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Chemical Pathology - Path > Calcium homeostasis > Flashcards

Calcium homeostasis Flashcards

1
Q

What are the different roles of calcium in the body?

A
  • Skeleton and bone growth/maintenance
  • Metabolic - Action potentials and IC signalling
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2
Q

Describe calcium handling in the body

A

99% of the body’s calcium is in the bones/skeleton. We can get calcium from our diet, where it is absorbed in the GI tract. However, we cannot fully absorb calcium without adquate vitamin D levels, which is dependent on sunlight exposure and diet, as well as renal function.

When Ca is low, PTH is produced by the parathyroid glands which acts to activate osteoblasts and suppress osteoclast activity, to increase break down of bone to release calcium. PTH also increases renal reabsorption of calcium and alpha 1 hydroxylase activation, and causes increased excretion of phosphate.

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3
Q

99% of calcium is in the bones, only 1% is found in the serum.

What are the 3 forms that calcium that can be found in the serum, and there approx amounts?

A
  • Free “ionized” - the only one that is biologically active (50%)
  • Protein-bound - bound to albumin (40%)
  • Complexed - with citrate/phosphate (10%)
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4
Q
  1. What is the reference range for total serum calcium?
  2. Why do we correct serum calcium levels, and whta is the formula?
A
  1. 2.2-2.6mmol/L
  2. Corrected calcium is reported to correct for albumin levels. If albumin levels are incorrect, can cause a false reading for calcium levels

corrected calcium = serum Ca + 0.02 *(40 - serum albumin in g/L)

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5
Q

What will happen to calcium levels if you have a low albumin?

A

If you have a low albumin, the bound calcium wil be low, but the free calcium will be normal. Therefore, corrected calcium can show you whether the problem is the low albumin or whether the ionized calcium level really is too low.

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6
Q

Why is calcium important?

A
  • Important for normal nerve and muscle function
  • Chronic calcium deficiency can result in loss of calcium from bone in order to maintain calcium.
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7
Q

PTH ‘obtains’ Ca from what 3 sources in the body?

A
  • Bone - stimulation of osteoblasts
  • Gut - absorption
  • Kidney - resorption and renal 1 alpha hydroxylase activation
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8
Q

What two hormones are involved in calcium homeostasis?

A
  • PTH
  • Vitamin D
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9
Q
  1. How many amino acids make up PTH?
  2. What are the roles of PTH in the body?
A
  1. 84 amino acids long
  2. Bone and renal Ca resorption, stimulates 1,25(OH)2 vitamin D synthesis (1 alpha hydroxylation) and stimulates phosphate wasting
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10
Q

Describe the process of vitamin D synthesis

A
  • 7-dehydrocholesterol in the skin, reacts with sunlight to produce
  • cholecalciferol D3 which is converted by 25 hydroxylase from the liver to produce
  • 25-hydroxycholecalciferol (25-OH D3) which is converted by 1 alpha hydroxylation in the kidney and the presence of PTH to produce
  • 1, 25-dihydroxycholecalciferol (1,25(OH)2 D3 which is the physiologically active form
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11
Q

Which of these is a PLANT product?

  1. Ergocalciferol
  2. Cholecalciferol
A
  1. Ergocalciferol
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12
Q

Where is vitamin D3 synthesized?

A

The skin

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13
Q

Where the following enzymes found and what do they do?

  1. 25 hydroxylase
  2. 1 alpha hydroxylase
A
  1. 25 hydroxylase - liver - 100% of absorbed vitamin D is hydroxylated at the 25 position by this enzyme. 25 hydroxy vitamin D is inactive and stored in the liver and measured form of vitamin D
  2. 1 alpha hydroxylase - kidney - next step after the liver, 25 hydroxy vitamin D is actiavted to its active form (1,25(OH)2D3) by 1 alpha hydroxylase. The kidney is the rate limiting step
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14
Q

What cells/conditions can ectopically secrete 1 alpha hydroxylase?

A
  • Lung cells
  • Sarcoid tissue
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15
Q

What is the role of 1,25(OH)2 D3?

A
  • Activated form of vitamin D
  • Intestinal Ca absorption
  • Also intestinal Phosphate absorption
  • Bone formation
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16
Q

Vitamin D deficiency

  1. What is it in adults and in children?
  2. What are the risk factors?
A
  1. Defective bone mineralization. In children vit D deficiency is called Rickets, and in adulthood it is Osteomalacia
  2. Lack of sunlight exposure, dark skin, dietary and malabsorption
17
Q

What are the clinical features of osteomalacia?

A
  • Bone and muscle pain
  • Increased risk of fracture
  • Low Ca and phosphate levels, raised ALP
  • Looser’s zones - pseudo fractures
18
Q

What are the clinical features of Rickets?

A
  • Bowed legs
  • Costochondral swelling
  • Widened epiphyses at the wrists
  • Myopathy
19
Q

What are the different causes of osteomalacia?

A
  • Bone is demineralised, most commonly caused by vitamin D deficiency
  • Renal failure
  • Anticonvulsants induce breakdown of vitamin D
  • Lackf of sunlight
  • Chappatis (phytic acid)
20
Q

What is osteoporosis?

A
  • Cause of pathological fracture
  • Loss of bone mass with increasing age, especially in post-menopausal women. Residual bone normal in structure but not in mass
  • Has a normal Ca/biochemistry
  • Aysmptomatic until a fracture, most commonly NOF
21
Q

How is osteoporosis diagnosed?

A
  • DEXA scan
  • A T score of <-2.5 is osteoporosis
  • A T scpre of between -1 & -2.5 is osteopenia
22
Q

What are the causes of osteoporosis?

A
  • Childhood illness
  • Early menopause
  • Lifestyle: sedentary, alcohol, smoking, low BMI/nutritional
  • Endocrine - hyperprolactinemia, thyrotoxicosis, Cushing’s
  • Drugs - steroids
23
Q

How is osteoporosis treated?

A
  • Lifestyle changes - increased weight bearing exercise, stop smoking and reduce alcohol intake
  • Drug therapy - vitamin D/Ca, bisphosphonates e.g. alendronate that reduces bone resporption, SERMs, Teriparatide (PTH derivative)
24
Q

What are the symptoms of hypercalcemia?

A
  • Polyuria/polydipsia
  • Constipation
  • Neurological - confusion/seizures/coma
25
Q

What is the normal hormonal response to hypercalcaemia?

A

PTH release should be suppressed

26
Q

Hypercalcemia and PTH is not suppressed. What could the cause be of this inappropriate response?

A

Primary problem with PTH regulation.

Primary hyperparathyroidism (common)

Familial hypocalciuric hypercalcaemia

27
Q

Hypercalcemia with a suppressed PTH.

What could the diagnosis be?

A

Malignancy

Less common

  • Sarcoid
  • Vitamin D excess
  • Thyrotoxicosis
  • Milk alkali syndrome
28
Q
  1. What are the underlying cases of primary hyperparathyroidism?
  2. Is primary hyperparathyroidism more common in men or women?
A
  • Parathyroid adenoma/hyperplasia/carcinoma (rare)
  • Hyperplasia associated with MEN1
  1. Women
29
Q

What would the biochemistry look like for primary hyperparathyroidism?

A
  • Increased serum Ca
  • Reduced serum phosphate
  • Increased urinary Ca (due to hypercalcaemia)
30
Q

Hypercalcemia in malignancy. What are the 3 “types”?

A
  • Humoral hypercalcemia of malignancy e.g. small cell lung Ca - increase in PTHrP
  • Bone metastases e.g. breast cancer - caused by local bone osteolysis
  • Haematological malignancy e.g. myeloma - cytokine driven
31
Q

What are the other causes of Non-PTH driven hypercalcemia? (not including malignancy)

5 conditions and their underlying mechanisms for causing hypercalcemia.

ST THE

A
  • Sarcoidosis - non-renal 1 alpha hydroxylation
  • Thyrotoxicosis - increased thryoxine leads to increased bone resoprtion and release of calcium
  • Hypoadrenalism - affecting renal Ca transport
  • Thiazide diuretics - affecting renal Ca transport
  • Excess vitamin D e.g sunbeds
32
Q

What is the acute management for hypercalcemia?

A

FLUIDS and more fluids

Should bisphosphonates be given? Unless known to be cancer avoid.

Then treat underlying cause.

33
Q

What are the main clinical signs of hypocalcemia?

A
  • Neuro-muscular excitability
  • Trousseau’s sign
  • Chvostek’s sign
  • Hyperreflexia
  • Laryngeal spasm - stridor
  • Prolonged QT interval on ECG
  • Convulsions
  • Choked disk on fundoscopy
34
Q

What are the main causes of non-PTH driven hypocalcemia?

A
  • Vitamin D deficiency - can be caused by dietary, malabsorption or lack of sunlight
  • Chronic kidney disease - 1 alpha hydroxylation - can progress into tertiary hyperparathyroidism
  • PTH resistance - pseudohypoparathyroidism
35
Q

What are the causes of hypocalcemia due to low PTH?

A
  • Surgical, included post thyroidectomy
  • Auto-immune hypoparathyroidism
  • Congenital absence of parathyroids e.g. DiGeorge syndrome
  • Magnesium deficiency - PTH regulation
36
Q
  1. What is Paget’s disease?
  2. Describe the signs and symptoms of Paget’s disease
  3. How is it diagnosed?
  4. What is the treatment?
A
  1. Focal disorder of bone remodeling
  2. Symptoms - Pain, warmth, fractures, S&S of SC compression. Mainly affects the pelvis, femur, skull and tibia. Signs include elevated alkaline phosphatase (marker of bone turnover)
  3. Nuclear med scan/ x-ray of affected bones
  4. Treatment = Bisphosphonates for pain
37
Q

What are other metabolic bone disorders that can occur because of the following conditions?

  1. Primary hyperparathyroidism
  2. Secondary hyperparathyroidism
A
  1. In primary hyperparathyroidism there is loss of cortical bone an increased fracture risk. Can lead to osteitis fibrosa
  2. Secondary hyperparathyrodism and retention of aluminum from dialysis can lead to renal osteodystrophy
38
Q

Describe the biochemistery for the folllowing conditions including, Primary defect, Ca, Phosphate, PTH, Vit D and ALP

For the following conditions:

  • Osteoporosis
  • Osteomalacia/rickets
  • Paget’s
  • Parathyroid bone disease
  • Renal bone disease

Draw a table

A

See table

39
Q
A

Chemical Pathology - Path (18 decks)

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