The document discusses disorders of the parathyroid glands and tetany. It notes that the parathyroid glands regulate calcium and phosphate levels and vitamin D metabolism. Disorders can cause hypercalcemia or hypocalcemia. Hypercalcemia symptoms include polyuria and renal problems. Hypocalcemia can cause tetany with muscle spasms. Primary causes, clinical features, investigations, and management are described for various parathyroid disorders including primary hyperparathyroidism and hypoparathyroidism. Tetany is defined as muscle spasms caused by parathyroid dysfunction and low calcium levels.

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PARATHYROID GLAND
DISORDERS AND
TETANY

2.  4 parathyroid glands lie behind the lobe of
thyroid gland
 Plays a key role in regulating calcium,
phosphate homeostasis and vitamin D
metabolism
 Chief cells respond directly to change in
calcium concentration, secreting PTH in
response to fall in ionised calcium

4. Investigations
 Measurement of calcium, phosphate, alkaline
phosphatase, renal function, PTH, and
25(OH)D
 Most of laboratories only measure total serum
calcium level and about 50% of calcium is
bound to organic ions
 If the serum albumin is reduced total calcium
concentration should be corrected by adjusting
the value of calcium upwards by 0,02 mmol/L
for each 1 g/L reduction in albumin below 40g/L

5. Presenting problems
in parathyroid disease
Hypercalcaemia
hypocalcaemia

6. Hypercalcaemia

7. Clinical assessment
 Usually asymptomatic
 Polyuria
 polydipsia
 renal colic
 Lethargy
 anorexia
 nausea
 Dyspepsia
 peptic ulceration
 Constipation
 Depression
 drowsiness
 impaired cognition

8.  Malignant hypercalcaemia:- rapid onset of
symptoms and clinical features that helps to
localize the tumour
 Primary hyperparathyroidism:- bones,
stones, and abdominal groans

9. Investigations
 Measurement of PTH
 If PTH levels are detectable or elevated in the
presence of hypercalcaemia primary
hyperparathyroidism
 High plasma phosphate + alkaline
phosphatase + renal tubular impairment
tertiary hyperparathyroidism

10.  Hypercalcaemia nephrocalcinosis and
renal tubular impairment Hyperuricemia and
hyperchloremia
 FHH
 present with similar biochemical picture to primary
hyperparathyroidism but have low urinary calcium
excretion.
 Confirmed by screening family members for
hypercalcaemia and/or a mutation in gene encoding
the calcium sensing receptor

11.  If PTH low and no other causes apparent then
malignancy with or without bony metastasis is
likely
 PTH related peptide is often responsible for
the hypercalcaemia associated malignancy.
Not detected by PTH assays
 Screened for malignancy with chest x
ray,melanoma screen and CT

12. Management
 IV 0.9% saline 2-4 L/ day
 IV bisphosphonates given to inhibit bone
resorption. Zoledronic acid 4mg IV or
pamidronate 60-90 MG IV
 Reduce the calcium level to normal with in 5
days but if not treatment repeated
 IM/SC calcitonin 100U 3 times daily for first 24-
48 hours in life threatening hypercalcaemia

13. Hypocalcaemia
 Less common
 Causes
 Hypoalbuminaemia
 alkalosis
 vitamin D deficiency
 chronic renal failure
 Hyperparathyroidis
 pseudohypoparathyroidism
 acute pancreatitis
 hypomagnesaemia

14. Clinical assessments
 Often asymptomatic
 Tetany - muscle spasms due to increased
excitability of peripheral nerves
 Children are more likely to develop tetany
 Triad of carpopedal spasm stridor and convulsions
 Papilloedema
 Prolonged QT interval ventricular arrhythmia

15.  Prolonged Hypocalcaemia and
hyperphosphataemia causes calcification of
basal ganglia, grand mal epilepsy, psychosis
and cataract
 Hypocalcaemia associated with
hyperphosphataemia as in vitamin D
deficiency cause rickets in children and
osteomalacia in adults

16. Management
 10-20mL 10% calcium Gluconate IV over 10-
20minutes
 Continuous IV infusion may be required for
several hours
 Cardiac monitoring is recommended
 If associated Hypomagnesaemia 50mmol
magnesium chloride IV over 24hrs
 Most parenteral magnesium will be excreted in the
urine, so further doses may be required to
replenish body store

17. Primary hyperparathyroidism
 Caused by autonomous secretion of PTH

18. Clinical and radiological features
 Osteitis fibrousa
 increased bone resorption by osteoclasts with
fibrous replacement in the lacuna.
 Bone pain and tenderness, fracture and deformity

19.  Chondrocalcinosis
 deposition of calcium pyrophosphate crystals
within articulate cartilage.
 Affect menisci at knee and can result in
secondary degenerative arthritis or predispose to
attacks of acute pseudogout

20. Management
 Surgery indicated in
 Individual aged less than 50 years
 Clear cut symptoms
 Documented complications - peptide ulcer, renal
stone, renal impairment or osteoporosis
 Significant Hypercalcaemia
 Cinacalcet – calcimimetic, enhance sensitivity
to calcium sensing receptor reduces PTH level

21. Familial hypocalciuric
hypercalcaemia
 Autosomal dominant disorder
 Inactivating mutation in one of the alleles of
calcium sensing receptor gene which reduces
the ability to sense the ionised calcium
concentration
 Higher than the normal calcium levls are
needed to supress PTH secretion
 Affect renal tubule cusing increased renal
tubular reabsorption of calcium and
hyperuricemia

22. Hypoparathyroidism
 Causes
 Parathyroid gland damage during thyroid surgery
 Infiltration of gland (haemochromatosis, Wilson’s
disease
 Congenital/inherited(autoimmune polyendocrine
syndrome type 1, autosomal dominant
hypoparathyroidism

23.  In pseudo hypoparathyroidism –tissue
resistance to PTH
 Clinical features
 Short statcure
 Short 4th metacarpals and metatarsals
 Rounded face
 Obesity
 Subcutaneous calcification
 Serum calcium and PTH are normal

24.  Results from inheritance of gene defect from
mother due to genomic imprinting

25. Management
 Oral calcium salts
 Vitamin D analogues (alfacalcidol,calcitriol)
 Monitoring of therapy required – iatrogenic
hypercalcaemia, hypercalciuria and
nephrocalcinosis

26. Tetany

27.  A condition marked by intermittent muscular
spasms, caused by malfunction of the
parathyroid glands and a consequent
deficiency of calcium
 Childrens are more likely to be affected

28. Clinical features
 Classical triad
 Carpopedal spasm:-characteristic position of
hand- flexion of metacarpophalangeal joint and
adduction of thumb
 Stridor :-spasm of glottis
 Convulsions

29. Signs
 Trousseau’s sign:- inflation of
sphygmomanometer cuff on the upper arm to
more than systolic blood pressure is followed
by carpopedal spasm within 3 minutes
 Chvostek’s sign :-tapping over branches of
facial nerve as they emerging from the parotid
gland produces twitching of the facial muscles

30.  Management same as that of hypocalcaemia

31. Thank you