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61 Cards in this Set
- Front
- Back
This is the single most important regulator of PTH is ?
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Serum ionized calcium
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What are two other things, besides calcium, that contribute to parathyroid hormone regulation?
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1. Vitamin D
2. Serum Phosphate |
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What are the three mechanisms by which parathyroid hormone causes an increase in calcium?
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1. Prolonged secretion of PTH increases the number and activity of osteoclasts
2. PTH stimulates the kidney to increase calcium and decrease phosphate resorption 3. PTH stimulates the synthesis of Vitamin D which induces an increase in intestinal calcium absorption. |
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This is more frequent in people over 50
Women are more affected than men Hypercalcemia of malignancy is seen with this |
Hyperparathyroidism
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The hypercalcemia of malignancy associated with hyperparathyroidism has two main factors, what are they?
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1. Tumors secrete PTH related protein (PTHrP)
2. Increase incidence associated with breast cancer and non-melanoma skin cancer - basal and squamous cell cancer |
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This is when there is excessive secretion of PTH by the parathyroid gland - labs will show increased PTH and calcium.
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Primary hyperparathyroidism
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What are the five main causes of PTH hypersecretion?
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1. Parathyroid gland adenoma
2. Hyperplasia of the parathyroid glands 3. Parathyroid cancer 4. Familial 5. Secondary to lithium therapy |
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Causes of hypersecretion of PTH from the parathyroid hormone can be secondary to what drug therapy?
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Lithium
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This is a cause of primary hyperparathyroidism. It accounts for approximately 80-90% of cases, the size of the adenoma correlates with the serum PTH level.
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Parathyroid gland adenoma
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This is a cause of primary hyperparathyroidism. It can involve one gland or all four, may develop independently or in response to chronic hypocalcemia.
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Hyperplasia of the parathyroid glands
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This accounts for less than 1 % of all primary hyperparathyroidism cases. There is a higher incidence when hyperparathyroidism occurs before the age of 30.
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Parathyroid cancer
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This is a familial disorder that causes primary hyperparathyroidism. It is associated with parathyroid hyperplasia, pancreatic tumors, and pituitary adenomas.
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MENI
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This is a familial disorder that causes primary hyperparathyroidism. It is associated with asymmetric parathyroid hyperplasia and medullary thyroid cancer.
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MEN2A
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This is a familial disorder that causes primary hyperparathyroidism. It is caused by a mutation of the calcium sensing receptors that shift to a higher set point for calcium.
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Familial hypocalciuric hypercalcemia
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Associated with primary hyperparathyroidism. This is seen in approxmiately 15-60% of patients taking this medication. Shifts the set point for calcium to a higher threshold. Often resolves when lithium is withdrawn.
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Lithium therapy
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This is hyperparathyroidism associated with chronic kidney disease (hypocalcemia, hyperphosphatemia, and Vitamin D deficiency), Vitamin D deficiencies, The primary defect is not with the parathyroid gland.
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Secondary hyperparathyroidism
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This is hyperparathyroidism, under chronic stimulation as seen with chronic kidney disease, the parathyroid glands hypertrophy and continue to secrete excess PTH even after correcting underlying calcium, most common in renal transplant patients.
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Tertiary Hyperparathyroidism
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These are usually not palpable in the physical exam?
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Parathyroid adenomas
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Approximately 50% of parathyroid cancers are associated with?
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a palpable mass
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This is a clinical manifestation of hyperparathyroidism. It can be asymptomatic, but it can also manifest as via thirst, annorexia, nausea, vomiting, constipation, fatigue, weakness.
Band Keratopathy: Calcium precipitates in the corneas Calciphylaxis: Calcium precipitates in soft tissue. |
Hypercalcemia
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This is a clinical manifestation of hyperparathyroidism. It can be seen as depression, psychosis, personality changes, confusion, hallucinations, paresthesias, decreased DTRs.
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Psychiatric/Neurologic manifestations of hyperparathyroidism
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What are the gastrointestinal manifestations of hyperparathyroidism?
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Constipation, nausea/vomiting, abdominal pain
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What are the clinical manifestations of hyperparathyroidism in the musculoskeletal system?
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Decreased bone mass
Osteitis Fibrosa Cystica |
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This is a musculoskeletal manifestation of hyperparathyroidism that is a loss of corticol bone predominately from the long bones. It is associated with bone pain, arthralgias, pathologic long bone fractures.
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Decreased bone mass
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This is a clinical manifestation of hyperparathyroidism that is an increased osteoclastic resorption of bone, pentrabicular fibrosis and cystic brown tumors. With X-Rays pathologic fractures, mottling of the skull "salt and pepper" appearance.
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Osteitis Fibrosa Cystica
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What is the most common presenting renal presentation of hyperparathyroidism?
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Nephrolithiasis
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Besides nephrolithiasis, what else manifests in the renal system in hyperparathyroidism?
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Hypercalcemia induced nephrogenic diabetes insipidus - polyuria and polydipsia
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What will the diagnostic tests show when looking for hyperparathyroidism?
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Hypercalcemia - serum total calcium >10.5mg/dL
Elevated PTH |
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Apart from hypercalcemia and elevated PTH, what else is associated with the lab findings for hyperparathyroidism?
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Elevated urine calcium
Hypophosphatemia - serum phosphate <2.5mg/dL Elevated urine phosphate Neck US or radionuclide imaging to identify adenoma or gland hyperplasia Elevated alkaline phosphatase if bone disease is present Check serum 25-OH vitamin D level |
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People affected by this typically have high normal or mildly elevated calcium levels with PTH levels that are inappropriately normal or only slightly elevated.
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Familial hypocalciuric hypercalcemia
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How do you test for familial hypocalciuric hypercalcemia?
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Check a 24 hour urine calcium excretion - Low in FHH, high in PHP
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With this you will see elevated PTH, normal to low calcium, vitamin D deficiency, and kidney disease/failure. Must check vitamin D level and BUN/creatinine, serum phosphate.
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Secondary hyperparathyroidism
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Mild asymptomatic primary hyperparathyroidism may only require ?
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1. Close follow up - check creatinine to make sure kidneys are working properly
2. Patient education |
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What are three things to tell all patients dealing with hyperparathyroidism?
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1. adequate hydration
2. moderate intake of calcium 3. avoid thiazide diuretics, large doses of vitamin A, calcium containing antacids or supplements |
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This is indicated for patients with symptomatic parathyroidhormone disease with an adenoma or with significant hyperplasia?
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Surgical treatment
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What are the other indications for surgical tx of hyperparathyroidism?
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Age < 50 years
Serum calcium >1mg/dL above the upper limit of normal Patients for whom medical follow up is not possible Marked hypercalciuria (>400mg daily) Reduction in bone mineral density at any site to a T score of <2.5 Decrease in Calcium:Creatinine (ClCr) to 70% of normal Pregnancy |
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What are the surgical complications associated with hyperparathyroid surgery?
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1. Post operative hypocalcemia - parasthesias - most common in first 24 hours
Treatment is calcium carbonate 2. Hungry bone syndrome Most common approximately 1 week after surgery, marked by profound hypocalcemia and increased PTH, treat with calcium and vitamin D |
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What is a medical treatment that can be used for hyperparathyroidism patients, it inhibits bone loss associated with PHP?
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Bisphosphonates - inhibits bone loss associated with PHP; cause a decline in calcium levels over days. Use IV pamidronate and Zoledronate. PO alendronate has been shown to increase bone density in the lumbar spine and hip.
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This is a medical treatment that can be used for hyperparathyroidism. It lowers PTH and calcium levels by enhancing the sensitivity of the calcium sensor receptors to calcium.
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Calcimimetics - Cinacalcet
FDA approved for the tx of secondary hyperparathyroidism in patients with CKD on dialysis and for patients with parathyroid carcinomas. |
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How do you TX Vit D deficiency in secondary hyperparathyroidism?
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Ergocalciferol (D2) 50,000 IU weekly or monthly - replace unitl 25(OH(D level is >30ng/ml
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How do you TX secondary hyperparathyroidism in chronic kidney disease?
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Maintain PTH levels based on stage of CKD - typically correct hyperphosphatemia first then control the calcium and finally correct for vitamin D.
IV vitamin D therapy (calcitrol) to patients on dialysis to suppress parathyroid hyperplasia Cinacalcet for patients on dialysis - dose reduction dependent reduction in PTH |
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What is involved in the follow up TX of someone dealing with parathyroid disease?
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check serum calcium level every six months
check creatinine every 6-12 months check bone density (distal radius, hip and spine) every 1-2 years. |
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This is inappropriate, low secretion of PTH for a given level of ionized calcium.
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Hypoparathyroidism
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This is when there is an inappropriately low secretion of PTH for a given level of ionized calcium.
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Hypoparathyroidism
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What are the five causes of hypoparathyroidism?
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1. Surgical - Most common after thyroidectomy
2. Damage from heavy metal or iron deposits 3. Magnesium deficiency - prevents secretion of PTH 4. Polyglandular Autoimmune Syndrome - Mucocutaneous candidiasis, hypoparathyroidism, adrenal insufficiency 5. Congenital hypoparathyroidism |
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What are the symptoms associated with acute hypoparathyroidism?
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Tetany
Tingling of circumoral area, hands and feet Carpopedial spasm Hyperactive DTRs Muscle cramps Irritability Convulsions |
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What are the symptoms associated with chronic hypoparathyroidism?
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Lethargy
Personality changes Anxiety Cataracts Parkinsonism Mental Retardation |
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This is an adduction of the thumb, flexion of the metacarpal joints, and flexion of the wrist seen with acute hypoparathyroidism
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Carpopedal spasms
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This is an ipsalateral facial muscle contraction caused by tapping of the facial nerve 2cm in front of the ear. This sign is associated with hypoparathyroidism.
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Chvostek's sign
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This is associated with hypoparathyroidism and is a carpal spasm after application of a cuff 20mmHg above systolic BP for 3 minutes.
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Trousseau's Phenomenon
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What are the dermatologic manifestations of hypoparathyroidism?
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Dry brittle nails
Dry skin Loss of hair (eyebrows) Impetigo herpetiformis - form of pustular psoriasis in a pregnant female with hypocalcemia |
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What is the classic laboratory presentation of hypoparathyroidism?
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Low serum calcium
Low PTH High serum phosphate Low urinary calcium Alkaline phosphatase normal |
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What are the EKG findings with hypoparathyroidism?
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Prolongation of the QT interval
T wave inversion |
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With hypoparathyroidism what is something that must be checked?
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Check serum magnesium level - hypomagnesemia and hypocalcemia are often found together.
Magnesium deficiency prevents the secretion of PTH Hypomagnesemia can exacerbate hypocalcemia |
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This is associated with hypoparathyroidism. This is a major binding protein of calcium.
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Hypoalbuminemia. Albumin is a major binding protein of calcium.
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This produces a low total serum calcium concentration because of the reduction in the bound fraction of calcium but the ionized calcium is normal.
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Low albumin
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How do you correct for hypoalbuminemia?
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By either measuring ionized calcium or using the calculation.
Corrected serum calcium = measured serum calcium (total) + (.8 X [4-measured serum albumin]) |
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What are the five steps in Tx acute hypoparathyroidism?
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1. Secure the airway
2. IV calcium gluconate or calcium chloride 3. Oral Calcium 4. Oral Vitamin D 5. Correct any underlying hypomagnesemia |
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What is the Tx for chronic hypoparathyroidism?
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Includes both oral calcium and Vitamin D.
Maintain serum calcium between 8-8.6mg/dL |
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This is a cluster of inherited disorders. Elevated PTH, low calcium, high phosphate, caused by a decreased end organ response to PTH.
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Pseudohypoparathyroidism
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What is the prognosis with hypoparathyroidism?
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Prognosis is good if discovered and treated early
Dental changes, cataract formation and brain calcifications are permanent Periodic serum levels for monitoring |