Download The parathyroid glands

The parathyroid glands
Dr. AMMAR SALIH ABBOOD
2016
The parathyroid glands
• Parathyroid hormone (PTH) plays a key role
in the regulation of calcium and phosphate
homeostasis and vitamin D metabolism
Anatomy and physiology
• Four glands lie behind the lobes of the
thyroid.
• The chief cells secret PTH which is a single
chain polypeptide of 84 amino acids
• Low ionised serum calcium will stimulate the
chief cells via a “calcium sensing receptor” to
secret PTH
Functions of PTH
• Increase calcium reabsorption from renal
tubules and decrease phosphate
reabsorption
• Increase osteoclastic bone resorption and
bone formation
• Stimulates alpha hydroxylase enzyme in the
kidney and promotes the conversion of 25
HCC to 1,25 DHCC
Calcium and phosphorus
Calcium
• Total body calcium is about 1200-2000 g.
* 99% in bones and teeth.
*1% circulates in the blood.
• 50% of circulating Ca is bounded to albumin.
• The free Ca”ionised” is the biologically active
form.
• Blood level of Ca is 2.2–2.6 mmol/L (8.5–10.5
mg/dL).
Functions of Calcium
• Bone mineralization.
• Regulates hormonal and neuromuscular
signaling.
• Important in cardiac contractility.
• Important for blood coagulation.
Hypocalcemia
Causes of Hypocalcemia:
• Hypoparathyroidism
• Pseudohypoparathyroidism
• Vitamin D deficiency.
• Chronic renal failure.
• Drugs ( loop diuretics, bisphosphonates).
• Acute pancreatitis.
• Acute rhabdomyolysis.
Clinical feature of hypocalcemia
• Mild : asymptomatic.
• Moderate : paresthesias mainly affect fingers
and perioral area (Chvostek's and Trousseau's
signs may be seen).
• Severe : seizures, carpopedal spasm,
bronchospasm and laryngospasm may occur.
• Clinical features of the underlying cause
Hypercalcemia
Causes of hypercalcemia:
• Primary and tertiary Hyperparathyroidism.
• Malignancies.
• Granulomatous diseases (sarcoidosis, tuberculosis)
• Endocrine disorders ( hyperthyroidism, Addison )
• Drugs (thiazides).
• Excessive calcium intake (Milk-alkali syndrome).
• Familial hypocalciuric hypercalcemia
Clinical features of hypercalcemia
• Mild : asymptomatic
• Moderate :
*nausea, anorexia, constipation, polyuria.
*Renal stones.
*Peptic ulcer disease.
* neuropsychiatric symptoms.
• Sever : lethargy, confusion and coma.
Investigations
• Serum calcium.
• Hypoalbuminaemia will falsely lower serum
calcium level , so level needs to be corrected
by adding 0.1 mmol/l (0.4 mg/dL) for each 5
g /L reduction in serum albumin below 40 g/L
(40 – Alb)* 0.02 + Ca++ mmol/L
(40 – Alb)* 0.08 + Ca++ mg/dL
Other investigations
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ECG : QT interval.
Serum phosphate
Alkaline phosphatase
Renal function tests
PTH
25 HCC
Treatment
• Correction of the underlying cause.
• IV calcium gluconate for acute symptomatic
hypocalcemia.
• Oral calcium for chronic hypocalcemia with
vitamin D.
• Rehydration with or without diuretics for
hypercalcemia
• Bisphosphonates for hypercalcemia
Phosphorus
• Total body phosphorus is about 600 g of
which 85% present in bones.
• It is also a component of structural proteins,
enzymes, transcription factors, energy stores
(ATP) and nucleic acids.
• Blood level is 0.75–1.45 mmol/L (2.5–4.5
mg/dL).
Food sources of phosphorus
Hypophosphatemia
Causes of hypophosphatemia :
• Primary hyperparathyroidism.
• Vitamin D deficiency.
• Renal loss of phosphate.
• Drugs like aluminum containing antacids.
Clinical features of hypophosphatemia
• With hypocalcemia : Bone pain, proximal
muscle weakness and pseudofractures.
• With hypercalcemia : renal stones ,
calcifications
• Lethargy, confusion, disorientation, ataxia,
Respiratory failure, cardiac dysfunction and
Rhabdomyolysis may occur in sever cases.
hyperphosphatemia
Causes of hyperphosphatemia:
• Renal insufficiency.
• Hypoparathyroidism.
• Extensive cellular injury or necrosis ( crush
injury, rhabdomyolysis)
Clinical features of hyperphosphatemia
• Widespread calcium phosphate precipitation
leading to:
*Renal stones.
*Seizures.
*Pulmonary and cardiac calcifications.
• Symptoms of hypocalcemia.
Diagnosis and treatment
• serum phosphorus, serum calcium
• Correct the underlying cause.
• Hypophosphatemia : Oral phosphate for mild
cases and IV phosphate for severe cases.
• Hyperphosphatemia : Rehydration, Phosphate
binders (sevalamer), Hemodialysis.
Hyperparathyroidism
Classification and Causes
Primary Hyperparathyroidism
Epidemiology
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Prevalence 1 in 800
2-3 times more common in women
90 % of patients are over 50 years old
May be part of familial MEN syndrome
Clinical features
• 50% asymptomatic
• Clinical features of hypercalcemia , polyuria,
polydipsia, recurrent renal pain, constipation,
dyspepsia, peptic ulceration, nausea,
anorexia, lethargy, depression and impaired
cognition
• “ bones, stones and abdominal groans”
Clinical features
• Osteitis fibrosa : bone resorption and fibrous
replacement in the lacunae
• Chondrocalcinosis: ca deposition in articular
cartilage and secondary OA and Pseudogout
• Nephrocalcinosis
• Soft tissue calcification, vessels walls, hands
and cornea
Investigations
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Hypercalcemia
Hypercalciuria
Hypophosphatemia,
Raised PTH (fasting)
Normal renal function tests
Investigations
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Skeletal X-rays:
Normal in early disease
Demineralization
Subperiosteal erosions and terminal
resorption of phalanges
Salt and paper appearance on lat. skull x-ray
Osteopenia and osteoporosis by DEXA
Localization of the adenoma
• Ultrasound
• Neck MRI
• 99m Tc-sestamibi scintigraphy
Treatment
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Surgery is indicated in :
Age <50
Ca >11.4 mg (2.85 mmol)
Presence of complications PU, stones etc.
Complications of surgery
• “hungry bone syndrome “ is a profound
hypocalcemia which develops after
parathyroidectomy due to rapid remineralisation
of bone before recovery of residual parathyroid
tissue
• This is prevented by calcium and active vitamin D
supplements in the immediate post-operative
period for 2-3 weeks
Treatment
• Asymptomatic patients need follow up 6-12
monthly
• Cinacalcet is a calcimimetic that enhance the
sensitivity of Ca sensing receptors used for
patients unfit for GA and for tertiary
hyperparathyroidism
Familial hypocalciuric hypercalcemia
• AD , defective Ca-sensing receptors
• Presents with hypercalcemia, increased PTH
and hypocalciuria
• The hypercalcemia is always asymptomatic
and no complications
• Diagnosis by urine Ca and genetic testing
• No treatment is required
Hypoparathyroidism
Causes
• Damage to the glands or their blood supply
during thyroid surgery 10% transient, 1%
permanent
• Polyendocine syndrome
• Di George syndrome
• Autosomal dominant hypoparathyrodism ADH
(Hypocalcaemic hypercalciuria)
• Abnormal infiltrations of the gland , Wilson's ,
hemochromatosis
Pseudohypoparathyroidism
• Tissue resistance to PTH , patients are
hypoparathyroid with elevated PTH , their
features are short stature with short 4th
metacarpals , round faces , obesity and
subcutaneous calcifications ‘’ Albright’s
hereditary osteodystrophy AHO “
Pseudo-pseudohypoparathyrodism
• Same as AHO with normal Ca and PTH
concentration
• This disorder is an example of genetic
imprinting, inheritance of defective gene
from the mother leads to pseudohypopara,
inheritance of the defective gene from the
father leads to pseudo-pseudohypopara
Clinical features of
hypoparathyrodism
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Symptoms of Hypocalcemia
Decrease Calcium level
Increase phosphate level
PTH
Treatment
• Oral calcium salts and vitamin D analogues
either alfacalcidol or Calcitriol
• Recombinant PTH is available.