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DR MOHAMMED SHAHID
 BLOOD: Hypercalcemia
Hypophosphatemia
ALP- increased
 URINE: Hypercalciuria
Hyperphosphaturia
 HPE: single adenoma-mc,
pale, clear-chief cells
 ECG: short QT interval
 USG & Tc99 SESTAMIBI SCAN
 24hr urinary calcium:
• Differentiates pHPT from familial hypocalciuric
hypercalcemia
 Phosphate excretion test:
• PTHdecreases net tubular phosphorous
reabsorptionphosphaturia.
 Phosphorous loading test:
• In case of poor intake or poor absorption, there is normal
phosphorous excretion
• Oral phosphorous (2-3g over 3days)  decreases tubular
phosphorous reabsorption phosphaturia
 Cortisone suppression test:
• Administration of steroids (150mg cortisone per day for
10days)  no effect on hypercalcemia of
hyperparathyroidism in contrast to sarcoidosis, multiple
myeloma, hypervit D
 Urinary Hydroxyproline: markedly raised. attributed to
increased bone turnover and collagen degradation.
 Isotope studies:
• Se-75 (selenomethionine) scan detects abnormal
parathyroid tissue
 RIA: radiolabelled antibodies directed against PTH. More
specific.
 M/C : generalized osteopenia
 Bone resorption- subperiosteal, intracortical,
trabecular, endosteal, subchondral, subligamentous, or
subtendinous.
 Bone sclerosis
 Brown tumors
 Chondrocalcinosis
 Soft tissue calcification and vascular calcification.
•M/c -Radial aspects of the
middle phalanges.
•Phalangeal tufts.
•Distal end of the clavicle
•Medial tibial & humeral
metaphysis.
•Medial femoral neck
•Superior & inferior margins
of ribs.
Spotty de-ossification- salt & pepper appearance
•Iliac side of SI joint.
•DIP joint(m/c- ring &
little fingers).
•MCP joint.
•Clavicular side of AC
joint.
Scalloping along the cortex
M/c in long bones
•Expansile lytic lesion with
well defined non sclerotic
margin
•Replacement of bone by
vascularized fibrous tissue-
osteoclastic activity
•m/c in secondary
hyperparathyroidism
• horizontal, bandlike
("rugger jersey")
sclerosis.
Ca PTH P ALP
PHPT
SECONDARY
HPT (CKD)
(soft
tissue
deposition)
MILK ALKALI /N N
MALIGNANCY /N
PAGET’S N N N
RICKETS
 Acute hypercalcemia -rehydration with normal saline,
reduced calcium intake, haemodialysis.
 Loop diuretics
 Avoid thiazide diuretics.
 Monitor serum creatinine levels
and calcium levels every 6 months.
 DEXA scan on an annual basis.
 Calcimimetics: mimics calcium by stimulating calcium
sensors -> less PTH release.
• Side effects: joint and muscle pain, diarrhea, nausea, and
respiratory infection.
 Bisphosphonates: decreases osteoclastic bone resorption,
osteo protective.
• Side effects: low blood pressure, fever and vomiting.
 Surgery :
- Symptomatic hyperparathyroidism
-Asymptomatic hyperparathyroidism with:
◦ 24-hour urinary calcium > 400 mg
◦ serum calcium > 1 mg/dl above upper limit of normal
◦ Creatinine clearance > 30% below normal for patient's age
◦ Bone density > 2.5 SD below peak (i.e., T-score of -2.5)
◦ People age < 50
 Minimally invasive surgery - solitary adenoma,
 Subtotal parathyroidectomy - diffuse hyperplasia.
 “Hungry Bone Syndrome”- postoperative, prolonged (>4days),
profound hypocalcemia (<8.4 mg/dL) -osteoblastic activity.
 Can also present in men metastatic prostate cancer.
 Presents with hypocalcemic tetany.
 Rx- bolus 10% ca. gluconate 10-20 mL in 50-100 mL of 5%-D IV
over 5-10 minutes(100 to 200 mg of elemental calcium.)
 Continuous infusion- 100cc of 10% ca.gluconate in 1L of
5%D (1 mg/mL of elemental calcium.)
 Start at 50 ml/hr and follow Ca, phosphorus, and magnesium
levels titrating every 4-6 hours.
SECONDARY HYPERPARATHYROIDISM:
 Correcting vitamin D deficiency.
 Treatment of chronic kidney disease (Calcium
supplementation)
TERTIARY HYPERPARATHYROIDISM:
 Total or subtotal parathyroidectomy.
 Autotransplantation
PATHOLOGICAL/STRESS FRACTURES:
 immediate immobilisation – treat the primary cause.
 Bisphosphonate therapy
THANK YOU

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Hyperprathyroidism- Dr Shahid

  • 2.  BLOOD: Hypercalcemia Hypophosphatemia ALP- increased  URINE: Hypercalciuria Hyperphosphaturia  HPE: single adenoma-mc, pale, clear-chief cells  ECG: short QT interval  USG & Tc99 SESTAMIBI SCAN
  • 3.  24hr urinary calcium: • Differentiates pHPT from familial hypocalciuric hypercalcemia  Phosphate excretion test: • PTHdecreases net tubular phosphorous reabsorptionphosphaturia.  Phosphorous loading test: • In case of poor intake or poor absorption, there is normal phosphorous excretion • Oral phosphorous (2-3g over 3days)  decreases tubular phosphorous reabsorption phosphaturia
  • 4.  Cortisone suppression test: • Administration of steroids (150mg cortisone per day for 10days)  no effect on hypercalcemia of hyperparathyroidism in contrast to sarcoidosis, multiple myeloma, hypervit D  Urinary Hydroxyproline: markedly raised. attributed to increased bone turnover and collagen degradation.  Isotope studies: • Se-75 (selenomethionine) scan detects abnormal parathyroid tissue  RIA: radiolabelled antibodies directed against PTH. More specific.
  • 5.  M/C : generalized osteopenia  Bone resorption- subperiosteal, intracortical, trabecular, endosteal, subchondral, subligamentous, or subtendinous.  Bone sclerosis  Brown tumors  Chondrocalcinosis  Soft tissue calcification and vascular calcification.
  • 6. •M/c -Radial aspects of the middle phalanges. •Phalangeal tufts. •Distal end of the clavicle •Medial tibial & humeral metaphysis. •Medial femoral neck •Superior & inferior margins of ribs.
  • 7. Spotty de-ossification- salt & pepper appearance
  • 8. •Iliac side of SI joint. •DIP joint(m/c- ring & little fingers). •MCP joint. •Clavicular side of AC joint.
  • 9. Scalloping along the cortex M/c in long bones
  • 10. •Expansile lytic lesion with well defined non sclerotic margin •Replacement of bone by vascularized fibrous tissue- osteoclastic activity
  • 11. •m/c in secondary hyperparathyroidism • horizontal, bandlike ("rugger jersey") sclerosis.
  • 12. Ca PTH P ALP PHPT SECONDARY HPT (CKD) (soft tissue deposition) MILK ALKALI /N N MALIGNANCY /N PAGET’S N N N RICKETS
  • 13.  Acute hypercalcemia -rehydration with normal saline, reduced calcium intake, haemodialysis.  Loop diuretics  Avoid thiazide diuretics.  Monitor serum creatinine levels and calcium levels every 6 months.  DEXA scan on an annual basis.
  • 14.  Calcimimetics: mimics calcium by stimulating calcium sensors -> less PTH release. • Side effects: joint and muscle pain, diarrhea, nausea, and respiratory infection.  Bisphosphonates: decreases osteoclastic bone resorption, osteo protective. • Side effects: low blood pressure, fever and vomiting.
  • 15.  Surgery : - Symptomatic hyperparathyroidism -Asymptomatic hyperparathyroidism with: ◦ 24-hour urinary calcium > 400 mg ◦ serum calcium > 1 mg/dl above upper limit of normal ◦ Creatinine clearance > 30% below normal for patient's age ◦ Bone density > 2.5 SD below peak (i.e., T-score of -2.5) ◦ People age < 50  Minimally invasive surgery - solitary adenoma,  Subtotal parathyroidectomy - diffuse hyperplasia.
  • 16.  “Hungry Bone Syndrome”- postoperative, prolonged (>4days), profound hypocalcemia (<8.4 mg/dL) -osteoblastic activity.  Can also present in men metastatic prostate cancer.  Presents with hypocalcemic tetany.  Rx- bolus 10% ca. gluconate 10-20 mL in 50-100 mL of 5%-D IV over 5-10 minutes(100 to 200 mg of elemental calcium.)  Continuous infusion- 100cc of 10% ca.gluconate in 1L of 5%D (1 mg/mL of elemental calcium.)  Start at 50 ml/hr and follow Ca, phosphorus, and magnesium levels titrating every 4-6 hours.
  • 17. SECONDARY HYPERPARATHYROIDISM:  Correcting vitamin D deficiency.  Treatment of chronic kidney disease (Calcium supplementation) TERTIARY HYPERPARATHYROIDISM:  Total or subtotal parathyroidectomy.  Autotransplantation PATHOLOGICAL/STRESS FRACTURES:  immediate immobilisation – treat the primary cause.  Bisphosphonate therapy