1 / 39

Followup

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

beck-russell
Télécharger la présentation

Followup

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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?

More Related