Calsium and bone Flashcards
What is hypoparathyroidism and what are its causes?
Hypoparathyroidism is the insufficient secretion or production of parathyroid hormone (PTH). Causes include congenital absence of parathyroid glands, neck surgery (e.g., thyroidectomy or parathyroid adenoma removal), autoimmune conditions like type 1 diabetes or Graves’ disease, and Hashimoto’s disease
What is hyperparathyroidism and its etiology?
Hyperparathyroidism is the excessive secretion of PTH, leading to hypercalcemia. It can be primary (due to parathyroid adenoma, hyperplasia, or carcinoma) or secondary (due to chronic kidney disease or vitamin D deficiency).
What is the pathophysiology of hypoparathyroidism?
Hypoparathyroidism leads to low PTH, causing low calcium and high phosphate levels. Reduced PTH impairs calcium absorption from bones, kidneys, and intestines, leading to hypocalcemia and hyperphosphatemia. This disrupts neuromuscular function.
What are the clinical manifestations of hypoparathyroidism?
Acute symptoms include tetany(involuntary muscle contractions), muscle cramps, spasms, convulsions, and paresthesias. Chronic symptoms include lethargy, anxiety, blurry vision (due to cataracts), and extrapyramidal signs.
What is the pathophysiology of primary hyperparathyroidism?
In primary hyperparathyroidism, excess PTH causes increased bone resorption, leading to hypercalcemia and weakened bones. It also causes decreased phosphate reabsorption in the kidneys, and increased calcium absorption in the intestines.
What are the clinical manifestations of primary hyperparathyroidism?
Symptoms include bone pain, fractures, osteoporosis, kidney stones, gastrointestinal issues, muscle weakness, fatigue, depression, and cognitive difficulties. The mnemonic “stones, bones, abdominal groans, and psychic moans” summarizes these symptoms.
What is secondary hyperparathyroidism, and what is its main cause?
Secondary hyperparathyroidism is a condition where the parathyroid glands secrete excessive parathyroid hormone (PTH) in response to low calcium levels, typically caused by chronic kidney disease (CKD) or vitamin D deficiency. Secondary hyperparathyroidism occurs as a compensatory response to an external cause.
What is the pathophysiology behind secondary hyperparathyroidism?
The main pathophysiology of secondary hyperparathyroidism involves:
Hypocalcemia: Due to impaired calcium absorption or kidney dysfunction.
Hyperphosphatemia: Because of decreased phosphate excretion by the kidneys.
Excessive PTH secretion: As a compensatory response to low calcium and high phosphate levels, the parathyroid glands secrete more PTH, leading to increased bone resorption to release calcium, further exacerbating bone disease.
What are the clinical manifestations of secondary hyperparathyroidism?
Bone pain: Due to bone resorption and weakened bone structure (renal osteodystrophy).
Fractures: Increased risk due to reduced bone density.
Muscle weakness and cramps: Often associated with imbalanced calcium and phosphate levels.
Pruritus (itching): Common in patients with kidney disease.
Fatigue and malaise: Often seen in patients with chronic kidney disease.
What is hypocalcemia and its relation to hypoproduction of calcitonin?
Hypocalcemia occurs when blood calcium levels fall below 8.5 mg/dL. Calcitonin, produced by the thyroid, lowers blood calcium by inhibiting bone resorption. A lack of calcitonin results in reduced calcium storage in bones and contributes to hypocalcemia.
What are the clinical manifestations of hypocalcemia due to calcitonin hypoproduction?
Symptoms include muscle cramps, spasms (tetany), tingling, seizures, and prolonged QT intervals, which increase the risk of arrhythmias. Positive Chvostek and Trousseau signs are key indicators.
What is hyperproduction of calcitonin and its pathophysiology?
Hyperproduction of calcitonin often occurs in medullary thyroid carcinoma. Excess calcitonin inhibits bone resorption, leading to decreased calcium levels in the blood (hypocalcemia). It may also reduce renal calcium reabsorption.
What are the clinical manifestations of hyperproduction of calcitonin?
Symptoms include muscle cramps, spasms, tingling, prolonged QT interval, increased bone density, and fatigue. In thyroid cancer, neck swelling or a palpable thyroid mass may also be present.
What is vitamin D deficiency (Hypoproduction) and its pathophysiology?
Vitamin D deficiency leads to reduced calcium absorption, causing hypocalcemia. This triggers increased PTH secretion, leading to bone resorption and conditions like osteomalacia (soft bones) or rickets (bone deformities in children).
What are the clinical manifestations of vitamin D deficiency (hypoprodution)?
Symptoms include bone pain, muscle weakness, fractures, rickets in children (bone deformities), and osteomalacia in adults (soft, painful bones).
What is hyperproduction of vitamin D and its pathophysiology?
Excess vitamin D increases calcium absorption, leading to hypercalcemia. It can cause soft tissue calcification, kidney stones, and bone pain. This condition may result from granulomatous diseases, lymphomas, or vitamin D toxicity.
What are the clinical manifestations of hyperproduction of vitamin D?
Symptoms include hypercalcemia (nausea, vomiting, constipation), kidney stones, bone pain, muscle weakness, fatigue, confusion, and osteoporosis.
What is osteoporosis and its pathophysiology?
Osteoporosis is characterized by weak, brittle bones due to an imbalance between bone resorption and formation, often influenced by factors like estrogen levels, vitamin D deficiency, and hypocalcemia. Increased osteoclast activity leads to bone mass loss and fractures.
What are the clinical manifestations of osteoporosis?
Osteoporosis often has no symptoms until fractures occur from minimal trauma. Common fractures affect the wrists, spine, and hips. Vertebral fractures can cause back pain, height loss, spinal deformities, and a stooped posture.
