• Parathyroid hormone (PTH) is a powerful regulator of extracellular calcium and phosphate concentrations.
• It controls these ions by regulating:
  • Intestinal absorption
  • Renal excretion
  • Exchange of calcium and phosphate between bone and extracellular fluid
• Excess parathyroid activity causes rapid release of calcium salts from bone.
• This increases extracellular calcium and produces hypercalcemia.
• Reduced parathyroid activity causes hypocalcemia.
• Severe hypocalcemia may produce tetany.

Physiological Anatomy of the Parathyroid Glands

• Humans normally have four parathyroid glands.
• They lie immediately behind the thyroid gland:
  • One behind each upper pole
  • One behind each lower pole
• Each parathyroid gland is approximately:
  • 6 mm long
  • 3 mm wide
  • 2 mm thick
• They appear macroscopically like dark brown fat.
• During thyroid surgery, parathyroid glands can be difficult to identify because they may resemble a small thyroid lobule.
• Therefore, they may accidentally be removed during thyroid surgery.
• Removal of half of the parathyroid glands usually causes no major physiological problem.
• Removal of three of the four glands may cause temporary hypoparathyroidism.
• However, even a small amount of remaining parathyroid tissue can hypertrophy and usually provide enough function.
• The adult parathyroid gland contains mainly chief cells and smaller numbers of oxyphil cells (Fig. 80.12).
• Chief cells secrete most, if not all, of the PTH.
• Oxyphil cells are absent in many animals and in young humans.
• Their exact function is uncertain.
• They are believed to be modified or depleted chief cells that no longer secrete hormone.

KEY CONCEPT

• PTH = major regulator of extracellular Ca²⁺ and phosphate.
• ↑ PTH → calcium released from bone → ↑ blood Ca²⁺.
• ↓ PTH → ↓ blood Ca²⁺ → possible tetany.
• Normally there are 4 parathyroid glands behind the thyroid.
• Chief cells → secrete PTH.

Conceptual Examples

• Excess PTH:
  ↑ PTH → ↑ release of calcium salts from bone → hypercalcemia.
• Low PTH:
  ↓ PTH → ↓ blood Ca²⁺ → increased nerve and muscle excitability → tetany.
• After loss of three glands:
  Small remaining parathyroid tissue → hypertrophy → may restore adequate PTH function.
• Cell type:
  Chief cell → PTH secretion.

Chemistry of Parathyroid Hormone

• PTH is first synthesized on ribosomes as a preprohormone containing 110 amino acids.
• It is then processed in the endoplasmic reticulum and Golgi apparatus: Prepro-PTH (110 amino acids) → Pro-PTH (90 amino acids) → PTH (84 amino acids)
• The final PTH is packaged into secretory granules inside the cell.
• Mature PTH has a molecular weight of about 9500.
• Smaller fragments containing as few as 34 amino acids near the N-terminal end can still produce full PTH activity.
• The kidneys remove the complete 84-amino-acid PTH from the blood within minutes.
• Many smaller PTH fragments remain in the circulation for hours.
• Therefore, a considerable part of prolonged PTH activity may come from these circulating fragments.

KEY CONCEPT

• PTH synthesis: 110-aa preprohormone → 90-aa prohormone → 84-aa active PTH
• N-terminal 34 amino acids can retain full biological activity.
• Whole PTH is cleared rapidly by the kidneys, whereas many fragments remain for much longer.

Conceptual Examples

• PTH formation:
  Ribosome → 110-aa prepro-PTH → processing in ER/Golgi → 84-aa PTH.
• Active fragment:
  N-terminal 34-amino-acid fragment → can still show full PTH activity.
• Blood persistence:
  Whole PTH → removed within minutes.
  PTH fragments → remain for hours → longer-lasting hormonal activity.

PARATHYROID HORMONE EFFECTS ON EXTRACELLULAR FLUID CALCIUM AND PHOSPHATE CONCENTRATIONS

• When PTH is suddenly increased, blood calcium begins to rise and reaches a plateau in about 4 hours (Fig. 80.13).
• Blood phosphate falls more rapidly, reaching a lower level within about 1–2 hours.
• PTH raises blood calcium mainly by:
  • Increasing release of calcium and phosphate from bone
  • Decreasing calcium excretion by the kidneys
• Therefore: ↑ PTH → ↑ bone calcium release + ↑ renal calcium conservation → ↑ blood Ca²⁺
• PTH lowers blood phosphate because it strongly increases phosphate excretion by the kidneys.
• Although PTH also releases phosphate from bone, the renal phosphate loss is greater.
• Therefore: ↑ PTH → ↑ renal phosphate excretion → ↓ blood phosphate

KEY CONCEPT

• PTH raises blood calcium but lowers blood phosphate.
• Calcium: rises more slowly, plateau in about 4 hours.
• Phosphate: falls faster, within about 1–2 hours.
• Main pattern: ↑ PTH → ↑ Ca²⁺ + ↓ phosphate

Conceptual Examples

• Calcium effect:
  ↑ PTH → calcium released from bone + less calcium lost in urine → blood Ca²⁺ rises.
• Phosphate effect:
  ↑ PTH → kidneys excrete more phosphate → blood phosphate falls.
• Easy memory:
  PTH saves Ca²⁺ but wastes phosphate.

Figure 80.13 — Effect of PTH on Calcium and Phosphate

🧠 Main Idea

Parathyroid hormone (PTH) does two important things in blood:

Calcium ↑
Phosphate ↓

Think: PTH = “Pushes calcium High, Throws phosphate out.”

📊 Axes

• X-axis = Hours → time during PTH infusion.
• Left Y-axis = Blood calcium (mmol/L).
• Right Y-axis = Blood phosphate (mmol/L).

⬇️ “Begin parathyroid hormone” arrow

At about 1 hour, PTH infusion begins.

Before this point:

🔴 Red line = Calcium

After PTH begins:

Calcium gradually rises ↑

~2.30 → ~2.40 mmol/L

It reaches a near plateau at about 4 hours.

Why?

PTH:

• releases calcium from bone ↑
• reduces calcium loss in urine ↑ renal Ca²⁺ reabsorption

➡️ Therefore blood calcium increases.

The slight flattening afterward means a new near-steady level is being reached.

🔵 Blue line = Phosphate

After PTH begins:

Phosphate falls rapidly ↓

It reaches its lowest level within about 1–2 hours after PTH starts, then rises slightly toward a lower steady level.

Why?

PTH causes the kidneys to:

↓ phosphate reabsorption → ↑ phosphate excretion in urine

➡️ Therefore blood phosphate decreases.

Even though PTH can release phosphate from bone, the kidney throws out so much phosphate that the overall blood phosphate level falls.

⭐ Most Important Comparison

Phosphate falls faster than calcium rises.

Why?

• Phosphate effect = rapid kidney excretion
• Calcium rise = bone release + kidney calcium conservation, which develops more gradually.

Easy Memory

PTH → Ca²⁺ ↑, PO₄³⁻ ↓

PTH saves calcium but wastes phosphate.

Parathyroid Hormone Mobilizes Calcium and Phosphate From Bone

• PTH releases calcium and phosphate from bone in two phases:
  • Rapid phase → begins within minutes and lasts for several hours.
  • Slow phase → develops over days to weeks.
• The rapid phase mainly activates already existing bone cells, especially osteocytes, to release calcium and phosphate.
• The slow phase increases osteoclast formation and bone resorption.

Rapid Phase of Calcium and Phosphate Mobilization From Bone—Osteolysis

• After large amounts of PTH are given, blood Ca²⁺ begins to rise within minutes.
• This occurs before new bone cells can form.
• PTH removes calcium salts mainly from:
  • Bone matrix surrounding osteocytes
  • Bone surfaces near osteoblasts
• Osteocytes and osteoblasts form an interconnected osteocytic membrane system throughout bone.
• A small amount of bone fluid lies between this membrane system and the bone.
• Normally, the osteocytic membrane pumps Ca²⁺ from bone fluid into the extracellular fluid.
• This keeps calcium concentration in bone fluid at about one-third of extracellular fluid calcium.
• When this calcium pump becomes strongly activated:
  • Bone-fluid Ca²⁺ falls.
  • Calcium phosphate salts dissolve from bone.
• This rapid removal of mineral salts without breakdown of the organic bone matrix is called osteolysis.
• When the pump is inactive, bone-fluid calcium rises and calcium phosphate can be redeposited in bone.
• Osteoblasts and osteocytes have PTH receptors.
• PTH strongly activates their calcium pump.
• PTH also increases calcium permeability on the bone-fluid side of these cells.
• Therefore: PTH → osteoblast/osteocyte receptor → ↑ Ca²⁺ movement from bone fluid → ↑ Ca²⁺ into extracellular fluid

Slow Phase of Bone Resorption and Calcium Phosphate Release—Activation of the Osteoclasts

• PTH also causes a slower increase in osteoclast activity.
• Osteoclasts themselves do not have PTH receptors.
• PTH acts on osteoblasts and osteocytes, which then send signals to osteoclast precursors.
• An important signal is RANKL.
• RANKL converts preosteoclasts into mature bone-resorbing osteoclasts.
• Osteoclast activation occurs in two stages:
  • Rapid activation of existing osteoclasts
  • Formation of new osteoclasts
• After several days of excess PTH, osteoclast activity becomes strongly increased.
• With prolonged PTH stimulation, this activity can continue increasing for months.
• After months of excess PTH, excessive bone resorption can cause weak bones.
• Osteoblast activity also increases in an attempt to replace lost bone.
• However, with continued excess PTH: Bone resorption > bone deposition
• Bone contains about 1000 times more calcium than all extracellular fluids combined.
• Therefore, short-term rises in blood calcium may not produce obvious structural changes in bone.
• But prolonged PTH excess for months or years can cause marked bone resorption and large osteoclastic cavities.

KEY CONCEPT

• PTH raises blood Ca²⁺ from bone in 2 phases.
• Rapid phase: osteocytes/osteoblasts → calcium pump activation → osteolysis.
• Osteolysis = mineral removal without destruction of organic bone matrix.
• Slow phase: PTH → osteoblast/osteocyte → ↑ RANKL → ↑ osteoclasts → true bone resorption.
• Chronic excess PTH → bone resorption exceeds bone formation → weak bones.

Conceptual Examples

• Within minutes:
  ↑ PTH → osteocytic calcium pump activated → calcium phosphate leaves bone → blood Ca²⁺ rises rapidly.
• After several days:
  ↑ PTH → ↑ RANKL → more mature osteoclasts → greater bone resorption.
• Long-term excess PTH:
  Persistent osteoclast activity → bone loss exceeds replacement → weak bones and bone cavities.

Parathyroid Hormone Decreases Calcium Excretion and Increases Phosphate Excretion By the Kidneys

• PTH rapidly increases phosphate loss in urine.
• It does this by decreasing phosphate reabsorption in the proximal renal tubules.
• At the same time, PTH increases renal calcium reabsorption.
• Therefore: ↑ PTH → ↓ phosphate reabsorption → ↑ phosphate excretion ↑ PTH → ↑ calcium reabsorption → ↓ calcium excretion
• PTH also increases renal reabsorption of:
  • Magnesium
  • Hydrogen ions
• PTH decreases renal reabsorption of:
  • Sodium
  • Potassium
  • Amino acids
• Increased calcium reabsorption occurs mainly in the:
  • Thick ascending loop of Henle
  • Distal tubules
• Without this calcium-conserving effect of PTH, continuous urinary calcium loss would eventually deplete calcium from both the extracellular fluid and bones.

Parathyroid Hormone Increases Intestinal Absorption of Calcium and Phosphate

• PTH increases intestinal absorption of both calcium and phosphate.
• This effect occurs mainly because PTH stimulates the kidneys to form more 1,25-dihydroxycholecalciferol (calcitriol) from vitamin D.
• Therefore: ↑ PTH → ↑ calcitriol → ↑ intestinal Ca²⁺ and phosphate absorption

Cyclic Adenosine Monophosphate Mediates the Effects of Parathyroid Hormone

• Many effects of PTH are mediated through the cAMP second-messenger system.
• Within minutes after PTH increases, cAMP rises in target cells.
• Increased cAMP contributes to effects such as:
  • Osteoclastic secretion of enzymes and acids → bone resorption
  • Increased formation of 1,25-dihydroxycholecalciferol in the kidneys
• Some PTH effects may also occur independently of cAMP.

KEY CONCEPT

• PTH saves calcium but wastes phosphate.
• Kidney:
  • ↑ Ca²⁺ reabsorption → ↓ urinary calcium
  • ↓ phosphate reabsorption → ↑ urinary phosphate
• PTH → kidney → ↑ calcitriol → ↑ intestinal Ca²⁺ + phosphate absorption.
• Many PTH actions occur through the cAMP second-messenger pathway.

Conceptual Examples

• Phosphate:
  ↑ PTH → ↓ proximal tubular phosphate reabsorption → more phosphate in urine.
• Calcium:
  ↑ PTH → ↑ renal Ca²⁺ reabsorption → less calcium lost in urine.
• Intestine:
  ↑ PTH → ↑ calcitriol → more calcium and phosphate absorbed from food.
• Second messenger:
  PTH binds target cell → ↑ cAMP → activates important PTH effects.

CONTROL OF PARATHYROID SECRETION BY CALCIUM ION CONCENTRATION

• Even a small fall in extracellular Ca²⁺ causes the parathyroid glands to increase PTH secretion within minutes.
• If low Ca²⁺ continues for a long time, the parathyroid glands enlarge (hypertrophy), sometimes up to 5-fold or more.
• Parathyroid enlargement occurs in:
  • Rickets → chronically reduced Ca²⁺
  • Pregnancy → increased calcium requirement
  • Lactation → calcium is used for milk formation
• In contrast, high extracellular Ca²⁺ decreases parathyroid activity and reduces gland size.
• This can occur with:
  • High dietary calcium
  • Increased vitamin D
  • Increased bone resorption from causes other than PTH, such as bone disuse
• Parathyroid cells detect extracellular Ca²⁺ through the calcium-sensing receptor (CSR).
• CSR is a G protein–coupled receptor.
• When extracellular Ca²⁺ rises: ↑ Ca²⁺ → activates CSR → activates phospholipase C → ↑ IP₃ + DAG → ↑ intracellular Ca²⁺ → ↓ PTH secretion
• When extracellular Ca²⁺ falls:
  • CSR stimulation decreases.
  • These intracellular pathways become less active.
  • PTH secretion increases.
• Therefore: ↓ Blood Ca²⁺ → ↑ PTH
  ↑ Blood Ca²⁺ → ↓ PTH
• This is unusual because, in many other endocrine cells, increased intracellular signaling and Ca²⁺ promote hormone secretion, whereas in parathyroid cells they suppress PTH secretion.
• Fig. 80.14 shows the inverse relationship between plasma Ca²⁺ and PTH.
• During an acute fall in Ca²⁺, even a small decrease can cause PTH to increase 2–3 times.
• During chronic low Ca²⁺ over many weeks, parathyroid hypertrophy makes the response even stronger.
• A decrease of only a fraction of 1 mg/dL in plasma Ca²⁺ can eventually double PTH secretion.
• This creates a very powerful long-term feedback system for maintaining normal plasma Ca²⁺.

KEY CONCEPT

• PTH secretion is inversely related to blood Ca²⁺.
• ↓ Ca²⁺ → ↑ PTH
• ↑ Ca²⁺ → ↓ PTH
• Chronic ↓ Ca²⁺ → parathyroid hypertrophy → even greater PTH secretion.
• Calcium is detected by the calcium-sensing receptor (CSR).
• Main feedback: ↓ Ca²⁺ → ↑ PTH → helps restore Ca²⁺ toward normal

Conceptual Examples

• Low calcium:
  ↓ Blood Ca²⁺ → less CSR activation → ↑ PTH secretion.
• High calcium:
  ↑ Blood Ca²⁺ → CSR activation → ↑ IP₃/DAG → ↓ PTH secretion.
• Long-term low calcium:
  Persistent ↓ Ca²⁺ → parathyroid glands enlarge → much greater PTH response.
• Lactation:
  Calcium used for milk → greater calcium requirement → parathyroid glands enlarge and increase PTH activity.

Figure 80.14 — How Blood Calcium Controls PTH and Calcitonin

🧠 Main idea

This graph shows that blood calcium is the main switch for 2 hormones:

• Low calcium → Parathyroid hormone (PTH) goes up
• High calcium → Calcitonin goes up

So remember:

Calcium low = PTH ON
Calcium high = Calcitonin ON

📊 First understand the axes

X-axis = Plasma calcium (mg/100 mL)

This is the amount of calcium in blood.

• Moving left = lower blood calcium
• Moving right = higher blood calcium

Left Y-axis = Parathyroid hormone (ng/mL)

This measures PTH.

Right Y-axis = Plasma calcitonin (pg/mL)

This measures calcitonin.

So the graph is showing 2 hormones on the same calcium scale.

🔴 Red solid line = PTH acute effect

This line shows what happens to PTH quickly/immediately when calcium changes.

What it means:

• When calcium is low (left side), PTH is very high
• As calcium rises, PTH falls sharply
• At high calcium, PTH becomes very low

Easy meaning:

The parathyroid gland is saying:

“Calcium is low! Release more PTH!”

Why?

Because PTH helps raise blood calcium by:

• increasing calcium release from bone
• increasing calcium reabsorption in kidney
• helping activate vitamin D, which increases calcium absorption from gut

Simple concept:

Low calcium → high PTH
High calcium → low PTH

🔴 Red dotted/dashed line = PTH chronic effect

This dotted line shows the long-term effect of calcium on PTH.

It is steeper than the acute line.

What does that mean?

Over a longer time, even a small change in calcium can cause a very big change in PTH.

Easy idea:

If calcium stays low for a long time, the parathyroid glands become more active and enlarged, so PTH response becomes even stronger.

So:

• Acute effect = quick response
• Chronic effect = stronger long-term response

Most important point:

The dotted line means PTH is extremely sensitive to calcium in the long run.

🔵 Blue line = Calcitonin

This line goes upward.

What it means:

• At low or normal calcium, calcitonin is low
• When calcium rises above normal, calcitonin rises quickly

Easy meaning:

The thyroid C cells are saying:

“Calcium is high! Release calcitonin!”

Calcitonin helps lower blood calcium, mainly by reducing bone resorption.

Simple concept:

High calcium → high calcitonin

✖ Black “Normal levels” mark

This black mark shows the normal blood calcium level, around 9–10 mg/100 mL.

At this point:

• PTH is present at a low-normal level
• Calcitonin is also around its normal level

This point is like the balance point.⭐ Compare all lines simply

When calcium falls:

• PTH rises a lot 🔴
• Calcitonin stays low 🔵

When calcium rises:

• PTH falls 🔴
• Calcitonin rises 🔵

So the 2 hormones work in opposite directions.

⭐ Final short memory

PTH

• Responds to low calcium
• Works to increase calcium

Calcitonin

• Responds to high calcium
• Works to decrease calcium

One-line memory:

Low Ca²⁺ → PTH up
High Ca²⁺ → Calcitonin up

2-Line Exam Recall — Figure 80.14

↓ Plasma Ca²⁺ → ↑ PTH → raises blood Ca²⁺.
↑ Plasma Ca²⁺ → ↓ PTH + ↑ calcitonin → opposes further rise in Ca²⁺.

Very Short MBBS Note

PTH: inversely related to plasma Ca²⁺; chronic PTH response is much more sensitive than the acute response.
Calcitonin: directly related to plasma Ca²⁺ and increases mainly when Ca²⁺ becomes high.

🔑 Memory

Low Ca²⁺ = PTH ON
High Ca²⁺ = Calcitonin ON

SUMMARY OF EFFECTS OF PARATHYROID HORMONE

• A decrease in extracellular Ca²⁺ stimulates increased PTH secretion (Fig. 80.15).
• PTH then raises extracellular calcium through three main actions.
• 1. Bone
  • PTH stimulates bone resorption.
  • Calcium is released from bone into the extracellular fluid.
  • Therefore:
  ↑ PTH → ↑ bone resorption → ↑ blood Ca²⁺
• 2. Kidneys
  • PTH increases calcium reabsorption by renal tubules.
  • Therefore, less calcium is lost in urine.
  • PTH decreases phosphate reabsorption.
  • Therefore, more phosphate is lost in urine.
  ↑ PTH → ↓ urinary Ca²⁺ + ↑ urinary phosphate
• 3. Vitamin D and Intestine
  • PTH is required for conversion of:
  25-hydroxycholecalciferol → 1,25-dihydroxycholecalciferol (calcitriol)
  • Calcitriol then increases intestinal calcium absorption.
  • Therefore:
  ↑ PTH → ↑ calcitriol → ↑ intestinal Ca²⁺ absorption
• Together, these actions provide a powerful mechanism for maintaining normal extracellular Ca²⁺ concentration.

KEY CONCEPT

• ↓ Blood Ca²⁺ → ↑ PTH
• PTH raises blood Ca²⁺ by:
  • Bone → ↑ calcium release
  • Kidney → ↑ calcium reabsorption
  • Kidney → ↑ calcitriol → intestine → ↑ calcium absorption
• At the same time: PTH → ↓ renal phosphate reabsorption → ↑ phosphate excretion
• Easy memory: PTH raises Ca²⁺ and lowers phosphate.

Conceptual Examples

• Bone:
  ↑ PTH → ↑ bone resorption → Ca²⁺ enters blood.
• Kidney:
  ↑ PTH → kidney saves Ca²⁺ but wastes phosphate → ↑ blood Ca²⁺ + ↓ blood phosphate.
• Intestine:
  ↑ PTH → ↑ calcitriol → more dietary Ca²⁺ absorbed.
• Overall:
  ↓ Ca²⁺ → ↑ PTH → bone + kidney + intestine work together → Ca²⁺ returns toward normal.

Figure 80.15 — How PTH Raises Blood Calcium

Easiest Concept

Think of PTH as the emergency hormone for low blood calcium.

↓ Ca²⁺ → ↑ PTH → bone + kidney + intestine work together → ↑ blood Ca²⁺

Follow the figure from top to bottom

• ↓ Ca²⁺
  • Blood calcium falls.
• CaSR = calcium-sensing receptor
  • Present in the parathyroid gland.
  • It detects the fall in Ca²⁺.
• Low Ca²⁺ causes:
  • ↑ PTH secretion

1. PTH effect on Bone

↑ PTH → ↑ bone resorption

• Bone calcium is released into blood.
• Therefore:
  • ↑ Ca²⁺ efflux from bone
  • ↑ plasma Ca²⁺

Think: Bone acts as a calcium bank. PTH withdraws calcium.

2. PTH effect on Kidney

PTH causes:

• ↑ Ca²⁺ reabsorption
  • Less calcium is lost in urine.
  • More Ca²⁺ stays in blood.
• ↓ PO₄³⁻ reabsorption
  • More phosphate is lost in urine.
  • This is called phosphaturia.
• ↑ 1,25-dihydroxycholecalciferol
  • Kidney makes more active vitamin D (calcitriol).

3. PTH effect on Intestine

PTH acts on the intestine mainly indirectly through active vitamin D.

Active vitamin D causes:

• ↑ Ca²⁺ absorption
• ↑ PO₄³⁻ absorption

So more dietary calcium enters the blood.

Final Result

All three organs increase blood calcium:

Bone releases Ca²⁺ + Kidney saves Ca²⁺ + Intestine absorbs more Ca²⁺ → ↑ plasma Ca²⁺

Important phosphate concept

PTH may increase phosphate release from bone and vitamin D increases intestinal phosphate absorption, but PTH makes the kidney excrete phosphate strongly.

So the classic overall effect of PTH is:

↑ Blood Ca²⁺
↓ Blood phosphate

🔑 KEY CONCEPT

Low Ca²⁺ → CaSR senses it → ↑ PTH

Then:

Bone: ↑ resorption
Kidney: ↑ Ca²⁺ reabsorption + ↓ phosphate reabsorption + ↑ active vitamin D
Intestine: ↑ Ca²⁺ absorption

One-line memory

“PTH raises calcium by taking it from bone, saving it in kidney, and absorbing more from intestine.”

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