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Followup

Followup. Nathanael Wood, MD December 20, 2005. CC: seizure-like activity HPI:

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Followup

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  1. Followup Nathanael Wood, MD December 20, 2005

  2. CC: seizure-like activity • HPI: 42 year old male was driving home after a soccer game when his arms began shaking. He pulled his car to the side of the road. When a police officer found him he was unable to talk, with rigid upper extremities. Symptoms lasted 15-20 minutes and began resolving spontaniously. He remembers the entire event. When seen in the ER, the patient was asymptomatic.

  3. ROS: Neg • PMH: None • PSH: None • Meds: None • Allergies: None • Social: No cigs, occasional EtOH, no drugs, professional, weekend recreational soccer player.

  4. Physical Exam • T 98.8, HR 75, BP 135/85, RR 16, O2 sat 99% • General: age appropriate male in nad • HEENT: normal • CV: normal • Resp: normal • Abd: normal • Neuro: normal • Everything else: normal

  5. Studies • EKG: neg • Head CT: neg

  6. Labs 141 103 12 124 19 4.1 1.5 Ca 11.0 Mg 2.4 Phos 0.8 PTH 81 (normal 0 - 50) Hyperparathyroidism

  7. Parathyroid Anatomy

  8. Parathyroid Anatomy

  9. Parathyroid Anatomy • Chief Cells make PTH

  10. Renal Effects of PTH • Increases Ca2+ reabsorption in distal tubule • Decreases PO4-  reabsorption in distal tubule • Increases 1-alpha-hydroxylase (which facilitates the production of 1,25-(OH)2-Vit D)

  11. Bone Effects of PTH • Increases bone resorption • Facilitates bone formation

  12. Regulators of PTH • Calcium and Phosphate • Low Serum Ca2+ → Increased PTH • High Serum PO4- → Increased PTH • High Serum Ca2+ → Decreased PTH • Low PO4- → Decreased PTH • The most important regulator is Ca2+.

  13. Pathophysiology ofHyperparathyroidism • Parathyroid adenoma • A single adenoma is found in 70-80% of primary hyperparathyroidism. • Benign tumor. • Unregulated release of PTH. • Double adenoma in 4-5%

  14. Pathophysiology • Parathyroid hyperplasia • Diffuse enlargement of all the parathyroid glands. • Unregulated release of PTH. • 10-15% of cases of primary hyperparathyroidism. • Difficult operative diagnosis.

  15. Pathophysiology • Parathyroid carcinoma • Less than 1% of cases of hyperparathyroidism

  16. Pathophysiology • Other etiologies • Multiple Endocrine Neoplasia Type 1 and 2 • Abnormalities of thyroid, adrenal, and parathyroid glands • Hyperplasia of the parathyroid glands • Radiation therapy to the head and neck during childhood for benign diseases. • Familial hyperparathyroidism has been observed • Rare.

  17. Secondary Hyperparathyroidism • Occurs when the parathyroid glands become hyperplastic after long-term stimulation to release PTH in response to chronically low circulating calcium. • Chronic renal failure, rickets, and malabsorption syndromes are the most frequent causes. • High levels of PTH do not cause hypercalcemia because the primary problem is hypocalcemia. • With long-term hyperstimulation, the glands eventually function autonomously and continue to produce high levels of PTH even if the chronic hypocalcemia has been corrected.

  18. Tertiary Hyperparathyroidism • Hypercalcemia caused by autonomous parathyroid function after long-term hyperstimulation.

  19. Differential Diagnosis of Hypercalcemia • Primary hyperparathyroidism (more common in out-patient) • Cancer (more common in in-patient) • Milk-alkali syndrome • Granulomatous disease • Hyperthyroidism • Drugs: thiazides, lithium • FHH (Familial hypocalciuric hypercalcemia)

  20. Clinical Presentation of Hyperparathyroidism • Manifestations can be subtle • May run a benign course for many years • Less commonly, hyperparathyroidism may worsen abruptly and cause severe hypercalcemic complications (eg, profound dehydration, neurologic symptoms, coma). This is referred to as hypercalcemic parathyroid crisis.

  21. Clinical Presentation ofHypercalcemia • At least half are asymptomatic • “Bones, Stones, Groans, and Psychic Moans” • Bones: Painful and tender bones • Stones: Nephrolithiasis • Groans: Abdominal pain • Psychic Moans: Changes in mental status

  22. Clinical Presentation • Renal • Thirst • Polydipsia • Polyuria

  23. Clinical Presentation • Gastrointestinal • Abdominal distress • Constipation • Vomiting • Anorexia • Weight loss

  24. Clinical Presentation • Skeletal and neuromuscular • Bone pain and/or tenderness, muscle fatigue, weakness • Spontaneous fractures

  25. Clinical Presentation • Mental • Anxiety • Depression • Psychosis • Apathy • Fatigue

  26. Clinical Presentations • Asymptomatic hypercalcaemia (50%) • Renal stones(28%) • Polyuria, polydipsia (5%) • Peptic ulcer (4%) • Hypertension(4%) • Bone disease(3%) • MEN 1 Syndrome(1%)

  27. Workup • The diagnosis of hyperparathyroidism is made by demonstrating elevated PTH in the setting of high serum calcium.

  28. Other Lab Findings • Elevated serum chloride levels. • Decreased serum phosphate level. • Decreased serum carbon dioxide • Hyperchloremic metabolic acidosis. • Increase in urine cyclic adenosine monophosphate (cAMP).

  29. Remember our patient… • Elevated PTH in setting of elevated Calcium • Decreased Phosphorus • Decreased CO2. 141 103 12 124 19 4.1 1.5 Ca 11.0 Mg 2.4 Phos 0.8 PTH 81 (normal 0 - 50)

  30. Complications ofHyperparathyroidism • Chondrocalcinosis and pseudogout are common. • Significant loss of cortical bone. • Maternal hyperparathyroidism can lead to profound hypocalcemia in newborns • Can lead to tetany, coma, and death • neonatal severe hyperparathyroidism. • Nocturia and polyuria • From the effects of calcium on the renal tubule. • Nephrolithiasis (20% of patients). • Most severe acute manifestation: • Hypercalcemia-induced altered mental status

  31. Osteitis Fibrosa Cystica • “Brown Tumor” • Indication of severe disease. • Increased osteoclastic resorption of calcified bone with replacement by fibrous tissue.

  32. Treatment • Profound hypercalcemia with severe alterations of mental status: • Normal saline and loop diuretics • Mild asymptomatic hypercalcemia: • Gentle Hydration

  33. Treatment • Surgical removal of adenoma vs. conservative for asymptomatic hyperparathyroidism. • For female patients who do not have surgery, estrogen may be beneficial to help maintain bone mass (controversial)

  34. Treatment, Surgical • Guidelines for recommendation for surgical treatment (from the 2002 NIH Workshop on Asymptomatic Primary Hyperparathyroidism): • Patients with a serum calcium concentration of 1.0 mg/dL or more above the upper limit of normal. • Patients with hypercalciuria. • Patients with a creatinine clearance that is 30 percent or lower than that of age-matched normal subjects. • Patients with bone density at the hip, lumbar spine, or distal radius that is more than 2.5 standard deviations below peak bone mass (T score <-2.5). • Patients who are less than 50 years old. • Patients in whom periodic follow-up will be difficult.

  35. Treatment, Non-Surgical •  Avoid factors that can aggravate hypercalcemia: • thiazide diuretic • lithium • volume depletion • prolonged bed rest or inactivity • high calcium diet • Encourage physical activity to minimize bone resorption. • Encourage adequate hydration.   • Maintain a moderate calcium intake (1000 mg/day). • Maintain moderate vitamin D intake.

  36. Treatment, Non-Surgical • Monitoring • Serum calcium every six months • Serum creatinine, and bone density (hip, spine, and forearm) every 12 months.

  37. Questions?

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