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Hypoparathyroidism: DR Gwer

Hypoparathyroidism is a condition caused by a deficiency of parathyroid hormone (PTH) which can result from genetic disorders, surgical removal of the parathyroid glands, or autoimmune disease. Symptoms include muscular cramps, numbness, seizures, and abnormalities in calcium and phosphate levels. Treatment involves emergency calcium supplementation and long-term vitamin D and calcium therapy to manage calcium levels and prevent complications.

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Malueth Angui
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50 views14 pages

Hypoparathyroidism: DR Gwer

Hypoparathyroidism is a condition caused by a deficiency of parathyroid hormone (PTH) which can result from genetic disorders, surgical removal of the parathyroid glands, or autoimmune disease. Symptoms include muscular cramps, numbness, seizures, and abnormalities in calcium and phosphate levels. Treatment involves emergency calcium supplementation and long-term vitamin D and calcium therapy to manage calcium levels and prevent complications.

Uploaded by

Malueth Angui
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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Hypoparathyroidism

Dr Gwer
Introduction
• The parathyroid glands are derived from the
pharyngeal pouches just like the thymus.
• Usually the 4 glands found next to 4 lobes of
the thyroid. 10% of the population have only 2
or 3 glands.
• Parathormone (PTH) levels are regulated by free
circulating levels of calcium ions. The hormone’s
effect is to increase circulating calcium.
functions of PTH
• PTH activates osteoclasts which mobilise
calcium from bone.
• It increases renal tubular re-absorption of
calcium
• It increases conversion of vit D to active form.
• It increases urinary phosphate excretion
• It augments GIT calcium absorption
Causes of hypoparathyroidism
• Genetic causes: aplasia/hypoplasia (Di-George syndrome),
chromosomal anomalies and mitochondrial DNA anomalies
(kearns-sayre syndrome)
• Suppression of maternal PTH due to maternal
hyperparathyroidism
• Surgical hypoparathyroidism – post surgical
• Auto-immune hypoparathyroidism; usually associated with
adrenal insufficiency and candidiasis (APS 1)
• Idiopathic hypoparathyroidism
• Excess copper or iron deposition in Wilsons disease and
thallasemia
Clinical manifestations

• Muscular pain/cramps • Features of raised ICP


• Numbness/stiffness • Late dental eruption
• Tingling extremities • Irregular enamel and soft
• +ve Chvostek sign teeth
• Trousseau sign • Dry scaly skin
• Laryngeal spasms
• Horizontal nail lines
• Convulsions
• Cataracts
• Abdominal pains
•
• Physical/mental retardation
Headaches
•
(may be permanent in
Tonic rigidity and head retraction
delayed treatment)
Laboratory findings
• Hypocalcemia
• Hyper phosphatemia
• Low or normal ALP
• Low active vitamin D ( may be high in severe disease}
• Immunometric assay of PTH show low levels
• Prolonged QT interval on ECG
• Slow activity on EEG
• Xray : increased metaphyseal density (heavy metal
poisoning) or increased density of lamina dura
Treatment
• Emergency treatment of tetany with calcium
gluconate and calcitriol (active vit D)
• After normocalcemia achieved continue
therapy with vit D2
• Supplement cacium
• Reduce dietary phosphorus (eg milk, eggs and
cheese)
• Monitor blood to avoid hypercalcemia.
Pseudohypoparathyroidism
• In this condition there is end-organ resistance
to PTH. Serum PTH are normal or high.
• Type 1A: is resistance to PTH, TSH and LH/FSH
and is a mutational disorder inherited from
maternal allele.
• Type 1B; inherited is inherited from paternal
allele and only PTH affected
HYPERPARATHYROIDISM
Introduction
• Primary hyperparathyroidism: autonomous
spontaneous over production of PTH usually due to
adenoma or hyperplasia (rare in childhood)
• Secondary hyperparathyroidism: excess production
of PTH as a compensatory reaction to hypocalcemic
states of diverse origins. (common)
• Tertiary hyperparathyroidism: rare occasions where
2 ͦhyperPTH becomes autonomous and excessive
Causes
1 ͦ hyper PTH 2 ͦ hyperPTH
• Adenoma • Renal failure
• Autosomal dominant • Vit D deficiency
adenoma • Steatorrhea
• MEN 1 • Dietary calcium lack
• Parathyroid hyperplasia of
infancy ( maternal hypoPTH)
• Ectopic PTH production
Clinicals of 1 ͦ dz
• May be asymptomatic and identified on routine chemistry
profile
• Muscular weakness, anorexia, nausea, emesis, polydypsia,
polyuria, constipation and fever.
• Nephrocalcinosis, renal calculi, back pain, fractures,
pancreatitis, gait disturbance
• In infants- failure to thrive, poor feeding hypotonia
• Parathyroid crisis: Ca²+ levels > 15mg/dl , oliguria, azotemia,
stupor, coma
• Long term: mental retardation, fits and blindness, cardiac
valvular calcifications
Lab findings
• Hypercalcemia , hypophosphatemia, hypoMg
• Elevated serum PTH
• Xray: resorption of subperiosteal bone,
rarefaction of bone, fractures, deformity/
bone cysts, rickets, renal calculi and
nephrocalcinosis
•
Treatment of 1 ͦ dz
• Surgical exploration in all cases with removal
of adenoma
• Severe dz require total removal
• Prognosis good with early treatment

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