, paralysis, convulsions
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15
Q

What is chronic hypercalcaemia and what does it result in?

A

Elevated calcium levels over a longer period of time

  • Kidney stones
  • Constipations
  • Dehydration
  • Kidney damage
  • Tiredness
  • Depression
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16
Q

What is responsible for the short and long term control of serum calcium concentration?

A
  • Short: parathyroid hormone

- Long: calcitriol

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17
Q

How is PTH synthesised?

A
  • Pro-pre-hormone cleaved
  • Regulated at the transcriptional and post transcriptional levels, so:

Low serum calcium = upregulated gene transcription, prolonged mRNA survival
High serum calcium = downregulated gene transcription

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18
Q

What is the half life of PTH and why?

A

4 1/2 minutes - means that the hormone is responding quickly

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19
Q

What is the function of chief cells?

A

Degradation and synthesis of PTH (cleavage initiated by high serum calcium levels)

20
Q

What are the target organs and the physiological effects of PTH?

A
  • Bone: increased osteoclast activation to release calcium and phosphate into blood
  • Intestine: activated vit. D and increases transcellular uptake
  • Kidney: decreases loss to urine (more reabsorption)
21
Q

What is the relationship between calcium and phosphate?

A

If more phosphate is excreted, more calcium is reabsorbed which reduces the likelihood of crystal formation

22
Q

How is bone deposited?

A

Osteoblasts producing collagen matrix mineralised by hydroxyapatite

23
Q

How is bone reabsorbed?

A

Osteoclasts producing an acid micro-environment to dissolve hydroxyapatite

24
Q

How does PTH act on the bone?

A
  • Stimulated osteolysis
  • Inducing osteoblastic cells to synthesise and secrete cytokines on cell surface
  • Decreased osteoblast activity exposes bony surface to osteoclasts
25
Q

What is the feedback regulation of serum calcium?*

A
  • Increase = lower PTH secretion
  • Less Ca2+ reabsorbed from gut
  • Less vit D and less Ca2+ from gut
  • More bone building

= Lower plasma Ca2+

26
Q

What are the symptoms of chronic hypercalcaemia?

A
  • Renal calculi
  • Kidney damage
  • Constipation
  • Tiredness
  • Depression

Stones, moans, groand

27
Q

When do symptoms of severe hypercalcaemia appear?

A
  • When serum calcium raises above 3.0 mmol/L
  • Lethargy
  • Weakness
  • Confusion
  • Coma
  • Renal failure
28
Q

How do you treat hypercalcaemia?

A

Rehydration

29
Q

What is the aetiology of hypercalcaemia?

A
  • Malignant osteolytic bone mets (big bone patches missing)
  • Multiple myeloma
  • Cancers that metastasise to bone (breast, lung, renal, thyroid)
30
Q

Why would prostate cancer mets not cause hypercalcaemia?

A

Rather than osteolytic mets, it causes osteoblastic mets and no calcium will be liberated so it would not cause hypercalcaemia

31
Q

What are the common sites for bone metastases?*

A
  • Vertebra
  • Pelvis
  • Proximal femur
  • Ribs
  • Proximal humerus
  • Skull
32
Q

What is primary hyperparathyroidism?

A

A condition where one of the four parathyroid glands develops an adenoma which secretes excess PTH
- Causes serum calcium rises and phosphate falls

33
Q

What is secondary hyperparathyroidism?

A

A condition where all 4 parathyroid glands become hyperplastic

34
Q

What causes secondary hyperparathyroidism?

A
  • Vitamin D deficiency

- Low serum calcium absorption so low calcium and therefore high PTH

35
Q

What are the symptoms of primary hyperparathyroidism?

A
  • Stones (kidney)
  • Moans (tiredness, depression)
  • Groans (constipation)
  • Bones (+ muscle aches)
36
Q

Why does hypercalcaemia lead to suppression of neuronal activity?

A

More is needed to fire the action potential, and therefore not as many will fire

37
Q

Why does hypocalcaemia lead to excitabe nerves?

A

Less contribution to RMP so less needed to reach threshold and more will fire

38
Q

When is symptomatic hypocalcaemia seen?

A
  • When serum calcium falls below 2.1 mmol/l
  • Most common in post-total thyroidectomy
  • Can start within 6 hours of thyroidectomy
39
Q

What are the symptoms of hypocalcaemia?*

A
  • Tingling in mouth and fingers
  • Tetany of muscles
  • Carpopedal spasm
40
Q

What is the difference between osteoporosis and osteomalacia?

A
  • Osteomalacia: normal bone structure that is under mineralised
  • Osteoporosis: structurally degraded bone that is fully mineralised
41
Q

What is the cause of osteomalacia?

A
  • Vitamin D deficiency
  • Rickets in children
  • Can be due to diet or renal disease
42
Q

What are the symptoms of osteomalacia?*

A
  • Bone pain
  • Muscle weakness
  • Deformity
43
Q

How is vitamin D obtained?

A

Sun exposure, food, supplements

44
Q

How is inert vitamin D converted into 1,25-dihydroxycalficerol?

A

By undergoing two hydroxylation reactions

45
Q

What is parathyroid hormone related peptide?

A

A peptide that is produced by tumours and mimics the action of PTH without increasing calcitriol concentration

Causes humeral hypercalcaemia of malignancy (HMM)

46
Q

What does PTHrP cause?

A
  • Increased calcium release from bone
  • Reduced renal calcium excretion
  • Reduced renal phosphate reabsorption

= Hypercalcaemia

47
Q

Why des PTHrP not increase calcitriol concentration?

A
  • Does not increase renal C-1 hydroxylase activity that catalyses the hydroxylation of calcifediol to calcitriol
  • Therefore cannot make calcitriol
  • So no increase in concentration

Metabolism, Endocrinology, Haematology (16 decks)

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