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Health Sciences > L48,49 parathyroid glands, calcium homeostasis and bone physiology > Flashcards

L48,49 parathyroid glands, calcium homeostasis and bone physiology Flashcards

1
Q

What are the main roles of calcium in the body?

A

Structural: Calcium is a major component of bones, teeth, and connective tissues.

Bone calcification: Essential for maintaining bone strength and structure via hydroxyapatite crystals.

Blood clotting: Acts as a cofactor (Factor IV) in the coagulation cascade.

Cell signalling: Functions as a second messenger in processes like hormone secretion, muscle contraction, and cell growth.

Muscle contraction: Required for smooth, skeletal, and cardiac muscle contractions by enabling actin-myosin interaction.

Neural transmission: Facilitates synaptic activity at the neuromuscular junction (NMJ), allowing nerves to stimulate muscles.

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2
Q

Where is calcium stored in the body and in what forms?

A

Total calcium in an adult is ~1 kg.

99% is stored in bones and teeth as hydroxyapatite (Ca₁₀(PO₄)₆(OH)₂).

The remaining 1% is:

Intracellular: Very low (0.1 μmol/L), tightly regulated for signalling.

Extracellular (plasma): 2.20–2.60 mmol/L, divided into:

50% ionised/free calcium (~1.4 mmol/L) – biologically active.

40% protein-bound (mostly albumin).

10% complexed with anions (e.g. phosphate, citrate).

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3
Q

Which hormones regulate plasma calcium, and how do they work?

A
  1. Parathyroid Hormone (PTH): Raises plasma calcium.
  • Released in response to low ionised calcium.
  • Increases calcium reabsorption in kidneys.
  • Stimulates bone resorption (via osteoclast activation).
  • Increases activation of vitamin D → enhances calcium absorption in intestines.
  1. Vitamin D (Calcitriol): Sustains long-term calcium levels.
  • Increases calcium and phosphate absorption in the intestines.
  • Promotes bone remodelling and mineralisation.
  1. Calcitonin: Lowers plasma calcium.
  • Released from thyroid C-cells when calcium is high.
  • Inhibits osteoclast activity → reduces bone resorption.
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4
Q

What is PTH and what are its effects on the body?

A

PTH is an 84-amino acid hormone produced by the parathyroid glands (4 glands behind the thyroid).

Responds to low ionised calcium or high phosphate levels.

A. Direct actions:

  • In bones: Stimulates osteoblasts to release RANK-L, which activates osteoclasts → bone resorption.
  • In kidneys:
  1. Increases calcium reabsorption (distal tubule).
  2. Decreases phosphate reabsorption (proximal tubule).

B. Indirect action:

  • Enhances vitamin D activation (via renal 1α-hydroxylase) → increases calcium absorption in the intestine.
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5
Q

How does calcium get mobilised from bone?

A

Fast release: Calcium moves from interstitial bone fluid via osteocyte activity.

Slow release (resorption):

  • PTH stimulates osteoblasts → release RANK-L → osteoclast activation.
  • Osteoclasts break down collagen and hydroxyapatite → calcium and phosphate released into blood.
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6
Q

How does PTH affect the kidney?

A

Increases calcium reabsorption in the distal tubule.

Inhibits phosphate reabsorption in the proximal tubule by blocking Na⁺/phosphate co-transporters.

Stimulates 1α-hydroxylase to activate vitamin D into calcitriol.

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7
Q

How is Vitamin D synthesised and activated?

A

Skin: UV light converts 7-dehydrocholesterol → cholecalciferol (D3).

Liver: D3 is hydroxylated → 25(OH)D3 (inactive storage form).

Kidney: Under PTH influence, 25(OH)D3 → 1,25(OH)₂D3 (Calcitriol) via 1α-hydroxylase.

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8
Q

What does calcitriol (active Vitamin D) do?

A

In intestines:

  • Binds to VDR (vitamin D receptors).
  • Increases transcription of calbindin, a protein that binds and transports calcium.
  • Enhances absorption of calcium and phosphate.

In bone: Promotes remodelling and mineralisation.

Negative feedback on PTH production.

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9
Q

What is calcitonin, and is it essential?

A

Secreted by C-cells (parafollicular cells) in the thyroid.

Released when calcium levels are high.

Inhibits osteoclast activity, reducing bone resorption.

Not essential for life – people without thyroids (e.g. post-thyroidectomy) maintain calcium balance via PTH and vitamin D.

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10
Q

What are the causes and symptoms of hypercalcaemia?

A

Causes:

  • Primary hyperparathyroidism (usually due to a parathyroid adenoma).
  • Malignancy (e.g. PTHrP from tumours).
  • Excess vitamin D or calcium intake.

Symptoms:

  • Kidney stones.
  • Constipation.
  • Dehydration.
  • Fatigue, depression.
  • In severe cases: confusion, cardiac arrhythmias.
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11
Q

What causes hypocalcaemia and what are its symptoms?

A

Causes:

  • Vitamin D deficiency or resistance.
  • Hypoparathyroidism.
  • Chronic kidney disease (reduced 1α-hydroxylase activity).
  • Pseudohypoparathyroidism (PTH resistance).

Symptoms:

  • Neuromuscular excitability (tetany).
  • Trousseau’s sign: hand spasm when blood pressure cuff inflated.
  • Chvostek’s sign: facial twitching when facial nerve tapped.
  • Severe: Convulsions, laryngospasm → can be fatal if untreated.
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12
Q

What is Vitamin D deficiency, and how does it affect the bones?

A

Causes:

  • Inadequate sunlight.
  • Poor dietary intake (lack of oily fish, liver, fortified foods).
  • Renal failure → can’t activate 25(OH)D3.

Effects:

  • Children: Rickets – bone deformities due to defective mineralisation.
  • Adults: Osteomalacia – soft bones, bone pain, muscle weakness.
  • Bone is sacrificed to maintain plasma calcium levels.

Treatment:

  • Vitamin D supplements.
  • Dietary changes.
  • Safe sunlight exposure.
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13
Q

How is calcium homeostasis summarised?

A

Short-term regulation: Handled by PTH acting on bone, kidney, and indirectly the intestine.

Long-term regulation: Managed by calcitriol, which promotes absorption and bone turnover.

Calcitonin: Has a minor, non-essential role in lowering calcium during hypercalcaemia.

Disruptions in this system can cause serious consequences like tetany, osteoporosis, kidney stones, or death in extreme cases.

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14
Q

What is the calcium-sensing receptor (CaSR) and how does it regulate PTH?

A

CaSR is a G-protein-coupled receptor found on parathyroid chief cells.

It detects ionised calcium levels in plasma.

When calcium is high → CaSR is activated → inhibits PTH release.

When calcium is low → reduced CaSR activation → stimulates PTH secretion.

Mutations in CaSR can cause calcium regulation disorders (e.g., FHH).

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15
Q

How does PTH exert its effects at the molecular level?

A

Binds to PTH1 receptors in kidneys and bone.

Activates Gs protein → ↑ cAMP → Protein Kinase A (PKA).

Also activates Gq pathway → PLC → IP₃ + DAG → ↑ intracellular Ca²⁺.

Stimulates transcription of genes like 1α-hydroxylase (in kidney).

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16
Q

How does calcitriol (1,25(OH)₂D₃) exert its effects?

A

Binds to Vitamin D Receptor (VDR) – a nuclear receptor.

Calcitriol-VDR complex binds DNA and modifies gene transcription.

Increases synthesis of calbindin, TRPV6 (Ca²⁺ channel), and PMCA (Ca²⁺ ATPase).

Enhances intestinal calcium and phosphate absorption.

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17
Q

How do acid-base disturbances affect calcium levels?

A

Acidosis: H⁺ competes with Ca²⁺ for albumin → ↑ free calcium (more ionised).

Alkalosis: More Ca²⁺ binds to albumin → ↓ free calcium → can lead to symptoms of hypocalcaemia (tetany, spasms).

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18
Q

How do medications affect calcium balance?

A

Loop diuretics: Inhibit Na⁺/K⁺/2Cl⁻ transporter → ↓ calcium reabsorption → hypocalcaemia.

Thiazide diuretics: Enhance calcium reabsorption → may help in kidney stones.

Glucocorticoids: ↓ intestinal absorption and ↑ urinary excretion of calcium → risk of osteoporosis.

Bisphosphonates: Inhibit osteoclasts → used to treat hypercalcaemia.

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19
Q

What is PTH-related peptide (PTHrP)?

A

Structurally similar to PTH, binds the same receptors.

Secreted by some cancers (e.g. lung squamous cell carcinoma).

Causes hypercalcaemia of malignancy.

Unlike PTH, does not activate 1α-hydroxylase, so calcitriol levels remain low.

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20
Q

Osteomalacia vs Osteoporosis

A

Osteomalacia:

  • Due to defective mineralisation.
  • Bone matrix is laid down, but poorly mineralised.
  • Commonly due to vitamin D deficiency.
  • Bone is soft, can bend.

Osteoporosis:

  • Normal mineralisation, but reduced bone mass.
  • More porous, brittle bones.
  • Seen in elderly, postmenopausal women.
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21
Q

A patient has a plasma calcium of 2.9 mmol/L and low PTH. What’s the likely cause?

A

Likely malignancy-associated hypercalcaemia (e.g. via PTHrP). The low PTH shows the parathyroids are suppressed.

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22
Q

A 50-year-old man with chronic kidney disease presents with low calcium and high phosphate. Explain the mechanism.

A

CKD reduces renal 1α-hydroxylase activity → ↓ calcitriol → ↓ calcium absorption.
Also ↓ phosphate excretion → hyperphosphataemia binds free calcium → worsens hypocalcaemia.

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23
Q

A child with bowed legs and poor growth has low vitamin D and calcium. Diagnosis?

A

Rickets – vitamin D deficiency leading to defective mineralisation at growth plates.

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24
Q

A patient on a thiazide diuretic has high calcium. Mechanism?

A

Thiazides increase calcium reabsorption in the distal tubule → risk of hypercalcaemia.

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25
Which of the following is not a function of PTH? A) Increases bone resorption B) Stimulates calcitonin secretion C) Increases renal calcium reabsorption D) Stimulates 1α-hydroxylase in kidneys
🟦 Correct Answer: B (Calcitonin is not regulated by PTH but by high calcium levels.)
26
28. What is the main storage form of calcium in the body? A) Calcium citrate B) Free ionised calcium C) Calcium phosphate in plasma D) Hydroxyapatite in bone
🟦 Correct Answer: D
27
Which condition shows high calcium, low phosphate, and high PTH? A) Rickets B) Chronic kidney disease C) Primary hyperparathyroidism D) Hypoparathyroidism
Correct Answer: C
28
30. Which hormone increases both calcium and phosphate absorption in the intestines? A) Calcitonin B) PTH C) 1,25(OH)₂D₃ D) Insulin
Correct Answer: C
29
A patient has low calcium and high PTH. Which is the least likely cause? A) Vitamin D deficiency B) Chronic renal failure C) Parathyroid adenoma D) PTH resistance (pseudohypoparathyroidism)
Correct Answer: C (Parathyroid adenoma would cause high calcium, not low.)
30
What is the normal reference range for total plasma calcium?
2.20 – 2.60 mmol/L (total plasma calcium).
31
What is the normal level for ionised calcium? Why is this important?
~1.1 – 1.4 mmol/L. This is the biologically active form, crucial for muscle function, nerve transmission, and enzyme activity.
32
What plasma calcium level indicates hypocalcaemia requiring urgent treatment?
<1.5 mmol/L: Carpopedal spasms, convulsions. <1.0 mmol/L: Risk of laryngospasm, respiratory arrest, and death.
33
What plasma calcium and PTH levels are expected in primary hyperparathyroidism?
↑ Calcium ↑ PTH ↓ Phosphate (due to renal phosphate wasting)
34
What labs are seen in hypoparathyroidism?
↓ Calcium ↓ PTH ↑ Phosphate (reduced excretion)
35
What is the classic lab profile in vitamin D deficiency?
↓ Calcium ↓ Phosphate ↑ PTH (secondary hyperparathyroidism) ↓ 25(OH)D₃ on blood test
36
What is the first-line blood test to assess Vitamin D status?
Serum 25(OH)D₃ (not calcitriol). It reflects body stores of vitamin D.
37
What labs are seen in chronic kidney disease affecting calcium balance?
↓ Calcium ↑ Phosphate ↑ PTH (secondary hyperparathyroidism) ↓ 1,25(OH)₂D₃ (due to low 1α-hydroxylase activity)
38
What does a low calcium + high PTH + normal vitamin D suggest?
Pseudohypoparathyroidism – resistance to PTH at the receptor level. PTH is produced but not effective.
39
Which of the following results would suggest primary hyperparathyroidism? A) High calcium, low PTH, low phosphate B) High calcium, high PTH, low phosphate C) Low calcium, high PTH, high phosphate D) Low calcium, low PTH, low phosphate
Correct Answer: B In primary hyperparathyroidism, the parathyroid gland autonomously secretes too much PTH. PTH increases calcium (via bone resorption and renal reabsorption). PTH decreases phosphate (via phosphaturia). Thus: ↑ calcium, ↑ PTH, ↓ phosphate.
40
Which test best assesses long-term vitamin D status? A) Serum 1,25(OH)₂D₃ B) Serum 25(OH)D₃ C) Urinary calcium D) Serum calcitonin
Correct Answer: B ✅ Explanation: 25(OH)D₃ is the storage form of vitamin D and reflects total body stores over time. 1,25(OH)₂D₃ (calcitriol) is the active form, but its levels can fluctuate and don’t reflect stores well.
41
A 65-year-old man with CKD has low calcium and high phosphate. What explains this? A) High calcitonin B) Increased intestinal calcium absorption C) Decreased 1α-hydroxylase activity D) High vitamin D levels
Correct Answer: C ✅ Explanation: In chronic kidney disease, there is reduced 1α-hydroxylase activity → less conversion of 25(OH)D₃ to active calcitriol → reduced calcium absorption. The failing kidney also retains phosphate, worsening hypocalcaemia via precipitation.
42
Which combination is most consistent with hypoparathyroidism? A) ↓ Calcium, ↑ PTH, ↓ Phosphate B) ↓ Calcium, ↓ PTH, ↑ Phosphate C) ↑ Calcium, ↓ PTH, ↓ Phosphate D) ↓ Calcium, ↑ PTH, ↑ Phosphate
Correct Answer: B ✅ Explanation: In hypoparathyroidism, PTH secretion is low → less calcium reabsorption and more phosphate reabsorption. So calcium is low, phosphate is high, and PTH is also low.
43
Which condition typically presents with high PTH but low calcium and low phosphate? A) Primary hyperparathyroidism B) Pseudohypoparathyroidism C) Vitamin D deficiency D) Hypervitaminosis D
Correct Answer: C ✅ Explanation: In vitamin D deficiency, calcium absorption from the gut is impaired → low plasma calcium. Low calcium stimulates secondary PTH release. Phosphate is also low because PTH promotes phosphate excretion.
44
Which lab pattern would support the diagnosis of pseudohypoparathyroidism? A) ↓ Calcium, ↓ PTH B) ↓ Calcium, ↑ PTH C) ↑ Calcium, ↑ PTH D) Normal calcium, ↑ PTH
Correct Answer: B ✅ Explanation: In pseudohypoparathyroidism, the body produces PTH, but target tissues don’t respond (receptor or post-receptor defect). So, despite high PTH, calcium remains low and phosphate stays high. This is a classic example of hormone resistance.
45
Which lab pattern would support the diagnosis of pseudohypoparathyroidism? A) ↓ Calcium, ↓ PTH B) ↓ Calcium, ↑ PTH C) ↑ Calcium, ↑ PTH D) Normal calcium, ↑ PTH
Correct Answer: B ✅ Explanation: In pseudohypoparathyroidism, the body produces PTH, but target tissues don’t respond (receptor or post-receptor defect). So, despite high PTH, calcium remains low and phosphate stays high. This is a classic example of hormone resistance.
46
What is osteoporosis?
Osteoporosis is a systemic skeletal disease characterised by: - Low bone mass - Micro-architectural deterioration These result in increased bone fragility and susceptibility to fractures. It differs from osteomalacia, where bone mass is normal but mineralisation is deficient.
47
What are the key bone cells and their roles?
Osteoclasts: Resorb bone (jellyfish-like structure; acidic microenvironment dissolves bone matrix). Osteoblasts: Form bone; secrete osteoid and mineralise it. Osteocytes: Mechanosensors; coordinate bone repair and response to stress. Bone lining cells: Inactive osteoblasts; help initiate bone remodelling.
48
What is the RANKL/OPG system?
RANKL (on osteoblasts): Binds RANK receptors on osteoclasts → promotes their activation/survival. OPG (osteoprotegerin): A decoy receptor that binds RANKL and prevents osteoclast activation. PTH: Increases RANKL expression → more bone resorption. High PTH levels = bad for bone.
49
What are common fracture sites in osteoporosis?
Vertebrae: Especially post-menopausal women. Colles’ fracture: Distal radius. Neck of femur: Hip fractures.
50
What causes osteoporosis?
- Oestrogen deficiency (e.g. menopause): ↑ RANKL → ↑ osteoclasts. - Glucocorticoids: ↓ osteoblasts, ↑ PTH, ↓ sex steroids. - Vitamin D/calcium deficiency: ↓ mineralisation → osteomalacia → eventually osteoporosis. - Ageing: ↓ androgens, IGF-1, growth factors.
51
How does vitamin D deficiency contribute to bone disease?
↓ Calcium absorption from intestines. Leads to compensatory ↑ PTH → bone resorption. Without enough calcium/phosphate, bone matrix remains unmineralised = osteomalacia. Chronic deficiency leads to structural deterioration = osteoporosis.
52
What is glucocorticoid-induced osteoporosis (GIO)?
Long-term steroids → osteoblast apoptosis, ↓ bone formation. Also ↑ PTH and ↓ IGF-1. Fracture risk increases within months of steroid use. Treated with bisphosphonates, and by minimising steroid use.
53
How do bisphosphonates work?
Analogues of pyrophosphate with high affinity for bone. Bind beneath osteoclasts → inhibit intracellular signalling → cause osteoclast apoptosis. Reduce spine and hip fracture risk.
54
What are side effects of bisphosphonates?
Osteonecrosis of the jaw (rare, serious). May delay repair of bone microfractures. Remain in the bone for years.
55
What are SERMs and how do they work?
Selective Oestrogen Receptor Modulators like Raloxifene. Oestrogen agonist in bone → ↑ bone density. Antagonist in breast/uterus → ↓ cancer risk. Not effective in men or premenopausal women.
56
What is Denosumab and how does it work?
Monoclonal antibody against RANKL. Prevents RANKL-RANK binding → inhibits osteoclast activation. Used in post-menopausal osteoporosis. Side effects: immune suppression, ↑ skin infections.
57
How do intermittent PTH injections work (e.g. Teriparatide)?
Low-dose, intermittent PTH → stimulates osteoblast differentiation and survival. Promotes bone formation, especially in trabecular bone. Only anabolic therapy. Used in severe osteoporosis. Long-term use risks osteosarcoma (seen in animal studies).
58
Role of calcium and vitamin D supplements?
Reduces secondary hyperparathyroidism. ↓ fracture risk in elderly/institutionalised. Combined therapy (Ca + Vit D) more effective than either alone.
59
Trabecular vs Cortical Bone in Osteoporosis
Trabecular bone: Found in vertebrae, ends of long bones; metabolically more active → affected first. - Responds better to anabolic therapy (e.g., Teriparatide) Cortical bone: Dense outer shell, found in femoral neck and forearm. - Slower turnover; still affected in prolonged disease or advanced age.
60
How is osteoporosis diagnosed and monitored?
Diagnosed using DEXA scan (dual-energy X-ray absorptiometry). T-score: ≤ -2.5 = osteoporosis -1 to -2.4 = osteopenia Repeat scans are done every 1–2 years to assess treatment efficacy. Also monitor serum calcium, phosphate, PTH, vitamin D levels, especially if on treatment.
61
What is the role of the Calcium-Sensing Receptor (CaSR) in bone health?
Found on parathyroid glands and osteoblasts. Senses extracellular calcium levels → influences PTH release. Dysfunction → abnormal PTH levels, altered bone remodelling. Related to familial hypocalciuric hypercalcaemia or autosomal dominant hypocalcaemia.
62
A 62-year-old woman with back pain has a T-score of -2.8 on a DEXA scan. What is the diagnosis? A) Normal B) Osteopenia C) Osteoporosis D) Osteomalacia
Correct Answer: C ✅ Explanation: A T-score of ≤ -2.5 indicates osteoporosis (WHO definition). Osteopenia is -1 to -2.4.
63
Which of the following increases osteoclast activity by upregulating RANKL? A) Oestrogen B) PTH C) Denosumab D) OPG
Correct Answer: B ✅ Explanation: PTH stimulates RANKL expression → activates osteoclasts → increases bone resorption.
64
Which of the following drugs promotes bone formation rather than inhibiting resorption? A) Alendronate B) Raloxifene C) Denosumab D) Teriparatide
Correct Answer: D ✅ Explanation: Teriparatide (intermittent PTH) is the only listed agent that stimulates osteoblasts and promotes bone formation.
65
Which bone type is most affected early in osteoporosis? A) Cortical bone B) Flat bone C) Trabecular bone D) Sesamoid bone
Correct Answer: C ✅ Explanation: Trabecular bone (e.g., spine, ends of long bones) has higher metabolic activity and is affected first in osteoporosis.
66
A 45-year-old man on chronic steroids for asthma presents with a Colles' fracture. What’s the best treatment? A) Raloxifene B) Teriparatide C) Bisphosphonates D) Oestrogen
Correct Answer: C ✅ Explanation: Glucocorticoid-induced osteoporosis (GIO) is treated first-line with bisphosphonates, unless severe or resistant.
67
Which of the following best describes the action of Denosumab? A) Mimics oestrogen to reduce osteoclast activity B) Blocks RANKL to prevent osteoclast activation C) Inhibits osteoblast function D) Increases OPG levels directly
Correct Answer: B ✅ Explanation: Denosumab is a monoclonal antibody against RANKL, preventing it from activating RANK on osteoclasts.
68
Which condition shows normal bone volume but poor mineralisation? A) Osteoporosis B) Osteomalacia C) Osteogenesis imperfecta D) Paget’s disease
Correct Answer: B ✅ Explanation: Osteomalacia is caused by impaired mineralisation, often due to vitamin D deficiency.
69
What is a significant risk of long-term bisphosphonate use? A) Skin rash B) Osteonecrosis of the jaw C) Hypercalcaemia D) Breast cancer
Correct Answer: B ✅ Explanation: Rare but serious, osteonecrosis of the jaw is a known complication of prolonged bisphosphonate therapy.
70
Which of the following is a feature of oestrogen deficiency-induced bone loss? A) Increased OPG B) Decreased RANKL C) Increased osteoclast survival D) Increased osteoblast activity
Correct Answer: C ✅ Explanation: Oestrogen suppresses RANKL. Its deficiency → ↑ RANKL → increased osteoclast activity and survival.
71
A patient discontinues Denosumab abruptly. What is the main concern? A) Hypocalcaemia B) Jaw necrosis C) Rebound vertebral fractures D) Osteomalacia
Correct Answer: C ✅ Explanation: Stopping Denosumab can cause rapid rebound in bone turnover, particularly leading to vertebral fractures.

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