hyperparathyroidism Flashcards
parathyroid and metabolic bone diseases objectives
-Identify and interpret the homeostatic mechanism of PTH on kidney, bone and intestine to maintain calcium blood concentration.
-Determine and assess etiology, clinical presentation, and dx, medical and surgical tx of primary and secondary hyperparathyroidism
-Compare and contrast inherited and acquired hypoparathyroidism
-Interpret acute and chronic symptoms that result from non-tx and determine tx options.
-Differentiate between the causes of hypercalcemia
-Determine the classifications of hypocalcemia, their differential diagnosis, and tx
-Explain the pathophysiology of osteoporosis; evaluate the classifications, clinical features, radiologic features, laboratory findings, differential diagnosis, prevention, and treatment.
-Explain the classifications of osteomalacia. Describe the pathogenesis, clinical findings, radiologic features, laboratory findings, and treatment options for each identified diagnosis.
-Determine the etiology, pathophysiology, clinical picture, radiologic changes, complications, and treatment of Paget’s disease.
-Differentiate benign and malignant bone tumors and their effect of serum calcium levels
hyperparathyroidism
-Excess production of PTH- Results in hypercalcemia
-Usually the result of- Autonomously functioning adenomas or hyperplasia
-Surgery is highly effective- Shown to reverse some of the deleterious effects of long-standing PTH excess on bone density
-Hypercalcemia of malignancy is also common - Usually due to the overproduction of parathyroid hormone–related peptide (PTHrP) by cancer cells
-Similarities in the biochemical characteristics of hyperparathyroidism and hypercalcemia of malignancy - Reflect the actions of PTH and PTHrP
primary hyperparathyroidism
-single adenoma- 80% *
-diffuse hyperplasia- 15%
-multiple adenoma - 4%
-prevalence - 0.1-0.5%
-incidence- 0.03%
-asymptomatic- 80%*
primary hyperparathyroidism
-Due to adenomas, - normal feedback on parathyroid hormone production by extracellular Ca – lost – therefore there is a change in the set point causing there to be increase in PTH
-Due to parathyroid hyperplasia - increase in the cell numbers is probably the cause of increased secretion of PTH -> Chronic excessive resorption of calcium from bone caused by excessive parathyroid hormone can result in osteopenia
-In severe cases - “osteitis fibrosa cystica”:
-Subperiosteal resorption of the distal phalange
-Tapering of the distal clavicles
-Salt-and-pepper skull
-Brown tumors of the long bones
hypercalcemia
-Parathyroid-related:
-Primary hyperparathyroidism
-Lithium therapy
-Familial hypocalciuric hypercalcemia [FHH]
-Multiple endocrine neoplasia 1
-Malignancy-related:
-Solid tumor with metastases (breast)
-Solid tumor with humoral mediation of hypercalcemia (lung, kidney)
-Hematologic malignancies (multiple myeloma, lymphoma, leukemia)
-PTHr
-Vitamin D-related
-Vitamin D intoxication
-↑ 1,25(OH)2D; sarcoidosis and other granulomatous diseases
-Idiopathic hypercalcemia of infancy
-Associated with high bone turnover
-Hyperthyroidism
-Immobilization
-Thiazides
-Vitamin A intoxication
-Associated with renal failure:
-Severe secondary hyperparathyroidism
-Aluminum intoxication
-Milk-alkali syndrome
-Primary hyperparathyroidism and cancer account for 90% of cases of hypercalcemia*
classic symptoms
-80% — Asymptomatic
St-ones:
-Nephrolithiasis – 20%
-Urinary tract obstruction
-Bones:
-Selective cortical bone loss - common
-Osteitis Fibrosa Cystica: rare now; salt and pepper skull appearance -> Increased osteoclasts & bone turnover and Reduced cortical bone density
-Fractures or radiographic findings – 2%
-Abdominal groans
-Psychic Moans: Neuropsychiatric impairment
other symptoms: neuro, renal, GI, cardio
-Neuro: proximal myopathy, weakness and easy fatigability, depression, inability to concentrate, and memory problems or subtle deficits that are often characterized poorly and may not be noted by the patient
-Renal: polyuria, kidney stones, hypercalciuria, and rarely nephrocalcinosis, nephrolithiasis, kidney disease
-GI: anorexia, nausea, vomiting, abdominal pain, constipation, PUD*, and acute pancreatitis
-Cardiovascular manifestations include: hypertension, bradycardia, QT interval shortening and left ventricular hypertrophy
parathyroid crisis
-severe
-life threatening hypercalcemia
-renal failure from nephrocalcinosis
-coma
-cardiac arrest
investigations
-calcium and phosphorus levels
-serum PTH:
-if elevated in the setting of hypercalcemia, then hyperparathyroidism is diagnosis
If low, check PTHrP, Vitamin A & D, TSH, Cortisol, ACE, 24h urine calcium clearance, review meds
-24-hour urine calcium excretion:
-Used to rule out familial hypocalciuric hypercalcemia
-Values below 100mg/24 hours or a calcium creatinine clearance ratio of <0.01 are suggestive of FHH
imaging
-wrist, spine, and hip DEXA
-consider KUB, IVP, or CT to evaluate for kidney stone
-imaging:
-99m technetium sestamibi radionuclide scan
-US: CT; MRI
interpretation
-Elevated serum PTH immunoassay (high sensitivity)
-High calcium
-Low or normal phosphate (decreased proximal tubular reabsorption)
-Elevated 1,25(OH)2D (low specificity)
surgical management
-Surgical Indications- Ca > 11.5, T-score < -2.5, renal stones
-Cure rate- 95% – 98%
-Perioperative morbidity- Up to 3%
-Permanent hypoparathyroidism- 2%
-Permanent laryngeal nerve injury- <1%
medical management
-Replace volume
-IV Bisphosphonates – decrease bone reabsorption [Pamidronate; Zoledronic acid]
-Calcitonin – rapid in emergent situation
-Facilitate calciuresis (loop diuretics)
-Hormonal Therapy (post menopasual):
-Estrogen
-Dose required is high
-Raloxifene
-Calcium/Vitamin D
-Calcimimetic agents (Cinacalcet)- Binds to the sites of the parathyroid glands – which bind extracellular calcium —therefore a decrease in PTH levels
-if mild or asymptomatic -> no therapy
secondary hyperparathyroid
-Vitamin D deficiency
-Primary decreased calcium absorption in elderly
-Increased phosphate in acute or chronic renal failure
-Renal Osteodystrophy:
-Osteomalacia (low Ca, Vitamin D)
-Osteitis fibrosa cystica (high PTH)
-Adynamic Bone Disease (low PTH)
secondary hyperparathyroid: dx
-Elevated PTH in the setting of low or normal serum calcium is diagnostic
-If phosphorous is elevated, cause is renal
-If phosphorous is low, other causes of vit D deficiency should be sought
-Prevention
-Vitamin D replacement
-Phosphorus binders [Sevelamer]
-Treatment
-Medical- Calcimimetic agents
-Surgical:
-Considered in cases of refractory
-Severe hypercalcemia, severe bone disease, severe pruritis, calciphylaxis, severe myopathy
