1. Calcium homeostasis is regulated by parathyroid hormone (PTH), calcitonin, vitamin D, and the kidneys and bones. Abnormalities can cause hypo- or hypercalcemia. 2. Hypocalcemia presents with symptoms like numbness, cramps, and seizures. It is diagnosed through blood tests and may be treated with oral calcium or IV calcium gluconate. 3. Hypercalcemia has various causes like primary hyperparathyroidism and can be asymptomatic or cause polyuria, nausea, and kidney stones. Treatment involves rehydration, calcitonin, and bisphosphonates.

1. Prof. Taj Jamshaid
Professor of Medicine
drjamshaid1@gmail.com
Parathyroid gland /
Parathormone and Calcium
metabolism

2. Calcium –
Homeostasis
PTH
STIMULUS: Falling
Plasma Ca++ levelStimulates Ca++
release from Bones
Stimulates Ca++
uptake in kidneysActive vitamin D
 Ca++ uptake
in intestines
Blood Ca++ level
rises to set point
STIMULUS: Rising
Plasma Ca++ level
Thyroid gland
releases CALCITONIN
CALCITONIN
Stimulates Ca++
deposition in bones
↓ Ca++ uptake
in kidneys
Blood Ca++ level
↓ to set point

3. Normal adult Calcium content:
20 – 25 gm/kg of body wt
Normal plasma calcium:
8.7 – 10.4 mg/dl
Ionized calcium (Biologically active
fraction): about 50%
Protein bound (mostly albumin): 50%
Do following tests to
investigate Calcium
Disorders:
• Calcium
• Phosphate
• Alkaline phosphate
• PTH (Parathormone)
• S/Albumin
Corrected Calcium = 0.8 x ( Normal Albumin – Pt’s Albumin) + Serum Calcium
Note: Calcium (mg/dl) Albumin (g/dl)

4. Presenting problems in Parathyroid
disease:
1. HYPOCALCEMIA
2. HYPERCALCEMIA

5. Misc:
 Hungry Bone syndrome
 Pancreatitis
 critical illness
Parathyroid
Disorder
Vitamin D
disorders
Magnessium
depletion and
Hypocalcemia
Hypo-functioning Parathyroid (>
99% of all cases)
• Surgical removal
• Idiopathic (congenital/ acquires)
Inability of kidney and
bone to respond to
PTH being produced
by normal PTH
Resistance to PTH
leading to raised PTH
but not effective
• pseudohypoparath
yroidism
Hyperphosphatemia
& Hypocalcemia
Medicines:
• Antiepiletics
• Anticancer
Facticious
Hypocalcemia
HYPOCALCEMIA:
(S/ Ca++ < 8.4 mg/dl)

6. CLINICAL FEATURES
 Perioral numbness
 Tingling parasthesias
 Muscle cramps
 Carpopedal spasm
 Seizures
 Laryngospasm/ stridor

7. Hyperreflexia
Hypotension
Bradycardia
Prolonged QT interval
Arrhythmias
Chvostek sign
Trousseau sign
(Last 2 signs for latent
hypocalcemia)
SIGNS

8. CHVOSTEK’S SIGN:
 Tell the patient to relax his facial muscles
 Stand directly in front of patient
 Tap the facial nerve;
 either just anterior to the ear-lobe and
below the zygomatic arch
 or between the zygomatic arch and corner
of his mouth
 Positive response varies depending on
the severity of hypocalcemia;
 Twitching of the lip at the corner of the
mouth
 Spasm of all facial muscles

9. TROUSSEAU
SIGN:
 Very uncomfortable and painful
 BP cuff inflated to a pressure
above systolic level
 Pressure continued for about 3
minutes
 Carpopedal spasm:
 flexion at the wrist
 flexion at the MP joints
 extension of the IP joints
 adduction thumbs/fingers

10. Most Hypocalcemic emergencies – mild, requiring only supportive
care and usually Oral Calcium preparations
Aggressive approach with supportive care and IV Calcium
Gluconate (10% 10cc 10minutes), if
Seizures
Tetany
Refractory hypotension
Arrhythmias
Stridor/ laryngospasm
 S/ Calcium < 7.6 mg /dl
MANAGEMENT OF HYPOCALCEMIA:
DEPENDS ON
SPEED OF ONSET, CAUSE, BIOCHEMICAL SEVERITY, AND CLINICAL FEATURES.

11. • One of the most common biochemical abnormality
• > 50% detected incidentally on during routine biochemical
analysis & asymptomatic.
• Can present with chronic symptoms, & occasionally as an
acute emergency with severe hypercalcemia & dehydration
HYPERCALCEMIA:
(S/ Ca++ > 10.4 mg/dl)

12. CLINICAL ASSESSMENT OF HYPERCALCEMIA
S/S of hypercalcaemia:
• Polyuria & polydipsia
• Renal colic
• Lethargy
• Anorexia, nausea, dyspepsia &
peptic ulceration
• Constipation
• Depression, drowsiness & impaired
cognition
Patients with malignant
hypercalcemia:
• Rapid onset of symptoms
• May have clinical features
that help to localize the
tumor

13. CLINICAL ASSESSMENT OF HYPERCALCEMIA

14. CAUSES & EVALUATION OF HYPERCALCEMIA:

15. Treatment of severe hypercalcaemia:
• Rehydration with normal saline.
• Calcitonin acts rapidly and can be added for the first 24–48 hrs in
patients with life threatening hypercalcaemia.
• Bisphosphonates (e.g. pamidronate 90 mg IV over 4 hrs) reduce
serum calcium to normal within 5 days, the effect lasting up to 4
wks.
• Repeated therapy can be given 3–4weekly as an outpatient.
Management Of Hyperparathyroidism:
MANAGEMENT OF HYPERCALCEMIA:
• ALLEVIATE THE SYMPTOMS
• TREAT THE CAUSE

16. Type Serum Calcium PTH
Primary:
• Single adenoma (90%)
• Multiple adenoma (4%)
• Nodular hyperplasia (5%)
• Carcinoma (1%)
↑ Not suppressed
Secondary:
• CRF
• Malabsorption
• Osteomalacia & Rickets
↓ ↑
Tertiary: ↑ Not suppressed

17. MEN type I (PPP)
 Parathyroid adenoma
 Pituitary adenoma
 Pancreatic Islet cell tumor
MEN type II (PTP)
 Parathyroid adenoma
 Thyroid Medullary Carcinoma
 Pheochromocytoma
Primary Hyperparathyroidism
Prevalence: 1 in 800
 2 – 3 times more common
 90% over 50 years
May be part of MEN (Multiple Endocrine Neoplasia)

18. CLINICAL PRESENTATION:
•Often ‘ASYMPTOMATIC’
• ↑Ca2+ on routine tests (> 10.4 mg/dl)
May have
•S/S of ↑Ca2+
•Skeletal & Radiological changes

19. •OSTEOPOROSIS: reduced bone
mineral density on DEXA scanning
• OSTEITIS FIBROSA CYSTICA: Due to severe bone
resorption by osteoclasts with fibrous replacement –
bone pains/ fractures/ deformity

20. ‘Pepper-pot’ skull
Acro-osteolytis – tuft
resorption with subperiosteal
bone resorption of radial
margins of middle phalanges of
2nd, 3rd & 4th fingers, and cysts or
brown tumors of the phalanges
X-Ray Changes:
Renal Calcifications

21. OTHER TESTS
•↑Ca2+ & ↑ or inappropriately normal PTH
•↓PO4 (unless in renal failure), ↑ALP from bone
activity, 24h urinary ↑ Ca2+.
•99mTc-sestamibi scintigraphy or USS:
•performed prior to surgery to localise the adenoma

22. RX (DEPENDING UPON SEVERITY / COMPLICATIONS)
•Rx of hypercalcemia
•Rx of choice for primary
hyperparathyroidism:
• surgical excision of a solitary
parathyroid adenoma or
hyperplastic glands
•Indications of surgery:
• Patients under 50
• With s/s or complications
(PUD, renal stones, renal
impairment or osteopenia)
Otherwise:
• Annual review, with assessment
of symptoms, renal function,
serum calcium and bone mineral
density.
Cinacalcet (calcimimetic that
enhances the sensitivity of calcium
sensing receptor, so ↓PTH levels)
• licensed for tertiary
hyperparathyroidism & for
primary hyperparathyroidism
unwilling or unfit to have surgery.

23.  ↑ PTH production in response
to ↓ Ca2+, (appropriately)
• Caused by conditions that
interfere with Calcium,
phosphate or vit D regulation:
• ↓ Vit D intake
• CRF
• Malnutrition
SECONDARY HYPERPARATHYROIDISM
 Rx:
 Correct causes
 Phosphate binders, Vit D
 Cinacalcet if PTH ≥ 85pmol/L &
parathyroidectomy tricky

24. • Occurs after prolonged secondary hyperparathyroidism,
causing glands to act autonomously having undergone
hyperplastic or adenomatous change.
 This causes ↑Ca2+ from ↑↑ secretion of PTH unlimited by
feedback control.
 Seen in CRF
TERTIARY HYPERPARATHYROIDISM

25. • Parathyroid gland damage
during thyroid surgery:
• transient hypocalcaemia in 10%,
permanent in 1%
• Infiltration of the glands:
• haemochromatosis, Wilson’s
disease
• Congenital/inherited (rare):
• autoimmune polyendocrine
syndrome (APS) type I
• autosomal dominant
hypoparathyroidism.
• ↓PTH
• ↓ Ca2+ and ↑ PO43- Equivocal
ALP
• Signs of hypocalcaemia or
features of polyendocrine
failure
• Rx: Ca2+ supplement +
calcitriol (vitamin D
analogue) or synthetic PTH
Primary Hypoparathyroidism

26. • Tissue resistance or failure of
target cell response to PTH
• Signs: Short metacarpals (4th &
5th), round face, short stature,
obesity, low IQ, calcified basal
ganglia, subcutaneous
calcification
• Tests: ↓ Ca2+ and ↑ PTH &
Equivocal ALP
• Rx: As for 1°
hypoparathyroidism.
PSEUDOHYPOPARATHYROIDISM

27. •Morphological features of Pseudohypoparathyroidism
but with normal serum calcium and PTH levels
PSEUDO-PSEUDOHYPOPARATHYROIDISM
Both are due to Genomic imprinting/ factors:
• gene defect from mother – Pseudohypoparathyroidism
• gene defect from father – Pseudo-pseudohypoparathyroidism