PARATHYROID

 Serum calcium is controlled by Parathyroid

Hormone & Vit D
 There are 4 Parathyroid glands derived from the
pharyngeal pouches
 Produce Parathormone (PTH)
 PTH levels rise as serum calcium levels fall
• Total serum calcium = ionized (biologically active)
+ protein bound
• Serum ca should be increased by 0.8 for each
1.0 g of albumin going down
 PTH
 PTH causes
 Osteoclastic
bone
resorption
 Increases
intestinal Ca
absorption
 Increases 1. ACTIVATES OSTEOCLASTS
synthesis of 2. INCREASES THE RENAL Ca REABSORPTION
3. INCREASES URINARY PO4 EXCRETION
Vit D
 Increases
renal Ca re-
absorption &
Po4 excretion
HYPERCALCEMIA
 HYPERCALCEMIA
 Most common cause of clinically
significant hypercalcemia is malignancy

 Common cause of asymptomatic

hypercalcemia is Primary
hyperparathyroidism

 Hyperparathyroidism can be Primary,

Secondary or Tertiary
 CAUSES OF HYPERCALCEMIA
 Excessive PTH secretion:
 Primary & tertiary hyperparathyroidism
 Malignancy:
 Myeloma, Metastasis, PTH- related peptide
 Bronchus, Esophagus, Prostate, Thyroid tumors
 Excess of Vit D:
 Self administered, Sarcoidosis, TB, Lymphoma
 Drugs:
 Thiazide, Chronic lithium
 Long term immobility
 Hypercalcemia
Raised PTH Decreased PTH
 Primary  Malignancy
hyperparathyroidism  Vitamin D toxicity
 Familial  Immobilization
hypercalcemia  drugs
 Primary Hyperparathyroidism
 Is one of the common endocrine
disorders
 Various pararthyroid lesions causes this
 Adenoma 75 – 80%
 Primary hyperplasia 10 – 15%
 Parathyroid carcinoma <5%
 Can be part of MEN type 1 or 2a
 MEN Type 1
 3 P’s
 Parathyroid Hyperplasia
 Pancreatic adenoma (ZES, Gastrinoma,
Insulinoma)
 Pituitary adenoma (prolactinoma)
MEN type 2A (Sipple syndrome)
 Medullary carcinoma of thyroid (100%)
 Pheochromocytoma (50%)
 Parathyroid hyperplasia (30%)

MEN type 2B (William syndrome)

 Medullary carcinoma thyroid
 Pheochromocytoma
 There is NO Parathyroid disease
 Also have Ganglioneuromas of GIT, Lips, tongue
 Marfan’s Habitus
 SECONDARY
HYPERPARATHYROIDISM
 Renal failure or Vit D deficiency giving rise
to Hypocalcemia causes raised PTH
levels due to feed back stimulation

 Parathyroid hyperplasia is seen

 Raised PTH levels with Low or Normal Ca

levels
 TERTIARY
HYPERPARATHYROIDISM
 Long standing secondary
hyperparathyroidism due to Renal failure
can give rise to autonomous parathyroid
hyperplasia

 Associated with raised Ca levels

 Parathyroidectomy is needed to manage

 CLINICAL FEATURES of
Hypercalcemia
 They present generally in one of the two
ways

1. Asymptomatic Hypercalcemia

2. Classic clinical manifestation associated

with mild or severe hypercalcemia
 SYMPTOMS & SIGNS
 Tiredness, fatigue, dehydration
 Bone disease – Osteoporosis leading to
fractures, brown tumor
 Nephrolithiasis
 GIT – Constipation, Peptic ulcers,
Pancreatitis, Gall stones
 CNS – Depression, Lethargy and Seizures
 CVS – Aortic or Mitral calcification.
 INVESTIGATIONS
 Serum Ca & Po4 levels
 Serum PTH levels
 Renal functions
 Protein electrophoresis for myeloma
 Serum TSH for thyroid status
 Abdominal X-ray for stones, DEXA for bone
osteoporosis
 USG scan, CT scan or MRI for Parathyroid
localization
 Radioisotope scan for parathyroid
 Sr Calcium Sr Po4 PTH levels

Primary
Hyperparat
hyroidism
Secondary N or

Tertiary
 HYPERCALCEMIA- RX
 Immediate Rx is mandatory if the patient is
ill or if Ca levels are > 13.5 mg/dl
 Normal Ca levels are: 8.5 – 10.5 mg/dl
 Adequate hydration
 TOC: IV biphosphonates infusion
(Pamidronate)
 IV calcitonin, prednisolone can be given
 SURGERY FOR
HYPERPARATHYROIDISM
 Controversial indications for surgery
 Pts with renal stones or impaired Renal fn
 Marked bone mineral abnormality
 Sustained marked hypercalcemia > 13.5
mg/dl
 Younger pt < age 50 yrs
 Previous episode of severe acute
hypeprcalcemia
 Post OP complications: Hypocalcemia,
vocal cord paralysis
 Hypoparathyroidism
 Is far less common than
hyperparathyroidism
 Etiology
 Surgically induced – During thyroidectomy
 Congenital absence of all the four glands
 Idiopathic hypoparathyroidism- Autoimmune
 Familial hypoparathyroidism- DiGeorge
syndrome
 PSEUDOHYPOPARATHYROIDISM
 End organ resistance to PTH
 Hypocalcemia, Hyperposphatemia, & Increased
PTH levels
 Short stature, rounded face, shortened fourth
metacarpals and other bones of the hand and
feet, obesity, dental hypoplasia, and soft tissue
calcifications/ossifications
 Pseudopseudohypoparathyroidism (PPHP) is
characterized by normal calcium homeostasis in
the setting of this PHP phenotype
CLINICAL FEATURES - Hypocalcemia
 Hallmark of hypocalcemia is Tetany
 Characterized by neuromuscular irritability –
parasthesia, numbness, Chvostek sign,
Trousseau sign.
 Mental changes – Emotional instability,
Anxiety, Confusion, Hallucination
 CVS – QT prolongation
 Dental changes – Dental hypoplasia,
failure of eruption.
 Convulsions, Tetany, stridor, psychosis.
 Investigations - Hypocalcemia
 serum and urine creatinine for renal disease
 PTH levels : absent or inappropriately low in
hypoparathyroidism, high in other causes of
hypocalcaemia
 parathyroid antibodies (present in idiopathic
hypoparathyroidism)
 25-hydroxy vit D level (low in vit D deficiency)
 magnesium level – severe hypomagnesaemia
results in functional hypoparathyroidism
 X-rays of metacarpals, showing short fourth
metacarpals which occur in
pseudohypoparathyroidism.
 Treatment

 Alpha-hydroxylated derivatives of vitamin

D are preferred for their shorter half-life,
and especially in renal disease as the
others require renal hydroxylation.
 0.25–2 μg/day for alfacalcidol (1α-OH-D3).
 Monitor Serum Ca level during treatment