Thyroid and parathyroid

Parathyroid Hormone
Physiological role

1. Production related to plasma Calcium

2. Control of Calcium levels
3. Target organs
a. Bone
• Increased Ca/PO4 release
b. Kidneys
• Increased reabsorption of Ca
• Increased excretion of PO4
c. Gut
• Indirect increase in calcium reabs by
stimulting activation of vit D metabolism
 Ca – Dietary Sources

• Milk – 100 ml =120mg

• Cheese – 15gm = 110mg
• Yoghurt pot – 80gm = 160mg
• Other sources
– Fish
– Meat
– Bread
– Cereal
– Broccoli
Synthesis and regulation of vit D3 (Calcitriol)
Bone
 Etiology of hypocalcaemia
• Failure of secretion or actions of PTH
• Disorders of vitamin D
• CaSR disorders
• Dietary Ca deficiency (CMPI)
• Malabsorption of Ca – coeliac disease, short
gut, tufting enteropathy
 Low PTH levels High PTH levels
(hypoparathyroidism) (secondary hyperparathyroidism)
Parathyroid Destruction PTH resistance
Surgery Pseudohypoparathyroidism
Auto-immune (isolated or polyglandular) Hypomagnesemia
Cervical irradiation
Infiltration by metastasis or systemic diseases
(Sarcoidosis, amyloidosis, hemochromatosis,
Wilson’s disease, thalassemia)

Reduced parathyroid function Vitamin D deficiency

Hypomagnesemia Nutritional
PTH gene defects Lack of sunlight
Calcium sensing receptor mutations Malabsorption
Vitamin D dependent rickets
type I (lack of activity of 1a-hydroxylase)
type II (Vitamin D receptor resistance)
Chronic renal disease
Parathyroid agenesis Drugs
 Low PTH levels High PTH levels
(hypoparathyroidism) (secondary hyperparathyroidism)
Parathyroid agenesis Drugs
DiGeorge Syndrome Bisphosphonates, cisplatin, ketoconazole, gallium
Isolated x-linked hypoparathyroidism nitrate, anticonvulsants
Kenny-Caffey syndrome
Mitochondrial neuropathies
Hyperphosphatemia
Renal insufficiency
Massive tumor lysis
Acute rhabdomyolysis
Acute pancreatitis
Hungry bone
Toxic shock syndrome
Acute severe illness
Calcium chelators (citrated blood transfusions,
phosphate
 Clinical features of Hypocalcaemia

1. Neuromuscular excitability
2. Paraesthesia (tingling sensation) around mouth,
fingers and toes
3. Muscle cramps, carpopedal spasms
4. Tetany
5. Seizures – focal or generalised
6. Laryngospasm, stridor and apneas (neonates)
7. Cardiac rhythm disturbances (prolonged QT interval)
8. Chvostek’s and Trousseau’s signs – latent
hypocalcemia
 Chvostek’s and Trousseau’s sign

• Svostex Trousseau’s sign

Chvostek I phenomenon
Chvostek II phenomenon
 Investigations
1. Ca and Pi
2. PTH
3. Vit D
a. 25 hydroxy vit D3
b. 1,25 dihydroxy vit D3
4. Mg
5. Urinary Ca/ Cr ratio
 Urine Ca/Cr
> 0.56 < 0.56
mmol/mmol mmol/mmol

Serum P
Hypocalcaemic
hypercalciuria
Low High

Vitamin D related causes

Serum 25 OH D Serum PTH

Normal Low Low High

Serum 1, 25
(OH)2 D Vit D Deficiency

Low High

VDDR VDDR Hypo-PTH Pseudo-

Type I Type II hypo-PTH
 Approach
1. Low PTH
Hypoparathyroidism (Primary/ secondary)
2. Normal/ low normal PTH
Mg deficiency
CaSR activating mutation
3. High PTH
Vit D deficiency
VDDR
Pseudohypoparathyroidism – types 1, 2
 Treatment of Hypocalcaemia

Severe Symptomatic:
• IV 10% Calcium Gluconate @ 0.11 mmol/kg
(0.5 mls/kg – max 20 mls) over 10 minutes

• Continuous IV infusion of Calcium Gluconate @

0.1 mmol/kg
(Max 8.8 mmols) over 24 hours

Severe Asymptomatic:
Oral Calcium Supplements @ 0.2 mmol/kg
(Max 10 mmols or 400 mg Ca) 4 x a day
 Calsium peroral
Milligrams of salt
Element needed in order to Parenteral preparation
Salt content obtain 1 g
elementary calcium
Calcium carbonate 40% 2500
Calcium phosphate 38% 2631
Calcium chloride 27% 3700 10% Solution =
273 mg/10 ml
Calcium citrate 21% 4762
Calcium lactate 13% 7700
Calcium gluconate 9% 11100 10% Solution =
93 mg/10 ml
 Treatment of Hypoparathyroidism

• Aim to keep serum Ca (2.0 - 2.2 mmol/l

• Oral Calcium supplements
• Active preparations of Vitamin D
• 1,25-dihydroxyvitamin D (Calcitriol)
• 1‑α‑hydroxyvitamin D (Alfacalcidiol)
@ 50 nanograms/kg (Max ~2micrograms/day)
• Monitoring
• Urine Ca/Cr (<0.7)
• Renal Ultrasound Scan
 Vit D3 analogue
Calciferol Calcidiol Calcitriol Alfacalcidol
D3 / D2 25(OH)D 1,25(OH)2D 1αOHD

 25-hydroxylation + – – –
necessary

 1α-hydroxylation + + – –
necessary

 Physiological 2.5–10 μg 1–5 μg 0.25–0.5 μg 1–3 μg

dose/dosage (1 μg= 40 UI) (1 μg= 40 UI)

 Pharmacological 0.625–5 mg 20–250 μg 0.5–3 μg 1–3 μg

dose/dosage

 Time needed to 4–8 weeks 2–4 weeks 3–7 days 7–14 days
normalize calcium

 Duration of effect 6–12 weeks 2–6 weeks 3–7 days 7–14 days
 Summary
• PTH is the primary regulator of blood calcium levels and bone
metabolism.
• Insufficient levels of PTH lead to hypoparathyroidism
(low serum calcium and elevated serum phosphate)
• The most commonly caused by damage to the parathyroid glands
during thyroid surgery.
• Its being treated with oral calcium and active vitamin D.
To avoid worsening hypercalciuria, target serum calcium levels
are normal.
• The recent FDA approval of recombinant human (rh) PTH(1-84)