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30 Cards in this Set

  • Front
  • Back
Which hormone increases the level of serum calcium?
A: (pth)|(para)
Which horomone drives down the level of serum calcium
E: Calcitonin
A: calci
What are the four mechanisms by which PTH increases serum calcium?
E: PTH is synthesized and secreted by the parathyroid glands in response to low serum levels of calcium. Its mechanisms of action include:

* Increases bone resorption
* Increases 1,25 (OH)2 vitamin D production
* Increases renal calcium retention
* Increases renal phosphate excretion

Which is the most active form of Vitamin D?
E: 1,25(OH)2 Vitamin D
A: 1,25
How does 1,25(OH)2 Vitamin D increase serum calcium levels?
E: The most active form is 1,25 (OH) 2 vitamin D, which is synthesized in the kidney by conversion of 25 (OH) vitamin D by 1-alpha hydroxylase. Its mechanisms of action include:

* Increases bone resorption
* Increases renal calcium and phosphate retention
* Enhances intestinal calcium absorption

E: resorption, phosphate, absorp
How does calcitonin decrease serum calcium levels?
E: Calcitonin is synthesized by thyroidal C cells. Its mechanisms of action include:

* Promotes calcium deposition in bone
* Inhibits osteoclastic bone resorption

A: deposition, osteocl
Which hormones drive up serum calcium?
E: Vitamin D and parathormone. 1. Calcium homeostasis is tightly regulated to keep calcium in a very narrow physiologic range.
2. The three organs involved in calcium homeostasis are the bone (storage), kidney (excretion), and intestine (absorption).
3. The three hormones involved in calcium homeostasis are parathyroid hormone, vitamin D, and calcitonin.
4. Parathyroid hormone and vitamin D work to increase calcium levels.
5. Calcitonin works to decrease calcium levels.

What happens to the QT interval in hypocalcemia (shortens/prolongs)?
E: Shortened QT interval and arrhythimas.
A: short
What happens to the QTc interval in hypocalcemia (shortens/prolongs)?
E: Prolongs
A: long
A patient presents with confusion, polyuria, renal impairment, nephrocalcinosis. What is the cause?
E: Hypercalcemia
A: hyper
What are the initial signs of hypocalcemia?
E: Perioral and peripheral paraesthesias.
A: thesia
What kind of arrhythmia do you get with hypocalcemia (brady/tachy)?
E: Bradyarrhythmia with prolonged QTc
A: brady
When can you get simultaneous dehydration and hypertension(hypocalcemia/hypercalcemia)?
E: Hypercalcemia causes polyuria and dehydration.
A: hyper
Of the three hormones affecting calcium and phosphate level, which one increases renal retention of calcium AND phosphate?
E: 1,25(OH)2 Vitamin D. The other two hormones (PTH, calcitonin) have mirror image actions on phosphate and calcium. PTH decreases phosphate, increases calcium; calcitonin does the reverse.
Which two signs are characteristic of hypocalcemia?
E: Chvostek and Trousseau
A: Chvos, Trous
What is the commonest cause of hypercalcemia?
E: Primary hyperparathyroidism(55%).
A: prim
What is the second commonest cause of hypercalcemia?
E: Malignancy accounts for 35%
A: (malign)|(cancer)
What are the uncommon causes of hypercalcemia (categories)?
E: Thyrotoxicosis, granulomatous disease (sarcoidosis, tuberculosis, histoplasmosis, coccidiomycosis), drug-induced (thiazides, lithium vitamins A and D intoxication, aluminum toxicity in renal failure, immobilization, renal insufficiency, tertiary hyperparathyroidism), and total parenteral nutrition. Another possibility is total parenteral nutrition.
A: thyrot, granulo, drugs, vit, (renal)|(fail)|(CR), TPN
What are some rare causes of hypercalcemia?
E: Adrenal insufficiency, pheochromocytosis, pancreatic islet-cell tumors, familial hypocalciuric hypercalcemia (FHH), and milk alkali syndrome.
A: adren, pheo, panc, FHH, milk-alk
What does the diagnosis of primary hyperparathyroidism depend upon?
E: Primary hyperparathyroidism is usually due to a single parathyroid adenoma. Diagnosis rests on elevated levels of calcium and PTH level and hypercalciuria.
A: hypercal, uria, PTH
What is the treatment of severe hyperparathyroidism?
E: urgery is recommended for patients with any of the severe complications (e.g., bone lesions, nephrolithiasis, nephrocalcinosis, or overt muscle disease). However, some patients do not present with classic signs and symptoms and are believed to have a mild form of the disease that has been termed asymptomatic hyperparathyroidism. Many of these patients have mild elevations in calcium and complain of mild cognitive symptoms or symptoms of depression that are not always clearly related to the disease. Since a large number of patients are "asymptomatic" and may be observed, a list of indications for surgery has been developed. Table 2-12 lists the guidelines as revised in 2002.
Bilezikian JP, et al: Summary statement from a workshop on asymptomatic primary hyperparathyroidism: a perspective from the 21st century. JCEM 87:5353-5361, 2002.

Serum calcium (amount above normal): 1 mg/dL
24-hr urine calcium: Greater than 400 mg/day
Creatinine clearance: Reduced 30%
Bone mineral density:T-score is 2.5 at any site (spine, hip, forearm)
Age:50 years
A: surg
What are the three categories of primary osteoporosis
E: Juvenile, idiopathic, and involutional. Involutional osteoporosis is further divided into type 1 (associated with menopause) and type 2 (associated with aging).
A: involutional,
What are the secondary causes of osteoporosis?
E: # Endocrine: DM, hyperthyroidism, hypogonadism, Cushing's syndrome, hyperparathyroidism, osteomalacia.
# Gastrointestinal: gastrectomy /malabsorption syndromes (patients may develop calcium and vitamin D deficiencies), malnutrition (also seen in anorexia nervosa), liver disease (patients may develop vitamin D deficiency).
# Malignancy: multiple myeloma, metastatic carcinoma.
# Renal disease
# Connective tissue disorders
# Medications: steroids (most common), thyroid hormone (chronic overreplacement), anticonvulsants, heparin, isoniazidView drug information, loop diuretics, cyclosporin A, transplant antirejection medications.
# Miscellaneous: lifestyle factors such as poor nutrition, use of alcohol and/or tobacco, immobilization
A: Endo, meds, malign, GI, renal, connect, misc
What testing will you perform to identify the cause of secondary osteoporosis?
E: It is important to perform a careful history and physical exam to assess fracture risk factors and symptoms suggestive of a secondary cause of osteoporosis. Approximately one third of osteoporotic women have an undiagnosed disorder of bone or mineral metabolism (usually calcium disorder). An initial laboratory evaluation with serum calcium, PTH, and TSH as well as 24-hour urine calcium has been shown to identify the majority of secondary causes.
A: serum, PTH, urine, TSH
Which drugs are available for use in osteoporosis besides the bisphosphantes and estrogen?
A: raloxifene, teriparatide
What are the key pathogenetic problems in familial hypocalciuric hypercalciuria?
E: page 86
page 87
FHH is a very rare autosomal dominant genetic disorder that has a high penetrance (nearly 100%). It is due to an inactivating germ-line mutation in the calcium-sensing receptor, resulting in insensitivity of the parathyroid cells to inhibition by calcium. Renal tubule cells are also insensitive to calcium.
A: renal, parathy
What is the management of Paget's disease?
E: Paget's disease is characterized by abnormal bone remodeling. It can affect one or more skeletal sites and begins with abnormal bone resorption followed by compensatory bone formation. This process results in disorganized bone remodeling that predisposes the affected region to deformity and fracture. The exact etiology is unknown. Patients may be asymptomatic and present only with elevated serum alkaline phosphatase levels, or they may present with bone pain and deformity.
What causes hypocalcemia?
E: Hypocalcemia can be divided into two broad categories: hypoparathyroidism or nonhypoparathyroidism. Hypoparathyroidism causes can be divided into PTH deficiency (e.g., surgical, autoimmune, congenital aplasia, radiation-induced, infiltrative diseases) or PTH resistance (PTH antibodies, pseudohypoparathyroidism). Nonhypoparathyroid causes include vitamin D deficiency or resistance (dietary deficiency, lack of sunlight, liver and renal disease), accelerated bone mineralization (hungry bone syndrome following parathyroidectomy), drugs (anticalcemic, antineoplastic), and acute complexing/sequestration of calcium (rhabdomyolysis, tumor lysis syndrome, pancreatitis, phosphate infusions, blood transfusions).
What is the treatment of acute hypocalcemia?
E: Treatment depends on the severity and duration of symptoms. Patients with acute hypocalcemia should be hospitalized with telemetry monitoring and given intravenous calcium supplementation. Patients with chronic hypocalcemic disorders are managed with oral calcium and vitamin D supplementation. Note: Never give calcium with phosphate.
What is the treatment of chronic hypocalcemia?
E: Treatment depends on the severity and duration of symptoms. Patients with acute hypocalcemia should be hospitalized with telemetry monitoring and given intravenous calcium supplementation. Patients with chronic hypocalcemic disorders are managed with oral calcium and vitamin D supplementation. Note: Never give calcium with phosphate.
A: calcium, vit.*D